Parkinson's disease and lower limb somatosensory evoked potentials: apomorphine-induced relief of the akinetic-rigid syndrome and vertex P37-N50 potentials.

We evaluated brainstem P30, vertex-central P37-N50 and contralateral frontal N37 somatosensory evoked potentials (SEPs) from the tibial nerve in 14 patients affected by Parkinson's disease (PD) with akinetic-rigid syndrome. In seven patients SEPs were recorded after administration of apomorphine. The cortical P37-N50 complex was either absent (five patients, eight tested sides) or significantly smaller in patients as compared to the control group (n = 18). There was a relationship between abnormalities of early vertex potentials and degree of motor impairment. Administration of apomorphine was followed by an increase in amplitude of P37-N50 response, which was maximal after 15-30 min and then progressively returned to basal values in parallel with clinical improvement. Amplitude of brainstem P30 and frontal N37 responses was within normal values and did not vary following drug administration. These results suggest that the P37-N50 complex arises from independent cortical generators, probably located in the pre-rolandic cortex, which may be selectively affected by basal ganglia dysfunction. Amplitude decrease of the P37-50 complex may reflect an abnormal processing of somatosensory inputs within the pre-central cortex due to defective modulation exerted by basal ganglia circuitry on cortical excitability. SEP potentiation following apomorphine, besides indicating that this dysfunction is partly reversible, might suggest objective method to measure therapeutic efficacy.     

SEPs in two patients with localized lesions of the postcentral gyrus.

Scalp distributions of median nerve SEPs were studied in normal controls and 2 patients with localized lesions of the postcentral gyrus. In controls, parieto-occipital electrodes registered N20-P27 while frontal electrodes registered P20-N27. Other small components, parieto-occipital P22 and frontal N22, were recognized in about half of the control records. The wave forms at a frontal and a parieto-occipital electrode, both distant from the central region, formed exact mirror images of each other concerning N20-(P22)-P27 and P20-(N22)-N27. Electrodes near the central region contralateral to the stimulation registered cP22-cN30 (central P22 and central N30). When the postcentral gyrus was damaged, N20/P20-P27/N27 and cP22-cN30 were eliminated and the only remaining components were a frontal negative wave (frN) and a contralateral parieto-occipital positive wave (poP). Digital nerve stimulation also evoked poP and frN in both cases. In case 2, poP coincided with P22 of the non-affected side. The following generators were proposed; N20/P20-P27/N27: area 3b, cP22-cN30: areas 1 and 2, poP/early frN (= P22/N22): area 4 at the anterior wall of the central sulcus (due to direct thalamic inputs to motor cortex), late frN: uncertain (SMA?, SII?).     

Topographical features of the sensory-evoked responses in malformed brains

To reveal the functional organization of the somatosensory area in the dysgenetic cortex, somatosensory-evoked potentials were examined in seven patients with congenital brain anomalies diagnosed by magnetic resonance imaging, including six patients in whom multichannel recordings over the scalp were used. In four patients with polymicrogyria/pachygyria and two with lissencephaly, the early cortical responses, frontal P20 and parietal N20, were absent in the cortex contralateral to the stimulated side. The first cortical response was a positive wave that appeared predominantly over the centroparietal area in five patients, and in the frontal area in the other patient with polymicrogyria/pachygyria. These findings suggest that the differentiated somatosensory function is distributed normally in the centroparietal cortex in most cases of widespread cortical dysplasia. However, the absence of P20/N20 may indicate a hypoplastic central sulcus or functionally undifferentiated subdivision of the somatosensory cortex in these patients. The absence of cortical responses in the patient with holoprosencephaly may correspond with growth failure of the thalamocortical afferent projections in this disorder.     

