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IMAGING MODALITIES Computerized Tomography Magnetic Resonance Imaging
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Advantages of C.T Detection of calcification and calvarial defects
No contraindication
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Disadvantages of CT Use of ionizing radiation
Reaction to iodinated contrast Nephrotoxicity
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Advantages of MRI No radiation Excellent soft tissue resolution
Multiplanar imaging
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Limitations of MRI Hyperacute bleed Evaluation of calcification
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Contraindications for MRI
Cochlear implants Cardiac pace maker Neuro stimulator
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Lissencephaly Most severe of neuronal migrational abnormalities
Generalized paucity of gyral and sulcal formation Vertically oriented sylvian fissures
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Torch Infections Toxoplasmosis Rubella Cytomegalovirus - Most common
cause of congenital CNS infection Herpes simplex virus
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Focal cortical dysplasia
Common location – temporal lobes Expanded gyrus with abnormally oriented sulci and thickened cortex Subcortical white matter hyperintensity Surgical excision of dysplastic focus when possible is often curative
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Cortical dysplasia – Balloon Cell Type of Taylor
Focal cortical thickening Blurring of the gray-white matter junction Hyperintensity (on T2-weighted images) of subcortical white matter often tapering toward the ventricle
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Unilateral megalencephaly
Hamartomatous overgrowth of a part or whole of cerebral hemisphere Ipsilateral migrational defects Hypoplastic / hyperplastic white matter Intractable seizures, hemiplegia and severe developmental delay
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Peri-Sylvian syndrome
Anomalous cortical development overlying underdeveloped sylvian fissures Dorsal perirolandic extension of sylvian fissures
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Septo-optic dysplasia (de Morsier syndrome)
Partial or complete absence of septum pellucidum Squared off appearance of frontal horns Hypoplasia of optic nerves and chiasm ( 40-80%) Hypoplasia of hypothalamus
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Tuberous sclerosis (Bourneville disease)
Incidence :10,000-50,000 Inheritance -- autosomal dominant -- low penetrance -- chromosomes: 9, q ; 11, ??
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Clinical - “classic” triad of:
Tuberous sclerosis Clinical - “classic” triad of: > Papular facial lesions > seizures > mental retardation- 50% of patients
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Tuberous sclerosis CNS lesions Non- CNS lesions - Subependymal nodules
- Giant cell astrocytoma - Cortical tubers - White matter lesions Non- CNS lesions - Skin, kidneys, cardiovascular, Liver, spleen, pancreas and Musculoskeletal
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Sturge-weber syndrome (Encephalotrigeminal angiomatosis)
Inheritance : none Clinical : port wine stain in CN - V distribution
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Sturge-weber syndrome
Aetiology - Normal cortical venous drainage fails to develop Pathology - Leptomeningeal angiomatous vascular plexus with secondary dystrophic cortical changes
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Sturge-weber syndrome
Calcification Atrophy Enlarged med, sub-epen veins Ocular lesions
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Periventricular leukomalacia
Commonly seen in premature infants Ischemic lesions are most obvious in parieto-occipital regions Paucity of white matter in the parieto-occipital regions Indentation of the lateral ventricles
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Hippocampus Mean volumes: Hippocampal sclerosis: 1.46+0.60cu.cm
Right Left Male cu.cm cu.cm Female cu.cm cu.cm Hippocampal sclerosis: cu.cm
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Hippocampus Normal: NAA/Cho:1.20 + 0.27 Hippocampal sclerosis:
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Hippocampus T2 Relaxometry Mean T2 time:110-115ms
Prolonged in Hippocampal sclerosis
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Dysembryoplastic Neuroepithelial Tumor
Slow growing superficial lesions usually within temporal lobe but always supratentorial Focal cortical lesion , hypointense on T1 & hyperintense on T2 Wt.images Surgery is curative
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