Shin-ichi Wada

Anatomical bases of binaural interaction in auditory brain-stem responses from guinea pig

There is a non-linear interaction of binaural stimulation on auditory brain-stem potentials in both human and animals. The interaction takes the form of the binaurally evoked ABR being of smaller amplitude than the sum of the monaurally evoked ABRs. In the guinea pig this interaction occurs at the time of components P4, N4 and P5. In order to investigate the generator sites of binaural interaction in the ABR, various lesions were made in the brain-stem auditory system in 29 guinea pigs. The effects of those lesions on binaural interaction were as follows: (1) unilateral lesion of lateral lemniscus or bilateral lesions of the inferior colliculi had no significant effect on binaural interaction; (2) transection of the lateral lemnisci bilaterally was associated with a loss of the component of binaural interaction associated in time with N4; (3) a lesion just lateral to the lateral superior olivary complex resulted in an attenuation of the component of binaural interaction associated in time with P4; (4) complete section of the decussating fibers of the trapezoid body or a complete unilateral lesion of the superior olivary complex led to a loss of all components of binaural interaction. These results suggest that binaural interaction in the guinea pig ABR requires the integrity of several distinct portions of the brain-stem auditory pathway, i.e., both lateral lemnisci are required for the interaction occurring at the time of N4; the brain-stem just lateral to the lateral superior olive participates in the interaction at the time of P4. The trapezoid body and superior olivary nucleus are required for binaural interaction at P4, N4 and P5.

Absence of spinal N13-P13 and normal scalp far-field P14 in a patient with syringomyelia

Short latency somatosensory evoked potentials to median or ulnar nerve stimulation were recorded in a patient with syringomyelia. Scalp-recorded far-field P14 was clearly preserved, but spinal N13-P13 components disappeared. Our findings support the hypothesis that spinal N13-P13 is generated by structures intrinsic to the cervical cord, most likely in the ventral central gray matter.

P30 and N33 of posterior tibial nerve SSEPs are analogous to P14 and N18 of median nerve SSEPs

Generator sources of far-field P30 and N33 components produced by posterior tibial nerve stimulation were compared with those of the P14 and N18 components of median nerve stimulated somatosensory evoked potentials. Intracranial spatio-temporal distributions of P30 and N33 were similar to those of the P14 and N18 obtained by median nerve stimulation. In clinical cases, the changes in P30 and N33 were correlated with those in P14 and N18, indicative that P30 and N33 are derived from activities similar to those that produce P14 and N18.

Effect of transcutaneous electrical nerve stimulation (TENS) on central nervous system amplification of somatosensory input

The effect of transcutaneous electrical nerve stimulation (TENS) on the central nervous system amplification process was investigated focusing on the dorsal column-medial lemniscal pathway, because the dorsal column nucleus was recently shown to receive multiple sources of sensory information, including pain. Short latency somatosensory evoked potentials (SSEPs) were recorded in ten healthy normal volunteers. Amplitude changes in each SSEP component (the N9 brachial plexus potential, the P14 potential that originates from the cervicomedullary junction, spinal N13/P13 generated by the cervical dorsal horn and the cortical N20/P25 potential) were studied at stimulus strenghts ranging from the threshold (40% maximum stimulus) to 2.5 times the threshold (maximum). The findings suggest that sensory amplification begins at the P14 generator source near the cuneate nucleus. There was no statistically significant difference in sensory amplification between P14 and cortical N20/P25, indicating that the cuneate nucleus is the main site of the central amplifying process. When TENS was applied to the palm distal to the median nerve stimulation used for SSEP, cortical N20/P25 amplification disappeared, evidence that TENS suppresses the central amplification phenomenon, most probably at the level of the cuneate nucleus.

Skin and epidural recording of spinal somatosensory evoked potentials following median nerve stimulation: correlation between the absence of spinal N13 and impaired pain sense

SummaryA clinical lesion study and intraoperative epidural recordings were made to test the origin and clinical significance of the spinal N13 and P13 of somatosensory evoked potentials (SEP) that follow median nerve stimulation. Intraoperatively, the respective peak latencies of spinal P13 and N13 coincided with those of the N1 component of the dorsal cord potential and its phase reversed positivity. On both the ventral and dorsal sides of the cervical epidural space, maximal amplitude was at the C5 vertebral level to which nerve input from the C6 dermatome is the main contributor. The modality of sensory impairment in the hand dermatome was examined in selected patients with cervical lesions, who showed such normal conventional SEP components as Erb N9, far-field P9, P11, P14, N18 and cortical N20, with or without loss of spinal N13. Statistically, the loss of spinal N13 was associated with decrease of pain sensation in the C6 dermatome. This was interpreted as being due to damage to the central grey matter of the cord, including the dorsal horn. Our results suggest the spinal N13 and P13 originate from the same source in the C6 spinal cord segment and that they are good indicators for the detection of centromedullary cervical cord damage.