Mapping of early and late human somatosensory evoked brain potentials to phasic galvanic painful stimulation

In the present study, we modeled the spatiotemporal evolution of human somatosensory evoked cortical potentials (SEPs) to brief median-nerve galvanic painful stimulation. SEPs were recorded (-50 to +250 ms) from 12 healthy subjects following nonpainful (reference), slight painful, and moderate painful stimulations (subjective scale). Laplacian transformation of scalp SEPs reduced head volume conduction effects and annulled electric reference influence. Typical SEP components to the galvanic nonpainful stimulation were contralateral frontal P20-N30-N60-N120-P170, central P22-P40, and parietal N20-P30-P60-P120 (N = negativity, P = positivity, number = latency in ms). These components were observed also with the painful stimulations, the N60, N120, P170 having a longer latency with the painful than nonpainful stimulations. Additional SEP components elicited by the painful stimulations were parietomedian P80 as well as central N125, P170 (cP170), and P200. These additional SEP components included the typical vertex negative-positive complex following transient painful stimulations. Latency of the SEP components exclusively elicited by painful stimulation is highly compatible with the involvement of A delta myelinated fibers/spinothalamic pathway. The topography of these components is in line with the response of both nociceptive medial and lateral systems including bilateral primary sensorimotor and anterior cingulate cortical areas. The role of attentive, affective, and motor aspects in the modulation of the reported SEP components merits investigation in future experiments.     

Distinct fronto-central N60 and supra-sylvian N70 middle-latency components of the median nerve SEPs as assessed by scalp topographic analysis, dipolar source modelling and depth recordings.

OBJECTIVES: To investigate the possible contribution of the second somatosensory (SII) area in the generation of the N60 somatosensory evoked potential (SEP).METHODS: In 7 epileptic patients and in 6 healthy subjects scalp SEPs were recorded by 19 electrodes placed according to the 10-20 system. All epileptic patients but one were also investigated using depth electrodes chronically implanted in the parieto-rolandic opercular cortex. Scalp SEPs underwent brain electrical source analysis.RESULTS: In both epileptic patients and healthy subjects, scalp recordings showed two middle-latency components clearly distinguishable on the basis of latency and scalp distribution: a fronto-central N60 potential contralateral to stimulation and a later bilateral temporal N70 response. SEP dipolar source modelling showed that a contralateral perisylvian dipole was activated in the scalp N70 latency range whereas separate perirolandic and frontal sources were activated at the scalp N60 latency. Depth electrodes recorded a biphasic N60/P90 response in the parieto-rolandic opercular regions contra- and ipsilateral to stimulation.CONCLUSIONS: Two different middle-latency SEP components N60 and N70 can be distinguished by topographic analysis and source modelling of scalp recordings, the sources of which are located in the fronto-central cortex contralateral to stimulation and in the supra-sylvian cortex on both sides, respectively. The source location of the scalp N70 in the SII area is strongly supported by its spatio-temporal similarities with SEPs directly recorded in the supra-sylvian opercular cortex.     

Comparison Between a Real Sequential Finger and Imagery Movements: An fMRI Study Revisited

Recently, much discussion has been centered on the brain networks of recall, memory, and execution. This study utilized functional magnetic resonance imaging to compare activation between a simple sequential finger movement (real task) and recalling the same task (imagery task) in 15 right-handed normal subjects. The results demonstrated a greater activation in the contralateral motor and somatosensory cortex during the real task, and a higher activation in the contralateral inferior frontal cortex, ipsilateral motor, somatosensory cortex, and midbrain during the imagery task. These real task-specific areas and imagery-specific areas, including the ipsilateral motor and somatosensory cortex, are consistent with recent studies. However, this is the first report to demonstrate that the imagery-specific regions involve the ipsilateral inferior frontal cortex and midbrain. Directly comparing the activation between real and imagery tasks demonstrated the inferior frontal cortex and midbrain to therefore play important roles in cognitive feedback.     

