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WHAT IS CEREBRAL PALSY

2020-11-16T09:27:00.000-08:00

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What Is Cerebral Palsy

The Nervous System

Human Brain Anatomy

Unique CP Symptoms

Severe CP

Aging with Cerebral Palsy

Driving and Cerebral Palsy

Living With AutismTV Show

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Chest Physical Therapy For CP new

What is the definition of cerebral palsy? Cerebral palsy is a term used to describe a group of chronic conditions affecting body movements and muscle coordination. It is caused by damage to one or more specific areas of the brain, usually occurring during fetal development or infancy. It also can occur before, during or shortly following birth.

"Cerebral" refers to the brain and "Palsy" to a disorder of movement or posture. If someone has cerebral palsy it means that because of an injury to their brain (cerebral) they are not able to use some of the muscles in their body in the normal way (palsy). Children with cerebral palsy may not be able to walk, talk, eat or play in the same ways as most other children.

Cerebral palsy is neither progressive nor communicable. It is also not "curable" in the accepted sense, although education, therapy and applied technology can help persons with cerebral palsy lead productive lives. It is important to know that cerebral palsy is not a disease or illness. It isn't contagious and it doesn't get worse. Children who have cerebral palsy will have it all their lives.

What Causes Cerebral Palsy?

Congenital cerebral palsy results from brain injury during a baby's development in the womb. It is present at birth, although it may not be detected for months. It is responsible for about 70% of children who have cerebral palsy. An additional 20% are diagnosed with congenital cerebral palsy due to a brain injury during the birthing process. In most cases, the cause of congenital cerebral palsy is unknown. Some other causes are

Infections during pregnancy

that may damage a fetus' developing nervous system. These include rubella (German measles), cytomegalovirus (a herpes-type virus), and toxoplasmosis (an infection caused by a parasite that can be carried in cat feces or inadequately cooked meat). Other infections in pregnant women that may go undetected are being recognized now as an important cause of developmental brain damage of the fetus.

Severe jaundice in the infant.

Jaundice is caused by excessive bilirubin in the blood. Normally, bilirubin is filtered out by the liver. But often, newborns' livers need a few days to start doing this effectively, so it's not uncommon for infants to have jaundice for a few days after birth. In most cases, phototherapy (light therapy) clears up jaundice, and there are no lasting health effects. However, in rare cases, severe, untreated jaundice can damage brain cells.
Rh incompatibility between mother and infant.
In this blood condition, the mother's body produces antibodies that destroy the fetus's blood cells. This, in turn, leads to a form of jaundice in the newborn and may cause brain damage.
The physical and metabolic trauma of being born. This can precipitate brain damage in a fetus whose health has been threatened during developmen

Autism (ASD) HOME

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Introduction

If you are the parent or caregiver of a school-age child who has

been diagnosed with an autism spectrum disorder (ASD), this

booklet is written for you.

Receiving a diagnosis of an autism spectrum disorder can be an

overwhelming experience. You may have received other diagnoses

before the ASD diagnosis was made, or this may be the first

diagnosis given to your child. Either way, an ASD diagnosis can

explain some of the differences you have observed during your

child’s development and can also provide a direction for appropriate

interventions at home, in school, and in the community.

Included in this booklet are questions that parents frequently

ask when their school-age child receives an ASD diagnosis,

and brief answers containing links to resources with more

detailed information.

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Important Topics

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Mentally Retarded Children

2019-03-10T23:48:00.000-07:00

THE MENTALLY RETARDED CHILDREN

The guidace about Mentally Retarded Children.

How does Mental Retardation affect the child? Developmental aspects .

support in various aspects to cope with basic needs in daily life.

Severe. Profound.

-------Important Topics-------

Chest Physical Therapy

2017-07-19T06:59:00.000-07:00

Chest Physical Therapy

(CPT) For Cerebral palsy Child

What is CPT?

Chest Physical Therapy (CPT) is something you can do to help your child
breathe better. Sometimes there is too much mucus, or it is too thick. It blocks
the air from moving in and out of your child’s lungs. Mucus makes it hard for
your child to breathe. Mucus that sits too long in the lungs can also grow germs
that can make your child sick. CPT helps to loosen your child’s mucus, so your
child can cough it up.
Think about how you would take Jell-O
out of a mold. You tilt the mold over,
then shake it and tap it to loosen the Jell-O
. Mucus is like that Jell-O , and CPT
helps to get it out.

Airways Air moves through these and into your lungs. The airways of the nose
and throat lead to the big airways in the chest. The big airways branch off into
smaller airways in the lungs. The big airways are like a trunk of a tree, and the
small airways, like the branches.
Chest Physical Therapy (CPT) is something you can do to loosen your child’s
mucus. The three parts to CPT are postural drainage, percussion and deep
breathing and coughing.Percussion is clapping the chest. Percuss
means to tap sharply. A drum is a percussion instrument.
Percussion in CPT can be done with either a cupped hand or an electric percussor.
The clapping shakes the inside of the chest and loosens mucus, so it is easier to cough out.
Postural Drainage moves the mucus by changing the child’s position. Mucus,
like water, moves from high places to low places. Tilting the child helps move
the mucus from the small airways at the bottom of the lungs to the large airways
in the middle. The most mucus moves into the large airways when you do
percussion and postural drainage together.
Deep breathing and coughing helps to move the loosened mucus.
Lobe is a section of the lung. The left lung has two lobes, and the right lung
has three lobes.

Before Doing CPT

• It is best to do CPT before meals or at least one to two hours after eating.
This will make it less likely that the child will feel sick to the stomach or
throw up.
• The best times for CPT are early morning and at bed time. Early morning
CPT helps remove the mucus that built up over night. Bed time CPT
takes out the mucus of the day, and helps the child cough less at night.
Your doctor may want you to do CPT more often.
• Your doctor may prescribe medicine to open the airways. This may come as an
SVN (small volume nebulizer) or an MDI (metered dose inhaler). This
medicine should be taken before CPT. The medicine, positioning and
percussion all work together to clear the mucus from the lungs.
• The person doing the CPT should take off all rings and jewelry on the hands or
wrists.
• If the child’s clothing is tight or has thick seams, remove it.
• If the child is wearing clothes with buttons, remove it.
• Have the child wear a t-shirt or put a soft cloth over the spot that will be
percussed.

What You Need:

• A place to do CPT. You will need a bed, pillows, a couch, ﬂoor or a special
table (slant board).
• Your hand or a percussor.
• A clock or a timer, to know how long to percuss.

How to do:

• Always percuss over the ribs. Never percuss below the ribs or on the stomach.
The lungs are in the chest, protected by the ribs. Never percuss on the
backbone, breast bone, nipples or on any IV tubes or feeding tubes.
• Do CPT in each spot for
p 2 minutes p 3 minutes or p ____ minutes.
(Health Care Provider: check one)
Your doctor will tell you how long to percuss.
One session of CPT should take 20 to 40 minutes.
• Usually, CPT is done in all the positions and percussion in all the spots.
Your doctor may have you do more in some areas, where the chest x-ray shows more mucus.
• If your child’s mucus has bright red blood in it, stop the CPT and call your
doctor.

1 Top Upper Lobes

• Sit the child up. Tilt the child half way between sitting up and laying ﬂat.
• Percuss between the nipple and collarbone on the left side of the chest for
2 minutes 3 minutes or minutes.
• Percuss between the nipple and collarbone on the right side of the chest for
2 minutes 3 minutes or minutes.

2 Back Upper Lobes

• Sit the child up. Tilt the child half way between sitting up and laying ﬂat.
• Percuss over the shoulder blade on the left side of the back for
2 minutes p 3 minutes or minutes.
• Percuss over the shoulder blade on the right side of the back for
2 minutes 3 minutes or minutes.

3 Front Upper Lobes

• Lie child on his or her back.
• Percuss between the nipple and the collarbone on the left side for 2 minutes 3 minutes or minutes.
• Percuss between the nipple and the collarbone on the right side for 2 minutes 3 minutes or minutes.

4 Front Right Middle Lobe

• Lie child down on his or her left side, feet higher than head.
• Percuss below the right arm, but above the bottom edge of the ribs, for
2 minutes 3 minutes or minutes.

5 Side of Right Lung

• Lie child on his or her back, feet higher than head.
• Turn the child to his or her left, half way between back and side.
• Percuss between the child’s right nipple and underarm for
2 minutes 3 minutes or minutes.

6 Front Left Lower Lobe•

Lie child on his or her back, feet higher than head.
• Turn the child to his or her right, half way between back and side.
• Percuss between the child’s left nipple and underarm for 2 minutes 3 minutes
or minutes.

7 Side of Left Lung

• Lie child down on his or her right side, feet higher than head.
• Percuss below the left arm but above the bottom edge of the ribs for
2 minutes 3 minutes or minutes.

8 Back Lower Lobes

• Lie child on his or her stomach, feet higher than head.
• Percuss over the middle of the right ribs, above the bottom edge of the ribs for
2 minutes 3 minutes or minutes.
• Percuss over the middle of the left ribs above the bottom edge of the ribs for
2 minutes 3 minutes
or minutes.

After the treatment:

• Your child may cough more during or after CPT. Coughing helps your child
get rid of the loosened mucus.
• Your child may cough up to one or two hours after CPT. Even if no mucus
comes up, the CPT is working.
• After swallowing a lot of mucus, your child may feel sick to the stomach or
throw up. As soon as your child is old enough to learn to spit, teach him
or her how to spit the mucus into a tissue.
• If your child does not stop throwing up, call your doctor.

Rights of Ageing People with Autism

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In recent years, the European Union has undertaken remarkable steps to enforce equal

rights for citizens with disabilities. The EU has ratifed the United Nations Convention on the

Rights of Persons with Disabilities in December 2010, and to date most of its Member States

have also ratifed it. The Convention on the Rights of Persons with Disabilities (UNCRPD)

is an international human rights instrument intended to protect the rights and dignity of

people with disabilities. Parties to the Convention are required to promote, protect, and

ensure the full enjoyment of human rights by people with disabilities on an equal basis with

others.

There are eight guiding principles that underlie the Convention and each one of its

specifc articles:

1. Respect for inherent dignity, individual autonomy including the freedom to make one’s

own choices, and independence of persons;

2. Non-discrimination;

3. Full and efective participation and inclusion in society;

4. Respect for diference and acceptance of persons with disabilities as part of human

diversity and humanity;

5. Equality of opportunity;

6. Accessibility;

7. Equality between men and women;

8. Respect for the evolving capacities of children with disabilities and respect for the right

of children with disabilities to preserve their identities.

