The Human Body

TREATMENT OF PEPTIC ULCER

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Peptic ulcer is defined as mucosal erosion equal to or greater than 0.5cm. It is the commonest ulcer in the gastrointestinal tract. Although the pathogenesis of peptic ulcer disease is not fully understood, three major causative factors are recognized: 1) Infection with gram negative Helicobacter pylori, 2) increased hydrochloric acid secretion and 3) inadequate mucosal defense against gastric acid. Treatment approaches include:

Eradicating the H. pylori infection
Reducing secretion of gastric acid or neutralizing the acid after it is released, and/or
Providing agents that protect the gastric mucosa from damage.

Above figure summarizes drugs that are effective in treating peptic ulcer disease.

INTRAMUSCULAR INJECTION SITES

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Intramuscular injections are used when rapid absorption is needed, because muscle has a good blood supply. Common sites are the buttock (gluteus medius), the lateral thigh (vastus lateralis), and the shoulder (deltoid).Since these muscles contain major muscles of the body, great care should be taken while giving the injection so that the nerves are not injured. These sites are shown in the given figure.

MUSCLES OF HIP AND LEGS

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The hip muscles that move the thigh are anchored to the pelvic bone and cross the hip joint to the femur. Among these are the gluteus maximus (extension), gluteus medius (abduction), and iliopsoas (flexion). The muscles that form the thigh include the quadriceps group anteriorly and the hamstring group posteriorly. For most people, the quadriceps is stronger than the hamstrings, which is why athletes more often have a “pulled hamstring” rather than a “pulled quadriceps.” Movement of the knee joint depends on thigh muscles and lower leg muscles. Movement of the foot depends on lower leg muscles such as the gastrocnemius (dorsiflexion or flexion) and the tibialis anterior (plantar flexion or extension). See table 4 for details.

MUSCLES OF SHOULDER AND ARMS

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The triangular deltoid muscle covers the point of the shoulder like a cap, and can pull the humerus to the side (abduction), forward (flexion), or backward (extension). You already know the functions of the biceps brachii and triceps brachii, the muscles that form the bulk of the upper arm. Other muscles partially in the upper arm help bend the elbow (flexion). The muscles that form the bulk of the forearm are the flexors and extensors of the hand and fingers. You can demonstrate this yourself by clasping the middle of your right forearm with your left hand, then moving your right hand at the wrist and closing and opening a fist; you can both feel and see the hand and finger muscles at work. See table 3 for details.

MAJOR MUSCLES OF THE TRUNK

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The muscles of the trunk cannot be described with one or two general functions. Some form the wall of the trunk and bend the trunk, such as the rectus abdominis (flexion) and the sacrospinalis group (extension). The trapezius (both together form the shape of a trapezoid) is a large muscle that can raise (shrug) the shoulder or pull it back, and can help extend the head. Other muscles found on the trunk help move the arm at the shoulder. The pectoralis major is a large muscle of the chest that pulls the arm across the chest (flexion and adduction). On the posterior side of the trunk, the latissimus dorsi pulls the arm downward and behind the back (extension and adduction). These muscles have their origins on the bones of the trunk, the sternum, the or vertebrae, which are strong, stable anchors. Another set of muscles forms the pelvic floor, where the muscles support the pelvic organs and assist with urination and defecation. Yet another category is the muscles that are concerned with breathing. These are the intercostal muscles between the ribs and the diaphragm that separates the thoracic and abdominal cavities. See table 2 for details.

MAJOR MUSCLES OF HEAD AND NECK

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Three general groups of muscles are found in the head and neck: those that move the head or neck, the muscles of facial expression, and the muscles for chewing. The muscles that turn or bend the head, such as the sternocleidomastoids (flexion) and the pair of splenius capitis muscles (extension), are anchored to the skull and to the clavicle and sternum anteriorly or the vertebrae posteriorly. The muscles for smiling or frowning or raising our eyebrows in disbelief are anchored to the bones of the head or to the undersurface of the skin of the face. The masseter is an important chewing muscle in that it raises the mandible (closes the jaw).See table 1 for details of muscles of head and neck.

TYPES OF NEURON

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Neurons may be classified into three groups: sensory neurons, motor neurons, and interneurons.

Sensory neurons (or afferent neurons) carry impulses from receptors to the central nervous system. Receptors detect external or internal changes and send the information to the CNS in the form of impulses by way of the afferent neurons. The central nervous system interprets these impulses as a sensation. Sensory neurons from receptors in skin, skeletal muscles, and joints are called somatic; those from receptors in internal organs are called visceral sensory neurons.

Motor neurons (or efferent neurons) carry impulses from the central nervous system to effectors. The two types of effectors are muscles and glands. In response to impulses, muscles contract or relax and glands secrete. Motor neurons linked to skeletal muscle are called somatic; those to smooth muscle, cardiac muscle, and glands are called visceral. Sensory and motor neurons make up the peripheral nervous system. Visceral motor neurons form the autonomic nervous system, a specialized subdivision of the PNS that will be discussed later in this chapter.

Interneurons are found entirely within the central nervous system. They are arranged so as to carry only sensory or motor impulses, or to integrate these functions. Some interneurons in the brain are concerned with thinking, learning, and memory. A neuron carries impulses in only one direction. This is the result of the neuron’s structure and location, as well as its physical arrangement with other neurons and the resulting pattern of synapses. The functioning nervous system, therefore, is an enormous network of “one-way streets,” and there is no danger of impulses running into and canceling one another out.

FACTORS AFFECTING BONE GROWTH

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1. Heredity—each person has a genetic potential for height, that is, a maximum height, with genes inherited from both parents. Many genes are involved, and their interactions are not well understood. Some of these genes are probably those for the enzymes involved in cartilage and bone production, for this is how bones grow.

2. Nutrition—nutrients are the raw materials of which bones are made. Calcium, phosphorus, and protein become part of the bone matrix itself. Vitamin D is needed for the efficient absorption of calcium and phosphorus by the small intestine. Vitamins A and C do not become part of bone but are necessary for the process of bone matrix formation (ossification). Without these and other nutrients, bones cannot grow properly. Children who are malnourished grow very slowly and may not reach their genetic potential for height.

3. Hormones—endocrine glands produce hormones that stimulate specific effects in certain cells. Several hormones make important contributions to bone growth and maintenance. These include growth hormone, thyroxine, parathyroid hormone, and insulin, which help regulate cell division, protein synthesis, calcium metabolism, and energy production. The sex hormones estrogen or testosterone help bring about the cessation of bone growth. The hormones and their specific functions are listed in Table.

4. Exercise or “stress”—for bones, exercise means bearing weight, which is just what bones are specialized to do. Without this stress (which is normal), bones will lose calcium faster than it is replaced. Exercise need not be strenuous; it can be as simple as the walking involved in everyday activities. Bones that do not get this exercise, such as those of patients confined to bed, will become thinner and more fragile.

EMBRYONIC GROWTH OF BONES

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During embryonic development, the skeleton is first made of cartilage and fibrous connective tissue, which are gradually replaced by bone. Bone matrix is produced by cells called osteoblasts (a blast cell is a “growing” or “producing” cell, and osteo means “bone”). In the embryonic model of the skeleton, osteoblasts differentiate from the fibroblasts that are present. The production of bone matrix, called ossification, begins in a center of ossification in each bone.

The cranial and facial bones are first made of fibrous connective tissue. In the third month of fetal development, fibroblasts (spindle-shaped connective tissue cells) become more specialized and differentiate into osteoblasts, which produce bone matrix. From each center of ossification, bone growth radiates outward as calcium salts are deposited in the collagen of the model of the bone. This process is not complete at birth; a baby has areas of fibrous connective tissue remaining between the bones of the skull. These are called fontanels, which permit compression of the baby’s head during birth without breaking the still thin cranial bones. The fontanels also permit the growth of the brain after birth. You may have heard fontanels referred to as “soft spots,” and indeed they are. A baby’s skull is quite fragile and must be protected from trauma. By the age of 2 years, all the fontanels have become ossified, and the skull becomes a more effective protective covering for the brain.

The rest of the embryonic skeleton is first made of cartilage, and ossification begins in the third month of gestation in the long bones. Osteoblasts produce bone matrix in the center of the diaphyses of the long bones and in the center of short, flat, and irregular bones. Bone matrix gradually replaces the original cartilage.

The long bones also develop centers of ossification in their epiphyses. At birth, ossification is not yet complete and continues throughout childhood. In long bones, growth occurs in the epiphyseal discs at the junction of the diaphysis with each epiphysis. An epiphyseal disc is still cartilage, and the bone grows in length as more cartilage is produced on the epiphysis side. On the diaphysis side, osteoblasts produce bone matrix to replace the cartilage. Between the ages of 16 and 25 years (influenced by estrogen or testosterone), all of the cartilage of the epiphyseal discs is replaced by bone. This is called closure of the epiphyseal discs (or we say the discs are closed), and the bone lengthening process stops.

Also in bones are specialized cells called osteoclasts (a clast cell is a “destroying” cell), which are able to dissolve and reabsorb the minerals of bone matrix, a process called resorption. Osteoclasts are very active in embryonic long bones, and they reabsorb bone matrix in the center of the diaphysis to form the marrow canal. Blood vessels grow into the marrow canals of embryonic long bones, and red bone marrow is established. After birth, the red bone marrow is replaced by yellow bone marrow. Red bone marrow remains in the spongy bone of short, flat, and irregular bones. For other functions of osteoclasts and osteoblasts,

CANCER- ABNORMAL CELLULAR FUNCTIONING

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There are more than 200 different types of cancer, all of which are characterized by abnormal cellular functioning. Normally, our cells undergo mitosis only when necessary and stop when appropriate. A cut in the skin, for example, is repaired by mitosis, usually without formation of excess tissue. The new cells fill in the damaged area, and mitosis slows when the cells make contact with surrounding cells. This is called contact inhibition, which limits the new tissue to just what is needed. Malignant (cancer) cells, however, are characterized by uncontrolled cell division. Our cells are genetically programmed to have particular life spans and to divide or die. One gene is known to act as a brake on cell division; another gene enables cells to live indefinitely, beyond their normal life span, and to keep dividing. Any imbalance in the activity of these genes may lead to abnormal cell division. Such cells are not inhibited by contact with other cells, keep dividing, and tend to spread.

A malignant tumor begins in a primary site such as the colon, then may spread or metastasize. Often the malignant cells are carried by the lymph or blood to other organs such as the liver, where secondary tumors develop. Metastasis is characteristic only of malignant cells; benign tumors do not metastasize but remain localized in their primary site.

What causes normal cells to become malignant? At present, we have only partial answers. A malignant cell is created by a mutation, a genetic change that brings about abnormal cell functions or responses and often leads to a series of mutations. Environmental substances that cause mutations are called carcinogens. One example is the tar found in cigarette smoke, which is definitely a cause of lung cancer. Ultraviolet light may also cause mutations, especially in skin that is overexposed to sunlight. For a few specific kinds of cancer, the trigger is believed to be infection with certain viruses that cause cellular mutations. Carriers of hepatitis B virus, for example, are more likely to develop primary liver cancer than are people who have never been exposed to this virus. Research has discovered two genes, one on chromosome 2 and the other on chromosome 3, that contribute to a certain form of colon cancer. Both of these genes are the codes for proteins that correct the “mistakes” that may occur when the new DNA is synthesized. When these repair proteins do not function properly, the mistakes (mutations) in the DNA lead to the synthesis of yet other faulty proteins that impair the functioning of the cell and predispose it to becoming malignant.

Once cells have become malignant, their functioning cannot return to normal, and though the immune system will often destroy such cells, sometimes it does not, especially as we get older. Therefore, the treatments for cancer are directed at removing or destroying the abnormal cells. Surgery to remove tumors, radiation to destroy cells, and chemotherapy to stop cell division or interfere with other aspects of cell metabolism are all aspects of cancer treatment.

New chemotherapy drugs are becoming more specific, with very precise targets. For example, the cells of several types of solid-tumor cancers have been found to have mutations in the gene for the cell membrane receptor for a natural growth factor (epidermal growth factor receptor, or EGFR). These altered receptors, when triggered by their usual growth factor, then cause the cell to divide uncontrollably, an abnormal response. Medications that target only these altered receptors have already been developed for some forms of lung cancer and breast cancer. Not only do they show promise in treating the cancer, they do not have the side effects of other forms of chemotherapy.

AGING

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Multicellular organisms, including people, age and eventually die; our cells do not have infinite life spans. It has been proposed that some cells capable of mitosis are limited to a certain number of divisions; that is, every division is sort of a tick-tock off a biological clock. We do not yet know exactly what this cellular biological clock is. There is evidence that the ends of chromosomes, called telomeres, may be an aspect of it. With each cell division, part of the telomeres is lost (rather like a piece of rope fraying at both ends), and eventually the telomeres are gone. With the next division, the ends of the chromosomes, actual genes, begin to be lost. This may be one signal that a cell’s life span has come to an end (there are probably many different kinds of signals).

Cellular aging also involves the inevitable deterioration of membranes and cell organelles. Just as the parts of a car break down in time, so too will cells. Unlike cars or machines, however, cells can often repair themselves, but they do have limits. As cells age, structural proteins break down and are not

replaced, or necessary enzymes are not synthesized. Proteins called chaperones, which are responsible for the proper folding of many other proteins and for the repair or disposal of damaged proteins, no

longer function as well as cells age. Without chaperones, damaged proteins accumulate within cells and

disrupt normal cellular processes. Clinical manifestations of impaired chaperones include cataracts and neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease.

Much about the chemistry of the aging process remains a mystery, though we can describe what happens to organs and to the body as a whole. Keep in mind that a system is the sum of its cells, in tissues and organs, and that all aging is ultimately at the cellular level.

ANEMIA

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Anemia is a deficiency of red blood cells, or insufficient hemoglobin within the red blood cells. There are many different types of anemia.

Iron-deficiency anemia is caused by a lack of dietary iron, and there is not enough of this mineral to form sufficient hemoglobin. A person with this type of anemia may have a normal RBC count and a normal hematocrit, but the hemoglobin level will be below normal.

A deficiency of vitamin B12, which is found only in animal foods, leads to pernicious anemia, in which the RBCs are large, misshapen, and fragile. Another cause of this form of anemia is lack of the intrinsic factor due to autoimmune destruction of the parietal cells of the stomach lining.

Sickle-cell anemia has already been discussed in previous post. It is a genetic disorder of hemoglobin, which causes RBCs to sickle, clog capillaries, and rupture.

Aplastic anemia is suppression of the red bone marrow, with decreased production of RBCs, WBCs, and platelets. This is a very serious disorder that may be caused by exposure to radiation, certain chemicals such as benzene, or some medications. There are several antibiotics that must be used with caution since they may have this potentially fatal side effect.

Hemolytic anemia is any disorder that causes rupture of RBCs before the end of their normal life span. Sickle-cell anemia and Rh disease of the newborn are examples. Another example is malaria, in which a protozoan parasite reproduces in RBCs and destroys them. Hemolytic anemias are often characterized by jaundice because of the increased production of bilirubin.

Apart from the above mentioned anemias, there are few others like megaloblastic anemia, sideroblastic anemia etc. These are somehow related to the above mentioned anemias. No matter whatever the cause of anemia be its signs and symptoms are similar. Cause is basically needed for the proper treatment of the disease.

SICKLE CELL ANEMIA- A GENETIC DISEASE

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A genetic disease is a hereditary disorder, one that may be passed from generation to generation. Although there are hundreds of genetic diseases, they all have the same basis: a mistake in DNA. Because DNA makes up the chromosomes that are found in eggs and sperm, this mistake may be passed from parents to children. Sickle-cell anemia is the most common genetic disorder among people of African descent and affects the hemoglobin in red blood cells. Normal hemoglobin, called hemoglobin A (HbA), is a protein made of two alpha chains (141 amino acids each) and two beta chains (146 amino acids each). In sickle-cell hemoglobin (HbS), the sixth amino acid in each beta chain is incorrect; valine instead of the glutamic acid found in HbA. This difference seems minor—only 2 incorrect amino acids out of more than 500—but the consequences for the person are very serious.

HbS has a great tendency to crystallize when oxygen levels are low, as is true in capillaries. When HbS crystallizes, the red blood cells are deformed into crescents (sickles) and other irregular shapes. These irregular, rigid red blood cells clog and rupture capillaries, causing internal bleeding and severe pain. These cells are also fragile and break up easily, leading to anemia and hypoxia (lack of oxygen). Treatment of this disease has improved greatly, but it is still incurable. What has happened to cause the formation of HbS rather than HbA? Hemoglobin is a protein; the gene for its beta chain is in DNA (chromosome 11). One amino acid in the beta chains is incorrect, therefore, one triplet in its DNA gene must be, and is, incorrect. This mistake is copied by mRNA in the cells of the red bone marrow, and HbS is synthesized in red blood cells.

Sickle-cell anemia is a recessive genetic disease, which means that a person with one gene for HbS and one gene for HbA will have “sickle-cell trait.” Such a person usually will not have the severe effects of sickle-cell anemia, but may pass the gene for HbS to children. It is estimated that 9% of African-Americans have sickle-cell trait and about 1% have sickle-cell anemia.

EPONYMS

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An eponym is a person for whom something is named, and an eponymous term is a term that uses that name or eponym. For example, fallopian tube is named for Gabriele Fallopio, an Italian anatomist of the 16th century. In recent years it has been suggested that eponymous terms be avoided because they are not descriptive and that they be replaced with more informative terms. Such changes, however, occur slowly, because the older terms are so familiar to those of us who teach. Some of us may even use them as opportunities to impart a little history, also known as “telling stories.”

In this post, the most familiar eponymous terms have been retained, with the newer term in parentheses

after the first usages. The list below is provided to show the extent of reclassification of eponymous terms as related to basic anatomy and physiology.

PREFIX AND SUFFIX USED IN MEDICAL TERMINOLOGY

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prefix

a-, an- absent, without (amenorrhea: absence of menstruation)

ab- away from (abduct: move away from the midline)

abdomin/o- abdomen (abdominal aorta: the portion of the aorta in the abdomen)

acou- hearing (acoustic nerve: the cranial nerve for hearing)

ad- toward, near, to (adduct: move toward the midline)

aden/o- gland (adenohypophysis: the glandular part of the pituitary gland)

af- to, toward (afferent: toward a center)

alba- white (albino: an animal lacking coloration)

alg- pain (myalgia: muscle pain)

ana- up, back (anabolism: the constructive phase of metabolism)

angi/o- vessel (angiogram: imaging of blood vessels, as in the heart)

ante- before (antenatal: before birth)

anti- against (antiemetic: an agent that prevents vomiting)

arthr/o- joint (arthritis: inflammation of a joint)

atel- imperfect, incomplete (atelectasis: incomplete expansion of a lung)

auto- self (autoimmune disease: a disease in which immune reactions are directed against part of one’s own body)

bi- two, twice (biconcave: concave on each side, as a red blood cell)

bio- life (biochemistry: the chemistry of living organisms)

blasto- growth, budding (blastocyst: a rapidly growing embryonic stage)

brachi/o- arm (brachial artery: the artery that passes through the upper arm)

brachy- short (brachydactyly: abnormally short fingers or toes)

brady- slow (bradycardia: slow heart rate)

bronch- air passage (bronchioles: small air passages in the lungs)

carcin/o- cancer (carcinogen: cancer-causing substance)

cardi/o- heart (cardiopathy: heart disease)

carp/o- wrist (carpals: bones of the wrist)

cata- down (catabolism: the breaking down phase of metabolism)

caud- tail (cauda equina: the spinal nerves that hang below the end of the spinal cord and resemble a horse’s tail)

celi/o- abdomen (celiac artery: a large artery that supplies abdominal organs)

cephal/o- head (cephaledema: swelling of the head)

cerebr/o- brain (cerebrum: the largest part of the human brain)

cervic- neck (cervical nerves: the spinal nerves from the neck portion of the spinal cord)

chem/o- chemical (chemotherapy: the use of chemicals to treat disease)

chondr/o- cartilage (chondrocyte: cartilage cell)

circum- around (circumoral: around the mouth)

co-, com-, with, together (congenital: born with)

con-, contra- opposite, against (contraception: the prevention of conception)

cost/o- ribs (intercostal muscles: muscles between the ribs)

crani/o- skull, head (cranial nerves: the nerves that arise from the brain)

cut- skin (cutaneous: pertaining to the skin)

cyan/o- blue (cyanosis: bluish discoloration of the skin due to lack of oxygen)

cyst- bladder, sac (cystic duct: duct of the gallbladder)

cyt/o- cell (hepatocyte: cell of the liver)

dactyl/o- digits, fingers or toes (polydactyly: more than five fingers or toes)

de- down, from (dehydration: loss of water)

derm- skin (dermatologist: a specialist in diseases of the skin)

di- two, twice (disaccharide: a sugar made of two monosaccharides)

diplo- double (diplopia: double vision)

dis- apart, away from (dissect: to cut apart)

duct- lead, conduct (ductus arteriosus: a fetal artery)

dys- difficult, diseased (dyspnea: difficult breathing)

ecto- outside (ectoparasite: a parasite that lives on the body surface)

edem- swelling (edematous: affected with swelling)

endo- within (endocardium: the innermost layer of the heart wall)

enter/o- intestine (enterotoxin: a toxin that affects the intestine and causes diarrhea)

epi- on, over, upon (epidermis: the outer layer of the skin)

erythr/o- red (erythrocyte: red blood cell)

eu- normal, good (eupnea: normal breathing)

ex- out of (excise: to cut out or remove surgically)

exo- without, outside of (exophthalmia: protrusion of the eyeballs)

extra- outside of, in addition to, beyond (extraembryonic membranes: the membranes that surround the embryofetus)

fasci- band (fascia: a fibrous connective tissue membrane)

fore- before, in front (forehead: the front of the head)

gastro/o- stomach (gastric juice: the digestive secretions of the stomach lining)

gluco-, glyco- sugar (glycosuria: glucose in the urine)

gyn/o-, gyne/co- woman, female (gynecology: study of the female reproductive organs)

haplo- single, simple (haploid: a single set, as of chromosomes)

hema-, hemato-, hemo- blood (hemoglobin: the protein of red blood cells)

hemi- half (cerebral hemisphere: the right or left half of the cerebrum)

hepat/o- liver (hepatic duct: the duct that takes bile out of the liver)

hetero- different (heterozygous: having two different genes for a trait)

hist/o- tissue (histology: the study of tissues)

homeo- unchanged (homeostasis: the state of body stability)

homo- same (homozygous: having two similar genes for a trait)

hydr/o- water (hydrophobia: fear of water)

hyper- excessive, above (hyperglycemia: high blood glucose level)

hypo- beneath, under, deficient (hypodermic: below the skin)

idio- distinct, peculiar to the individual (idiopathic: of unknown cause, as a disease)

inter- between, among (interventricular septum: the wall between the ventricles of the heart)

intra- within (intracellular: within cells)

is/o- equal, the same (isothermal: having the same temperature)

kinesi/o- movement (kinesthetic sense: muscle sense)

labi- lip (herpes labialis: cold sores of the lips)

lacri- tears (lacrimal glands: tear-producing glands)

lact/o- milk (lactation: milk production)

leuc/o, leuk/o- white (leukocyte: white blood cell)

lip/o- fat (liposuction: removal of fat with a suctioning instrument)

macr/o- large (macromolecule: a large molecule such as a protein)

mal- poor, bad (malnutrition: poor nutrition)

medi- middle (mediastinum: a middle cavity, as in the chest)

mega- large (megacolon: abnormally dilated colon)

meta- next to, beyond (metatarsal: bone of the foot next to the ankle)

micr/o- small (microcephaly: small head)

mon/o- one (monozygotic twins: identical twins, from one egg)

morph/o- shape, form (amorphous: without definite shape)

multi- many (multicellular: made of many cells)

my/o- muscle (myocardium: heart muscle)

narco- sleep (narcotic: a drug that produces sleep)

nat/a- birth (neonate: a newborn infant)

neo- new (neoplasty: surgical restoration of parts)

nephr/o- kidney (nephrectomy: removal of a kidney)

neur/o- nerve (neuron: nerve cell)

non- not (non-communicable: unable to spread)

ocul/o- eye (oculomotor nerve: a cranial nerve for eye movement)

olig/o- few, scanty (oliguria: diminished amount of urine)

oo- egg (oogenesis: production of an egg cell)

ophthalmo- eye (ophthalmoscope: instrument to examine the eye)

orth/o- straight, normal, correct (orthostatic: related to standing upright)

oste/o- bone (osteocyte: bone cell)

ot/o- ear (otitis media: inflammation of the middle ear)

ovi-, ovo- egg (oviduct: duct for passage of an egg cell, fallopian tube)

path/o- disease (pathology: the study of disease)

ped/ia- child (pediatric: concerning the care of children)

per- through (permeate: to pass through)

peri- around (pericardium: membranes that surround the heart)

phag/o- eat (phagocyte: a cell that engulfs pariculate matter)

phleb/o- vein (phlebitis: inflammation of a vein)

pleuro-, pleura- rib (pleurisy: inflammation of the pleural membranes of the chest cavity)

pneumo- lung (pneumonia: lung infection)

pod- foot (pseudopod: false foot, as in ameboid movement)

poly- many (polysaccharide: a carbohydrate made of many monosaccharides)

post- after (postpartum: after delivery of a baby)

pre- before (precancerous: a growth that probably will become malignant)

pro- before, in front of (progeria: premature old age, before its time)

pseudo- false (pseudomembrane: false membrane)

py/o- pus (pyogenic: pus producing)

pyel/o- renal pelvis (pyelogram: an x-ray of the renal pelvis and ureter)

quadr/i- four (quadriceps femoris: a thigh muscle with four parts)

retro- behind, backward (retroperitoneal: located behind the peritoneum)

rhin/o- nose (rhinoviruses that cause the common cold)

salping/o- fallopian tube (salpingitis: inflammation of a fallopian tube)

sarc/o- flesh, muscle (sarcolemma: membrane of a muscle cell)

sclero- hard (sclerosis: deterioration of tissue with loss of function)

semi- half (semilunar valve: a valve shaped like a half-moon)

steno- narrow (aortic stenosis: narrowing of the aorta)

sub- below, beneath (subcutaneous: below the skin)

supra- above (suprarenal gland: gland above the kidney, the adrenal gland)

sym- together (symphysis: a joint where two bones meet)

syn- together (synapse: the space between two nerve cells)

tachy- fast (tachycardia: rapid heart rate)

thorac/o- chest (thoracic cavity: chest cavity)

thromb/o- clot (thrombosis: formation of a blood clot)

tox- poison (toxicology: the study of poisons)

trans- across (transmural: across the wall of an organ)

tri- three (trigone: a three-sided area on the floor of the urinary bladder)

ultra- excessive, extreme (ultrasonic: sound waves beyond the normal hearing range)

un/i- one (unicellular: made of one cell)

uria-, uro- urine (urinary calculi: stones in the urine)

vas/o- vessel (vasodilation: dilation of a blood vessel)

viscera-, viscero- organ (visceral pleura: the pleural membrane that covers the lungs)

suffix

-ac pertaining to (cardiac: pertaining to the heart)