Frontal component of the somatosensory evoked potential

Electric stimulation of the median nerve at the wrist evokes a series of electric potentials that can be recorded from the scalp or directly from the cortex. These somatosensory evoked potentials (SEP) include a parietal negativity with a maximum 20 ms after the stimulus, which originates in the somatosensory cortex, probably area 3b (Allison et al. [1991a], Brain 114:2465–2503 and Desmedt et al. [1987], Electroenceph Clin Neurophysiol 68:1–19). Thirty milliseconds after the stimulus, a negative potential (N30) occurs at frontal recording sites. Recently it was observed that the amplitude of this potential is altered in patients with dystonia, Parkinson's disease, and Huntington's chorea. It has been argued that the N30 potential stems from cortical areas other than the somatosensory cortex, for example, the supplementary motor area. We used multichannel recordings to investigate the scalp distribution of the N20 and the N30 potentials in healthy subjects. We found that the N20 as well as the N30 potentials were accompanied by a corresponding positivity at frontal and parietal recording sites, respectively. The N20/P20 and the N30/P30 potential fields had a mirrorlike appearance, and both showed a polarity reversal near the central sulcus. This and the results of correlation analyses led us to the conclusion that the N30 generator is located near the central sulcus. © 1995 Wiley-Liss, Inc.     

Stereotactic recordings of median nerve somatosensory-evoked potentials in the human pre-supplementary motor area

Median nerve somatosensory-evoked potentials (SEPs) have been recorded using intracortical electrodes stereotactically implanted in the frontal lobe of eight epileptic patients in order to assess the waveforms, latencies and surface-to-depth distributions of somatosensory responses generated in the anterior subdivision of supplementary motor areas (SMAs), the so-called pre-SMA. Intracortical responses were analysed in two latency ranges: 0--50 ms and 50--150 ms after stimulus. In all patients, we recorded in the first 50 ms after stimulus two positive P14 and P20 potentials followed by a N30 negativity. In the hemisphere contralateral to stimulation, the P20--N30 potentials showed a clear amplitude decrease from the outer to the inner aspect of the frontal lobe with minimal amplitudes in the pre-SMA. In the hemisphere ipsilateral to stimulus, P20 and N30 amplitudes were decreasing from mesial to lateral frontal cortex. In the 50--150 ms latency range, contacts implanted in the pre-SMA recorded a negative potential in the 60--70 ms latency range which, in five patients, was followed by a positive response peaking 80--110 ms after stimulus. These potentials were not picked up by more superficial contacts. We conclude that no early SEP is generated in pre-SMA in the first 50 ms after stimulation, while some potentials peaking in the 60--100 ms after stimulus are likely to originate from this cortical area. The latency of the pre-SMA responses recorded in our patients supports the hypothesis that the pre-SMA does not receive short-latency somatosensory inputs via direct thalamocortical projections. More probably the pre-SMA receives somatosensory inputs mediated by a polysynaptic transcortical transmission through functionally secondary motor and somatosensory areas.     

Somatosensory tibial nerve evoked potentials with parasagittal tumours: a contribution to the problem of generators

Somatosensory evoked potentials following stimulation of the median nerve at the wrist and the tibial nerve at the ankle were recorded in 5 patients with parasagittal tumours, 4 in the fronto-parietal and 1 in the frontal region. Three had intracerebral tumours and 2 parasagittal meningiomas. The extent of each lesion was determined by CT scan, showing a unilateral process involving predominantly the paracentral lobule and adjacent parts of the post- and precentral gyri ("Mantelkante') in 4 patients and a more frontal location of one meningioma affecting mainly the superior frontal gyrus. SEPs recorded from the patients with fronto-parietal tumours showed a uniform pattern with a complete absence of the wave N70 of the tibial SEP elicited by stimulating the nerve contralateral to the lesion. All other waves, including the P40-N50 complex on both sides and the median SEP, were in the normal range. In contrast, the frontal meningioma led to an only slightly altered from of the waves immediately following the initial P40-N50 complex. It is concluded that the tumour abolished the generators of the wave N70 which are apparently located in the cortical somatosensory leg area. Therefore unilateral loss of the wave N70 is indicative of parasagittal lesions. The results may give good evidence that the P40-N50 complex is generated in the thalamus or thalamo-cortical connections.     

