Peripheral Neuropathies HIGH YIELD Flashcards
subtypes of neuropathy
1) axonal
2) demyelinating
3) wallerian degeneration
________ transport is necessary to maintain the axon itself
ANTEROGRADE transport is necessary to maintain the axon itself (and thus the muscle too since denervated muscles atrophy)
what happens to denervated muscle?
atrophy
Wallerian degeneration
“dying forward”
- axonal injury occurs
- axon dies from site of injury to the end of the axon (peripherally)
- chromatolysis
- muscle atrophy
- can regenerate if myelin sheath is intact
axonal degeneration
“dying back”
- metabolic derangement
- distal part dies first (due to lack of nutrients etc)
- proximal direction
- chromatolysis
- muscle atrophy
segmental demyelination
- myelin is stripped off in some places
- AP dies out
- axon is still intact, just missing myelin
- NO chromatolysis
- NO muscle atrophy
nerve conduction studies
- used to diagnose peripheral neuropathies
- measure nerve function
- measure evoked action potentials (either motor or sensory)
does NOT look at overall nerve function
-just between cell body and end organ
-helps distinguish between types of lesions
Peripheral nerve injury: appearance on nerve conduction studies
Motor: abnormal
Sensory: abnormal
- lesion distal to dorsal root ganglion
- both axons are cut between cell body and muscle
- neither trigger an AP
nerve root injury: appearance on nerve conduction studies
Motor: abnormal
Sensory: normal
- axon bringing sensory info to cell body is still intact; still transmits AP
- motor axon is cut between anterior horn cells and muscle; degenerates; no AP
patterns involved in diagnosis of peripheral neuropathies
- Focal v. Systemic
- Motor v. Sensory v. Autonomic v. Mixed
- Chronic v. Acute
- Axonal v. Demyelinating
- weakness: myotomal or peripheral nerve pattern
- atrophy?
- distal weakness (axonal) or proximal weakness (demyelinating)?
muscles atrophy suggests
axonal damage
as opposed to demyelinating
no atrophy suggests
demyelinating damage
as opposed to axonal damage
distal weakness suggests
axonal damage
proximal weakness suggests
demyelinating damage
OR myopathy
symptoms of axonal neuropathy
- slow, chronic
- stocking glove distribution
- loss of reflexes distally
- muscle wasting distally
- low amplitude CMAPs (muscle AP)
- absent SNAPs (sensory AP)
Guillian-Barre Syndrome
- acute demyelinating polyneuropathy
- segmental demyelination
- primarily motor (some sensory)
- cause: autoimmune: Abs cause inflammation, destroy myelin
- rapidly progressive
- no reflexes (afferent pathology)
- ataxia (afferent pathology)
- conduction block
- treatment: immune modulating therapy (IVIg)
histological sign of chronic demyelinating neuropathy
onion bulb sign
-myelin grows, dies, grows, dies…
ischemic mononeuritis multiplex
- commonly seen in polyarteritis nodosa (vasculitis)
- fascicular injury –> individual fascicles are injured by interruption of microcirculation of nerve
- confluent mononeuritis makes it look like generalized neuropathy
- biopsy: arteritis, fascicular injury
-tx: steroids (vasculitis), cyclophosphamide (immune modulating drug)
fascicular injury
- Individual fascicles are injured, not the whole nerve.
- Due to interruption of the microcirculation of the nerve.
types of focal neuropathies
- Compressive/traumatic
- Ischemic: diabetic or vasculitic – fascicular injury
- autoimmune; brachial plexopathy
-Injury: wallerian degeneration
injury associated with focal neuropathies
wallerian degeneration
- disruption of anterograde transport so axon dies backward
- retrograde transport starts chromatolysis, increases metabolic activity for axonal regeneration
- axonal sprouting occurs
- regeneration depends on if schwann cell sheaths are disrupted or not
traumatic nerve injury classification
CLASS 1: Neurapraxia
- compression with focal demyelination
- no denervation (no atrophy)
- quick recovery
CLASS 2: Axonotmesis
- axonal damage
- intact nerve sheath for sprouting to occur through
- slower recovery (sometimes incomplete)
CLASS 3: Neurotmesis
- scarred/disrupted nerve sheath
- no recovery
neurotmesis
- scarred/disrupted nerve sheath
- no recovery
Axonotmesis
- axonal damage
- intact nerve sheath for sprouting to occur through
- slower recovery (sometimes incomplete)
Neurapraxia
- compression with focal demyelination
- no denervation (no atrophy)
- quick recovery
