Brain Imaging. IC calcifications. Mamdouh mahfouz MD
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1 Brain Imaging IC calcifications Mamdouh mahfouz MD
2 CT Hyper dense [ more than100 HU ] MRI Low signal in T1 and T2 WIs [non mobile protons]
3 Exceptions Minute calcifications are seen on CT but not on MRI High signal in T1 and low signal in T2 WIs DD Fat Early subacute blood (intracellular met Hb)
4 Physiological intracranial calcifications Choriod plexus Pineal body Falx Tentorium Diaphragma sellae Petroclinoid ligament
5 Pathological Intracranial Calcifications Diagnostic Non diagnostic Bilateral symmetrical basal ganglia calcification Periventricular calcification Gyral calcifications
6 Diagnostic Calcifications Bilateral symmetrical basal ganglia calcification Periventricular calcification Gyral calcifications
7 Basal ganglia calcifications Idiopathic Hypoparathyroidism Pseudohypoparathyroidism Pseudo pseudohypoparathyroidism Fahr disease [Ferro calcinosis] Parkinsonism Radiation therapy Encephalitis Carbon monoxide intoxication Familial Hyperparathyroidism Bilateral patchy almost symmetrical calcifications Mainly affecting the basal ganglia
8 Basal ganglia calcifications
9 Basal ganglia calcifications
10 Periventricular calcifications Spotty non symmetrical periventricular calcific foci [ Congenital Intracranial infections] CT CT Cytomegalovirus inclusion bodies Toxoplasmosis Cysticercosis Tuberous sclerosis
11 Congenital brain infection
12 Cysticercosis
13 Congenital and neonatal Infections The classic TORCH infections include: Toxoplasmosis Rublla Cytomegalovirus (CMV) Herpes simplex virus (HSV) type2 Toxoplasmosis
14 Transmission through three major routes Hematogenous / transplacental ( toxoplasmosis, most viruses except HSV type2) Ascending cervical infection ( most bacteria) During delivery through birth canal (HSV type2) The pattern of dystrophic calcification is not entirely specific, CMV calcifications are usually central with predilection for periventricular location, whereas toxoplasmosis calcifications are more widespread with slight predilection for basal ganglia
15 Tuberous sclerosis Neuro ectodermal disorder 1:150,000 live births Adenoma sebaceum 30% Seizures 80% Mental retardation 70%
16 Subependymal hamartomas Calcification with age progression 88% Subependymal Giant cell astrocytoma 5-15% F 35Y Tuberous sclerosis with Subependymal GCA
17
18 Tuberous sclerosis
19 Subependymal Giant Cell Astrocytoma Very rare 0.3% Develops from the nodules Usually in the frontal horn near the foramen of Monro Hydrocephalus Low grade lesion [ No recurrence ] CT Isodense or slightly hyper dense Calcification Homogenous enhancement
20 Tuberous sclerosis with giant cell astrocytoma
21 Tuberous sclerosis with giant cell astrocytoma operated upon with intraventricular hemorrhage
22 Sturge- Webber syndrome Vascular malformation with capillary venous angioma in the face, ocular choroid, leptomeninges Gyral calcification after 2 years of age Parietooccipital more than frontal Bilateral lesions in 20% of cases Cortical hemi atrophy Choroid plexus enlargement Thickened skull and orbits
23 Sturge- Webber syndrome
24 Sturge webber syndrome
25 Non diagnostic calcification Vascular Metabolic Inflammatory Neoplastic AVM, aneyrysm hemangioma arteriosclerosis Carbon monoxide poisoning Folic acid deficiency Hypervitaminosis D Homocystinuria Lead poisoning Wilson s disease healed brain abscess Fungal cerebritis Parasitic disease Cysticercosis, hydatid TB, Toxoplasma Traumatic Hematoma scarring and needle tracts Meningioma, glioma, deposits, neurofibromatosis, treated lymphoma and leukaemia
26 Multiple tuberculomata Multiple tuberculomata
27 Multiple tuberculomas
28 Oligodendroglioma
29 Oligodendroglioma M 50Y
30 Subfrontal meningioma
31 سبحانك اللهم و بحمدك نشهد ان ال اله اال انت نستغفرك و نتوب اليك ssr-eg.net Thank you Mamdouh Mahfouz MD
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