Bilateral basal ganglia & thalamic abnormalities

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Bilateral basal ganglia & thalamic abnormalities

  1. 1. Dr / Hytham Nafady
  2. 2.  Bilateral globus pallidus abnormal signal.  Bilateral corpus striatum abnormal signal.  Bilateral thalamic abnormal signal.
  3. 3. Basal ganglia Globus pallidus Globus pallidus interna Globus pallidus externa Striatum Caudate Putamen Subthalamus Substantia nigra
  4. 4.  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.
  5. 5. Acute:  CO poisoning.  Ischemia (heroin abuse).  Kernictreus  Hemolytic uremic syndrome Chronic:  Chronic hepatic encephalopathy.  Chronic renal dialysis.  Non ketotic hyperglycemia.  Kernictreus.  Neurofibromatosis.  Hallervorden Spatz syndrome.  Methyl malonic aciduria.  Fucosidosis.
  6. 6. 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
  7. 7. 2 month
  8. 8.  Globus pallidus.  Deep white matter.  Hippocampus. Pathogenesis: CO is colourless, odorless, tas tless gas generated through incomplete consumption of carbon containing products. Mechanism of brain injury: Hypoxia.
  9. 9. Pathogenesis:  Old diabetic patient.  Unknown mechanism. Location:  Corpus striatum unilaterally.  Globus pallidus bilaterally. C.P:  Chorea.  Hemiballisums.
  10. 10. Pathogenesis: Manganese toxicity. Location:  Globus pallidus.  Subthalamus  Substantia nigra.
  11. 11. Pathogenesis: Manganese toxicity. Location:  Globus pallidus.  Subthalamus  Substantia nigra.
  12. 12.  (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.
  13. 13. Pathogenesis:  Lysosomal storage disease characterized by deficiency of enzyme fucosidase. Location:  White matter hypomyelination.  Bilateral globus pallidusT2 low signal.  Bilateral substantia nigraT2 low signal.
  14. 14. Pathogenesis: Defective incorporation of copper into ceruloplasmin. Location: Putamina. Caudate nuclei. Globus pallidus (hepatic patients). Midbrain. Dentate nucleus.
  15. 15. 3 years
  16. 16. 3 years
  17. 17. Pathogenesis:  Hamartomas.  Myeline vacuolation. Location:  Globus pallidus.  Brain stem.  Cerebellum.
  18. 18. Acute:  Acute hepatic encephalopathy.  Hypoxia.  Hypoglycemia.  PRES.  Encephalitis.  Osmotic myelinolysis. Chronic:  Leigh disease.  Wilson disease.  Huntigton disease.  Glutaric aciduria.  Gangliosidosis.  Urea cycle disorders.
  19. 19. Bilateral corpus striatum abnormalities Acute Hypoxia Hypoglycemia Osmotic myelinolysis Encephalitis Acute hepatic encephalopathy Chronic Pediatric Leigh disease Wilson disease Glutaric aciduria Urea cycle disorders Adult Huntington disease
  20. 20. Pathogenesis:  Hyperammonemia. Location (Grey matter):  Basal ganglia.  Insular cortex.  Cingulate gyrus. MRS: Elevated gluatamine/glutamate complex.
  21. 21. Mild HIE involve water shed zones. Sever HIE involve grey matter  Cerebral cortex.  Basal ganglia.  Thalami.  Hippocampus.
  22. 22. 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.
  23. 23. 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.
  24. 24. Location:  50% basis pontis (central pontine myelinolysis)  50% basal ganglia (extra-pontine myelinolysis)
  25. 25. Pathogenesis:  Mitochondrial disorder characterized by neurodegeneration. Location:  Putamina.  Caudate nuclei.  Periaqueductal grey matter.  Cerebral peduncles.  Thalami.
  26. 26. Leigh disease
  27. 27. Leigh disease
  28. 28. Leigh disease
  29. 29. Leigh disease
  30. 30. Leigh disease
  31. 31. Leigh disease
  32. 32. Leigh disease
  33. 33. Leigh disease
  34. 34. Leigh disease
  35. 35. Leigh disease
  36. 36.  Bilateral lentiform nucleiT1 bright signal onT1.  Bilateral globus pallidusT2 low signal.  Bilateral putaminalT2 bright signal.  Bilateral insular & bilateral perirolandicT1 bright signal. MRS:  Glutamine shoulder on the left of NAA.
  37. 37. Acute: Ischemia (arterial). Ischemia (venous). Hypoxia. PRES Encephalitis. Wernick’s encephalopathy Osmotic myelinolysis. Chronic: Fabry disease. Fahr disease. Leigh disease. Wilson disease. Gangliosidosis. Krabbe’s disease. Bilateral thalamic glioma.
  38. 38. Pathogenesis: Thiamine (Vit. B1) deficiency.  Alcoholism.  Hyperemesis gravidarum. Location: Medial thalami. Mammillary bodies. Hypothalamus. Fornix. Periaqueductal grey. Tectal plate.
  39. 39. Limbic encephalitis
  40. 40. Pathogenesis:  Inborn error of metabolism characterized by deficiency of galactosidase enzyme.
  41. 41.  Decreased NAA/Cr.  Increased mI/Cr.  Normal choline/Cr.

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