Case 1

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Case 1
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• A-What are the finding ?
• B-What is the expected history ?
• C-What is the diagnosis?

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• FINDING 5- MARKES
• 1- there are of confluent patchy area of large
  scattered abnormal T2 signal developing in
  multiple areas of subcortical white matter
  bilaterally.
• 2- the lesion is bright on diffusion WI(active
  disease)
• B- The expected history is post vaccination or
  post viral infection. 2- MARKES
• DxADEM 3- MARKES

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adem

• Findings  Since the prior normal study, there
  has been interval development of scattered
  abnormal T2 signal developing in multiple areas
  of white matter bilaterally. Specific areas
  involved include the periventricular white
  matter, the centrum semiovale, the middle
  cerebellar peduncles, and the subcortical white
  matter of the frontal and temporal cortices
  bilaterally. These abnormal white matter foci do
  not enhance and do not demonstrate restricted
  diffusion. MRA images are normal. The visualized
  intracranial vessels are free of aneurysmal
  dilatation or stenosis. Vessel morphology and
  distribution is normal. There is no evidence of
  vasculitis.

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adem

• ADEM represents an abnormal immune response to
  viral illness or vaccination. The disease is most
  commonly seen in children, often with an abrupt
  onset following a viral infection or recent
  vaccination. Common viral infections causing ADEM
  include measles, mumps, rubella, and chicken pox.
  Less commonly, ADEM develops following a
  disseminated bacterial infection (usually
  mycoplasma).
• ADEM typically presents with seizure activity or
  focal neurological signs 4-7 days following the
  clinical onset of a viral infection. Other signs
  and symptoms include headache, fever,
  irritability, dizziness, vomiting, and nuchal
  rigidity. Symptoms often spontaneously resolve
  spontaneously over several weeks, though 10-20
  of patients experience permanent neurological
  deficits.
• Grossly, ADEM appears as patchy perivenous
  inflammation and demyelination throughout the
  brain, most commonly within the deep nuclei and
  deep white matter. The etiology of ADEM is
  unclear, but it is believed to result from an
  antigen-antibody response against CNS proteins,
  mainly myelin. Gross specimens have shown marked
  similarities to experimentally induced cases of
  allergic encephalitis mediated by anti-myelin.
• Radiologic Overview of the Diagnosis

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• Radiologic Overview of the Diagnosis
• CT images may demonstrate large patchy foci of
  decreased attenuation within the sub-cortical
  white matter, and to a lesser extent, the deep
  brain nuclei, corresponding to area of
  demyelination. More commonly, however, CT will
  fail to demonstrate any evidence of
  demyelination.
• MR again demonstrates areas of demyelination
  within the subcortical white matter, as well as
  the deep nuclei, which are affected in
  approximately 50 of cases. One or both
  hemispheres may be involved, though distribution
  is commonly asymmetric. The brainstem, cerebellar
  white matter, and spinal cord may be involved, as
  well. Foci of demyelination are seen as irregular
  areas of T1 and T2 prolongation, with various
  patterns of enhancement in the acute phase. Foci
  of acute and subacute demyelination also
  demonstrate restricted diffusion.
• Key points
• Scattered demyelination which develops several
  days after the onset of a viral prodrome or
  vaccination.
• Typically involves sub-cortical white matter and
  deep brain nuclei.
• May demonstrate enhancement and restricted
  diffusion in the acute phase.

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Case 2
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• A-What are the finding ?
• B-What is the expected history ?
• C-What is the diagnosis or differentials Dx?

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• Finding 5- MARKES
• 1-there is oval shape small complex mass at
  medial aspect of left temporal lobe .
• 2- there is small tiny internal cystic changes.
• Daignosis DNET 3- MARKES
• DNET ,a low-grade astrocytoma or a ganglioglioma,
  which are the more common supratentorial tumors
  seen in young patients.

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• They occur in young patients (age range one week
  to thirty years) who usually present with
  intractable partial complex seizures.  2- MARKES
• Because DNET does not recur after resection,
  postoperative radiation or chemotherapy is not
  needed.