In this context, the rights of ageing people with disabilities should not be forgotten. People

with autism, their families or representatives, and relevant organisations must gain a strong

understanding of their rights and governments must fulfl their obligations under the

UNCRPD.

The intersection of age and disability has not yet been taken into account by the European

Union and its Member States’ legislators and policy makers in the context of implementing

the UNCRPD. Across Europe, people with disabilities currently face a gap between policy and

practice, for example, in France – a country which has ratifed the UNCRPD – a person over

the age of 60 years is no longer considered a person with a disability in relation to welfare

payments. Instead, a person aged over 60 years is simply considered an older person,

regardless of their disability and individual needs. In this case, government allowances are

signifcantly lower and the individual may be required to pay up to 90 percent of their long-

term care costs. Therefore, in France, older people have an interest in becoming incapacitated

before the age of 60 years.

This gap in understanding and addressing the needs of older

people with disabilities must be addressed as part of the implementation of the UNCRPD.

Taking due account of the United Nations Convention on the Rights of Persons with

Disabilities, the Council of Europe has adopted the Recommendation on ageing and disability

in the 21st

century35

in 2009. In its recommendation, the Council of Europe indicates that the

ageing of people with disabilities, particularly of those requiring more intensive support,

compels Member States to adopt innovative approaches. In this regard, the Council of

Europe notes that “the quantity and quality of community-based and residential support

services in this feld have been unsatisfactory, especially for people with learning disabilities.

Older people with disabilities have sufered a double disadvantage, as seen in their relatively

low priority in health- and social-care policies and provision.”

With due regard for their own national, regional or local structures and respective

responsibilities, the Council of Europe Member States should contribute to the creation of

sustainable frameworks to enable greater quality of life in an inclusive society for ageing

people with disabilities.

The following recommendations formulated by Autism-Europe take into account the United

Nations Convention on the Rights of Persons with Disabilities, the articles 25 and 26 of the

Charter of Fundamental Rights of the European Union (on the rights of the elderly and

people with disabilities), as well as the Recommendation of the Council of Europe on ageing

and disability in the 21st century. They are also based on Autism-Europe’s position paper on

ageing that was published in 2003. These recommendations are addressed to policy makers

as guidance in fulflling their obligations to older people with autism.

The right to an independent life and self-determination (art. 19 of the UNCRPD)

People with autism and other types of disabilities requiring a high level of support have

the right to make decisions for their own future, and to ask for the provisions of the UN

Convention on the Rights of Persons with Disabilities to be respected.

The right to maintain or improve the quality of health (art. 25 of the UNCRPD)

People with autism should be provided with the necessary means to ensure:

• Prevention of health problems related to ageing, notably through regular check-ups and
screenings;
• Accurate diagnosis and accurate information on their specifc health condition;
• Prevention of problems related to their specifc health conditions (e.g. osteoarthritis due to stereotypy);
•Treatment of individual health conditions.

The right to maintain and improve communication and social interaction (art 9 and art 26 of the UNCRPD)

Older people with autism should be provided with access to adapted/alternative means of

communication and visual information.

Where possible, inter-generational dialogue involving older people with autism should be

fostered by:

• Participation in cultural events and other leisure or sports activities with younger people

in the broader community;

• Facilitatation of contact between schools, youth organisations and structures for older

people with autism.

The right to appropriate intervention (art 26 of the UNCRPD)

Multidisciplinary assessment and co-ordination of interventions should be provided for

people with autism throughout their lifespan, including during old age, while taking into

account:

• The functional abilities of the older person;

•The interests and wishes of the older person and his/her family.

Individualised support plans for people with autism should be designed and put into practice

with the main objectives of:

• Improving and maintaining skills for autonomy in the home or residence;

• Improving and maintaining social skills in community activities

The right to have services to provide a good quality of life (art 26 of the UNCRPD)

Older people with autism should be fully and directly involved throughout the process of

designing, implementing and evaluating services that aim to meet their needs. Families, care

providers and friends should also be involved in these processes, as appropriate services

should be the result of a dialogue between relevant stakeholders. A diversity of accredited

services must also be available.

Service users with autism and their families/representatives must have permanent contact

and dialogue with the staf, the opportunity to express their needs, priorities, hopes and

desires, and to participate fully in the development, monitoring and review of individual

support plans.

In order to achieve these goals, services should provide specifc, qualifed interventions

consequent to contemporary knowledge in the feld of autism. Services should also have

a stable and reliable structure that adopts quality standards related to the quality of life

of the users and is based on a set of rules defning responsibilities, day-to-day routines and procedures.

These measures will enable family and staf members to identify the individual needs of

people with autism. These measures will also provide a way of reducing the risk of isolation

and exclusion.

The right to education and lifelong learning (art 24 of the UNCRPD)

Relevant services must provide a learning environment and education facilities adapted

to older people with autism. For people with autism, throughout their lifespan, education

represents a lot more than a basic right. Lifelong education is necessary to compensate

for the great difculties that people with autism have in extracting meaning from simple

experiences (something most other people are capable of without specifc educational

support) and to attain the highest possible degree of self-sufciency.

The right to housing facilities (art 19 and 23 of UNCRPD)

People with autism must be supported to remain in their own homes as long as they can,

like other ageing people, or live in places where they were accustomed to spending time

before retiring from ’active life’. Preparation for the changes in living arrangements must be

carefully planned. New environments must be adapted to the specifc needs of each person with autism.

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Challenges faced by ageing people with autism and their families

2017-03-14T04:16:00.000-07:00

It is important to refect on the defnition of elderly’ or ‘old age’ when applied to people

with autism. General chronological and biological age do not always coincide when people

age, thus it is difcult to defne old age’ by a specifc age range. The health status,capacities,

level of social interaction, etc., of people with autism can vary widely, even within the same

age group. Thus, the heterogeneity of older people should be taken into account when

determining the age-specifc care that should be available and some people with

autism may

need specifc attention in relation to ageing at an earlier stage than the general population.

While the overall life expectancy of people with autism remains lower than for other

individuals, their life expectancy is increasing along with the general population.

According

to various surveys, individuals with learning disabilities have a reduced life expectancy,

however, as for the general population, the life expectancy for this group is increasing.

These studies are also indicative of increased life expectancy for people with autism, who

can have diferent degrees’ of learning disability.

Who will care?

Most older adults with disabilities no longer have their parents to take care of them and

support them to voice their needs. This raises an essential question: what will happen to

3.3 million older people who have autism when their parents are no longer able to care for

them or have passed away?

One of the biggest concerns for the families of adults with autism is who will care for them

when their parents are no longer able to do so. The results of a survey conducted by the

National Autistic Society in 2012 showed that 96 percent of parents who responded are

worried about their son/daughter’s future when they are no longer able to support them.

Of these, 68 percent described themselves as ‘very worried’, and 28 percent said they are

quite worried’.30

Among the survey respondents, 35 percent had made some plans for what will happen if

they are no longer able to support their son/daughter, but only 4 percent said they had

planned a lot. This leaves a large number of people worried about what will happen to their

son or daughter when they are unable to support them, but very few who have made plans

for them.

Recently in France, a 49 year-old man with a mental disability (who had been left without support after the death of his mother last year) died alone in their apartment. The man’s

body was found, months later, mummifed. This case involving a man with a mental disability

illustrates the same problem that people who have autism face: a severe lack of services

that leave people alone and vulnerable.

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Symptoms of Autism

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Autism affects the way an individual perceives the
world and makes communication and social interac-
tion diffcult. Autism spectrum disorders (ASD) are
characterized by social-interaction diffculties,
communication challenges and a tendency to engage
in repetitive behaviors. However, symptoms and their
severity vary widely across these three core areas.
Taken together, they may result in relatively mild
challenges for someone on the high functioning end
of the autism spectrum. For others, symptoms may
be more severe, as when repetitive behaviors and
lack of spoken language interfere with everyday life.
While autism is usually a life long condition, all
children and adults beneft from interventions, or
therapies, that can reduce symptoms and increase
skills and abilities. Although it is best to begin inter-
vention as soon as possible, the benefts of therapy
can continue throughout life. The long term outcome
is highly variable. A small percentage of children
lose their diagnosis over time, while others remain
severely affected. Many have normal cognitive
skills, despite challenges in social and language
abilities. Many individuals with autism develop
speech and learn to communicate with others.
Early intervention can make extraordinary differ-
ences in your child’s development. How your child
is functioning now may be very different from how
he or she will function later on in life.

Social symptoms

Typically developing infants are social by nature.
They gaze at faces, turn toward voices, grasp a
fnger and even smile by 2 to 3 months of age. By
contrast, most children who develop autism have
diffculty engaging in the give-and-take of everyday
human interactions. By 8 to 10 months of age, many
infants who go on to develop autism are showing
some symptoms such as failure to respond to their
names, reduced interest in people and delayed
babbling. By toddlerhood, many children with autism
have diffculty playing social games, don’t imitate the
actions of others and prefer to play alone. They may
fail to seek comfort or respond to parents’ displays
of anger or affection in typical ways.
Research suggests that children with autism are
attached to their parents. However, the way they
express this attachment can be unusual. To parents,
it may seem as if their child is disconnected. Both
children and adults with autism also tend to have diff-
culty interpreting what others are thinking and feeling.
Subtle social cues such as a smile, wave or grimace
may convey little meaning. To a person who misses
these social cues, a statement like “Come here!”
may mean the same thing, regardless of whether the
speaker is smiling and extending her arms for a hug or frowning and planting her fsts on her hips.
Without the ability to interpret gestures and facial
expressions, the social world can seem bewildering.
Many people with autism have similar diffculty
seeing things from another person’s perspective.
Most fve-year-olds understand that other people
have different thoughts, feelings and goals than they
have. A person with autism may lack such under-
standing. This, in turn, can interfere with the ability to
predict or understand another person’s actions.
It is common – but not universal – for those with
autism to have diffculty regulating emotions. This
can take the form of seemingly “immature” behavior
such as crying or having outbursts in inappropriate
situations. It can also lead to disruptive and physically
aggressive behavior. The tendency to “lose control”
may be particularly pronounced in unfamiliar, over-
whelming or frustrating situations. Frustration can
also result in self-injurious behaviors such as head
banging, hair pulling or self-biting.
Fortunately, children with autism can be taught how
to socially interact, use gestures and recognize facial
expressions. Also, there are many strategies that
can be used to help the child with autism deal with
frustration so that he or she doesn’t have to resort
to challenging behaviors. We will discuss this later.

