PNS disorders Flashcards
Nerve anatomy
- endometrium: around axon
- perineurium: around a bundle of axons (fascicles)
- epineurium: around a bundle of fascicles)
- epieneural sheath: around a nerve (has blood vessels)
What can be damaged in the PNS and what degeneration occurs
- can occur to myelin, axons, different CT etc
- damage to an axon = anything distally will degenerate and can have some healin g
- wallerian degeneration (distal degeneration)
Effects of Aging on the PNS
- number of fascicles
- effect on CT
- cross sectional area
- myelinated and non-myelinated fibers
- blood vessels = plaques
- processing speed of nociceptive signals
- protein production
- motor units decrease
Aging neuropathy
- loss of motor and sensory cell bodies
- fibers and receptors decrease
- nerve damage from a lifetime of trauma
Classification of nerve injury/neuropathy
- Demyelination: neurapraxia (least sever/grade 1)
- Axonotmesis: degeneration; damage to axon but CT is intact (stage 2)
- Stage 3: damage to axon and endoneurium
- stage 4: damage to axon, perineurium
- stage 5: neutromesis: complete severance of axon; damage to all layers of CT
Neuropathy types
- mononeuropathy: one nerve
- polyneuropathy: more than 1 nerve
- myopathy: muscle signs and symptoms
Signs and symptoms of peripheral nerve pathology
- loss of sensory function
- paresis or paralysis
- vascular control and sweating (dry skin, scaly, blue etc)
Mechanical injuries to PNS
- median neuropathy
- thoracic outlet syndrome
- tardy ulnar palsy/retroepicondylar palsy
- Saturday night palsy/sleep palsy (radial nerve)
- parsonage-turner syndrome
- morton neuroma
- idiopathic fascial paralysis/bell palsy
Thoracic outlet syndrome
- can be nerve or vascular
- can cause changes peripheral
- brachial plexus involvement due to compression in thoracic outlet
- pain, paresthesia, motor weakness
- raynauds
- color, temperature changes, ischemia and trophic changes
Tardy ulnar palsy
- ulnar nerve
- could occur after a fracture, direct force or trauma
- leads to benediction hand
Charcot-marie tooth disease
- Hereditary motor and sensory neuropathy
- progressive muscular (peroneal) atrophy
Clinical manifestations of Charcot-marie tooth disease
- distal symmetrical weakness, atrophy, and diminished DTR
- weak DF, evertors
- steppage gait
- progression causes wasting in intrinsics of hands and eventually forearm
- poor proprioception and cutaneous sensation (risk of falls)
- pes cavus (high arch) and hammer toes
- Saturday night palsy/sleep palsy
(radial nerve)
- in radial groove
- wake up/slept on arm wrong
parsonage-turner syndrome
- what is it + a differential diagnosis
- neuralgia amyotrophy affecting LMN of brachial plexus
- Differential: cervical radiculopathy, rotator cuff, TOS
- morton neuroma
- benign mass between 2nd and 3rd metatarsals that presses on the nerve
- idiopathic fascial paralysis/bell palsy
- facial nerve compression
- facial nerve motor for facial expression
- can be caused by an exposure to virus/infection
Hammer toe
- extended MTP and flexion of PIP
Metabolic neuropathies
- diabetic neuropathy
- alcoholic neuropathy: over consumption for long time
- chronic renal failure: changes in electrolytes
- stocking and glove pattern
Diabetic neuropathy etiology
- hyperglycemia
Diabetic neuropathy risk factors
- type 1 - 54%
- type 2 - 30 %
Diabetic neuropathy types
- rapidly reversible neuropathy (acute and goes away)
- generalized symmetric polyneuropathies
- focal neuropathies
Diabetic neuropathy treatmetn
- general-control hyperglycemia
- specific-symptomatic management
- meds include anticonvulsants and antidepressants (treat the pain/is not reversible)
Gullian Barre syndrome
- inflammatory infectous disorder
- typicall follows bacterial/viral infection
- more common in males than females
- Radipdly ascending bilateral symmetric motor weakness and distal sensory impairments
- paresthesia in toes that quickly spreads to leg within hours or days
Postpolio syndrome/postpolio muscular atrophy
- had pollio and stays dormit
- muscular atrophy
- can be asymtomatic
- nonparayltic infection that produced GI, flu-like symptoms and muscular pain
- virus invades anterior horn cell bodies
Trigeminal Neuralgia/tic douloureux