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• Pearls
• DNET is a pathologically benign tumor occurring
  in young patients who usually present with
  partial complex seizures.
• The tumors are usually in the temporal lobe and
  are of low density on CT. On MR, lesions are Tl
  hypointense and T2 hyperintense and may display
  cystic features.
• Imaging alone cannot distinguish DNET from a
  low-grade astrocytoma or a ganglioglioma, which
  are the more common supratentorial tumors seen in
  young patients.
• Selected References

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• Dysembryoplastic neuroepithelial tumor (DNET) is
  a recently described, pathologically benign tumor
  arising within the supratentorial cortex.  Tumors
  are occasionally cystic and demonstrate at least
  one of the following three characteristics
• a specific glioneuronal component
• multinodular lesion consisting of glial nodules
• association with focal cortical dysplasia.
• They occur in young patients (age range one week
  to thirty years) who usually present with
  intractable partial complex seizures.  Because
  DNET does not recur after resection,
  postoperative radiation or chemotherapy is not
  needed.
• Diagnosis  CT and MRI for characterization.
  Diagnosis requires biopsy.
• Treatment Curable by excision.
• Radiology The majority of tumors occur in the
  temporal lobe with the frontal lobe being the
  second most common location.  On CT, they appear
  as a low-density, well-demarcated lesion which
  may appear cystic.  The margins of the tumor are
  well -circumscribed and may remodel the adjacent
  calvarium.  On MR, they demonstrate low signal on
  T1-weighted and high signal on T2-weighted
  images.  Little peritumoral edema is seen. 
  Differentiation from ganglioglioma or low-grade
  astrocytoma is not possible by imaging.

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• CT   Hypo-attenuating lesion in the left
  temporal lobe demonstrating peripheral
  enhancement and thin corona of surrounding edema.
• MR   Tl-hypointense, T2-hyperintense 3 cm
  temporal lobe mass with little surrounding
  edema.   The mass demonstrates circumferential
  enhancement and appears cystic centrally.

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• CT   Hypo-attenuating lesion in the left
  temporal lobe demonstrating peripheral
  enhancement and thin corona of surrounding edema.
• MR   Tl-hypointense, T2-hyperintense 3 cm
  temporal lobe mass with little surrounding
  edema.   The mass demonstrates circumferential
  enhancement and appears cystic centrally.

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Case 3
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• What are the finding?
• What is the diagnosis?

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• Finding(6 mrks)
• 1-There is extensive Sino nasal disease filling
  and causing of all the Para nasal sinuses
  especially the maxillary, ethmoid as well as
  sphenoid air sinus (2 mrks)
• It appear moderately hyper intense on T1WI and
  signal void( fungal ball )on T2WI with peripheral
  enhancement in post contrast study of the fungal
  ball (2 mrks)

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• There is bulging of the lamina papyrasia
  bilaterally abutting the medial rectus
  bilaterally more marked on the right side. (2
  mrks)
• No Intracranial extension .
• Diagnosis fungal sinusitis (4mrks)

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Case 4
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• What are the finding?
• What is the diagnosis?

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• Finding (6 mrks)
• 1- left MCA hyper dense sign
• 2- blurring of the left basal ganglia
• 3- effacement of left cortical sulci (MCA
  territory.
• 4-Mild mass effect on left frontal horn
• Diagnosis (4 mrks) acute infarction of
• MCA territory .

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Case 3
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Case 5
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• What are the finding?
• What is the diagnosis?
• Mention three clinical or radiological signs?

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• 1- fusiform enlargement of the optic chiasma
• 2- there are altered signal intensity
• Of the white matter around the fourth ventricle.
  (HAMARTOMA)
• Diagnosis NF 1

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• Intracranial manifestations of NF1 include
  development of optic pathway gliomas, cerebral
  gliomas, hydrocephalus, schwannomas of the
  cranial nerves, vascular dysplasias, hamartomas,
  craniofacial plexiform neurofibromas, and
  spongiotic myelinopathy.
• NF1 can involve the spine, musculoskeletal
  system, and the gastrointestinal (GI) tract, and

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• Criteria for diagnosis
• Six or more café au lait macules larger than 5 mm
  in the greatest diameter in prepubertal children
  and larger than 1.5 cm in postpubertal
  individuals
• Two or more neurofibromas of any type or one
  plexiform neurofibroma
• Multiple freckles (Crowe sign) in the axillary or
  inguinal region
• A distinctive osseous lesion, such as sphenoid
  dysplasia or thinning of long bone cortex, with
  or without pseudoarthrosis
• Optic glioma
• Two or more iris hamartomas (Lisch nodules) seen
  on slitlamp or biomicroscopy examination
• A first-degree relative (parent, sibling,
  offspring) with NF1, as diagnosed by using the
  criteria above