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What causes autism?

2017-03-14T03:44:00.000-07:00

Not long ago, the answer to this question would have

been “we have no idea.” Research is now delivering

the answers. First and foremost, we now know that

there is no one cause of autism, just as there is no

one type of autism. Over the last fve years, scien-

tists have identifed a number of rare gene changes

or mutations associated with autism. Research has

identifed more than 100 autism risk genes. In around

15% of cases, a specifc genetic cause of a person’s

autism can be identifed. However, most cases in-

volve a complex and variable combination of genetic

risk and environmental factors that infuence early

brain development.

In other words, in the presence of a genetic pre-

disposition to autism, a number of non-genetic or

environmental infuences further increase a child’s

risk. The clearest evidence of these environmental

risk factors involves events before and during birth.

They include advanced parental age at time of con-

ception (both mom and dad), maternal illness during

pregnancy, extreme prematurity, very low birth weight

and certain diffculties during birth, particularly those

involving periods of oxygen deprivation to the baby’s

brain. Mothers exposed to high levels of pesticides

and air pollution may also be at higher risk of having

a child with ASD. It is important to keep in mind that

these factors, by themselves, do not cause autism.

Rather, in combination with genetic risk factors, they

appear to modestly increase risk.

A small but growing body of research suggests that

autism risk is lower among children whose mothers

took prenatal vitamins (containing folic acid) in the

months before and after conception.

Increasingly, researchers are looking at the role of

the immune system in autism. Autism Speaks is

working to increase awareness and investigation of

these and other issues where further research has

the potential to improve the lives of those who

struggle with autism.

While the causes of autism are complex, it is abun-

dantly clear that it is not caused by bad parenting.

Dr. Leo Kanner, the psychiatrist who frst described

autism as a unique condition in 1943, believed that

it was caused by cold, unloving mothers. Bruno

Bettelheim, a renowned professor of child develop-

ment, perpetuated this misinterpretation of autism.

Their promotion of the idea that unloving mothers

caused their children’s autism created a generation of

parents who carried the tremendous burden of guilt

for their child’s disability. In the 1960s and 70s,

Dr. Bernard Rimland, the father of a son with autism

who later founded the Autism Society of America and

the Autism Research Institute, helped the medical

community understand that autism is a biological

disorder and is not caused by cold parents.

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What is Autism?

2017-03-13T23:51:00.000-07:00

Autism spectrum disorder (ASD) and autism are

both general terms for a group of complex disorders

of brain development. These disorders are charac-

terized, in varying degrees, by diffculties in social

interaction, verbal and nonverbal communication and

repetitive behaviors. With the May 2013 publication

of the ffth edition of the American Psychiatric

Association’s Diagnostic and Statistical Manual

of Mental Disorders (commonly referred to as the

DSM-5), all autism disorders were merged into

one umbrella diagnosis of ASD. Previously, they

were recognized as distinct subtypes, including

autistic disorder, childhood disintegrative

disorder, pervasive developmental disorder-not

otherwise specifed (PDD-NOS) and Asperger

Syndrome. The DSM is the main diagnostic

reference used by mental health professionals and

insurance providers in the United States.

You may also hear the terms Classic Autism or

Kanner’s Autism (named after the frst psychiatrist to

describe autism) used to describe the most severe

form of the disorder. Under the current DSM-5, the

diagnosis of autism requires that at least six develop-

mental and behavioral characteristics are observed,

that problems are present before the age of three and

that there is no evidence of certain other conditions

that are similar.

What is Common is Autism?

Autism statistics from the U.S. Centers for Disease

Control and Prevention (CDC) released in March

2014 identify around 1 in 68 American children as on

the autism spectrum – a ten-fold increase in preva-

lence in 40 years. Careful research shows that this

increase is only partly explained by improved diag-

nosis and awareness. Studies also show that autism

is four to fve times more common among boys than

girls. An estimated 1 out of 42 boys and 1 in 189 girls

are diagnosed with autism in the United States.

ASD affects over 2 million individuals in the U.S.

and tens of millions worldwide. Moreover, govern-

ment autism statistics suggest that prevalence rates

have increased 10% to 17% annually in recent

years. There is no established explanation for this

continuing increase, although improved diagnosis

and environmental infuences are two reasons

often considered.

Behaviour

Children with autism often engage in a restricted range of behaviours, interests and activities

in a repetitive and stereotypic way. For example, they may concentrate intensively on an activ-

ity such as spinning the wheels on a toy car or lining up toys time and time again, but much

more seldom engage in spontaneous and varying games of pretend and role playing. Fixations

on different objects are common, as well as fxations on very complicated habits and routines

that must be repeated in exactly the same way each time. A departure from such a routine or

ritual can cause an outburst of despair or rage. Any sort of change, such as something being in

a different place or something being done in a different order than usual, can also be hard to

tolerate for a person with autism. Slightly older, more well-gifted children may especially have

periods of one-sided and narrow interests such as time tables, others’ birth dates, the popula-

tion of all Swedish towns, etc. It is also common for children with autism to continuously wave

their hands, rock back and forth and walk on tiptoe.

In addition to the diagnosed-based behaviours in the three areas named above, other symp-

toms are also common with autism: over-sensitivity or under-sensitivity for certain sounds,

touches, odours etc; periods of hyperactivity; sleeping and eating disorders, etc. None of these

are required for a diagnosis of autism.

What can be done?

Autism is a life-long disability. There is currently no known cure for autism. On the other hand,
many children with autism can develop signifcantly with early, well-planned and individu-
ally tailored educational efforts in specially adapted settings. One of the primary objectives is
to help the child develop functional communication. The educational approaches must focus
on knowledge about the unique ways that children with autism learn. Various ABA strategies
(Applied behaviour analysis) as well as the structured teaching method in the TEACCH-model
(Treatment and Education of Autistic and related Communication Handicapped Children) are
examples of such specially-tailored educational strategies for persons with autism.
Early identifcation, assessment and diagnosis are the frst step. The next step is to provide ac-
curate information for, and education of, parents and other concerned persons as soon as pos-
sible. These, together with promptly applied supportive measures that are both well-planned
and individually tailored, are the long-term basis for being able to help the child to develop. A
specially adapted nursery school and subsequent schooling are important prerequisites for the
child; similarly an adapted home environment and daily activities are equally important for the
adults. Adolescents and adults may need continued access to educational measures to further
develop skills that aim to increase independence and participation, even if these measures had been introduced early. High-functioning persons may require different types of assistance in
organizing their studies and access to various forms of tailored daily activities.
As adults, and for the rest of their lives, most persons with autism are in need of extensive as-
sistance and support. However, some persons may become relatively independent.

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Questions about the treatment of mental illness in children

2017-03-11T00:33:00.001-08:00

A few questions answer, that must you get
in your mind about Mentally Retarded Children.

Q. How do I know if my child’s problems are serious?

A. Not every problem is serious. In fact,
many everyday stresses can cause
changes in your child’s behavior. For
example, the birth of a sibling may
cause a child to temporarily act much
younger than he or she is. It is impor
tant to be able to tell the difference
between typical behavior changes and
those associated with more serious
problems. Pay special attention to
behaviors that include:
Problems across a variety of settings,
such as at school, at home, or with
peers
Changes in appetite or sleep
Social withdrawal, or fearful behavior
toward things your child normally is not
afraid of Returning to behaviors more common
in younger children, such as bed-
wetting, for a long time
Signs of being upset, such as sadness
or tearfulness
Signs of self-destructive behavior, such
as head-banging, or a tendency to get
hurt often
Repeated thoughts of death.

--------------------

Q.- Can symptoms be caused by a death in the family, illness in a parent, family inancial problems, divorce, or other events?

A. Yes. Every member of a family is
affected by tragedy or extreme stress,
even the youngest child. It’s normal for
stress to cause a child to be upset.
Remember this if you see mental, emo
tional, or behavioral symptoms in your
child. If it takes more than one month
for your child to get used to a situation,
or if your child has severe reactions,
talk to your child’s doctor.
Check your child’s response to stress.
Take note if he or she gets better with
time or if professional care is needed.
Stressful events are challenging, but
they give you a chance to teach your
child important ways to cope.
------------------------------

Q -Will my child get better with time?

A. Some children get better with time. But
other children need ongoing profes
sional help. Talk to your child’s doctor
or specialist about problems that are
severe, continuous, and affect daily
activities. Also, don’t delay seeking
help. Treatment may produce better
results if started early.

<---------------------///

Q.- How do I work with my child’s school?

A. If your child is having problems in
school, or if a teacher raises concerns,
you can work with the school to ind a
solution. You may ask the school to
conduct an evaluation to determine
whether your child qualiies for special
education services. However, not all
children diagnosed with a mental
illness qualify for these services.
Start by speaking with your child’s
teacher, school counselor, school
nurse, or the school’s parent organiza
tion. These professionals can help you
get an evaluation started. Also, each
state has a Parent Training and Infor
mation Center and a Protection and
Advocacy Agency that can help you
request the evaluation. The evaluation
must be conducted by a team of pro
fessionals who assess all areas related
to the suspected disability using a
variety of tools and measures.

<---------------------------///-

Q. What else can I do to help my child?

A. Children with mental illness need guid
ance and understanding from their par
ents and teachers. This support can
help your child achieve his or her full
potential and succeed in school. Before
a child is diagnosed, frustration, blame,
and anger may have built up within a
family. Parents and children may need
special help to undo these unhealthy
interaction patterns. Mental health pro
fessionals can counsel the child and
family to help everyone develop new
skills, attitudes, and ways of relating to
each other.
Parents can also help by taking part
in parenting skills training. This helps
parents learn how to handle dificult
situations and behaviors. Training
encourages parents to share a pleasant
or relaxing activity with their child, to
notice and point out what their child
does well, and to praise their child’s
strengths and abilities. Parents may
also learn to arrange family situations
in more positive ways. Also, parents
may beneit from learning stress-
management techniques to help them
deal with frustration and respond
calmly to their child’s behavior.
Sometimes, the whole family may need
counseling. Therapists can help family
members ind better ways to handle
disruptive behaviors and encourage
behavior changes. Finally, support
groups help parents and families con
nect with others who have similar prob
lems and concerns. Groups often meet
regularly to share frustrations and suc
cesses, to exchange information about
recommended specialists and strate
gies, and to talk with experts.

