Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Sensorimotor Cortex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,639 records · Page 91Linked to original sources
PubMed1987

Cerebral magnetic responses to stimulation of ulnar and median nerves.

We have compared spatial patterns of somatosensory evoked magnetic fields (SEFs) to stimulation of the ulnar and median nerves at the wrist. An oddball paradigm was used additionally to examine whether an infrequent change in the stimulation site would alter the field pattern. The response consisted of 3 parts: an early small deflection at 22-28 msec, a large deflection peaking between 34 and 86 msec, and a late deflection at 110-180 msec. The wave forms and amplitudes of the responses to ulnar and median nerve stimulation were similar, without any additional deflections for the infrequent stimuli. The field patterns, which were interpreted in terms of the dipole model, could be explained by activation of the primary sensorimotor cortex during all peaks of the response. For the early parts of the response at 22-46 msec, the locations of the equivalent sources for median and ulnar nerve stimulation differed from each other, in agreement with the known somatotopy of SI. No somatotopical order was found for the sources of the later deflections.

Adult↗
PubMed1988

Motor and somatosensory evoked potentials recorded from the rat.

An accurate neurophysiological technique that is able to monitor both the sensory and motor tracts of the spinal cord is required to assess patients with injury or other lesions of the cord, and for the evaluation of experimental studies of cord injury. We have recorded and characterized the motor and somatosensory evoked potentials (MEPs and SSEPs) from 20 normal rats and from 16 rats with cord lesions. MEPs were elicited by applying constant current anodal stimuli to the sensorimotor cortex (SMC) with the responses recorded from microelectrodes in the spinal cord at T10 (MEP-C) and from a bipolar electrode placed on the contralateral sciatic nerve (MEP-N). SSEPs were elicited by stimulating the sciatic nerve and were recorded from the cord at T10 and the contralateral SMC. The MEP-C consisted of an initial D wave (mean latency 1.21 +/- 0.12 msec and 4 subsequent I waves, 11-14). The D wave was elicited at stimulation frequencies exceeding 100 Hz. The initial positive wave of the MEP-N (mean latency 3.09 +/- 0.19 msec) was followed by several slower components which were attenuated by repetition rates exceeding 8.2 Hz. The grand mean SSEP consisted of 7 peaks. Sectioning of the dorsal columns abolished the SSEP but spared the MEP. Complete cord transection abolished both the MEP and SSEP. These experiments demonstrate that the combined recording of MEPs and SSEPs is an accurate and easily performed method of monitoring the functional integrity of the rat cord, and suggest that this technique would be of value in patients, especially those undergoing operative treatment of spinal lesions.

Animals↗
PubMed1991

Myoclonic epilepsy in an HIV positive patient: neurophysiological findings.

An HIV-positive patient is described who presented with action myoclonus. Unusually, focal sinusoidal EEG burst complexes with a frequency of 40 and 55 Hz could be recorded over the sensorimotor cortex. Activity having a similar frequency was evoked in this area by posterior tibial nerve stimulation in the affected leg, and jerk-locked averaging showed that myoclonic jerks were preceded by similar cortical sinusoidal waves.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Spatiotemporal modeling of cerebral evoked magnetic fields to median nerve stimulation.

We measured somatosensory evoked magnetic fields during median nerve stimulation in 6 normal subjects. We applied multiple dipole models to study the spatiotemporal structure of early somatosensory evoked magnetic fields (SEFs), as well as the number, 3-dimensional location and time activity of their underlying neuronal sources. Two dipole sources were necessary to model the first 40 msec of SEFs explaining 85% of the data variance. Source 1 was located deeper than source 2, showed primarily a tangential orientation, and accounted for a larger part of the variance; source 2 showed no consistent orientation across subjects. Both sources showed biphasic time activities corresponding to the previously described N20-P30 and P25-N35 components. Spatiotemporal modeling could identify sources which could not be modeled consistently above noise by single moving dipoles (P25 component), revealed small latency differences of the two sources in some subjects suggesting parallel activation of these sources, and allowed separation of sources overlapping considerably both in space and time. We conclude that spatiotemporal modeling of SEFs may be useful to study functional anatomy of human sensorimotor cortex non-invasively.

