Bilateral basal ganglia & thalamic abnormalities
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Transcript of Bilateral basal ganglia & thalamic abnormalities
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Bilateral basal ganglia & thalamic abnormalities
Dr / Hytham Nafady
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Bilateral globus pallidus abnormal signal.
Bilateral corpus striatum abnormal signal.
Bilateral thalamic abnormal signal.
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Basal ganglia
Globus pallidus
Globus pallidus interna
Globus pallidus externa
Striatum
Caudate Putamen
Subthalamus
Substantia nigra
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Globus = sphere.Pallidus = pale relative to the
surrounding brain substance.Caudate = (head, body and tail).Lentiform = lens shaped.Striatum = stripped. Substantia nigra = pigmented
nerve cells.
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Substantia nigra
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What are the basal ganglia?
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What are the basal ganglia?Basal ganglia Vs basal nuclei.
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Subthalamus
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Corpus striatum
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Bilateral globus pallidus normal variants
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Bilateral globus pallidus abnormalities
Acute: CO poisoning. Ischemia (heroin abuse). Kernictreus Hemolytic uremic syndromeChronic: Chronic hepatic encephalopathy. Chronic renal dialysis. Non ketotic hyperglycemia. Kernictreus. Neurofibromatosis. Hallervorden Spatz syndrome. Methyl malonic aciduria. Fucosidosis.
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Bilateral globus pallidus
abnormalities
Acute
Adult
CO
Ischemia (heroin)
Pediatric Kernicterus
chronic
Adult
Chronic hepatic encephalopathy
Chronic renal dialysis
Non ketotic hyperglycemia
Pediatric
Kernicterus
NF1
Hallorverden Spatz syndrome
Wilson disease
Fucosidosis
T1
T1
T1
T2
T2
T2
T2
T2
T2
T1
T1
T1
T2
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CO poisoning
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Monoxide mania
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CO delayed leukoencephalopathy
2 month
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Areas involved with CO
Globus pallidus. Deep white matter. Hippocampus.Pathogenesis:CO is colourless, odorless,
tastless gas generated through incomplete consumption of carbon containing products.
Mechanism of brain injury:
Hypoxia.
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Non ketotic hyperglycemia
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Non ketotic hyperglycemia
Pathogenesis: Old diabetic patient. Unknown mechanism.Location: Corpus striatum unilaterally. Globus pallidus bilaterally.C.P: Chorea. Hemiballisums.
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Non ketotic hyperglycemia
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Non ketotic hyperglyemia
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Non ketotic hyperglycemia
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Chronic hepatic encephalopathy
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Chronic hepatic encephalopathyPathogenesis:Manganese toxicity.Location: Globus pallidus. Subthalamus Substantia nigra.
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Chronic renal dialysis
Pathogenesis:Manganese toxicity.Location: Globus pallidus. Subthalamus Substantia nigra.
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Heroin abuse(bilateral globus pallidus ischemia)
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Kernicterus
(Yellow nuclear region of the brain)Acute: Increased T1 signal intensity in globus
pallidus, substantia nigra & dentate nucleus.Chronic: Increased T2 signal intensity in globus
pallidus.C.P (triad):Choreoathetosis.Deafness.Upward gaze palsy.
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Chronic kernicterus
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Hallervorden Spatz syndrome
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Hallervorden Spatz syndrome
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Fucosidosis
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Pathogenesis: Lysosomal storage disease
characterized by deficiency of enzyme fucosidase.
Location: White matter hypomyelination. Bilateral globus pallidus T2 low
signal. Bilateral substantia nigra T2 low
signal.
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Methyl malonic aciduria
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Hepatic Wilson disease
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Hepatic Wilson disease
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Wilson disease:
Pathogenesis:Defective incorporation of copper into
ceruloplasmin.Location:Putamina.Caudate nuclei.Globus pallidus (hepatic patients).Midbrain.Dentate nucleus.
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Neuropsychatric Wilson disease
3 years
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Neuropsychatric Wilson disease
3 years
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Wilson disease
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NF1
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Neurofibromatosis type 1
Pathogenesis: Hamartomas. Myeline vacuolation.Location: Globus pallidus. Brain stem. Cerebellum.
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Bilateral corpus striatum abnormalities
Acute: Acute hepatic encephalopathy. Hypoxia. Hypoglycemia. PRES. Encephalitis. Osmotic myelinolysis.Chronic: Leigh disease. Wilson disease. Huntigton disease. Glutaric aciduria. Gangliosidosis. Urea cycle disorders.
