MedPath Lecture 10

Nerve Compression or Repetitive Motion Can Cause Mechanical Nerve injury
Nerve Injuries can Fall into 3 categories:
Neurapraxia (axon intact) - segmental demyelination, temporary loss of function (recover in weeks or months when schwann cells regrow)
Usually caused by compression or ischemia
Axonotmesis - axonal injury that does not damage epi-, peri-, or endoneurium (recover in months or years)
Usually caused by prolonged compression or ischemia
Neurotmesis - severing of axon and outer coverings, worst prognosis (surgery may not even fix it)
Caused by profound physical trauma
Neuropathies affect longer axons first
Mononeuropathy - one nerve
Polyneuropathy - several nerves
Radiculoneuropathy - nerve root
Polyradiculitis - several nerve roots
Mechanical Neuropathy Disease Mechanism
Acutely, pressure causes demyelination (neurapraxia) and if pressure increases, blood vessels can be compressed and cause ischemia
Demyelinated axons fails to conduct AP’s along their length so the acute symptoms of weakness and sensory loss begin
Pain is a common symptom due to
Mechanical stimulation - ion channels are forced open which depolarizes C fibers
Inflammation - nociceptive afferents are excited by cytokines
Positive feedback loop - formation of scar tissue makes nerve sticky and cannot move as well and causes more pressure
Ephaptic transmission - because of demyelination, teh insulation is removed between axons so K is released and depolarizes nearby axons. AP’s excite nearby C fibers
Combination of demyelination and ischemia can lead to axonotmesis
If pressure persists, remyelination is not an option and ion channels cannot keep inserting so the AP are slower and can lead to oxidative stress
Trigeminal Neuralgia - chronic pain condition that occurs when non-painful stimuli activate nociceptive afferents in the trigeminal nerve (near the entry site at the pons)
Prevalence: 5 per 100,000
Incidence: 5.5 per 100,000 per year
Risk factors: hypertension, atherosclerosis, 1.74:1 F:M, 50-70 years of age, multiple sclerosis (demyelination of trigeminal root), family hx (1-2% autosomal dominant), viral infection
Pathophysiology: between 80-90% of the cases are caused by compression by an adjacent artery or vein
Superior cerebellar artery causes 75-80% of cases
Pain is caused by ephaptic transmission
Clinical symptoms: sharp sensation of pain in the face (mostly over cheek)
Diagnosis: normal light touch sensation and strength, imaging to visualize cause
Prognosis: depends on cause (may be able to fix it)
Treatment: surgery or medications (carbamazepine or phenytoin) to inhibit ion channels so the nerves cannot fire like they are supposed to
Bell’s Palsy - facial paralysis caused by entrapment of the facial nerve
Incidence: 23 per 100,000 per year
Risk factors: viral infection, vascular ischemia, autoimmune inflammatory disorders, family hx, other neuropathies, conditions that cause swelling
This is not painful
Clinical symptoms: inability to wrinkle eyebrow, drooping eyelid, inability to close eye, inability to puff cheek, asymmetrical smile, drooping corner of mouth, dry mouth
Diagnose: observation
Prognosis: 85% had signs of recovery in 3 weeks
Better prognosis with less initial paralysis
Treatment: spontaneous recovery happens or can use augment with EMG feedback and give facial exercises
Thoracic Outlet Syndrome - caused by pressure on the brachial plexus or vasculature in the thoracic outlet
Incidence: 2.5-4 per 100,000 per year
Surgeons are more likely to diagnose especially with private insurance or workers comp
Risk factors: repetitive upper limb elevation and use (especially with weight)
Common causes: traumatic injury, skeletal abnormalities (extra rib), muscular abnormalities, hypertrophy, tumorigenesis, osteomyelitis
Clinical symptoms: pain, tingling, paresthesia occur with overhead activities and worsen throughout the day
C5-7: neck, face, chest
C7-T1: neck, shoulder, medial arm, ulnar digits
Diagnose: rule out other causes by doing MRI/x-ray or can put in provocative position to see if symptoms are reproduced
Prognosis: fix it or it gets worse
Once muscle wasting occurs, it becomes difficult for functional recovery
Treatment: conservative approach or 1st rib resection
Postural retraining, breathing, strengthen/stabilize shoulder girdle, modify activities
No 1st rib mobilization
Saturday Night Palsy - caused by prolonged compression of radial nerve at upper medial arm or axilla
Incidence: 2.5 per 100,000 per year
Risk factors: prolonged pressure on axilla
Sleeping with arm on back of chair, using crutches improperly, compressive clothing or accessories, prolonged blood pressure cuff use
Clinical symptoms: wrist drop
Diagnose: clinical symptoms, NCS
Prognosis: 67-100% recovery within 3 months
Treatment: cock-up splint
Tardy Ulnar Palsy - caused by ulnar nerve entrapment at the elbow
Incidence: 20-25 per 100,000 per year
Risk factors: repeated elbow trauma or shallow ulnar groove
Elbow fx’s lead to callus formation or displacement of bones which stretches the nerve causing neurapraxia and axonotmesis
Clinical symptoms: claw hand
Diagnosis: percussion, elbow flexion
Prognosis: the sooner the treatment, the better
Treatment: mild - nerve/tendon glides, moderate to severe - decompression surgery
Carpal Tunnel Syndrome - pain, numbness, weakness, tingling in the hand and arm caused by compression of medial nerve at the carpal tunnel