Electric Stimulation↗
PubMed1992

Cortical somatosensory magnetic responses in multiple sclerosis.

Somatosensory evoked magnetic fields (SEFs) to contralateral median and ulnar nerve stimulation were analyzed in 10 patients with multiple sclerosis and in 8 healthy controls. SEFs were recorded with a 24-channel SQUID gradiometer over both hemispheres. Seven patients showed abnormally large-amplitude SEF deflections at 60-80 msec; 5 of them had multiple lesions around lateral ventricles in magnetic resonance imaging. In 2 patients with plaques at the level of 3rd and 4th ventricles and medulla, the 30 msec responses were enlarged. The equivalent sources of 20 msec and 30-80 msec responses were in the primary hand sensorimotor cortex both in patients and in control subjects. The results suggest that early and middle-latency SEFs reflect parallel processing of somatosensory input. Recording of middle-latency evoked responses, electric or magnetic, may give additional information about the somatosensory function in multiple sclerosis.

Adult↗
PubMed1993

Source analysis of scalp-recorded movement-related electrical potentials.

We used brain electric source analysis to study the sources generating the movement-related cortical potentials during the interval from 200 msec before to 200 msec after the movement onset. Dipole solutions were obtained for the peak of the negative slope (pNS') and the frontal peak of the motor potential (fpMP) on scalp-recorded movement-related electrical potentials elicited by self-paced, repetitive unilateral finger movements in 10 normal volunteers. Two sources in homologous areas on each side of a spherical head model provided a satisfactory solution for the activity occurring at the instant of the pNS' in all subjects. The fpMP was modeled by a contralateral source and a midline source in 6 subjects and by a single contralateral source in the remaining 4 subjects. The percentage of the residual variance, or goodness-of-fit, over the interval from -200 to 200 msec, using the derived at pNS' and fpMP, was low. The results support the hypothesis that the NS' originates from the activity of bilateral generators in the sensorimotor cortex, and the motor potential arises from the combined activity of sources in the contralateral postcentral regions and the supplementary motor area.

Adult↗
PubMed1980

Effect of L-cycloserine on cortical neurons in the rat.

L-Cycloserine but not D-cycloserine, depressed the firing of neurons in the sensorimotor cortex of the rat with a relatively slow time course when administered by microionophoresis or i.p. injection. The effects of GABA applied by microionophoresis or released synaptically were not modified by i.p. injections and microionophoretic administration of L-cycloserine. It is concluded that L-cycloserine depresses cell firing not by potentiation of the action of GABA but by elevating GABA-levels.

Animals↗
PubMed1986

Effects of the indirect dopaminomimetic diethylpemoline on local cerebral glucose utilization and local cerebral blood flow in the conscious rat.

The changes in local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) following the systemic application of the indirect dopaminomimetic diethylpemoline (50 mg/kg i.v.) were measured in conscious rats using the autoradiographic [14C]2-deoxyglucose and the [14C] iodoantipyrine technique. Increased rates of glucose utilization were observed in the sensorimotor cortex, parafascicular nucleus, ventrolateral nucleus of the thalamus, substantia nigra, caudate nucleus, globus pallidus, red nucleus, subthalamic nucleus, cerebellar cortex and vermis. Cingulate cortex, anteromedial, anteroventral nucleus of the thalamus, habenula and nucleus accumbens showed a decreased LCGU. The determination of LCBF revealed a similar pattern of altered blood flow values. Statistical evaluation of the relationship between glucose utilization and blood flow by regression analysis did not reveal any distinguishable difference between diethylpemoline-treated rats and controls. The data suggest that it is mainly the altered neuronal activity and metabolic demand after dopaminergic stimulation that effect the changes in blood flow rather than a direct dopaminergic effect on brain vasculature.

Animals↗
PubMed1991

Effects of intracisternal endothelin-1 injection on blood flow to the lower brain stem.

