The Third Eye - Radiology site

Periventricular Leukomalacia

2012-01-30T17:00:00.000+05:30

MRI images of a five year old baby with spastic quadriparesis were shown below. He had history of preterm birth with low birth weight and birth asphyxia.

FLAIR images shows periventricular gliosis with wavy margins of bilateral ventricles.

Periventricular cysts on coronal T2 Weighted images.

Periventricular leukomalacia results from hypoxic-ischemic injury to watershed zones of arterial supply in the periventricular white matter of the immature brain .

These watershed zones are most prominent in the posterior periventricular white matter at the trigone of the lateral ventricles and in white matter adjacent to the foramina of Monro .

The anatomic location of PVL determines the characteristic neurologic sequelae observed in many survivors of low birth weight. Thus, lesions may affect either the geniculocalcarine tract and cause visual impairment or the corticospinal tracts in the corona radiata and damage the motor fibers, which control the function of lower limbs and trunk. Consequently, the classical neurologic sequelae of PVL include spastic diplegia or quadriplegia, and cortical blindness with relative preservation of cognitive functions, except in severe cases. In severe cases, the cerebral injury is more diffuse and results in multiple neurologic handicaps .

Radiologic features of PVL, includes

(1) ventriculomegaly with irregular outline of body and trigone of lateralventricles

(2) Reduced amounts of periventricular white matter at the trigone and, in more severe cases, the entire centrum semiovale; and

(3) Deep and prominent sulci with subcortical gray matter abutting the ventricles directly without interposed white matter .

(4) Thinning of corpus callosum.

Reference- MR imaging of periventricular leukomalacia in childhood, American Journal of Radiology.

Osgood-Schlatter disease

2012-01-27T16:38:00.000+05:30

An adolescent boy presented with pain, soft tissue swelling, and tenderness in the anterior knee in the

proximity of the tibial tuberosity.

The distal patellar tendon is edematous and swollen with loss of the sharp margination. There is
fragmentation of the tibial tuberosity. Bone marrow edema is seen as well in proximal tibia.

Osgood-Schlatter disease is a common, self-limiting, but painful and disabling disorder involving the patellar tendon-tibial tubercle complex in adolescent individuals.

Distinctively, the disease is most frequently encountered in adolescents between 11 and 15 years of age.

A common misconception is that Osgood-Schlatter disease represents avascular necrosis of the developing tibial tuberosity. The pathologic abnormalities are most consistent with inflammatory changes at the distal patellar tendon.

Recently, the MRI findings have been categorized into five stages, consisting of normal, early, progressive, terminal, and healing. In the early stage, MRI signs of marrow edema can be seen in one third of cases with a low signal on T1- and high signal on T2-weighted studies. Progression is noted by the partial avulsion of the secondary ossification center, whereas the terminal stage consists of complete separation. Healing is characterized most significantly by resolution of the soft tissue changes. Persistence of the ossicles may be asymptomatic but, infrequently, may precipitate persistence of pain into adulthood. Rarely, genu recurvatum and patella alta may complicate the disorder.

References

Essentials of Skeletal Radiology 3rd Edition by Yochum & Rowe.

Musculoskeletal Imaging: THE REQUISITES, 3rd edition.

Aicardi-Goutières syndrome and pseudo TORCH lesions.

2012-01-24T18:00:00.000+05:30

Six month infant with jitteriness, feeding problems ,hypertonia and stiffness came for imaging evaluation for delayed mile stones.

Toxoplasmosis, rubella, cytomegalovirus, and herpes virus (TORCH) studies were negative.

There is diffuse cerebral atrophy and hypomyelination

Thinning of corpus callosum

Hypomyelination on T1WI

Aicardi-Goutières syndrome is a rare syndrome characterized by autosomal recessive inheritance Genetic studies show genetic heterogeneity with one locus at chromosome 3p21 . Most affected children are normal at birth, but show progressive microcephaly and encephalopathy (including spasticity, dystonia, visual inattention, abnormal eye movements, and cognitive delay) . Seizures are uncommon . Although most affected children show rapid progression of symptoms during the first year of life, some have a slowly progressive course characterized mainly by dystonia, dyskinesia, or cognitive delay.

Current diagnostic criteria are as follow: (a) progressive neurological disorder with onset in first year of life; (b) normal head circumference at birth; (c) calcification involving the basal ganglia and sometimes white matter; (d) CSF pleocytosis (>5 cells/mL); and (e) negative TORCH studies .

Imaging findings are primarily those of punctate calcifications of the putamen and, sometimes, the subcortical white matter. Progressive atrophy is typical but is variable in severity. Although myelination may be delayed, frank leukoencephalopathy is not seen .

Numerous forms of childhood leukoencephalopathy with calcifications can be a differential diagnosis,

1. Main one is TORCH infections, which is excluded by TORCH serology,

2. Pseudo-TORCH Syndrome of Baraitser and Reardon in which patients are microcephalic at birth. In our case, the baby had normal head circumference.

4. Cockayne syndrome, in which cerebellar atrophy is also a predominant feature, which is not a feature in our case.

5. Metabolic causes like Biotinidase deficiency & carbonic anhydrase II deficiency.

6. Cree encephalitis, reported among the Cree Indians, leads to microcephaly, intracerebral calcifications, hepatosplenomegaly, and thrombocytopenia.

7. HIV infection, which is again excluded by serology.

b By excluding each other and with the diagnostic criterias, presumed diagnosis is Aicardi-Goutières syndrome ( chromosomal diagnosis awaited).

r References

1 1.Pediatric neuroimaging James Barkovich.