- intense paroxysms of lancinating pain within nerve distribtuion (face)
- can arise from herpes zoster, MS, vascular lesions or tumors
- sudden onset of sharp knifelike pain/lightning bold
Human immunodeficiency Virus Advenaced disease (AIDS) - PNS symptoms
- peripheral neuropathy,
- disease or drug indiuced myopathy
- MSK pain syndrome
occur in advanced stages of HIV
Vasculitic Neuropathy
causes
- primary cause: inflammation and necrosis of blood vessel walls
- secondary: process associated with autoimmune responses, infections, toxins or drug exposure
- peripheral nerves or even in CNS can sustain ischemia
herpes zoster/postherpetic neuralgia
- occurs in dermatomal pattern
- painful, sensory symptoms
- red lesions
Paraneoplastic neuropathies
- associated with carinomas
- numbeness/paresthesias initialy assymetric but progress
- weakness that is generally related to inability to sustain contraction secondary to proprioceptive feedback
Lead neuropathy
- primarily affects neurons innervating muscules in UE
- wrist drop,
- trouble grasping
Pesticides and organophosphates
- inhibit cholinesterase activity = creating an acute cholinergic crisis
- nausea/vomiting
- diarrhea
- muscule fasciculations
- weakness
- paralysis
- sudden paralysis of respiratory musculature
Myasthenia Gravis
- motor end plate disorder (NMJ)
- autoimmune
- number of ACh receptors are decreased and others are flattened
myasthenia gravis cardinal features
- muscule weakness and fatigability
- normal neurological findings
- eyes dont close
- speech is nasal
- aspiration of food (controlling epiglottis is hard)
4 categories of myasthenia gravis
- ocular,
- mild generalized
- acute fulminating
- later severe
myasthenia gravis diagnosis
- immunological: presence of anti-ACh receptor antibodies
- Pharmacologic: tensilon inhitis AChE (leaves ACh in junction)
- electrophysiological testing = normal EMG at rest
myasthenia gravis treatment
- ACh
- surgical removal of thymus = successful in 85%
- immunosuppressants
- long-term corticosteriods
What is Complex regional pain syndrome/reflex sympathetic dystrophy
- sensory, autonomic, motor and dystrophic signs and symptoms with or without known trauma
CRPS 1
- formerly RSD
- there was a known injury
- absence of known traumatic nerve injury
CRPS 2
- formerly causalgia
- known traumatic nerve injury
CRPS-NOS
- no other explanation
Complex regional pain syndrome/reflex sympathetic dystrophy: etiology/pathogenesis
- may follow medical procedures or injury
- no apparent soft tissue inflammaiton
- represents a reflex neurogenic inflammation
- migrains
CRPS: stage 1
- acute inflammation: denervation and sympathetic hypoactivity
- begins up to 10 days following injury and lasts 3-6 months
CRPS: stage 1 signs and symptoms
- Abnormalities in pain
- pain: more severe than expected; burning or aching character; increased by dependent position
- hyperalgesia (lower pain threshold)
- allodynia: all stimuli = pain
- hyperpathia: threshold to pain increased once exceeded sensation intensity increased more radiply than expected
- edema: soft and localized
CRPS: stage 2
- dystrophic paradoxic sympathetic hyperactivity
- occurs 3-6 months after onset of pain and lasts about 6 months
CRPS: stage 2 Signs and symptoms
- skin color and temperature changes
- pain: worsens, constant, burnging and aching
- allodynia, hyperalgesia and hyperpathia almost always present
- edema: becomes thicker and more fibrotic causing joint stiffness
- vasomotor/thermal changes: neither warm nor cold
- skin: thin, glossy, cool and sweating, thin ridgiied nails
- osteoporosis,cyctic and subchondral bone erosion
CRPS: stage 3
- atrophic
- begins about 6-12 months
CRPS: stage 3 signs and symptoms
- **Edema, Vasomotor and sudomotor abnormalities and motor dysfunction and trophic changes **
- pain: spreads proximally occasionally to entire skin surrounding face and plateaus joint stiffness progresses
- edema: hardens
- vasomotor/thermal: sympathetic NS regulation is decreased and affected extremity, affected limb is cooler
- skin: thin, shiny, cyanotic and dry
- fingers and toes are involved extremity are atropic
- fascia is thickened and contracutres may occur
- demineralization and ankylosis