<-------------------------------------///-

Q. Where can I go for help?

A. If you are unsure where to go for help,
ask your family doctor. Others who can
help are listed below.
Mental health specialists, such as psy
chiatrists, psychologists, social work
ers, or mental health counselors
Health maintenance organizations
Community mental health centers
Hospital psychiatry departments and
outpatient clinics
Mental health programs at universities
or medical schools
State hospital outpatient clinics
Family services, social agencies,
or clergy Peer support groups
Private clinics and facilities
Employee assistance programs
Local medical and/or psychiatric
societies.
You can also check the phone book
under “mental health,” “health,” “social
services,” “hotlines,” or “physicians”
for phone numbers and addresses. An
emergency room doctor can also pro
vide temporary help and can tell you
where and how to get further help.
<-----------------------------------///-

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What Are the Signs of Mental Retardation?

2017-03-11T00:19:00.000-08:00

There are many signs of mental retardation.
For example, children with mental retardation may:

• sit up, crawl, or walk later than other children;
• learn to talk later, or have trouble speaking,
• find it hard to remember things,
• not understand how to pay for things,
• have trouble understanding social rules,
• have trouble seeing the consequences of their
actions,
• have trouble solving problems, and/or
• have trouble thinking logically.
About 87% of people with mental retardation
will only be a little slower than average in learning
new information and skills. When they are chil-
dren, their limitations may not be obvious. They
may not even be diagnosed as having mental
etardation until they get to school. As they
become adults, many people with mild retarda-
ion can live independently. Other people may not
even consider them as having mental retardation.
The remaining 13% of people with mental
retardation score below 50 on IQ tests. These
people will have more difficulty in school, at
home, and in the community. A person with
more severe retardation will need more inten-
sive support his or her entire life.
Every child with mental retardation is able
to learn, develop, and grow. With help, all
children with mental retardation can live a
satisfying life...

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What Causes Mental Retardation?

2017-03-11T00:11:00.001-08:00

Doctors have found many causes of mental
retardation. The most common are
• Genetic conditions. Sometimes mental retardation
is caused by abnormal genes inherited from
parents, errors when genes combine, or other
reasons. Examples of genetic conditions are
Down syndrome, fragile X syndrome, and
phenylketonuria (PKU).
• Problems during pregnancy. Mental retardation
can result when the baby does not develop inside
the mother properly. For example, there may be
a problem with the way the baby’s cells divide as
it grows. A woman who drinks alcohol or gets
an infection like rubella during pregnancy may
also have a baby with mental retardation.
• Problems at birth. If a baby has problems during
labor and birth, such as not getting enough
oxygen, he or she may have mental retardation.
• Health problems. Diseases like whooping cough,
the measles, or meningitis can cause mental
retardation. Mental retardation can also be
caused by extreme malnutrition (not eating
right), not getting enough medical care, or by
being exposed to poisons like lead or mercury.
Mental retardation is not a disease. You can’t
catch mental retardation from anyone. Mental
retardation is also not a type of mental illness, like
depression. There is no cure for mental retardation.
However, most children with mental retardation can
learn to do many things. It just takes them more time
and effort than other children.

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What is Mental Retardation Child?

2017-03-11T00:00:00.000-08:00

Mental retardation is a term used when a person

has certain limitations in mental functioning and in

skills such as communicating, taking care of him or

herself, and social skills. These limitations will cause

a child to learn and develop more slowly than a

typical child. Children with mental retardation may

take longer to learn to speak, walk, and take care of

their personal needs such as dressing or eating. They

are likely to have trouble learning in school. They

will learn, but it will take them longer. There may be

some things they cannot learn.

BACK TO MEAN PAGE

My legs condition

2013-10-18T22:00:00.000-07:00

As I've very severe spastic cp. I want to show my legs condition, aspecially when i am laying on bed.
It has too hot summer, that's why, i am sleeping out of room, open area my house.

ARY TV News Channel

2013-10-18T21:45:00.000-07:00

I given an interview to local TV channel about 2 week ago.
They asked many questions about my this situation.
i was a little nervous. because it was first i given live interview

Central Nervous System

2013-05-10T22:10:00.002-07:00

IMPOERTANT POINTS

General functions of the CNS

The Limbic System and Higher Mental Functions

Overview of the entire nervous system

The central nervous system is the control center for the body. It regulates organ function, higher thought, and
movement of the body. The central nervous system consists of the brain and spinal cord.

Generation & propagation of an action potential

The Nerve Impulse
When a nerve is stimulated the resting potential changes. Examples of such stimuli are pressure, electricity,
chemicals, etc. Different neurons are sensitive to different stimuli(although most can register pain). The stimulus
causes sodium ion channels to open. The rapid change in polarity that moves along the nerve fiber is called the
"ACTION POTENTIAL." This moving change in polarity has several stages:

Depolarization

The upswing is caused when positively charged sodium ions(Na+) suddenly rush through open sodium gates
into a nerve cell.The membrane potential of the stimulated cell undergoes a localized change from-65
millivolts to 0 in a limited area. As additional sodium rushes in, the membrane potential actually reverses its
polarity so that the outside of the membrane is negative relative to the inside. During this change of polarity
the membrane actually develops a positive value for a moment(+40 millivolts). The change in voltage
stimulates the opening of additional sodium channels (called a voltage-gated ion channel). This is an example
of a positive feedback loop.

Repolarization

(The downswing) is caused by the closing of sodium ion channels and the opening of potassium ion channels.
Release of positively charged potassium ions (K+) from the nerve cell when potassium gates open. Again,
these are opened in response to the positive voltage--they are voltage gated. This expulsion acts to restore the
localized negative membrane potential of the cell (about -65 or -70 mV is typical for nerves).
Refractory phase
is a short period of time after the depolarization stage. Shortly after the sodium gates open they close and go
into an inactive conformation. The sodium gates cannot be opened again until the membrane is repolarized to
its normal resting potential. The sodium-potassium pump returns sodium ions to the outside and potassium
ions to the inside. During the refractory phase this particular area of the nerve cell membrane cannot be
depolarized. This refractory area explains why action potentials can only move forward from the point of
stimulation.
Increased permeability of the sodium channel occurs when there is a deficit of calcium ions. when there is a deficit
of calcium ions (Ca+2) in the interstitial fluid the sodium channels are activated (opened) by very little increase of
the membrane potential above the normal resting level. The nerve fiber can therefore fire off action potentials
spontaneously, resulting in tetany. Could be caused by the lack of hormone from parathyroid glands. could be caused
by hyperventilation, which leads to a higher pH, which causes calcium to bind and become unavailable. Speed of
conduction. This area of depolarization/repolarization/recovery moves along a nerve fiber like a very fast wave. In
myelinated fibers, conduction is hundreds of times faster because the action potential only occurs at the nodes of
Ranvier (pictured below in 'types of neurons') by jumping from node to node. This is called "saltatory" conduction.
Damage to the myelin sheath by the disease can cause severe impairment of nerve cell function. Some poisons and
drugs interfere with nerve impulses by blocking sodium channels in nerves. See discussion on drug at the end of this
outline.

Brain

The brain is found in the cranial cavity. Within it are found the higher
nerve centers responsible for coordinating the sensory and motor
systems of the body (forebrain). The brain stem houses the lower nerve
centers (consisting of midbrain, pons, and medulla),

Medulla

The medulla is the control center for respiratory, cardiovascular and
digestive functions.

Pons

The pons houses the control centers for respiration and inhibitory functions. Here it will interact with the cerebellum.

Cerebrum

The cerebrum, or top portion of the brain, is divided by a deep crevice, called the longitudinal sulcus. The
longitudinal sulcus separates the cerebrum in to the right and left hemispheres. In the hemispheres you will find the
cerebral cortex, basal ganglia and the limbic system. The two hemispheres are connected by a bundle of nerve fibers
called the corpus callosum. The right hemisphere is responsible for the left side of the body while the opposite is true
of the left hemisphere. Each of the two hemispheres are divided into four separated lobes: the frontal in control of
specialized motor control, learning, planning and speech; parietal in control of somatic sensory functions; occipital in
control of vision; and temporal lobes which consists of hearing centers and some speech. Located deep to the
temporal lobe of the cerebrum is the insula.

Cerebellum

The cerebellum is the part of the brain that is located posterior to the medulla oblongata and pons. It coordinates
skeletal muscles to produce smooth, graceful motions. The cerebellum receives information from our eyes, ears,
muscles, and joints about what position our body is currently in (proprioception). It also receives output from the
cerebral cortex about where these parts should be. After processing this information, the cerebellum sends motor
impulses from the brainstem to the skeletal muscles. The main function of the cerebellum is coordination. The
cerebellum is also responsible for balance and posture. It also assists us when we are learning a new motor skill, such
as playing a sport or musical instrument. Recent research shows that apart from motor functions cerebellum also has

READ MORE

General functions of the CNS

The Limbic System and Higher Mental Functions

Overview of the entire nervous system

General functions of the CNS

2013-05-10T00:14:00.001-07:00

CNS:
The "Central Nervous System", comprised of brain, brainstem, and
spinal cord.
The central nervous system (CNS) represents the largest part of the
nervous system, including the brain and the spinal cord. Together, with
he peripheral nervous system (PNS), it has a fundamental role in the
control of behavior.
The CNS is conceived as a system devoted to information processing,
where an appropriate motor output is computed as a response to a
sensory input. Many threads of research suggest that motor activity
exists well before the maturation of the sensory systems, and senses
only influence behavior without dictating it. This has brought the
conception of the CNS as an autonomous system.

