SEARCH · PubMed Health

Results for “Motor Cortex”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 469 records · Page 26Linked to original sources

PubMed1997

[Motor cortex stimulation therapy in patients with thalamic pain].

Seven patients with thalamic pain were treated by electrical stimulation of the motor cortex. Patients ranged from 55 to 71 years of age. There were six men and one woman. Causes of thalamic pain were thalamic infarction in 2 patients and thalamic hemorrhage in five. Six patients had intractable pain associated with dysesthesia in the upper and lower limb (upper limb dominant). One patient had intractable pain in the face contralateral to the lesion. Magnetic resonance images (MRI) were performed in 5 patients and showed the deposit of hemosiderin in the internal capsule, posterolateral nucleus and pulvinar. Electrodes were placed on the motor cortex epidurally in seven patients. Electrodes were implanted permanently in six patients and removed in one patient after an unsatisfactory result of test stimulation. Motor cortex stimulation provided satisfactory pain relief in all six patients for a month after the beginning of stimulation, however, by the time three months had passed, pain relief had become gradually unsatisfactory in five patients. We compared pain relief between 10 Hz and 100 Hz of stimulus rate in four patients and observed that all patients complained of fatigue in the upper extremity at the 100 Hz of stimulus rate, though no differences in pain relief was obtained according to which of these two stimulus rates were used. We concluded that motor cortex stimulation brought about pain inhibition in patients with thalamic pain, but pain control tended to become less gradual within several months after the beginning of stimulation.

Aged↗

PubMed1988

[Functional interneuronal connections in the motor cortex of waking and anesthetized cats].

Neuronal interconnections in the motor cortex of alert and anesthetized cats were studied using the techniques of multiunit activity recording and cross-correlative histograms. The number of neuronal interconnections did not decrease in cortical microareas during the deepening of anesthesia, but their reconstruction and levelling of inputs and outputs of all microareas' cells occurred. During the reconstruction of interrelationships among functional microareas an activation occurred in the neurons which had been rather inert in the cortex of alert cats. The data obtained suggest differential participation of the cat motor cortex' neurons in information processing at the level of microareas.

Action Potentials↗

PubMed2002

Transcranial magnetic stimulation study of plastic changes of human motor cortex after repetitive simple muscle contractions.

Studies of use-dependent changes in neural activation have recently focused on the primary motor cortex. To detect the excitability changes in the primary motor cortex after practice in human subjects, motor-evoked potentials by transcranial magnetic stimulation during motor imagery after just 10 sessions of simple index finger abduction were examined. The present results indicate that width of the output map and amplitudes of motor-evoked potential became progressively larger until practice ended. These flexible short-term modulations of human primary motor cortex seem important and could lead to structural changes in the intracortical networks as the skill becomes more learned and automatic, i.e., 'adaptation' as one of the neural mechanisms related to motor learning.

Adult↗

PubMed2006

Partial tuning of motor cortex neurons to final posture in a free-moving paradigm.

Motor cortex neurons in the monkey brain were tested with a diverse and naturalistic arm movement set. Over this global set of movements, the neurons showed a limited but significant degree of tuning to the multijoint posture attained by the arm at the end of each movement. Further supporting the hypothesis that the neurons are partially tuned to end posture, the postures preferred by the neurons significantly matched the postures evoked by electrical stimulation of the same cortical sites. However, much of the variance in neuronal activity remained unexplained even by the end-posture model, and thus other variables must have contributed to the response profile of the neurons. One possibility is that motor cortex neurons become tuned to the wide variety of movement parameters that are relevant to the animal's normal behavioral repertoire, and, therefore, any one parameter accounts for only a limited amount of neuronal variance.

Animals↗

PubMed2004

Repetitive TMS of the motor cortex improves ipsilateral sequential simple finger movements.

