Yoshiyuki Murai

Toxic polyneuropathy due to glue sniffing

Four cases of toxic polyneuropathy due to glue-sniffing were reported. Neurological examination revealed motor predominant mixed type polyneuropathy. The cause of polyneuropathies in these cases was considered to be due to the inhalation of the vaporized elements of the adhesive agent, which contain mainly n-hexane and toluene. N-hexane is considered to be chiefly responsible for the polyneuropathy, though toluene also could have some influence on the illness.

Motor potentials evoked by magnetic stimulation of the motor cortex in normal subjects and patients with motor disorders

Motor evoked potentials (MEPs) elicited by magnetic coil stimulation of motor cortex were studied at rest and during maximum voluntary muscle contraction in 20 normal subjects and 42 patients with motor disorders. MEP parameters employed in this study included: onset latency, amplitude, MEP/M wave amplitude ratio and background EMG/MEP area ratio. Maximum voluntary contraction increased the amplitude of MEPs compared to the size of M waves elicited by peripheral nerve stimulation. A reduced MEP/M wave amplitude ratio had a higher correlation with pyramidal tract involvement than did a prolonged MEP onset latency. Analysis of MEP parameters may help in the differential diagnosis of cerebral infarction, ALS and cervical spondylotic radiculomyelopathy. The inhibitory period which follows MEPs during voluntary contraction was observed in all subjects; the mean duration in normal subjects was 126.6 +/- 29.5 msec. The mean duration of the inhibitory period in patients with cerebral infarction, ALS and cervical spondylotic radiculomyelopathy was 73.9 +/- 41.7 msec, 79.5 +/- 54.5 msec and 85.1 +/- 36.5 msec, respectively. These values were significantly shorter than in normal subjects.

Inhibitory period following motor potentials evoked by magnetic cortical stimulation

Following motor potentials evoked (MEPs) by magnetic cortical stimulation, there is a transient suppression of muscle action potentials (inhibitory period). We recorded MEPs, the inhibitory period, V1 waves and F waves from the abductor pollicis brevis muscle in 20 normal subjects and in 17 patients with spastic hyperreflexia due to cerebral infarction. The duration of the inhibitory period increased in correspondence with increasing stimulus intensity and did not necessarily depend on the amplitude of the MEPs. The duration of the inhibitory period elicited by a twin coil, which can stimulate the motor cortex locally, was shorter than by a single coil. The mean duration of the inhibitory period was significantly shorter in patients with spastic hyperreflexia than in normal subjects, and it correlated with the amplitude of F waves. The effects of the inhibitory period on V1 waves were different from its effects on F waves in one patient with large V1 and F waves. The amplitudes of V1 waves recorded during the inhibitory period were approximately 30-50% of the maximal amplitude of V1 waves, but F waves were not smaller. The inhibitory period is probably caused primarily by central inhibitory mechanisms.

Beriberi neuropathy: Morphometric study of sural nerve

Seven biopsied sural nerves from patients with beriberi were morphometrically evaluated. In teased fiber analysis the mean frequency of myelinated fibers showing axonal degeneration and segmental demyelination was 37.5 and 5.3%, respectively. In two cases with frequency of segmental demyelination higher than 5%, segmental demyelination was shown by statistical criteria to have occurred on certain fibers in a clustered fashion. Therefore, the segmental demyelination in beriberi may be secondary to axonal degeneration. Electromyographic findings and slow improvement of muscle weakness were compatible with axonal degeneration of motor fibers. Determinations of fiber densities revealed preferential decrease of the density of large myelinated fibers with the preservation of the density of small myelinated and unmyelinated fibers. The preferential nerve fiber involvement in beriberi was not associated with pain in the lower limbs and this fact is contrary to the expectation of the proponents of the gate control theory.

Age-dependent changes in physiological threshold asymmetries for the motor evoked potential and silent period following transcranial magnetic stimulation

OBJECTIVE To study the effect of age on the physiological threshold asymmetries for the motor evoked potential (MEP) and silent period (SP) following transcranial magnetic stimulation. METHODS We studied 63 right-handed subjects and 13 young left-handed subjects (19-39 years). The right-handers were classified into three age groups; 22 young (20-38 years), 20 middle-aged (40-58 years) and 21 old (61-82 years) subjects. We measured the MEP thresholds at rest and during voluntary contraction (VC), and the SP thresholds from the right and left abductor pollicis brevis (APB) muscles. We also measured the side to side differences of the F wave persistency and the F wave/M wave amplitude ratio from the same muscles. RESULTS Among young subjects, all of the MEP and SP thresholds for the right APB were significantly lower than those for the left APB in the right-handers, and the reverse was true in the left-handers. The results in the middle-aged right-handers were similar to those in the young right-handers, but in the old right-handers, none of the thresholds were different between the two sides. We did not find any asymmetries of the F wave in the subjects of any age group. CONCLUSION We speculate that the age-dependent threshold asymmetries are preferentially related to functional asymmetries at the cortical level.