-al pertaining to (intestinal: pertaining to the intestine)

-an, -ian characteristic of, pertaining to, belonging to (ovarian cyst: a cyst of the ovary)

-ar relating to (muscular: relating to muscles)

-ary relating to, connected with (salivary: relating to saliva)

-ase enzyme (sucrase: an enzyme that digests sucrose)

-atresia abnormal closure (biliary atresia: closure or absence of bile ducts)

-blast grow, produce (osteoblast: a bone-producing cell)

-cele swelling, tumor (meningocele: a hernia of the meninges)

-centesis puncture of a cavity (thoracocentesis: puncture of the chest cavity to remove fluid)

-cide kill (bactericide: a chemical that kills bacteria)

-clast destroy, break down (osteoclast: a bone-reabsorbing cell)

-desis binding, stabilizing, fusion (arthrodesis: the surgical immobilization of a joint)

-dipsia thirst (polydipsia: excessive thirst)

-dynia pain (gastrodynia: stomach pain)

-ectasia, -ectasis expansion (atelectasis: without expansion)

-ectomy excision, cutting out (thyroidectomy: removal of the thyroid)

-emia pertaining to blood (hypokalemia: low blood potassium level)

-form structure (spongiform: resembling a sponge)

-gen producting (carcinogen: a substance that produces cancer)

-genesis production of, origin of (spermatogenesis: production of sperm)

-globin protein (myoglobin: a muscle protein)

-gram record, writing (electroencephalogram: a record of the electrical activity of the brain)

-graph an instrument for making records (ultrasonography: the use of ultrasound to produce an image)

-ia condition (pneumonia: condition of inflammation of the lungs)

-iasis diseased condition (cholelithiasis: gallstones)

-ic pertaining to (atomic: pertaining to atoms)

-ile having qualities of (febrile: feverish)

-ism condition, process (alcoholism: condition of being dependent on alcohol)

-ist practitioner, specialist (neurologist: a specialist in diseases of the nervous system)

-itis inflammation (hepatitis: inflammation of the liver)

-lepsy seizure (narcolepsy: a sudden onset of sleep)

-lith stone, crystal (otoliths: stones in the inner ear)

-logy study of (virology: the study of viruses)

-lysis break down (hemolysis: rupture of red blood cells)

-megaly enlargement (splenomegaly: enlargement of the spleen)

-meter a measuring instrument (spirometer: an instrument to measure pulmonary volumes)

-ness state of, quality (illness: state of being ill)

-oid the appearance of (ovoid: resembling an oval or egg)

-ole small, little (arteriole: small artery)

-oma tumor (carcinoma: malignant tumor)

-opia eye (hyperopia: farsightedness)

-ory pertaining to (regulatory: pertaining to regulation)

-ose having qualities of (comatose: having qualities of a coma)

-osis state, condition, action, process (keratosis: abnormal growth of the skin)

-ostomy creation of an opening (colostomy: creation of an opening between the intestine and the abdominal wall)

-otomy cut into (tracheotomy: cut into the trachea)

-ous pertaining to (nervous: pertaining to nerves)

-pathy disease (retinopathy: disease of the retina)

-penia lack of, deficiency (leukopenia: lack of white blood cells)

-philia love of, tendency (hemophilia: a clotting disorder; “love of blood”)

-phobia an abnormal fear (acrophobia: fear of heights)

-plasia growth (hyperplasia: excessive growth)

-plasty formation, repair (rhinoplasty: plastic surgery on the nose)

-plegia paralysis (hemiplegia: paralysis of the right or left half of the body)

-poiesis production (erythropoiesis: production of red blood cells)

-ptosis dropping, falling (hysteroptosis: falling of the uterus)

-rrhage burst forth (hemorrhage: loss of blood from blood vessels)

-rrhea discharge, flow (diarrhea: frequent discharge of feces)

-scope instrument to examine (microscope: instrument to examine small objects)

-spasm involuntary contraction (blepharospasm: twitch of the eyelid)

-stasis to be still, control, stop (hemostasis: to stop loss of blood)

-sthenia strength (myasthenia: loss of muscle strength)

-stomy surgical opening (colostomy: a surgical opening in the colon)

-taxia muscle coordination (ataxia: loss of coordination)

-tension pressure (hypertension: high blood pressure)

-tic pertaining to (paralytic: pertaining to paralysis)

-tomy incision, cut into (phlebotomy: incision into a vein)

-tripsy crush (lithotripsy: crushing of stone such as gallstones)

-trophic related to nutrition or growth (autotrophic: capable of making its own food, such as a green plant)

-tropic turning toward (chemotropic: turning toward a chemical)

-ula, -ule small, little (venule: small vein)

-uria urine (hematuria: blood in the urine)

-y condition, process (healthy: condition of health)

SHOCK

2011-08-17T15:16:00.000+05:30

Shock can be defined as a state of imbalance between the demand for oxygenated blood and its supply. It is a clinical syndrome typified by a restless patient who is cool and clammy and has a blood pressure 50mm Hg lower than the normal. Though usually associate with an absolute diminution in cardiac output, shock may still be present even in higher output states when shunting of blood from the arterial to the venous side of the circulation deprives critical organs of flow.

Classification of Shock by Causes

Though the final clinical events are similar in all types of shock, there are several general causes.

Hypovolemic Shock: Hypovolemia is most often due to hemorrhage and is characterized by a reduction in blood volume as a precipitating event; effective hypovolemia may also be due to “third spacing” of fluid, as in peritonitis or burns, which results in lowering of blood volume.
Cardiogenic Shock: This type of shock is due to major myocardial infaraction an dresults from an abrupt drop in cardiac output.
Vascular shock: Types of shock resulting from lowered peripheral resistance include the following:-

Gram-negative shock is caused by the vasodilating properties of endotoxin, decreasing peripheral resistance, the initial effect of which is to increase the cardiac output(“warm shock”). Though cardiac output is increased initially, the associated sustained increase in venous pooling ultimately results in a lower venous return, a consequent drop in cardiac output, and more typical appearance of “cool shock” with vasoconstriction and pallor as noted above.
Anaphylactic shock, though most notable for its effect on the airways, is characterized by a profoundly low peripheral resistance; refractory hypotension can be a cause of death in this situation, which is best known for its occurrence after penicillin injection or bee sting.
Toxic shock is caused by a staphylococcal exotoxin usually resulting from vaginal organism growth associated with tampon use. Fever, rash, hypotension, and occasional central nervous system and hepatorenal dysfunction are observed.

Clinical manifestations

The clinical picture depends on whether hypovolemia, reduced cardiac output, or lowered vascular resistance was the primary event.

Treatment

Management varies with the cause of shock, but volume resuscitation is common to all. Military antishock trousers (MAST) markedly redistribute intravascular fluid into the upper circulation, and this is potentially valuable in all forms except cardiogenic shock. The fluid of choice to replace volume is a matter of dispute, but there is probably no important difference between crystalloid (eg, normal saline) and colloid (eg, albumin); in hemorrhage, it is just important to replace volume as it is to transfuse erythrocytes. In all types of shock, dopamine and dobutamine are the pressor agents of choice; any pressor therapy should be reserved for situations where blood volume has been shown to be adequate but ineffective. In gram-negative shock, there is new information favoring the use of the narcotic antagonist naloxone because of the proposed mediator role of endogenous opiates in causing the hypotension of the shock state. The role of corticosteroids remains controversial, though they are in widespread use in this type of Shock.

To monitor all patients with all types of shock, central venous pressure determination is widely used and has a good positive correlation with left ventricular filling pressure, except in patients with preexisting cardiac disease; thus, in suspected cardiogenic shock or in shock states in patients with underlying cardiovascular disease it is essential to monitor therapy by using the Swan-Ganz catheter to measure the pulmonary artery wedge pressure. In addition, an indwelling arterial line is placed to monitor mean blood pressure, and cardiac output can be calculated easily using the thermodilution technique.

ELECTROCARDIOGRAPHY-II (Basic terminology)

2011-06-16T09:55:00.000+05:30

This article explains the genesis of and normal values for the individual components of the wave forms that are seen in an electrocardiogram. To recognise electrocardiographic abnormalities the range of normal wave patterns must be understood.

P wave
The sinoatrial node lies high in the wall of the right atrium and initiates atrial depolarisation, producing the P wave on the electrocardiogram. Although the atria are anatomically two
distinct chambers, electrically they act almost as one. They have relatively little muscle and generate a single, small P wave. P wave amplitude rarely exceeds two and a half small squares
(0.25 mV). The duration of the P wave should not exceed three small squares (0.12 s).

The wave of depolarisation is directed inferiorly and towards the left, and thus the P wave tends to be upright in leads I and II and inverted in lead aVR. Sinus P waves are usually most prominently seen in leads II and V1. A negative P wave in lead I may be due to incorrect recording of the electrocardiogram (that is, with transposition of the left and right arm electrodes), dextrocardia, or abnormal atrial rhythms.

The P wave in V1 is often biphasic. Early right atrial forces are directed anteriorly, giving rise to an initial positive deflection; these are followed by left atrial forces travelling posteriorly, producing a later negative deflection. A large negative deflection (area of more than one small square) suggests left atrial enlargement.

Normal P waves may have a slight notch, particularly in the precordial (chest) leads. Bifid P waves result from slight asynchrony between right and left atrial depolarisation. A pronounced notch with a peaktopeak interval of > 1 mm (0.04 s) is usually pathological, and is seen in association with a left atrial abnormality—for example, in mitral stenosis.

PR interval
After the P wave there is a brief return to the isoelectric line, resulting in the “PR segment.” During this time the electrical impulse is conducted through the atrioventricular node, the
bundle of His and bundle branches, and the Purkinje fibres.

The PR interval is the time between the onset of atrial depolarisation and the onset of ventricular depolarisation, and it is measured from the beginning of the P wave to the first
deflection of the QRS complex (see next section), whether this be a Q wave or an R wave.The normal duration of the PR interval is three to five small squares (0.120.20 s). Abnormalities of the conducting system may lead to transmission delays, prolonging the PR interval.

QRS complex
The QRS complex represents the electrical forces generated by ventricular depolarisation. With normal intraventricular conduction, depolarisation occurs in an efficient, rapid fashion.The duration of the QRS complex is measured in the lead with the widest complex and should not exceed two and a half small squares (0.10 s). Delays in ventricular depolarisation—for
example, bundle branch block—give rise to abnormally wide QRS complexes (>0.12 s).

The depolarisation wave travels through the interventricular septum via the bundle of His and bundle branches and reaches the ventricular myocardium via the Purkinje fibre network. The
left side of the septum depolarises first, and the impulse then spreads towards the right. Lead V1 lies immediately to the right of the septum and thus registers an initial small positive
deflection (R wave) as the depolarisation wave travels towards this lead.

When the wave of septal depolarisation travels away from the recording electrode, the first deflection inscribed is negative. Thus small “septal” Q waves are often present in the lateral
leads, usually leads I, aVL, V5, and V6.

These nonpathological Q waves are less than two small squares deep and less than one small square wide, and should be < 25% of the amplitude of the corresponding R wave. The wave of depolarisation reaches the endocardium at the apex of the ventricles, and then travels to the epicardium, spreading outwards in all directions. Depolarisation of the right and left ventricles produces opposing electrical vectors, but the left ventricle has the larger muscle mass and its depolarization dominates the electrocardiogram. In the precordial leads, QRS morphology changes depending on whether the depolarisation forces are moving towards or away from a lead. The forces generated by the free wall of the left ventricle predominate, and therefore in lead V1 a small R wave is followed by a large negative deflection (S wave). The R wave in the precordial leads steadily increases in amplitude from lead V1 to V6, with a corresponding decrease in S wave depth, culminating in a predominantly positive complex in V6. Thus, the QRS complex gradually changes from being predominantly negative in lead V1 to being predominantly positive in lead V6. The lead with an equiphasic QRS complex is located over the transition zone; this lies between leads V3 and V4, but shifts towards the left with age. The height of the R wave is variable and increases progressively across the precordial leads; it is usually < 27 mm in leads V5 and V6. The R wave in lead V6, however, is often smaller than the R wave in V5, since the V6 electrode is further from the left ventricle. The S wave is deepest in the right precordial leads; it decreases in amplitude across the precordium, and is often absent in leads V5 and V6. The depth of the S wave should not exceed 30 mm in a normal individual, although S waves and R waves > 30 mm are occasionally recorded in normal young male adults.

ST segment
The QRS complex terminates at the J point or ST junction. The ST segment lies between the J point and the beginning of the T wave, and represents the period between the end of ventricular
depolarisation and the beginning of repolarisation. The ST segment should be level with the subsequent “TP segment” and is normally fairly flat, though it may slope upwards slightly before merging with the T wave.

In leads V1 to V3 the rapidly ascending S wave merges directly with the T wave, making the J point indistinct and the ST segment difficult to identify. This produces elevation of the ST segment, and this is known as “high takeoff.”

Nonpathological elevation of the ST segment is also associated with benign early repolarisation (see article on acute myocardial infarction later in the series), which is particularly common in young men, athletes, and black people. Interpretation of subtle abnormalities of the ST segment is one of the more difficult areas of clinical electrocardiography; nevertheless, any elevation or depression of the ST segment must be explained rather than dismissed.

T wave
Ventricular repolarisation produces the T wave. The normal Twave is asymmetrical, the first half having a more gradual slope than the second half.

T wave orientation usually corresponds with that of the QRS complex, and thus is inverted in lead aVR, and may be inverted in lead III. T wave inversion in lead V1 is also common. It is occasionally accompanied by T wave inversion in lead V2, though isolated T wave inversion in lead V2 is abnormal. T wave inversion in two or more of the right precordial leads is known as a persistent juvenile pattern; it is more common in black people. The presence of symmetrical, inverted T waves is highly suggestive of myocardial ischaemia, though asymmetrical inverted T waves are frequently a nonspecific finding.

No widely accepted criteria exist regarding T wave amplitude. As a general rule, T wave amplitude corresponds with the amplitude of the preceding R wave, though the tallest T waves are seen in leads V3 and V4. Tall T waves may be seen in acute myocardial ischaemia and are a feature of hyperkalaemia.

QT interval
The QT interval is measured from the beginning of the QRS complex to the end of the T wave and represents the total time taken for depolarisation and repolarisation of the ventricles.

The QT interval lengthens as the heart rate slows, and thus when measuring the QT interval the rate must be taken into account. As a general guide the QT interval should be 0.35 0.45 s, and should not be more than half of the interval between adjacent R waves (RR interval). The QT interval increases slightly with age and tends to be longer in women than in men. Bazett's correction is used to calculate the QT interval corrected for heart rate (QTc): QTc = QT/RR (seconds).

Prominent U waves can easily be mistaken for T waves, leading to overestimation of the QT interval. This mistake can be avoided by identifying a lead where U waves are not prominent—for example, lead aVL.

U wave
The U wave is a small deflection that follows the T wave. It is generally upright except in the aVR lead and is often most prominent in leads V2 to V4. U waves result from repolarisation of the midmyocardial cells—that is, those between the endocardium and the epicardium—and the
HisPurkinje system. Many electrocardiograms have no discernible U waves. Prominent U waves may be found in athletes and are associated with hypokalaemia and hypercalcaemia.

ELECTROCARDIOGRAPHY (1)

2011-06-11T09:15:00.000+05:30

Electrocardiography is a fundamental part of cardiovascular assessment. It is an essential tool for investigating cardiac arrhythmias and is also useful in diagnosing cardiac disorders such as myocardial infarction. Familiarity with the wide range of

patterns seen in the electrocardiograms of normal subjects and an understanding of the effects of noncardiac disorders on the trace are prerequisites to accurate interpretation.

The contraction and relaxation of cardiac muscle results

from the depolarisation and repolarisation of myocardial cells. These electrical changes are recorded via electrodes placed on the limbs and chest wall and are transcribed on to graph paper to produce an electrocardiogram (commonly known as an

ECG).

The sinoatrial node acts as a natural pacemaker and initiates atrial depolarisation. The impulse is propagated to the ventricles by the atrioventricular node and spreads in a coordinated fashion throughout the ventricles via the specialised conducting tissue of the HisPurkinje system. Thus, after delay in the atrioventricular mode, atrial contraction is followed by rapid and coordinated contraction of the ventricles.

The electrocardiogram is recorded on to standard paper

travelling at a rate of 25 mm/s. The paper is divided into large squares, each measuring 5 mm wide and equivalent to 0.2 s. Each large square is five small squares in width, and each small square is 1 mm wide and equivalent to 0.04 s.

The electrical activity detected by the electrocardiogram

machine is measured in millivolts. Machines are calibrated so that a signal with an amplitude of 1 mV moves the recording stylus vertically 1 cm. Throughout this text, the amplitude of waveforms will be expressed as: 0.1 mV = 1 mm = 1 small square.

The amplitude of the waveform recorded in any lead maybe influenced by the myocardial mass, the net vector of depolarisation, the thickness and properties of the interveningtissues, and the distance between the electrode and the myocardium. Patients with ventricular hypertrophy have a relatively large myocardial mass and are therefore likely to have

high amplitude waveforms. In the presence of pericardial fluid, pulmonary emphysema, or obesity, there is increased resistance to current flow, and thus waveform amplitude is reduced.

The direction of the deflection on the electrocardiogram

depends on whether the electrical impulse is travelling towards

or away from a detecting electrode. By convention, an electrical

impulse travelling directly towards the electrode produces an

upright (“positive”) deflection relative to the isoelectric baseline,

whereas an impulse moving directly away from an electrode

produces a downward (“negative”) deflection relative to the

baseline. When the wave of depolarisation is at right angles to

the lead, an equiphasic deflection is produced.

The six chest leads (V1 to V6) “view” the heart in the

horizontal plane. The information from the limb electrodes is

combined to produce the six limb leads (I, II, III, aVR, aVL, and

aVF), which view the heart in the vertical plane. The

information from these 12 leads is combined to form a

standard electrocardiogram.

The arrangement of the leads produces the following

anatomical relationships: leads II, III, and aVF view the inferior

surface of the heart; leads V1 to V4 view the anterior surface;

leads I, aVL, V5, and V6 view the lateral surface; and leads V1

and aVR look through the right atrium directly into the cavity

of the left ventricle.

Rate

The term tachycardia is used to describe a heart rate greater than 100 beats/min. A bradycardia is defined as a rate less than 60 beats/min (or < 50 beats/min during sleep). One large square of recording paper is equivalent to 0.2 seconds; there are five large squares per second and 300 per minute. Thus when the rhythm is regular and the paper speed is running at the standard rate of 25 mm/s, the heart rate can be calculated by counting the number of large squares between two consecutive R waves, and dividing this number into 300.

Alternatively, the number of small squares between two consecutive R waves may be divided into 1500.

Some countries use a paper speed of 50 mm/s as standard; the heart rate is calculated by dividing the number of large squares between R waves into 600, or the number of small squares into 3000.

“Rate rulers” are sometimes used to calculate heart rate; these are used to measure two or three consecutive RR intervals, of which the average is expressed as the rate equivalent. When using a rate ruler, take care to use the correct scale according to paper speed (25 or 50 mm/s); count the correct numbers of beats (for example, two or three); and restrict the technique to regular rhythms.

When an irregular rhythm is present, the heart rate may be calculated from the rhythm strip (see next section). It takes one second to record 2.5 cm of trace. The heart rate per minute can be calculated by counting the number of intervals between QRScomplexes in 10 seconds (namely, 25 cm of recording paper)

and multiplying by six.

Rhythm

To assess the cardiac rhythm accurately, a prolonged

recording from one lead is used to provide a rhythm strip. Lead II, which usually gives a good view of the P wave, is most commonly used to record the rhythm strip.

The term “sinus rhythm” is used when the rhythm originates in the sinus node and conducts to the ventricles.

Young, athletic people may display various other rhythms, particularly during sleep. Sinus arrhythmia is the variation in the heart rate that occurs during inspiration and expiration.

There is “beat to beat” variation in the RR interval, the rate

increasing with inspiration. It is a vagally mediated response to

the increased volume of blood returning to the heart during

inspiration.

Cardiac axis

The cardiac axis refers to the mean direction of the wave of

ventricular depolarisation in the vertical plane, measured from a zero reference point. The zero reference point looks at the heart from the same viewpoint as lead I. An axis lying above this line is given a negative number, and an axis lying below the line is given a positive number. Theoretically, the cardiac axis may lie anywhere between 180 and - 180°. The normal range for the cardiac axis is between - 30° and 90°. An axis lying beyond - 30° is termed left axis deviation, whereas an axis > 90° is termed right axis deviation.

Several methods can be used to calculate the cardiac

axis, though occasionally it can prove extremely difficult to

determine. The simplest method is by inspection of leads I, II,

and III.

A more accurate estimate of the axis can be achieved if all

six limb leads are examined. The hexaxial diagram shows each lead's view of the heart in the vertical plane.

The direction of current flow is towards leads with a positive deflection, away from leads with a negative deflection, and at 90° to a lead with an equiphasic QRS complex. The axis is determined as follows:

1. Choose the limb lead closest to being equiphasic. The axis lies about 90° to the right or left of this lead

2. With reference to the hexaxial diagram, inspect the QRS complexes in the leads adjacent to the equiphasic lead. If the

lead to the left side is positive, then the axis is 90° to the

equiphasic lead towards the left. If the lead to the right side is

positive, then the axis is 90° to the equiphasic lead towards the

right.

INTELLIGENCE

2010-05-11T07:06:00.000+05:30

Intelligence, term usually referring to a general mental capability to reason, solve problems, think abstractly, learn and understand new material, and profit from past experience. Intelligence can be measured by many different kinds of tasks. Likewise, this ability is expressed in many aspects of a person’s life. Intelligence draws on a variety of mental processes, including memory, learning, perception, decision-making, thinking, and reasoning.

DEFINING INTLLIGENCE
Most people have an intuitive notion of what intelligence is, and many words in the English language distinguish between different levels of intellectual skill: bright, dull, smart, stupid, clever, slow, and so on. Yet no universally accepted definition of intelligence exists, and people continue to debate what, exactly, it is. Fundamental questions remain: Is intelligence one general ability or several independent systems of abilities? Is intelligence a property of the brain, a characteristic of behavior, or a set of knowledge and skills?

