Nerve conduction velocity and electromyography (EMG)

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  1. In carpal tunnel syndrome
    1. measure amplitude (axon), conduction velocity (myelin) and width of action potential
      1. the velocity of an action potential increases with high transmembrane resistance, low internal resistance, and low membrane capacitance
        1. myelin increases transmembrane resistance and decreases membrane capacitance
      2. compound motor action potential (CMAP) – size of amplitude is decreased due to fewer motor fibers firing
        1. in carpal tunnel syndrome, initial compound muscle action potential produced by electrical stimulation is slightly reduced or normal then after a train of 4-10 stimuli at rates of 2-5 Hz the amplitude of the potentials decreases by 25% or more and then after more stimuli may increase slightly; this is similar to the effect of curare or other nondepolarizing neuromuscular blockers and can be corrected with neostigmine; similar effect with progressive stimulation can also be seen in polio and ALS
          1. alpha component of the CMAP is produced by the rapid conduction of myelinated A fibers; the beta component is produced by slower conducting B fibers – separation between the alpha and beta waves increases further down the muscle due to the differences in conduction velocity
        2. presynaptic myasthenic syndrome of Lambert-Eaton is characterized by a different type of response: with successive stimulation, muscle action potentials which are at first small or practically absent with the first stimulus, increase in voltage with successive response until a more nearly normal amplitude is attained; neostigmine has little effect on this
      3. distal motor latency (DML) – measure of conduction velocity; in peripheral motor nerve it typically takes 4 msec to go 8 cm (50 m/sec)
      4. width of the action potential measures temporal dispersion of impulse over innervated muscles, indication of poor or dispersed conduction
      5. measures of EMG show motor unit activity (i.e. anterior horn cell and all muscle fibers connected to it – 10-12 muscle fibers in upper extremity to hundreds of muscle fibers in lower extremity)
      6. after an EMG study, creatinine kinase levels will increase to 1.5 x normal about 6 hours after the test
      7. in carpal tunnel typically see denervation and reinnervation signs:
        1. polyphasic waves, increased amplitude, wider duration, fibrillation, fasciculation due to recruiting more fibers over a larger area (reinnervation branches out over a larger area recruiting more fibers with more amplitude but larger width of action potential)
          1. in lower motor neuron disease, surviving motor neurons must fire at a rapid rate to compensate for the loss of other motor units
          2. fasciculation and fibrillation are associated with lower motor neuron disease
          3. fasciculation is a sign of motor nerve fiber irritability and has 3-5 phases
          4. fibrillation potentials last 1-5 msec, have a di or triphasic pattern and may take the form of positive sharp waves; usually seen 10-25 days following the death of an axon
    2. myopathy
      1. see polyphasic waves with low amplitude and decreased duration
        1. polymyositis and the muscular dystrophies reduce the population of muscle fibers per motor unit thus the potential is of lower voltage and shorter duration than normal and may also appear polyphasic
    3. denervated muscle
      1. see positive sharp waves; number of motor unit potentials (MUP) appearing during contraction are reduced but the remaining ones are normal; in time, the remaining MUPs increase in amplitude (2-3 times normal) and become longer in duration and sometimes polyphasic (more than 4 phases)
        1. thought to arise from greater than usual number of muscle fibers that are spread out over a greatly enlarged territory within the muscle; presumably, the new nerve twigs have sprouted from nodal points and terminals of undamaged axons and reinnervated previously denervated muscle fibers
        2. after reinnervation, the MUPs will be low in amplitude, prolonged and polyphasic while increased amplitude is associated with very chronic, proximal axon loss as in remote poliomyelitis, syringomyelia and chronic cervical radiculopathy; an increase in the size of the motor unit potential reflects anatomic reorganization of denervated muscle as in chronic lower motor neuron disease
        3. muscle biopsy of acutely denervated tissue typically shows target fibers
    4. fibrillation
      1. low amplitude, spontaneous activity from a single muscle fiber degeneration; occurs when the muscle fiber has lost its nerve supply; is not visible through the skin
      2. the presence of fibrillation in a paralyzed muscle after 2-3 weeks is a good prognostic sign when there was initially no EMG evidence of motor unit activity with effort
    5. fasciculation
      1. anterior horn cell phenomenon (not from nerve or muscle fibers); occurs from the spontaneous firing of a motor unit causing contraction of a group of muscle fibers that may be visible through the skin