2 2.M.S. van der Knaap, J.Valk Magnetic Resonance of Myelination and Myelin Disorders

third Edition

PLAGIOCEPHALY

2012-01-21T03:56:00.000+05:30

Premature cranial suture synostosis signifies premature closure of one or more of the cranial sutures from any cause. Primary cranial synostoses occur in the absence of underlying brain or metabolic disease. Secondary cranial synostoses occur as the indirect consequence of reduced intracranial volume, often after shunting of hydrocephalus or a cerebral insult.

Normally, the sutures become narrower and the fontanelles become smaller as the skull matures. The sagittal suture begins to close at 22 years, the coronal suture at 24 years, and the lambdoid suture at 26 years. These sutures may become fully closed only at 35, 41, and 47 years, respectively.

Unilateral or bilateral fusion of the coronal suture is the second most common form of craniosynostosis ( after scaphocephaly) and accounts for 20%–30% of all craniosynostosis cases.

Unilateral coronal synostosis in infancy is considered sporadic and nonsyndromic, while bilateral coronal synostosis is commonly syndromic.

Patients with unilateral coronal synostosis present with a palpable suture, ipsilateral exophthalmos, uplifting of the ipsilateral eyebrow, and ﬂattening of the frontal bone, resulting in anterior plagiocephaly. Patients with bilateral coronal synostosis have symmetric bone growth along the sagittal and metopic sutures, resulting in brachycephaly.

left coronal synostosis

The most consistent imaging feature of coronal synostosis, the harlequin deformity of the orbit, occurs because of superior elevation of the lesser wing of the sphenoid with resultant proptosis and exophthalmos, which can be severe. Anterior ﬂattening of the ipsilateral forehead and orbit and compensatory bulging of the contralateral side is a common presentation leading to anterior plagiocephaly.

plagiocephaly

References

1.Head and Neck Imaging- Peter Som & Hugh Curtin

2. Imaging of Craniosynostosis from Diagnosis through Reconstruction Hesham Attaya, MD, Joel Thomas, MD, and Anthony Alleman, MD, MPH Neurographics Volume 1, Number 3, December 2011

Enchondroma

2012-01-18T18:50:00.000+05:30

Incidentally detected lesion in a young female who came for cervical spine evaluation

PDFS image show chondroid matrix- geographic hyperintense lesion with signal voids.

T2WI better shows the calcifications- signal voids.

No permeation of cortex- T1WI Axial

matrix calcifications well seen in CT.

Diagnosis of enchondroma is quite obvious in this case- differentials in any case may include marrow infarct ( which is excluded by MRI here) / low grade chondrosarcoma.

However in many cases,Differentiation between enchondroma and low grade chondrosarcoma is a major challenge for several reasons. The following guidelines may be helpful in tricky situations.

Lesions with the typical radiographic appearance of an enchondroma in a typical localisation and without symptoms can be diagnosed by plain radiography and do not need further workup. Certain criteria, however, do not belong to the typical presentation of an enchondroma and should initiate further workup. These are:

Ø Lesion-related pain, especially when not explained by the mechanical situation of the parent bone, i.e. if the lesion is not likely to cause a stress phenomenon.
Ø Atypical localisation.
Ø Large lesion size, e.g. larger than 5 cm.
Ø Any radiographic change in the mature skeleton.
Ø Penetration of the cortex.
Ø Deep cortical scalloping, more than two thirds of the cortical thickness.
Ø Periosteal reaction or cortical remodelling, except for a thin neocortex.
Ø Different calcification patterns within a lesion.
Ø Different signal patterns within a lesion in MR imaging.
Ø Soft tissue extension.
Ø Marked uptake of radionuclide (greater than the anterior iliac crest).

Reference-

Imaging of Bone Tumors and Tumor-Like Lesions Techniques and Applications : SPRINGER: A. M. Davies ∙ M. Sundaram ∙ S. L. J. James page numb 246-248.

Persistent Trigeminal Artery

2012-01-14T21:52:00.000+05:30

In fetal life,communications between the carotid and posterior circulation occur during vascular development. Persistence of these embryonic vascular communications occasionally occur.

The persistent trigeminal artery is the most cephalically located and frequently occurring persistent carotid–vertebrobasilar anastomosis. It is called as the trigeminal artery as it courses in proximity to the trigeminal nerve. Its incidence is reported to be 0.1–0.6% in large angiographic series.

The persistent trigeminal artery usually arises from the presellar ICA as it exits the carotid canal and enters the cavernous sinus. It extends posteriorly to join the distal third of the basilar artery usually between the origins of the superior and anterior inferior cerebellar arteries.

The persistent trigeminal artery has two types, the lateral type and the medial type. Both are equally common.

The persistent trigeminal artery is classified according to the configuration of the ipsilateral posterior cerebral artery.

In the Saltzman type 1 persistent trigeminal artery, the posterior communicating artery is absent.

In the Saltzman type 2 persistent trigeminal artery, the ipsilateral posterior cerebral artery arises directly from the ICA and the P1 segment is absent, which indicates a fetal origin of the posterior cerebral artery.

The basilar artery is usually hypoplastic caudad to the anastomosis in both Saltzman types.

The tau sign refers to the unusual conﬁguration of signal voids in the presellar ICA and in a persistent trigeminal artery, as viewed on parasagittal T1-weighted MR images.The combination of the vertical and horizontal segments of the ICA and the proximal portion of the trigeminal artery creates the outline of the Greek letter tau.

TAU SIGN

References-

1.The Tau Sign Manish Goyal, MD September 2001 Radiology,220, 618-619.

