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30 patients with moderate diabetic polyneuropathy (Stage 2 according to Dyck) were evaluated for autonomic symptoms, sympathetic skin response (SSR) and Valsalva index. Their SSR were compared to a control group of 30 healthy normal subjects. Neuropathy was confirmed by history, clinical examination and nerve conduction measurements. Although our patients had only moderate polyneuropathy autonomic dysfunction was frequent. Two thirds reported autonomic symptoms. Impotence was present in 60% of males. SSR amplitudes were significantly lower in diabetics (changed in 53%, absent in 20%) than in the controls. SSR abnormality correlated to some clinical and electroneurographic signs of neuropathy, suggesting similar affection of sympathetic and somatic fibres. Valsalva index was abnormal in 37% of patients showing no correlation to clinical, electroneurographic or SSR changes.

Intraoperative monitoring of spinal cord evoked potentials (SCEP) evoked by tibial nerve stimulation was performed in six patients who underwent junctional coagulation lesion of the dorsal root entry zone for relief of intractable pain. The pain was secondary to complete brachial plexus avulsion. Normal spinal cord evoked potentials showed an initial positive wave and two negative waves, then a group of high frequency conducted waves. On the avulsion side, incomplete spinal cord evoked injury potentials were recorded in all cases and in one on the normal side also. The incomplete spinal cord evoked injury potential consisted of a high-amplitude positive wave with a sharp rising phase and slower falling phase that led to a long lasting, low-amplitude, negative deflection. Several high-frequency components were superimposed onto the monophasic positive wave. The duration of these superimposed components was approximately the same as the duration of the normal spinal cord evoked potentials, but the incomplete spinal cord evoked injury potentials were longer than normal spinal cord evoked potentials for the negative afterwave. Incomplete spinal cord evoked injury potential amplitude was 3-11 times higher than the normal spinal cord evoked potentials. Our results suggest two possible sources of incomplete spinal cord evoked injury potential: the chronic subclinical spinal cord injury produced by the avulsion and the effect of subpial placement of the recording electrodes.

Intraoperative spinal cord evoked potentials (SCEPs) to median nerve stimulation were detected subpially from the dorsal surface of the cervical spinal cord in 5 patients with cervical syringomyelia and were compared to normal SCEPs obtained from the unaffected side in 6 patients during intraoperative monitoring of dorsal root entry zone lesion. Normal SCEP began with a positive deflection P9 and a complex N11/N13 with several low amplitude short potentials superimposed on the N11/N13. The complex was followed by a second negative potential N2 and a late prolonged positivity, P. In the 4 patients in whom median nerve somatosensory evoked potentials (SEPs) were present preoperatively, SCEP consisted of the N11 potential and the following low amplitude short (LAS) potentials, while the N13 wave was missing. In the fifth patient, in whom the preoperative median nerve SEP was missing, SCEPs were of much lower amplitude and shorter duration than normal. The potentials N2 and P were not recorded in any of our 5 patients. Changes in N13 wave, N2 and P potentials noted in syringomyelia were presumed to be the result of destruction of the spinal cord dorsal horn neurons caused by spinal cord central cavitation.

Cortico-spinal potentials (CSPs) to transcutaneous motor cortex stimulation were recorded epidurally and subpially in 8 patients undergoing spinal cord surgery. In 6 patients without cortico-spinal tract involvement, a CSP consisted of a direct (D) wave, which was followed by indirect (I) waves at a higher stimulus intensity. The D wave appeared at 25-50% of the maximum stimulus intensity. With increasing stimulus its amplitude levelled off between 10 and 30 microV when recorded epidurally. At high stimulus a prominent indirect potential (I' wave) appeared which followed the D wave after 2.2-3.6 msec. The D and I' wave conduction velocities calculated in 3 cases were identical -65, 70 and 80 m/sec. Subpial records had larger amplitudes than epidural ones but were of the same configuration. In 2 patients with spastic paraparesis the CSP changes were detected below the site of the cord lesion.

Seven patients with complete avulsion of the brachial plexus underwent junctional coagulation lesions of the dorsal root entry zone (DREZ) for relief of intractable pain in the paralyzed arm. Intra-operative monitoring by recording spinal cord somatosensory evoked potentials (SEP) resulting from tibial nerve stimulation was done using subpial recording electrodes situated dorsal to the posterior median sulcus at the C4 and T2 segment. SEP on the normal side showed an initial positive wave and two negative waves followed by a group of high frequency waves of relatively high amplitude which continued into high frequency, low amplitude potentials. The conduction velocity of the fastest spinal evoked potential components were, on average, 86 m/s. Recordings from the side of avulsion revealed a steep positive potential of high amplitude which appeared in five patients prior to the creation of the DREZ lesion. This effect was assumed to be secondary to spinal cord damage caused by avulsion. During the DREZ coagulation the SEP from the unaffected side did not change. On the side of DREZ coagulation the velocity of the fastest fibres decreased. Four patients reported sensory deficits after the operation, which were transient in three. In one of these patients, the first two negative potentials disappeared. In the fourth patient, who had permanent sensory deficits, the positive steep potential appeared after generation of the lesion. Our results point to the usefulness of the subpial SEPs monitoring during microneuro-surgical procedures on the spinal cord to provide further insight into evoked electrical activity of the normal and injured spinal cord, and to minimize post-operative neurological morbidity.

The new method of transcranial electrical and magnetic brain stimulation was tested in 41 normal subjects. Stimulation on the scalp excites corticospinal neurones in the motor cortex while stimulation over the spine excites spinal nerve roots. The difference between EMG response latencies after both stimulations represents conduction in the central motor pathways and is called central motor latency (CML). The aim of out experiments was to investigate certain methodological aspects of the technique in order to standardize the procedure. Recordings were done from slightly contracted abductor digiti minimi and tibialis anterior muscles after electrical stimulation on the scalp and from the relaxed and contracted abductor digiti minimi and biceps brachii muscles after magnetic brain stimulation. Stimulation over the spine (C7/T1 interspace in case of upper limb muscles stimulation and T12/L1 interspace in case of tibialis anterior stimulation) was always electrical. Using a rather weak non-commercial magnetic stimulator we were not able to activate lower limb muscles, neither we succeeded to evoke responses from the relaxed arm muscles in all subjects. Electrical scalp stimulation proved successful in all cases. Muscle response after cortical stimulation in contracting muscles and shorter latencies and provided more accurate estimate of conduction time in the central motor pathways than responses in the relaxed muscles. Latencies should be measured from several superimposed responses and not from averaged ones. The intensity of stimulation over the neck did not affect CML. We nevertheless suggest that the strongest stimulus intensities should not be used in order to avoid CML overestimation.