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In this study the authors suggest that MR neurography is an effective means of both confirming compression of the median nerve and its successful surgical decompression in patients with carpal tunnel syndrome. This modality may prove useful in the assessment of unconfirmed or complex cases of carpal tunnel syndrome both before and after surgery.

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Each digital branch of the median nerve was stimulated in turn in 34 women (55 hands) with carpal tunnel syndrome (CTS). The amplitude and conduction velocity of the sensory nerve action potential (SNAP) recorded at the wrist, and the threshold for patient perception of the electrical stimulus on the median innervated sides of each digit, were compared with the corresponding values in a group of asymptomatic, age-matched women. Sensory conduction velocity or SNAP amplitude were abnormal in more than 80% of all digital nerves studied apart from those in the index finger. Stimulation of digital nerves in the index finger proved the least sensitive means of detecting the electrophysiological abnormality. We conclude that selective digital nerve stimulation is a sensitive technique in the diagnosis of CTS. If ring electrodes are preferred, our results suggest that the middle rather than the index finger should be used.

In 15 patients with neurogenic muscular disorders, including cases of motor neuron disease, Wohlfart-Kugelberg-Welander disease, Davidenkow's scapuloperoneal syndrome, peripheral neuropathy and traumatic neuropathies, muscle biopsies were carried out, usually after EMG or single fibre EMG investigation. Enzyme histochemical and electronmicroscopic techniques were used to study longitudinal fibre splitting and its quantitative relation to the general changes in the biopsies. In 9 cases serial sections were used to study the longitudinal extent and character of fibre splitting. Longitudinal fibre splitting was found in 14 cases. It was prominent in Type 1 fibres, and in those biopsies in which hypertrophy was most marked. It was often associated with central migration of sarcolemmal nuclei. Ultrastructurally there was evidence that splitting consisted of mechanical disruption of the myofibrillar pattern, followed by an active process of membrane formation. We suggest that longitudinal splitting of muscle fibres, induced by overload of poorly innervated, hypertrophied fibres, can account for many of the "myopathic" changes found in neurogenic muscular disorders.

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Two healthy men with McLeod syndrome, a rare X-linked recessive phenotype characterized by acanthocytosis and weakened red blood cell antigenicity in the Kell blood group system, have been investigated. Both men showed raised blood creatine kinase levels, with myopathic EMG abnormalities. Biopsies of the quadriceps muscle showed the features of an active myopathy although there was no clinical evidence of muscular abnormality. The combination of the association of membrane abnormalities in red blood cells and a myopathy in both McLeod phenotype and Duchenne muscular dystrophy suggests that these syndromes may be due to related genetic abnormalities. The genetic locus for McLeod phenotype is situated near the end of the short arm of the X chromosome. The locus for Duchenne muscular dystrophy is unknown but it has been postulated that it is also situated on the short arm of the X chromosome at Xp 21. The occurrence of a subclinical X-linked myopathy with acanthocytosis (McLeod phenotype) thus raises the possibility of a new approach to genetic investigations in Duchenne muscular dystrophy, and in the related milder forms of this disease.