After an acute nerve transection, nerve fibres
degenerate from the site of the lesion distally. Muscle fibres themselves remain viable but after a
period of 7–10 days become supersensitive and fibrillations will be detectable. Acutely
denervated muscle fibres have acetylcholine receptors over the whole of the muscle fibre membrane rather
than these being limited to the neuromuscular junction. The effect is to make the
fibre supersensitive with the result that it discharges spontaneously. This is detected by the EMG
needle as a single fibre discharge or fibrillation Fibrillation is not visible through the skin and is an
electrical sign not a clinical sign. Positive sharp waves have the same
origin as fibrillation and have the same significance. They arise when the needle tip damages a
fibre and spontaneous action potentials propagate up to the needle tip and then are
extinguished. Fibrillation may persist for many months after a nerve lesion. Any nerve lesion,
complete or partial, from the spinal motor neurone to the intramuscular nerve branches can give rise to
fibrillation. Fibrillations are not found exclusively in neurogenic disease, however; they also
occur in inflammatory and dystrophic muscle disease. |
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Fasciculations arise from the discharge of part or the
whole of a single motor unit . They are larger and more complex than fibrillation potentials. Fasciculations
are isolated discharges that recur at irregular intervals,
usually in the order of several seconds. Fasciculations near
the surface of a muscle may be visible at the skin; those
deep within the muscle and detected by an EMG needle are
not. Fasciculations are not under voluntary control, a
useful point in distinguishing them from motor units discharging
due to poor relaxation. Fasciculations probably arise within
the fine terminal arborisation of a single motor axon within
the muscle. It has been shown, for example, that there may
be more than one generator of a single fasciculation as evidenced by subcomponents of the potential occurring
in a different order on different discharges.
Fasciculations occur in motor neurone diseases, other neurogenic diseases
such as radiculopathy and neuropathy, thyroid disease, and
peripheral nerve hyperexcitability syndromes, and may be
benign. The significance of fasciculations is judged by the
company they keep in the muscle; benign fasciculations are not accompanied by denervation changes but malign
fasciculations usually are.‘‘ping’’ sound from the EMG machine.
Neuromyotonia occurs in autoimmune anti-voltage gated potassium nerve axon channelopathy and Morvan’s syndrome.  |
  MYOTONIA: Clinical myotonia is accompanied by myotonic
discharges on EMG ; once heard, never forgotten. Discharges are provoked by needle movement, tapping the muscle and
after a short voluntary contraction, and vary in frequency
and amplitude producing the characteristic ‘‘dive bomber’’
sound. They occur in muscle fibre membrane channelopathies, including dystrophia myotonica, congenital myotonias,
proximal myotonic dystrophy, and hypokalaemic periodic
paralysis. |
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