The simplest definition proposed is that intelligence is whatever intelligence tests measure. But this definition does not characterize the ability well, and it has several problems. First, it is circular: The tests are assumed to verify the existence of intelligence, which in turn is measurable by the tests. Second, many different intelligence tests exist, and they do not all measure the same thing. In fact, the makers of the first intelligence tests did not begin with a precise idea of what they wanted to measure. Finally, the definition says very little about the specific nature of intelligence.

Whenever scientists are asked to define intelligence in terms of what causes it or what it actually is, almost every scientist comes up with a different definition. For example, in 1921 an academic journal asked 14 prominent psychologists and educators to define intelligence. The journal received 14 different definitions, although many experts emphasized the ability to learn from experience and the ability to adapt to one’s environment. In 1986 researchers repeated the experiment by asking 25 experts for their definition of intelligence. The researchers received many different definitions: general adaptability to new problems in life; ability to engage in abstract thinking; adjustment to the environment; capacity for knowledge and knowledge possessed; general capacity for independence, originality, and productiveness in thinking; capacity to acquire capacity; apprehension of relevant relationships; ability to judge, to understand, and to reason; deduction of relationships; and innate, general cognitive ability.

People in the general population have somewhat different conceptions of intelligence than do most experts. Laypersons and the popular press tend to emphasize cleverness, common sense, practical problem solving ability, verbal ability, and interest in learning. In addition, many people think social competence is an important component of intelligence.

Most intelligence researchers define intelligence as what is measured by intelligence tests, but some scholars argue that this definition is inadequate and that intelligence is whatever abilities are valued by one’s culture. According to this perspective, conceptions of intelligence vary from culture to culture. For example, North Americans often associate verbal and mathematical skills with intelligence, but some seafaring cultures in the islands of the South Pacific view spatial memory and navigational skills as markers of intelligence. Those who believe intelligence is culturally relative dispute the idea that any one test could fairly measure intelligence across different cultures. Others, however, view intelligence as a basic cognitive ability independent of culture.

In recent years, a number of theorists have argued that standard intelligence tests measure only a portion of the human abilities that could be considered aspects of intelligence. Other scholars believe that such tests accurately measure intelligence and that the lack of agreement on a definition of intelligence does not invalidate its measurement. In their view, intelligence is much like many scientific concepts that are accurately measured well before scientists understand what the measurement actually means. Gravity, temperature, and radiation are all examples of concepts that were measured before they were understood.

MEASURING INTELLINGENCE
The first intelligence tests were short-answer exams designed to predict which students might need special attention to succeed in school. Because intelligence tests were used to make important decisions about people’s lives, it was almost inevitable that they would become controversial. Today, intelligence tests are widely used in education, business, government, and the military. However, psychologists continue to debate what the tests actually measure and how test results should be used.

A. Early test
Interest in measuring individual differences in mental ability began in the late 19th century. Sir Frances Galton, a British scientist, was among the first to investigate these differences. In his book Hereditary Genius (1869), he compared the accomplishments of people from different generations of prominent English families. No formal measures of intelligence existed at the time, so Galton evaluated each of his subjects on their fame as judged by encyclopedia entries, honors, awards, and similar indicators. He concluded that eminence of the kind he measured ran in families and so had a hereditary component. Believing that some human abilities derived from hereditary factors, Galton founded the eugenics movement, which sought to improve the human species through selective breeding of gifted individuals.

Between 1884 and 1890 Galton operated a laboratory at the South Kensington Museum in London (now the Victoria and Albert Museum) where, for a small fee, people could have themselves measured on a number of physical and psychological attributes. He tried to relate intellectual ability to skills such as reaction time, sensitivity to physical stimuli, and body proportions. For example, he measured the highest and lowest pitch a person could hear and how well a person could detect minute differences between weights, colors, smells, and other physical stimuli. Despite the crude nature of his measurements, Galton was a pioneer in the study of individual differences. His work helped develop statistical concepts and techniques still in use today. He also was the first to advance the idea that intelligence can be quantitatively measured.

In the 1890s American psychologist James McKeen Cattell, who worked with Galton in England, developed a battery of 50 tests that attempted to measure basic mental ability. Like Galton, Cattell focused on measurements of sensory discrimination and reaction times. Cattell’s work—and by association, Galton’s—was unsupported in 1901, when a study showed that the measurements had no correlation with academic achievement in college. Later researchers, however, pointed out that Cattell’s test subjects were limited to Columbia University students, whose high academic performance was not representative of the general population. Better-designed tests given to broader samples have shown that reaction time and processing speed on perceptual tasks do correlate with academic achievement.

B. The Binet-simon test
Alfred Binet, a prominent French psychologist, was the first to develop an intelligence test that accurately predicted academic success. In the late 19th century, the French government began compulsory education for all children. Prior to this time, most schoolchildren came from upper-class families. With the onset of mass education, French teachers had to educate a much more diverse group of children, some of whom appeared mentally retarded or incapable of benefiting from education. Teachers had no way of knowing which of the “slow” students had true learning problems and which simply had behavioral problems or poor prior education. In 1904 the French Ministry of Public Instruction asked Binet and others to develop a method to objectively identify children who would have difficulty with formal education. Objectivity was important so that conclusions about a child’s potential for learning would not be influenced by any biases of the examiner. The government hoped that identifying children with learning problems would allow them to be placed in special remedial classes in which they could profit from schooling. Binet and colleague Théodore Simon took on the job of developing a test to assess each child’s intelligence.

As Binet and Simon developed their test, they found that tests of practical knowledge, memory, reasoning, vocabulary, and problem solving worked better at predicting school success than the kind of simple sensory tests that Galton and Cattell had used. Children were asked, among other tasks, to perform simple commands and gestures, repeat spoken digits, name objects in pictures, define common words, tell how two objects are different, and define abstract terms. Similar items are used in today’s intelligence tests. Binet and Simon published their first test in 1905. Revisions to this test followed in 1908 and 1911.

Binet and Simon assumed that all children follow the same course of intellectual development but develop at different rates. In developing their test, they noted which items were successfully completed by half of seven-year-olds, which items by half of eight-year-olds, and so on. Through these observations they created the concept of mental age. If a 10-year-old child succeeded on the items appropriate for 10-year-olds but could not pass the questions appropriate for 11-year-olds, that child was said to have a mental age of 10. Mental age did not necessarily correspond with chronological age. For example, if a 6-year-old child succeeded on the items intended for 9-year-olds, then that child was said to have a mental age of 9.

To judge how effectively the test predicted academic achievem ent, Binet asked teachers to rate their students from best to worst. The results showed that students who had been rated higher by their teachers also scored higher on the test. Thus, Binet’s test successfully predicted how students would perform in school.

C. The IQ test
Binet’s test was never widely used in France. Henry Goddard, director of a New Jersey school for children with mental retardation, brought it to the United States. Goddard translated the test into English and began using it to test people for mental retardation. Another American psychologist, Lewis Terman, revised the test by adapting some of Binet’s questions, adding questions appropriate for adults, and establishing new standards for average performance at each age. Terman’s first adaptation, published in 1916, was called the Stanford-Binet Intelligence Scale. The name of the test derived from Terman’s affiliation with Stanford University.

Instead of giving a person’s performance on the Stanford-Binet as a mental age, Terman converted performance into a single score, which he called the intelligence quotient, or IQ. A quotient is the number that results from dividing one number by another. The idea of an intelligence quotient was first suggested by German psychologist William Stern in 1912. To compute IQ, Stern divided mental age by the actual, chronological age of the person taking the test and then multiplied by 100 to get rid of the decimal point. For example, if a 6-year-old girl scored a mental age of 9, she would be assigned an IQ of 150 (9/6 × 100). If a 12-year-old boy scored a mental age of 6, he would be given an IQ of 50 (6/12 × 100). The IQ score, as originally computed, expressed a person’s mental age relative to his or her chronological age. Although this formula works adequately for comparing children, it does not work well for adults because intelligence levels off during adulthood. For example, a 40-year-old person who scored the same as the average 20-year-old would have an IQ of only 50.

Modern intelligence tests—including the current Stanford-Binet test—no longer compute scores using the IQ formula. Instead, intelligence tests give a score that reflects how far the person’s performance deviates from the average performance of others who are the same age. Most modern tests arbitrarily define the average score as 100. By convention, many people still use the term IQ to refer to a score on an intelligence test.

D. Creation of group test
During World War I (1914-1918) a group of American psychologists led by Robert M. Yerkes offered to help the United States Army screen recruits using intelligence tests. Yerkes and his colleagues developed two intelligence tests: the Army Alpha exam for literate recruits, and the Army Beta exam for non-English speakers and illiterate recruits. Unlike previous intelligence tests, which required an examiner to test and interact with each person individually, the Army Alpha and Beta exams were administered to large groups of recruits at the same time. The items on the tests consisted of practical, short-answer problems. The Alpha exam included arithmetic problems, tests of practical judgment, tests of general knowledge, synonym-antonym comparisons, number series problems, analogies, and other problems. The Beta exam required recruits to complete mazes, complete pictures with missing elements, recognize patterns in a series, and solve other puzzles. The army assigned letter grades of A through D- based on how many problems the recruit answered correctly. The army considered the highest-scoring recruits as candidates for officer training and rejected the lowest-scoring recruits from military service. By the end of World War I, psychologists had given intelligence tests to approximately 1.7 million recruits. Modern critics have pointed out that the army tests were often improperly administered. For example, different test administrators used different standards to determine which recruits were illiterate and should be assigned to take the nonverbal Beta exam. Thus, some recruits mistakenly assigned to the Alpha exam may have scored poorly because of their limited English skills, not because of low intelligence.

The use of intelligence tests by the United States military enhanced the credibility and visibility of group mental tests. Following World War I these tests grew in popularity. Most were short-answer tests modeled on the army tests or the Stanford-Binet. For example, Yerkes and Terman developed the National Intelligence Test, a group test for schoolchildren, around 1920. The Scholastic Aptitude Test, or SAT, was introduced in 1926 as a multiple-choice exam to aid colleges and universities in their selection of prospective students.

E. Modern intelligence test
The most widely used modern tests of intelligence are the Stanford-Binet, the Wechsler Intelligence Scale for Children (WISC), the Wechsler Adult Intelligence Scale (WAIS), and the Kaufman Assessment Battery for Children (Kaufman-ABC). Each of the tests consists of a series of 10 or more subtests. Subtests are sections of the main test in which all of the items are similar. Examples of subtests include vocabulary (“Define happy”), similarities (“In what way are an apple and pear alike?”), digit span (repeating digit strings of increasing length from memory), information (“Who was the first president of the United States?”), object assembly (putting together puzzles), mazes (tracing a path through a maze), and simple arithmetic problems. Each item has scoring criteria so the examiner can determine if the answer given is correct.

Items on each subtest are given in order of difficulty until the person being tested misses a certain number of items. Each subtest provides a score. The subtest scores are then added together to obtain a total raw score, which is then converted into an IQ score. Some tests, such as the Wechsler tests, give separate verbal and performance (nonverbal) scores as well as an overall score.

Other intelligence tests, like the Peabody Picture Vocabulary Test or Raven’s Progressive Matrices, consist of only one item type. In the Peabody Picture Vocabulary Test, the test taker must define a word by deciding which picture out of four pictures best represents the meaning of the word said by the examiner. In Raven’s Progressive Matrices, a person is shown a matrix of patterns with one pattern missing. The person must figure out the rules governing the patterns and then use these rules to pick the item that best fills in the missing pattern. The Raven’s test was designed to minimize the influence of culture by relying on nonverbal problems that require abstract reasoning and do not require knowledge of a particular culture.

All of the tests mentioned so far can be individually administered. An examiner tests one person at a time for a specific amount of time, ranging from 20 to 90 minutes. There are also group-administered tests. The Army Alpha test described above was one of the earliest group-administered tests. This test developed into what is now known as the Armed Services Vocational Achievement Battery (ASVAB), which is used to select and classify military recruits. Group tests usually are not as reliable as individually administered tests. They are often shorter and have less variety in item types because of restrictions inherent in group administration. Furthermore, the administrator of an individual test can more fully supervise the test taker’s performance. For example, the administrator can make sure the test taker is motivated and provide additional information when necessary. But group tests are efficient because they can be given to large numbers of people in a short time and at a relatively low cost.

Achievement tests and aptitude tests are very similar to intelligence tests. An achievement test is designed to assess what a person has already learned, whereas an aptitude test is designed to predict future performance or assess potential for learning. Usually the items on achievement tests and aptitude tests relate to a specific area of knowledge, such as mathematics or vocabulary. Because intelligence tests frequently include these same areas of knowledge, many experts believe that it is impossible to distinguish between intelligence tests, achievement tests, and aptitude tests. Often, test makers call their tests achievement tests or aptitude tests to avoid the word intelligence, which can be frightening to some test takers. Examples of achievement and aptitude tests that are widely used include the SAT, the Graduate Record Exam (GRE), the California Achievement Test, the Law School Admissions Test (LSAT), and the Medical College Admission Test (MCAT).

F. Standardization, reliabillity, and validity of tests
An intelligence test, like any other psychological test, must meet certain criteria in order to be accepted as scientific and accurate. A test must be standardized, reliable, and valid.

Standardization refers to the process of defining norms of performance to which all test takers are compared. Before an intelligence test can be used to make meaningful comparisons, the test makers first give the test to a sample of the population representative of the individuals for whom the test is designed. This sample of people is called a normative sample, because it is used to establish norms (standards) of performance on the test. Normative samples usually consist of thousands of people from all areas of the country and all strata of society. Test scores of people in the sample are statistically analyzed to compile the test norms. When the test is made available for general use, these norms are used to determine a score for each person who takes the test. The IQ score or overall score reflects how well the person did compared to people of the same age in the normative sample.

Reliability refers to the consistency of test scores. A reliable test yields the same or close to the same score for a person each time it is administered. In addition, alternate forms of the test should produce similar results. By these criteria, modern intelligence tests are highly reliable. In fact, intelligence tests are the most reliable of all psychological tests.

Validity is the extent to which a test predicts what it is designed to predict. Intelligence tests were designed to predict school achievement, and they do that better than they do anything else. For example, IQ scores of elementary school students correlate moderately with their class grades and highly with achievement test scores. IQ tests also predict well the number of years of education that a person completes. The SAT is somewhat less predictive of academic performance in college. Educators note that success in school depends on many other factors besides intelligence, including encouragement from parents and peers, interest, and motivation.

Intelligence tests also correlate with measures of accomplishment other than academic success, such as occupational status, income, job performance, and other measures of vocational success. However, IQ scores do not predict occupational success as well as they predict academic success. Twenty-five percent or less of the individual differences in occupational success are due to IQ. Therefore, a substantial portion of the variability in occupational success—75 percent or more—is due to factors other than intelligence.

Validity also refers to the degree to which a test measures what it is supposed to measure. A valid intelligence test should measure intelligence and not some other capability. However, making a valid intelligence test is not a straightforward task because there is little consensus on a precise definition of intelligence. Lacking such a consensus, test makers usually evaluate validity by determining whether test performance correlates with performance on some other measure assumed to require intelligence, such as achievement in school.
G. Distribution of IQ scores
IQ scores, like many other biological and psychological characteristics, are distributed according to a normal distribution, which forms a normal curve, or bell curve, when plotted on a graph. In a normal distribution, most values fall near the average, and few values fall far above or far below the average. Although raw scores are not exactly normally distributed, test makers derive IQ scores using a formula that forces the scores to conform to the normal distribution. The normal distribution is defined by its mean (average score) and its standard deviation (a measure of how scores are dispersed relative to the mean). Usually the mean of an IQ test is arbitrarily set at 100 with a standard deviation of 15. Other tests use different values. For example, the SAT originally used a mean of 500 and a standard deviation of 100, although these are now recomputed annually.

Because IQs are distributed along a normal curve, a fixed percentage of scores fall between the mean and any standard deviation value. For example, 34 percent of IQ scores fall between the mean and one standard deviation. For a standard IQ distribution with a mean of 100 and a standard deviation of 15, 34 percent of the cases would fall between 100 and 115. Since the normal curve is symmetrical about the mean, 34 percent of the scores would also fall between 85 and 100, which represents one standard deviation below the mean. To interpret the score of any test, it is important to know the mean and standard deviation of the test. Along with knowledge of the standard deviation and the normative sample used for the test, one can then interpret the score in terms of the percentage of the population scoring higher or lower. If a person obtains a score of 115 on an IQ test, approximately 16 percent of the population will score higher and 84 percent will score lower.

When an IQ test is revised, it is restandardized with a new normative sample. The distribution of raw scores in the sample population determines the IQ that will be assigned to the raw scores of others who take the test. By analyzing the performance over the years of different normative samples on the same tests, researchers have concluded that performance on intelligence tests has risen significantly over time. This phenomenon, observed in industrialized countries around the world, is known as the Flynn effect, named after the researcher who discovered it, New Zealand philosopher James Flynn. Scores on some tests have increased dramatically. For example, scores on the Raven’s Progressive Matrices, a widely used intelligence test, increased 15 points in 50 years when scored by the same norms. In other words, a representative sample of the population that took the test in 1992 scored an average of 15 points higher on the test than a representative sample that took the test in 1942.

It appears that people are getting smarter. However, only some tests show these changes. Tests of visual-spatial reasoning, like the Raven’s test, show the largest changes, while vocabulary and verbal tests show almost no change. Some psychologists believe that people are not really getting smarter but are only becoming better test takers. Others believe the score gains reflect real increases in intelligence and speculate they may be due to improved nutrition, better schooling, or even the effects of television and video games on visual-spatial reasoning.

H. Uses of intelligence tests
Intelligence tests and similar tests are widely used in schools, business, government, the military, and medicine. In many cases, intelligence tests are used to avoid the biases more arbitrary methods of selection introduce. For example, it was once common for colleges to admit students whose parents had attended the college or who came from socially prominent families. By using tests, colleges could select students based on their ability instead of their social position.

Intelligence tests were originally designed for use in schools. In elementary and secondary schools, educators use tests to assess how well a student can be expected to perform and to determine if special educational programs are necessary. Intelligence tests can help to identify students with mental retardation and to determine an appropriate educational program for these students (see Education of Students with Mental Retardation). Intelligence tests may also be required for admission into programs for the gifted or talented (see Education of Gifted Students). Institutions of higher education use achievement or aptitude tests, which are very similar to intelligence tests, for the selection and placement of students.

In business, employers frequently use intelligence and aptitude tests to select job applicants. Since World War I, the United States military has had one of the most comprehensive testing programs for selection and job assignment. Anyone entering the military takes a comprehensive battery of tests, including an intelligence test. For specialized and highly skilled jobs in the military, such as jet pilot, the testing is even more rigorous. Intelligence tests are helpful in the selection of individuals for complex jobs requiring advanced skills. The major reason intelligence tests work in job selection is that they predict who will learn new information required for the job. To a lesser extent, they predict who will make “smart” decisions on the job.

In medicine, physicians use intelligence tests to assess the cognitive functioning of patients, such as those with brain damage or degenerative diseases of the nervous system. Psychiatrists and psychologists may use intelligence tests to diagnose the mental capacities of their clients.

I. Criticisms of intelligence tests
Properly used, intelligence tests can provide valuable diagnostic information and insights about intellectual ability that might otherwise be overlooked or ignored. In many circumstances, however, intelligence testing has become extremely controversial, largely because of misunderstandings about how to interpret IQ scores.

1. Validity: One criticism of intelligence tests is that they do not really measure intelligence but only a narrow set of mental capabilities. For example, intelligence tests do not measure wisdom, creativity, common sense, social skills, and practical knowledge—abilities that allow people to adapt well to their surroundings and solve daily problems. The merit of this criticism depends on how one defines intelligence. Some theorists consider wisdom, creativity, and social competence aspects of intelligence, but others do not. Psychologists know little about how to objectively measure these other abilities. Another criticism of IQ tests is that some people may not perform well because they become anxious when taking any timed, standardized test. Their poor performance may reflect their anxiety rather than their true abilities. However, test anxiety is probably not a major cause of incorrect scores.

2. Misintrepretation and misuse: Critics of intelligence testing argue that IQ tests tend to be misinterpreted and misused. Because IQ tests reduce intelligence to a single number, many people mistakenly regard IQ as if it were a fixed, real trait such as height or weight, rather than an abstract concept that was originally designed to predict performance in school. Furthermore, some people view IQ as a measurement of a person’s intrinsic worth or potential, even though many factors other than those measured by IQ tests contribute to life success.

Critics also note that intelligence testing on a large scale can have dangerous social consequences when the results are misused. For example, during the 1920s IQ tests were used to identify “feeble-minded” persons. These persons were then subject to forced sterilization. In the 1927 case Buck v. Bell, the United States Supreme Court upheld the right of states to sterilize individuals judged to be feeble-minded.

In judging the uses of intelligence tests, one must compare how decisions would be made without using the tests. When tests are used to make a decision, there should be evidence that the decision made using the test is better with the test than without it. For example, if schools did not use intelligence or aptitude tests to determine which students need remedial education, teachers would be forced to rely on more subjective and unreliable criteria, such as their personal opinions.

In some cases, institutions use tests when they do not need to. Some colleges and universities require students to take admission tests but then admit 80 percent or more of applicants. Tests are of little use in selection decisions when there is little or no selection. Another criticism of intelligence tests is that they sometimes lead to inflexible cutoff rules. In some states, for example, a person with mental retardation must have an IQ of 50 or below before being allowed to work in a special facility known as a sheltered workshop. Although intelligence is important in determining performance, it is not the only determinant. People with an IQ of 50 vary widely in their skills and abilities. Using an arbitrary cutoff of 50 can make it difficult for people whose IQ is 51 to get essential services.

3. Bias: Psychologists have long known that ethnic and racial groups differ in their average scores on intelligence tests. For example, African Americans as a group consistently average 15 points lower than whites on IQ tests. Such differences between groups have led some people to believe that intelligence tests are culturally biased. Many kinds of test items appear to require specialized information that might be more familiar to some groups than to others. Defenders of IQ tests argue, however, that these same ethnic group differences appear on test items in which cultural content has been reduced.

The question of bias in tests has led intelligence researchers to define bias very precisely and find ways of explicitly assessing it. An intelligence test free of bias should predict academic performance equally well for African Americans, Hispanics, whites, men, women, and any other subgroups in the population. Based on this definition of bias, experts agree that intelligence tests in wide use today have little or no bias for any groups that have been assessed. Many psychologists believe that group differences in performance exist not because of inherent flaws in the tests, but because the tests merely reflect social and educational disadvantages experienced by members of certain racial and ethnic groups in school and other settings. For more information on IQ differences between groups, see the Racial and Ethnic Differences section of this article.

Because they are used for educational and employment testing, tests have been challenged in many court cases. In the 1979 case Larry P. v. Wilson Riles, a group of black parents in California argued that intelligence tests were racially biased. As evidence they cited the fact that black children were disproportionately represented in special education classes. Placement in these classes depended in part on the results of IQ tests. A federal judge hearing the case concluded that the tests were biased and should not be used to place black children in special education. The judge also ordered the state of California to monitor and eliminate disproportionate placement of black children in special education classes. In a 1980 case, PASE v. Hanon, brought in Chicago on the same grounds, a federal judge ruled that the IQ tests being used were not biased (except for a few items). In employment cases, a number of rulings have specified how tests can be used. For example, it is not legal to test applicants for an ability that is not required to do the job.

THEORIES OF INTELLIGENCE
Scholars have tried to understand the nature of intelligence for many years, but they still do not agree on a single theory or definition. Some theorists try to understand intelligence by analyzing the results of intelligence tests and identifying clusters of abilities. Other theorists believe that intelligence encompasses many abilities not captured by tests. In recent years, some psychologists have tried to explain intelligence from a biological standpoint.
A. GENERAL INTELLIGNCE
Efforts to explain intelligence began even before Binet and Simon developed the first intelligence test. In the early 1900s British psychologist Charles Spearman made an important observation that has influenced many later theories of intelligence: He noted that all tests of mental ability were positively correlated. Correlation is the degree to which two variables are associated and vary together (see Psychology: Correlational Studies). Spearman found that individuals who scored high on any one of the mental tests he gave tended to score high on all others. Conversely, people who scored low on any one mental test tended to score low on all others.

Spearman reasoned that if all mental tests were positively correlated, there must be a common variable or factor producing the positive correlations. In 1904 Spearman published a major article about intelligence in which he used a statistical method to show that the positive correlations among mental tests resulted from a common underlying factor. His method eventually developed into a more sophisticated statistical technique known as factor analysis. Using factor analysis, it is possible to identify clusters of tests that measure a common ability.

Based on his factor analysis, Spearman proposed that two factors could account for individual differences in scores on mental tests. He called the first factor general intelligence or the general factor, represented as g. According to Spearman, g underlies all intellectual tasks and mental abilities. The g factor represented what all of the mental tests had in common. Scores on all of the tests were positively correlated, Spearman believed, because all of the tests drew on g. The second factor Spearman identified was the specific factor, or s. The specific factor related to whatever unique abilities a particular test required, so it differed from test to test. Spearman and his followers placed much more importance on general intelligence than on the specific factor.

