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IMAGING MODALITIES Computerized Tomography Magnetic Resonance Imaging.

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Presentation on theme: "IMAGING MODALITIES Computerized Tomography Magnetic Resonance Imaging."— Presentation transcript:

1 IMAGING MODALITIES Computerized Tomography Magnetic Resonance Imaging

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

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

4 Advantages of MRI No radiation Excellent soft tissue resolution
Multiplanar imaging

5 Limitations of MRI Hyperacute bleed Evaluation of calcification

6 Contraindications for MRI
Cochlear implants Cardiac pace maker Neuro stimulator

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

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

9 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

10 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

11 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

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

13 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

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

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

16 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

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

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

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

20 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

21 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

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

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

24 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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