Somatosensory disinhibition in dystonia.

Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease.     

The relationship between human long-latency somatosensory evoked potentials recorded from the cortical surface and from the scalp.

In scalp recordings, stimulation of the median nerve evokes a number of long-latency (40-300 msec) somatosensory evoked potentials (SEPs) whose neural origins are unknown. We attempted to infer the generators of these potentials by comparing them with SEPs recorded from the cortical surface or from within the brain. SEPs recorded from contralateral sensorimotor cortex can be characterized as "precentral," "postcentral," or "pericentral." The scalp-recorded P45, N60 and P100 potentials appear to correspond to the pericentral P50, N90 and P190 potentials and are probably generated mainly in contralateral area 1 of somatosensory cortex. The scalp-recorded N70-P70 appear to correspond to the precentral and postcentral N80-P80 and are generated mainly in contralateral area 3b of somatosensory cortex. The scalp-recorded N120-P120 appear to correspond to the intracranial N100-P100 and are probably generated bilaterally in the second somatosensory areas. N140 and P190 (the "vertex potentials") are probably generated bilaterally in the frontal lobes, including orbito-frontal, lateral and mesial (supplementary motor area) cortex. The supplementary sensory area probably generates long-latency SEPs, but preliminary recordings have yet to confirm this assumption. Most of the proposed correspondences are speculative because the different conditions under which scalp and intracranial recordings are obtained make comparison difficult. Human recordings using chronically implanted cortical surface electrodes, and monkey studies of SEPs which appear to be analogs of the human potentials, should provide better answers regarding the precise generators of human long-latency SEPs.     

The N30 component of somatosensory evoked potentials in patients with dystonia.

We recorded short-latency median nerve somatosensory evoked potentials (SEPs) in 10 patients with dystonia (6 with focal dystonia, 3 with generalized dystonia, and 1 with segmental dystonia) and compared them with those of 10 normal controls. The EEG was recorded from 29 sites on the scalp with linked earlobe electrodes for reference. Latencies and amplitudes of P15, postcentral N20 and P45, and frontal N30 were evaluated. The latencies of all potentials were the same in patients and controls. The amplitudes of P15, N20 and P45 were also the same in both groups, but the N30 amplitude of the patients was larger than of the controls. The amplitude of N30 did not vary from the affected side to the unaffected side. Previous work has shown decreased N30 amplitude in patients with Parkinson's disease. Changes in N30 amplitude may be indicative of abnormal excitatory effects on cortex resulting from disorders of the basal ganglia.     

Non-invasive evaluation of input-output characteristics of sensorimotor cerebral areas in healthy humans

The topography of scalp SEPs to mixed and sensory median nerve (MN) and to musculocutaneous nerve stimulation was examined in 20 healthy subjects through multichannel (12-36) recording in a 50 msec post-stimulus epoch. MN-SEPs in both frontal leads were characterized by an N18, P20, N24, P28 complex showing maximal amplitude at contralateral parasagittal sites. This was sometimes partly obscured by a wide wave N30 having a fixed latency, but a steep amplitude gradient moving toward the scalp vertex. A P40 component followed, having longer peak latencies, moving the recording sites from contralateral medial parietal toward the vertex and frontal ipsilateral positions. MN-SEPs in contralateral parietal leads contained a widespread N20 with a maximum source posterior to the Cz-ear line. The following P25 enveloped two subcomponents - early and late P25 - having different distributions. The late P25 showed a maximum - coincident with that of wave N20 - which was localized more posteriorly than that of the early P25. An inconstant wave N33 with progressively longer peak latencies from sagittal toward lateral positions was then recorded. MN-SEPs in contralateral central positions showed a well-localized P22 wave in which both the parietal early P25 and the frontal P20 were vanishing. Common or separate generators for frontal, central and parietal SEPs were discriminated by evaluating the influence of stimulus rate and intensity, as well as of general anesthesia and transient CBF deficits, investigated in 7 patients undergoing carotid endarterectomy. Unifocal anodal threshold shocks were separately delivered to each of the scalp electrodes and motor action potentials were recorded from the target muscle in order to delineate the scalp representation of the motor strip for the upper limb and, consequently, to monitor, through SEP tracings, the short-latency sensory input to the motor cortex for hand and shoulder muscles. This was characterized by a boundary zone separating the parietal N20-early P25 complex, from the fronto-central N18-P22 one. This zone had an oblique direction strongly resembling that of the central sulcus.     