Structure and function of neurons

Structure

Neurons are highly specialized for the processing and transmission of
cellular signals. Given the diversity of functions performed by neurons in different parts of the nervous system, there
is, as expected, a wide variety in the shape, size, and electrochemical properties of neurons. For instance, the soma of
a neuron can vary in size from 4 to 100 micrometers in diameter.
The soma (cell body) is the central part of the neuron. It contains the nucleus of the cell, and therefore is where most
protein synthesis occurs. The nucleus ranges from 3 to 18 micrometers in diameter. The dendrites of a neuron are
cellular extensions with many branches, and metaphorically this overall shape and structure is referred to as a
dendritic tree. This is where the majority of input to the neuron occurs. However, information outflow (i.e. from
dendrites to other neurons) can also occur (except in chemical synapse in which backflow of impulse is inhibited by
the fact that axon do not possess chemoreceptors and dendrites cannot secrete neurotransmitter chemical). This
explains one way conduction of nerve impulse. The axon is a finer, cable-like projection which can extend tens,
hundreds, or even tens of thousands of times the diameter of the soma in length. The axon carries nerve signals away
from the soma (and also carry some types of information back to it). Many neurons have only one axon, but this
axon may - and usually will - undergo extensive branching, enabling communication with many target cells. The part
of the axon where it emerges from the soma is called the 'axon hillock'. Besides being an anatomical structure, the
axon hillock is also the part of the neuron that has the greatest density of voltage-dependent sodium channels. This
makes it the most easily-excited part of the neuron and the spike initiation zone for the axon: in neurological terms it
has the greatest hyperpolarized action potential threshold. While the axon and axon hillock are generally involved in
information outflow, this region can also receive input from other neurons as well. The axon terminal is a specialized
structure at the end of the axon that is used to release neurotransmitter chemicals and communicate with target
neurons. Although the canonical view of the neuron attributes dedicated functions to its various anatomical
components, dendrites and axons often act in ways contrary to their so-called main function.
Axons and dendrites in the central nervous system are typically only about a micrometer thick, while some in the
peripheral nervous system are much thicker. The soma is usually about 10–25 micrometers in diameter and often is
not much larger than the cell nucleus it contains. The longest axon of a human motor neuron can be over a meter
long, reaching from the base of the spine to the toes. Sensory neurons have axons that run from the toes to the dorsal
columns, over 1.5 meters in adults. Giraffes have single axons several meters in length running along the entire
length of their necks. Much of what is known about axonal function comes from studying the squids giant axon, an
ideal experimental preparation because of its relatively immense size (0.5–1 millimeters thick, several centimeters
long).

Function

Sensory afferent neurons convey information from tissues and organs into the central nervous system. Efferent
neurons transmit signals from the central nervous system to the effector cells and are sometimes called motor
neurons. Interneurons connect neurons within specific regions of the central nervous system. Afferent and efferent
can also refer generally to neurons which, respectively, bring information to or send information from brain region.
Classification by action on other neurons
Excitatory neurons excite their target postsynaptic neurons or target cells causing it to function. Motor neurons and
somatic neurons are all excitatory neurons. Excitatory neurons in the brain are often glutamatergic. Spinal motor
neurons, which synapse on muscle cells, use acetylcholine as their neurotransmitter. Inhibitory neurons inhibit their
target neurons. Inhibitory neurons are also known as short axon neurons, interneurons or microneurons. The output
of some brain structures (neostriatum, globus pallidus, cerebellum) are inhibitory. The primary inhibitory
neurotransmitters are GABA and glycine. Modulatory neurons evoke more complex effects termed
neuromodulation. These neurons use such neurotransmitters as dopamine, acetylcholine, serotonin and others. Each
synapses can receive both excitatory and inhibitory signals and the outcome is determined by the adding up of
summation.

Summation

When excitatory synapses exceed the amount of inhibitory synapses there are, then the excitatory synapses will
prevail over the other. The same goes with inhibitory synapses, if there are more inhibitory synapses than excitatory,
the synapses will be inhibited. To determine all of this is called summation.
Classification by discharge patterns:
Neurons can be classified according to their electrophysiological characteristics (note that a single action potential is
not enough to move a large muscle, and instead will cause a twitch).
Tonic or regular spiking: Some neurons are typically constantly (or tonically) active. Example: interneurons in
neurostriatum.
Phasic or bursting: Neurons that fire in bursts are called phasic.
Fast spiking: Some neurons are notable for their fast firing rates. For example, some types of cortical inhibitory
interneurons, cells in globus pallidus.
Thin-spike: Action potentials of some neurons are more narrow compared to the others. For example, interneurons
in prefrontal cortex are thin-spike neurons.
Classification by neurotransmitter released:
Some examples are cholinergic, GABAergic, glutamatergic and dopaminergic neurons.

The Limbic System and Higher Mental Functions

2013-05-10T00:05:00.000-07:00

The Limbic System

The Limbic System is a complex set of structures found just beneath
the cerebrum and on both sides of the thalamus. It combines higher
mental functions, and primitive emotion, into one system. It is often
referred to as the emotional nervous system. It is not only responsible
for our emotional lives, but also our higher mental functions, such as
learning and formation of memories. The Limbic system explains why
some things seem so pleasurable to us, such as eating and why some
medical conditions are caused by mental stress, such as high blood
pressure. There are two significant structures within the limbic system
and several smaller structures that are important as well. They are:

1. The Hippocampus
2. The Amygdala
3. The Thalamus
4. The Hypothalamus
5. The Fornix and Parahippocampus
6. The Cingulate Gyrus

Structures of the Limbic System

Hippocampus

The Hippocampus is found deep in the temporal lobe, shaped like a seahorse. It consists of two horns that
curve back from the amygdala. It is situated in the brain so as to make the prefrontal area aware of our past
experiences stored in that area. The prefrontal area of the brain consults this structure to use memories to
modify our behavior. The hippocampus is responsible for memory.

Amygdala

The Amygdala is a little almond shaped structure, deep inside the anteroinferior region of the temporal lobe,
connects with the hippocampus, the septi nuclei, the prefrontal area and the medial dorsal nucleus of the
thalamus. These connections make it possible for the amygdala to play its important role on the mediation and
control of such activities and feelings as love, friendship, affection, and expression of mood. The amygdala is
the center for identification of danger and is fundamental for self preservation. The amygdala is the nucleus
responsible for fear.

Thalamus

Lesions or stimulation of the medial, dorsal, and anterior nuclei of the thalamus are associated with changes in
emotional reactivity. However, the importance of these nuclei on the regulation of emotional behavior is not
due to the thalamus itself, but to the connections of these nuclei with other limbic system structures. The
medial dorsal nucleus makes connections with cortical zones of the prefrontal area and with the hypothalamus.
The anterior nuclei connect with the mamillary bodies and through them, via fornix, with the hippocampus and
the cingulated gyrus, thus taking part in what is known as the Papez's circuit.

Hypothalamus

The Hypothalamus is a small part of the brain located just below
the thalamus on both sides of the third ventricle. Lesions of the
hypothalamus interfere with several vegetative functions and
some so called motivated behaviors like sexuality,
combativeness, and hunger. The hypothalamus also plays a role
in emotion. Specifically, the lateral parts seem to be involved
with pleasure and rage, while the medial part is linked to
aversion, displeasure, and a tendency to uncontrollable and loud
laughing. However, in general the hypothalamus has more to do
with the expression of emotions. When the physical symptoms
of emotion appear, the threat they pose returns, via the
hypothalamus, to the limbic centers and then the prefrontal
nuclei, increasing anxiety.

The Fornix and Parahippocampal

These small structures are important connecting pathways for the limbic system.

The Cingulate Gyrus

The Cingulate Gyrus is located in the medial side of the brain between the cingulated sulcus and the corpus
callosum. There is still much to be learned about this gyrus, but it is already known that its frontal part
coordinates smells and sights, with pleasant memories of previous emotions. The region participates in the
emotional reaction to pain and in the regulation of aggressive behavior.

Memory and Learning

Memory is defined as : The mental faculty of retaining and recalling past experiences, the act or instance of
remembering recollection. Learning takes place when we retain and utilize past memories.
Overall, the mechanisms of memory are not completely understood. Brain areas such as the hippocampus, the
amygdala, the striatum, or the mammillary bodies are thought to be involved in specific types of memory. For
example, the hippocampus is believed to be involved in spatial learning and declarative learning (learning
information such as what you're reading now), while the amygdala is thought to be involved in emotional memory.
Damage to certain areas in patients and animal models and subsequent memory deficits is a primary source of
information. However, rather than implicating a specific area, it could be that damage to adjacent areas, or to a
pathway traveling through the area is actually responsible for the observed deficit. Further, it is not sufficient to
describe memory, and its counterpart, learning, as solely dependent on specific brain regions. Learning and memory
are attributed to changes in neuronal synapses, thought to be mediated by long-term potentiation and long-term
depression.

There are three basic types of memory:

1. Sensory Memory
2. Short Term Memory
3. Long Term Memory

Sensory Memory

The sensory memories act as a buffer for stimuli through senses. A sensory memory retains an exact copy of
what is seen or heard: iconic memory for visual, echoic memory for aural and haptic memory for touch.
Information is passed from sensory memory into short term memory. Some believe it lasts only 300
milliseconds, it has unlimited capacity. Selective attention determines what information moves from sensory
memory to short term memory.

Short Term Memory

Short Term Memory acts as a scratch pad for temporary recall of the information under process. For instance,
in order to understand this sentence you need to hold in your mind the beginning of the sentence as you read
the rest. Short term memory decays rapidly and also has a limited capacity. Chunking of information can lead
to an increase in the short term memory capacity, this is the reason why a hyphenated phone number is easier
to remember than a single long number. The successful formation of a chunk is known as closure. Interference
often causes disturbance in short term memory retention. This accounts for the desire to complete a task held
in short term memory as soon as possible.

Within short term memory there are three basic operations:

1. Iconic memory - the ability to hold visual images
2. Acoustic memory - the ability to hold sounds. Can be held longer than iconic.
3. Working memory - an active process to keep it until it is put to use. Note that the goal is not really to move the
information from short term memory to long term memory, but merely to put it to immediate use.

The process of transferring information from short term to long term memory involves the encoding or consolidation
of information. This is not a function of time, that is, the longer the memory stays in the short term the more likely it
is to be placed in the long term memory. On organizing complex information in short term before it can be encoded
into the long term memory, in this process the meaningfulness or emotional content of an item may play a greater
role in its retention in the long term memory. The limbic system sets up local reverberating circuits such as the
Papez's Circuit.