BACKGROUND: Disruption of cortical function can improve behavior. Motor cortex (M1) transcallosal interactions are mainly inhibitory; after unilateral damage to M1, there is increased excitability of the unaffected M1. Repetitive transcranial magnetic stimulation (rTMS) of M1 produces a temporary reduction in cortical excitability in the same M1 that outlasts the duration of the rTMS train. The authors hypothesize that reducing cortical excitability of M1 by rTMS may improve motor performance in the ipsilateral hand by releasing the contralateral M1 from transcallosal inhibition. METHODS: Sixteen healthy volunteers participated. Using a sequential key-pressing task with the index finger, motor performance was monitored before and after rTMS (1 Hz for 10 minutes with the intensity below motor threshold) applied to the ipsilateral M1, contralateral M1, ipsilateral premotor area, or vertex (Cz). RESULTS: rTMS of M1 shortened execution time of the motor task with the ipsilateral hand without affecting performance with the contralateral hand. This effect outlasted rTMS by at least 10 minutes, was specific for M1 stimulation, and was associated with increased intracortical excitability in the unstimulated M1. CONCLUSIONS: The authors' results support the concept of an interhemispheric "rivalry." They demonstrate the utility of repetitive transcranial magnetic stimulation to explore the functional facilitation of the unstimulated counterpart motor cortex, presumably via suppression of activity in the stimulated motor cortex and transcallosal inhibition.

Adult↗

PubMed2003

Pain-related modulation of the human motor cortex.

Pain is a complex multi-dimensional phenomenon that influences a wide variety of nervous system functions, including sensory--discriminative, affective--motivational and cognitive--evaluative components. So far, these components have been studied in both patients with chronic pain and in normal subjects in whom pain was induced experimentally. The interaction between pain and motor function is not fully understood, although from everyday life it is known that pain affects movements. The effects of pain on motor control are typically seen as a limited or impaired ability to perform movements. Most studies have dealt with the effects of pain on the spinal cord reflexes, but in recent years, several lines of evidence suggest that the interaction between motor and pain systems in conditions of pain induced experimentally, rather than a simple spinal reflex, is a more complex process that involves also supraspinal brain areas. Although pain-motor interaction shows different features and time course depending on different pain variables, such as duration (tonic versus phasic pain), submodalities (deep versus superficial pain) and location (distal versus proximal pain), a common finding is that pain is able to inhibit the motor cortex. This motor cortex inhibition may act as a sort of motor 'decerebration' so as to allow the spinal motor system to freely develop protective responses to noxious stimulation. Further studies are required to assess the effects of pain on the motor system in patients suffering from chronic pain, in order to develop innovative rational therapeutic strategies to reduce both pain and motor disability.

Electric Stimulation↗

PubMed2005

Interactions between long latency afferent inhibition and interhemispheric inhibitions in the human motor cortex.

Various inhibitory pathways exist in the human brain which are crucial in modulating motor cortex output and they can be investigated non-invasively using transcranial magnetic stimulation. Interhemispheric inhibition (IHI) is one form of cortical inhibition. It can be elicited by stimulation of the opposite motor cortex at interstimulus intervals (ISIs) of 10 ms (IHI10) or 40 ms (IHI40) and inhibitions at these intervals are probably mediated by different mechanisms. Peripheral sensory stimulation can also inhibit the motor cortex. Median nerve stimulation produces long latency afferent inhibition (LAI) at ISI 200 ms. LAI inhibits another form of cortical inhibition known as long interval intracortical inhibition (LICI) and a study that examined the interaction between IHI10 and LICI hypothesized that they are mediated by an overlapping population of inhibitory neurones. We tested this hypothesis by examining the interaction between IHI10, IHI40 and LAI. With increasing test MEP amplitude LAI, IHI10 and IHI40 all decreased. There was no correlation between the strength of LAI, IHI10 and IHI40. In the presence of LAI, IHI10 was slightly but significantly reduced compared to IHI10 alone. There was no correlation between the reduction in IHI10 in the presence of LAI and the strength of LAI or IHI10. In the presence of LAI, IHI40 was significantly reduced compared to IHI40 alone. LAI produced a greater decrease in IHI40 than in IHI10. The decrease in IHI40 in the presence of LAI strongly correlated with the strength of LAI but not with the strength of IHI40. Reducing the strength of LAI, IHI10 and IHI40 still resulted in similar interaction between IHI10 and LAI but markedly decreased the effect of LAI on IHI40. We conclude that LAI and IHI10 do not directly inhibit each other but LAI probably inhibits IHI40. LICI is more likely to be related to IHI40 than to IHI10.

