Peripheral Neuropathies 1 Flashcards
Wallerian degeneration
distal part of a cut n. dies and macrophages destroy it
axonal degeneration
long n. at the ends start to die and degenerates backward form the end
small v. large fiber nn.
small fiber: poorly myelinated, primarily sensory and autonomic; symptoms = burning, tingling, numbness, pain
large fiber: heavily myelinated; primarily motor and sensory; symptoms = weakness, vibratory and position sense loss, numbness, areflexia
peripheral symmetric polyneuropathy
- usually affects longest nn. first; start in feet and then works up to hands; glove/stocking distribution; ex: diabetes
motor neuropathies
- Guillain Barre syndrome and motor neuron disease most commonly seen
- also includes porphyria and tick paralysis (more in western US like Rocky Mt. area)
S&S of peripheral neuropathy
- weakness - areflexia
- cramps - ataxias
- deformities - numbness
- pain - spasms
- trophic changes - autonomic dysfunction
- S&S will depend on the nn. involved
sensory +/- autonomic neuropathies
- diabetes mellitus = #1 risk factor in US
- amyloid
- inherited
- thallium poisoning
- alcohol = #2 risk factor
- leprosy –> depends where you practice; would see it mostly among immigrants
- carcinoma
- pyridoxine –> too much can damage nn. but deficiency can also cause n. damage
neuropathy symptom terminology:
hypesthesia; hyperesthesia; dysesthesia; paresthesia
hypesthesia = decreased sensation hyperesthesia = increased sensation dysesthesia = unpleasant, abnormal sensation produced by normal stimulus paresthesia = perverted, abnormal sensation like burnin, prickling, formication (crawling)
What are the 2 cranial neuropahies?
- Guillain-Barre syndrome
- diphtheria
Examples of autonomic neuropathies? (5)
- diabetes mellitus
- amyloid
- Guillain-Barre (not sure why it’s also listed as cranial)
- porphyria
- thallium poisoning –> rare but could be environment/work-related toxicology as an etiology
mononeuropathy multiplex examples? (6)
- diabetes mellitus
- vasculitis = rheumatoid arthritis, polyarteritis nodosa
- trauma
- plasma cell dyscrasia
- leprosy
- sarcoidosis
palpably enlarged nn. - possibly causes/diseases associated? (5)
- inherited disease like charcot marie tooth or neurofibromatosis
- leprosy
- amyloid
- acromegaly
- chronic inflammatory demyelinating polyneuropathy
Guillain-Barre syndrome
- acute idiopathic inflammatory polyneuropathy
- primarily demyelinating motor polyneuropathy
- ascending paralysis: goes from legs up to arms then breathing mm./nn.
- may begin cranially
- happens more in spring and fall
- unknown etiology but thought to be triggered by infectious agents or cancers -> something triggers an autoimmune response
GB possible etiologies
- viral illness like respiratory or GI
- CMV, EBV, HIV
- mycoplasma
- campylobacter jejuni –> causes special kind of GB that attacks the myelin and takes longer recovery time
- lymphoma
- vaccines/immunizations
GB pathologies
- lymphocytic infiltration
- segmental demyelination
- axonal degeneration
- can start w/ ill-defined back pain and tingling; biggest feature = weakness usually ascending
- axon can be damaged if not dx or tx ASAP; want to catch GB in the demyelination phase = faster recovery
GB clinical features
- paresthesias: tingling, ill-defined back pain
- weakness
- areflexia: starts in ankles and works up
- facial diplegia - both sides of face get weak
- autonomic instability: pts in ICU; could induce heart block
ddx for Guillain-Barre
- poliomyelitis: very unlikely in US but it’s asymmetric weakness
- myelitis: inflamed spinal cord so should have hyperreflexia not areflexia like GB
- diphtheria
- tick paralysis: geographically unlikely
- heavy metal poisoning
- botulism: can cause weakness and autonomic issues but usually starts cranially
- toxin
- porphyria
- HIV
- **overall the 2 most likely are GB and myelitis and they can be differentiated by the reflexes; GB = areflexia and myelitis = hyperreflexia
GB workup/dx procedure
- H&P; lumbar puncture, EMG, serology, toxicology
- LP –> looking for normal cell count and high protein = cytoalbuminal dissociation
- EMG –> n. conduction part and transmission part; in GB the transmission slows down; you would also do a m. biopsy
GB tx
- supportive care: prevent bed sores, DVTs, m. atrophy, pneumonia, etc.; thinking of all the complications and how you can prevent them
- plasmapheresis: take the proteins out of the blood and give the blood back to pt w/o the antibodies
- IV IgG: blood donor then take IgG out of the donor blood and give to pt; floods the system w/ antibodies and the immune system gets overloaded and slows down its response
- NEVER USE STEROIDS!!
GB prognosis
- mortality = 5% but 20% can be left w/ neurological deficits
- poor outcome predictors = older age, rapid onset, ventilator use, severely reduced distal cMAP on EMG
- best to catch GB in the demyelination phase; better prognosis the earlier you catch it
uremic polyneuropathy
- most common complication of chronic renal failure
- usually painless, progressive, symmetric sensorimotor peripheral neuropathy
- can be burning, cramping, crawling, itching, creeping which is worse at night; “restless legs”
- caused by diabetes, HTN; accumulation of 300-2000MW toxins
- tx = symptomatic (dialysis) and best = renal transplant - nothing beats a real kidney, not even dialysis
alcoholic polyneuropathy
- 2nd most common cause of neuropathy
- pathogenesis = direct toxic effect or nutritional (B1, B3, B6, B12, folic acid, zinc)
- symmetric sensorimotor polyneuropathy
- tx = stop drinking and get proper nutrition
diabetic neuropathy: what type of neuropathy does it fall into?
- mononeuropathy
- mononeuropathy multiplex
- symmetric sensorimotor polyneuropathy
- autonomic
- thoracoabdominal radiculopathy
- amyotrophy
- basically it can be anything!
DM as mononeuropathy & mononeuropathy multiplex
- cause = compression or infarct (occlusion of vasa nervorum [blood vessels for nn.]
- CN III, VI, VII can all be affected; CNVII most common
- peripheral nn. = femoral, sciatic, peroneal, radial, ulnar, median