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Neurologists are absurdly fond of impenetrable jargon that only those initiated into the club can understand. The more obscure the Latin or Greek etymology the better, and preferably with plenty of syllables (dentatorubral-pallidoluysian atrophy, anyone?). In neurophysiology, we are no different; our reports are peppered with terms that only a card-carrying neurophysiologist would understand, and we are equally partial to a juicy acronym. If you are lucky, the bottom couple of lines might sum up what it all means. If you are not, then how do you sort your CMAPs from your SNAPs and your F-waves from your A-waves? At the risk of being ostracised by my colleagues, here is my attempt to unmask some of the dark secrets of nerve conduction studies (NCS) handed down through countless generations of neurophysiologists.
The scope of NCS
Broadly speaking, NCS are used to investigate diffuse processes such as polyneuropathies and motor neuron disease, multi-focal processes such as mononeuritis multiplex and focal neuropathies such as carpal tunnel syndrome. They are highly sensitive in detecting peripheral nervous system disease, allow the precise anatomical localisation of the lesion and are central to the classification of the underlying pathophysiology.
As with any other functional test, the specificity is relatively poor. Although some specific patterns do exist, in general one ‘dying back’ neuropathy, for example, looks pretty like another, irrespective of the aetiology. So, while NCS can narrow down the underlying pathophysiology (eg, axonal vs demyelinating), and give an idea of the severity of the process, they are an adjunct to other more specific tests to determine the final diagnosis. Similarly, since they give a snapshot of peripheral nerve function, a single study gives little or no information as to whether the process is static or progressive. For this information, repeated studies over time may be needed.
NCS use electrical stimulation …
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