Adult↗

PubMed1992

Sensory characteristics of monkey thalamic and motor cortex neurones.

1. Extracellular single-cell recordings were made from the cerebellar thalamus, the ventro-posterior lateralis par caudalis (VPLc) and motor cortex of three conscious monkeys. Recordings were made from the thalamus as well as the cortex in two monkeys. In all, recordings were made from the thalamus in four hemispheres and from the motor cortex in four hemispheres. The animals were trained to permit a detailed examination when relaxed. Unexpected perturbations were applied to the wrist. Seventy-seven wrist-related neurones were recorded in the cerebellar thalamus, forty-two neurones from the VPLc and eighty-four neurones in motor cortex. 2. Cerebellar nuclear stimulation was used to physiologically identify thalamic neurones receiving input from the cerebellum. The location of all neurones was verified histologically. 3. The majority of cerebellar thalamic neurones had deep sensory receptive fields related to a single muscle, a group of synergists or a single joint. There was a distinct topographical organization. These fields were similar to sensory fields in motor cortical neurones, but had higher thresholds. 4. VPLc neurones had discrete deep or cutaneous sensory fields, or a combination of these fields, which suggests convergence. VPLc neurones had fields with lower thresholds than cerebellar thalamic neurones. The somatotopically located forelimb area in the VPLc was posterior to and continuous with the forelimb area in the cerebellar thalamus. 5. VPLc neurones responded with a shorter latency to wrist perturbations than did cerebellar thalamic neurones. VPLc neurones with deep sensory fields changed firing significantly earlier than those with cutaneous fields. The VPLc is likely to be the major source of sensory input to the motor cortex, and based on the results of this study we suggest that the VPLc is the thalamic nucleus best placed to transmit short-latency afferent input from the forelimb. 6. The timing of the neuronal discharge of cerebellar thalamic and VPLc cells, which resulted from perturbations of the wrist, was best linked to the duration of movement rather than its amplitude. The cells began firing as soon as the velocity changed sign and continued firing until the sign of the velocity changed again. In subsequent corrective movements neuronal discharge in the VPLc appeared to also encode movement acceleration.

Animals↗

PubMed1997

Reevaluation of ipsilateral corticocortical inputs to the orofacial region of the primary motor cortex in the macaque monkey.

An anatomical approach to possible areas in the cerebral cortex involved in somatic motor behavior is to analyze the cortical areas containing neurons that connect directly to the primary motor cortex (MI). To define the cortical areas related to orofacial movements, we examined the distribution of cortical neurons that send their axons to the orofacial region of the MI in the macaque monkey. Injections of retrograde tracers into the electrophysiologically identified orofacial region of the MI revealed that labeled neurons were distributed in the following cortical areas: the orbital cortex (area 12), insular cortex, frontoparietal operculum (including the deep part of the cortical masticatory area and the secondary somatosensory cortex), ventral division of the premotor cortex (especially in its lateral part), orofacial region of the supplementary motor area, rostral division of the cingulate motor area (CMA), and CMA on the ventral bank. A number of labeled neurons were also seen in the MI around the injection sites and in the parietal cortex (including the primary somatosensory cortex and area 7b). No labeled neurons were found in the dorsal division of the premotor cortex. Fluorescent retrograde double labeling further revealed virtually no overlap of distribution between cortical neurons projecting to the orofacial and forelimb regions of the MI. Based on the present results, we discuss the functional diversity of the cortical areas related to orofacial motor behavior and the somatotopical organization in the premotor areas of the frontal cortex.

Animals↗

PubMed2005

Depressed mood, index finger force and motor cortex stimulation: a transcranial magnetic stimulation (TMS) study.

