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Diagnosis of chronic peripheral neuropathy
  1. RICHARD A C HUGHES
  1. Department of Neuroimmunology, Guy's, King's and St Thomas' School of Medicine, Guy's Campus, London SE1 9RT, UK

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    “The golden rule is that there are no golden rules.” (George Bernard Shaw: Maxims for Revolutionists)

    The annual incidence of peripheral neuropathy is at least 118/100 000,1 sufficiently common to justify investigating more efficient strategies for its assessment. The Amsterdam Neuromuscular Centre2 (pp 205–209 of this issue) are to be congratulated on their pioneering audit of their own guidelines for diagnosing chronic polyneuropathy. They have castigated themselves for doing neurophysiological studies, which did not contribute to the diagnosis in 48%, and ancillary investigations, which were unhelpful in 51%. They conclude that in the presence of a known diagnosis—for instance, of diabetes mellitus—the occurrence of a typical polyneuropathy does not require further investigation. If the diagnosis is not obvious, investigations (or, one might say, more thorough history taking) should be aimed at revealing diabetes, alcohol misuse, renal failure, drug toxicity, and possibly HIV infection. In their revised guidelines the Amsterdam goup defer neurophysiological studies until after these investigations, considering their value to be in identifying demyelinating neuropathies and the presence of subclinical motor involvement in clinically pure sensory neuropathies.

    No one would disagree that the process should begin with a thorough clinical assessment in which the history and examination will often reveal the diagnosis, as with the history of pes cavus in a parent or the stigmata of liver disease in the alcoholic.1However there is a danger in accepting a coincident systemic illness as the cause of a neuropathy. For example, both vasculitic neuropathy and chronic inflammatory demyelinating polyradiculoneuropathy may occur in diabetes mellitus. Many would argue that the neurophysiological distinction of axonal from demyelinating neuropathy helps to direct the subsequent investigations and should be retained at an earlier stage in the process and not relegated as now proposed by the Amsterdam group. Furthermore the value of the negative investigation should not be underestimated. The symptoms of peripheral neuropathy are distressing and patients want to be reassured that all treatable causes have been considered.

    The authors set out guidelines for chronicpolyneuropathy assuming that the first step in the assessment, the identification of a multiple mononeuropathy, has been undertaken. Unfortunately vasculitic neuropathy may present as a symmetric polyneuropathy rather than a multiple mononeuropathy3 and the Amsterdam algorithm would risk missing such a diagnosis before disabling deficits have accumulated. Pointers to a diagnosis of vasculitis would be asymmetry, stepwise progression, pain, systemic illness and a raised erythrocyte sedimentation rate but sometimes all these are absent and the diagnosis can only be made by nerve biopsy. However, sural nerve biopsy should only be performed if the diagnosis cannot be achieved by other means because of the risk of persistent pain at the biopsy site in a third of patients.4

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