The prevalence of clinical and electrophysiological signs of peripheral nerve disease was evaluated in 151 patients with chronic obstructive pulmonary disease. Patients with concomitant disorders affecting the peripheral nervous system were excluded. Thirty patients had clinical signs of a mild sensorimotor and distal neuropathy and 13 additional patients had only electrophysiological abnormalities. The rate and the severity of the neuropathy correlated with the severity of chronic hypoxaemia. Three out of 20 patients with mild hypoxaemia (PaO2 less than 15 mm Hg below normal) had polyneuropathy as compared with 15 out of 36 with severe hypoxaemia (PaO2 more than 30 mm Hg below normal (rates different at the 10% level)). PaO2 and age were the only variables discriminating between patients with and without peripheral neuropathy.

A total of 103 patients (40 with pure sensory disturbances, 63 with sensory and motor deficits) with ulnar nerve lesions at the elbow were examined neurophysiologically. The measurement of motor conduction velocity across the cubital tunnel alone did not completely localize the lesion. The latency to an ulnar-innervated flexor muscle was of outstanding importance. The measurement of amplitudes was only rarely of localizing significance. The results of sensory recording proved to be important in patients with pure sensory disturbances. In cases with additional motor deficits, sensory recordings were too often abnormal in all segments of the ulnar nerve to be of substantial localizing value.

Blink reflexes elicited by electrical stimulation of the supraorbital nerves, by monoaurally presented 1 kHz sine wave bursts of 20-ms duration, and by flashes of light presented monocularly were investigated in 32 healthy controls. Absolute latencies of the individual components and side differences were measured. An outline of possible anatomical pathways which might be involved in the transmission of these reflexes is given.

Relative and absolute refractory periods were determined in sensory fibres of 24 median nerves and in 19 sural nerves of 30 volunteers aged 20–60 years, who had no sign of a neuromuscular disorder. The critical interval of conduction (absolute refractory period) was found to be about 0.7 msec. In median as well as in sural nerve the relative refractory periods were about 5 times the absolute refractory period, measuring the amplitude, and about 3.5 times the absolute refractory period, measuring the latencies. Reasons for the reduction of amplitude and prolongation of latency during the relative refractory period are discussed. Slightly significant differences between the two age groups (20–35 and 40–60 years) have been found with respect to the relative amplitude in median nerves, but not in sural nerves and not with respect to the relative latency in either median or sural nerves.

The bulbocavernosus reflex (BCR) was examined in 39 normal potent men and in 252 patients with impaired potency of varying aetiology. For BCR evaluation minimum, maximum and mean latencies, the temporal dispersion in ten successive responses, together with minimum and maximum side differences from simultaneous recordings of the left and right bulbocavernosus muscles were determined. Pathological findings were detected in 125 patients. Somatosensory evoked potentials (SSEPs) recorded from the scalp after stimulation of the penile dorsal nerves and the terminal branches of the pudendal nerve were investigated in 30 controls and in 246 patients. An abnormal SSEP was found in 63 patients.