The present study utilized transcranial magnetic stimulation (TMS) of the motor cortex to understand basic motor processes associated with depressive symptoms independent of cognitive requirements or diagnostic category. To assess the integrity of the basic cortical-spinal-motor circuit associated with depressed mood, TMS to the motor cortex was used to initiate motor evoked potentials (MEPs) in forearm EMG and force production measured in the right (dominant) index finger. While at rest, a group with more depressive symptoms showed less force response in the index finger following stimulations compared with a group endorsing less depressive symptoms. A negative correlation between force response in the index finger at baseline (rest) following stimulation and the Beck depression inventory indicated that depressive mood symptom elevations were associated with less response to stimulations. The results argue for a greater importance placed on the relationship between depressive mood symptoms and basic motor processes.

Affect↗

PubMed2000

Muscarinic receptor blockade has differential effects on the excitability of intracortical circuits in the human motor cortex.

The aim of the present study was to investigate whether muscarinic receptor blockade with scopolamine modifies the excitability of specific cortical networks of the human motor cortex as tested with transcranial magnetic stimulation. The effects of scopolamine on the excitability of human motor cortex were investigated in four healthy subjects using transcranial magnetic stimulation before and after an intravenous dose of scopolamine (0.006 mg/kg). We measured the threshold for motor responses, amplitude of motor responses, the duration of the cortical silent period, intracortical inhibition and facilitation, and short-latency inhibition produced by somatosensory input from the hand. In addition, we evaluated the amplitude of motor responses evoked by electrical anodal stimulation, since these responses originate from direct activation of corticospinal axons in the white matter and are not sensitive to changes in cortical excitability. Scopolamine decreased the threshold to magnetic stimuli and increased the amplitude of motor responses evoked by magnetic stimulation. In contrast, motor responses evoked by electrical stimulation were unaffected by administration of scopolamine. Scopolamine also led to a highly significant reduction in the amount of short-latency inhibition produced by somatosensory input from the hand. In contrast, short-latency intracortical inhibition and facilitation were not modified by scopolamine. The differential effect of scopolamine on motor responses evoked by magnetic and electrical stimulation of the motor cortex and the selective effect on somatosensory inhibition demonstrate that muscarinic blockade modifies the excitability of specific cortical networks in the human motor cortex.

Acetylcholine↗

PubMed2003

Functional reorganization of the motor cortex in adult rats after cortical lesion and treatment with monoclonal antibody IN-1.

We previously reported anatomical plasticity in the adult motor cortex after a unilateral sensorimotor cortex (SMC) lesion and treatment with monoclonal antibody (mAb) IN-1, which permits neurite outgrowth from the intact, opposite cortex into deafferented subcortical targets. This study was designed to investigate whether treatment with the mAb IN-1 after SMC lesion in the adult leads to functional reorganization of the intact, opposite motor cortex. Adult rats underwent unilateral SMC aspiration lesion and treatment with either mAb IN-1 or control antibody, or no treatment. After a 6 week survival period, the intact, opposite forelimb motor cortex was explored using intracortical microstimulation to evoke forelimb movements. A dramatic increase in ipsilateral movements of the lesion-impaired forelimb was found in animals treated with mAb IN-1 compared with control animals. These results resembled our previous findings of cortical reorganization in the spared hemisphere after neonatal cortical lesion and without any additional treatment. These results show that, after adult cortical lesion, treatment with mAb IN-1 induces a functional reorganization of the intact, opposite motor cortex.

Animals↗

PubMed1991

[Dislocated neurons and neural network: hodological study of the motor cortex of the reeler mutant mouse].