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• Skull
• Many skull abnormalities are well demonstrated on
  plain radiographs. These include macrocephaly,
  absence of the greater and lesser wings of the
  sphenoid, absence of the orbital floor,
  hypoplasia of the lesser wings of the sphenoid,
  enlarged orbits, enlargement of cranial foramina,
  enlargement of orbital margins, sclerosis in the
  vicinity of the optic foramen (optic nerve sheath
  meningioma), facial asymmetry, hypoplasia of the
  paranasal sinuses, mandibular abnormalities,
  mandibular hypoplasia with flattening of the
  external contour, thinning of the ramus, coronoid
  hyperplasia, widening of the lateral and medial
  coronoid spaces, and calvarial defects adjacent
  the left lambdoid suture.
• Multiple frontobasal osseomeningeal defects
  causing cerebrospinal fluid (CSF) rhinorrhea and
  meningoencephalocele can occur, and the osseous
  defects may be depicted on plain radiographs.

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• Chest
• Plain radiograph findings include inferior rib
  notching, twisted and ribbonlike ribs in the
  upper thoracic cage, posterior mediastinal masses
  secondary to intrathoracic meningoceles,
  mediastinal and lung masses secondary to
  neurofibromas, and dumbbell neurofibromas.
• Reported changes of lung parenchyma include
  progressive pulmonary interstitial fibrosis
  leading to formation of bullae and honeycomb
  lung.
• The incidence of spontaneous pneumothorax and
  hemothorax is increased.
• Changes of interstitial lung disease and
  pulmonary hypertension may be seen, such as
  dilatation/enlargement of the central pulmonary
  arteries and peripheral pruning of vessels.

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• Appendicular skeleton
• Bowing or an S-shaped deformity of long bones,
  hyperplasia or hypoplasia of long and short
  bones, pseudoarthrosis, erosions, periosteal
  dysplasia, intramedullary longitudinal
  osteosclerotic streaks, single or multiple cystic
  bone lesions, and focal gigantism may be
  depicted.
• Joint abnormalities reported include protrusio
  acetabuli, dislocation of the hip, dislocation of
  the radius and ulna, absence of a patella, and
  neuropathic arthropathy of the knee.

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• Spine
• A sharply angled kyphoscoliosis centered at the
  thoracolumbar junction is seen in 50 of
  patients. The kyphosis is more pronounced than
  the scoliosis, and the incidence increases with
  advancing age.
• Enlargement of the intervertebral foramina,
  scalloping of the vertebral bodies (anterior,
  posterior, lateral), hypoplasia of the vertebral
  pedicles, wedged-shaped vertebrae,
  spondylolisthesis, spinal clefts, osteolysis, and
  spindling of the transverse processes may be
  depicted.
• Spinal fusion may be complicated by
  pseudoarthrosis and curve progression.
• Spinal segments may be unstable, leading to
  subluxation or dislocation.

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Case 6
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• What is the study?
• What are the finding?
• What is the diagnosis?

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• 1- sagittal TIWI
• 2-sagittal T2WI FAT SAT.
• 3-Post contrast T1WI FAT SAT
• 4- MRV

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• Finding
• 1-MR images nicely show this vascular channel in
  the right occipital region traversing the
  calvarium
• 2-this venous channel communication with superior
  sagittal sinus to the dilated diploic veins of
  the skull
• diagnosis Sinus pericranii

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• Sinus pericranii is a rare disorder characterized
  by a congenital or acquired epicranial
  blood-filled nodule of the scalp that is in
  communication with an intracranial dural sinus
  through dilated diploic veins of the skull.
  Simply put, it connects the intracranial and
  extracranial venous systems. Sinus pericranii
  usually present in the pediatric age group as a
  focal swelling on the scalp. They are felt to be
  predominantly congenital in origin. Sinus
  pericranii are mostly located near the midline.
  The frontal region is most commonly involved,
  followed by the parietal and the occipital region
  (as in our case). It is soft and mobile and may
  be mistaken for a lipoma or subcutaneous cyst.
  Treatment is usually surgical.
• Radiologic Overview of the Diagnosis
• The plain film was ordered to assess for osseous
  involvement. The ultrasound was indicated as a
  vascular malformation was in the differential
  given the soft nature of the nodule. It was
  fortunate that this was done prior to biopsy as
  the ultrasound demonstrated communication with
  the transverse sinus.
• Key points
• Vascular malformation that connects the
  intracranial and extracranial venous systems.
• Ultrasound helpful for pre-biopsy
  characterization of soft tissue abnormalities.