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Bilateral corpus striatum abnormalities
Acute
Hypoxia
Hypoglycemia
PRES
Osmotic myelinolysis
Encephalitis
Acute hepatic encephalopathy
Chronic
Pediatric
Leigh disease
Wilson disease
Glutaric aciduria
Gangliosidosis
Urea cycle disorders
Adult
Huntington disease
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Acute hepatic encephalopathy
Pathogenesis: Hyperammonemia.Location (Grey matter): Basal ganglia. Insular cortex. Cingulate gyrus.MRS:Elevated gluatamine/glutamate
complex.
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Acute hepatic encephalopathy
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MRS in a patient with hepatic failure & after hepatic transplantation
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Hypoxia
Mild HIE involve water shed zones.Sever HIE involve grey matter Cerebral cortex. Basal ganglia. Thalami. Hippocampus.
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Sever hypoxic ischemic encephalopathy
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Hypoxia
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Hypoglycemia
Mild hypoglycemia:Transient white matter abnormalities: Splenium of corpus callosum. Internal capsule. Corona radiata.Sever hypoglycemia:Diffuse grey matter abnormalities: Cortical grey matter Basal ganglia.
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Mild hypoglycemia
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Sever Hypoglycemia
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Osmotic myelinolysis
Pathogenesis: Osmotic insult (change in osmotic gradient). Endothelial damage. Break BBB. Accumulation of Na in ECF Release of myelin toxins.Causes: Rapid correction of hyponatremia (classic). Hyperglycemia. Hypokalaemia. Ketoacidosis.Comorbid conditions: Hepatic, renal or paraneoplastic disease. Neutritional (alcohol, malnutrition, vomiting). Burn, transplantation, other surgical patient.
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Osmotic myelinolysis
Location:50% basis pontis (central pontine
myelinolysis)50% basal ganglia (extra-pontine
myelinolysis)
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Osmotic myelinolysis
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Osmotic myelinolysis
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Osmotic myelinolysis
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Central pontine myelinolysis
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Extrapontine myelinolysis
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Herpes encephalitis
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Herpes encephalitis
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Leigh disease
Pathogenesis: Mitochondrial disorder characterized
by neurodegeneration.Location: Putamina. Caudate nuclei. Periaqueductal grey matter. Cerebral peduncles. Thalami.
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Leigh disease
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Leigh disease
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Leigh disease
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Leigh disease
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Leigh disease
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Leigh disease
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Leigh disease
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Leigh disease
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Leigh disease
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Leigh disease
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Glutaric aciduria type 1
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Glutaric aciduria type 1
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Urea cycle disordershyperammonic encephalopathy
Bilateral lentiform nuclei T1 bright signal on T1.
Bilateral globus pallidus T2 low signal. Bilateral putaminal T2 bright signal. Bilateral insular & bilateral perirolandic
T1 bright signal.
MRS: Glutamine shoulder on the left of NAA.
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Bilateral thalamic lesions
Acute:Ischemia (arterial).Ischemia (venous).Hypoxia.PRESEncephalitis.Wernick’s encephalopathyOsmotic myelinolysis.Chronic:Fabry disease.Fahr disease.Leigh disease.Wilson disease.Gangliosidosis.Krabbe’s disease.Bilateral thalamic glioma.
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Artery of Percheron infarct
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Deep venous thrombosis
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Deep venous thrombosis
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Deep venous thrombosis
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Deep venous thrombosis
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Deep venous thrombosis
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Deep venous thrombosis
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PRES
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Wernicke’s encephalopathyPathogenesis:Thiamine (Vit. B1) deficiency. Alcoholism. Hyperemesis gravidarum.Location:Medial thalami.Mammillary bodies.Hypothalamus. Fornix.Periaqueductal grey.Tectal plate.
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Wernicke’s encephalopathy
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Wernicke’s encephalopathy
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Wernicke’s encephalopathy
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Wernicke’s encephalopathy
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Wernicke’s encephalopathy
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Wernicke’s encephalopathy
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Wernicke’s encephalopathy
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Wernicke’s encephalopathy
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West Nile viral encephalitis
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Streptococcal encephalitis
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Viral encephalitis
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Viral encephalitis
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Limbic encephalitis
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Fabry disease
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Fabry disease
Pathogenesis: Inborn error of metabolism
characterized by deficiency of galactosidase enzyme.
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Gangliosidosis
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Gangliosidosis
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Gangliosidosis
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Gangliosidosis
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Gangliosidosis
Decreased NAA/Cr.
Increased mI/Cr.
Normal choline/Cr.
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Krabbe’s diseasegloboid cell leukodystrophy
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Bilateral thalamic glioma