2. MR Angiography of Anomalous Branches of the Internal Carotid Artery AJR November 2003 vol. 181 no. 5 1409-1414

Pilomatrixoma of the scalp

2012-01-11T20:26:00.000+05:30

Pilomatrixoma, or calcifying epithelioma of Melherbe, is a rare benign tumor of hair-follicle origin that usually arises in the head and neck region, most commonly in the first two decades of life.

scalp lesion with calcifications

partly cystic, partly calcified scalp lesion T2WI

T1WI PILOMATRIXOMA

It is a benign calcifying tumor that is thought to arise from skin appendages. The lesion arises in the dermis from primitive cells that normally differentiate into hair matrix cells.

These lesions are small (usually less than 3 cm in diameter), grow slowly, are conﬁned to the subcutaneous tissue and are seen most commonly on the face, neck, and arms.

Calciﬁcation, which is more typically central, is seen in about 85% of lesions.

Reference-Superﬁcial Soft-Tissue Masses: Analysis, Diagnosis, and Differential Considerations , Radiographics March-April 2007 27:509-523.

Hemiconvulsion-hemiplegia-epilepsy syndrome

2012-01-09T23:51:00.000+05:30

A 3 year old girl child with prolonged unilateral (left) partial seizures developed left hemiplegia and she came for MR evaluation.

There is diffuse cortical edema in entire right cerebral hemisphere not confining to any specific vascular territory.

DWI and ADC maps reveal diffusion restriction suggesting cytotoxic edema in these areas as well in right thalamus.

MR angiography shows dilatation of right middle cerebral artery representing hyperperfusion.

Hemiconvulsion-hemiplegia-epilepsy syndrome (HHE) was first described by Gastaut and colleagues almost 50 years ago. It is defined by a prolonged unilateral febrile seizure or seizures followed by the development of a transient or permanent hemiparesis ipsilateral to the side of the convulsion occurring in a young child (<4 years of age). The imaging and pathologic features of HHE include acute edema of the affected hemisphere, often followed by the development of volume loss in that hemisphere. Following initial presentation, children may then develop partial epilepsy at a time remote from the initial presentation.

The pathogenesis is believed to be an interplay among genetic predisposition; viral infection (e.g., influenza, HHV 6) or toxin (theophylline) exposure; excitotoxicity due to prolonged ictal activity; and contributory systemic factors such as cytokine excess, hypoxia, ischemia, and fever.

References-

1. Hemiconvulsion-hemiplegia-epilepsy syndrome Another case for epilepsy surgery Neurology May 27, 2008

2. Diffusion-Weighted MR Imaging of the Brain Second Edition T. Moritani S. Ekholm,P.-L. Westesson

Atrophic rhinitis

2012-01-06T16:30:00.000+05:30

Also called as ozena (Greek for 'the stench'), Atrophic rhinitis is a chronic and troublesome disorder of nasal cavity of tropics characterised by progressive nasal mucosal atrophy with resorption of underlying cartilage.

Atrophy of the middle and inferior turbinates.

Roomy (enlarged) nasal cavities with bowing of lateral nasal walls

Mucoperiosteal thickening of the nasal cavity and paranasal sinuses

Often patients have intractable nasal secretions in earlier stages followed by dry bloody crusts later in the course of the disease giving rise to merciful anosmia( the patient has anosmia despite the fetid odour). on imaging, the patients have roomy nasal cavities with bowing of lateral nasal wall,mucoperiosteal thickening of nasal cavity and paranasal sinuses and loss of definition of the osteomeatal complex secondary to resorption of the ethmoid bulla and uncinate process.

Hypoplasia of the maxillary sinuses.

Multiple organisms have been claimed for these, but Klebsiella ozenae is frequently cultured from the nasal discharge.

Reference- Pace-Balzan A, Shankar L, Hawke M. Computed tomographic findings in atrophic rhinitis. J Otolaryngol 20: 428-32, 1991.

cervical rib with accessory articulation

2012-01-03T23:15:00.001+05:30

cervical ribs are one of the incidentally detected thing and are asymptomatic most of the times.

cervical ribs may be complete, when they articulate with sterum or may be rudimentary(incomplete).

A young lady with features of thoracic outlet syndrome had these findings.

There is complete cervical rib on the right side: The left cervical rib has an accessory articulation with the

typical first rib ( synostosis). There is pseudoarthrosis in the midst of the fusion.

INFANTILE CORTICAL HYPEROSTOSIS (CAFFEY’ S DISEASE)

2011-12-27T02:26:00.000+05:30

A four month baby presented to us with swelling of right cheek.

There is diffuse cortical thickening of body,ramus and coronoid process of mandible, more on the right side seen as periosteal thickening.

Caffey’s disease or Infantile Cortical Hyperostosis (ICH) is a mostly self limiting condition affecting young infants. It is characterized by acute inflammation of the periosteum and the overlying soft tissue and is accompanied by systemic changes of irritability and fever. Diagnosis may be delayed as this disorder mimics a wide range of diseases including osteomyelitis, hypervitaminosis A, scurvy, bone tumors and child abuse. A high index of suspicion in a typical clinical setting can avoid protracted investigations for this otherwise self-limiting illness.

The most commonly involved bones are the mandible, clavicle, and ribs, in which involvement is frequently symmetric.

There is soft tissue prominence of masticator muscles and parotid on the right side.

Patients usually manifest a clinical triad of hyperirritability, swelling of the soft tissues, and palpable hard masses over affected bones. Fever is nearly always present, along with an increased erythrocyte sedimentation rate and elevated serum alkaline phosphatase levels. More than half of Caffey’s patients show reduced hemoglobin and red blood cell levels.

Periosteal new bone formation takes place within the soft tissue swelling adjacent to the cortex. This new bone may be dense and may increase to the extent that the bone doubles its original size. The hyperostosis usually persists for some time after evidence of soft tissue swelling has subsided. During the healing phase, the new bone formation may have a laminated appearance, but this is not noted during the acute stage.

