1. Where does coup, contracoup injury occur?
    • On site of impact, usually convex brain
    • Opposite side (against skull), more severe.
  2. What are the patterns of skull fracture?
    • Linear
    • Depressed
    • Comminuted: large fracture with multiple fragments
    • Diastatic: Opens or reaches suture.
  3. What is a concussion, what function is most often affected?
    • Traumatically induced alterarion in mental status (+/- loss of conciousness)
    • Memory.
  4. What is a contusion?
    • Bruise, usually on crest of gyri
    • Often found in temporal or frontal lobes.
  5. Where is, what causes an epidural hemorrhage?
    • Between dura and calvarium
    • Rupture of meningeal (often middle meningeal) arteries due to trauma.
  6. What causes a subdural hematoma?
    • Rupture of bridging veins
    • Acceleration/deceleration injury (eg. shaken baby syndrome)
    • Symptoms: nausea, vomiting, dizziness, sleepiness.
  7. Subarachnoid hemorrhages may be caused by?
    • Trauma, contusion
    • Rupture of berry aneurysm
    • Rupture of leptomeningeal blood vessels
    • High mortality.
  8. What causes diffuse axonal lesions?
    Acceleration/deceleration result in axonal damage due to shearing stress.
  9. What is the time course of diffuse axonal injury?
    • 4-5hrs: accumulation of Amyloid Precursor Protein (APP)
    • 12-24hrs: Axonal bulbs/varicosities on H&E
    • 24hrs-2mo: Axonal spherules (with ubiquitin, APP, NF+)
  10. What is the hallmark lesion of MS, what does it represent?
    • Plaque
    • Area of demyelination
    • Often found in:
    • -periventricular white matter
    • -subcortical white matter
    • -cerebral cortex and gray matter
    • -optic nerves
    • -brainstem
    • -spinal cord.
  11. What stains are used for myelin?
    Luxol Fast Blue: lack of staining identifies myelin loss.
  12. What other cells may be found in active plaques, how can you stain for them?
    • Macrophages- parenchymal and perivascular with myelin debris
    • CD68
    • Lipid containing macrophages: oil-red-O.
  13. Name three pathological processes in MS?
    • Edema
    • Cytokines: lymphotoxin, TNFa, IL-6
    • Endothelial activation: upregulation of ICAM-1 and VCAM-1.
  14. What are the three types of cortical lesions in MS?
    • Gray/white matter junction
    • Within cortex: No B or T lymphocytes
    • Cortex abutting the pia: Microglial activation prominent.
  15. What do shadow plaques represent?
    • Remyelination
    • Incomplete process early in MS.
  16. What is the Marburg type of MS?
    • Acute MS
    • Fulminant of rapid course
    • Children and young adults
    • large conluent areas of demyelination
    • Massive macrophage infiltration
    • axonal swelling
    • necrosis.
  17. What is tumefactive MS?
    Acute inflammatory demyelinating mass presenting as a neoplasm.
  18. What is Devic's disease?
    • Neuromyelitis optica: optic neuritis + acute transverse myelitis
    • CSF: Aquaforin 4 + Ig perivascular deposition.
  19. What is acute dissmeinated encephalomyelitis (ADEM)?
    • Acute, monophasic (demyelinating)
    • In children
    • may follow infections
    • Affects white matter more.
  20. What causes subacute sclerosing pan encephalitis (SSPE)?
    Infection of oligodendrocytes by defective measles virus.
  21. What is the clinical disease and pathology of SSPE?
    • Global loss of higher brain functions and death
    • Perivascular lymphoid infiltrate
    • Intranuclear inclusions of measles virus.
  22. What causes central pontine myelinolysis?
    Rapid correction of hyponatremia.
  23. What can cause toxic leukoencephalopathy?
    A number of drugs, prescription and recreational.
  24. Thymic hyperplasia or thymoma may be found in what NMJ condition?
    • Myasthenia Gravis
    • Women affected twice as often as men.
  25. Is MG acquired or congenital?
    • Acquired, autoimmune, humoral
    • Anti-AchR antibodies bind to alpha subunit.
  26. What is Lambert Eaton Myasthenic Syndrome (LEMS) associated with?
    • Small cell lung carcinoma - paraneoplastic syndrome (60%)
    • Men twice as much as women.
  27. What is the pathology of LEMS?
    • Decreased pre-synaptic release of Ach
    • Antibodies against presynaptic voltage gated Ca2+ channel.
  28. What are the clinical presentations of muscle strength in MG and LEMS?
    • MG: decreased strength throughout the day, increased with rest
    • LEMS: Increased strength with more contractions.
  29. What are leukodystrophies?
    • Inherited demyelinating diseases in which the clincial sympoms derive from abnormal myelin synthesis or turnover
    • Mostly Autosomal Recessive, some X-linked.
Card Set
exam 2