The compound nerve action potential (CNAP) of the superficial peroneal nerve of dogs was investigated to determine: (1) the influence of the stimulation technique on the configuration of the CNAP, with particular attention to late components; (2) the fiber diameter (FD) distribution; and (3) the relationship between FD distribution and CNAP configuration, by reconstruction of CNAP made on the basis of FD distributions. The CNAP were evoked in 9 dogs under halothane anesthesia by 2 stimulation methods: percutaneous needle electrode stimulation and direct stimulation of the exposed superficial peroneal nerve. Recordings were made with percutaneous needle electrodes. Full nerve cross sections of 7 superficial peroneal nerves were prepared for FD morphometric analysis. Reconstruction of CNAP were made on the basis of the FD distributions. Late components of the CNAP could be evoked with either stimulation method, but only with a stimulus intensity of 3 to 5 times maximal for the main (early) component of the CNAP. The FD histograms of 7 analyzed nerves had bimodal distribution. In 5 nerves, peaks were at 4.2 to 4.5 micrometer and 9.0 to 10.0 micrometer with 60% of the fibers in the small-diameter group. In 2 nerves with lower maximal conduction velocities, peaks were shifted toward smaller values. The CNAP reconstructions made by use of FD data closely resembled actual recordings when a fifth-order polynomial function was applied to the relationship between nerve conduction velocity and FD. Reconstructions made by use of 1 or 2 linear functions did not accurately resemble actual recordings. The results indicate clinical sensory electroneurographic recordings can provide accurate information regarding both large- and small-diameter fibers, if adequate stimulus intensities are used. To understand the recorded potential more completely, further studies are needed to determine the effects of volume conduction on configuration of the CNAP. It should then be possible to estimate FD distributions even more accurately by analyzing CNAP of normal nerves, or of diseased nerves in which the normal relation between FD and conduction velocity is preserved.

Evoked potentials were induced by transcranial stimulation and recovered from the spinal cord, and the radial and sciatic nerves in six dogs. Stimulation was accomplished with an anode placed on the skin over the area of the motor cortex. Evoked potentials were recovered from the thoracic and lumbar spinal cord by electrodes placed transcutaneously in the ligamentum flavum. Evoked potentials were recovered from the radial and sciatic nerves by surgical exposure and electrodes placed in the perineurium. Signals from 100 repetitive stimuli were averaged and analyzed. Waveforms were analyzed for amplitude and latency. Conduction velocities were estimated from wave latencies and distance traveled. The technique allowed recovery of evoked potentials that had similar characteristics among all dogs. Conduction velocities of potentials recovered from the radial and sciatic nerves suggested stimulation of motor pathways; however, the exact origin and pathway of these waves is unknown.

Recordings of visual-evoked potentials that were induced by flashes of white light were obtained from 13 Beagle pups to document the development of the response from age 7 to 100 days. Responses were recorded between needle electrodes placed on the nuchal crest and the interorbital line, with ground at the vertex. Five alternating positive (P) and negative (N) peaks were observed in most visual-evoked potentials: P1, N1, P2, N2, and P3. Responses were recorded from 2 pups prior to opening of the eyelids. Recordings were performed without sedation or dark adaptation. Peak latencies were essentially mature (equal to those of adult dogs) by day 11 for P1, and by day 38 for N1, and P2. The latencies to N2 and P3 did not reach adult values by day 100, but did reach plateau values by day 43. The P1-N1, amplitude measurements reached mature levels by day 14, whereas N1-P2 amplitudes were mature by day 32. The P2-N2 and N2-P3 amplitudes reached plateaus that greatly exceeded adult amplitudes by days 50 and 58, respectively. Maturation of visual-evoked potential responses paralleled reported morphologic development of the visual cortex. All of the measured latency and amplitude values had significant (P less than or equal to 0.004) linear regression lines of latency vs age or amplitude vs age.

Somatosensory-evoked potentials (SEP) and spinal cord-evoked potentials (SCEP) were recorded in clinically normal adult cats in response to electrical stimulation of pudendal and tibial nerves to provide normative data that can be used in a clinical evaluation of pudendal nerve function in cats after sacral or sacrococcygeal luxations or fractures. Responses to tibial nerve stimulation were included in the study as an internal control because it is usually not involved in these types of injuries and because its SEP and SCEP are easily recorded. Evoked potentials were characterized by the latencies (ms) of positive (P or p) and negative (N or n) peaks. The SEP resulting from percutaneous pudendal nerve stimulation consisted of a prominent P-N-P potential in the 30- to 80-ms range. The pudendal SCEP was not successfully recorded because of large muscle artifacts evoked from the sacral area. The tibial SEP was similar to the pudendal SEP, except that the prominent P-N-P series in the 35- to 81-ms range was preceded by a smaller p-n-p-n sequence in the 7- to 23-ms range. The tibial SCEP consisted of a P-N-P series in the 2- to 4-ms range.

Somatosensory-evoked potentials (SEP) and spinal cord-evoked potentials (SCEP) were recorded in clinically normal adult cats in response to electrical stimulation of pudendal and tibial nerves to provide normative data that can be used in a clinical evaluation of pudendal nerve function in cats after sacral or sacrococcygeal luxations or fractures. Responses to tibial nerve stimulation were included in the study as an internal control because it is usually not involved in these types of injuries and because its SEP and SCEP are easily recorded. Evoked potentials were characterized by the latencies (ms) of positive (P or p) and negative (N or n) peaks. The SEP resulting from percutaneous pudendal nerve stimulation consisted of a prominent P-N-P potential in the 30- to 80-ms range. The pudendal SCEP was not successfully recorded because of large muscle artifacts evoked from the sacral area. The tibial SEP was similar to the pudendal SEP, except that the prominent P-N-P series in the 35- to 81-ms range was preceded by a smaller p-n-p-n sequence in the 7- to 23-ms range. The tibial SCEP consisted of a P-N-P series in the 2- to 4-ms range.

Brain stem auditory-evoked potentials (BAEP) were recorded in 4 dogs to analyze the relationship between acoustic stimulus intensities and peak latencies of each wave, and to investigate the relative effects of xylazine-atropine-ketamine, and xylazine-atropine-pentobarbital combinations and the time-course effects of the latter 2 drug combinations on BAEP. Click stimulations fixed at a stimulus rate of 10/s and a frequency of 4 kHz were delivered at intensities ranging from 10- to 110-dB sound pressure level (SPL) in 10-dB steps for analyzing the relationship between the acoustic stimulus intensities and the peak latencies and at an intensity of 110-dB SPL for investigating the effects of the sedative and the anaesthetic drug combinations and their time-course effects on BAEP. Waves I and VI were identified with stimulus intensity of greater than or equal to 50-dB SPL. Wave VII was observed in some records, but was excluded from statistical analysis. As intensity was increased from 50- to 110-dB SPL, the latency decreased for all waves during xylazine-atropine-ketamine anesthesia. There were no statistically significant differences in the peak latencies of each wave in BAEP among xylazine-atropine, xylazine-atropine-ketamine, and xylazine-atropine-pentobarbital combinations 20 minutes after drug administration, except that the latency of wave VI during xylazine-atropine sedation was significantly (P < 0.01) shorter than that detected during xylazine-atropine-ketamine or xylazine-atropine-pentobarbital anesthesia. There were no significant changes in peak latencies of waves I, II, III, V, and VI for 90 minutes after administration of the xylazine-atropine-ketamine combination and for 120 minutes after administration of the xylazine-atropine-pentobarbital combination. It was concluded that BAEP did not change over time after xylazine-atropine-ketamine or xylazine-atropine pentobarbital administration.