Residual changes—including facial asymmetry, disturbances in longitudinal growth, medullary expansion, and undertubulation of long bones—are often associated with severe and chronic cases.

Reference-

Essentials of Skeletal Radiology 3rd Edition- Yochum & Rowe

Direct Carotico Cavernous Fistula

2011-12-22T13:23:00.000+05:30

Carotid–cavernous fistulas represent a direct communication between the intracavernous portion of the internal carotid artery and the cavernous venous sinus. The typical clinical presentation of a carotid–cavernous fistula is ophthalmologic symptoms, including pulsatile proptosis, pain, chemosis,and orbital bruit

PROPTOSIS IN A GIRL POST TRAUMA

DILATED RT SUPERIOR OPHTHALMIC VEIN

MULTIPLE VESSELS IN RT CAV SINUS

MRA- FLOW RELATED ENHANCEMENT IN
RIGHT CAVERNOUS SINUS & RT SUPERIOR OPHTHALMIC VEIN.

There are two basic types of carotid–cavernous vascular malformations, direct (type A) and indirect (dural, types B–D), each of which has a different etiology.

Direct high flow carotid–cavernous fistulas are most commonly the result of head trauma; however,spontaneous carotid–cavernous fistulas may be seen in a spectrum of disorders, including atherosclerosis in the elderly, rupture of a carotid–cavernous aneurysm, or in association with underlying vascular dysplasias.

Indirect low flow carotid–cavernous vascular malformation, otherwise known as a dural arteriovenous fistula, is a shunt between cavernous sinuses and

meningeal branches of the cavernous internal carotid artery (type B),

meningeal branches of the external carotid artery (type C) or

meningeal branches of both the intracavernous carotid artery and the external carotid artery (type D)

DILATED SUP OPTHALMIC VEIN

MULTIPLE FLOW VOIDS IN CAV SINUS

References

1.Barrow DL, Spector RH, Braun IF, et al: Classification and treatment of spontaneous carotid-cavernous sinus fistulas, J Neurosurg 62:248–256, 1985.

2.Neuroradiology: THE REQUISITES, 2nd edition.

Parkinsonism & Basal ganglia T1 hyperintensity- an interesting association.

2011-12-17T21:31:00.000+05:30

We came across a patient with clinical diagnosis of parkinsonism, and his MR images were given below.

BILATERAL SYMMETRICAL HYPERINTENSITIES

IN GLOBUS PALLIDUS.

Liver disease and parenteral nutrition are two major conditions in which an excess of circulating manganese exists. For unknown reasons, the excess may accumulate in the anterior pituitary lobe and globus pallidus .Therefore, the association of homogeneous T1 signal hyperintensity of the adenohypophysis and globus pallidus bilaterally is a common pattern at cerebral MR imaging in patients receiving parenteral nutrition in an intensive-care unit, or in patients with chronic liver deficiency.

NOTE THE T1 HYPERINTENSE ANTERIOR PITUITARY.

Most of the time , radiologists who come across T1 hyperintensities in anterior pituitary and bilateral globus pallidus ascribe it to be due to hepatocerebral degeneration/ hypermanganesemia secondary to total parenteral nutrition. Yeah, in most of these instances the scenario ends with this however with some exceptions…..

Retrospectively,our patient had imaging features of chronic hepatic failure . And is there any relationship with parkinsonism ? and if so how it differs from idiopathic parkinsonism?

Answer is…

Parkinsonism has been recognized as a unique neurologic complication of chronic liver failure .

It is suggested that this form of parkinsonism may be distinguished from idiopathic Parkinson disease (PD) by early gait and balance dysfunction, relative absence of resting tremor, characteristically increased T1 signal in the basal ganglia on brain magnetic resonance (MR)imaging, and elevated serum manganese levels.

Similar symptoms, including parkinsonism, cognitive dysfunction,tremor, and personality change, have been observed in welders, called MANGANISM. Manganese exposure scenarios in the last century generally have changed from the acute, high-level exposure conditions responsible for the occurrence of manganism to chronic exposure to much lower levels. Such chronic exposures may progressively extend the site of manganese deposition and toxicity from the globus pallidus to the entire area of the basal ganglia, including the substantia nigra pars compacta involved in Parkinson's disease. The mechanisms of manganese neurotoxicity from chronic exposure to very low levels are not well understood.

The difference in treatment between these types of Parkinson diseases and their responses to levodopa are evolving and we have to still wait for it.

References

1.T1 Signal Hyperintensity in the Sellar Region: Spectrum of Findings- January 2006 RadioGraphics.

2. Neurologic Spectrum of Chronic Liver Failure and Basal Ganglia T1 Hyperintensity on Magnetic Resonance Imaging- ARCH NEUROL / VOL 62, SEP 2005

3. From manganism to manganese-induced parkinsonism: a conceptual model based on the evolution of exposure.Neuromolecular Med. 2009;11(4):311-21. Epub 2009 Dec 10.

Coke bottle in Eyes - Dysthyroid Ophthalmopathy

2011-12-11T21:01:00.000+05:30

Thyroid orbitopathy, or Graves’ dysthyroid ophthalmopathy, is the most common cause of unilateral and bilateral exophthalmos in the adult population.

About 90% of patients with thyroid orbitopathy have bilateral CT or MR imaging abnormalities even if the clinical involvement is unilateral.

coke bottle in ice !!!!!

coke bottle in eyes !!!!

Typically, enlargement involves the muscle belly, sparing the anterior tendinous insertion thus resembling coke bottles- termed aptly COKE- BOTTLE SIGN.

