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Neurophysiology - membrane potentials and EMG

Resting and action potentials, neuromuscular junction transmission and EMG interpretation

15 questions 3 source pages 1 fact-check flags

Images appear with the first question taken from each source page — tap a question to open it.

15 questions
Q1What is EMG and what is its aim?▸
  • Studies the electrical activity of individual muscle fibres and motor units
  • Aim: differentiate a nerve or muscle problem
  • Assess reinnervation
Q2Describe the EMG procedure.▸
  • Intramuscular needle over different spots for resting and insertional activity
  • Voluntary contraction for MUAP
  • Maximal voluntary contraction for interference pattern
Q3What is measured on EMG and how do neuropathy and myopathy differ?▸
  • Insertional activity: increase in neuropathy, decrease in myopathy
  • Spontaneous activity (fibrillation, positive sharp wave): increased in neuropathy, decreased in myopathy
  • Amplitude: normal in neuropathy, reduced in myopathy
  • Recruitment: reduced in neuropathy, increased in myopathy
  • Interference pattern: neuropathy reduced with fibrillation; myopathy full but low amplitude
  • Duration: increased in neuropathy, decreased in myopathy
Q4What are the EMG findings after nerve injury (axonotmesis/neurotmesis)?▸
  • Immediately after section the EMG in supplied muscle is normal
  • 5-14 days: positive sharp waves consistent with denervation
  • 15-30 days: denervation, fibrillation potentials present
  • Evidence of re-innervation: highly polyphasic motor unit potentials
Q5Compare EMG findings of denervation and myopathy.▸
  • Resting: both have fibrillation
  • Slight contraction: denervation giant unit; myopathy small polyphasic unit
  • Maximal contraction: denervation reduced interference pattern; myopathy full pattern but decreased magnitude
Q6What is a normal interference pattern on EMG?▸
  • A disorderly group of action potentials of varying rates and amplitudes
Q7What is the resting membrane potential and ionic distribution?▸
  • Resting potential -70mV
  • Intracellular: high K, organic ions
  • Extracellular: high Na, high Cl-
Q8What maintains the resting potential?▸
  • Lipid membrane with selective permeability to ions (more permeable to K)
  • Active Na/K pump (needs ATP)
  • Donnan equilibrium - impermeable proteins alter distribution of permeable ions to restore osmotic equilibrium
Q9Describe the action potential.▸
  • Threshold stimulus (can be summation of smaller stimuli)
  • Na channels open, Na influx -> depolarisation (-70mV to +30mV); close spontaneously after 1ms
  • K channels open, K efflux -> repolarisation (below -70mV)
  • Na/K exchange pump restores resting potential
  • Refractory period from Na inactivation and K hyperpolarisation ensures unilateral propagation
  • Myelinated nerves propagate at nodes of Ranvier (saltatory conduction)
Q10What determines conduction velocity and how do local anaesthetics work?▸
  • Conduction velocity depends on the type of nerve fibre and myelination
  • Local anaesthetics work at Na channels, blocking propagation and initiation of the AP by plugging the Na channels
Q11Describe the events when an action potential arrives at the NMJ.▸
  • Resting potential changes from -70mV to +30mV
  • Ca influx into neuron via voltage-gated calcium channels
  • Release of Ach
  • Ach binds postsynaptic nicotinic sodium channels
  • Increased Na influx -> AP propagates along the sarcolemma and down the T tubules
  • Ca release from the sarcoplasmic reticulum; Ca binds troponin C, moves tropomyosin, exposing the myosin binding site on actin
Q12How does Botox act at the NMJ?▸
  • inhibit SNAP 25 protein
  • SNAP 25 is important in production of Ach vesicles and migration of the vesicles to the junction
  • Therefore prevents release of Ach
Q13Compare depolarising and non-depolarising neuromuscular blockers.▸
  • Depolarising - succinylcholine: hyperpolarises the sarcolemma (per speaker notes)
  • Non-depolarising - rocuronium: prevents depolarisation of the sarcolemma
Q14What is the pathophysiology of myasthenia gravis?▸
  • Antibodies against the receptor
Q15Which other toxin acts at the neuromuscular junction?▸
  • Tetanus (toxin) is also mentioned alongside Botox as acting at the NMJ

Fact check

Depolarising NM blockade with succinylcholine hyperpolarises the sarcolemma — error - mechanism wrong — succinylcholine is an ACh receptor agonist causing persistent depolarisation of the motor endplate (inactivating sodium channels), not hyperpolarisation — source
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