Throughout his life, Spearman argued that g, as he had mathematically defined it using factor analysis, was really what scientists should mean by intelligence. He was also aware that his mathematical definition of general intelligence did not explain what produced g. In the 1920s he suggested that g measured a mental “power” or “energy.” Others who have continued to investigate g speculate that it may relate to neural efficiency, neural speed, or some other basic properties of the brain.
B. PRIMARY MENTAL ABILITIES
Much of the research on mental abilities that followed Spearman consisted of challenges to his basic position. In the early 20th century, a number of psychologists produced alternatives to Spearman’s two-factor theory by using different methods of factor analysis. These researchers identified group factors, specific abilities thought to underlie particular groups of test items. For example, results from tests of vocabulary and similarities (“How are an apple and orange alike?”) tend to correlate with each other but not with tests of spatial ability. Both the vocabulary and similarities tests contain verbal content, so psychologists might identify a verbal factor based on the correlation between the tests. Although most psychologists agreed that specialized abilities or group factors existed, they debated the number of factors and whether g remained as an overall factor.

In 1938 American psychologist Louis L. Thurstone proposed that intelligence was not one general factor, but a small set of independent factors of equal importance. He called these factors primary mental abilities. To identify these abilities, Thurstone and his wife, Thelma, devised a set of 56 tests. They administered the battery of tests to 240 college students and analyzed the resulting test scores with new methods of factor analysis that Thurstone had devised. Thurstone identified seven primary mental abilities: (1) verbal comprehension, the ability to understand word meanings; (2) verbal fluency, or speed with verbal material, as in making rhymes; (3) number, or arithmetic, ability; (4) memory, the ability to remember words, letters, numbers, and images; (5) perceptual speed, the ability to quickly distinguish visual details and perceive similarities and differences between pictured objects; (6) inductive reasoning, or deriving general ideas and rules from specific information; and (7) spatial visualization, the ability to mentally visualize and manipulate objects in three dimensions.

Others who reanalyzed Thurstone’s results found two problems with his conclusions. First, Thurstone used only college students as subjects in his research. College students perform better on intelligence tests than do individuals in the general population, so Thurstone’s subjects did not represent the full range of intellectual ability. By restricting the range of ability in his sample, he drastically reduced the size of the correlations between tests. These low correlations contributed to his conclusion that no general intelligence factor existed. To understand why restricting the range of ability reduces the size of correlations, consider an analogy. Most people would agree that in basketball, height is important in scoring. But in the National Basketball Association (NBA), the correlation between players’ scoring and heights is zero. The reason is that NBA players are heavily selected for their height and average 15 cm (6 in) taller than the average height in the general population. When Thurstone gave his tests to a more representative sample of the population, he found larger correlations among his tests than he had found using only college students.

A second problem with Thurstone’s results was that, even in college students, the tests that Thurstone used were still correlated. The method of factor analysis that Thurstone had devised made the correlations harder to identify. When other researchers reanalyzed his data using other methods of factor analysis, the correlations became apparent. The researchers concluded that Thurstone’s battery of tests identified the same g factor that Spearman had identified.

C. FLUID INTELLIGENCE AND CRYSTALLIZED INTELLIGENCE
In the 1960s American psychologists Raymond Cattell and John Horn applied new methods of factor analysis and concluded there are two kinds of general intelligence: fluid intelligence (gf) and crystallized intelligence (gc). Fluid intelligence represents the biological basis of intelligence. Measures of fluid intelligence, such as speed of reasoning and memory, increase into adulthood and then decline due to the aging process. Crystallized intelligence, on the other hand, is the knowledge and skills obtained through learning and experience. As long as opportunities for learning are available, crystallized intelligence can increase indefinitely during a person’s life. For example, vocabulary knowledge is known to increase in college professors throughout their life span.

In addition to identifying the two subtypes of general intelligence, Cattell also developed what he called investment theory. This theory sought to explain how an investment of biological endowments (fluid intelligence) could contribute to learned skills and knowledge (crystallized intelligence). As one might expect, it is very difficult to separate the biological basis of intelligence from what is learned. As Cattell was aware, nearly all mental tests draw on both crystallized and fluid intelligence. Consequently, crystallized and fluid abilities are correlated with each other. Some researchers interpret this correlation between the two factors as evidence of Spearman’s factor of general intelligence, g. They see Cattell’s theory as a refinement of Spearman’s original theory, not a departure from it.

D. MULTIPLE INTELLIGENCE
In 1983 American psychologist Howard Gardner proposed a theory that sought to broaden the traditional definition of intelligence. He felt that the concept of intelligence, as it had been defined by mental tests, did not capture all of the ways humans can excel. Gardner argued that we do not have one underlying general intelligence, but instead have multiple intelligences, each part of an independent system in the brain.

In formulating his theory, Gardner placed less emphasis on explaining the results of mental tests than on accounting for the range of human abilities that exist across cultures. He drew on diverse sources of evidence to determine the number of intelligences in his theory. For example, he examined studies of brain-damaged people who had lost one ability, such as spatial thinking, but retained another, such as language. The fact that two abilities could operate independently of one another suggested the existence of separate intelligences. Gardner also proposed that evidence for multiple intelligences came from prodigies and savants. Prodigies are individuals who show an exceptional talent in a specific area at a young age, but who are normal in other respects. Savants are people who score low on IQ tests—and who may have only limited language or social skills—but demonstrate some remarkable ability, such as extraordinary memory or drawing ability. To Gardner, the presence of certain high-level abilities in the absence of other abilities also suggested the existence of multiple intelligences.

Gardner initially identified seven intelligences and proposed a person who exemplified each one. Linguistic intelligence involves aptitude with speech and language and is exemplified by poet T. S. Eliot. Logical-mathematical intelligence involves the ability to reason abstractly and solve mathematical and logical problems. Physicist Albert Einstein is a good example of this intelligence. Spatial intelligence is used to perceive visual and spatial information and to conceptualize the world in tasks like navigation and in art. Painter Pablo Picasso represents a person of high spatial intelligence. Musical intelligence, the ability to perform and appreciate music, is represented by composer Igor Stravinsky. Bodily-kinesthetic intelligence is the ability to use one’s body or portions of it in various activities, such as dancing, athletics, acting, surgery, and magic. Martha Graham, the famous dancer and choreographer, is a good example of bodily-kinesthetic intelligence. Interpersonal intelligence involves understanding others and acting on that understanding and is exemplified by psychiatrist Sigmund Freud. Intrapersonal intelligence is the ability to understand one’s self and is typified by the leader Mohandas Gandhi. In the late 1990s Gardner added an eighth intelligence to his theory: naturalist intelligence, the ability to recognize and classify plants, animals, and minerals. Naturalist Charles Darwin is an example of this intelligence. According to Gardner, each person has a unique profile of these intelligences, with strengths in some areas and weaknesses in others.

Gardner’s theory found rapid acceptance among educators because it suggests a wider goal than traditional education has adopted. The theory implies that traditional school training may neglect a large portion of human abilities, and that students considered slow by conventional academic measures might excel in other respects. A number of schools have formed with curriculums designed to assess and develop students’ abilities in all of the intelligences Gardner identified.

Critics of the multiple intelligences theory have several objections. First, they argue that Gardner based his ideas more on reasoning and intuition than on empirical studies. They note that there are no tests available to identify or measure the specific intelligences and that the theory largely ignores decades of research that show a tendency for different abilities to correlate—evidence of a general intelligence factor. In addition, critics argue that some of the intelligences Gardner identified, such as musical intelligence and bodily-kinesthetic intelligence, should be regarded simply as talents because they are not usually required to adapt to life demands.

E. TRIARCHIC THEORY OF INTELLIGENCE
In the 1980s American psychologist Robert Sternberg proposed a theory of intelligence that, like Gardner’s theory of multiple intelligences, attempted to expand the traditional conception of intelligence. Sternberg noted that mental tests are often imperfect predictors of real-world performance or success. People who do well on tests sometimes do not do as well in real-world situations. According to Sternberg’s triarchic (three-part) theory of intelligence, intelligence consists of three main aspects: analytic intelligence, creative intelligence, and practical intelligence. These are not multiple intelligences as in Gardner’s theory, but interrelated parts of a single system. Thus, many psychologists regard Sternberg’s theory as compatible with theories of general intelligence.

Analytic intelligence is the part of Sternberg’s theory that most closely resembles the traditional conception of general intelligence. Analytic intelligence is skill in reasoning, processing information, and solving problems. It involves the ability to analyze, evaluate, judge, and compare. Analytic intelligence draws on basic cognitive processes or components.

Creative intelligence is skill in using past experiences to achieve insight and deal with new situations. People high in creative intelligence are good at combining seemingly unrelated facts to form new ideas. According to Sternberg, traditional intelligence tests do not measure creative intelligence, because it is possible to score high on an IQ test yet have trouble dealing with new situations.

Practical intelligence relates to people’s ability to adapt to, select, and shape their real-world environment. It involves skill in everyday living (“street smarts”) and in adapting to life demands, and reflects a person’s ability to succeed in real-world settings. An example given by Sternberg of practical intelligence is of an employee who loved his job but hated his boss. An executive recruiter contacted the employee about a possible new job. Instead of applying for the job, the employee gave the recruiter the name of his boss, who was subsequently hired away from the company. By getting rid of the boss he hated instead of leaving the job he loved, the employee showed adaptation to his real-world environment. People with high practical intelligence may or may not perform well on standard IQ tests.

In Sternberg’s view, “successfully intelligent” people are aware of their strengths and weaknesses in the three areas of intelligence. They figure out how to capitalize on their strengths, compensate for their weaknesses, and further develop their abilities in order to achieve success in life.

Sternberg’s theory has drawn praise because it attempts to broaden the domain of intelligence to more exactly correspond to what people frequently think intelligence is. On the other hand, some critics believe that scientific studies do not support Sternberg’s proposed triarchic division. For example, some propose that practical intelligence is not a distinct aspect of intelligence, but a set of abilities predicted by general intelligence.

F. OTHER APPROACHES
Many researchers have taken new approaches to understanding intelligence based on advances in the neurological, behavioral, and cognitive sciences. Some studies have found that differences in IQ correspond with various neurological measures. For example, adults with higher IQs tend to show somewhat different patterns of electrical activity in the brain than do people with lower IQs. In addition, PET (positron emission tomography) scans show that adults with higher IQs have lower rates of metabolism for cortical glucose as they work on relatively difficult reasoning problems than people with lower IQs. That is, people with higher IQs seem to expend less energy in solving difficult problems than those with lower IQs. Other researchers have sought to understand human intelligence by using the computer as a metaphor for the mind and studying how artificial intelligence computer programs relate to human information processing. These new approaches are extremely promising, but their ultimate value has yet to be determined.

In recent years a number of theorists have proposed the existence of emotional intelligence that is complementary to the type of intelligence measured by IQ tests. American psychologists Peter Salovey and John Mayer, who together introduced the concept in 1990, define emotional intelligence as the ability to perceive, understand, express, and regulate emotions. Emotionally intelligent people can use their emotions to guide thoughts and behavior and can accurately read others’ emotions. Daniel Goleman, an American author and journalist, popularized the concept in his book Emotional Intelligence (1995). He expanded the concept to include general social competence.

An American psychologist, Douglas Detterman, has compared general intelligence to a complex system, like a university, city, or country. In this view, IQ tests provide a global rating reflective of the many cognitive processes and learning experiences that compose intelligence, just as a rating of a university is based on an evaluation of its components, such as library size, faculty quality, and size of endowment. Mental tests tend to correlate with each other because they are part of a unified system that works together. The implication of this theory is that understanding general intelligence will require understanding how the cognitive processes of the brain actually work.

INFLUENCE OF HEREDITY AND ENVIRONMENT
Few topics in the social sciences have produced more controversy than the relative influences of nature and nurture on intelligence. Is intelligence determined primarily by heredity or by one’s environment?

The issue has aroused intense debate because different views on the heritability of intelligence lead to different social and political implications. The strictest adherents of a genetic view of intelligence believe that every person is born with a fixed amount of intelligence. They argue that there is little one can do to improve intelligence, so special education programs should not be expected to produce increases in IQ. On the other hand, those who see intelligence as determined mostly by environmental factors see early intervention programs as critical to compensate for the effects of poverty and other disadvantages. In their view, these programs help to create equal opportunities for all people. Perhaps the most controversial issue surrounding intelligence has been the assertion by some people that genetic factors are responsible not only for differences in IQ between individuals, but also for differences between groups. In this view, genetic factors account for the poorer average performance of certain racial and ethnic groups on IQ tests. Others regard genetic explanations for group differences as scientifically indefensible and view as racist the implication that some racial groups are innately less intelligent than others.

Today, almost all scientists agree that intelligence arises from the influence of both genetic and environmental factors. Careful study is required in order to attribute any influence to either environment or heredity. For example, one measure commonly used to assess a child’s home environment is the number of books in the home. But having many books in the home may be related to the parents’ IQ, because highly intelligent people tend to read more. The child’s intelligence may be due to the parents’ genes or to the number of books in the home. Further, parents may buy more books in response to their child’s genetically influenced intelligence. Which of these possibilities is correct cannot be determined without thorough studies of all the factors involved.
A. GENETIC INFLUENCES
In behavioral genetics, the heritability of a trait refers to the proportion of the trait’s variation within a population that is attributable to genetics. The heritability of intelligence is usually defined as the proportion of the variation in IQ scores that is linked to genetic factors. To estimate the heritability of intelligence, scientists compare the IQs of individuals who have differing degrees of genetic relationship. Scientists have conducted hundreds of studies, involving tens of thousands of participants, that have sought to measure the heritability of intelligence. The generally accepted conclusion from these studies is that genetic factors account for 40 to 80 percent of the variability in intelligence test scores, with most experts settling on a figure of approximately 50 percent. But heritability estimates apply only to populations and not to individuals. Therefore, one can never say what percentage of a specific individual’s intelligence is inherited based on group heritabilities alone.

Although any degree of genetic relationship can and has been studied, studies of twins are particularly informative. Identical twins develop from one egg and are genetically identical to each other. Fraternal twins develop from separate eggs and, like ordinary siblings, have only about half of their genes in common. Comparisons between identical and fraternal twins can be very useful in determining heritability. Scientists have found that the IQ scores of identical twins raised together are remarkably similar to each other, while those of fraternal twins are less similar to each other. This finding suggests a genetic influence in intelligence. Interestingly, fraternal twins’ IQ scores are more similar to each other than those of ordinary siblings, a finding that suggests environmental effects. Some researchers account for the difference by noting that fraternal twins are probably treated more alike than ordinary siblings because they are the same age.

Some of the strongest evidence for genetic influences in intelligence comes from studies of identical twins adopted into different homes early in life and thus raised in different environments. Identical twins are genetically identical, so any differences in their IQ scores must be due entirely to environmental differences and any similarities must be due to genetics. Results from these studies indicate that the IQ scores of identical twins raised apart are highly similar—nearly as similar as those of identical twins raised together. For adoption studies to be valid, placement of twin pairs must be random. If brighter twin pairs are selectively placed in the homes of adoptive parents with higher intelligence, it becomes impossible to separate genetic and environmental influences.

Another way of studying the genetic contribution to intelligence is through adoption studies, in which researchers compare adopted children to their biological and adoptive families. Adopted children have no genetic relationship to their adoptive parents or to their adoptive parents’ biological children. Thus, any similarity in IQ between the adopted children and their adoptive parents or the parents’ biological children must be due to the similarity of the environment they all live in, and not to genetics.

There are two interesting findings from studies of adopted children. First, the IQs of adopted children have only a small relationship to the IQs of their adoptive parents and the parents’ biological children. Second, after the adopted child leaves home, this small relationship becomes smaller. In general, the IQs of adopted children are always more similar to their biological parents’ IQs than to their adoptive parents’ IQs. Further, once they leave the influence of their adoptive home, they become even more similar to their biological parents. Both of these findings suggest the importance of hereditary factors in intelligence.

People sometimes assume that if intelligence is highly heritable, then it cannot be changed or improved through environmental factors. This assumption is incorrect. For example, height has very high heritability, yet average heights have increased in the 20th century among the populations of many industrialized nations, most likely because of improved nutrition and health care. Similarly, performance on IQ tests has increased with each generation (see the Distribution of IQ Scores section of this article), yet few scientists attribute this phenomenon to genetic changes. Thus, many experts believe that improved environments can, to some degree, increase a person’s intelligence.

Some genetic disorders, such as phenylketonuria (PKU) and Down syndrome, may result in mental retardation and low IQ. But evidence for genetic influences should not be interpreted as evidence of a direct connection between genes and intelligence. In PKU, for example, a rare combination of recessive genes sets the stage for a series of biochemical interactions that ultimately results in low IQ. These interactions only occur, however, in the presence of the amino acid phenylalanine. If the disorder is detected early and phenylalanine is withheld from the infant’s diet, then large IQ deficits do not develop.
B. ENVIRONMENTAL INFLUENCES
If genetic influences account for between 40 and 80 percent of the variation in intelligence, then environmental influences account for between 20 and 60 percent of the total variation. Environmental factors comprise all the stimuli a person encounters from conception to death, including food, cultural information, education, and social experiences. Although it is known that environmental factors can be potent forces in shaping intelligence, it is not understood exactly how they contribute to intelligence. In fact, scientists have identified few specific environmental variables that have direct, unambiguous effects on intelligence. Many environmental variables have small effects and differ in their effect on each person, making them difficult to identify.

Schooling is an important factor that affects intelligence. Children who do not attend school or who attend intermittently score more poorly on IQ tests than those who attend regularly, and children who move from low-quality schools to high-quality schools tend to show improvements in IQ. Besides transmitting information to students directly, schools teach problem solving, abstract thinking, and how to sustain attention—all skills required on IQ tests.

Many researchers have investigated whether early intervention programs can prevent the lowered intelligence that may result from poverty or other disadvantaged environments. In the United States, Head Start is a federally funded preschool program for children from families whose income is below the poverty level. Head Start and similar programs in other countries attempt to provide children with activities that might enhance cognitive development, including reading books, learning the alphabet and the numbers, learning the names of colors, drawing, and other activities. These programs often have large initial effects on IQ scores. Children who participate gain as much as 15 IQ points compared to control groups of similar children not in the program. Unfortunately, these gains seem to last only as long as the intervention lasts. When children from these programs enter school, their IQ declines to the level of control groups over a period of several years. This has come to be known as the “fade-out” effect.

Even though early intervention preschool programs do not seem to produce lasting IQ gains, some studies suggest they may have other positive long-term effects. For example, the Consortium for Longitudinal Studies reported that participants are less likely to repeat grades, less likely be placed in remedial classes, and more likely to finish high school than comparable nonparticipants—even though both groups show about the same levels of academic achievement. Preschoolers in early intervention programs may also benefit from improved health and nutrition, and their mothers may sometimes benefit from additional education that the programs provide. Because a substantial portion of the variation in intelligence is due to environmental factors, early intervention programs should be able to produce significant and lasting IQ gains once the specific environmental variables that influence IQ have been identified. Researchers continue to search for the interventions that will increase IQ and, ultimately, academic achievement.

Two environmental variables known to affect intelligence are family size and birth order. Children from smaller families and children who are earlier-born in their families tend to have higher intelligence test scores. These effects, however, are very small and amount to only a few IQ points. They are detectable only when researchers study very large numbers of families.

Although there has been substantial debate about the effects of other environmental variables, certain substances in the prenatal environment may influence later intelligence. For example, some pregnant women who consume large amounts of alcohol give birth to children with fetal alcohol syndrome, a condition marked by physical abnormalities, mental retardation, and behavioral problems. Even exposure to moderate amounts of alcohol may have some negative influence on the development of intelligence, and to date no safe amount of alcohol has been established for pregnant women. Scientists have also discovered that certain substances encountered during infancy or childhood may have negative affects on intelligence. For example, children with high blood levels of lead, as a result of breathing lead-contaminated air or eating scraps of lead-based paint, tend to have lower IQ scores. Prolonged malnutrition during childhood also seems to influence IQ negatively. In each of these cases, a correlation exists between environmental factors and measured intelligence, but one cannot conclude that these factors directly influence intelligence. Other environmental variables in this category include parenting styles and the physical environment of the home.

Although the nature-nurture debate has raged for some time, research points to a conclusion that appeals to common sense: Intelligence is about half due to nature (heredity) and about half due to nurture (environment). The exact mechanisms by which genetic and environmental factors operate remain unknown. Identifying the specific biological and environmental variables that affect intelligence is one of the most important challenges facing researchers in this field.
C. SEX DIFFERENCES
Are women smarter or are men smarter? Psychologists have studied sex differences in intelligence since the beginning of intelligence testing. The question is a very complicated one, though. One problem is that test makers sometimes eliminate questions that show differences between males and females to eliminate bias from the test. Intelligence tests, therefore, may not show gender differences even if they exist. Even when gender differences have been explicitly studied, they are hard to detect because they tend to be small.

There appear to be no substantial differences between men and women in average IQ. But the distribution of IQ scores is slightly different for men than for women. Men tend to be more heavily represented at the extremes of the IQ distribution. Men are affected by mental retardation more frequently than are women, and they also outnumber women at very high levels of measured intelligence. Women’s scores are more closely clustered around the mean.

Although there are no differences in overall IQ test performance between men and women, there do seem to be differences in some more specialized abilities. Men, on average, perform better on tests of spatial ability than do women. Spatial ability is the ability to visualize spatial relationships and to mentally manipulate objects. The reason for this difference is unknown. Some psychologists speculate that spatial ability evolved more in men because men were historically hunters and required spatial ability to track prey and find their way back from hunting forays. Others believe that the differences result from parents’ different expectations of boys’ and girls’ abilities.

Many studies have examined whether gender differences exist in mathematical ability, but the results have been inconsistent. In 1990 American researchers statistically combined the results of more than 100 studies on gender differences in mathematics using a technique known as meta-analysis. They found no significant differences in the average scores of males and females on math tests. Research also indicates that the average girl’s grades in mathematics courses equal or exceed those of the average boy. Other studies have found that boys and girls perform equally well on math achievement tests during elementary school, but that girls begin to fall behind boys in later years. For example, male high school seniors average about 45 points higher on the math portion of the SAT than do females.

A 1995 study examined the performance of more than 100,000 American adolescents on various mental tests. The study found that on average, females performed slightly better than males on tests of reading comprehension, writing, perceptual speed, and certain memory tasks. Males tended to perform slightly better than girls on tests of mathematics, science, and social studies. In almost all cases, the average sex differences were small.

Are differences in abilities between men and women biologically based or are they due to cultural influences? There is some evidence on both sides. On the biological side, researchers have studied androgenized females, individuals who are genetically female but were exposed to high levels of testosterone, a male hormone, during their gestation. As these individuals grow up, they are culturally identified as female, but they tend to play with “boys’ toys,” like blocks and trucks, and have higher levels of spatial ability than females who were not exposed to high levels of testosterone. Further evidence for a biological basis for spatial gender differences comes from comparisons of the brains of men and women. Even when corrected for body size, males tend to have slightly larger brains than females. Some scientists speculate that this extra brain volume in males may be devoted to spatial ability.

On the cultural side, many social scientists argue that differences in abilities between men and woman arise from society’s different expectations of them and from their different experiences. Girls do not participate as extensively as boys do in cultural activities thought to increase spatial and mathematical ability. As children, girls are expected to play with dolls and other toys that develop verbal and social skills while boys play with blocks, video games, and other toys that encourage spatial visualization. Later, during adolescence, girls take fewer math and science courses than boys, perhaps because of stereotypes of math and science as masculine subjects and because of less encouragement from teachers, peers, and parents. Many social scientists believe cultural influences account for the relatively low representation of women in the fields of mathematics, engineering, and the physical sciences.

It is important to remember that sex differences, where they exist, represent average differences between men and women as groups, not individuals. Knowing whether an individual is female or male reveals little about that person’s intellectual abilities.

D. RACIAL AND ETHNIC DIFFERENCES
Numerous studies have found differences in measured IQ between different self-identified racial and ethnic groups. For example, many studies have shown that there is about a 15-point IQ difference between African Americans and whites, in favor of whites. The mean scores of IQ scores of the various Hispanic American subgroups fall roughly midway between those for blacks and whites. Although these differences are substantial, there are much larger differences between people within each group than between the means of the groups. This large variability within groups means that a person’s racial or ethnic identification cannot be used to infer his or her intelligence.

