[An analysis of A-wave with slowed conduction in its afferent and efferent pathways below the branching point].

Motor nerve conduction study was carried out in a 59-year-old woman with 20 years' history of diabetes mellitus. When her right ulnar nerve was stimulated at the wrist, the needle electrode penetrated into the first dorsal interosseous muscle revealed an existence of A-wave. Following characteristics were observed: (1) A-wave appeared with more than 20 mA of the stimuli, in a all-or-none manner at the latency of 54 msec; (2) when stimulated more than 50 mA, A-wave jumped at 10 msec of the latency and were superimposed upon the M-wave; (3) A-wave had a stable latency; (4) when stimulated at the more proximal site, A-wave had longer latency (direct pathway) by strong stimuli, and the potential had shorter latency (indirect pathway) by weak stimuli; and (5) A-wave was not collided by paired stimuli. A-wave conduction velocity was slower than 10 m/sec in the distal part of the reflecting point both in afferent and efferent pathways. This report is the first to show strikingly slowed conduction of A-wave distal to the reflecting point compared to the proximal portion. This fact supports the thesis that A-wave is generated from the branching of immature regenerating fibers. M-wave conduction velocity also decreased around the reflecting point of the A-wave, suggesting that, in addition to moderate diabetic polyneuropathy, entrapment at the cubital tunnel may be involved in generating this A-wave.

[Stimulus effect of submaximal trains of impulses on nerves].

Although the occurrence of rate-dependent conduction block upon exposure to supramaximal stimuli is a well-known phenomenon, changes in the stimulus effect of submaximal trains of impulses on nerves remain unknown. To investigate changes in the stimulus effect, we evaluated median nerve action potentials using various frequencies of impulse trains. The subjects were 12 healthy controls and 9 patients with diabetic polyneuropathy. A tungsten microelectrode was inserted into the median nerve trunk at the elbow. Weak stimuli that produced 10 microV compound nerve action potentials were repeated. Each value recorded is the average of 20 trials. Repetition of 1- to 5-Hz stimuli yielded the same average wave, but above 7-Hz, the stimuli produced a diminution in amplitude and slight prolongation of the latency of each peak. This was most prominent with 50-Hz or 100-Hz repeated stimuli. The potentials changed amplitude with a waxing and waning pattern, and gradually stabilized at a lower level. The averaged wave corresponded to the record of reduced stimuli at 0.6 mA, maximally. Paired stimuli at an interval of less than 5 msec were equivalent to a relative refractory period, whereas at an interval of 4-18 msec they were equivalent to a supernormal period, and at 12-90 msec, to a subnormal period. The 'jumping' (unexpected shortening of the latency of a potential in response to increased stimulus intensity) of a single nerve unit was provoked or released corresponding to these periods. No differences were found between healthy individuals and patients with diabetic polyneuropathy. As a consequence of electrogenic Na+/K+ pumping, a three-Na+ ion efflux occurred instead of a two-K+ ion influx. Thus, repeated high-frequency impulses induced membrane hyperpolarization that reduced the stimulus effect on nerves. With trains of impulses at a frequency of 100-Hz, which corresponds to a stimulus every 10 msec, the second response was greater than the first, reflecting the supernormal period, but impulse trains provoked hyperpolarization, as mentioned above, and reduced the amplitude of nerve action potentials. The results of this study show that the stimulus effect on nerves decreased at submaximal stimuli greater than 7-Hz, which reduced the amplitude of compound nerve action potentials. Therefore, averaging should be done at a stimulus frequency below 6-Hz.

[Electrophysiological assessment of median sensory nerve function in HMSN type I by intraneural neurography].

Microneurography (MNG) performed in the forearm segment of the median nerve enabled us to assess compound nerve action potentials reflecting the density of large myelinated sensory fibers around the microelectrode. We examined sensory nerve function of the median nerve in seven patients with hereditary motor and sensory neuropathy type I (HMSN-I) with conventional surface-electrode technique and MNG. In six of seven patients sensory nerve action potentials were not elicited with the surface-electrode method. In contrast, compound nerve action potentials (CNAPs) were evoked in all seven patients with MNG. Although the normal waveform of CNAP is characterized by a large triphasic wave with subsequent small multiphasic waves, the triphasic wave was diminished and prolonged small multiphasic waves were prominent in the patients. Maximal nerve conduction velocity and amplitude of the wave were decreased to 69% and 9% of age-matched control values, respectively. These changes detected in patients with HMSN-I could be interpreted as a result of large myelinated fiber loss and segmental demyelination of sensory nerves. We showed that sensory fiber dysfunction in HMSN-I could be quantitatively evaluated with MNG, even though the sensory action potential was not elicited with the surface-electrode method.

[Midmotoraxonal reexcitation observed in a patient with hereditary motor and sensory neuropathy (HMSN) type IA].

We report a unique late motor unit potential observed in a patient with hereditary motor and sensory neuropathy (HMSN) type IA. The characteristics of the potential were as follows; (1) constant appearance with more than 20 mA of the stimuli, without disappearance with supramaximal stimuli, (2) constant wave-form and amplitude, (3) shorter latency with more proximal stimulation (indirect pathway), (4) remarkable fluctuation of the latency, and (5) disappearance with paired stimuli. The characteristics (1)-(3) correspond to Tomasulo's "peripheral late wave". But our late potential had fluctuation in its latency and was cancelled by paired stimuli, which indicates that this potential originated from the reflection at the midmotoraxonal demyelinating portion. Demyelinating portion is electrically unstable, where the duration of action potential is elongated. Consequently, nerve action potential at that site continues even after the refractory period is over at the adjacent distal portion, which might be the reason that this reflecting potential was evoked.