Cortical and subcortical somatosensory evoked potentials to median nerve stimulation in man

In order to define the precise locations of precentral and postcentral gyri during neurosurgical operations, somatosensory evoked potentials to contralateral median nerve stimulation were recorded from the cerebral cortex in 19 cases with organic cerebral lesions which located near the central sulcus. In addition to that, distribution patterns of early components of SEPs were displayed by Nihonkoden Atac 450 in 3 cases who had bone defects after wide decompressive craniectomy but were without any sensory disturbances In 4 cases, in whom deep electrodes were inserted for the stereotaxic operations or other reasons, frontal subcortical SEPs were recorded in order to know the origins of frontal components of SEPs. From the parietal cortex, N19, P22 and P23 were observed. And from the frontal cortex, P20 and N25 were obtained. Their average peak latencies were as follows; (table; see text) Because all subjects had organic lesion in the brain, the peak latencies were a little bit longer, and their standard deviations were larger than those in normal cases. Usually, clear-cut phase reversal could be observed between N19 and P20 across the central sulcus. So, the precentral and postcentral gyri were easily identified during the operations. N19 and P23 appeared over the wide areas of the parietal cortex. Also, P20 and N25 were recorded almost whole areas of the frontal cortex. On the other hand, P22 appeared from relatively restricted part of the postcentral gyrus where sensory hand area might have been located. Depth recording from the frontal subcortical area revealed that P20 could be recorded from the bilateral frontal subcortical areas and there observed no phase reversal between the cortical and subcortical SEPs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Somatosensory evoked potentials in minor cerebral ischaemia: diagnostic significance and changes in serial records

Frontal, central and parietal short and middle latency somatosensory evoked potentials (SEPs) arising after stimulation of the contralateral median nerve were studied in 10 normal adults. Stable SEPs were recorded: a frontal P21-N30 complex and an N20-P23-P28-N35-P42 complex in the centro-parietal region. The use of a chin reference electrode allowed identification of (the thalamic) P15 and N18. SEP studies of 20 patients with unilateral cerebral ischaemia were also performed, about 4 and 18 days after the stroke. In 13 out of 18 patients with a minor stroke (TIA, RIND and PNS) abnormalities of the frontal and/or parietal SEPs were demonstrated. Improvement in these SEPs occurred in 5 cases. In two patients who suffered from a major ischaemic deficit, the SEPs were highly abnormal and did not show any change in the course of time. SEP studies may be useful for the diagnosis of minor cerebral ischaemia as well as quantification of recovery; an even more important indication for this neurophysiological method might be detection of subclinical lesions in patients who have suffered from transient cerebral ischaemia even weeks before the SEP studies are carried out.     

"Gating" of human short-latency somatosensory evoked cortical responses during execution of movement. A high resolution electroencephalography study.

The present study aimed at investigating gating of median nerve somatosensory evoked cortical responses (SECRs), estimated during executed continuous complex ipsilateral and contralateral sequential finger movements. SECRs were modeled with an advanced high resolution electroencephalography technology that dramatically improved spatial details of the scalp recorded somatosensory evoked potentials. Integration with magnetic resonance brain images allowed us to localize different SECRs within cortical areas. The working hypothesis was that the gating effects were time varying and could differently influence SECRs. Maximum statistically significant (p<0. 01) time-varying gating (magnitude reduction) of the short-latency SECRs modeled in the contralateral primary motor and somatosensory and supplementary motor areas was computed during the executed ipsilateral movement. The gating effects were stronger on the modeled SECRs peaking 30-45 ms (N30-P30, N32, P45-N45) than 20-26 ms (P20-N20, P22, N26) post-stimulus. Furthermore, the modeled SECRs peaking 30 ms post-stimulus (N30-P30) were significantly increased in magnitude during the executed contralateral movement. These results may delineate a distributed cortical sensorimotor system responsible for the gating effects on SECRs. This system would be able to modulate activity of SECR generators, based on the integration of afferent somatosensory inputs from the stimulated nerve with outputs related to the movement execution.     

