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Describe the pathophysiology of chronic nerve compression

  • Disruption to Blood-Nerve-Barrier (from traction, compression, tethering, pressure, excessive excursion)
  • Endoneurial edema
  • Perineurial thickening, fibrosis, scar
  • Deposition of renault bodies
  • Further increase endoneurial pressure/edema
  • Disruption to microneural circulation
  • Dynamic ischemia
    • at 30-50% ischemia --> reduction in oxidative phosphorylation --> decrease ion exchange and protein transport --> impaired nerve conduction


Describe the progression of clinical pathology

  • Intermittent paresthesia
  • Continuous paresthesia
  • abnormal monofilament testing
  • Local demyelination, remyelination
  • vibration sensory disturbance
  • abnormal static then dynamic 2PD
  • Wallerian degeneration
  • Muscle weakness
  • Muscle atrophy


define double crush and reverse double crush

  • Anecdote: double crush phenomenon is like 2 kinks in a hose
  • Definition: proximal site of compression places distal nerve more susceptible to damage (lower threshold for impairment with compression)
  • Reverse double crush - distal site of compression results in decreased transport of neurotrophic substances back proximally to neuron, results in overall decreased production and distal transport


What are predisposing factors to compression neuropathy:

  • Patient:
    • PMHx: DM, RA/OA/inflammatory arthropahty, obesity, renal disease, hypothyroid, trauma, space occupying lesion
    • Situational: pregnancy
    • Posture and position and repetition: sleep, work, study
    • Controversial: smoking occupation (related to psoture, position, repitition)
    • genetic: hereditary demyelinating polyneuropathies (charcot-marie-tooth) - hereditatry and heterogeneous motor and sensory neuropathy that affect myelin and axon
      • also heridatry neuroapthy with liability to pressure neuropathy - AD demyelinating neuropathy


what is a differential diagnosis to a peripheral compression neuropathy?

  • Central lesion
  • Proximal site of compression: cervical radiculopathy
  • Neuropathy/myopathy secondary to chronic systemic illness or malnutrition: DM, renal disease, hypothyroidism, B12/folate/thiamine, chronic alcoholism, MS
  • Inflammatory - parsonage turner, brachial plexus poly/mononeuritis
  • Autoimmune/inflammatory - RA, SLE, PAN, GBS
  • Vascular insufficiency - vasculitis , DM
  • Space occupying lesion: tumour (benign, malignant), vascular lesion
  • Trauma
  • Infection: HIV, lyme disease, leprosy
  • Toxin: gold, arsenic
  • Psychological


Describe components of physical exam for compression neuropathy

  • Motor
    • inspect for atrophy
    • test strength of all innervated muscle, last innervated muscle, (measure on MRC)
    • examine for contracture or limited ROM
  • Sensory
    • examine peripheral nerve distribution for:
      • Threshold - minimum for nerve response
        • Early - slowly adapting - cutaneous pressure / Semmes Weinstein monofilament
        • Later - fast adapting - vibration
      • Tactile - innervation density
        • Early - slowly adapting - static 2 point discrimination
        • Later - fast adapting - dynamic 2 point discriminiation
      • Other: TENS, gross sensation compared with other nerve distribution, otherside
  • Provocative tests
    • Tinel: indicates regenerating axons
    • Specific for nerves / sites of compression (see table)
  • "Scratch collapse"


Describe provocative tests for various peripheral nerve compression neuropathy

  • Median Nerve
    • Pronator: elbow flexion 120-135 + pronation, pain induced
    • CTS: Durkan pressure >30sec
    • CTS: Phallen wrist flexed, elbow extended, >60sec
    • CTS: Tinels
  • Ulnar Nerve
    • Cubital tunnel: elbow flexion, supination and pressure proximal to tunnel >60sec, paresthesia induced


Describe purpose and indication of electrodiagnostic tests in evaluation of chronic compression neuropathy

  • Purpose: to localize and characterize nerve injury
    • tests MYELINATED motor and sensory nerves
    • first nerves affected wiht chronic compression are demyelinated nerves, so symptomatic patients may have normal EDS early in disease
  • Indications:
    • many chronic compression neuropathy can be diagnosed with history and physcial exam alone
    • patients with unclear history or physical
    • patients with suspected multiple points of compression
    • define/document severity of compression (controversial)
    • monitor progression or recovery
    • some specific presentations do warrent use of EDS: consider for proximal median nerve (differentiate btwn AIN and pronator); cubital tunnel (w/ motor complaints); ulnar tunnel; differentiate btwn radial tunnel and PIN


describe NCS

  • measure large myelinated motor and sensory nerves
  • measure complex motor action potentials and sensory nerve action potentials when an voltage stimulator is placed on skin (overlying nerve) and evoked potential measured when electrode is placed over muscle (CMAP) or nerve (SNAP)
  • Measure latency, amplitude and conduction velocity
    • demyelinating injury: normal values when stimulated distal (ie not across lesion); abnormal (low) values when stimulated proximal (ie across lesion/site)
    • axonal injury: abnormal amplitude values along nerve (proximal/across or distal/not across); requires significant threshold value of axonal loss before abnormal conduction velocity or latency findings


describe EMG

  • assess only motor component of nerve damage, also can assess myopathy
  • assess factors such as insertional activity (fibrillations) and voluntary motor unit potentials (MUPS) to assess recruitment, amplitude, duration
    • demylinating injury: decreased recruitment (maybe initially decreased / no MUPS) but normal insertioanl activity (no fibrillations)
    • axonal injury: shows abnormal insertional activity (fibrillations) and abnormal recruitment (low/no MUPS)


describe the progression of findings on EDS with increasing severity of compression neuropathy