Another helpful finding in thyroid myopathy is the presence of hyperintense areas within the muscle bellies.

These are probably the result of focal accumulation of lymphocytes and mucopolysaccharide deposition. Other MR imaging findings in thyroid orbitopathy are increased orbital fat, enlargement (engorgement) of the lacrimal glands, edema (fullness) of the eyelids, proptosis, anterior displacement of the orbital septum, and stretching of the optic nerve with or without associated ‘‘tenting’’ of the posterior globe.

Compression of the optic nerve can be best evaluated on oblique sagittal MRI, obtained along (parallel to) the optic nerve as well as on axial MR images. contrast study shows homogenous enhancement of these muscle bullies as shown in the picture below.

Image courtesy- coca cola logo, google for green frogs.

where smooother becomes undesirable- Classical Lissencephaly

2011-12-01T12:23:00.000+05:30

Clinical data- term neonate with feeding difficulty and infantile spasms.

Images

Findings- Imaging reveals smooth brain surface with near complete agyric cortex and sylvian fissure with figure- of-eight appearance. The agyric frontal cortex were thicker and has trilayered cortex-outer thin gray matter, central thin cell sparse white matter and an inner thick band of grey matter ( band heterotopia). Pachygyric cortex were also seen in posterior parietal cortex. Corpus callosum is hypogenetic

Diagnosis- Classical Lissencephaly

Discussion-The term lissencephaly means “smooth brain” and refers to a paucity of gyral and sulcal development on the surface of the brain. Agyria is defined as an absence of gyri on the surface of the brain in association with a thick cortex and is synonymous with “complete lissencephaly,” whereas pachygyria is defined as the presence of a few broad, flat gyri with thickened cortex, and is used interchangeably with the term “incomplete lissencephaly.” These definitions adopt the concepts of Hennekam and Barth that proper use of the terms agyria and pachygyria requires a thick cortex be present and that these malformations result from an arrest of neuronal migration.

Reference- Pediatric neuroimaging A.James Barkovich fourth edition.

PLANTAR FASCIITIS

2011-11-29T18:11:00.001+05:30

Clinical data - Left heel pain.

Images

Findings- There is thickening of medial cord of plantar fascia with detachment of medial cord seen as a clear fluid filled gap between the fascia and os calcis.

Altered intrafascial signal intensity ( hyperintense areas on PDFS images) with perifascial edema.

Subcutaneous edema is seen both superficial and deep to the plantar fascia.

The lateral cord of plantar fascia is intact.

Reactive calcaneal marrow edema noted at the attachment site.

Diagnosis- Plantar fasciitis with rupture of medial cord. prominent calcaneal enthesophyte.

Discussion-

The plantar fascia is a fibrous aponeurosis originating from the calcaneal tuberosity and inserting onto the deep short transverse ligaments of the metatarsal heads. Of the medial, lateral, and central components, the central component is the strongest, largest, and most typically involved by plantar fasciitis.

Plantar fasciitis is a chronic degeneration and inflammation that occurs in response to micro tears in the fascia. Etiology is most commonly repetitive trauma as in athletes and less commonly inflammatory arthritides such as ankylosing spondylitis, Reiters syndrome, and psoriasis.

Other possible risk factors include obesity, hard walking surfaces, and age over 40. The site usually involved is the calcaneal origin but plantar fasciitis can also occur moredistally. Diagnosis is more often clinical, but MRI does demonstrate abnormalities in the plantar fascia.

FAMILIAL CAVERNOMATOSIS

2011-11-29T03:14:00.001+05:30

clinical data- Headache under evaluation.

Images-

T2WI- RETICULATED POPCORN APPEARANCE

T2WI- PERIPHERAL HEMOSIDERIN RIM

T1WI- HETEOINTENSE LESIONS

SWI

Diagnosis- Multiple cavernomas in a patient with familial cavernomatosis.

Cavernomas may occur sporadically, after radiation therapy and hereditarily following an autosomal dominant trait. The hallmark of the familial form is multiplicity of cavernomas within the brain. Recently, genes causing cavernomas were mapped on chromosomes 7q, 7p,and 3q in a group of families.

Typically, cavernomas have a popcorn-like appearance with a well-delineated complex reticulated core of mixed signal intensities representing hemorrhage in different stages of evolution and/or different velocities of blood flow. Typical is a low signal hemosiderin rim,which completely surrounds the lesion.

The dark signal “blooms” on T2-weighted images, and is best visible on gradient echo T2*-weighted studies.

Multiple cavernomas occur in up to 90% of familial cases and in around 25% of sporadic cases.

Therefore,whenever you see a single cavernoma on the MR scan of a patient, make sure that this is the only one!

Idiopathic Intracranial Hypertension

2011-11-29T01:13:00.001+05:30

clinical data- Headache with visual complaints

DISTENSION OF PRIOPTIC SUBARACHNOID SPACE WITH TORTUOSITY

Findings- There is flattening 0f posterior sclera,distension of perioptic
subarachnoid space with vertical tortuosity of jntraorital optic nerves. note is made of
partial empty sella. MR Venogram shows bilateral transverse sinus stenosis.

Diagnosis - Idiopathic intracranial hypertension

Discussion-

IIH, also known as pseudotumor cerebri and benign intracranial hypertension, is a syndrome characterized by increased CSF pressure and papilledema in patients without focal neurologic findings,except for occasional CN VI palsy. It is a diagnosis of exclusion, and radiologic examinations are traditionally performed to help exclude lesions that produce intracranial hypertension, such as obstructive hydrocephalus, tumor, chronic meningitis, arteriovenous fistula, internal jugular vein stenosis,and dural sinus thrombosis.
Imaging shows flattening of the posterior sclera, distension of the perioptic subarachnoid space, vertical tortuosity of the orbital optic nerve, and a partially empty sella .