The debate about racial and ethnic differences in IQ scores is not about if the differences exist but what causes them. In 1969 Arthur Jensen, a psychology professor at the University of California at Berkeley, ignited the modern debate over racial differences. Jensen published a controversial article in which he argued that black-white differences in IQ scores might be due to genetic factors. Further, he argued that if IQ had a substantial genetic component, remedial education programs to improve IQ should not be expected to raise IQ as they were currently being applied. In 1994 American psychologist Richard Herrnstein and American social analyst Charles Murray renewed the debate with the publication of The Bell Curve (1994). Although only a small portion of the book was devoted to race differences, that portion of the book received the most attention in the popular press. Among other arguments, Herrnstein and Murray suggested it was possible that at least some of the racial differences in average IQ were due to genetic factors. Their arguments provoked heated debates in academic communities and among the general public.

As discussed earlier, research supports the idea that differences in measured intelligence between individuals are partly due to genetic factors. However, psychologists agree that this conclusion does not imply that genetic factors contribute to differences between groups. No one knows exactly what causes racial and ethnic differences in IQ scores. Some scientists maintain that these differences are in part genetically based. Supporters of this view believe that racial and ethnic groups score differently on intelligence tests partly because of genetic differences between the groups. Others think the cause is entirely environmental. In this view, certain racial and ethnic groups do poorer on IQ tests because of cultural and social factors that put them at a disadvantage, such as poverty, less access to good education, and prejudicial attitudes that interfere with learning. Representing another perspective, many anthropologists reject the concept of biological race, arguing that races are socially constructed categories with little scientific basis (see Race). Because of disagreements about the origins of group differences in average IQ, conclusions about these differences must be evaluated cautiously.

Some research indicates that the black-white differential in IQ scores might be narrowing. Several studies have found that the difference in average IQ scores between African Americans and whites has shrunk to 10 points or less, although research has not established this trend clearly. The National Assessment of Educational Progress, a national longitudinal study of academic achievement, also shows that the performance of African Americans on math and science achievement tests improved between 1970 and 1996 when compared to whites.

Educators and researchers have focused much attention on explaining why some ethnic groups perform more poorly than others on measures of intelligence and academic achievement. Another topic of research is why some ethnic groups, particularly Asian Americans, perform so well academically. Compared to other groups, Asian American students get better grades, score higher on math achievement and aptitude tests, and are more likely to graduate from high school and college. The exact reasons for their high academic performance are unknown. One explanation points to Asian cultural values and family practices that place central importance on academic achievement and link success in school with later occupational success. Critics counter that this explanation does not explain why Asian Americans excel in specific kinds of abilities.

The academic and occupational successes of Asian Americans have caused many people to presume Asian Americans have higher-than-average IQs. However, most studies show no difference between the average IQ of Asian Americans and that of the general population. Some studies of Asians in Asia have found a 3 to 7 point IQ difference between Asians and whites, in favor of Asians, but other studies have found no significant differences.

REFLEX ACTION

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Of the many kinds of neural activity, there is one simple kind in which a stimulus leads to an immediate action. This is reflex activity. The word reflex (from Latin reflexus, “reflection”) was introduced into biology by a 19th-century English neurologist, Marshall Hall, who fashioned the word because he thought of the muscles as reflecting a stimulus much as a wall reflects a ball thrown against it. By reflex, Hall meant the automatic response of a muscle or several muscles to a stimulus that excites an afferent nerve. The term is now used to describe an action that is an inborn central nervous system activity, not involving consciousness, in which a particular stimulus, by exciting an afferent nerve, produces a stereotyped, immediate response of muscle or gland.

The anatomical pathway of a reflex is called the reflex arc. It consists of an afferent (or sensory) nerve, usually one or more interneurons within the central nervous system, and an efferent (motor, secretory, or secreto-motor) nerve.

Most reflexes have several synapses in the reflex arc. The stretch reflex is exceptional in that, with no interneuron in the arc, it has only one synapse between the afferent nerve fibre and the motor neuron. The flexor reflex, which removes a limb from a noxious stimulus, has a minimum of two interneurons and three synapses.

Probably the best-known reflex is the pupillary light reflex. If a light is flashed near one eye, the pupils of both eyes contract. Light is the stimulus; impulses reach the brain via the optic nerve; and the response is conveyed to the pupillary musculature by autonomic nerves that supply the eye. Another reflex involving the eye is known as the lacrimal reflex. When something irritates the conjunctiva or cornea of the eye, the lacrimal reflex causes nerve impulses to pass along the fifth cranial nerve (trigeminal) and reach the midbrain. The efferent limb of this reflex arc is autonomic and mainly parasympathetic. These nerve fibres stimulate the lacrimal glands of the orbit, causing the outpouring of tears. Other reflexes of the midbrain and medulla oblongata are the cough and sneeze reflexes. The cough reflex is caused by an irritant in the trachea and the sneeze reflex by one in the nose. In both, the reflex response involves many muscles; this includes a temporary lapse of respiration in order to expel the irritant.

The first reflexes develop in the womb. By seven and a half weeks after conception, the first reflex can be observed; stimulation around the mouth of the fetus causes the lips to be turned toward the stimulus. By birth, sucking and swallowing reflexes are ready for use. Touching the baby's lips induces sucking, and touching the back of its throat induces swallowing.

Although the word stereotyped is used in the above definition, this does not mean that the reflex response is invariable and unchangeable. When a stimulus is repeated regularly, two changes occur in the reflex response—sensitization and habituation. Sensitization is an increase in response; in general, it occurs during the first 10 to 20 responses. Habituation is a decrease in response; it continues until, eventually, the response is extinguished. When the stimulus is irregularly repeated, habituation does not occur or is minimal.

There are also long-term changes in reflexes, which may be seen in experimental spinal cord transections performed on kittens. Repeated stimulation of the skin below the level of the lesion, such as rubbing the same area for 20 minutes every day, causes a change in latency (the interval between the stimulus and the onset of response) of certain reflexes, with diminution and finally extinction of the response. Although this procedure takes several weeks, it shows that, with daily stimulation, one reflex response can be changed into another. Repeated activation of synapses increases their efficiency, causing a lasting change. When this repeated stimulation ceases, synaptic functions regress, and reflex responses return to their original form.

Although a reflex response is said to be rapid and immediate, some reflexes, called recruiting reflexes, can hardly be evoked by a single stimulus. Instead, they require increasing stimulation to induce a response. The reflex contraction of the bladder, for example, requires an increasing amount of urine to stretch the muscle and to obtain muscular contraction.

Reflexes can be altered by impulses from higher levels of the central nervous system. For example, the cough reflex can be suppressed easily, and even the gag reflex (the movements of incipient vomiting resulting from mechanical stimulation of the wall of the pharynx) can be suppressed with training.

The so-called conditioned reflexes are not reflexes at all but complicated acts of learned behaviour. Salivation is one such conditioned reflex; it occurs only when a person is conscious of the presence of food or when one imagines food.

PHYSIOLOGY OF REFLEX
Many reflexes of placental mammals appear to be innate. They are hereditary and are a common feature of the species and often of the genus. Reflexes include not only such simple acts as chewing, swallowing, blinking, the knee jerk, and the scratch reflex, but also stepping, standing, and mating. Built up into complex patterns of many coordinated muscular actions, reflexes form the basis of much instinctive behaviour in animals.

Humans also exhibit a variety of innate reflexes, which are involved with the adjustment of the musculature for optimum performance of the distance receptors (i.e., eye and ear), with the orientation of parts of the body in spatial relation to the head, and with the management of the complicated acts involved in ingesting food. Among the innate reflexes involving just the eyes, for example, are: (1) paired shifting of the eyeballs, often combined with turning of the head, to perceive an object in the field of vision; (2) contraction of the intraocular muscles to adjust the focus of the retina for the viewing of near or far objects; (3) constriction of the pupil to reduce excessive illumination of the retina; and (4) blinking due to intense light or touching of the cornea.

In its simplest form, a reflex is viewed as a function of an idealized mechanism called the reflex arc. The primary components of the reflex arc are the sensory-nerve cells (or receptors) that receive stimulation, in turn connecting to other nerve cells that activate muscle cells (or effectors), which perform the reflex action. In most cases, however, the basic physiological mechanism behind a reflex is more complicated than the reflex arc theory would suggest. Additional nerve cells capable of communicating with other parts of the body (beyond the receptor and effector) are present in reflex circuits. As a result of the integrative action of the nervous system in higher organisms, behaviour is more than the simple sum of their reflexes; it is a unitary whole that exhibits coordination between many individual reflexes and is characterized by flexibility and adaptability to circumstances. Many automatic, unconditioned reflexes can thus be modified by or adapted to new stimuli, making possible the conditioning of reflex responses. The experiments of the Russian physiologist Ivan Petrovich Pavlov, for example, showed that if an animal salivates at the sight of food while another stimulus, such as the sound of a bell, occurs simultaneously, the sound alone can induce salivation after several trials. The animal's behaviour is no longer limited by fixed, inherited reflex arcs but can be modified by experience and exposure to an unlimited number of stimuli.

REFLEX IS AN INSTINCT
A variety of what may be called simple instinctive behaviour has long been known as reflex action. When this term was introduced, it meant the simple and almost invariable response of a simple organ system (e.g., a single muscle) to a simple stimulus, such as a touch or a flash of light. In its most elementary versions, this activity has been seen as the function of an idealized mechanism that has been called the reflex arc. The primary components of the reflex arc have been identified as the sensory-nerve cell (or receptor) that receives the stimulation, in turn connecting (hence the term arc) to another nerve cell that activates the muscle cell (or effector).

Although such a reflex arc might be the simplest imaginable mechanism for inflexibly automatic behaviour, it is, as noted above, a theoretical minimum rather than an actually observed functional arrangement of cells in the body of the animal; nevertheless, a mechanism but little more complicated than this helps to account for the locomotion of such animals as millipedes. In some insects, for example, the stepping movement of one limb or muscle provides stimuli that set off another limb or muscle on a similar course of movement, providing a kind of feedback system or chain of reflex arc activities. In most cases of this sort, however, the basic physiological mechanism is more complicated than the simple arc theory would suggest. Additional nerve cells capable of communicating with other parts of the body (beyond the receptor and effector) are invariably present in reflex circuits. Such connections are what make possible the conditioning of reflex responses.

Among higher animals, and perhaps many others (such as insects), what once were thought to be chain reflexes are not systems simply linked or chained together; they are systems under the precise control of coordinated complexes of nerve cells in particular parts of the nervous system, such as the spinal cord and brain. Even without evidence of a chain of feedback (or reafferent) stimuli, performance may be smoothly integrated. This is well illustrated by the complex movements of swallowing in mammals; in the dog, for example, 11 separate muscles or muscular systems are found to discharge one after the other, precisely timed to a matter of milliseconds, and all under the control of the central nervous system (CNS: brain and spinal cord). Such complexes of precisely controlled movement, known as fixed action patterns (FAP's), are thought to form the hard core of the inborn movement forms of instincts. When such sequences of uniform stereotyped responses seem to constitute an end point or goal-directed climax of some sort, they are known as consummatory acts.

AUTONOMIC NERVOUS SYSTEM

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The autonomic nervous system is the part of the peripheral nervous system that regulates the basic visceral processes needed for the maintenance of normal bodily functions. It operates independently of voluntary control, although certain events, such as stress, fear, sexual excitement, and alterations in the sleep-wake cycle, change the level of autonomic activity.

The autonomic system usually is defined as a motor system that innervates three major types of tissue: cardiac muscle, smooth muscle, and glands. However, it also relays visceral sensory information to the central nervous system and processes it so that alterations can be made in the activity of specific autonomic motor outflows, such as those that control the heart, blood vessels, and other visceral organs. It also stimulates the release of certain hormones involved in energy metabolism (e.g., insulin, glucagon, and epinephrine [also called adrenaline]) or cardiovascular functions (e.g., renin and vasopressin). These integrated responses maintain the normal internal environment of the body in an equilibrium state called homeostasis.

The autonomic system consists of two major divisions: the sympathetic nervous system and the parasympathetic nervous system. These often function in antagonistic ways. The motor outflow of both systems is formed by two serially connected sets of neurons. The first set, called preganglionic neurons, originates in the brainstem or the spinal cord, and the second set, called ganglion cells or postganglionic neurons, lies outside the central nervous system in collections of nerve cells called autonomic ganglia. Parasympathetic ganglia tend to lie close to or within the organs or tissues that their neurons innervate, whereas sympathetic ganglia are located at more distant sites from their target organs. Both systems have associated sensory fibres that send feedback into the central nervous system regarding the functional condition of target tissues.

A third division of the autonomic system, the enteric nervous system, consists of a collection of neurons embedded within the wall of the gastrointestinal tract and its derivatives. This system controls gastrointestinal motility and secretion.

SYMPATHETIC NERVOUS SYSTEM

The sympathetic nervous system normally functions to produce localized adjustments (such as sweating as a response to an increase in temperature) and reflex adjustments of the cardiovascular system. Under conditions of stress, however, the entire sympathetic nervous system is activated, producing an immediate, widespread response called the fight-or-flight response. This response is characterized by the release of large quantities of epinephrine from the adrenal gland, an increase in heart rate, an increase in cardiac output, skeletal muscle vasodilation, cutaneous and gastrointestinal vasoconstriction, pupillary dilation, bronchial dilation, and piloerection. The overall effect is to prepare the individual for imminent danger.

Sympathetic preganglionic neurons originate in the lateral horns of the 12 thoracic and the first 2 or 3 lumbar segments of the spinal cord. (For this reason the sympathetic system is sometimes referred to as the thoracolumbar outflow.) The axons of these neurons exit the spinal cord in the ventral roots and then synapse on either sympathetic ganglion cells or specialized cells in the adrenal gland called chromaffin cells.

Sympathetic ganglia
Sympathetic ganglia can be divided into two major groups, paravertebral and prevertebral (or preaortic), on the basis of their location within the body. Paravertebral ganglia generally are located on each side of the vertebrae and are connected to form the sympathetic chain, or trunk. There are usually 21 or 22 pairs of these ganglia—3 in the cervical region, 10 or 11 in the thoracic region, 4 in the lumbar region, and 4 in the sacral region—and a single unpaired ganglion lying in front of the coccyx, called the ganglion impar. The three cervical sympathetic ganglia are the superior cervical ganglion, the middle cervical ganglion, and the cervicothoracic ganglion (also called the stellate ganglion). The superior ganglion innervates viscera of the head, and the middle and stellate ganglia innervate viscera of the neck, thorax (i.e., the bronchi and heart), and upper limbs. The thoracic sympathetic ganglia innervate the trunk region, and the lumbar and sacral sympathetic ganglia innervate the pelvic floor and lower limbs. All the paravertebral ganglia provide sympathetic innervation to blood vessels in muscle and skin, arrector pili muscles attached to hairs, and sweat glands.

The three preaortic ganglia are the celiac, superior mesenteric, and inferior mesenteric. Lying on the anterior surface of the aorta, preaortic ganglia provide axons that are distributed with the three major gastrointestinal arteries arising from the aorta. Thus, the celiac ganglion innervates the stomach, liver, pancreas, and the duodenum, the first part of the small intestine; the superior mesenteric ganglion innervates the small intestine; and the inferior mesenteric ganglion innervates the descending colon, sigmoid colon, rectum, urinary bladder, and sexual organs.

Neurotransmitter and receptors

Upon reaching their target organs by traveling with the blood vessels that supply them, sympathetic fibres terminate as a series of swellings close to the end organ. Because of this anatomical arrangement, autonomic transmission takes place across a junction rather than a synapse. “Presynaptic” sites can be identified because they contain aggregations of synaptic vesicles and membrane thickenings; postjunctional membranes, on the other hand, rarely possess morphological specializations, but they do contain specific receptors for various neurotransmitters. The distance between pre- and postsynaptic elements can be quite large compared with typical synapses. For instance, the gap between cell membranes of a typical chemical synapse is 30–50 nanometres, while in blood vessels the distance is often greater than 100 nanometres or, in some cases, 1–2 micrometres (1,000–2,000 nanometres). Owing to these relatively large gaps between autonomic nerve terminals and their effector cells, neurotransmitters tend to act slowly; they become inactivated rather slowly as well. To compensate for this inefficiency, many effector cells, such as those in smooth and cardiac muscle, are connected by low-resistance pathways that allow for electrotonic coupling of the cells. In this way, if only one cell is activated, multiple cells will respond and work as a group.

At a first approximation, chemical transmission in the sympathetic system appears simple: preganglionic neurons use acetylcholine as a neurotransmitter, whereas most postganglionic neurons utilize norepinephrine (noradrenaline)—with the major exception that postganglionic neurons innervating sweat glands use acetylcholine. On closer inspection, however, neurotransmission is seen to be more complex, because multiple chemicals are released, and each functions as a specific chemical code affecting different receptors on the target cell. In addition, these chemical codes are self-regulatory, in that they act on presynaptic receptors located on their own axon terminals.

The chemical codes are specific to certain tissues. For example, most sympathetic neurons that innervate blood vessels secrete both norepinephrine and neuropeptide Y; sympathetic neurons that innervate the submucosal neural plexus of the gut contain both norepinephrine and somatostatin; and sympathetic neurons that innervate sweat glands contain calcitonin gene-related peptide, vasoactive intestinal polypeptide, and acetylcholine. In addition, other chemicals besides the neuropeptides mentioned above are released from autonomic neurons along with the so-called classical neurotransmitters, norepinephrine and acetylcholine. For instance, some neurons synthesize a gas, nitric oxide, that functions as a neuronal messenger molecule. Thus, neural transmission in the autonomic nervous system involves the release of combinations of different neuroactive agents that affect both pre- and postsynaptic receptors.

Neurotransmitters released from nerve terminals bind to specific receptors, which are specialized macromolecules embedded in the cell membrane. The binding action initiates a series of specific biochemical reactions in the target cell that produce a physiological response. In the sympathetic nervous system, for example, there are five types of adrenergic receptors (receptors binding epinephrine): α1, α2, β1, β2, and β3. These adrenoceptors are found in different combinations in various cells throughout the body. Activation of α1- adrenoceptors in arterioles causes blood-vessel constriction, whereas stimulation of α2 autoreceptors (receptors located in sympathetic presynaptic nerve endings) functions to inhibit the release of norepinephrine. Other types of tissue have unique adrenoceptors. Heart rate and myocardial contractility, for example, are controlled by β1-adrenoceptors; bronchial smooth muscle relaxation is mediated by β2-adrenoceptors; and the breakdown of fat (lipolysis) is controlled by β3-adrenoceptors.

Cholinergic receptors (receptors binding acetylcholine) also are found in the sympathetic system (as well as the parasympathetic system). Nicotinic cholinergic receptors stimulate sympathetic postganglionic neurons, adrenal chromaffin cells, and parasympathetic postganglionic neurons to release their chemicals. Muscarinic receptors are associated mainly with parasympathetic functions and are located in peripheral tissues (e.g., glands and smooth muscle). Peptidergic receptors exist in target cells as well.

The length of time that each type of chemical acts on its target cell is variable. As a rule, peptides cause slowly developing, long-lasting effects (one or more minutes), whereas the classical transmitters produce short-term effects (about 25 milliseconds).

PARASYMPATHETIC NERVOUS SYSTEM

The parasympathetic nervous system primarily modulates visceral organs such as glands. Responses are never activated en masse as in the fight-or-flight sympathetic response. While providing important control of many tissues, the parasympathetic system, unlike the sympathetic system, is not crucial for the maintenance of life.

The parasympathetic nervous system is organized in a manner similar to the sympathetic nervous system. Its motor component consists of preganglionic and postganglionic neurons. The preganglionic neurons are located in specific cell groups (also called nuclei) in the brainstem or in the lateral horns of the spinal cord at sacral levels (segments S2–S4). (Because parasympathetic fibres exit from these two sites, the system is sometimes referred to as the craniosacral outflow.) Preganglionic axons emerging from the brainstem project to parasympathetic ganglia that are located in the head (ciliary, pterygopalatine [also called sphenopalatine], and otic ganglia) or near the heart (cardiac ganglia), embedded in the end organ itself (e.g., the trachea, bronchi, and gastrointestinal tract), or situated a short distance from the urinary bladder (pelvic ganglion). Both pre- and postganglionic neurons secrete acetylcholine as a neurotransmitter, but, like sympathetic ganglion cells, they also contain other neuroactive chemical agents that function as cotransmitters.

The third cranial nerve (oculomotor nerve) contains parasympathetic nerve fibres that regulate the iris and lens of the eye. From their origin in the Edinger-Westphal nucleus of the midbrain, preganglionic axons travel to the orbit and synapse on the ciliary ganglion. The ciliary ganglion contains two types of postganglionic neurons: one innervates smooth muscle of the iris and is responsible for pupillary constriction, and the other innervates ciliary muscle and controls the curvature of the lens.

Various secretory glands located in the head are under parasympathetic control. These include the lacrimal gland, which supplies tears to the cornea of the eye; salivary glands (sublingual, submandibular, and parotid glands), which produce saliva; and nasal mucous glands, which secrete mucus throughout the nasal air passages. The parasympathetic preganglionic neurons that regulate these functions originate in the reticular formation of the medulla oblongata. One group of parasympathetic preganglionic neurons belongs to the superior salivatory nucleus and lies in the rostral part of the medullary reticular formation. These neurons send axons out of the medulla in a separate branch of the seventh cranial nerve (facial nerve) called the intermediate nerve. Some of the axons innervate the pterygopalatine ganglion, and others project to the submandibular ganglion. Pterygopalatine ganglion cells innervate the vasculature of the brain and eye as well as the lacrimal gland, nasal glands, and palatine glands, while neurons of the submandibular ganglion innervate the submandibular and sublingual salivary glands. A second group of parasympathetic preganglionic neurons belongs to the inferior salivatory nucleus, located in the caudal part of the medullary reticular formation. Neurons of this group send axons out of the medulla in the ninth cranial (glossopharyngeal) nerve and to the otic ganglion. From this site, postganglionic fibres travel to and innervate the parotid salivary gland.

Preganglionic parasympathetic fibres of the 10th cranial (vagus) nerve arise from two different sites in the medulla oblongata. Neurons that slow heart rate arise from a part of the ventral medulla called the nucleus ambiguus, while those that control functions of the gastrointestinal tract arise from the dorsal vagal nucleus. After exiting the medulla in the vagus nerve and traveling to their respective organs, the fibres synapse on ganglion cells embedded in the organs themselves. The vagus nerve also contains visceral afferent fibres that carry sensory information from organs of the neck (larynx, pharynx, and trachea), chest (heart and lungs), and gastrointestinal tract into a visceral sensory nucleus located in the medulla called the solitary tract nucleus.

Enteric nervous system

The enteric nervous system is composed of two plexuses, or networks of neurons, embedded in the wall of the gastrointestinal tract. The outermost plexus, located between the inner circular and outer longitudinal smooth-muscle layers of the gut, is called the Auerbach, or myenteric, plexus. Neurons of this plexus regulate peristaltic waves that move digestive products from the oral to the anal opening. In addition, myenteric neurons control local muscular contractions that are responsible for stationary mixing and churning. The innermost group of neurons is called the Meissner, or submucosal, plexus. This plexus regulates the configuration of the luminal surface, controls glandular secretions, alters electrolyte and water transport, and regulates local blood flow.

Three functional classes of intrinsic enteric neurons are recognized: sensory neurons, interneurons, and motor neurons. Sensory neurons, activated by either mechanical or chemical stimulation of the innermost surface of the gut, transmit information to interneurons located within the Auerbach and the Meissner plexi, and the interneurons relay the information to motor neurons. Motor neurons in turn modulate the activity of a variety of target cells, including mucous glands, smooth muscle cells, endocrine cells, epithelial cells, and blood vessels.

Extrinsic neural pathways also are involved in the control of gastrointestinal functions. Three types exist: intestinofugal, sensory, and motor. Intestinofugal neurons reside in the gut wall; their axons travel to the preaortic sympathetic ganglia and control reflex arcs that involve large portions of the gastrointestinal tract. Sensory neurons relay information regarding distention and acidity to the central nervous system. There are two types of sensory neurons: sympathetic neurons, which originate from dorsal-root ganglia found at the thoracic and lumbar levels; and parasympathetic neurons, which originate in the nodose ganglion of the vagus nerve or in dorsal-root ganglia at sacral levels S2–S4. The former innervate the gastrointestinal tract from the pharynx to the left colic flexure, and the latter innervate the distal colon and rectum. Each portion of the gastrointestinal tract receives a dual sensory innervation: pain sensations travel via sympathetic afferent fibres, and sensations that signal information regarding the chemical environment of the gut travel by way of parasympathetic fibres and are not consciously perceived.

The third extrinsic pathway, exercising motor control over the gut, arises from parasympathetic preganglionic neurons found in the dorsal vagal nucleus of the medulla oblongata and from sympathetic preganglionic neurons in the lateral horns of the spinal cord. These pathways provide modulatory commands to the intrinsic enteric motor system and are nonessential in that basic functions can be maintained in their absence.