  • clinical findings but normal EDS
  • increased latency and decreased CV
  • decreased SNAP
  • decreased CMAP
  • abnormal insertional activity and fibrillations
  • abnormal MUPS, giant MUPS
  • with decompression and remyelination/axonal regeneration - EDS may or may not return to normal


differentiate between clinical findings of pronator syndrome and AIN syndrome

  • both are proximal median nerve compression neuropathy
  • pronator syndrome is characterized by aching pain in proximal volar forearm, numbness and tingling in median nerve distrubtion including palmar cutaneous branch (ie palm, thenar eminence) and ABSENCE of motor neuropathy
  • AIN syndrome is characterized by ABSENCE of sensory neuropathy and presence of motor neuropathy of FPL, FPD D2,D3, PQ; usually no pain


list sites of compression of proximal median nerve

  • supracondylar process
  • ligament of struthers (from medial epicondyle to supracondylar process)
  • lacertus fibrosis (from biceps tendon to flexor fascia)
  • between ulnar and humeral heads of PT
  • underbelly of FDS ~ 6.5cm distal to elbow (aponeurotic arch)
  • occassionally from anamalous head of FPL (Ganzer's muscle; more in AIN)


what are the borders of the carpal tunnel

  • roof = transverse carpal ligament
  • floor = carpal bones
  • radial = scaphoid, trapezium
  • ulnar = triquetrum, hamate


How do you diagnose CTS?

  • 6 classic findings - numbess/tingling in median n distribution; nocturnal paresthesias and wakening; weakness/atrophy of thenar muscles; positive phalen; positive tinel; abnormal 2pd
  • also on history: hand shaking, clumsiness, aching/pain; long finger involved first
  • 85% specificity w/ positive phalen, tinel and objective sensory disturbance
  • rarely require EDS


discuss treatment for CTS

  • Non-operative
    • nocturnal wrist splint in neutral
    • local steroid injection
    • both
    • others: NSAID, activity modification, PT/stretching/nerve gliding
  • Operative
    • endoscopic
    • open
    • combined


describe incision and procedure for open CTR

  • markings: Kaplan's cardinal line (parallel to adductor crease/ulnar thumb border to hook of hamate) and distal wrist crease, along radial border of D4
  • remain ulnar to PL to avoid palmar cutaneous branch injury
  • divide superficial palmar fascia
  • hold incision on stretch
  • under direct vision sharply divide the TCL distally from palmar fat (be ware of superficial palmar arch) and proximally to antebrachial fascia


discuss complications for CTR

  • early
    • hematoma
    • dehiscence
    • infection
    • injury to adjacent structures: median n proper, RMB, digital nerve, palmar cutaneous nerve; superficial palmar arch; tendon
  • Late
    • incomplete release / persistent or recurrent symptoms
    • recurrence
    • pillar pain
    • scar, scar tenderness
    • CRPS
    • bowstringing
    • stiffness


List points of compression of ulnar nerve proximally

  • Arcade of struthers 8cm proximal to medial epicondyle
  • Medial IM septum
  • Medial epicondyle pathology: abnormal medial epicondyle, anconeous epitrochlearis
  • Osborne ligament (=roof of cubital tunnel)
  • Elbow joint pathology (osteophyte, HO, cubitus valgus) 
  • leading edge of FCU fascia
  • distal edge of FCU fascia
  • fascial band btwn FCU and FDS d4 (Lig. of Spinner)


list signs of ulnar nerve denervation

  • sensory abnormalities in ulnar nerve distrubtion
    • DSUn - 4-6cm proximal to wrist crease
  • abnormal motor findings: proximal (FDP D4,5, FCU), distal (hypothenar, intrinsic weakness), intrinsic wasting
  • signs:
    • Duchenne/claw - hyperext at MCP wiht flxn at IPJ
    • Wartenberg - abduction of D5
    • Masse - flattening of MC arch
    • Froment - thumb IPJ flexion when attempting to adduct paper betwn thumb pad and lateral index
    • Jeanne - thumb hyperextension with adduction due to activation of APL when attempting to adduct btwn pad and lateral index
    • Pollock's test - inability to activate D4,5 FDP
    • Pitres-Testut - can't abduct/adduct long finger
    • Can't do finger cross
  • Provocative tests: elbow flexion +/- compression, tinel


what are treatment options for cubital tunnel

  • non-operative: nocturnal splinting, activity modification
  • operative:
    • medial epicondylectomy
    • simple decompression
    • subcutaneous transposition
    • intramuscular transposition
    • submuscular transposition


describe steps of intra-muscular transpotision of ulnar nerve at elbow

§ avoid injury to MABC (3.5cm distal to medial epicondyle)