The central effects of endothelin-1 (Et-1, 10-30 pmol in 2.5 microliters injected intracisternally) have been investigated in the conscious rat. With 10 and 20 pmol Et-1, no significant change in blood pressure was observed. With 30 pmol Et-1, mean arterial blood pressure rose by 40 +/- 10 mm Hg with an accompanying modest, short-lived bradycardia at 2 min post-injection. Cerebral blood flow [( 14C]iodoantipyrine autoradiography), measured simultaneously with the hypertensive response, was markedly reduced throughout the caudal medulla and cerebellum (by up to 85%), while significant hyperaemia was evident in a number of forebrain structures (e.g. an increase of 78% in sensorimotor cortex). These observations have relevance to two distinct scientific areas. Concerning the significant effect of Et-1 in central cardiovascular control, these results caution against drawing conclusions from ventricular application with knowledge only of cardiovascular parameters. These results also illustrate the profound effects of Et-1 which is uniquely capable of overriding cerebral autoregulatory mechanisms.

Animals↗
PubMed1992

Increased acetylcholine and quisqualate responsiveness after blockade of GABAB receptors.

The aim of this study was to gain further insight into the function of cortical GABAB receptors. In chloral hydrate-anaesthetized rats, microiontophoretic administration of the GABAB receptor blocker CGP 35348 induced a moderate increase in firing of spontaneously active neurons in the rostral and caudal sensorimotor cortex. This increase in cell firing was accompanied by a reduction in the baclofen-induced inhibition of cell activity. In contrast to the GABAA receptor antagonist bicuculline methiodide, CGP 35348 did not induce any paroxysmal discharges. The excitatory responses of rostral cortical neurons elicited by iontophoretically applied acetylcholine and quisqualate were potentiated in most neurons after both microiontophoretic and intravenous administration of CGP 35348. The potentiation was observed in the absence of any change in the spontaneous firing rate. These effects were dose-dependent for both routes of administration. The potentiation of the quisqualate response was reversed by intravenously applied baclofen. In conclusion, these findings suggest that cortical GABAB receptors are involved in the control of cortical neuronal excitability.

Acetylcholine↗
PubMed1986

Histopathologic evaluation of prolonged intracortical electrical stimulation.

Chronic stimulating microelectrodes fabricated from platinum-30% iridium (Pt-30%Ir) or activated iridium were implanted in assemblies of three in the left sensorimotor cortex of the cat and pulsed continuously at currents of 10 to 320 microA (100 to 3200 microC/cm2 X ph, 2 to 64 nC/ph) for periods of 24 h or for 23 h/day for 7 days. The microelectrodes had beveled tips with uninsulated geometric surface areas of 20 X 10(-6) cm2. Neuronal activity evoked by the focal stimulation was monitored by recording compound action potentials from the ipsilateral pyramidal tract. By this criterion neuronal activation thresholds were 5 to 15 microA (50 to 150 microC/cm2 X ph, 1 to 3 nC/ph) for both types of electrodes. Histologic evaluations of tissue surrounding the electrode tips were carried out by either light or electron microscopy. No neural damage was induced by 24 or 161 h of pulsing using either type of electrode at currents of 10 to 80 microA. Neural damage attributable to electrical stimulation per se was observed in a few sites pulsed with 320 microA (3200 microC/cm2 X ph, 64 nC/ph, 16 A/cm2) with Pt-30%Ir but not activated iridium electrodes of the same size. Electrode dissolution appears to be best correlated with charge density and current density. Dissolution of the Pt-30%Ir microelectrode tip was observed by scanning electron microscopy at charge densities as low as 200 microC/cm2 X ph (1 A/cm2), whereas erosion of activated iridium microelectrodes occurred only at the highest charge and current densities (3200 microC/cm2 X ph, 16 A/cm2). Thus, the activated iridium electrode is superior to Pt-30%Ir for chronic stimulations, from the standpoint of electrode tip stability, because with the former, in contrast to the alloy, detectable erosion occurred only at an intensity well above that required for activation of nearby neurons.

Animals↗
PubMed1987

Epispinal stimulation of the spinal cord: a proposed method of operative monitoring.