The effects of stimulus rates on high frequency oscillations of median nerve somatosensory-evoked potentials – direct recording study from the human cerebral cortex

OBJECTIVES To study the effects of different stimulus rates on high-frequency oscillations (HFOs) of somatosensory-evoked potentials (SEPs), we recorded median nerve SEPs directly from the human cerebral cortex. METHODS SEPs were recorded from subdural electrodes in 5 patients with intractable epilepsy, under the conditions of low (3.3Hz) and high (12.3Hz) stimulus rates. RESULTS Increased stimulus rates to the median nerve from 3.3 to 12.3Hz showed a pronounced amplitude reduction of HFOs when compared with the primary N20-P20, area 3b, and P25, area 1, responses. CONCLUSIONS HFOs were more sensitive to a high stimulus rate than the primary cortical responses, suggesting that the post-synaptic intracortical activities may greatly contribute to the HFO generation.

Quantitative analysis of reversible dysfunction of brain-stem midline structures caused by disturbance of basilar artery blood flow with the auditory brain-stem responses

To clarify the effects of disturbances in basilar artery blood flow, basilar artery angiospasm was induced in 2 cats and 4 guinea pigs and auditory brain-stem responses (ABRs) were continuously recorded preceding, during and following the angiospasm. The angiospasm caused specific ABR changes in that waves II (P2-N2) and III (P3-N3) were attenuated without any corresponding amplitude reduction of P4. Those changes were equivalent following stimulation of either ear. Moreover, the ABR changes gradually recovered within 5 h. On the basis of the animal experiments, 52 patients with subarachnoid hemorrhage, supratentorial tumor showing increased intracranial pressure or hydrocephalus were selected for repeated ABR examinations. ABR abnormalities similar to those observed in the animal experiment were obtained especially from the patients exhibiting grade 3 or 4 symptomatology with subarachnoid hemorrhage. In these cases, the wave III to wave IV-V amplitude ratio was significantly decreased. In some cases the ABR abnormalities and the wave III to wave IV-V amplitude ratio recovered as the clinical course improved. These results support the conclusion that specific ABR changes (wave III to wave IV-V amplitude ratio) reflect transient ischemic dysfunction of the midline portion of the brain-stem caused by disturbances of basilar artery blood flow.

Amplitude abnormalities in the scalp far-field N18 of SSEPs to median nerve stimulation in patients with midbrain-pontine lesion

Various amplitude ratios were measured in 20 normal controls and 36 patients with midbrain-pontine, thalamic or putaminal lesions in order to evaluate the amplitude abnormalities in scalp far-field N18 following median nerve stimulation. A study of normal controls showed that the distributions of P9/N18, P14/N18 and N18/P14 + N18 resembled a gaussian distribution and could be used as criteria for determining the decrease in N18 amplitude in each patient. There was a decrease in N18 amplitude, or the absence of N18, in patients with midbrain-pontine lesions, but not in those with thalamic or putaminal lesions. Nine amplitude ratios (P11/P9, P14/P9, N18/P9, P9/P11, P9/P14, P9/N18, N18/P14, P14/N18 and N18/P14 + N18) were compared statistically for normal controls and 3 groups of patients based on non-parametric, Wilcoxons non-pairs and signed-rank tests. A decrease in N18 amplitude in midbrain-pontine lesion was shown by significant changes in N18/P9, P9/N18, N18/P14, P14/N18 and N18/P14 + N18, no amplitude decreases in P11 and P14 being found from the amplitude ratios of P11/P9, P9/P11, P14/P9 and P9/P14. No significant changes were seen in any of the 9 amplitude ratios when the normal controls and patients with thalamic and putaminal lesions were compared. The amplitude ratios of N18 can be used to detect a decrease in N18 amplitude in patients with midbrain-pontine lesions. The data obtained support the hypothesis that N18 originates in the midbrain-pontine region and that neither the thalamus nor thalamocortical radiation make major contributions to the formation of the N18 peak.

Spinal intramedullary recording of human somatosensory evoked potentials

We here report the first description of the intramedullary spatial distribution of evoked dorsal horn potentials in a human spinal cord. Somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded within the cervical spinal cord of a patient with syringomyelia. Spinal intramedullary recording demonstrated a negative slow wave of the same polarity as the dorsal spinal surface response and a complex wave interpreted as the summation of its negativity and phase-reversed positivity. These two wave forms may depend on the locations at which the recording electrodes are attached to the dorsal horn.

Dynamic changes in area 1 somatosensory cortex during transient sensory deprivation: a preliminary study.

Summary To investigate the neural plasticity in the somatosensory cortex, changes in somatosensory evoked potentials (SSEPs) during finger ischemia were evaluated and compared with those affected by touch or movement interference. Somatosensory evoked potentials were recorded in the vicinity of the central sulcus in four patients with intractable epilepsy. During electrical stimulation to a selected finger, ischemic anesthesia was induced in another finger. Effects of tactile or movement interference were examined during electrical stimulation to the selected finger by applying tactile stimulation to or inducing voluntary movement of the other finger. Dynamic SSEPs were recorded during varying levels of sensory deprivation and different types of interference, and the dynamic nature of the SSEP changes within an individual was studied in detail. Somatosensory evoked potential changes appeared during finger ischemia and tended to persist during the postischemic stage, which is indicative of sensory plasticity and the maintenance of new conditioning. Amplitudes of the early and late cortical components increased when complete finger anesthesia was induced—a sign of the unmasking phenomenon. Amplitudes of early cortical SSEPs decreased when ischemic anesthesia was incomplete, similar to the findings when tactile or movement interference was applied. Surrounding inhibition, therefore, may become dominant before the unmasking phenomenon appears in early cortical SSEPs.