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SUMMARY Morphological findings in sural nerves were related to nerve conduction in 12 patients with diabetic neuropathy, five with mainly sensory involvement, four with severe, symme,trical sensory-motor polyneuropathy, and three with multiple mononeuropathy. All had loss of large and small myelinated and of unmyelinated fibres, even early in the disease; segmental remyelination was the most prominent myelin alteration in teased fibres, segmental demyelination was found in only a few fibres. Axonal degeneration and Schwann cell damage seem to proceed independently of each other. The relation between recorded conduction velocity and that expected from the diameter of the largest fibres indicated that slowing of 20 to 30% was due to causes other than fibre loss; a grossly diminished conduction velocity was caused mainly by fibre loss. Electrophysiological findings in the sural nerve were largely representative of findings in other nerves, though abnormalities were less marked in the median nerve. In half the endoneurial vessels from diabetic neuropathy the perivascular space was thickened or contained more layers of basal laminae than normal. The same abnormalities were found in one-quarter of the endoneurial vessels from other acquired neuropathies.

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Twitches were recorded in situ in muscles of normal humans by small transducers connected to a needle in the tendon. The twitches were elicited by stimuli in the endplate zone, the force of the smallest twitches corresponding to the average of one or two motor units. The time to peak contraction was measured of 20–30 bundles of fibres in each muscle examined. The histograms of contraction times agreed with histochemical findings; contraction times longer than 60 msec corresponded to the proportion of fibres rich in mitochondria. Thus, long contraction times predominated in the soleus and gastrocnemius muscles, comprised half the times in the anterior tibia], a third in the brachial biceps (long head) and a few per cent in the brachial triceps muscle (lateral head). Bundles of fibres with short contraction times, those poor in mitochondria had a higher temperature coefficient of the time to peak than bundles with long contraction times. During hypoxia the contraction times shortened. The contraction time of motor units first activated voluntarily lay near the mean of bundles activated electrically. The contraction times of fasciculating fibres were in the range of electrically evoked twitches; the force was about three times that of voluntarily activated units.

In a previous study2 a method was

SUMMARY In 30 patients with diabetic neuropathy sensory potentials in the median nerve, motor conduction in the lateral popliteal and median nerves, and electromyographic findings in distal and proximal muscles were compared with the severity of symptoms and signs. All patients had abnormalities in at least one of the electrophysiological parameters. The sensory potentials were the most sensitive indicator of subclinical involvement; abnormalities were found in 24 patients, 12 of whom had no sensory symptoms or signs and five of whom had no other clinical or electrophysiological evidence of neuropathy in the upper extremities. This indicates that sensory nerve fibres may be affected before motor. The next most sensitive parameter was the presence offibrillation potentials, found in more than half the distal muscles examined. Slowing in motor conduction in the lateral popliteal nerve was the only electrophysiological change correlated to the severity of the neuropathy, and no other electrophysiological parameter was correlated to the duration or the severity of the neuropathy or the diabetes. An onset of neuropathy before or simultaneously with the manifestations of the diabetes, as well as the frequent occurrence of asymptomatic changes in sensory conduction, support the evidence at hand that the neuropathy develops concomitantly with and as an integral part of the metabolic disturbance rather than as a consequence of the vascular complications of diabetes. Of three patients with clinical signs or symptoms of a diabetic amyotrophy, two had asymptomatic electrophysiological abnormalities in distal nerves and muscles, consistent with widespread involvement of the peripheral nerves. The third patient had electromyographic changes in the medial vastus muscles suggestive of a myopathy. Motor and sensory conduction in distal and proximal nerves were normal.Previous studies of electrophysiological changes in diabetic neuropathy have dealt with fibrillation potentials, polyphasic potentials, or conduction velocity in motor and, in a few instances, mixed and distal sensory nerves

Electromyography (EMG), histology, and histochemistry were related in 264 patients with neuromuscular disorders classified according to history and clinical and other laboratory findings. Electromyography and histological and histochemical abnormalities were divided in specific and nonspecific criteria. Specific histochemical criteria alone identified 28% of neurogenic lesions. Criteria of myopathy, obtained from the pattern of electrical activity during 30% of maximal effort, helped to delineate a myopathy when the only abnormality was an increased incidence of polyphasic potentials together with a pattern of full recruitment during maximal effort. Histology, histochemistry, or both, and EMG were concordant with clinical findings in 77% of 188 patients with myopathy and in 91% of 64 patients with neurogenic lesions. The electromyogram was concordant with the clinical classification in 87% of patients with myopathy and in 91% of patients with neurogenic impairment. The biopsy was in agreement with or contributed to the classification in 79% of patients with myopathy and in 92% of patients with neuropathy.

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