Most common upper limb neuropathy
Incidence: 7,100 per 100,000 people; 250-360 per 100,000 per year
Risk factors: repetitive use (typing, gripping, vibrating tools), working in extreme cold, 2.5:1 F:M, other neuropathies, conditions that cause swelling of the joints and hands
Prolonged flexion or extension of wrist causes compression of median nerve
Clinical symptoms: tingling, numbness, shooting pain, weakened grip
worsen at night, decrease by shaking wrist
Diagnose: NCS show slowed conduction, special tests
Prognosis: more severe, worse prognosis
Treatment: modify lifestyle, steroids for pain, surgery to cut ligament (must have symptoms for > 1 year), splinting, tendon glides, generalized conditiong
Sciatica - radiculopathy caused by sciatic nerve root compression or inflammation
Incidence: 1,000-5,000 per 100,000 per year
Risk factors: peaks at age 40-60, jobs where workers are subject to physically awkward positions
Common causes: lumbosacral disc herniation, abscess, tumor, blood clots
Clinical symptoms: sensory deficits first then motor
Diagnose: MRI can rule out tumor but will also show other issues that can be blames for sciatica
Prognosis: good if responds well to PT, surgery
Treatment: PT, epidural injections for pain, discectomy
Postpolio Syndrome is caused by oxidative stress in surviving motor neurons
Prevalence: 40% of polio survivors
Risk factors: prior polio infection, initial severity predicts future severity
Disease mechanism:
Initial polio virus: kills motor neurons in spinal cord, brain, and cortex by disrupting protein synthesis or activating pro-apoptotic proteins
PPS occurs due to a second round of motor neuron loss likely from overuse
Surviving motor neurons innervate denervated muscle fibers (have to work harder)
Hyperactivity increases metabolic stress and leads to cell death (ATP → free radicals → apoptosis)
Clinical symptoms: new onset of weakness, fatigue, pain
Slow progression
Diagnostic criteria: prior paralytic polio, period of partial/complete recovery with at least 15 years of stable function, new symptoms last < 1 year
PT: non-fatiguing protocol
Look for signs of overwork or fasciculations
If they originally had bulbar involvement: SOB, dysphagia, cardiopulmonary insufficiency
May need assistive devices or bracing
Charcot-Marie Tooth Disease is caused by axonal impairments (demyelination or impaired axonal transport)
Prevalence: 40 per 100,000
Risk factors: family hx (most are autosomal dominant), other neuropathies could worsen symptoms
Disease mechanism: 2 main variants
CMT1 (mutations in myelin proteins) - abnormalities in myelin sheath
Mutations create segmental demyelination of peroneal nerve
Remyelination leads to formation of “onion ball” enlargements on nerves
CMT2 (impaired axonal transport) - starves the axon of new proteins and organelles so neurons can’t survive
Clinical symptoms: distal limb weakness and wasting, sensory loss, foot deformity (high arch & curled toes)
Diagnose: genetic testing or nerve biopsy to determine type
Prognosis: unimpacted lifespan but deformity results in balance loss and can progress to forearms/hands
PT: bracing
Articulating AFO: allows some ankle movement, helps with foot drop and mediolateral instability
Dynamic AFO: helps with foot drop only, energy efficient
Posterior leaf spring AFO: helps with foot drop only
Rigid AFO: most supportive, helps with foot drop and mediolateral instability
Diabetic Neuropathy - sensory, motor, and autonomic neuropathy that develops as a result of diabetes mellitus
Prevalence: 50-66% of people with DM develop peripheral neuropathy
Risk factors: age, DM duration, elevated hemoglobin, hypertension, dyslipidemia, and other microvascular complications
Cause: insulin insensitivity
Neurons cannot grow without insulin (anti-apoptotic Bcl-2 proteins)
Insulin regulates vasodilation
Insufficiency can lead to ischemia
Insulin regulates glucose uptake
Insufficiency can lead to excitotoxicity
Clinical symptoms: burning and tingling feet, numbness, impaired balance, shooting pain, hot and cold sensitivity, foot deformity
3 types

  1. Diabetic polyneuropathy - gradual onset, burning hands/feet, loss of tactile sensation
  2. Hyperglycemic neuropathy - rapid and reversible
  3. Acute sensory neuropathy - rapid, deep burning pain in the feet
    Diagnosis: combination of NCS, monofilament testing, and tuning fork (see if they can feel vibration)
    Prognosis: impact on health is widespread, 50% of amputations occur in people with diabetes
    Treatment: control glucose levels, gabapentin for nerve pain, podiatry
    PT: balance, skin inspection, task-specific training
    <70 no exercise
    15-15 rule
    Organophosphate Neurotoxin - common in pesticides
    Mechanism: inhibits cholinesterase
    Cholinergic crisis - hyper activation of skeletal muscles leads to paralysis, hyperactivation of parasympathetic target leads to bradycardia, drop in BP, pupillary constriction, salivation, lacrimation, urination, defecation, GI distress and emesis
    Treatment: atropine (mAChR antagonist) and cholinesterase activators
    Botulism - condition caused by anaerobic bacteria (entered by food or wounds)
    Mechanism: clostridial toxins destroy proteins that release neurotransmitters so synaptic transmission is impaired
    Clinical symptoms: motor weakness/paralysis, blurred vision, fatigue, dysarthria, dysphagia, difficulty breathing
    Treatment: botulinum antitoxins