Reference- MR Imaging of Idiopathic Intracranial Hypertension,AJNR Am J Neuroradiol 22:196–199, January 2001

MISSED TORSION

2011-06-24T19:50:00.000+05:30

A teenager presented with clinical history of scrotal pain for the past six days.

Torsion knot seen as a dark stalk at the inferior aspect of testis

DISCUSSION

Spermatic cord torsion typically occurs in the teens and twenties.

The classic presentation is waking up with testicular pain radiating to the abdomen or

groin that gradually worsens. Torsion may, however, present with acute onset of pain that can be so

severe as to cause nausea and vomiting.

The affected hemiscrotum appears indurated, enlarged and tender, mimicking epididymitis and leading to clinical misdiagnosis in a large percentage of cases.

If torsion is suspected, immediate surgery is required, because salvage of testicular function

decreases with time. Although nearly all testes can be salvaged if ischemic for 5 hours or less, the salvage rate decreases to 20% if surgery is done at or beyond 12 hours.

When patients present in the subacute phase (24 hours or later), surgery is still required to remove the torsed testis and fix the contralateral testis to the scrotum. The torsed testis should be removed to establish the diagnosis, stop the pain, which would otherwise last for 3 to 4 weeks, and prevent the development of infertility in the contralateral testis owing to the possible development of antisperm antibodies, although this latter reason is controversial.

Acute torsion can be adequately diagnosed with color Doppler imaging, particularly when the

equipment is sensitive to slow flow. Experience with MRI has been limited to subacute torsion (greater

than 24 hours) in which several characteristic findings have been observed, three of which are specific,

allowing for 100% accuracy.

The first is the appearance of the point of twist itself. The twisted stalk, which contains vessels,

lymphatics, tubules, and fat, is usually near the posterior aspect of the scrotum. The point of

twist is quite dark, presumably owing to the water being squeezed out of the tissues, similar to the

wringing of a wet towel .From this dark point (point of twist) emanates several

curvilinear dark lines, presumably representing the spiraling facial planes resembling a whirlpool.

From the point of twist several curvilinear dark lines, presumably representing the spiraling fascial planes resembling whirl pool.

The second finding is the appearance of the testis and epididymis. The epididymis is

markedly thickened with areas of swelling and areas of subacute hemorrhage (intermediate signal

intensity on proton-density-weighted and darker on T2-weighted images).

The testis in the subacute phase (more than 5 days) was smaller than the contralateral testis.

Left epididymis is in abnormal position It is swollen and markedly thickened with areas of sub acute hemorrhage

NORMALLY ENHANCING RIGHT TESTIS

TUNICAL THICKENING, NONENHANCING LEFT TESTIS

The third finding is the appearance of the proximal cord, which was thickened.( not shown here). The cord

had absent or diminished vascularity .Its signal intensity was diminished and inhomogeneous.

NONENHANCING LEFT TESTIS

This is the subtraction images obtained after contrast study. Loss of parenchymal enhancement observed in left testis.

THE MUSICAL LYRE & THE NOTES ONE CAN GET.....

2011-03-27T17:54:00.000+05:30

LYRE

Lyre ( in India called as Ektara) is a stringed musical instrument used by ancient Greeks. It is a Well-known decorative "parlor" instruments of the 1800s.

In Greek mythology, Amphion, king of Thebes, fortified the city with a wall. It is said that when he played on his golden lyre the stones moved of their own accord and took their places in the wall.

In imaging, LYRE SIGN represents splaying of external and internal carotid artery by carotid body tumor.

Glomus vagale paraganglioma, carotid body tumor, schwannoma of carotid space can give similar imaging appearances. knowledge of essential functional anatomy and behavior of the growth can very well differentiate these lesions by imaging.

Glomus vagale paraganglioma typically causes anterior and medial displacement of internal carotid artery without widening of carotid bifurcation.

Carotid body tumor presents as avidly enhancing mass in the carotid bifurcation with splaying of ECA and ICA.

INTENSELY ENHANCING CAROTID BODY TUMOR

Schwannoma of the carotid space presents as well circumscribed soft tissue density mass. Internal carotid artery (ICA) is usually bowed over anteromedial surface. The absence of flow voids can differeniate them from paragangliomas.

Occasionally salivary gland tumors of parapharyngeal space can mimic these lesions as well : but as a rule, these salivary gland tumors displaces ICA posteriorly.

CT ANGIOGRAM LYRE SIGN

Well, we will come back to the lyre, what tunes one can expect?

I mean, what is expected in the imaging of carotid body tumors by vascular surgeons ?

The preferred treatment for carotid body tumors is surgery and it is challenging being the mass is often densely adherent to the carotid bifurcation.

Shamblin et al classified carotid body tumors into 3 groups based on the operative notes and gross specimen examination and established that the risk of surgical intervention depends mainly on the relationship of the tumor with the carotid vessels . The importance of this classification increases significantly if preoperative (noninvasive) cross-sectional imaging can accurately predict the Shamblin group.

In short,
Type 1 - were minimally attached to the vessels and easily resectable: a tumor-ICA maximum degree of circumference of contact less than or equal to 180°.
Type 2- seemed to partially surround the vessel and were more adherent to vessel adventitia. These tumors were difficult to dissect but amenable to careful resection. Circumferential contact of tumor- ICA would be more than 180 and less than 270.

