ClinNeuro- Thalamocortex

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Mawad
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312320
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ClinNeuro- Thalamocortex
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2015-12-02 09:45:14
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vetmed clinneuro
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vetmed clinneuro
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  1. What are functions of the cerebral cortex? (4)
    personality/behavior, conscious awareness, perception of visual stimuli (occipital cortex), pyramidal motor system (frontal cortex)
  2. Functions of the diencephalon (thalamus). (3)
    relay system, ascending reticular activating system, homeostasis (pituitary hormone regulation, thirst, appetite, sleep/wake, temperature regulation)
  3. Clinical signs of cerebral cortex lesions. (7)
    seizures, behavior changes, circling (toward lesion), menace deficit (contralateral), decreased nasal sensation, postural reaction deficits (with relatively normal gait), head turn
  4. Clinical signs of a lesion in the thalamus/hypothalamus. (7- 2 thalamus, 5 hypothalamus)
    many same as cortical, decreased consciousness (somnolence), [hypothalamus] abnormal water consumption, abnormal appetite, abnormal temperature regulation, abnormal heart rate, narcolepsy
  5. Differential diagnoses for forebrain disease.
    • Degenerative
    • Anomalous
    • Metabolic
    • Neoplastic
    • Idiopathic/infectious/inflammatory
    • Trauma/toxin
    • Vascular
  6. With cerebral cortex lesions, patient that are circling are circling _________ the lesion.
    toward
  7. With cerebral cortex lesions, menace deficit is ___________ to the lesion.
    contralateral
  8. With cerebral cortical disease, nasal sensation is decreased ___________ to the lesion.
    contralateral
  9. What are anomalous forebrain diseases? (2)
    hydrocephalus, quadrigeminal cistern cyst
  10. What causes congenital hydrocephalus?
    malformation(s) that interfere with CSF flow or reabsorption, most commonly stenosis of the mesencephalic aqueduct (fluid accumulation in third and lateral ventricles)
  11. What animals are predisposed to congenital hydrocephalus?
    toy breeds, brachycephalics; clinical signs by 3-12 months of age
  12. Even severe cases of __________ can be an incidental finding, ie. no profound clinical signs.
    congenital hydrocephalus
  13. Clinical signs of congenital hydrocephalus. (9)
    excessively domed cranial vault, "sunset strabismus" (eyes go ventral and lateral), open fontanels, seizures, abnormal behavior (difficulty house training, etc), mentation change, circling, postural reaction deficits, hear turn, central blindness
  14. How do you diagnose congenital hydrocephalus?
    CT or MRI, US if fontanels are open
  15. Describe medical management of congenital hydrocephalus. (3)
    diuretics (decrease CSF), low-dose prednisone (decrease vasogenic edema), proton pump inhibitor (Omprazole- decrease CSF)
  16. What is the prognosis for congenital hydrocephalus with medical management?
    • mild to moderate cases- may do well
    • severe cases- poor, should go to surgery
  17. What is the surgical treatment for congenital hydrocephalus?
    ventriculoperitoneal shunting
  18. What complications can occur with ventriculoperitoneal shunting? (3)
    acute over-shunting (collapse of cortex and subdural hematoma), infection, blockage
  19. A quadrigeminal cistern cyst is a(n) _____________.
    intracranial arachnoid cyst
  20. In what dogs are quadrigeminal cistern cysts (QCC) most common?
    toy breed dogs, congenital (since birth)--> +/- progressive
  21. What are the most common clinical signs of QCCs?
    • none-incidental finding
    • generalized seizures--> compression of occipital lobe
  22. What is the treatment for QCCs?
    symptomatic (seizure management)
  23. Metabolic causes of forebrain disease. (3)
    hypoglycemia, hepatic encephalopathy, electrolyte imbalances
  24. Clinical signs associated with hepatic encephalopathy. (5)
    [signs often bilateral and symmetrical] obtunded mentation, visual deficits, head pressing, circling, seizure activity (relatively uncommon)
  25. What diseases can cause hepatic encephalopathy? (4)
    • young- portosystemic shunts
    • older- liver failure
    • any age- hepatitis, toxin (ammonia) exposure
  26. What biochem changes can be associated with portosystemic shunts? (7)
    low albumin, low glucose, low cholesterol, low BUN [decreased liver synthetic function], normal ALP and ALT, bile acids > 100 (very high) post-prandial
  27. How do you treat hepatic encephalopathy? (5)
    eliminate gut-derived neurotoxins with lactulose and antibiotics, treat GI bleeding if present, low protein diet, control seizures if present
  28. How does lactulose help with txt of hepatic encephalopathy?
    decreases colon pH to prevent ammonia absorption
  29. What is the cause of hypoglycemic encephalopathy?
    brain has absolute glucose requirement--> neuronal energy depletion rapidly results in neurologic signs
  30. Clinical signs of hypoglycemia encephalopathy. (3)
    weakness/lethargy, behavioral changes, seizures (acute and severe presentation)
  31. What are the top 4 causes of hypoglycemic encephalopathy?
    • young animals- primary hypoglycemia (lower glycogen stores in the liver, if they miss a meal their BG will drop more severely than an older animal)
    • older patients- insulinoma
    • Diabetic patient- insulin overdose
    • Xylitol toxicity (causes profound release of insulin from the pancreas in dogs)
  32. What is the treatment for hypoglycemic encephalopathy?
    IV dextrose
  33. What are the most common primary brain tumors?
    meningioma
  34. What is the most common metastatic brain tumor?
    hemangiosarcoma
  35. What is the most common inflammatory disease of the forebrain in dogs?
    idiopathic immune-mediated
  36. What is the most common cause of forebrain inflammation in cats?
    infectious- FIP, FIV, FeLV
  37. Paradoxical sleep accompanied by atonia of the skeletal muscles, resulting in collapse.
    narcolepsy
  38. What causes narcolepsy?
    low CSF hypocretin levels--> hypocretin normally keeps the brainstem reticular center (hypothalamus) in check to maintain wakefulness
  39. What breeds have a predilection for congenital narcolepsy? (3)
    dachshund, doberman, weimaraner
  40. How do you diagnose narcolepsy? (3, 1 definitive)
    clinical presentation, food-elicited cataplexy response test (food and excitement often stimulate an attack), CSF hypocretin levels [definitive dx]
  41. How do you treat narcolepsy?
    drug that modulate the RAS by increasing serotonin levels

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