Scalp topography and distribution of cortical somatosensory evoked potentials to median nerve stimulation

Topographies and distributions of cortical SEPs to median nerve stimulation were studied in 8 normal adults and 5 neurological patients. SEPs recorded from C4, P4, Pz, T6-A1A2 derivations to left median nerve stimulation were composed of 2 early negative (N16, N20) and 2 positive components (P12, P23), whereas those recorded from frontal electrodes (Fz, Fp1, Fp2) disclosed 2 early negativities (N16, N24) and 2 early positivities (P12, P20). N20 and P20, and P23 and N24, reversed across the rolandic fissure with no significant difference in their peak latencies. P23 was of slightly shorter latency at C4 than at more posterior electrodes (P4, T6, Pz). In 3 patients with complete hemiplegia but normal sensation, all the early SEP components were normal in scalp distribution and peak latencies except for a decrease of N24 amplitude. In 2 patients with complete hemiplegia and sensory loss no early cortical SEPs were seen. These findings suggest that N20 and P20 are generated as a single horizontal dipole in the central fissure, whereas P23 and N24 are a reflection of multiple generators in pre- and postrolandic regions.

Effect of sleep stage on somatosensory evoked potentials by median nerve stimulation.

The effects of sleep stage on early cortical somatosensory evoked potentials (SEPs) and short-latency components elicited by median nerve stimulation were studied in 12 normal volunteers. The latency of P13 in the awake stage was not significantly different from that in any sleep stage. The latencies of N16, N20 and P20 were significantly prolonged while the amplitude of N20 was decreased during the non-rapid eye movement (NREM) sleep stage. P22, P23 and N24 components showed double peaks (P23a, P23b, N24a, N24b) during the NREM sleep stage in 6 subjects, while N24 showed a single peak and only P22 and P23 showed double peaks in 5 other subjects. The latencies and morphologies of SEPs during rapid eye movement sleep stage were almost the same as those during the awake stage. These findings suggest that NREM sleep affects the latency, amplitude and morphology of N16 and early cortical components.

Sympathetic skin responses evoked by magnetic stimulation of the neck

We studied sympathetic skin responses (SSRs) following magnetic stimulation of the neck in 40 normal subjects and 54 patients with neurological diseases and active sweat gland densities (ASGDs) at the foot induced by pilocarpine in 39 patients. SSRs at the hand following magnetic stimulation showed the lowest coefficients of variability of the latencies and amplitudes in eight consecutive responses compared with SSRs following other types of stimuli (electrical and auditory stimulation, and deep inspiration) in 12 normal subjects. Fourteen of 38 patients with neuropathies (37%) showed the presence of SSRs after magnetic stimulation, but not after median nerve stimulation, although SSRs to magnetic stimulation corresponded with those to nerve stimulation in all patients with multiple sclerosis or multiple system atrophy. These results suggest that the absence of SSRs after nerve stimulation in patients with neuropathies may be due to abnormalities of the peripheral sensory afferent fibers. ASGDs significantly correlated with SSRs at the foot following magnetic stimulation, but not with those following nerve stimulation in patients with neuropathies. Magnetic stimulation of the neck is the highly reproducible method of evoking SSRs because this technique is able to produce strong sensory afferent inputs proximally. Furthermore, SSRs following magnetic stimulation, little influenced by sensory afferent fiber involvement, are very useful for evaluating the postganglionic sympathetic function in patients with neuropathies.

Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions

Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23). In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.

Frontal distribution of early cortical somatosensory evoked potentials to median nerve stimulation

The topography of early frontal SEPs (P20 and N26) to left median nerve stimulation was studied in 30 normal subjects and 3 patients with the left frontal bone defect. The amplitudes of P20 and N26 were maximum at the frontal electrode (F4) contralateral to the stimulation and markedly decreased at frontal electrodes ipsilateral to the site of stimulation. There was, however, no latency difference of P20 and N26 between ipsilateral and contralateral frontal electrodes. These results suggest that the origin of the ipsilateral and contralateral P20 and N26 is the same. The wide distribution of P20 and N26 over both frontal areas could be explained by assuming a smearing effect from generators actually located in the rolandic fissure and motor cortex.