By monitoring spinal cord function during surgical procedures in and around the spinal cord, vital information can be obtained regarding the integrity of this structure. However, the techniques currently used have several limitations. This paper describes a system of monitoring in the cat, whereby, using electrodes placed outside the spine for stimulation of the cord, reproducible responses can be recorded from a midline electrode tapped into the calvarium overlying the sensorimotor cortex. The levels of activation of the spinal cord achieved by direct stimulation of the cord through epidural electrodes and by the epispinal method were found to be similar. By studying the effects of various lesions on the epispinal evoked response, components in the recorded response were identified that were carried in all three funiculi of the cord; the changes produced by these lesions in the epispinal evoked response were immediate. In addition, the sensitivities of the epispinal evoked response and of the somatosensory evoked response to the lesions were compared. When the dorsal blood supply was interrupted, it became evident that, unlike the somatosensory evoked response, which monitors only the dorsal blood supply, the epispinal evoked response monitors both the dorsal and ventral blood supply. By evaluating the recorded response obtained using this method of monitoring, it was possible to identify the particular quadrant of spinal cord injury.

Animals↗
PubMed1987

Changes of activity of cortical neurons induced by acetylcholine in adult and young rats.

Acetylcholine was applied microiontophoretically by means of multibarrel electrodes to neurons in the sensorimotor cortex of adult, 18-, 15-, 12-, and 9-day-old rats anesthetized with urethane. A total of 229 neurons was recorded; only 22 of them were in 18- and 15-day-old rats because of similarity of results with those from adult as well as 12-day-old animals. In adult rats 43 of 58 neurons recorded in infragranular layers responded to acetylcholine with a marked increase in their firing. In 12-day-old rats the incidence of excitatory responses to acetylcholine was also high: 59 of 86 cells again were localized predominantly in deep cortical layers (V and VI). A marked difference was observed in 9-day-old rats: only 15 of 63 neurons were excited by acetylcholine. A majority of cells did not respond at all--including units localized in infragranular layers. Two cells in layer V responded to acetylcholine by an inhibition. Our results indicate that there is a marked increase in cholinoceptivity of cortical neurons between postnatal days 9 and 12. This finding is in agreement with the finding that local application of acetylcholine can elicit an epileptogenic focus in 12-day but not in 9-day-old rat pups.

Acetylcholine↗
PubMed1988

Naloxone facilitates sensory precipitation of focal and generalized seizures: evoked potentials and power spectral analysis in the cat.

To analyze the role of endogenous opioids on epileptogenesis the effect of repeated doses of naloxone alone (NA) (2, 4, and 8 mg/kg every 15 min) or along with intermittent photic stimulation (NPS) (1, 3, and 10 Hz) was tested on acute "Encephale isolé" cats. The electrical activity recordings of sensorimotor cortex (SMC), visual cortex, and right and left amygdalae revealed progressive changes as naloxone was administered: (A) slow spindle activity (4-6 Hz) in SMC, (B) 12 Hz rhythmic activity in both amygdalae, (C) generalized paroxysms, and (D) spontaneous tonic-clonic electrographic seizures. These changes occurred in both experimental groups (NA, NPS), and their onset was dose-related. Photic stimulation precipitated these phenomena. The amplitude of the visual evoked potential components (N1-P1, P1-N2, N2-P2) and power spectral analysis of spontaneous and evoked activity underwent progressive changes. Our results confirm a facilitatory effect of naloxone on epileptogenesis and suggest a possible role of endogenous opioids in this process and on sensory pathways' excitability.

Amygdala↗
PubMed1987

Cerebral magnetic responses to stimulation of tibial and sural nerves.

We report somatosensory evoked magnetic fields (SEFs) to stimulation of the mixed posterior tibial nerve (PTN) and the sensory sural nerve (SN) in 6 healthy subjects. The first peak of the responses occurred at 39-50 ms (P40m), with a 2-3 ms longer latency for SN than PTN stimulation. Within 200 ms several other deflections followed, with interindividually varying waveforms and latencies. Magnetic field mappings indicated that the source of P40m for PTN can be modelled by a single equivalent current dipole at the primary sensorimotor cortex; for the smaller responses to SN stimulation the single dipole model was less applicable. Field patterns for later deflections differed from those of P40m, indicating that several current sources within or near the primary foot projection area are sequentially activated after stimulation of both a mixed and a sensory lower limb nerve. These late deflections could not always be satisfactorily explained by single current dipoles, suggesting more complex geometries for the underlying neural activity.

