10-08 L1 Neuronal reaction to injury Flashcards

1
Q

Cytotoxic (Brain Edema)

A
  • **Minutes to hours **
  • Swelling of cellular elements
  • Ion pumps fail
  • Rapid accumulation of sodium with cells
  • Water follows to maintain osmotic equilibrium
  • Leads to glutamate excitotoxicity (Glutamate binds to NMDA receptors and stays bound –>Ca influx causing apoptosis)
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2
Q

Vasogenic (Brain Edema)

A
  • Hours to days
  • Increase in extracellular fluid volume (resulting from increased permeability of brain; endothelial cells to macromolecular serum proteins)
  • Brain herniation
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3
Q

Central chromatolysis

A
  • (swelling 2 times the size and increase in nissel bodies)
  • Reaction to axonal injury
  • Affects cell body
  • Swelling, nuclear displacement
  • Dispersion of Nissl bodies
  • Regenerative response
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4
Q

What are the eight different cytoplasmic accumulations and what are they associated with?

A
  1. _Neurofibillary tangle (AD) _
  2. Granulovacuolar bodies (AD)
  3. Hirano body (AD, CJD)
  4. Lewy bodies (PD, Lewy body dementia)
  5. Pick body (Pick’s disease)
  6. Negri bodies (Rabies)
  7. Psammoma bodies (meningioma)
  8. Verocay bodies (schwannoma)
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5
Q

**Wallerian degeneration **

A

** Wallerian degeneration
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  • occurs in distal part of the axon (when its cell body is destroyed or separated from the (axotomy) by disease or injury
  • both CNS & PNS (axon can not survive when it is seperated from its cell body)
  • Most axonal debris disappears within a month
  • CNS process is much slower and lipid
    • laden marcrophages may remain for months or even years.
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6
Q

Process of Wallerian Degeneration

A

A. Normal axon

B. Transected axon

C. Degradation of the meylin in the distal portion of the axon

D. Macrophages removing myelin and axonal debris

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7
Q

Dying Back (Distal axonopathy)

A
  • “Dying-back” results in **axonal degeneration at the most distal extent of the axon. **
  • Axonal degnerative polneuropathies are usually symmetric, and as the disorder progresses, the axons typically degenerate in a distal-to-proximal gradient.
  • Axonal degeneration is the most common type of pathologic reaction in generalized polyneuropathies
    • often attributed to a “metabolic etiology (diabetes, renal failure, etc.).
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8
Q

Trans-synaptic (transneuronal) degeneration

A
  • **Anterograde: ** target of injured cell undergoes atrophy or death
  • Retrograde: inputs to an injured neuron deprived of trophic substances
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9
Q

Neurapraxia

A
  • Block in conduction
  • Recover takes place w/o Wallerian degeneration
  • Biochemical lesoin caused by a concussion or shock-like injury to the nerve fiber
  • Common examples:
    • crossing the legs (peroneal parylis from prolonged cross-legged position)
    • radial or Saturday night paralysis caused by compression of the axilla (sleeping on your arm)
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10
Q

Axonotmesis

A
  • Involves loss of the relative continuity of the axon and its covering of myelin preservation of the connective framework of the nerve (endoneurial tube)
  • Wallerian degeneration occurs due to loss of axonal continuity
  • This is usually a severe crush or contusion injury
  • The potential for regeneration is excellent
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11
Q

Neurotmesis

A
  • cut thorugh both the axon and the endoneural tube
  • This result from more severe contusion, stretch, or laceration and _not only axons, but the investing connective tissues lose their continuity _
  • Both the endoneurial and perineurial connective tissue layers and the axon are disrupted
  • Regenerating axons reach the distal stump but fail to find their preinjury pathways
  • No function regeneration (if they are not brought back together).
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12
Q

Oligodenrocytes

A
  • Myelinated CNS
  • Inujury results in demylination
    • Viruses, immunologic mechanisms, aging
  • Leukodystrophies
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13
Q

Microglia

A
  • Resident macrophages (ontologically related to cells of the mononuclear phagocyte lineage)
  • Resting vs actived
  • Infarcts, demyelinating processes, infection, injury
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