Long Term Memory

Long Term Memory is used for storage of information over a long time. Information from short to long term
memory is transferred after a short period. Unlike short term memory, long term memory has little decay.
Long term potential is an enhanced response at the synapse within the hippocampus. It is essential to memory
storage. The limbic system isn't directly involved in long term memory necessarily but it selects them from
short term memory, consolidates these memories by playing them like a continuous tape, and involves the
hippocampus and amygdala.
There are two types of long term memory:

1. Episodic Memory
2. Semantic Memory

Episodic memory represents our memory of events and experiences in a serial form. It is from this memory that we
can reconstruct the actual events that took place at a given point in our lives. Semantic memory, on the other hand, is
a structured record of facts, concepts, and skills that we have acquired. The information in the semantic memory is
derived from our own episode memory, such as that we can learn new facts or concepts from experiences.
There are three main activities that are related to long term memory:

1. Storage
2. Deletion
3. Retrieval

Information for short term memory is stored in long term memory by rehearsal. The repeated exposure to a stimulus
or the rehearsal of a piece of information transfers it into long term memory. Experiments also suggest that learning
is most effective if it is distributed over time. Deletion is mainly caused by decay and interference. Emotional factors
also affect long term memory. However, it is debatable whether we actually ever forget anything or whether it just
sometimes becomes increasingly difficult to retrieve it. Information may not be recalled sometimes but may be
recognized, or may be recalled only with prompting. This leads us to the third operation of memory, information
retrieval.
There are two types of information retrieval:

1. Recall
2. Recognition

In recall, the information is reproduced from memory. In recognition the presentation of the information provides the
knowledge that the information has been seen before. Recognition is of lesser complexity, as the information is
provided as a cue. However, the recall may be assisted by the provision of retrieval cues which enable the subject to
quickly access the information in memory.

Long-term Potentiation

. Long-term potentiation (LTP) is the lasting enhancement of connections between two neurons that results from
stimulating them simutaneously. Since neurons communicate via chemical synapses, and because memories are
believed to be stored within these synapses, LTP and it's opposing process, long-term depression, are widely
considered the major cellular mechanisms that underlie learning and memory. This has been proven by lab
experiments. When one of the chemicals involved (PKMzeta, it will be discussed later) is inhibited in rats, it causes
retrograde amnesia with short term memory left intact (meaning they can't recall events from before the inhibitor was
given).
By enhancing synaptic transmission, LTP improves the ability of two neuron, one presynaptic and the other
postsynaptic, to communicate with one another across a synapse. The precise mechanism for this enhancement isn't
known, but it varies based on things like brain region, age and species. This will focus on LTP in the CA1 section of
the hippocampus, because that's what is well known.
The end result of LTP is a well established neural circuit that can be called upon later for memory.
LTP in the CA1 hippocampus is called NMDA receptor-dependent LTP. It has four main properties.
• Rapid induction
LTP can be rapidly induced by applying one or more brief, high-frequency, stimulus to a presynaptic cell.
• Input specificity
Once induced, LTP at one synapse does not spread to other synapses; rather LTP is input specific. LTP is only
propagated to those synapses according to the rules of associativity and cooperativity.
• Associativity
Associativity refers to the observation that when weak stimulation of a single pathway is insufficient for the
induction of LTP, simultaneous strong stimulation of another pathway will induce LTP at both pathways.
• Cooperativity
LTP can be induced either by strong tetanic stimulation of a single pathway to a synapse, or cooperatively via
the weaker stimulation of many. When one pathway into a synapse is stimulated weakly, it produces
insufficient postsynaptic depolarization to induce LTP. In contrast, when weak stimuli are applied to many
pathways that converge on a single patch of postsynaptic membrane, the individual postsynaptic
depolarizations generated may collectively depolarize the postsynaptic cell enough to induce LTP
cooperatively. Synaptic tagging, discussed later, may be a common mechanism underlying associativity and
cooperativity.
LTP is generally divided into three parts that occur sequentially: Short-term potentiation, early LTP (E-LTP) and late
LTP (L-LTP). Short-term potentiation isn't well understood and will not be discussed.
E-LTP and L-LTP phases of LTP are each characterized by a series of three events: induction, maintenance and
expression. Induction happens when a short-lived signal triggers that phase to begin. Maintenance corresponds to the
persistent biochemical changes that occur in response to the induction of that phase. Expression entails the
long-lasting cellular changes that result from activation of the maintenance signal.
Each phase of LTP has a set of mediator molecules that dictate the events of that phase. These molecules include
protein receptors, enzymes, and signaling molecules that allow progression from one phase to the next. In addition to
mediators, there are modulator molecules that interact with mediators to fine tune the LTP. Modulators are a bit
beyond the scope of this introductory book, and won't be discussed here.

Early Phase

Induction
E-LTP induction begins when the calcium inside the postsynaptic cell exceeds a threshold. In many types of LTP,
the flow of calcium into the cell requires the NMDA receptor, which is why these types of LTP are considered
NMDA receptor-dependent.
When a stimulus is applied to the presynaptic neuron, it releases a neurotransmitter, typically glutamate, onto the
postsynaptic cell membrane where it binds to AMPA receptors, or AMPARs. This causes an influx of sodium ions
into the postsynaptic cell, this short lived depolarization is called the excitatory postsynaptic potential (EPSP) and
makes it easier for the neuron to fire an action potential.
A single stimulus doesn't cause a big enough depolarization to trigger an E-LTP, instead it relies on EPSP
summation. If EPSPs are reaching the cell before the others decay, they will add up. When the depolarization reaches
a critical level, NMDA receptors lose the magnesium molecule they were originally plugged with and let calcium in.
The rapid rise in calcium within the postsynaptic neuron trigger the short lasting activation of several enzymes that
mediate E-LTP induction. Of particular importance are some protein kinase enzymes, including CaMKII and PKC.
To a lesser extent, PKA and MAPK activation also contribute.
Maintenance
During the maintenance stage of E-LTP, CaMKII and PKC lose their dependence on calcium and become
autonomously active. They then carry out phosphorylation that underlies E-LTP expression.
Expression
CaMKII and PKC phosphorylate existing AMPA receptors to increase their activity, and mediate the insertion of
additional AMPA receptors onto the postsynaptic cell membrane. This is achieved by having a pool of nonsynaptic
AMPA receptors adjacent to the postsynaptic membrane. When the appropriate stimulus arrives, the nonsynaptic
AMPA receptors are brought into the postsynaptic membrane under the influence of protein kinases.
AMPA receptors are one of the most common type of receptors in the brain. Their effect is excitatory. By adding
more AMPA receptors, and increasing their activity, future stimuli will generate larger postsynaptic responses.

Late Phase

Late LTP is the natural extension of E-LTP. L-LTP requires gene transcription and protein synthesis in the
postsynaptic cell, unlike E-LTP. Late LTP is also associated with the presynaptic synthesis of synaptotagmin and an
increase in synaptic vesicle number, suggesting that L-LTP induces protein synthesis not only in postsynaptic cells,
but in presynaptic cells as well. This is discussed under "retrograde messenger" below.
Induction
Late LTP is induced by changes in gene expression and protein synthesis brought about by persistent activation of
protein kinases activated during E-LTP, such as MAPK. In fact, MAPK--Specifically the ERK subfamily of
MAPKs--may be the molecular link between E-LTP and L-LTP, since many signaling cascades involved in E-LTP,
including CaMKII and PKC, can converge on ERK.
Maintenance
Upon activation, ERK may phosphorylate a number of cytoplasmic and nuclear molecules that ultimately result in
the protein synthesis and morphological changes associated with L-LTP. These chemicals may include transcription
factors such as CREB. ERK-mediated changes in transcription factor activity may trigger the synthesis of proteins
that underlie the maintenance of L-LTP. PKMzeta is one such molecule. When this molecule is inhibited in rats, they
experience retrograde amnesia (where you can't recall previous events but short term memory works fine).
Expression
Aside from PKMzeta, many of the proteins synthesized during L-LTP are unknown. They are though to increase
postsynaptic dendritic spine number, surface area and sensitivity to the neurotransmitter associated with L-LTP
expression.

Retrograde Signaling

Retrograde signaling is a hypothesis that attempts to explain that, while LTP is induced and expressed
postsynaptically, some evidence suggests that it is expressed presynaptically as well. The hypothesis gets its name
because normal synaptic transmission is directional and proceeds from the presynaptic to the postsynaptic cell. For
induction to occur postsynaptically and be partially expressed presynaptically, a message must travel from the
postsynaptic cell to the presynaptic cell in a retrograde (reverse) direction. Once there, the message presumably
initiates a cascade of events that leads to a presynaptic component of expression, such as the increased probability of
neurotransmitter vesicle release.
Retrograde signaling is currently a contentious subject as some investigators do not believe the presynaptic cell
contributes at all to the expression of LTP. Even among proponents of the hypothesis there is controversy over the
identity of the messenger.
Language and Speech
Language depends on semantic memory so some of the same areas in the brain are involved in both memory and
language. Articulation, the forming of speech, is represented bilaterally in the motor areas. However, for most
individuals, language analysis and speech formation take place in regions of the left hemisphere only. The two
regions involved are:

1. Broca's Area
2. Wernicke's Area

Broca's area is located just in front of the voice control area of the left motor cortex. This region assembles the motor
of speech and writing. For example, patients with lesions in this area:

1. Understand language perfectly
2. May be able to write perfectly
3. Seldom speak spontaneously

Wernicke's area is part of the auditory and visual associations cortex. This region is responsible for the analysis and
formation of language content. For example, patients with lesions in this area:

1. Are unable to name objects
2. Are unable to understand the meaning of words
3. Articulate speech readily but usually nonsensically
Diseases of the Limbic System

There are several well known diseases that are disorders of the limbic system. Several are discussed here.
Schizophrenia
An increased dopamine (DA) response in the limbic system results in schizophrenia. DA may be synthesized or
secreted in excess, DA receptors may be supersensitive, and DA regulatory mechanism may be defective. Symptoms
are decreased by drugs which block DA receptors. Symptoms of schizophrenia are:

1. Loss of touch with reality
2. Decreased ability to think and reason
3. Decreased ability to concentrate
4. Decreased memory
5. Regress in child-like behavior
6. Altered mood and impulsive behavior
7. Auditory hallucinations

Symptoms may be so severe that the individual cannot function.

