Differential gating of slow postsynaptic and high-frequency spike-like components in human somatosensory evoked potentials under isometric motor interference.

Human cortical somatosensory evoked potentials (SEP) can be modified by concomitant motor tasks ('gating'), through peripheral occlusion and/or central mechanisms. The present study aimed (1) at refining earlier results concerning motor-gating of the primary cortical EPSP-related N20 response after electric median nerve stimulation, and (2) at providing first data on motor-gating of the 600 Hz SEP wavelet burst which occurs superimposed onto N20 and primarily reflects repetitive cerebral population spikes. In 12 healthy subjects median nerve SEP were elicited, using electrical stimuli with intensities below, at and above motor threshold, under either rest or an isometric fist clenching task. Amplitude and latency modifications were analysed for the peripheral compound action potential (CAP), low-frequency SEP components (N20, P25, N35 and P70) and the high-frequency burst. While the peripheral CAP remained unchanged, isometric motor innervation significantly attenuated N20, P25 and P70 amplitudes and shortened peak latencies progressively for all components after N20. In contrast, the high-frequency 600 Hz burst was modulated neither in amplitude nor in latency. Regular amplitude recruitment occurred for all components independent from the motor task, excluding channel saturation as an explanation for gating. We suggest that SEP gating under isometric motor innervation is a central process which selectively operates on specific SEP components and could partly reflect an "efference copy" mechanism.

Propofol narcosis dissociates human intrathalamic and cortical high-frequency (> 400 hz) SEP components.

Human somatosensory evoked potentials (SEP) contain a brief burst of high-frequency wavelets (>400 Hz) presumably reflecting rapidly repeated population spikes of as-yet undetermined origin. To study state-dependent response changes, SEP after electric median nerve stimulation were recorded in six Parkinson's disease patients perioperatively from intrathalamic electrode implants, and in five non-implanted patients from scalp electrodes, before and under propofol narcosis. In all intrathalamic recordings burst amplitude and intraburst frequency (approximately 950 Hz) proved to be almost stable under propofol administration. In strong contrast, the scalp burst (640 Hz) was significantly slowed (480 Hz) under propofol narcosis, and its amplitude reduced to 28% of the pre-propofol baseline. Low-frequency SEP components which underly the burst at thalamic (P16) and cortical level (N20) did not change significantly. This dissociation of bursts indicates neuronal generators showing different sensitivities to propofol narcosis, with a robust thalamic response and a state-dependent cortical contribution, possibly from pyramidal chattering cells and/or inhibitory interneurons.

Double-pulse stimulation dissociates intrathalamic and cortical high-frequency (>400Hz) SEP components in man.

Human somatosensory evoked potentials (SEP) contain high-frequency (600 Hz) wavelet bursts possibly reflecting repetitive population spikes in thalamocortical axons and/or postsynaptic responses. To dissociate thalamic and cortical burst components the recovery of intrathalamic SEP (derived from electrodes implanted for movement disorder therapy in seven patients) was compared with scalp SEP in six age-matched Parkinsonian patients and six healthy younger subjects. Upon electric median nerve double-pulse stimulation conditioned scalp bursts were found attenuated in both groups, more for 10ms than 20ms interstimulus intervals; moreover, intraburst frequencies decreased from 690Hz to 590Hz. By contrast, intrathalamic burst amplitudes and frequencies (around 1 kHz) remained largely stable. These dissociations indicate functionally distinct generator mechanisms for scalp and intrathalamic high-frequency SEP bursts.

Changes of forearm EMG and cerebral evoked potentials following sudden muscle stretch in patients with Huntington's disease.

Various investigators have reported that the late-reflex electromyographic (EMG) activity following muscle stretch is decreased in Huntington's disease. To explore the basis of this decreased activity, we recorded the late EMG responses together with associated cerebral responses following muscle stretch in patients with Huntington's disease. Five patients and seven controls voluntarily participated in two sets of experiments in which they grasped a handle attached to a torque motor and maintained the wrist isometrically against a constant flexor force of 2.3 newtons (N). The force was changed unpredictably (first set of experiments) or predictably (second set) to 10.4 N, causing a stretch of wrist extensors or flexors. Rectified surface EMG from the extensor and flexor carpi radialis muscles was integrated for the M2 and M3 components of the late responses. Cerebral responses were recorded from F3, F4, C3, C4, and Cz and averaged separately depending upon condition. The late muscle responses to unpredictable muscle stretch were decreased or absent in patients with Huntington's disease. The cerebral responses recorded at Cz differed markedly between patients and controls, beginning approximately 15 ms prior to the onset of the late M2 muscle response. Although the initial positivity was similar in amplitude, all other cerebral components were markedly reduced in the patient group. Both controls and patients showed a markedly attenuated cerebral response when the muscle stretch was predictable. The electrocerebral response to muscle stretch is thus altered prior to the onset of M2 in patients with Huntington's disease, suggesting that the long-latency reflex involves transcerebral pathways that are affected in this disease.

