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