Kaoru Iwayama

Origin of frontal N15 component of somatosensory evoked potential in man

Origin of the frontal somatosensory evoked potential (SEP) by median nerve stimulation was investigated in normal volunteers and in patients with localized cerebrovascular diseases, and the following results were obtained. (1) In normal subjects, SEPs recorded at F3 (or F4) contralateral to the stimulating median nerve were composed of P12, N15, P18.5 and N26. Similar components were recognized in SEP recorded at Fz. (2) In patients in whom putaminal or thalamic hemorrhages had destroyed the posterior limbs of the internal capsules, frontal N15 and parietal N18 (N20) disappeared. These components were also absent in patients with cortical (parietal) infarctions. Among these patients, the thalamus was not affected in cases with putaminal hemorrhages and cortical infarctions. These facts indicate that the generator of the frontal N15 does not exist in the thalamus but that it originates from the neural structure central to the internal capsule, which suggests a similarity to the generator of the parietal N18. Because N15 was recorded in the midline of the frontal region with shorter latency than parietal N18, the frontal N15 might represent a response to the sensory input of the frontal lobe via the non-specific sensory system.

Neurones with Epileptiform Discharge in the Central Nervous System and Chronic Pain

Epileptiform discharge was recorded from neurons in the thalamic nuclei of chronic pain patients during stereotactic surgery. Hyperactive neurons showed regular firing of 3-5 trains of epileptic-like group discharges with a frequency of 4 to 5 Hz. As described by Lombard et al. (1979), we operated on the dorsal root unilaterally, sectioning C5 to Thl in male Wistar rats. One to three months after the operation, hyperactive neurons were examined in the contra-lateral thalamic nuclei (VP, zona incerta), and lemniscus medialis. The firing patterns and distribution of hyperactive neurons in these animals was very similar to those of humans. The hyperactive neuron was unaffected by electrical stimulation of the nucleus raphe dorsalis (NRD) and locus ceruleus (LC). Administration of phenytoin and diazepam reduced the firing. However, no effect was seen with valproic acid. During spreading depression of the sensorimotor cortex, a remarkable reduction was seen on the firing of thalamic hyperactive neurons. This suggested that hyperactive neurons of the thalamic nuclei received facilitory effects from the sensorimotor cortex with little influence from adrenergic or serotoenergic systems.

Origin of the initial negative potential (N15) recorded on the skull by superficial radial nerve stimulation in the cat

The origin of the initial prominent negative potential with a latency of about 15 msec (N15), recorded on the skull by superficial radial nerve stimulation was studied in the cat, and the following results were obtained. In the direct recording from the cortex, SEPs were elicited from the SI and SII areas, as well as the lateral gyrus and anterior suprasylvian gyrus. Among various wave forms recognized in the SI area, diphasic positive-negative (P-N) potential obtained from the postero-lateral part was most distinct, representing the primary evoked potential. Responses recorded on the dura and those directly on the cortex showed similar wave patterns over many sites. Although different forms of evoked potentials were recorded extensively over the skull, the most prominent negative potential was elicited at the site corresponding to the postero-lateral part of the SI area. The latency of this potential was approximately in agreement with that of the negative component of the P-N potential recorded on the cortex. Based on the intracortical laminar analysis of P-N potential, the positive component of this potential was assumed to reflect the activity of cells in the deeper layer of the cortex. The negative component, on the other hand, might represent activities of apical dendrites of the cortex. From the result of functional elimination of the cortex, however, this positive component was thought to contain potentials from far field neural structures. N15 recorded on the skull completely disappeared during cortical spreading depression.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes of somatosensory evoked potential accompanying ischaemia and hypoxia in cats

Changes of evoked potential accompanying haemorrhagic hypotension and hypoxia were investigated on cats to evaluate the usefulness of SEP as a monitor in an intensive care unit (ICU), and the following results were obtained. Positive-negative diphasic potential was elicited at posterior sigmoid gyrus(PSG) by contralateral superficial radial nerve stimulation. This potential was recorded at the restricted area of the posterior border of PSG and regarded as primary somatosensory evoked potential. In the initial stage of haemorrhagic hypotension, both positive and negative components of SEP occasionally increased in amplitude. In profound hypotension in which CBF fell to less than the critical level of 30 ml 100 g-1 min-1, the latency was retarded and the amplitude was decreased. At CBE less than 10 ml 100 g-1 min-1, SEP disappeared. Within the range of CBF between 10 and 30 ml 100 g-1 min, a close correlation was noted between CBF and SEP amplitude. Transient increase of SEP amplitude was also observed during hypoxia induced by inhalation of nitrogen gas. (3) In normal state SEP was decreased in amplitude by conditioning stimulation of the nucleus lateralis posterior (LP nucleus) of the thalamus. This might be explained by the fact that intracortical inhibitory interneurons were activated by stimulation of LP nucleus. After haemorrhagic hypotension and hypoxia, however, the inhibitory effect on SEP elicited by LP nucleus stimulation attenuated or disappeared. Because of the initial impairment of the inhibitory interneurons by ischaemia and hypoxia, the amplitude of SEP might increase transiently. In conclusion, the authors thought that SEP might be less useful than EEG in ICU, because of its insensible change to hypoxia and ischaemia.