Central apnea and acute cardiac ischemia in a sheep model of epileptic sudden death.

The etiology of sudden death in patients with epilepsy remains unclear. Previous studies in a well-established sheep model of status epilepticus showed that more than one-third of the unsedated animals died within 5 minutes of seizure onset due to hypoventilation. The relative contributions of airway obstruction and central hypoventilation could not be determined because airway flow and respiratory effort were not monitored. In this study, status epilepticus was induced in unsedated sheep with tracheostomies monitored by electrocardiography, electroencephalography, arterial line, serial blood gases, and airway flowmeter. All 8 animals demonstrated central apnea and hypoventilation, which resulted in the death of 1 and contributed to the death of another. A third animal died of acute heart failure within 2 minutes of seizure onset, accompanied by a large septal myocardial hemorrhage, contraction bands, and signs of global cardiac ischemia. More subtle contraction bands, subendocardial hemorrhage, and signs of acute myocardial ischemia were seen in other animals as well, none of which died of cardiac causes. Malignant arrhythmia was not seen in any of the sheep. Central hypoventilation and apnea accompany generalized status epilepticus and may be an important cause of sudden death in epileptics. Acute cardiac failure may also be a cause of epileptic sudden death.

Changes of forearm EMG and cerebral evoked potentials following sudden muscle stretch during isometric contractions in patients with Parkinson's disease.

Various investigators have reported that the late reflex EMG activity following muscle stretch is increased in patients with Parkinson's disease. To explore the basis of this increased activity, we have now recorded the late EMG responses together with associated cerebral responses following muscle stretch in parkinsonian patients. Nine patients and eight controls participated in two sets of experiments in which they grasped a handle attached to a torque motor and maintained the wrist isometrically against a constant flexor force. The force was changed unpredictably (first set) or predictably (second set of experiments), causing a stretch of wrist extensors or flexors. Cerebral responses and muscle responses from the forearm were recorded and averaged separately depending upon condition. The late muscle responses to unpredictable muscle stretch were enhanced in parkinsonian patients while the cerebral responses were attenuated when compared to controls. The alteration of the electrocerebral response began approx. 25 ms prior to the late M2 muscle response. Both controls and patients showed a markedly attenuated cerebral response when the muscle stretch was predictable. These results indicate that the electrocerebral response to muscle stretch is altered prior to the onset of M2 in patients with Parkinson's disease, and suggest that these cerebral events reflect components of a long-latency transcerebral reflex pathway that is affected in this disorder.

Comparison of late components in simultaneously recorded event-related electrical potentials and event-related magnetic fields.

We have attempted to define the late components of the event-related magnetic field (ERF) and to relate them to the late components of the event-related electrical potential (ERP). Simultaneous multichannel electroencephalogram (EEG) and magnetoencephalogram (MEG) were recorded in 13 subjects during an auditory oddball paradigm in two series of experiments. EEG responses to frequent tones consisted of the N1 and P2 components of the auditory vertex potential. Responses to rare tones consisted of N1, apparent P2, N2 and P3 components. All EEG components were best seen in the midline and were highly reproducible for all subjects. MEG responses to frequent tones consisted of N1m and P2m components that were highly reproducible only when recorded over the temporal region. By contrast, the ERF to rare tones was less well defined and only the N1m component could be identified satisfactorily. There was little consistent activity in the MEG at the time of occurrence of the N2 and P3 components of the ERP.

Laser-evoked potentials: exogenous and endogenous components.

The aim of this study was to distinguish the exogenous component (related to the physical properties of the stimulus) and the endogenous component (reflecting event-related cognitive processing) of the laser-evoked potential (LEP). Short painful radiant heat pulses generated by a CO2-laser were applied to the dorsum of the right and left foot. LEPs were recorded with 5 scalp electrodes in the midline versus linked earlobes in 26 healthy subjects. In order to identify the exogenous component, the LEP was recorded during a standardised distraction task (reading a short story). To identify the endogenous component P3 for the LEP, a 2-stimulus oddball paradigm was used (20% probability of targets). When the task of the oddball paradigm consisted of pressing a button, a movement-related long-latency negativity (N 1200) was recorded in frontal leads that was absent in a counting task. The LEP of targets, frequent non-targets and during distraction was dominated by a single large positivity. The amplitude of this positivity was task-dependent and increased the more attention the subject payed to the laser stimuli (distraction < neutral < non-target < target). The laser-evoked positivity during distraction had a peak latency of about 400 msec (P400) and a maximum amplitude at the vertex, which was independent of inter-stimulus interval. The P3 following laser stimulation had a significantly later peak at about 570 msec (P570) and a different scalp topography with a parietal maximum. Its amplitude decreased when the interstimulus interval was reduced from 10 to 6 sec. Under neutral instructions, the LEP positivity consisted of a superposition of both the exogenous P 400 and the endogenous P570.