IMAGING MODALITIES Computerized Tomography Magnetic Resonance Imaging

Advantages of C.T Detection of calcification and calvarial defects No contraindication

Disadvantages of CT Use of ionizing radiation Reaction to iodinated contrast Nephrotoxicity

Advantages of MRI No radiation Excellent soft tissue resolution Multiplanar imaging

Limitations of MRI Hyperacute bleed Evaluation of calcification

Contraindications for MRI Cochlear implants Cardiac pace maker Neuro stimulator

Lissencephaly Most severe of neuronal migrational abnormalities Generalized paucity of gyral and sulcal formation Vertically oriented sylvian fissures

Torch Infections Toxoplasmosis Rubella Cytomegalovirus - Most common cause of congenital CNS infection Herpes simplex virus

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

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

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

Peri-Sylvian syndrome Anomalous cortical development overlying underdeveloped sylvian fissures Dorsal perirolandic extension of sylvian fissures

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

Tuberous sclerosis (Bourneville disease) Incidence -- 1:10,000-50,000 Inheritance -- autosomal dominant -- low penetrance -- chromosomes: 9, q32 - 34; 11, ??

Clinical - “classic” triad of: Tuberous sclerosis Clinical - “classic” triad of: > Papular facial lesions > seizures > mental retardation- 50% of patients

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

Sturge-weber syndrome (Encephalotrigeminal angiomatosis) Inheritance : none Clinical : port wine stain in CN - V distribution

Sturge-weber syndrome Aetiology - Normal cortical venous drainage fails to develop Pathology - Leptomeningeal angiomatous vascular plexus with secondary dystrophic cortical changes

Sturge-weber syndrome Calcification Atrophy Enlarged med, sub-epen veins Ocular lesions

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

Hippocampus Mean volumes: Hippocampal sclerosis: 1.46+0.60cu.cm Right Left Male - 2.20+0.47cu.cm 2.17+0.72cu.cm Female- 2.27+0.47cu.cm 2.23+0.48cu.cm Hippocampal sclerosis: 1.46+0.60cu.cm

Hippocampus Normal: NAA/Cho:1.20 + 0.27 Hippocampal sclerosis:

Hippocampus T2 Relaxometry Mean T2 time:110-115ms Prolonged in Hippocampal sclerosis

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