Depression

Depression is the most common major mental illness and is characterized by both emotional and physical symptoms.
Symptoms of depression are:

1. Intense sadness and despair
2. Anxiety
3. Loss of ability to concentrate
4. Pessimism
5. Feelings of low self esteem
6. Insomnia or hypersomnia
7. Increased or decreased appetite
8. Changes in body temperature and endocrine gland function

10 to 15% of depressed individuals display suicidal behavior during their lifetime.
The cause of depression and its symptoms are a mystery but we do understand that it is an illness associated with
biochemical changes in the brain. A lot of research goes on to explain that it is associated with a lack of amines
serotonin and norephinephrine. Therefore pharmacological treatment strategies often try to increase amine
concentrations in the brain.
One class of antidepressants is monoamine oxidase inhibitors. Mono amine oxidase is a enzyme that breaks down
your amines like norephinephrine and serotonin. Because the antidepressants inhibit their degradation they will
remain in the synaptic cleft for a longer period of time making the effect just as if you had increased theses types of
neurotransmitters.
A newer class of antidepressants is selective serotonin reuptake inhibitors (SSRI's). With SSRI's decreasing the
uptake of serotonin back into the cell that will increase the amount of serotonin present in the synaptic cleft. SSRI's
are more specific than the monoamine oxidase inhibitors because they only affect serotonergic synapses. You might
recognize these SSRI's by name as Prozac and Paxil.

Bipolar Disorder

Another common form of depression is manic depression. Manic is an acute state characterized by:

1. Excessive elation and impaired judgment
2. Insomnia and irritability
3. Hyperactivity
4. Uncontrolled speech

Manic depression, also known as bipolar disorder, displays mood swings between manic and depression. The limbic
system receptors are unregulated. Drugs used are unique mood stabilizers.
The hippocampus is particularly vulnerable to several disease processes, including ischemia, which is any
obstruction of blood flow or oxygen deprivation, Alzheimer’s disease, and epilepsy. These diseases selectively attack
CA1, which effectively cuts through the hippocampal circuit.
An Autism Link
A connection between autism and the limbic system has also been noted as well. URL: http:/ / www. autism. org/
limbic. html

Case Study

Central Pain Syndrome

I was 42 years old when my life changed forever. I had a stroke. As an avid viewer of medical programs on
television I assumed that I would have physical therapy for my paralyzed left side and get on with my life. No one
ever mentioned pain or the possibility of pain, as a result of the stroke. I did experience unusual sensitivity to touch
while still in the hospital, but nothing to prepare me for what was to come.
The part of my brain that is damaged is the Thalamus. This turns out to be the pain center and what I have now is an
out of control Thalamus, resulting in Thalamic Pain syndrome, also called Central Pain Syndrome. This means that
24 hours a day, seven days a week, my brain sends messages of pain and it never goes away. I am under the care of
physicians, who not only understand chronic pain, but are also willing to treat it with whatever medications offer
some help. None of the medications, not even narcotic medications, take the pain away. They just allow me to
manage it so I can function.

Overview of the entire nervous system

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The nervous system has three main functions: sensory input,
integration of data and motor output. Sensory input is when the body
gathers information or data, by way of neurons, glia and synapses. The
nervous system is composed of excitable nerve cells (neurons) and
synapses that form between the neurons and connect them to centers
throughout the body or to other neurons. These neurons operate on
excitation or inhibition, and although nerve cells can vary in size and
location, their communication with one another determines their
function. These nerves conduct impulses from sensory receptors to the
brain and spinal cord. The data is then processed by way of integration
of data, which occurs only in the brain. After the brain has processed
the information, impulses are then conducted from the brain and spinal
cord to muscles and glands, which is called motor output. Glia cells are
found within tissues and are not excitable but help with myelination,
ionic regulation and extracellular fluid.
The nervous system is comprised of two major parts, or subdivisions,
the central nervous system (CNS) and the peripheral nervous system
(PNS). The CNS includes the brain and spinal cord. The brain is the
body's "control center". The CNS has various centers located within it that carry out the sensory, motor and integration of data. These centers can be subdivided to Lower Centers
(including the spinal cord and brain stem) and Higher centers communicating with the brain via effectors. The PNS
is a vast network of spinal and cranial nerves that are linked to the brain and the spinal cord. It contains sensory
receptors which help in processing changes in the internal and external environment. This information is sent to the
CNS via afferent sensory nerves. The PNS is then subdivided into the autonomic nervous system and the somatic
nervous system. The autonomic has involuntary control of internal organs, blood vessels, smooth and cardiac
muscles. The somatic has voluntary control of skin, bones, joints, and skeletal muscle. The two systems function
together, by way of nerves from the PNS entering and becoming part of the CNS, and vice versa.

Cerebrospinal fluid

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Cerebrospinal fluid (CSF) is a watery liquid similar in composition to blood plasma. It is
formed in the choroid plexuses and circulates through the ventricles into the subarachnoid
space, where it is returned to the dural venous sinuses by the arachnoid villi. The prime
purpose of the CSF is to support and cushion the brain and help nourish it. Figure 2–4
illustrates the flow of CSF through the central nervous system.

Major regions of the brain and their functions

The major regions of the brain (Figure 2–5) are the cerebral hemispheres, diencephalon,
brain stem and cerebellum

Cerebral hemispheres

The cerebral hemispheres (Figure 2–6), located on the most superior part of the brain, are
separated by the longitudinal fissure. They make up approximately 83% of total brain mass,
and are collectively referred to as the cerebrum. The cerebral cortex constitutes a 2-4 mm
thick grey matter surface layer and, because of its many convolutions, accounts for about
40% of total brain mass. It is responsible for conscious behaviour and contains three
different functional areas: the motor areas, sensory areas and association areas. Located
internally are the white matter, responsible for communication between cerebral areas and
between the cerebral cortex and lower regions of the CNS, as well as the basal nuclei (or
basal ganglia), involved in controlling muscular movement.
Diencephalon
The diencephalon is located centrally within the forebrain. It consists of the thalamus,
hypothalamus and epithalamus, which together enclose the third ventricle. The thalamus
acts as a grouping and relay station for sensory inputs ascending to the sensory cortex and
association areas. It also mediates motor activities, cortical arousal and memories. The
hypothalamus, by controlling the autonomic (involuntary) nervous system, is responsible
for maintaining the body’s homeostatic balance. Moreover it forms a part of the limbic
system, the ‘emotional’ brain. The epithalamus consists of the pineal gland and the CSF-
producing choroid plexus.

Blood supply to the brain

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Figure 2–7 shows an overview of the arterial system supplying the brain. The major arteries
are the vertebral and internal carotid arteries. The two posterior and single anterior
communicating arteries form the circle of Willis, which equalises blood pressures in the
brain’s anterior and posterior regions, and protects the brain from damage should one of the
arteries become occluded. However, there is little communication between smaller arteries
on the brain’s surface. Hence occlusion of these arteries usually results in localised tissue
damage.

Cerebral haemodynamics

The cardiac output is about 5 l/min of blood for a resting adult. Blood flow to the brain is
about 14% of this, or 700 ml/min. For any part of the body, the blood flow can be calcu-
lated using the simple formula
Resistance
Pressure
= flow Blood (2.1)
Pressure in the arteries is generated by the heart which pumps blood from its left ventricle
into the aorta. (Since pressure was historically measured with a mercury manometer, the
units are commonly expressed in terms of [mm Hg], although the official SI unit is the
Pascal [Pa].) Resistance arises from friction, and is proportional to the following expression
4
Diameter) (Vessel
Length Vessel
Viscosity Resistance × ∝ (2.2)
Hence blood flow is slowest in the small vessels of the capillary bed, thus allowing time for
the exchange of nutrients and oxygen to surrounding tissue by diffusion through the
capillary walls.
Approximately 75% of total blood volume is ‘stored’ in the veins which, because of
their high capacity, act as reservoirs. Their walls distend and contract in response to the
amount of blood available in the circulation. However, the function of cerebral veins,

formed from sinuses in the dura mater, is somewhat different from other veins of the body,
as they are non-collapsible.

Autoregulation

[Panerai 1998] describes autoregulation of blood flow in the cerebral vascular bed as the
mechanism by which cerebral blood flow (CBF) tends to remain relatively constant despite
changes in cerebral perfusion pressure (CPP). With a constant metabolic demand, changes
in CPP or arterial blood pressure that would increase or reduce CBF, are compensated by
adjusting the vascular resistance. This maintains a constant O2 supply and constant CBF.
Therefore cerebral autoregulation allows the blood supply to the brain to match its
metabolic demand and also to protect cerebral vessels against excessive flow due to arterial
hypertension. Cerebral blood flow is autoregulated much better than in almost any other
organ. Even for arterial pressure variations between 50 and 150 mm Hg, CBF only changes
by a few percent. This can be accomplished because the arterial vessels are typically able to
change their diameter about 4-fold, corresponding to a 256-fold change in blood flow. Only
when the brain is very active is there an exception to the close matching of blood flow to
metabolism, which can rise by up to 30-50% in the affected areas. It is an aim of PET,
functional MRI, near infrared spectroscopy (NIRS), and, possibly, near infrared imaging, to
detect or image such localised changes in cortical activity and associated blood flow.

Structure and pathologies of the neonatal brain

Having introduced some basics of the anatomy and physiology of the adult brain, this
section focuses on the specific differences in the neonate, as well as common neonatal
pathologies which have motivated the construction of an instrument capable of imaging
cerebral oxygenation, blood volume and, possibly, myelination.
The embryonic brain and spinal cord develop from the neural tube, which is formed by
the fourth week of pregnancy. The brain grows immensely in both size and complexity
during pregnancy and even soon after birth. Because a membranous skull restricts expan-
sion, the forebrain is bent towards the brain stem, and the cerebral hemispheres almost
completely envelop the diencephalon and midbrain. Moreover, the spatial restrictions cause
the cerebral hemispheres to increase their surface area by becoming highly convoluted such
that about two thirds of its surface are hidden in its folds. The skull bones of the foetus and
neonate are soft and the sutures are not yet fused. Hence the skull is very flexible and
deforms under light pressure. Brain development of the foetus, neonate and infant are more
thoroughly reviewed by [Herschkowitz 1988].
Compared to the adult, neonates have a smaller head size (ca. 6-12 cm in diameter),
thinner surface tissue, skull and CSF layers, lower scattering coefficients of grey and white
matter (due to lesser myelination in the case of white matter), as well as a comparatively
small mismatch between the two (see also Table 4–1). These anatomical features are all
favourable to NIR imaging. The neonatal skull, because it is less mineralised, may also have
a lower scattering coefficient, but there is no data at present. All these factors greatly
benefit penetration of light deep into the white matter and enable measurements to be made
across the head, which is essential for tomographic imaging.
Arterial and venous haemoglobin saturation values for the foetus in utero are relatively
low at 56 % and 18% [Rooth 1963], respectively, compared to about 97% and 67% for
adults. This is because there is a gradient in oxygen concentration across the placenta which
ensures diffusion of sufficient amounts of oxygen from maternal blood into the foetal
bloodstream. A higher oxygen affinity of neonatal haemoglobin (dissociation curve shifted
to the ‘left’, c.f. Figure 4–3) compensates for this. Over a period of about 6 months after