Through the pathways described above, the parasympathetic system activates digestive processes while the sympathetic system inhibits them. The sympathetic system inhibits digestive processes by two mechanisms: (1) contraction of circular smooth muscle sphincters located in the distal portion of the stomach (pyloric sphincter), small intestine (ileo-cecal sphincter), and rectum (internal anal sphincter), which act as valves to prevent the oral-to-anal passage (as well as reverse passage) of digestive products; and (2) inhibition of motor neurons throughout the length of the gut. In contrast, the parasympathetic system provides messages only to myenteric motor neurons.

PERIPHERAL NERVOUS SYSTEM

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The peripheral nervous system is a channel for the relay of sensory and motor impulses between the central nervous system on one hand and the body surface, skeletal muscles, and internal organs on the other hand. It is composed of (1) spinal nerves, (2) cranial nerves, and (3) certain parts of the autonomic nervous system. As in the central nervous system, peripheral nervous pathways are made up of neurons (that is, nerve cell bodies and their axons and dendrites) and synapses, the points at which one neuron communicates with the next. The structures commonly known as nerves (or by such names as roots, rami, trunks, and branches) are composed of orderly arrangements of the axonal and dendritic processes of many nerve cell bodies.

The cell bodies of peripheral neurons are often found grouped into clusters called ganglia. On the basis of the type of nerve cell bodies found in ganglia, they may be classified as either sensory or motor. Sensory ganglia are oval swellings located on the dorsal roots of spinal nerves and on the roots of certain cranial nerves. The sensory neurons making up these ganglia are unipolar. Shaped much like a golf ball on a tee, they have round or slightly oval cell bodies with concentrically located nuclei, and they give rise to a single fibre that undergoes a T-shaped bifurcation, one branch going to the periphery and the other entering the brain or spinal cord. There are no synaptic contacts between neurons in a sensory ganglion.

Motor ganglia are associated with neurons of the autonomic nervous system, the part of the nervous system that controls and regulates the internal organs. Many motor ganglia are located in the sympathetic trunks, two long chains of ganglia stretching along each side of the vertebral column from the base of the skull to the coccyx; these are referred to as paravertebral ganglia. Prevertebral motor ganglia are located near internal organs innervated by their projecting fibres, while terminal ganglia are found on the surfaces or within the walls of the target organs themselves. Motor ganglia have multipolar cell bodies, which have irregular shapes and eccentrically located nuclei and which project several dendritic and axonal processes. Preganglionic fibres originating from the brain or spinal cord enter motor ganglia, where they synapse on multipolar cell bodies. These postganglionic cells, in turn, send their processes to visceral structures.

SPINAL NERVE

Sensory input from the body surface, from joint, tendon, and muscle receptors, and from internal organs passes centrally through the dorsal roots of the spinal cord. Fibres from motor cells in the spinal cord exit via the ventral roots and course to their peripheral targets (autonomic ganglia or skeletal muscle). Each spinal nerve is formed by the joining of a dorsal root and a ventral root, and it is the basic structural and functional unit of the peripheral nervous system.

STRUCTURAL COMPONENTS OF THE SPINAL NERVE
There are 31 pairs of spinal nerves; in descending order from the most rostral end of the spinal cord, there are 8 cervical (designated C1–C8), 12 thoracic (T1–T12), 5 lumbar (L1–L5), 5 sacral (S1–S5), and 1 coccygeal (Coc1). Each spinal nerve exits the vertebral canal through an opening called the intervertebral foramen. The first spinal nerve (C1) exits the vertebral canal between the skull and the first cervical vertebra; consequently, spinal nerves C1–C7 exit above the correspondingly numbered vertebrae. Spinal nerve C8, however, exits between the 7th cervical and first thoracic vertebrae, so that, beginning with T1, all other spinal nerves exit below their corresponding vertebrae.

Just outside the intervertebral foramen, two branches, known as the gray and white rami communicantes, connect each spinal nerve with the sympathetic trunk. These rami, along with the sympathetic trunk and more distal ganglia, are involved with the innervation of visceral structures. In addition, small meningeal branches leave each spinal nerve and gray ramus and reenter the vertebral canal, where they innervate the dura mater (the outermost of the meninges) and blood vessels.More peripherally, each spinal nerve divides into ventral and dorsal rami. All dorsal rami (with the exception of those from C1, S4, S5, and Coc1) have medial and lateral branches, which innervate deep back muscles and overlying skin. The medial and lateral branches of the dorsal rami of spinal nerves C2–C8 supply both the muscles and the skin of the neck. Those of T1–T6 are mostly cutaneous (that is, supplying only the skin), while those from T7–T12 are mainly muscular. Dorsal rami from L1–L3 have both sensory and motor fibres, while those from L4–L5 are only muscular. Dorsal rami of S1–S3 may also be divided into medial and lateral branches, serving deep muscles of the lower back as well as cutaneous areas of the lower buttocks and perianal area. Undivided dorsal rami from S4, S5, and Coc1 also send cutaneous branches to the gluteal and perianal regions.

Ventral rami of the spinal nerves carry sensory and motor fibres for the innervation of the muscles, joints, and skin of the lateral and ventral body walls and the extremities. Both dorsal and ventral rami also contain autonomic fibres.

FUNCTIONAL TYPES OF SPINAL NERVES
Because spinal nerves contain both sensory fibres (from the dorsal roots) and motor fibres (from the ventral roots), they are known as mixed nerves. When individual fibres of a spinal nerve are identified by their specific function, they may be categorized as one of four types: (1) general somatic afferent, (2) general visceral afferent, (3) general somatic efferent, and (4) general visceral efferent. The term somatic refers to the body wall (broadly defined to include skeletal muscles as well as the surface of the skin), and visceral refers to structures composed of smooth muscle, cardiac muscle, glandular epithelium, or a combination of these. Efferent fibres carry motor information to skeletal muscle and to autonomic ganglia (and then to visceral structures), and afferent fibres carry sensory information from them.

General somatic afferent receptors are sensitive to pain, thermal sensation, touch and pressure, and changes in the position of the body. (Pain and temperature sensation coming from the surface of the body is called exteroceptive, while sensory information arising from tendons, muscles, or joint capsules is called proprioceptive.) General visceral afferent receptors are found in organs of the thorax, abdomen, and pelvis; their fibres convey, for example, pain information from the digestive tract. Both types of afferent fibre project centrally from cell bodies in dorsal-root ganglia.

General somatic efferent fibres originate from large ventral-horn cells and distribute to skeletal muscles in the body wall and in the extremities. General visceral efferent fibres also arise from cell bodies located within the spinal cord, but they exit only at thoracic and upper lumbar levels or at sacral levels (more specifically, at levels T1–L2 and S2–S4). Fibres from T1–L2 enter the sympathetic trunk, where they either form synaptic contacts within a ganglion, ascend or descend within the trunk, or exit the trunk and proceed to ganglia situated closer to their target organs. Fibres from S2–S4, on the other hand, leave the cord as the pelvic nerve and proceed to terminal ganglia located in the target organs. Postganglionic fibres arising from ganglia in the sympathetic trunk rejoin the spinal nerves and distribute to blood vessels, sweat glands, and the arrector pili muscles of the skin, while postganglionic fibres arising from prevertebral and terminal ganglia innervate viscera of the thorax, abdomen, and pelvis.

CERVICAL PLEXUS
Cervical levels C1–C4 are the main contributors to the group of nerves called the cervical plexus; in addition, small branches of the plexus link C1 and C2 with the vagus nerve, C1 and C2 with the hypoglossal nerve, and C2–C4 with the accessory nerve. Sensory branches of the cervical plexus are the lesser occipital nerve (to the scalp behind the ear), the great auricular nerve (to the ear and to the skin over the mastoid and parotid areas), transverse cervical cutaneous nerves (to the lateral and ventral neck surfaces), and supraclavicular nerves (along the clavicle, shoulder, and upper chest). Motor branches of the plexus serve muscles that stabilize and flex the neck, muscles that stabilize the hyoid bone (to assist in actions like swallowing), and muscles that elevate the upper ribs.

Originating from C4, with small contributions from C3 and C5, are the phrenic nerves, which carry sensory information from parts of the pleura of the lungs and pericardium of the heart as well as motor impulses to muscles of the diaphragm.

BRACHIAL PLEXUS
Cervical levels C5–C8 and thoracic level T1 contribute to the formation of the brachial plexus; small nerve bundles also arrive from C4 and T2. Spinal nerves from these levels converge to form superior (C5 and C6), middle (C7), and inferior (C8 and T1) trunks, which in turn split into anterior and posterior divisions. The divisions then form cords (posterior, lateral, and medial), which provide motor, sensory, and autonomic fibres to the shoulder and upper extremity.

Nerves to shoulder and pectoral muscles include the dorsal scapular (to the rhomboid muscles), suprascapular (to supraspinatus and infraspinatus), medial and lateral pectoral (to pectoralis minor and major), long thoracic (to serratus anterior), thoracodorsal (to latissimus dorsi), and subscapular (to teres major and subscapular). The axillary nerve carries motor fibres to the deltoid and teres minor muscles as well as sensory fibres to the lateral surface of the shoulder and upper arm. The biceps, brachialis, and coracobrachialis muscles, as well as the lateral surface of the forearm, are served by the musculocutaneous nerve.

The three major nerves of the arm, forearm, and hand are the radial, median, and ulnar. The radial nerve innervates the triceps, anconeus, and brachioradialis muscles, eight extensors of the wrist and digits, and one abductor of the hand; it is also sensory to part of the hand. The median nerve branches in the forearm to serve the palmaris longus, two pronator muscles, four flexor muscles, thenar muscles, and lumbrical muscles; most of these serve the wrist and hand. The ulnar nerve serves two flexor muscles and a variety of small muscles of the wrist and hand.

Cutaneous innervation of the upper extremity originates, via the brachial plexus, from spinal cord levels C3–T2. The shoulder is served by supraclavicular branches (C3, C4) of the cervical plexus, while the anterior and lateral aspects of the arm and forearm have sensory innervation via the axillary (C5, C6) nerve as well as the dorsal (C5, C6), lateral (C5, C6), and medial (C8, T1) antebrachial cutaneous nerves. These same nerves have branches that wrap around to serve portions of the posterior and medial surfaces of the extremity. The palm of the hand is served by the median (C6–C8) and ulnar (C8, T1) nerves. The ulnar nerve also wraps around to serve medial areas of the dorsum, or back, of the hand. An imaginary line drawn down the midline of the ring finger represents the junction of the ulnar-radial distribution on the back of the hand and the ulnar-median distribution on the palm. A small part of the thumb and the distal thirds of the index, middle, and lateral surface of the ring finger are served by the median nerve. The inner arm and the armpit is served by the intercostobrachial and the posterior and medial brachial cutaneous nerves (T1–T2).

LUMBAR PLEXUS
Spinal nerves from lumbar levels L1–L4 contribute to the formation of the lumbar plexus, which, along with the sacral plexus, provides motor, sensory, and autonomic fibres to gluteal and inguinal regions and to the lower extremities. Lumbar roots are organized into dorsal and ventral divisions.

Minor cutaneous and muscular branches of the lumbar plexus include the iliohypogastric, genitofemoral, and ilioinguinal (projecting to the lower abdomen and to inguinal and genital regions) and the lateral femoral cutaneous nerve (to skin on the lateral thigh). Two major branches of the lumbar plexus are the obturator and femoral nerves. The obturator enters the thigh through the obturator foramen; motor branches proceed to the obturator internus and gracilis muscles as well as the adductor muscles, while sensory branches supply the articular capsule of the knee joint. An accessory obturator nerve supplies the pectineus muscle of the thigh and is sensory to the hip joint.

The sartorius muscle and medial and anterior surfaces of the thigh are served by branches of the anterior division of the femoral nerve. The posterior division of the femoral nerve provides sensory fibres to the inner surface of the leg (saphenous nerve), to the quadriceps muscles (muscular branches), to the hip and knee joints, and to the articularis genu muscle.

SACRAL PLEXUS
The ventral rami of L5 and S1–S3 form the sacral plexus, with contributions from L4 and S4. Branches from this plexus innervate gluteal muscles, muscles forming the internal surface of the pelvic basin (including those forming the levator ani), and muscles that run between the femur and pelvis to stabilize the hip joint (such as the obturator, piriformis, and quadratus femoris muscles). These muscles lend their names to the nerves that innervate them. Cutaneous branches from the plexus serve the buttocks, perineum, and posterior surface of the thigh.

The major nerve of the sacral plexus, and the largest nerve in the body, is the sciatic. Formed by the joining of ventral and dorsal divisions of the plexus, it passes through the greater sciatic foramen and descends in back of the thigh. There, sciatic branches innervate the biceps femoris, semitendinosus and semimembranosus muscles, and part of the adductor magnus muscle. In the popliteal fossa (just above the knee), the sciatic nerve divides into the tibial nerve and the common fibular (or peroneal) nerve. The tibial nerve (from the dorsal division) continues distally in the calf and innervates the gastrocnemius muscle, deep leg muscles such as the popliteus, soleus, and tibialis posterior, and the flexor muscles, lumbrical muscles, and other muscles of the ankle and plantar aspects of the foot. The peroneal nerve, from the ventral division, travels to the anterior surface of the leg and innervates the tibialis anterior, the fibularis muscles, and extensor muscles that elevate the foot and fan the toes. Cutaneous branches from the tibial and common fibular nerves serve the outer sides of the leg and the top and bottom of the foot and toes.

COCCYGEAL PLEXUS
The ventral rami of S4, S5, and Coc1 form the coccygeal plexus, from which small anococcygeal nerves arise to innervate the skin over the coccyx (tailbone) and around the anus.

CRANIAL NERVES

Cranial nerves can be thought of as modified spinal nerves, since the general functional fibre types found in spinal nerves are also found in cranial nerves but are supplemented by special afferent or efferent fibres. Fibres conveying olfaction (in cranial nerve I) and taste (in cranial nerves VII, IX, and X) are classified as special visceral afferent, while the designation of special somatic afferent is applied to fibres conveying vision (cranial nerve II) and equilibrium and hearing (cranial nerve VIII). Skeletal muscles that arise from the branchial arches are innervated by fibres of cranial nerves V, VII, IX, and X; these are classified as special visceral efferent fibres.

The 12 pairs of cranial nerves are identified either by name or by Roman or Arabic numeral.

Olfactory nerve (CN I or 1): Bipolar cells in the nasal mucosa give rise to axons that enter the cranial cavity through foramina in the cribriform plate of the ethmoid bone. These cells and their axons, totaling about 20 to 24 in number, make up the olfactory nerve. Once in the cranial cavity, the fibres terminate in a small oval structure resting on the cribriform plate called the olfactory bulb. As stated above, the functional component of olfactory fibres is special visceral afferent. Injury or disease of the olfactory nerve may result in anosmia, an inability to detect odours; it may also dull the sense of taste.

Optic nerve (CN II or 2): Rods and cones in the retina of the eye receive information from the visual fields and, through intermediary cells, convey this input to retinal ganglion cells. Ganglion cell axons converge at the optic disc, pass through the sclera, and form the optic nerve. A branch from each eye enters the skull via the optic foramen, and they join to form the optic chiasm. At the chiasm, fibres from the nasal halves of each retina cross, while those from the temporal halves remain uncrossed. In this way the optic tracts, which extend from the chiasm to the thalamus, contain fibres conveying information from both eyes. Injury to one optic nerve therefore results in total blindness of that eye, while damage to the optic tract on one side results in partial blindness in both eyes.

Optic fibres also participate in accommodation of the lens and in the pupillary light reflex. Since the subarachnoid space around the brain is continuous with that around the optic nerve, increases in intracranial pressure can result in papilledema, or damage to the optic nerve, as it exits the bulb of the eye.

Oculomotor nerve (CN III or 3): The oculomotor nerve arises from two nuclei in the rostral midbrain. These are (1) the oculomotor nucleus, the source of general somatic efferent fibres to superior, medial, and inferior recti muscles, to the inferior oblique muscle, and to the levator palpebrae superious muscle, and (2) the Edinger-Westphal nucleus, which projects general visceral efferent preganglionic fibres to the ciliary ganglion.

The oculomotor nerve exits the ventral midbrain, pierces the dura mater, courses through the lateral wall of the cavernous sinus, and exits the cranial cavity via the superior orbital fissure. Within the orbit it branches into a superior ramus (to the superior rectus and levator muscles) and an inferior ramus (to the medial and inferior rectus muscles, the inferior oblique muscles, and the ciliary ganglion). Postganglionic fibres from the ciliary ganglion innervate the sphincter pupillae muscle of the iris as well as the ciliary muscle.

Oculomotor neurons project primarily to orbital muscles on the same side of the head. A lesion of the oculomotor nerve will result in paralysis of the three rectus muscles and the inferior oblique muscle (causing the eye to rotate downward and slightly outward), paralysis of the levator palpebrae superious muscle (drooping of the eyelids), and paralysis of the sphincter pupillae and ciliary muscles (so that the iris will remain dilated and the lens will not accommodate).

Trochlear nerve (CN IV or 4): The fourth cranial nerve is unique for three reasons. First, it is the only cranial nerve to exit the dorsal side of the brainstem. Second, fibres from the trochlear nucleus cross in the midbrain before they exit, so that trochlear neurons innervate the contralateral (opposite side) superior oblique muscle of the eye. Third, trochlear fibres have a long intracranial course before piercing the dura mater.

The trochlear nucleus is located in the caudal midbrain; the functional component of these cells is general somatic efferent. After exiting at the dorsal side of the midbrain, the trochlear nerve loops around the midbrain, pierces the dura mater, and passes through the lateral wall of the cavernous sinus. It then enters the orbit through the superior orbital fissure and innervates only the superior oblique muscle, which rotates the eye downward and slightly outward. Damage to the trochlear nerve will result in a loss of this eye movement and may produce double vision (diplopia).

Trigeminal nerve (CN V or 5): The trigeminal nerve is the largest of the cranial nerves. It has both motor and sensory components, the sensory fibres being general somatic afferent and the motor fibres being special visceral efferent. Most of the cell bodies of sensory fibres are located in the trigeminal ganglion, which is attached to the pons by the trigeminal root. These fibres convey pain and thermal sensations from the face, oral and nasal cavities, and parts of the dura mater and nasal sinuses, sensations of deep pressure, and information from sensory endings in muscles. Trigeminal motor fibres, projecting from nuclei in the pons, serve the muscles of mastication (chewing). Lesions of the trigeminal nerve result in sensory losses over the face or in the oral cavity. Damage to the motor fibres results in paralysis of the masticatory muscles; as a result, the jaw may hang open or deviate toward the injured side when opened. Trigeminal neuralgia, or tic douloureux, is an intense pain originating mainly from areas supplied by sensory fibres of the maxillary and mandibular branches of this nerve.

The trigeminal ganglion gives rise to three large nerves: the ophthalmic, maxillary, and mandibular.
1.Ophthalmic nerve: The ophthalmic nerve passes through the wall of the cavernous sinus and enters the orbit via the superior orbital fissure. Branches in the orbit are (1) the lacrimal nerve, serving the lacrimal gland, part of the upper eyelid, and the conjunctiva, (2) the nasociliary nerve, serving the mucosal lining of part of the nasal cavity, the tentorium cerebelli and some of the dura mater of the anterior cranial fossa, and skin on the dorsum and tip of the nose, and (3) the frontal nerve, serving the skin on the upper eyelid, the forehead, and the scalp above the eyes up to the v ertex of the head.
2.Maxillary nerve: The maxillary nerve courses through the cavernous sinus below the ophthalmic nerve and passes through the foramen rotundum into the orbital cavity. Branches of the maxillary nerve are (1) the meningeal branches, which serve the dura mater of the middle cranial fossa, (2) the alveolar nerves, serving the upper teeth and gingiva and the lining of the maxillary sinus, (3) the nasal and palatine nerves, which serve portions of the nasal cavity and the mucosa of the hard and soft palate, and (4) the infraorbital, zygomaticotemporal, and zygomaticofacial nerves, serving the upper lip, the lateral surfaces of the nose, the lower eyelid and conjunctiva, and the skin on the cheek and the side of the head behind the eye.
3.Mandibular nerve: The mandibular nerve exits the cranial cavity via the foramen ovale and serves (1) the meninges and parts of the anterior cranial fossae (meningeal branches), (2) the temporomandibular joint, skin over part of the ear, and skin over the sides of the head above the ears (auriculotemporal nerve), (3) oral mucosa, the anterior two-thirds of the tongue, gingiva adjacent to the tongue, and the floor of the mouth (lingual nerve), and (4) the mandibular teeth (inferior alveolar nerve). Skin over the lateral and anterior surfaces of the mandible and the lower lip is served by cutaneous branches of the mandibular nerve.

Trigeminal motor fibres exit the cranial cavity via the foramen ovale along with the mandibular nerve. They serve the muscles of mastication (temporalis, masseter, medial and lateral pterygoid), three muscles involved in swallowing (anterior portions of the digastric muscle, the mylohyoid muscle, and the tensor veli palatini), and the tensor tympani, a muscle that has a damping effect on loud noises by stabilizing the tympanic membrane.

Abducens nerve (CN VI or 6): From its nucleus in the caudal pons, the abducens nerve exits the brainstem at the pons-medulla junction, pierces the dura mater, passes through the cavernous sinus close to the internal carotid artery, and exits the cranial vault via the superior orbital fissure. In the orbit the abducens nerve innervates the lateral rectus muscle, which turns the eye outward. Damage to the abducens nerve results in a tendency for the eye to deviate medially, or cross. Double vision may result on attempted lateral gaze. The nerve often is affected by increased intracranial pressure.

Facial nerve (CN VII or 7): The facial nerve is composed of a large root that innervates facial muscles and a small root (known as the intermediate nerve) that contains sensory and autonomic fibres.

From the facial nucleus in the pons, facial motor fibres enter the internal auditory meatus, pass through the temporal bone, exit the skull via the stylomastoid foramen, and fan out over each side of the face in front of the ear. Fibres of the facial nerve are special visceral efferent; they innervate the small muscles of the external ear, the superficial muscles of the face, neck, and scalp, and the muscles of facial expression.

The intermediate nerve contains autonomic (parasympathetic) as well as general and special sensory fibres. Preganglionic autonomic fibres, classified as general visceral efferent, project from the superior salivatory nucleus in the pons. Exiting with the facial nerve, they pass to the pterygopalatine ganglion via the greater petrosal nerve (a branch of the facial nerve) and to the submandibular ganglion by way of the chorda tympani nerve (another branch of the facial nerve, which joins the lingual branch of the mandibular nerve). Postganglionic fibres from the pterygopalatine ganglion innervate the nasal and palatine glands and the lacrimal gland, while those from the submandibular ganglion serve the submandibular and sublingual salivary glands. Among the sensory components of the intermediate nerve, general somatic afferent fibres relay sensation from the caudal surface of the ear, while special visceral afferent fibres originate from taste buds in the anterior two-thirds of the tongue, course in the lingual branch of the mandibular nerve, and then join the facial nerve via the chorda tympani branch. Both somatic and visceral afferent fibres have cell bodies in the geniculate ganglion, which is located on the facial nerve as it passes through the facial canal in the temporal bone.

Injury to the facial nerve at the brainstem produces a paralysis of facial muscles known as Bell palsy as well as a loss of taste sensation from the anterior two-thirds of the tongue. If damage occurs at the stylomastoid foramen, facial muscles will be paralyzed but taste will be intact.
Vestibulocochlear nerve or Auditory nerve (CN VIII or 8): This cranial nerve has a vestibular part, which functions in balance, equilibrium, and orientation in three-dimensional space, and a cochlear part, which functions in hearing. The functional component of these fibres is special somatic afferent; they originate from receptors located in the temporal bone.

Vestibular receptors are located in the semicircular canals of the ear, which provide input on rotatory movements (angular acceleration), and in the utricle and saccule, which generate information on linear acceleration and the influence of gravitational pull. This information is relayed by the vestibular fibres, whose bipolar cell bodies are located in the vestibular (Scarpa) ganglion. The central processes of these neurons exit the temporal bone via the internal acoustic meatus and enter the brainstem alongside the facial nerve.

Auditory receptors of the cochlear division are located in the organ of Corti and follow the spiral shape (about 2.5 turns) of the cochlea. Air movement against the eardrum initiates action of the ossicles of the ear, which, in turn, causes movement of fluid in the spiral cochlea. This fluid movement is converted by the organ of Corti into nerve impulses that are interpreted as auditory information. The bipolar cells of the spiral, or Corti, ganglion branch into central processes that course with the vestibular nerve. At the brainstem, cochlear fibres separate from vestibular fibres to end in the dorsal and ventral cochlear nuclei.