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• These findings are compatible with a sinus
  pericranii. MR images nicely show this vascular
  channel in the right occipital region traversing
  the calvarium.
•  Head CT demonstrates left frontal vascular
  anomaly with thinning of the calvarium. MRI
  demonstrates communication of the intracranial
  and extracranial circulations.

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• There is a small, oval-shaped flow-void within
  the mid-anterior parietal scalp. This lesion
  communicates with the superior sagittal sinus and
  an adjacent dilated scalp vein, thus creating an
  abnormal communication between the intracranial
  and extracranial venous systems. Within this
  midline lesion, Differential Diagnosis  Lytic
  lesion in the skull of a child
• Congenital anomaly (e.g., Sinus pericranii)
• Eosinophilic granuloma 
• Fibrous Dysplasia
• Hemangioma
• Infection
• Metastases

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CASE 7
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• 1-WHAT ARE THE FINDINGS ?
• 2-MENTION THE IMPORTANT CLINCAL FINDING?
• 3-what is the diagnosis?

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• 1- The cerebral hemispheres demonstrate
  asymmetric atrophy, marked on the right, with
  enlargement of the subjacent subarachnoid spaces
• 2- Thin, gyriform calcification is present in the
  distribution of the right occipital lobe.

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• Clinical features of Sturge-Weber include facial
  port-wine stain nevi ipsilateral to the cerebral
  findings, mental retardation, hemianopsia and
  hemiplegia

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• The causative etiology is unknown, but the
  disease is characterized by angiomata in the
  distribution of the fifth cranial nerve and in
  the leptomeninges, most commonly in the parietal
  and occipital lobes.

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Sturge weber

• Findings  The cerebral hemispheres demonstrate
  asymmetric atrophy, marked on the left, with
  enlargement of the subjacent subarachnoid spaces.
  Bulky, gyriform calcification is present in the
  distribution of the left posterior temporal,
  parietal and occipital lobes. A smaller focus of
  calcification is seen in the left frontal lobe as
  well. There is no evidence of acute hemorrhage or
  infarct.

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• Sturge-Weber syndrome is sporadic disease known
  descriptively as encephalotrigeminal
  angiomatosis.  The causative etiology is unknown,
  but the disease is characterized by angiomata in
  the distribution of the fifth cranial nerve and
  in the leptomeninges, most commonly in the
  parietal and occipital lobes.  This focal
  abnormal development of venous drainage results
  in vascular congestion, ischemia, atrophy and
  eventually calcification.  "Port-wine" vascular
  nevus flammeus in the trigeminal nerve
  distribution (most commonly in V1) is a commonly
  encountered cutaneous finding.  Patients
  frequently present with seizure in the first year
  of life.  These are usually focal and involve the
  side of the body contralateral to the nevus. 
  Focal cerebral ischemia may result in dystrophic
  calcification, seizure (80), mental retardation
  (gt50), hemianopsia, and hemiplegia.  About one
  third of patients will have ocular involvement,
  with buphthalmos and glaucoma.

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• Radiology 
• Calcification may be seen on plain film of the
  skull, and on the CT scanogram.  Significant
  calcium deposition before the age of 2 is
  uncommon.  Tram-tracking is the characteristic
  finding, resulting from calcification of apposing
  gyri surrounding a dilated sulcus.  CT
  demonstrates gyriform, curvilinear calcification,
  most prominent in the parietal and occipital
  lobes ipsilateral to the facial nevus.  Secondary
  changes in the skull are sometimes present, such
  as enlargement of the paranasal sinuses and
  mastoid air cells.  Strong post-contrast
  enhancement may be seen in both the angiomata, as
  well as the ipsilateral choroid plexus. 
  Prominent collateral drainage through
  subependymal and medullary veins may be seen,
  particularly with angiography or MR venography.
• Pearls
• Clinical features of Sturge-Weber include facial
  port-wine stain nevi ipsilateral to the cerebral
  findings, mental retardation, hemianopsia and
  hemiplegia.
• Atrophy and dystrophic calcification is secondary
  to venous congestion.
• Parieto-occipital distribution is most common.
• Calcifications are gyriform.

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Case 4 ???? ?????