delivery the neonatal haemoglobin is gradually substituted by the adult haemoglobin, which
has a lower oxygen affinity.
The autoregulation mechanism of the (adult) brain was discussed in the previous sec-
tion. However, in the newborn infant, and particularly in the very preterm infant, there is no
consensus on whether, or to what extent, autoregulation in the brain occurs. It is also not
clear what effect ischaemia has on cerebral blood flow and the evolution of haemorrhage.
Neurodevelopmental disorders in some preterm infants are due to either hypoxic-
ischaemic damage to the periventricular white matter, or to intraventricular haemorrhage
and its consequences. The period of highest risk is between 26 and 32 weeks of gestation.
In preterm infants the majority of haemorrhages occur into the ventricles and the surround-
ing white matter, the periventricular region. Hypoxic-ischaemic damage is caused by
cerebral underperfusion, often combined with a global oxygen deficiency due to an
impaired lung function. It also affects the periventricular white matter, which is thought to
be a result of the following two effects:
• Increased vulnerability due to high metabolic demands at this phase of the brain
development.
• The area is at a ‘watershed’ of perfusion from the territories of the posterior and middle
cerebral arteries (c.f. Figure 2–7).
Enduring neurodevelopmental disorders can lead to diminished neurological function in
later life, and in particular spasticity, since motor fibres run through this region of the white
matter. Given the potential of the premature infant’s developing brain to repair some
damage, spasticity is often restricted to stiff limbs and/or subtle learning disabilities.
Cerebral damage in the mature infant is most commonly a result of perinatal (‘birth’)
asphyxia, leading initially to cerebral oedema (resulting in compressed ventricles and
flattening of the convolutions of the brain), and later to tissue necrosis (tissue death) and
apoptosis (cell suicide). The subcortical white matter, basal ganglia, cerebellum and
brainstem are the areas predominantly affected, frequently leading to learning disabilities or
global developmental delay and cerebral palsy.
Sample neonatal brain images, including that of a patient with hypoxic-ischaemia
(Figure 3–4), can be found in chapter 3, which describes various conventional imaging
modalities. A comprehensive review of common neurologic disorders is given by [Hill
1996].

Brain stem

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The brain stem is similarly structured as the spinal cord: it consists of grey matter sur-
rounded by white matter fibre tracts. Its major regions are the midbrain, pons and medulla
oblongata. The midbrain, which surrounds the cerebral aqueduct, provides fibre pathways
between higher and lower brain centres, contains visual and auditory reflex and subcortical
motor centres. The pons is mainly a conduction region, but its nuclei also contribute to the
regulation of respiration and cranial nerves. The medulla oblongata takes an important role
as an autonomic reflex centre involved in maintaining body homeostasis. In particular,
nuclei in the medulla regulate respiratory rhythm, heart rate, blood pressure and several
cranial nerves. Moreover, it provides conduction pathways between the inferior spinal cord
and higher brain centres.

Cerebellum

The cerebellum, which is located dorsal to the pons and medulla, accounts for about 11% of
total brain mass. Like the cerebrum, it has a thin outer cortex of grey matter, internal white
matter, and small, deeply situated, paired masses (nuclei) of grey matter. The cerebellum
processes impulses received from the cerebral motor cortex, various brain stem nuclei and
sensory receptors in order to appropriately control skeletal muscle contraction, thus giving
smooth, coordinated movements.

The cerebral circulatory system

Blood is transported through the body via a continuous system of blood vessels. Arteries
carry oxygenated blood away from the heart into capillaries supplying tissue cells. Veins
collect the blood from the capillary bed and carry it back to the heart. The main purpose of
blood flow through body tissues is to deliver oxygen and nutrients to and waste from the
cells, exchange gas in the lungs, absorb nutrients from the digestive tract, and help forming
urine in the kidneys. All the circulation besides the heart and the pulmonary circulation is
called the systemic circulation.
Since it is the ultimate aim of this research project to image cerebral oxygenation and
haemodynamics some aspects of the cerebral circulatory system are described below.

Human Skull

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Depending on their shape, bones are classified as long, short, flat or irregular. Bones of
different types contain different proportions of the two types of osseous tissue: compact and
spongy bone. While the former has a smooth structure, the latter is composed of small
needle-like or flat pieces of bone called trabeculae, which form a network filled with red or
yellow bone marrow. Most skull bones are flat and consist of two parallel compact bone
surfaces, with a layer of spongy bone sandwiched between. The spongy bone layer of flat
bones (the diploë) predominantly contains red bone marrow and hence has a high concen-
tration of blood.
The skull is a highly complex structure consisting of 22 bones altogether. These can be
divided into two sets, the cranial bones (or cranium) and the facial bones. While the latter
form the framework of the face, the cranial bones form the cranial cavity that encloses and
protects the brain. All bones of the adult skull are firmly connected by sutures. Figure 2–2
shows the most important bones of the skull. The frontal bone forms the forehead and
contains the frontal sinuses, which are air filled cells within the bone. Most superior and
lateral aspects of the skull are formed by the parietal bones while the occipital bone forms
the posterior aspects. The base of the occipital bone contains the foramen magnum, which
is a large hole allowing the inferior part of the brain to connect to the spinal cord.
remaining bones of the cranium are the temporal, sphenoid and ethmoid bones.

Meninges

The meninges (Figure 2–3) are three connective tissue membranes enclosing the brain
the spinal cord. Their functions are to protect the CNS and blood vessels, enclos
venous sinuses, retain the cerebrospinal fluid, and form partitions within the skull.
outermost meninx is the dura mater, which encloses the arachnoid mater and the inner
pia mater.

The Brain Skin

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The skin constitutes a protective barrier against physical damage of underlying tissues,
invasion of hazardous chemical and bacterial substances and, through the activity of its
sweat glands and blood vessels, it helps to maintain the body at a constant temperature.
Together with the sweat and oil glands, hairs and nails it forms a set of organs called the
integumentary system. Figure 2–1 shows a cross-section of the skin and underlying
subcutaneous tissue. The skin consists of an outer, protective layer, the epidermis and an
inner layer, the dermis. While the top layer of the epidermis, the stratum corneum, consists
of dead cells, the dermis is composed of vascularised fibrous connective tissue. The
subcutaneous tissue, located underneath the skin, is primarily composed of adipose tissue
(fat).

Basic Anatomy and Physiology of the Human Brain

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Main Points

The Brain Skin

Human Skull

Brain stem

Blood supply to the brain

Cerebrospinal fluid

The human nervous system consists of the central nervous system (CNS) and peripheral
nervous system (PNS). The former consists of the brain and spinal cord, while the latter
composes the nerves extending to and from the brain and spinal cord. The primary
functions of the nervous system are to monitor, integrate (process) and respond to informa-
tion inside and outside the body. The brain consists of soft, delicate, non-replaceable neural
tissue. It is supported and protected by the surrounding skin, skull, meninges and cerebro-
spinal fluid.

The brain

Ø Human brain weighs about 1.2 to 1.4kg.
Ø It consumes 25% of the body oxygen supply to generate energy;
Ø It is covered by a membrane called the Meninges.
Ø It is enclosed in a bony case called the skull or cranium.
Ø It is made up of 2 types of nervous tissues, (Nerves cells or grey matter and Nerves fibers or white matter.)

Human brain is divided into 3 parts

a. Fore brain (i.e. Large, forward part).
b. Mid brain (i.e. narrow brain).
c. Hind brain (i.e. rare path).

Fore Brain: - it consist mainly cerebrum, thalamus and hypothalamus.

Midbrain: links the forebrain to the hindbrain. It controls auditory and visual reflexes.

Hindbrain: composed of 3 parts

(A) Cerebellum

(B) Pons varolii

SELF-ASSESSMENT EXERCISE 1

i. The autonomic nervous system consists of -- and --------
ii. Mention two portions of the hind brain.

Functions of the parts of the brain
Cerebrum controls all the bodies’ voluntary action and
consciousness.
Frontal lobe – seat of intelligence, Memory, Imagination,
thought, judgment, emotional reaction and movement of
skeletal muscles.
. Parietal lobe – Receives and interprets the sensations of pressure,
temperature and position.
Temporal lobe is concerned with hearing, memory and
understanding of speech.

Integration with other Systems

To function effectively, every cell in the body must communicate with
its neighbors and with cells and tissues in distant portions of the body.
In a few specialized cases, cellular activities are coordinated by the
exchange of ions and molecules from one cell to the next across gap
junctions. This direct communication occurs between cells of the same
type, and the two cells must be in extensive physical contact. The two
cells communicate so closely that they function as single entity. For
example, gap junctions (1) coordinate ciliary movement among
epithelial cells, (2) coordinate the contractions of cardiac muscle cells,
and (3) facilitate the propagation of action potentials from one neuron to
the next at electrical synapses.
Direct communications is highly specialized and relatively rare. Most of
the communications between cells involves the release and receipt of
chemical messages. Each cell continuously “talks” to its neighbors by
releasing chemicals into the extra cellular fluid. These chemicals tell
what their neighbors are doing at any moment; the result is the
coordination of tissue function at the local level. The use of chemical
messengers to transfer information from cell to cell within a single
tissue is called paracrine communications. The chemicals involved are
called paracrine factors, also known as cytokines, or local hormones.
Examples of paracrine factors include the prostaglandins.

SELF-ASSESSMENT EXERCISE B

(I) What is the function of the temporal lobe?
(II) --------------- is an example of paracrine factors.

CONCLUSION

The nervous system includes the neural tissues that make up the
autonomic nervous system and the peripheral nervous system. The
neurons are the basic functional unit. The nervous system and the
endocrine systems are closely linked.

SUMMARY

In this unit we have learnt the two major anatomical divisions of the
nervous system; (1) the central nervous system (II) peripheral nervous
system; their divisions and various functions.

The Brain Skin

Human Skull

Brain stem

Blood supply to the brain

Cerebrospinal fluid