Lesions of the vestibular root result in eye movement disorders (nystagmus), unsteady gait with a tendency to fall toward the side of the lesion, nausea, and vertigo. Damage to the cochlea or cochlear nerve results in complete deafness, ringing in the ear (tinnitus), or both.

Glossopharyngeal nerve (CN IX or 9): The ninth cranial nerve, which exits the skull through the jugular foramen, has both motor and sensory components. Cell bodies of motor neurons, located in the nucleus ambiguus in the medulla oblongata, project as special visceral efferent fibres to the stylopharyngeal muscle. The action of the stylopharyngeus is to elevate the pharynx, as in gagging or swallowing. In addition, the inferior salivatory nucleus of the medulla sends general visceral efferent fibres to the otic ganglion via the lesser petrosal branch of the ninth nerve; postganglionic otic fibres innervate the parotid salivary gland.

Among the sensory components of the glossopharyngeal nerve, special visceral afferent fibres convey taste sensation from the back third of the tongue via lingual branches of the nerve. General visceral afferent fibres from the pharynx, the back of the tongue, parts of the soft palate and eustachian tube, and the carotid body and carotid sinus have their cell bodies in the superior and inferior ganglia, which are situated, respectively, within the jugular foramen and just outside the cranium. Sensory fibres in the carotid branch detect increased blood pressure in the carotid sinus and send impulses into the medulla that ultimately reduce heart rate and arterial pressure; this is known as the carotid sinus reflex.

Vagus nerve (CN X or 10): The vagus nerve has the most extensive distribution in the body of all the cranial nerves, innervating structures as diverse as the external surface of the eardrum and internal abdominal organs. The root of the nerve exits the cranial cavity via the jugular foramen. Within the foramen is the superior ganglion, containing cell bodies of general somatic afferent fibres, and just external to the foramen is the inferior ganglion, containing visceral afferent cells.

Pain and temperature sensations from the eardrum and external auditory canal and pain fibres from the dura mater of the posterior cranial fossa are conveyed on general somatic afferent fibres in the auricular and meningeal branches of the nerve. Taste buds on the root of the tongue and on the epiglottis contribute special visceral afferent fibres to the superior laryngeal branch. General visceral afferent fibres conveying sensation from the lower pharynx, larynx, trachea, esophagus, and organs of the thorax and abdomen to the left (splenic) flexure of the colon converge to form the posterior (right) and anterior (left) vagal nerves. Right and left vagal nerves are joined in the thorax by cardiac, pulmonary, and esophageal branches. In addition, general visceral afferent fibres from the larynx below the vocal folds join the vagus via the recurrent laryngeal nerves, while comparable input from the upper larynx and pharynx is relayed by the superior laryngeal nerves and by pharyngeal branches of the vagus. A vagal branch to the carotid body usually arises from the inferior ganglion.

Motor fibres of the vagus nerve include special visceral efferent fibres arising from the nucleus ambiguus of the medulla oblongata and innervating pharyngeal constrictor muscles and palatine muscles via pharyngeal branches of the vagus as well as the superior laryngeal nerve. All laryngeal musculature (excluding the cricothyroid but including the muscles of the vocal folds) are innervated by fibres arising in the nucleus ambiguus. Cells of the dorsal motor nucleus in the medulla distribute general visceral efferent fibres to plexuses or ganglia serving the pharynx, larynx, esophagus, and lungs. In addition, cardiac branches arise from plexuses in the lower neck and upper thorax, and, once in the abdomen, the vagus gives rise to gastric, celiac, hepatic, renal, intestinal, and splenic branches or plexuses.

Damage to one vagus nerve results in hoarseness and difficulty in swallowing or speaking. Injury to both nerves results in increased heart rate, paralysis of pharyngeal and laryngeal musculature, atonia of the esophagus and intestinal musculature, vomiting, and loss of visceral reflexes. Such a lesion is usually life-threatening, as paralysis of laryngeal muscles may result in asphyxiation.

Accessory nerve (CN XI or 11): The accessory nerve is formed by fibres from the medulla oblongata (known as the cranial root) and by fibres from cervical levels C1–C4 (known as the spinal root). The cranial root originates from the nucleus ambiguus and exits the medulla below the vagus nerve. Its fibres join the vagus and distribute to some muscles of the pharynx and larynx via pharyngeal and recurrent laryngeal branches of that nerve. For this reason, the cranial part of the accessory nerve is, for all practical purposes, part of the vagus nerve.

Fibres that arise from spinal levels exit the cord, coalesce and ascend as the spinal root of the accessory nerve, enter the cranial cavity through the foramen magnum, and then immediately leave through the jugular foramen. The accessory nerve then branches into the sternocleidomastoid muscle, which tilts the head toward one shoulder with an upward rotation of the face to the opposite side, and the trapezius muscle, which stabilizes and shrugs the shoulder.

Hypoglossal nerve (CN XII or 12): The hypoglossal nerve innervates certain muscles that control movement of the tongue. From the hypoglossal nucleus in the medulla oblongata, general somatic efferent fibres exit the cranial cavity through the hypoglossal canal and enter the neck in close proximity to the accessory and vagus nerves and the internal carotid artery. The nerve then loops down and forward into the floor of the mouth and branches into the tongue musculature from underneath. Hypoglossal fibres end in intrinsic tongue muscles, which modify the shape of the tongue (as in rolling the edges), as well as in extrinsic muscles that are responsible for changing its position in the mouth.

A lesion of the hypoglossal nerve on the same side of the head results in paralysis of the intrinsic and extrinsic musculature on the same side. The tongue atrophies and, on attempted protrusion, deviates toward the side of the lesion.

ANATOMY:CNS-SPINAL CORD

2010-02-05T08:19:00.000+05:30

The spinal cord is an elongated cylindrical structure, about 45 cm (18 inches) long, that extends from the medulla oblongata to a level between the first and second lumbar vertebrae of the backbone. The terminal part of the spinal cord is called the conus medullaris. The spinal cord is composed of long tracts of myelinated nerve fibres (known as white matter) arranged around the periphery of a symmetrical butterfly-shaped cellular matrix of gray matter. The gray matter contains cell bodies, unmyelinated motor neuron fibres, and interneurons connecting either the two sides of the cord or the dorsal and ventral ganglia. Many interneurons have short axons distributed locally, but some have axons that extend for several spinal segments. Some interneurons may modulate or change the character of signals, while others play key roles in transmission and in patterned reflexes. The gray matter forms three pairs of horns throughout most of the spinal cord: (1) the dorsal horns, composed of sensory neurons, (2) the lateral horns, well defined in thoracic segments and composed of visceral neurons, and (3) the ventral horns, composed of motor neurons. The white matter forming the ascending and descending spinal tracts is grouped in three paired funiculi, or sectors: the dorsal or posterior funiculi, lying between the dorsal horns; the lateral funiculi, lying on each side of the spinal cord between the dorsal-root entry zones and the emergence of the ventral nerve roots; and the ventral funiculi, lying between the ventral median sulcus and each ventral-root zone.

Associated with local regions of the spinal cord and imposing on it an external segmentation are 31 pairs of spinal nerves, each of which receives and furnishes one dorsal and one ventral root. On this basis the spinal cord is divided into the following segments: 8 cervical (C), 12 thoracic (T), 5 lumbar (L), 5 sacral (S), and 1 coccygeal (Coc). Spinal nerve roots emerge via intervertebral foramina; lumbar and sacral spinal roots, descending for some distance within the subarachnoid space before reaching the appropriate foramina, produce a group of nerve roots at the conus medullaris known as the cauda equina. Two enlargements of the spinal cord are evident: (1) a cervical enlargement (C5 through T1), which provides innervation for the upper extremities, and (2) a lumbosacral enlargement (L1 through S2), which innervates the lower extremities. (The spinal nerves and the area that they innervate are described in the section The peripheral nervous system: Spinal nerves.)

CELLULAR LAMINAE
The gray matter of the spinal cord is composed of nine distinct cellular layers, or laminae, traditionally indicated by Roman numerals. Laminae I to V, forming the dorsal horns, receive sensory input. Lamina VII forms the intermediate zone at the base of all horns. Lamina IX is composed of clusters of large alpha motor neurons, which innervate striated muscle, and small gamma motor neurons, which innervate contractile elements of the muscle spindle. Axons of both alpha and gamma motor neurons emerge via the ventral roots. Laminae VII and VIII have variable configurations, and lamina VI is present only in the cervical and lumbosacral enlargements. In addition, cells surrounding the central canal of the spinal cord form an area often referred to as lamina X.

All primary sensory neurons that enter the spinal cord originate in ganglia that are located in openings in the vertebral column called the intervertebral foramina. Peripheral processes of the nerve cells in these ganglia convey sensation from various receptors, and central processes of the same cells enter the spinal cord as bundles of nerve filaments. Fibres conveying specific forms of sensation follow separate pathways. Impulses involved with pain and noxious stimuli largely end in laminae I and II, while impulses associated with tactile sense end in lamina IV or on processes of cells in that lamina. Signals from stretch receptors (i.e., muscle spindles and tendon organs) end in parts of laminae V, VI, and VII; collaterals of these fibres associated with the stretch reflex project into lamina IX.

Virtually all parts of the spinal gray matter contain interneurons, which connect various cell groups. Many interneurons have short axons distributed locally, but some have axons that extend for several spinal segments. Some interneurons may modulate or change the character of signals, while others play key roles in transmission and in patterned reflexes.

ASCENDING SPINAL TRACT
Sensory tracts ascending in the white matter of the spinal cord arise either from cells of spinal ganglia or from intrinsic neurons within the gray matter that receive primary sensory input.
Dorsal column: The largest ascending tracts, the fasciculi gracilis and cuneatus, arise from spinal ganglion cells and ascend in the dorsal funiculus to the medulla oblongata. The fasciculus gracilis receives fibres from ganglia below thoracic 6, while spinal ganglia from higher segments of the spinal cord project fibres into the fasciculus cuneatus. The fasciculi terminate upon the nuclei gracilis and cuneatus, large nuclear masses in the medulla. Cells of these nuclei give rise to fibres that cross completely and form the medial lemniscus; the medial lemniscus in turn projects to the ventrobasal nuclear complex of the thalamus. By this pathway, the medial lemniscal system conveys signals associated with tactile, pressure, and kinesthetic (or positional) sense to sensory areas of the cerebral cortex.

Spinothalamic tracts: Fibres concerned with pain, thermal sense, and light touch enter the lateral-root entry zone and then ascend or descend near the periphery of the spinal cord before entering superficial laminae of the dorsal horn—largely parts of laminae I, IV, and V. Cells in these laminae then give rise to fibres of the two spinothalamic tracts. Those fibres crossing in the ventral white commissure (ventral to the central canal) form the lateral spinothalamic tract, which, ascending in the ventral part of the lateral funiculus, conveys signals related to pain and thermal sense. The anterior spinothalamic tract arises from fibres that cross the midline in the same fashion but ascend more anteriorly in the spinal cord; these fibres convey impulses related to light touch. At medullary levels the two spinothalamic tracts merge and cannot be distinguished as separate entities. Many of the fibres, or collaterals, of the spinothalamic tracts terminate upon cell groups in the reticular formation, while the principal tracts convey sensory impulses to relay nuclei in the thalamus.

Spinocerebellar tracts: Impulses from stretch receptors are carried by fibres that synapse upon cells in deep laminae of the dorsal horn or in lamina VII. The posterior spinocerebellar tract arises from the dorsal nucleus of Clarke and ascends peripherally in the dorsal part of the lateral funiculus. The anterior spinocerebellar tract ascends on the ventral margin of the lateral funiculus. Both tracts transmit signals to portions of the anterior lobe of the cerebellum and are involved in mechanisms that automatically regulate muscle tone without reaching consciousness.

DESCENDING SPINAL TRACTS
Tracts descending to the spinal cord are involved with voluntary motor function, muscle tone, reflexes and equilibrium, visceral innervation, and modulation of ascending sensory signals. The largest, the corticospinal tract, originates in broad regions of the cerebral cortex. Smaller descending tracts, which include the rubrospinal tract, the vestibulospinal tract, and the reticulospinal tract, originate in nuclei in the midbrain, pons, and medulla oblongata. Most of these brainstem nuclei themselves receive input from the cerebral cortex, the cerebellar cortex, deep nuclei of the cerebellum, or some combination of these.

In addition, autonomic tracts, which descend from various nuclei in the brainstem to preganglionic sympathetic and parasympathetic neurons in the spinal cord, constitute a vital link between the centres that regulate visceral functions and the nerve cells that actually effect changes.

Corticospinal tract: The corticospinal tract originates from pyramid-shaped cells in the premotor, primary motor, and primary sensory cortex and is involved in skilled voluntary activity. Containing about one million fibres, it forms a significant part of the posterior limb of the internal capsule and is a major constituent of the crus cerebri in the midbrain. As the fibres emerge from the pons, they form compact bundles on the ventral surface of the medulla, known as the medullary pyramids. In the lower medulla about 90 percent of the fibres of the corticospinal tract decussate and descend in the dorsolateral funiculus of the spinal cord. Of the fibres that do not cross in the medulla, approximately 8 percent cross in cervical spinal segments. As the tract descends, fibres and collaterals branch off at all segmental levels, synapsing upon interneurons in lamina VII and upon motor neurons in lamina IX. Approximately 50 percent of the corticospinal fibres terminate within cervical segments.

At birth, few of the fibres of the corticospinal tract are myelinated; myelination takes place during the first year after birth, along with the acquisition of motor skills. Because the tract passes through, or close to, nearly every major division of the neuraxis, it is vulnerable to vascular and other kinds of lesions. A relatively small lesion in the posterior limb of the internal capsule, for example, may result in contralateral hemiparesis, which is characterized by weakness, spasticity, greatly increased deep tendon reflexes, and certain abnormal reflexes.

Rubrospinal tract: The rubrospinal tract arises from cells in the caudal part of the red nucleus, an encapsulated cell group in the midbrain tegmentum. Fibres of this tract decussate at midbrain levels, descend in the lateral funiculus of the spinal cord (overlapping ventral parts of the corticospinal tract), enter the spinal gray matter, and terminate on interneurons in lamina VII. Through these crossed rubrospinal projections, the red nucleus exerts a facilitating influence on flexor alpha motor neurons and a reciprocal inhibiting influence on extensor alpha motor neurons. Because cells of the red nucleus receive input from the motor cortex (via corticorubral projections) and from globose and emboliform nuclei of the cerebellum (via the superior cerebellar peduncle), the rubrospinal tract effectively brings flexor muscle tone under the control of these two regions of the brain.

Vestibulospinal tract: The vestibulospinal tract originates from cells of the lateral vestibular nucleus, which lies in the floor of the fourth ventricle. Fibres of this tract descend the length of the spinal cord in the ventral and lateral funiculi without crossing, enter laminae VIII and IX of the anterior horn, and terminate upon both alpha and gamma motor neurons, which innervate ordinary muscle fibres and fibres of the muscle spindle (see below Functions of the human nervous system: Movement). Cells of the lateral vestibular nucleus receive facilitating impulses from labyrinthine receptors in the utricle of the inner ear and from fastigial nuclei in the cerebellum. In addition, inhibitory influences upon these cells are conveyed by direct projections from Purkinje cells in the anterior lobe of the cerebellum. Thus, the vestibulospinal tract mediates the influences of the vestibular end organ and the cerebellum upon extensor muscle tone.

A smaller number of vestibular projections, originating from the medial and inferior vestibular nuclei, descend ipsilaterally in the medial longitudinal fasciculus only to cervical levels. These fibres exert excitatory and inhibitory effects upon cervical motor neurons.

Reticulospinal tract: The reticulospinal tracts arise from relatively large but restricted regions of the reticular formation of the pons and medulla oblongata—the same cells that project ascending processes to intralaminar thalamic nuclei and are important in the maintenance of alertness and the conscious state. The pontine reticulospinal tract arises from groups of cells in the pontine reticular formation, descends ipsilaterally as the largest component of the medial longitudinal fasciculus, and terminates among cells in laminae VII and VIII. Fibres of this tract exert facilitating influences upon voluntary movements, muscle tone, and a variety of spinal reflexes. The medullary reticulospinal tract, originating from reticular neurons on both sides of the median raphe, descends in the ventral part of the lateral funiculus and terminates at all spinal levels upon cells in laminae VII and IX. The medullary reticulospinal tract inhibits the same motor activities that are facilitated by the pontine reticulospinal tract. Both tracts receive input from regions of the motor cortex.

Autonomic tracts: Descending fibres involved with visceral and autonomic activities emanate from groups of cells at various levels of the brainstem. For example, hypothalamic nuclei project to visceral nuclei in both the medulla oblongata and the spinal cord; in the spinal cord these projections terminate upon cells of the intermediolateral cell column in thoracic, lumbar, and sacral segments. Preganglionic parasympathetic neurons originating in the oculomotor nuclear complex in the midbrain project not only to the ciliary ganglion but also directly to spinal levels. Some of these fibres reach lumbar segments of the spinal cord, most of them terminating in parts of laminae I and V. Pigmented cells in the isthmus, an area of the rostral pons, form a blackish-blue region known as the locus ceruleus; these cells distribute the neurotransmitter norepinephrine to the brain and spinal cord. Fibres from the locus ceruleus descend to spinal levels without crossing and are distributed to terminals in the anterior horn, the intermediate zone, and the dorsal horn. Other noradrenergic cell groups in the pons, near the motor nucleus of the facial nerve, project uncrossed noradrenergic fibres that terminate in the intermediolateral cell column (that is, lamina VII of the lateral horn). Postganglionic sympathetic neurons associated with this system have direct effects upon the cardiovascular system. Cells in the nucleus of the solitary tract project crossed fibres to the phrenic nerve nucleus (in cervical segments three through five), the intermediate zone, and the anterior horn at thoracic levels; these innervate respiratory muscles.

ANATOMY:CNS-THE BRAIN

2010-01-31T16:00:00.000+05:30

The central nervous system consists of the brain and spinal cord, both derived from the embryonic neural tube. Both are surrounded by protective membranes called the meninges, and both float in a crystal-clear cerebrospinal fluid. The brain is encased in a bony vault, the neurocranium, while the cylindrical and elongated spinal cord lies in the vertebral canal, which is formed by successive vertebrae connected by dense ligaments.

THE BRAIN

The brain weighs about 1,500 grams (3 pounds) and constitutes about 2 percent of total body weight. It consists of three major divisions: (1) the massive paired hemispheres of the cerebrum, (2) the brainstem, consisting of the thalamus, hypothalamus, epithalamus, subthalamus, midbrain, pons, and medulla oblongata, and (3) the cerebellum.

CEREBRUM

The cerebrum, derived from the telencephalon, is the largest, uppermost portion of the brain. It is involved with sensory integration, control of voluntary movement, and higher intellectual functions, such as speech and abstract thought. The outer layer of the duplicate cerebral hemispheres is composed of a convoluted (wrinkled) outer layer of gray matter, called the cerebral cortex. Beneath the cerebral cortex is an inner core of white matter, which is composed of myelinated commissural nerve fibres connecting the cerebral hemispheres via the corpus callosum, and association fibres connecting different regions of a single hemisphere. Myelinated fibres projecting to and from the cerebral cortex form a concentrated fan-shaped band, known as the internal capsule. The internal capsule consists of an anterior limb and a larger posterior limb and is abruptly curved, with the apex directed toward the centre of the brain; the junction is called the genu. The cerebrum also contains groups of subcortical neuronal masses known as basal ganglia.

The cerebral hemispheres are partially separated from each other by a deep groove called the longitudinal fissure. At the base of the longitudinal fissure lies a thick band of white matter called the corpus callosum. The corpus callosum provides a communication link between corresponding regions of the cerebral hemispheres.

Each cerebral hemisphere supplies motor function to the opposite, or contralateral, side of the body from which it receives sensory input. In other words, the left hemisphere controls the right half of the body, and vice versa. Each hemisphere also receives impulses conveying the senses of touch and vision, largely from the contralateral half of the body, while auditory input comes from both sides. Pathways conveying the senses of smell and taste to the cerebral cortex are ipsilateral (that is, they do not cross to the opposite hemisphere).

In spite of this arrangement, the cerebral hemispheres are not functionally equal. In each individual, one hemisphere is dominant. The dominant hemisphere controls language, mathematical and analytical functions, and handedness. The nondominant hemisphere controls simple spatial concepts, recognition of faces, some auditory aspects, and emotion.

LOBES OF CEREBRAL CORTEX

The cerebral cortex is highly convoluted; the crest of a single convolution is known as a gyrus, and the fissure between two gyri is known as a sulcus. Sulci and gyri form a more or less constant pattern, on the basis of which the surface of each cerebral hemisphere is commonly divided into four lobes: (1) frontal, (2) parietal, (3) temporal, and (4) occipital. Two major sulci located on the lateral, or side, surface of each hemisphere distinguish these lobes. The central sulcus, or fissure of Rolando, separates the frontal and parietal lobes, and the deeper lateral sulcus, or fissure of Sylvius, forms the boundary between the temporal lobe and the frontal and parietal lobes.

The frontal lobe: The frontal lobe, the largest of the cerebral lobes, lies rostral to the central sulcus (that is, toward the nose from the sulcus). One important structure in the frontal lobe is the precentral gyrus, which constitutes the primary motor region of the brain. When parts of the gyrus are electrically stimulated in concious patients (under local anesthesia), they produce localized movements on the opposite side of the body that are interpreted by the patients as voluntary. Injury to parts of the precentral gyrus results in paralysis on the contralateral half of the body. Parts of the inferior frontal lobe (close to the lateral sulcus) constitute the Broca area, a region involved with speech.

The parietal lobe: The parietal lobe, posterior to the central sulcus, is divided into three parts: (1) the postcentral gyrus, (2) the superior parietal lobule, and (3) the inferior parietal lobule. The postcentral gyrus receives sensory input from the contralateral half of the body. The sequential representation is the same as in the primary motor area, with sensations from the head being represented in inferior parts of the gyrus and impulses from the lower extremities being represented in superior portions. The superior parietal lobule, located caudal to (that is, below and behind) the postcentral gyrus, lies above the intraparietal sulcus. This lobule is regarded as an association cortex, an area that is not involved in either sensory or motor processing, although part of the superior parietal lobule may be concerned with motor function. The inferior parietal lobule (composed of the angular and supramarginal gyri) is a cortical region involved with the integration of multiple sensory signals.

In both the parietal and frontal lobes, each primary sensory or motor area is close to, or surrounded by, a smaller secondary area. The primary sensory area receives input only from the thalamus, while the secondary sensory area receives input from the thalamus, the primary sensory area, or both. The motor areas receive input from the thalamus as well as the sensory areas of the cerebral cortex.

The temporal lobe: The temporal lobe, inferior to the lateral sulcus, fills the middle fossa, or hollow area, of the skull. The outer surface of the temporal lobe is an association area made up of the superior, middle, and inferior temporal gyri. Near the margin of the lateral sulcus, two transverse temporal gyri constitute the primary auditory area of the brain. The sensation of hearing is represented here in a tonotopic fashion—that is, with different frequencies represented on different parts of the area. The transverse gyri are surrounded by a less finely tuned secondary auditory area. A medial, or inner, protrusion near the ventral surface of the temporal lobe, known as the uncus, constitutes a large part of the primary olfactory area.

The occipital lobe: The occipital lobe lies caudal to the parieto-occipital sulcus, which joins the calcarine sulcus in a Y-shaped formation. Cortex on both banks of the calcarine sulcus constitutes the primary visual area, which receives input from the contralateral visual field via the optic radiation. The visual field is represented near the calcarine sulcus in a retinotopic fashion—that is, with upper quadrants of the visual field laid out along the inferior bank of the sulcus and lower quadrants of the visual field represented on the upper bank. Central vision is represented mostly caudally and peripheral vision rostrally.

Insular or central lobe: Not visible from the surface of the cerebrum is the insular, or central, lobe, an invaginated triangular area on the medial surface of the lateral sulcus; it can be seen in the intact brain only by separating the frontal and parietal lobes from the temporal lobe. The insular lobe is thought to be involved in sensory and motor visceral functions as well as taste perception.

The limbic lobe: The limbic lobe is a synthetic lobe located on the medial margin (or limbus) of the hemisphere. Composed of adjacent portions of the frontal, parietal, and temporal lobes that surround the corpus callosum, the limbic lobe is involved with autonomic and related somatic behavioral activities. The limbic lobe receives input from thalamic nuclei that are connected with parts of the hypothalamus and with the hippocampal formation, a primitive cortical structure within the inferior horn of the lateral ventricle.