§ decompress: cubital tunnel fascia (Osborne’s ligament)

§ proximal neurolysis

§ excision medial intermuscular septum proximal to cubital tunnel

§ mark step-lengthening pattern on flexor pronator fascia, incise and elevate 2 flaps

§ identify  and resect “T” fascia in midportion of flexor pronator mass, PT separating from FCU, leading edge of FCU

§ making a groove in the flexor pronator mass, connect to FCU release and fascia release

§ excise septum btwn FCU and PT

§ elevate muscle flap (proximally based) and fascial flap (distally based)

§ transpose nerve in tension free

§ loose approximation of distal and prox flaps


what are complications of surgical intervention for cubital tunnel syndrome?


  • Hematoma, seroma, infection
  • Sensitive scar
  • Wound dehiscence
  • Injury to FCU motor branch
  • Incomplete release/persistent symptoms


  • Stiffness/elbow contractures
  • Injury to branches of the MABCn (neuroma) 
  • Weakness of elbow flexion
  • Devascularization of the nerve 
  • Medial epicondylitis
  • Ulnar nerve subluxation/irritation
  • Heterotopic ossification
  • Elbow instability
  • CRPS


what are 3 zones of ulnar nerve in guyon's canal


  • zone one is proximal, mixed motor and sensory
  • zone two is distal, just before H of H, as DMB travels deep and radial around hook and towards hypothenar, intrinsics
  • zone three is distal, just before H of H and more superficial, lateral as sensory branch travels to innervate D5 and ulnar D4


describe steps for operative decompression of ulnar nerve at guyon's canal

o  Chevron over Guyon’s and extends proximal to the wrist crease

o  Identify ulnar n (and artery) proximally

o  Release the volar carpal ligament and pisohamate ligament (all structures above NV bundle); palmaris brevis

o  Excise any space occupying lesion

o  Follow the ulnar nerve into the hypothenar muscles and release any fibrous bands FDQ

o  Explore superficial arch


describe sites of compression of radial nerve at the elbow

  • Fibrous bands radiocapitellar joint (attached to, & superficial to the joint)
  • Vascular leash of Henry (radial recurrent artery & venae comitantes)
  • Tendinous margin of ECRB
  • Arcade of Frohse (most common) – proximal fibrous edge of supinator muscle
  • Fascial border at distal edge of Supinator
  • Others: lateral head of triceps, intermuscular septum, exostoses 


differentiate between radial tunnel syndrome and PIN syndrome

  • both compression neuropathy of radial nerve more proximally
  • radial tunnel is characterized by aching pain of extensor/supinator mass in proximal forearm +/- tinel; usually ABSENT sensory and motor findings
  • PIN is characterized predominantly of motor findings - radial wrist deviation with extension (preserved ECRL, not ECRB); absent finger/thumb extension; also similar proximal pain and heaviness in forearm but notably ABSENT sensory findings


what is wartenberg's syndrome?

·   Compression of the superficial sensory branch of the radial nerve (aka cheiralgia paresthetica)


what is the differential diagnosis of wartenberg syndrome, and how to differentiate?

o  Compression/neuritis of the LABC nerve (overlaps the RSN distribution)

o  Intersection Syndrome (inflammation between tendons of 1st and 2nd compartments)

o  DeQuervain’s tenosynovitis


Classify nerve injuries

Sunderland 1st ', Seddon Neuropraxia

  • Focal conduction block
  • No disruption of axon/wallerian 
  • EMG = Lantency increased
  • Tinels absent
  • Recovery Full

Sunderland 2nd', Seddon Axonootmesis

  • Demyelination
  • Axon disruption, Wallerian degeneration
  • EMG = Decreased amplitude + fibrillation
  • TInels present, progressive
  • Recovery Full 

Sunderland 3rd', Seddon Axonotmesis

  • Demyelination
  • Axon, endoneurium disrupted, WD
  • EMG= decreased amplitude + fibrillations
  • TInels present progressive
  • Recovery variable

Sunderland 4th', Seddon Axonotmesis

  • Demyelination
  • Axon, endoneurium, perineurium disrupted, WD
  • EMG = NO transmission
  • Tinels positiove, NO PROGRESSION
  • Recovery incomplete
  • NIC present

Sunderland 5th ;, Seddon neurotmesis

  • Axon, endoneurium, perineurium, epineurium disrupted, WD
  • EMG = no transmission
  • Tinels positive, NO PROGRESSION
  • Recovery not expected
  • Neuroma + glioma present

Sunderland 6th', McKinnon Mixed