Movement-related cortical potentials in writer's cramp

Movement-related cortical potentials in response to simple, self-paced, brisk index finger abduction movements were recorded in patients with simple and complex writer's cramp and compared with those of age-matched control subjects. Analysis of the movement-related cortical potential waveforms showed that the Bereitschaftspotential, the peak of the negative slope, and the frontal peak of the motor potential did not differ in the two groups, except for the average amplitude of the early part of the negative-slope peak, which was decreased in the patient group during the interval of 300 to 200 msec prior to electromyographic onset. This finding was restricted to the electrodes overlying the contralateral and midline central electrodes. Movement-related cortical potentials from patients and control subjects could be equally accounted for by a four-dipole source model with sources located in the contralateral and ipsilateral sensorimotor regions and the supplementary motor area. There was a trend for a reduction in the strength of the sensorimotor sources active during the premotor period in the patient group, but the difference did not reach a significant level for any individual source. No differences were found between the movement-related cortical potentials elicited by movements of the affected and unaffected hand, or between those of patients with simple or complex hand cramps. This result suggests a deficiency of contralateral motor cortex activation just prior to the initiation of voluntary movements in patients with focal dystonia.     

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.     

Crossed inhibition of sensory cortex by 0.3 Hz transcranial magnetic stimulation of motor cortex.

Low-frequency repetitive transcranial magnetic stimulation (rTMS) of motor cortex causes persistent inhibitory effects in the targeted area. rTMS of motor cortex impairs sensory perception and results in a persistent change in cortical function at remote sites. The ability of rTMS to induce sustained changes in cortical function has led to studies testing its therapeutic efficacy in neurologic disorders, including epilepsy. Studies on the effect of low-frequency rTMS of motor cortex on the contralateral motor cortex have provided evidence for both inhibitory and excitatory changes. This study was designed to determine the effect of low-frequency rTMS of the right motor cortex on the contralateral sensory cortex. Before and after 0.3-Hz rTMS of right motor cortex, perception of ipsilateral threshold of cutaneous stimuli was assessed and somatosensory evoked potentials (SEPs) recorded after stimulation of the right thumb in eight normal subjects. In a control group of six subjects, sensory responses were assessed after rTMS anterior to the right motor cortex. After rTMS of motor cortex, detection of threshold sensory stimuli decreased by more than 50% compared with pre-rTMS (P < 0.05). The change in sensory perception lasted at least 30 minutes. No change was detected in the control group. Amplitude of the N20-P25 waveform of the SEP decreased from a mean of 0.84 muV before rTMS to 0.54 muV immediately after rTMS of motor cortex (P < 0.05). 0.3 Hz rTMS of motor cortex inhibits the contralateral sensory cortex.     

Methyl bromide myoclonus: an electrophysiological study

We report a case of myoclonus from overnight exposure to methyl bromide. Myoclonus was either spontaneous or induced by somatosensory stimulation or voluntary movements, multifocal and sometimes generalized. Median SEP showed normal size P14-N20, but giant parietal P25, N33 and frontal P22-N30 waves. Back-averaging showed a biphasic EEG spike of maximal amplitude at the central region contralateral to the corresponding myoclonic jerk recorded from abductor pollicis brevis and preceding it by a short interval consistent with conduction in corticospinal pathways. Long latency reflexes from cutaneous and mixed nerve stimulation were enhanced. The above electrophysiological findings suggest that myoclonus following methyl bromide poisoning belongs to the cortical reflex myoclonus category.