        1. the firing irregularly of a number of motor units seen as a rippling of the skin is called myokymia
    6. diabetic neuropathy
      1. generally see denervation due to axonal disease distally but good proximal
      2. sensory delays both proximal and distal
      3. in most neuropathies, only a part of the axon is affected and nerve conduction velocities are relatively uninformative; however, motor and particularly the sensory nerve amplitudes are usually diminished and there may be fibrillations and changes in motor unit potentials on needle examination of the more distal muscles
      4. in contrast, neuropathies of the acute and chronic inflammatory types such as metachromatic leukodystrophy, Krabbe disease, and Charcot Marie Tooth disease affect Schwann cells primarily and produce segmental demyelination with markedly slow conduction velocities or dispersion of the action potential below the conduction block
    7. M, H, and F response
      1. M reflex = stimulation of sensory-motor nerve with pure motor response
      2. H reflex = equivalent of Achilles reflex; single synapse response; low amplitude antedromic stimulation of mixed motor/sensory Ia nerve (spindle afferent fiber) with orthodromic conduction down motor unit
      3. F wave = high amplitude stimulus of mixed motor/sensory nerve with measurement of motor conduction antedromic and orthodromic
      4. NOTE: both H and F wave are normal in primary muscle diseases
    8. sensory nerve conduction velocity (NCV)
      1. antedromic – against physiologic direction of nerve
      2. orthodromic – in physiologic direction of nerve (microtubule response)
      3. conductance down the nerve is proportional to the length constant
        1. length constant = membrane resistance (myelination) divided by axial resistance (cytoplasmic resistance); this is equal to the distance along the nerve where a change in membrane potential produced by the current traveling through the nerve decays to 1/3rd of its original value
        2. NCV is faster in proximal segments between the ages of 5 and 40 (decreases about 10 m/sec between ages 60 and 80), in shorter individuals, and at warmer limb temperatures (loss of 2.4 m/sec/degree Celsius)
        3. Nerve conduction velocities increase as myelination occurs with peak velocities in adolescence and young adulthood and begin to decline after age 30-40
      4. sensory nerve action potential (SNAP) – evaluation of amplitude, width, temporal dispersion of motor response from stimulation of sensory nerve
        1. normal sensory action potential in a patient with sensory loss may indicate a poor prognosis for recovery since damage to preganglionic nerves precludes regeneration of sensory fibers; this typically occurs in nerve root avulsion or syringomyelia
        2. temporal dispersion occurs due to impulses of slow conducting fibers that lag behind those of fast conducting fibers over a long conduction path producing an action potential of greater duration and smaller amplitude; affects sensory nerves more than motor nerves
      5. in carpal tunnel typically see decreased NCV across the wrist but normal above the wrist
    9. brachial plexus injuries and EMG
      1. demyelinating conduction block is detectable during the first weeks after injury unless the injury is so severe that the axons are interrupted
        1. in the case of trauma, the presence of a demyelinating conduction block denotes a good prognosis
        2. if denervation changes are found in the paraspinal muscles, the source of weakness and pain is in the intraspinal roots
      2. types of brachial nerve injuries
        1. upper trunk brachial plexus (Erb-Duchenne palsy) – due to injury to the 5th and 6th cervical nerves and roots usually due to forceful separation of the head and shoulder during a difficult delivery
          1. muscles affected = biceps, deltoid, supinator, supraspinatus and infraspinatus and rhomboids
          2. arm is rotated internally and extended at the elbow; movements of the hand and forearm are unaffected
        2. lower trunk brachial plexus paralysis (Dejerine-Klumpke paralysis) – usually the result of traction on the abducted arm in a fall or during an operation on the axilla or compression by tumors arising from the apex of the lung
          1. weakness and wasting of the small muscles of the hand and a characteristic claw hand deformity; sensory loss is limited to the ulnar border and the hand and inner forearm; if the first thoracic motor root is involved there may be an associated Horner’s syndrome
        3. lateral cord – causes weakness of the muscles supplied by the musculocutaneous nerve and the lateral root of the median nerve; manifests as weakness of flexion and pronation of the forearm
        4. medial cord – causes weakness of muscles supplied by the medial root of the median nerve and ulnar nerve; effect is a combined median nerve and ulnar nerve palsy
        5. posterior cord – causes weakness of the deltoid muscle, extensors of the elbow, wrist, and fingers, and sensory loss on the outer surface of the upper arm
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