Chapter 2: Cranial and Peripheral Nerve Disorders = Peripheral Nerve Disease/Injury

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dmshaw9
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Chapter 2: Cranial and Peripheral Nerve Disorders = Peripheral Nerve Disease/Injury
Updated:
2015-03-10 23:50:59
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Cranial Peripheral Nerve Disorders
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NPTE,Chapter2
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NPTE: Chapter 2
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  1. Etiology
    Wide range of etiological factors
  2. Basic Pathological Processes
    • Wallerian degeneration
    • Segmental demyelination
    • Axonal degeneration
  3. Wallerian Degeneration
    • Transection (neurotmesis) results in degeneration of the axon and myelin sheath distal to site of axonal interruption
    • Chromatolysis and repair processes occurs in nerve cell body
    • Endoneurium (sheath) does not degenerate but forms tube directing regeneration
  4. Segmental Demyelination
    • Axons are preserved (no wallerian degeneration)
    • Remyelination restores function (i.e. Guillain-Barre syndrome)
  5. Axonal Degeneration
    • Degeneration of axon cylinder and myelin
    • Progresses from distal to proximal 
    • "Dying back" of nerves (i.e. peripheral neuropathy)
  6. Neuropathy (Peripheral Neuropathy)
    • Any disease of nerves characterized by deteriorating neural function (i.e. diabetic neuropathy, alcoholic neuropathy) 
    • Polyneuropathy: bilateral symmetrical involvement of peripheral nerves (usually legs > arms, distal segments earlier and more involved than proximal)
    • Mononeuropathy: involvement of a single nerve
  7. Radiculopathy
    Involvement of nerve roots
  8. Traumatic Nerve Injury
    • Neurapraxia (Class 1)
    • Axonotmesis (Class 2)
    • Neurotmesis (Class 3)
  9. Neurapraxia
    • Injury to nerve that causes transit loss of function (conduction block ischemia)
    • Nerve dysfunction may be rapidly reversed or persist a few weeks
    • Example = compression
  10. Axonotmesis
    • Injury to nerve interrupting the axon and causing loss of function and wallerian degeneration distal to the lesion
    • With no disruption of endoneurium --> regeneration is possible (i.e. crush injury)
  11. Nuerotmesis
    • Cutting of the nerve with severance of all structures and complete loss of function
    • Reinnervation typically fails without surgical intervention because of aberrant regeneration (failure of regenerating axon to find terminal end)
  12. Clinical Symptoms LMN Syndrome
    • Weakness/paresis of denervated muscle
    • Hyporeflexia/hypotonia
    • Atrophy
    • Fatigue
    • Sensory loss (corresponds to motor weakness)
    • Proprioceptive losses may yield sensory ataxia
    • Autonomic dysfunction
    • Hyperexcitability of remaining nerve fibers 
    • Muscle pain (myalgia) with inflammatory myopathies (i.e. postpolio syndrome)
  13. Autonomic Dysfunction in LMN Syndrome
    • Vasodilation
    • Loss of vasomotor tone 
    • Dryness
    • Warm skin
    • Edema
    • Orthostatic hypotension
  14. Hyperexcitability of Remaining Nerve Fibers in LMN Syndrome
    • Sensory dysesthesias: hyperalgesia, pins and needles, numbness, tingling, burning
    • Motor: fasciculations, spasms
  15. Diagnostic Tests
    • NCV studies: conduction times (motor and sensory) are slowed or complete conduction block may be evident
    • EMG (motor nerve function): signs of widespread denervation atrophy (spontaneous fibrillation potentials); evidence of reinneravtion (low-amplitude, short-duration, polyphasic motor unit potentials)

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