Abstract

Human muscles are composed of motor units and each motor (MU) unit is composed of a specific α-motor neuron and the muscle fibres it innervates. A motor neuron innervates the muscle fibres of a MU via the neuromuscular junction (NMJ) formed at the terminal end of each branch of its axon. Voluntary muscle contractions are initiated when the central nervous system recruits MUs by activating their motor neurons, which in turn, via their NMJs, activate their muscle fibres. At each NMJ, a region of transmembrane current is produced across the sarcolemma membrane of its corresponding fibre when the motor neuron is activated (i.e. discharges an action potential). This transmembrane current creates a change in transmem‐ brane potential (or action potential) which propagates along the fibre and initiates/co-ordinates its contraction [1]. The currents creating the action potentials of the activated fibres of recruited MUs summate to create dynamic electric fields in the volume conductor in and around muscles. Electrodes placed in these electric fields detect time changing voltage signals which are the electromyographic (EMG) signals discussed in this chapter. When a muscle is affected by a neuromuscular disorder, characteristics of its action potentials, and as a result of the EMG signals they create, change depending on whether the muscle is affected by a myopathic or neurogenic disorder and the extent to which the muscle is affected. Therefore, quantitative EMG signal analysis can be used to support the diagnosis of neuromuscular disorders. Clinical quantitative electromyography (QEMG) attempts to use the information contained in an EMG signal to characterize the muscle from which it was detected to support clinical decisions related to the diagnosis, treatment or management of neuromuscular disorders.

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