Neuro - Pns Disorders

Front 1

LMN Syndrome

Back 1

• Flaccid paralysis/hypotonia (loss of muscle spindle/α-motor neurons reflex arc)
• Fasciculations (spontaneous α-neuron APs)
• Areflexia/hyporeflexia (spinal loop is broken)
• Myotomal weakness/Dermatomal paraesthesia (nerves are involved, not spinal levels)
• Disuse atrophy

Front 2

What are the two primary responses to peripheral nerve injury?

Back 2

• Segmental demyelination due to external compression where the axon remains intact
  
• Wallerian degeneration due to axon disruption, results in anterograde degeneration from the point of lesion

Front 3

• What are the classes of peripheral nerve injury? What constitutes each? What type of recovery is possible?

Back 3

• Neurapraxia, compression of myelin with concurrent axon sparing; allows remyelination by Schwann cell mitosis and full recovery
• Axonotmesis, damage to axon with connective tissue intact, regeneration is slow, possible
• Complete severing of nerve fibers/support structure

Front 4

• What happens to muscle following neurotmesis/axonotmesis?
  
• Why does this happen?
  

Back 4

• Atrophy of the motor units
  
• Wallerian degeneration leads to the neuron being unable to transmit trophic controls to the previously innervated muscle fibers
  

Front 5

• In peripheral nerve disease states, which nerves tend to be involved first?
  
• What does this lead to, clinically?

Back 5

• The longest nerves
  
• PW-PNS diseases present with distal symptoms first
  

Front 6

• What is an alternative name for Acute Inflammatory Demyelinating Polyneuropathy?
• What is it similar to in terms of pathologenesis? Why?
• Who is most at risk?

Back 6

• Guillain-Barre syndrome
• It is similar to MS in that it involves autoimmune demyelination and ↓ internodal distance with remyelination
• White women, 40-70 y.o.

Front 7

• What typically preceded onset of AIDP/GBS?
• What is its typical course?
• What symptoms are typical at clinical presentation?

Back 7

• Viral infection, surgery, or vaccination
• Quick onset with peak impairment at 4 weeks, then plateau and slow improvement; Sensory symptoms improve before motor
• Distal-to-proximal, symmetrical motor/sensory deficits; LMN syndrome; Sparing of extraocular muscles

Front 8

• What symptoms may present medically in AIDP/GBS?
• In what pattern is recovery seen?
• What is of note regarding PT treatment?
• What outcomes may be expected?

Back 8

• Cardiac changes (tachy, BP, rhythm changes) and respiratory failure, mechanical ventilation
• Proximal to distal
• Pseudo-exacerbations possible with over-work
• 67% fully recover/20% significantly disabled at 1 year

Front 9

• What is the general pathogenesis of polio?
  
• Which areas are most commonly affected?
• How does weakness present?

Back 9

• Virus attacks anterior horn cells
  
• Cervical and lumbosacral segments in the SC, though 10-15% of cases occur in brainstem
• Assymetrical weakness, proximal > distal, LE > UE

Front 10

Signs and symptoms of polio

Back 10

• Flaccid paralysis with atrophy
• Hyporeflexia
• Dysarthria/dysphagia
• Extraocular sparing
• Respiratory involvement (may lead to death)

Front 11

• Why might giant motor units develop in PW-polio?
  
• What may this contribute to? Why? What is this?

Back 11

• Collateral sprouting from remaining neurons innervate additional muscle fibers
• Post-polio snydrome, which is the new onset of pain/weakness/fatigue, in part caused by long-term overstress of giant motor units

Front 12

• What is diabetic neuropathy? What causes it?
• How does it change with time?
• Most common S&S?

Back 12

• Loss/atrophy of peripheral nerve fibers, caused by metabolic abnormality
• Motor and sensory function diminish progressively in a symmetrical, distal-to-proximal fashion
• Painless distal paraesthesia, loss of vibration sense, diminished DTRs

Front 13

• What is affected in PW-myasthenia gravis? Why does this happen?
• Most common presenting symptom?
• Which muscles tend to be most affected?
• How do symptoms change t/o the day?

Back 13

• The immune system develops antibodies that bind to ACh receptors at the neuromuscular junction
• Extraocular muscle weakness and/or ptosis
• Proximal muscles
• They worsen