CEREBRAL VENTRICLES

Deep within the white matter of the cerebral hemispheres are cavities filled with cerebrospinal fluid that form the ventricular system. These cavities include a pair of C-shaped lateral ventricles with anterior, inferior, and posterior “horns” protruding into the frontal, temporal, and occipital lobes, respectively. Most of the cerebrospinal fluid is produced in the ventricles, and about 70 percent of it is secreted by the choroid plexus, a collection of blood vessels in the walls of the lateral ventricles. The fluid drains via interventricular foramina, or openings, into a slitlike third ventricle, which, situated along the midline of the brain, separates the symmetrical halves of the thalamus and hypothalamus. From there the fluid passes through the cerebral aqueduct in the midbrain and into the fourth ventricle in the hindbrain. Openings in the fourth ventricle permit cerebrospinal fluid to enter subarachnoid spaces surrounding both the brain and the spinal cord.

BASAL GANGLIA

Deep within the cerebral hemispheres, large gray masses of nerve cells, called nuclei, form components of the basal ganglia. Four basal ganglia can be distinguished: (1) the caudate nucleus, (2) the putamen, (3) the globus pallidus, and (4) the amygdala. Phylogenetically, the amygdala is the oldest of the basal ganglia and is often referred to as the archistriatum; the globus pallidus is known as the paleostriatum, and the caudate nucleus and putamen are together known as the neostriatum, or simply striatum. Together, the putamen and the adjacent globus pallidus are referred to as the lentiform nucleus, while the caudate nucleus, putamen, and globus pallidus form the corpus striatum.

The caudate nucleus and the putamen are continuous rostrally and ventrally, and they have similar cellular compositions, cytochemical features, and functions but slightly different connections. The putamen lies deep within the cortex of the insular lobe, while the caudate nucleus has a C-shaped configuration that parallels the lateral ventricle. The head of the caudate nucleus protrudes into the anterior horn of the lateral ventricle, the body lies above and lateral to the thalamus, and the tail is in the roof of the inferior horn of the lateral ventricle. The tail of the caudate nucleus ends in relationship to the amygdaloid nuclear complex, which lies in the temporal lobe beneath the cortex of the uncus.

There are an enormous number of neurons within the caudate nucleus and putamen; they are of two basic types: spiny and aspiny. Spiny striatal neurons are medium-size cells with radiating dendrites that are studded with spines. Axons of these cells project beyond the boundaries of the caudate nucleus and putamen. All nerves providing input to the caudate nucleus and the putamen terminate upon the dendritic spines of spiny striatal neurons, and all output is via axons of the same neurons. Chemically, spiny striatal neurons are heterogeneous; that is, most contain more than one neurotransmitter. Gamma-aminobutyric acid (GABA) is the primary neurotransmitter contained in spiny striatal neurons. Other neurotransmitters found in spiny striatal neurons include substance P and enkephalin.

Aspiny striatal neurons have smooth dendrites and short axons confined to the caudate nucleus or putamen. Small aspiny striatal neurons secrete GABA, neuropeptide Y, somatostatin, or some combination of these. The largest aspiny neurons are evenly distributed neurons that also secrete neurotransmitters and are important in maintaining the balance of dopamine and GABA.

Because the caudate nucleus and putamen receive varied and diverse inputs from multiple sources that utilize different neurotransmitters, they are regarded as the receptive component of the corpus striatum. Most input originates from regions of the cerebral cortex, with the connecting corticostriate fibres containing the excitatory neurotransmitter glutamate. In addition, afferent fibres originating from a large nucleus located in the midbrain called the substantia nigra or from intralaminar thalamic nuclei project to the caudate nucleus or the putamen. Neurons in the substantia nigra are known to synthesize dopamine, but the neurotransmitter secreted by thalamostriate neurons has not been identified. All striatal afferent systems terminate in patchy areas called strisomes; areas not receiving terminals are called the matrix. Spiny striatal neurons containing GABA, substance P, and enkephalin project in a specific pattern onto the globus pallidus and the substantia nigra.

The globus pallidus, consisting of two cytologically similar wedge-shaped segments, the lateral and the medial, lies between the putamen and the internal capsule. Striatopallidal fibres from the caudate nucleus and putamen converge on the globus pallidus like spokes of a wheel. Both segments of the pallidum receive GABAergic terminals, but in addition the medial segment receives substance P fibres, and the lateral segment receives enkephalinergic projections. The output of the entire corpus striatum (i.e., the caudate nucleus, putamen, and globus pallidus together) arises from GABAergic cells in the medial pallidal segment and in the substantia nigra, both of which receive fibres from the striatum. GABAergic cells in the medial pallidal segment and the substantia nigra project to different nuclei in the thalamus; these in turn influence distinct regions of the cerebral cortex involved with motor function. The lateral segment of the globus pallidus, on the other hand, projects almost exclusively to the subthalamic nucleus, from which it receives reciprocal input. No part of the corpus striatum projects fibres to spinal levels.

Pathological processes involving the corpus striatum and related nuclei are associated with a variety of specific diseases characterized by abnormal involuntary movements (collectively referred to as dyskinesia) and significant alterations of muscle tone. Parkinson disease and Huntington disease are among the more prevalent syndromes; each appears related to deficiencies in the synthesis of particular neurotransmitters.

The amygdala, located ventral to the corpus striatum in medial parts of the temporal lobe, is an almond-shaped nucleus underlying the uncus. Although it receives olfactory inputs, the amygdala plays no role in olfactory perception. This nucleus also has reciprocal connections with the hypothalamus, the basal forebrain, and regions of the cerebral cortex. It plays important roles in visceral, endocrine, and cognitive functions related to motivational behaviour.

BRAIN STEM

The brainstem is made up of all the unpaired structures that connect the cerebrum with the spinal cord. Most rostral in the brainstem are structures often collectively referred to as the diencephalon. These structures are the epithalamus, the thalamus, the hypothalamus, and the subthalamus. Directly beneath the diencephalon is the midbrain, or mesencephalon, and beneath the midbrain are the pons and medulla oblongata, often referred to as the hindbrain.

Epithalamus: The epithalamus is represented mainly by the pineal gland, which lies in the midline posterior and dorsal to the third ventricle. This gland synthesizes melatonin and enzymes sensitive to daylight. Rhythmic changes in the activity of the pineal gland in response to daylight suggest that the gland serves as a biological clock.

Thalamus: The thalamus has long been regarded as the key to understanding the organization of the central nervous system. It is involved in the relay and distribution of most, but not all, sensory and motor signals to specific regions of the cerebral cortex. Sensory signals generated in all types of receptors are projected via complex pathways to specific relay nuclei in the thalamus, where they are segregated and systematically organized. The relay nuclei in turn supply the primary and secondary sensory areas of the cerebral cortex. Sensory input to thalamic nuclei is contralateral for the sensory, or somesthetic, and visual systems, bilateral and contralateral for the auditory system, and ipsilateral for the gustatory and olfactory systems.

The sensory relay nuclei of the thalamus, collectively known as the ventrobasal complex, receive input from the medial lemniscus (originating in the medulla oblongata), from spinothalamic tracts, and from the trigeminal nerve. Fibres within these ascending tracts that terminate in the central core of the ventrobasal complex receive input from deep sensory receptors, while fibres projecting onto the outer shell receive input from cutaneous receptors. This segregation of deep and superficial sensation is preserved in projections of the ventrobasal complex to the primary sensory area of the cerebral cortex.

The metathalamus is composed of the medial and lateral geniculate bodies, or nuclei. Fibres of the optic nerve end in the lateral geniculate body, which consists of six cellular laminae, or layers, folded into a horseshoe configuration. Each lamina represents a complete map of the contralateral visual hemifield. Cells in all layers of the lateral geniculate body project via optic radiation to the visual areas of the cerebral cortex. The medial geniculate body receives auditory impulses from the inferior colliculus of the midbrain and relays them to the auditory areas of the temporal lobe. Only the ventral nucleus of the medial geniculate body is laminated and tonotopically organized; this part projects to the primary auditory area and is finely tuned. Other subdivisions of the medial geniculate body project to the belt of secondary auditory cortex surrounding the primary area.

Most output from the cerebellum projects to specific thalamic relay nuclei in a pattern similar to that for sensory input. The thalamic relay nuclei in turn provide input to the primary motor area of the frontal lobe. This system appears to provide coordinating and controlling influences that result in the appropriate force, sequence, and direction of voluntary motor activities. Output from the corpus striatum, on the other hand, is relayed by thalamic nuclei that have access to the supplementary and premotor areas. The supplementary motor area, located on the medial aspect of the hemisphere, exerts modifying influences upon the primary motor area and appears to be involved in programming skilled motor sequences. The premotor area, rostral to the primary motor area, plays a role in sensorially guided movements.

Other major thalamic nuclei include the anterior nuclear group, the mediodorsal nucleus, and the pulvinar. The anterior nuclear group receives input from the hypothalamus and projects upon parts of the limbic lobe (i.e., the cingulate gyrus). The mediodorsal nucleus, part of the medial nuclear group, has reciprocal connections with large parts of the frontal lobe rostral to the motor areas. The pulvinar is a posterior nuclear complex that, along with the mediodorsal nucleus, has projections to association areas of the cortex.

Output ascending from the reticular formation of the brainstem is relayed to the cerebral cortex by intralaminar thalamic nuclei, which are located in laminae separating the medial and ventrolateral thalamic nuclei. This ascending system is involved with arousal mechanisms, maintaining alertness, and directing attention to sensory events.
Hypothalamus: The hypothalamus lies below the thalamus in the walls and floor of the third ventricle. It is divided into medial and lateral groups by a curved bundle of axons called the fornix, which originate in the hippocampal formation and project to the mammillary body. The hypothalamus controls major endocrine functions by secreting hormones (i.e., oxytocin and vasopressin) that induce smooth muscle contractions of the reproductive, digestive, and excretory systems; other neurosecretory neurons convey hormone-releasing factors (e.g., growth hormone, corticosteroids, thyrotropic hormone, and gonadotropic hormone) via a vascular portal system to the adenohypophysis, a portion of the pituitary gland. Specific regions of the hypothalamus are also involved with the control of sympathetic and parasympathetic activities, temperature regulation, food intake, the reproductive cycle, and emotional expression and behaviour.

Subthalamus: The subthalamus is represented mainly by the subthalamic nucleus, a lens-shaped structure lying behind and to the sides of the hypothalamus and on the dorsal surface of the internal capsule. The subthalamic region is traversed by fibres related to the globus pallidus. Discrete lesions of the subthalmic nucleus produce hemiballismus, a violent form of dyskinesia in which the limbs are involuntarily flung about.

MID BRAIN

The midbrain (mesencephalon) contains the nuclear complex of the oculomotor nerve as well as the trochlear nucleus; these cranial nerves innervate muscles that move the eye and control the shape of the lens and the diameter of the pupil. In addition, between the midbrain reticular formation (known here as the tegmentum) and the crus cerebri is a large pigmented nucleus called the substantia nigra. The substantia nigra consists of two parts, the pars reticulata and the pars compacta. Cells of the pars compacta contain the dark pigment melanin; these cells synthesize dopamine and project to either the caudate nucleus or the putamen. By inhibiting the action of large aspiny striatal neurons in the caudate nucleus and the putamen (described above in the section Basal ganglia), the dopaminergic cells of the pars compacta influence the output of the neurotransmitter GABA from spiny striatal neurons. The spiny neurons in turn project to the cells of the pars reticulata, which, by projecting fibres to the thalamus, are part of the output system of the corpus striatum.

At the caudal midbrain, crossed fibres of the superior cerebellar peduncle (the major output system of the cerebellum) surround and partially terminate in a large centrally located structure known as the red nucleus. Most crossed ascending fibres of this bundle project to thalamic nuclei, which have access to the primary motor cortex. A smaller number of fibres synapse on large cells in caudal regions of the red nucleus; these give rise to the crossed fibres of the rubrospinal tract (see the section The spinal cord: Descending spinal tracts). The roof plate of the midbrain is formed by two paired rounded swellings, the superior and inferior colliculi. The superior colliculus receives input from the retina and the visual cortex and participates in a variety of visual reflexes, particularly the tracking of objects in the contralateral visual field. The inferior colliculus receives both crossed and uncrossed auditory fibres and projects upon the medial geniculate body, the auditory relay nucleus of the thalamus.

PONS

The pons (metencephalon) consists of two parts: the tegmentum, a phylogenetically older part that contains the reticular formation, and the pontine nuclei, a larger part composed of masses of neurons that lie among large bundles of longitudinal and transverse nerve fibres.

Fibres originating from neurons in the cerebral cortex terminate upon the pontine nuclei, which in turn project to the opposite hemisphere of the cerebellum. These massive crossed fibres, called crus cerebri, form the middle cerebellar peduncle and serve as the bridge that connects each cerebral hemisphere with the opposite half of the cerebellum. The fibres originating from the cerebral cortex constitute the corticopontine tract.

The reticular formation (an inner core of gray matter found in the midbrain, pons, and medulla oblongata) of the pontine tegmentum contains multiple cell groups that influence motor function. It also contains the nuclei of several cranial nerves. The facial nerve and the two components of the vestibulocochlear nerve, for example, emerge from and enter the brainstem at the junction of the pons, medulla, and cerebellum. In addition, motor nuclei of the trigeminal nerve lie in the upper pons. Long ascending and descending tracts that connect the brain to the spinal cord are located on the periphery of the pons.

MEDULLA OBLONGATA

The medulla oblongata (myelencephalon), the most caudal segment of the brainstem, appears as a conical expansion of the spinal cord. The roof plate of both the pons and the medulla is formed by the cerebellum and a membrane containing a cellular layer called the choroid plexus, located in the fourth ventricle. Cerebrospinal fluid entering the fourth ventricle from the cerebral aqueduct passes into the cisterna magna, a subarachnoid space surrounding the medulla and the cerebellum, via openings in the lateral recesses in the midline of the ventricle.

At the transition of the medulla to the spinal cord, there are two major decussations, or crossings, of nerve fibres. The corticospinal decussation is the site at which 90 percent of the fibres of the medullary pyramids cross and enter the dorsolateral funiculus of the spinal cord. Signals conveyed by this tract provide the basis for voluntary motor function on the opposite side of the body (see the section The spinal cord: Descending spinal tracts). In the other decussation, two groups of ascending sensory fibres in the fasciculus gracilis and the fasciculus cuneatus of the spinal cord terminate upon large nuclear masses on the dorsal surface of the medulla. Known as the nuclei gracilis and cuneatus, these masses give rise to fibres that decussate above the corticospinal tract and form a major ascending sensory pathway known as the medial lemniscus that is present in all brainstem levels. The medial lemniscus projects upon the sensory relay nuclei of the thalamus.

The medulla contains nuclei associated with the hypoglossal, accessory, vagus, and glossopharyngeal cranial nerves. In addition, it contains portions of the vestibular nuclear complex, parts of the trigeminal nuclear complex involved with pain and thermal sense, and solitary nuclei related to the vagus, glossopharyngeal, and facial nerves that subserve the sense of taste.

CEREBELLUM

The cerebellum (“little brain”) overlies the posterior aspect of the pons and medulla oblongata and fills the greater part of the posterior fossa of the skull. This distinctive part of the brain is derived from the rhombic lips, thickenings along the margins of the embryonic hindbrain. It consists of two paired lateral lobes, or hemispheres, and a midline portion known as the vermis. The cerebellar cortex appears very different from the cerebral cortex in that it consists of small leaflike laminae called folia. The cerebellum consists of a surface cortex of gray matter and a core of white matter containing four paired intrinsic (i.e., deep) nuclei: the dentate, globose, emboliform, and fastigial. Three paired fibre bundles—the superior, middle, and inferior peduncles—connect the cerebellum with the midbrain, pons, and medulla, respectively.

On an embryological basis the cerebellum is divided into three parts: (1) the archicerebellum, related primarily to the vestibular system, (2) the paleocerebellum, or anterior lobe, involved with control of muscle tone, and (3) the neocerebellum, known as the posterior lobe. Receiving input from the cerebral hemispheres via the middle cerebellar peduncle, the neocerebellum is the part most concerned with coordination of voluntary motor function.

The three layers of the cerebellar cortex are an outer synaptic layer (also called the molecular layer), an intermediate discharge layer (the Purkinje layer), and an inner receptive layer (the granular layer). Sensory input from all sorts of receptors is conveyed to specific regions of the receptive layer, which consists of enormous numbers of small nerve cells (hence the name granular) that project axons into the synaptic layer. There the axons excite the dendrites of the Purkinje cells, which in turn project axons to portions of the four intrinsic nuclei and upon dorsal portions of the lateral vestibular nucleus. Because most Purkinje cells are GABAergic and therefore exert strong inhibitory influences upon the cells that receive their terminals, all sensory input into the cerebellum results in inhibitory impulses' being exerted upon the deep cerebellar nuclei and parts of the vestibular nucleus. Cells of all deep cerebellar nuclei, on the other hand, are excitatory (secreting the neurotransmitter glutamate) and project upon parts of the thalamus, red nucleus, vestibular nuclei, and reticular formation.

The cerebellum thus functions as a kind of computer, providing a quick and clear response to sensory signals. It plays no role in sensory perception, but it exerts profound influences upon equilibrium, muscle tone, and the coordination of voluntary motor function. Because the input and output pathways both cross, a lesion of a lateral part of the cerebellum will have an ipsilateral effect on coordination.

DEVELOPMENT OF HUMAN NERVOUS SYSTEM

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It is a system that conducts stimuli from sensory receptors to the brain and spinal cord and that conducts impulses back to other parts of the body. As with other higher vertebrates, the human nervous system has two main parts: the central nervous system (the brain and spinal cord) and the peripheral nervous system (the nerves that carry impulses to and from the central nervous system). In humans the brain is especially large and well developed.

PRENATAL AND POSTNATAL DEVELOPMENT OF HUMAN NERVOUS SYSTEM

Almost all nerve cells, or neurons, are generated during prenatal life, and in most cases they are not replaced by new neurons thereafter. Morphologically, the nervous system first appears about 18 days after conception, with the genesis of a neural plate. Functionally, it appears with the first sign of a reflex activity during the second prenatal month, when stimulation by touch of the upper lip evokes a withdrawal response of the head. Many reflexes of the head, trunk, and extremities can be elicited in the third month.

During its development the nervous system undergoes remarkable changes to attain its complex organization. In order to produce the estimated 1 trillion neurons present in the mature brain, an average of 2.5 million neurons must be generated per minute during the entire prenatal life. This includes the formation of neuronal circuits comprising 100 trillion synapses, as each potential neuron is ultimately connected with either a selected set of other neurons or specific targets such as sensory endings. Moreover, synaptic connections with other neurons are made at precise locations on the cell membranes of target neurons. The totality of these events is not thought to be the exclusive product of the genetic code, for there are simply not enough genes to account for such complexity. Rather, the differentiation and subsequent development of embryonic cells into mature neurons and glial cells are achieved by two sets of influences: (1) specific subsets of genes and (2) environmental stimuli from within and outside the embryo. Genetic influences are critical to the development of the nervous system in ordered and temporally timed sequences. Cell differentiation, for example, depends on a series of signals that regulate transcription, the process in which deoxyribonucleic acid (DNA) molecules give rise to ribonucleic acid (RNA) molecules, which in turn express the genetic messages that control cellular activity. Environmental influences derived from the embryo itself include cellular signals that consist of diffusible molecular factors (see below Neuronal development). External environmental factors include nutrition, sensory experience, social interaction, and even learning. All of these are essential for the proper differentiation of individual neurons and for fine-tuning the details of synaptic connections. Thus, the nervous system requires continuous stimulation over an entire lifetime in order to sustain functional activity.

Neuronal development
In the second week of prenatal life, the rapidly growing blastocyst (the bundle of cells into which a fertilized ovum divides) flattens into what is called the embryonic disk. The embryonic disk soon acquires three layers: the ectoderm (outer layer), mesoderm (middle layer), and endoderm (inner layer). Within the mesoderm grows the notochord, an axial rod that serves as a temporary backbone. Both the mesoderm and notochord release a chemical that instructs and induces adjacent undifferentiated ectoderm cells to thicken along what will become the dorsal midline of the body, forming the neural plate. The neural plate is composed of neural precursor cells, known as neuroepithelial cells, which develop into the neural tube (see below Morphological development). Neuroepithelial cells then commence to divide, diversify, and give rise to immature neurons and neuroglia, which in turn migrate from the neural tube to their final location. Each neuron forms dendrites and an axon; axons elongate and form branches, the terminals of which form synaptic connections with a select set of target neurons or muscle fibres.

The remarkable events of this early development involve an orderly migration of billions of neurons, the growth of their axons (many of which extend widely throughout the brain), and the formation of thousands of synapses between individual axons and their target neurons. The migration and growth of neurons are dependent, at least in part, on chemical and physical influences. The growing tips of axons (called growth cones) apparently recognize and respond to various molecular signals, which guide axons and nerve branches to their appropriate targets and eliminate those that try to synapse with inappropriate targets. Once a synaptic connection has been established, a target cell releases a trophic factor (e.g., nerve growth factor) that is essential for the survival of the neuron synapsing with it. Physical guidance cues are involved in contact guidance, or the migration of immature neurons along a scaffold of glial fibres.

In some regions of the developing nervous system, synaptic contacts are not initially precise or stable and are followed later by an ordered reorganization, including the elimination of many cells and synapses. The instability of some synaptic connections persists until a so-called critical period is reached, prior to which environmental influences have a significant role in the proper differentiation of neurons and in fine-tuning many synaptic connections. Following the critical period, synaptic connections become stable and are unlikely to be altered by environmental influences. This suggests that certain skills and sensory activities can be influenced during development (including postnatal life), and for some intellectual skills this adaptability presumably persists into adulthood and late life.

Morphological development
By 18 days after fertilization, the ectoderm of the embryonic disk thickens along what will become the dorsal midline of the body, forming the neural plate and, slightly later, the primordial eye, ear, and nose. The neural plate elongates, and its lateral edges rise and unite in the midline to form the neural tube, which will develop into the central nervous system. The neural tube detaches from the skin ectoderm and sinks beneath the surface. At this stage, groupings of ectodermal cells, called neural crests, develop as a column on each side of the neural tube. The cephalic (head) portion of the neural tube differentiates into the prosencephalon (forebrain), mesencephalon (midbrain), and rhombencephalon (hindbrain), and the caudal portion becomes the spinal cord. The neural crests develop into most of the elements (e.g., ganglia and nerves) of the peripheral nervous system. This stage is reached at the end of the first embryonic month.

The cells of the central nervous system originate from the ventricular zone of the neural tube—that is, the layer of neuroepithelial cells lining the central cavity of the tube. These cells differentiate and proliferate into neuroblasts, which are the precursors of neurons, and glioblasts, from which neuroglia develop. With a few exceptions, the neuroblasts, glioblasts, and their derived cells do not divide and multiply once they have migrated from the ventricular zone into the gray and white matter of the nervous system. Most neurons are generated before birth, although not all are fully differentiated. (One exception is the neurons of the olfactory nerve, which are generated continuously throughout life.) This effectively implies that an individual is born with a full complement of nerve cells.

By mid-fetal life the slender primordial brain of the neural-tube stage differentiates into a globular-shaped brain. Although fully mature size and shape are not obtained until puberty, the main outlines of the brain are recognizable by the end of the third fetal month. This early development is the product of several factors: the formation of three flexures (cephalic, pontine, and cervical); the differential enlargement of various regions, especially the cerebrum and the cerebellum; the massive growth of the cerebral hemispheres over the sides of the midbrain and of the cerebellum at the hindbrain; and the formations of convolutions (sulci and gyri) in the cerebral cortex and folia of the cerebellar cortex. The central and calcarine sulci are discernible by the fifth fetal month, and all major gyri and sulci are normally present by the seventh month. Many minor sulci and gyri appear after birth.

Postnatal changes

The postnatal growth of the human brain is rapid and massive, especially during the first two years. By two years after birth, the size of the brain and the proportion of its parts are basically those of an adult. The typical brain of a full-term infant weighs 350 grams (12 ounces) at birth, 1,000 grams at the end of the first year, about 1,300 grams at puberty, and about 1,500 grams at adulthood. This increase is attributable mainly to the growth of preexisting neurons, new glial cells, and the myelination of axons. The trebling of weight during the first year (a growth rate unique to humans) may be an adaptation that is essential to the survival of humans as a species with a large brain. Birth occurs at a developmental stage when the infant is not so helpless as to be unable to survive, yet is small enough to be delivered out of the maternal pelvis. If the brain was much larger (enough, say, to support intelligent behaviour), normal delivery would not be possible.

Between the ages of 20 and 75, it is estimated that an average of 50,000 neurons atrophy or die each day. In a healthy person, this loss is roughly equal to 10 percent of the original neuronal complement. By the age of 75, the weight of the brain is reduced from its maximum at maturity by about one-tenth, the flow of blood through the brain by almost one-fifth, and the number of functional taste buds by about two-thirds. A loss of neurons does not necessarily imply a comparable loss of function; however, some loss may be compensated for by the formation from viable neurons of new branches of nerve fibres and by the formation of new synapses.