Effect of midbrain raphe nucleus stimulation on somatosensory evoked potential in cat

Experiments were carried out to clarify the effect of serotonin [5-hydroxytryptamine (5-HT)] upon the somatosensory evoked potential (SEP) elicited by superficial radial nerve stimulation in cat, and the following results were obtained: (i) in untreated (control) animals, a significant reduction occurred in amplitude of the SEP in response to conditioning stimulation of the dorsal raphe nucleus in the midbrain, within 100 ms of the interval between conditioning and test stimuli; (ii) in 5-HT depleted animals prepared by intraperitoneal injection of p-chlorophenylalanine (PCPA), the amplitude of SEP significantly increased in comparison with that of nontreated animals. Conditioning stimulation of the raphe nucleus in 5-HT depleted animals failed to cause any remarkable change in the SEP; (iii) the diminuation of the SEP by raphe nucleus conditioning reappeared following intraventricular administration of a large dose of 5-HT (200 micrograms) in the PCPA-treated animals. These results have demonstrated that the serotonergic system with its cell bodies located in the raphe nucleus of the midbrain has the function of reducing the amplitude of the SEP, thus suggesting that it acts as a suppressive control on the excitability of the cortex to sensory input.

Influence of the ipsilateral hemisphere upon somatosensory evoked potential in cats

Somatosensory evoked potentials (SEPs) were recorded on the skull corresponding to the (left) SI area by (right) superficial radial nerve stimulation. Amongst the various components of the SEP, special attention was directed to the negative component (N15) with a latency of approximately 15 ms. Changes in this potential followed by conditioning stimulation of the ipsilateral (right) hemisphere were observed and the following results were obtained: (i) when conditioning stimuli were applied to the contralateral (left) superficial radial nerve, the ipsilateral (right) thalamic VPL nucleus and the ipsilateral (right) sensory cortex, the amplitude of N15 decreased to 65-80% of the control level at C-T intervals less than 100 ms and (ii) following functional elimination of the unilateral sensory cortex by KCl application, the amplitude of N15 recorded at the opposite side significantly increased. In this condition, the inhibitory effects of the ipsilateral thalamus and contralateral peripheral nerve disappeared. From these observations, ipsilateral homologous cortex may well have an inhibitory influence upon the near field potential (N15) of the SEP.

Origin of short latency somatosensory evoked potential in cats: especially potentials derived from thalamus and cortex

Short latency somatosensory evoked potential (SSEP) was recorded in cats to identify the potentials originating from the cortex and the thalamus, and the following results were obtained. When SSEP was elicited on the bregma by stimulation of the contralateral superficial radial nerve, P2, P4, P4.5, P5.5, P7, P8, N8.5, P11, P9.5, N11.5, N12.5 and N14 were recognized. Of these components N11.5, N12.5 and N14 consisted of large negative potential (LNP). When KCl was applied to the sensorimotor cortex to induce spreading depression, the positive component of the primary evoked potential was markedly decreased and the negative component disappeared. In SSEP, components preceding N8.5 were unchanged. N8.5-P11 and P11-N12.5, however, markedly diminished or disappeared. The latency of the first component of the field potential recorded in the VPL nucleus of the thalamus was about 5 ms. When a small amount of Nembutal was injected into VPL nucleus, components between P2 and P4.5 remained unchanged, but P5.5 disappeared. P7, P8 and N8.5 were preserved. The amplitude of N8.5-P11 was markedly decreased and LNP disappeared. From these results, among various components of SSEP, P5.5 should originate from the thalamus, and P7, P8 and N8.5 from the extralemniscal system. N8.5-P11 should mainly represent post-synaptic potential (PSP) in the deep somatic layer, and P11-N12.5 represent PSP in the apical dentrites of the sensorimotor cortex. N14 probably represents PSP via the diffuse projection system. Thus, LNP should consist of complex potentials of specific and non-specific sensory systems.

Simultaneous recording of steady potential, extracellular potassium activity and unitary behavior on penicillin-focus in cats.

In order to clarify the fundamental factor for manifestation of the steady potential (SP) shifts observed in ECoG paroxysms, the following investigations were conducted. The epileptogenic focus was produced by applying Penicillin-G(Pc) on one side of the pericruciate gyrus in cats. The animal was paralyzed with gallamine triethiodide and maintained on artificial respiration. Surface SP was recorded by a modified pore electrode of Marshall.fi Deep SP was recorded by a glass-pipette Ag-AgCI electrode. In all experiments, the reference electrode was placed on the surface of the frontal bone.