Type 3- tumors had an intimate adherent relationship to the entire circumference of the carotid bifurcation, and surgical dissection was impossible even in the hands of experienced vascular surgeons. This group, therefore, required sacrifice of the ICA with vessel replacement. Circumferential contact of tumor- ICA would be greater than or equal to 270°

T2WI MRI SHAMBLIN TYPE 3 TUMOR

In our case, the circumferential contact of tumour –ICA was measured to be 310⁰ to 330^0,hence belongs to SHAMBLIN ‘ S type 3 lesion.

References

1. Carotid Body Paraganglioma Management and Outcome-European Journal of Scientific Research ISSN 1450-216X Vol.37 No.4 (2009), pp.567-574

2. Carotid Body Tumors: Objective Criteria to Predict the Shamblin Group on MR Imaging-Published April 16, 2008 as 10.3174/ajnr.A1092

Cysticercosis

2010-12-05T11:19:00.000+05:30

Cysticercosis in humans is infection with the larval form (cysticercus cellulosae) of the pork tapeworm T solium. It is endemic in Southeast Asia, Mexico, Central and South America, and Africa. Humans normally act as definitive hosts. Ingestion of inadequately cooked infected pork, the intermediate host, leads to the development of the adult worm in the small bowel of humans. The eggs of the worm are excreted with the feces, which are ingested by the pig, the intermediate host. Once ingested, the eggs hatch in the small intestine and result in the cysticercosis, completing the cycle. However, humans can occasionally be intermediate hosts, manifesting cysticercosis. It is transmitted to humans by ingestion of eggs from contaminated water or food, such as vegetables, or by internal regurgitation of eggs into the stomach due to reverse peristalsis, when the intestine harbors a gravid worm. The eggs hatch in the small intestine, releasing oncospheres that penetrate the bowel mucosa and enter the bloodstream to reach various tissues, where they develop to form a cysticercus cellulosae, which is the encysted larval form of T Solium. These can remain viable in this stage for as long as 10 years in humans. Living larvae evade immune recognition and do not elicit inflammation. When the larva dies, it induces a vigorous granulomatous inflammatory response that may produce symptoms, depending on the anatomic location.

Although most reported cases of cysticercosis involve the brain and orbit, the general belief is that the subcutaneous and muscular forms are as common as or more common than the other forms. However, most cases of subcutaneous and muscular cysticercosis are asymptomatic.

In the muscular form, 3 distinct types of clinical manifestations have been described: the myalgic type; the masslike, pseudotumor, or abscesslike type. During the death of the larva, there is leakage of fluid from the cyst. The resulting acute inflammation may result in local pain and myalgia. Alternatively, degeneration of the cyst may result in intermittent leakage of fluid, eliciting a chronic inflammatory response, with collection of fluid around the cyst, resulting in the masslike, pseudotumor, or abscesslike type. Alternatively, the cyst retracts, its capsule thickens, and the scolex calcifies. Later on, the cyst is completely calcified. When multiple, they give a “starry night” appearance on computed tomography. These are seen as multiple millet seed–shaped elliptical calcifications in the soft tissues on plain radiography.

25 year old male presenting with pain & swelling in the right sternocleidomastoid muscle . panoramic view showing focal swelling within the muscle.

Longitudinal view shows cystic lesion with an echogenic scolex inside.

Doppler evaluation shows the surrounding inflammatory response.

X- ray pelvis reveals multiple millet seed–shaped elliptical calcifications in the soft tissues.

In the muscles, cysticerci may calcify and become asymptomatic. Concomitant cerebral and muscular locations of cysticercosis are nearly always simultaneous; therefore, a combined search by brain CT and limb radiography or even CT should be performed in either situation. Subcutaneous involvement was reported in 17–78.5% of cases of neurocysticercosis, depending on geographic location.

Ultrasound can demonstrate an intramuscular or subcutaneous cyst or calcific nodule, which could be single or multiple. The cyst represents the cysticercus vesicle containing the characteristic invaginated scolex. The size of the cyst is about 10 mm. Identification of the scolex helps to differentiate the disease. An inflammatory reaction could be demonstrated using color Doppler techniques. Peculiarly, the live cysticerci evade the immunoreaction of the body. However, during the death of the larva, the leakage of fluid from the cyst may trigger an inflammatory response, leading to one of four clinical forms: the myalgic form, the myopathic form, the nodular mass-like lesion, or the pseudohypertrophic type. The finding of diffuse millet seed elliptical calcifications in the subcutaneous tissues and muscles is pathognomonic of cysticercosis.

Pituitary Apoplexy.

2010-11-16T20:50:00.000+05:30

Pituitary apoplexy is defined as a clinical syndrome that may include headache, visual deficits, ophthalmoplegia, or altered mental status. It may occur either due to rapid expansion of an infarcted/hemorrhagic pituitary adenoma.

Clinical risk factors are trauma, increased intracranial pressure, anticoagulation, bromocriptine therapy and diabetic ketoacidosis. Apoplexy in pituitary adenomas may vary from 2% to 7%. Nearly 50% of apoplectic events seem to occur in patients who were not known to harbor pituitary lesion previously. Imaging findings vary with age of hemorrhage.

30 year old female patient presents with severe headache and visual deficits - coronal T1 & T2 WI shows hemorrhage in to a pituitary macroadenoma.

Noncontrast CT may show sellar/suprasellar mass with patchy hyperdensities. MR imaging findings may vary depending upon age of hemorrhage. Early/late subacute hemorrhage may show increased signal as seen in our case. Acute compression of the hypothalamus and/or optic chiasm may cause increase signal on T2 along the optic tracts. Presence of restricted diffusion within an adenoma may suggest an early sign of apoplexy in the form of acute hemorrhage or associated infarction. Early diagnosis and treatment is necessary to prevent significant morbidity and mortality.