Adult↗
PubMed1991

Influence of stimulus repetition rate on cortical somatosensory potentials evoked by median nerve stimulation: implications for generation mechanisms.

Despite growing clinical and experimental interest in the cortical components of somatosensory evoked potentials (SEPs) little is known about their physiological dynamics, e.g. with changing stimulation parameters. This paper reports the influence of varying stimulus repetition rate from 0.5 to 5 Hz on cortical SEPs up to 60-msec latency after right median nerve stimulation, separately analyzed at frontal (F3), central (C3) and parietal (P3) electrodes. The amplitudes of early frontal P20 and N25, central P14 and N18, and parietal N20 did not change with stimulation rate. Later deflections were significantly modified when their amplitudes were determined with respect to the baseline: at F3 negative N30 and N60 diminished and positive P40 was enhanced with increasing rate of stimulation. At P3 the effects were the reverse, so that positive P27 and P45 were attenuated while negative N34 and N60 were enhanced. At C3 both positive P22 and P40 and negative N60 were reduced. However, the corresponding peak-to-peak amplitudes changed much less. We conclude that SEP waveforms following the earliest cortical deflections are very sensitive to small changes in stimulation frequency. The opposite changes at F3 compared with P3 probably represent the opposite scalp field poles from horizontally oriented generator(s) located within the primary sensorimotor cortex (SMI). We suggest that the rate effects are partly due to selective sensitivity of postexcitatory inhibitory postsynaptic potentials to stimulation frequency.

Adult↗
PubMed1982

Convulsant and anticonvulsant effects of opioids: relationship to GABA-mediated transmission.

The convulsant benzodiazepine Ro 5-3663, bicuculline and picrotoxin induced electroencephalographic (EEG) and behavioural convulsions. In rabbits, the EEG modifications consisted, with increasing doses, of three different patterns: slow waves in the optic lead, spike- and wave-complexes in the sensorimotor cortex, and grand-mal generalized seizures. These EEG effects were terminated by administration of diazepam (1 mg/kg) and morphine (0.25-1.0 mg/kg). Naloxone, in doses of 5-10 mg/kg, potentiated the effects of the three convulsant drugs. This potentiating phenomenon was also antagonized by the administration of diazepam and morphine. In membrane preparations, obtained from rat cortex, deprived of endogenous modulators of [3H]GABA binding, naloxone but not morphine, was able to inhibit [3H]GABA binding to its specific recognition sites. These data agree with previous findings indicating a GABA-antagonistic effect of naloxone, and support the hypothesis that the anticonvulsant effect of morphine might be, at least in part, due to an increase in GABAergic activity at the synaptic level.

Animals↗
PubMed1983

Effect of diphenylhydantoin on unit activity in a cortical epileptogenic focus in the rat.

The correlation between discharges of a penicillin focus and unit activity was studied in the sensorimotor cortex of 30 adult male curarized rats under urethane anaesthesia. Among 43 units, three types of activity could be differentiated: (1) units without any relationship to focal discharges (7% of neurones); (2) units with a biphasic reaction, a burst of spikes during the main negative deflection of the focal discharge followed by a period of inhibition (72%); (3) units inhibited during the whole duration of the focal discharge (21%). The effects of diphenylhydantoin (60 mg/kg i.p.) were studied on 35 units--20 of them were also recorded before administration of diphenylhydantoin and thus included in the above group. Diphenylhydantoin led to decreased representation in groups (1) and (2), whereas the percentage of units inhibited during the focal discharge was increased from 21 to 31%. A decrease in number of spikes in the excitatory burst and/or the prolongation of the inhibitory phase was a consequence of diphenylhydantoin administration in 18 out of 20 neurones with long-lasting recording. A direct action of diphenylhydantoin on the primary epileptogenic focus was thus demonstrated.

Animals↗