Pleomorphic Adenoma

2010-10-17T15:56:00.000+05:30

Salivary gland neoplasms are relatively rare. Most of them are benign (70%–80%) and found in the parotid glands (80%–90%). About 10%–12% of all salivary gland neoplasms are located in the submandibular glands, but almost half of these neoplasms may be malignant.

Pleomorphic adenomas occur most often in the parotid gland (60%–90%) in people in the fourth and fifth decades of life but may arise at any age . There is a slight predominance in women . Pleomorphic adenomas are usually solitary and unilateral . They grow slowly and may be asymptomatic. Nontreated pleomorphic adenomas may undergo malignant transformation after decades. In exceptional cases, pleomorphic adenomas may be clinically aggressive; they may metastasize and even be fatal.

A 33 year old female patient presented with slowly progressing swelling of the right sub mandibular gland - USG reveals a well defined round homogeneously hypo echoic mass lesion with posterior acoustic enhancement.

On color Doppler - predominantly peripheral vascularity noted without any intralesional vascularity.

At US, pleomorphic adenomas are hypoechoic, well-defined, lobulated tumors with posterior acoustic enhancement and may contain calcifications . The feature of lobulated shape is being emphasized in differential diagnosis . Many authors add also a feature of homogeneity, but it seems to depend on the composition of the tumor; when high-resolution transducers are used, more and more internal inhomogeneities are being found . Vascularization in pleomorphic adenomas is often poor or absent (even when the sensitive power Doppler mode is used) but may be abundant.

Malignant salivary gland tumors will have irregular shape, irregular borders, blurred margins, and a hypo echoic inhomogeneous structure. Colour Doppler may also aid in the assessment of malignancy; tumors demonstrating an increased intratumoral vascularity with RI >0.8, PI > 2 is more likely to be malignant.

Dysembryoplastic Neuroepithelial Tumor (DNET)

2010-05-15T23:14:00.000+05:30

DNET (WHO grade I) is a very uncommon, extremely slow growing, and even quasi-hamartomatous lesion found mainly during the first few decades of life.On gross pathology, gyral expansion and often small nodular elevations are seen due to the multinodular composition of the mass.

The superficial location, usually in the temporal lobe but always supratentorial in location, allows skull remodeling to occur due to the slow growth of the lesion. This cortical mass usually presents with long-standing seizures .

DNET in a 15-year-old patient with long-standing seizures. T2-weighted image shows hyperintense cortical mass with focally brighter areas , with out any surrounding edema/mass effect.

Axial T1 WI shows low signal intensity cortical mass .No enhancement is seen after gadolinium.

Axial diffusion WI shows lack of restricted diffusion with increased ADC.

Axial CECT scan shows a non enhancing wedge shaped cortical hypodense mass lesion with Scalloped inner table.

Imaging findings include Well circumscribed ,Wedge-shaped "bubbly" cortical mass with lack of surrounding edema and mass effect. CT findings include Wedge-shaped low density Cortical/subcortical lesion with Scalloped inner table. Calcification seen in 20-36% cases.on MR imaging the mass is low intensity on T1-weighted images and markedly hyperintense on T2-weighted images giving a "pseudocystic" or bubbly appearance. On diffusion they do not restrict , but show increased motion of water.

Imaging allows the diagnosis to be made with only few differential diagnosis considerations. Because the lesions can be partially cystic and calcified, the DNET is often indistinguishable from oligodendroglioma on CT and MR imaging when the oligodendroglioma is low grade and not associated with edema. Ganglioglioma , Pleomorphic xanthoastrocytoma are also a consideration, as are superficially located infiltrative astrocytomas, but these low grade tumors characteristically shows restricted diffusion.

Cerebellar Pilocytic Astrocytoma

2010-05-07T13:38:00.000+05:30

Pilocytic astrocytoma of the cerebellum, is the second most common posterior fossa neoplasm among children.

Most (85%) cerebellar astrocytomas are of the pilocytic variety and are pathologically similar to the hemispheric pilocytic found in the supratentorial region.Grossly, the pilocytic cerebellar astrocytoma is a well-circumscribed partially cystic mass, often with a mural nodule of vascular solid tissue, situated anywhere in the cerebellum.

The peak incidence is within the first two decades between 5 to 15 years of age. These lesions are seen with a higher frequency in patients with neurofibromatosis type I.

Axial NECT shows mixed cystic/solid cerebellar mass in 14 year old patient, The cerebellar astrocytoma displaces and effaces, rather than fills, the fourth ventricle, resulting in obstructive hydrocephalus.

Axial CECT shows enhancement of the solid portion and around wall of cyst, indicating tumoral origin of cyst.

At imaging, the classic appearance of pilocytic astrocytomas are Cystic cerebellar mass with enhancing mural nodule. On CT hypo- to isodense cystic/solid mass with little or no surrounding edema. Solid portion of the tumor should densely enhance with intravenous contrast, whereas the cyst wall may or may not enhance.

MR imaging has inarguably become the clear choice for evaluating all posterior fossa tumors, and the cerebellar astrocytoma is no exception. The typical findings on MR imaging of the pilocytic type include a mass, either midline or hemispheric, comprised of a single large cyst with a nodular solid portion, often located in the wall of the cyst. Solid portions is hyperintense on T2WI and hypointense on T1WI.

Pilocytic astrocytomas should be differentiated from medulloblastoma(PNET), although cyst can be seen with in the tumors, they are less a feature of PNET and more typical of PA.The solid portion of Pilocytic astrocytomas is more hyperintense on T2WI than the solid component of otherwise similarly appearing cystic PNET. On diffusion WI solid portion of PA shows increased motion of water with increased ADC, whereas in PNET solid portion shows Restricted diffusion.