Reeler, an autosomal recessive mutation in mice, causes cytoarchitectonic abnormalities of cerebral cortex, which are characterized by malposition of neurons. We examined hodological systems of the reeler motor cortex. The results are described as follows. (1) In normal controls, corticospinal tract neurons retrogradely labeled after the injection of HRP ioto the lumbar cord were situated only in layer V (layer of large pyramids: LP). In the reeler, by contrast, the labeled corticospinal tract neurons were scattered diffusely throughout all levels of the corresponding area. (2) In the normal controls, callosal commissural neurons retrogradely labeled after the HRP injection into the motor cortex were distributed in a bilaminar pattern such that the largest number of cells were located in the supragranular layers II (layer of small pyramids; SP) and III (layer of medium pyramids; MP), and in the infragranular layer V (LP). In the reeler mutant mice, callosal commissural neurons were found in all cortical layers, but two-thirds were situated in the lower half of the cortex. (3) In the normal controls, most of the thalamocortical neurons labeled after HRP injection into the motor cortex were located in the ventrolateral nucleus, the lateral division of the ventrobasal nucleus, the central lateral, paracentral and central intralaminar nuclei, and the medial division of the posterior complex. In the reeler mutant mice, retrogradely labeled neurons were again found in the nuclei referred to above, and the distribution pattern and morphology of HRP-filled neurons were also similar to those of normal controls. In the reeler, thalamocortical fibers took an abnormal course within the motor cortex: they ascended obliquely from the white matter to the pial surface and then descended obliquely to the deeper layers. These results strongly suggest that dislocated neurons project correctly to normally-situated and/or abnormally situated target(s).

Animals↗

PubMed1999

Effects of red nucleus microstimulation on the locomotor pattern and timing in the intact cat: a comparison with the motor cortex.

Effects of red nucleus microstimulation on the locomotor pattern and timing in the intact cat: a comparison with the motor cortex. To determine the extent to which the rubrospinal tract is capable of modifying locomotion in the intact cat, we applied microstimulation (cathodal current, 330 Hz; pulse duration 0.2 ms; maximal current, 25 microA) to the red nucleus during locomotion. The stimuli were applied either as short trains (33 ms) of impulses to determine the capacity of the rubrospinal tract to modify the level of electromyographic (EMG) activity in different flexors and extensors at different phases of the step cycle or as long trains (200 ms) of pulses to determine the effect of the red nucleus on cycle timing. Stimuli were also applied with the cat at rest (33-ms train). This latter stimulation evoked short-latency (average = 11.8-19.0 ms) facilitatory responses in all of the physiological flexor muscles of the forelimb that were recorded; facilitatory responses were also common in the elbow extensor, lateral head of triceps but were rare in the physiological wrist and digit extensor, palmaris longus. Responses were still evoked in most muscles when the current was decreased to near threshold (3-10 microA). Stimulation during locomotion with the short trains of stimuli evoked shorter-latency (average = 6.0-12.5 ms) facilitatory responses in flexor muscles during the swing phase of locomotion and, except in the case of the extensor digitorum communis, evoked substantially smaller responses in stance. The same stimuli also evoked facilitatory responses in the extensor muscles during swing and produced more complex effects involving both facilitation and suppression in stance. Increasing the duration of the train to 200 ms modified the amplitude and duration of the EMG activity of both flexors and extensors but had little significant effect on the cycle duration. In contrast, whereas stimulation of the motor cortex with short trains of stimuli during locomotion had very similar effects to that of the red nucleus, increasing the train duration to 200 ms frequently produced a marked reset of the step cycle by curtailing stance and initiating a new period of swing. The results suggest that whereas both the motor cortex and the red nucleus have access to the interneuronal circuits responsible for controlling the structure of the EMG activity in the step cycle, only the motor cortex has access to the circuits responsible for controlling cycle timing.

Animals↗

PubMed1995

Somatotopic mapping of the human primary motor cortex with functional magnetic resonance imaging.

We applied functional magnetic resonance imaging (FMRI) to map the somatotopic organization of the primary motor cortex using voluntary movements of the hand, arm, and foot. Eight right-handed healthy subjects performed self-paced, repetitive, flexion/extension movements of the limbs while undergoing echo-planar imaging. Four subjects performed movements of the right fingers and toes, while the remaining subjects performed movements of the right fingers and elbow joint. There was statistically significant functional activity in the left primary motor cortex in all subjects. The pattern of functional activity followed a topographic representation: finger movements resulted in signal intensity changes over the convexity of the left motor cortex, whereas toe movements produced changes either at the interhemispheric fissure or on the dorsolateral surface adjacent to the interhemispheric fissure. Elbow movements overlapped the more medial signal intensity changes observed with finger movements. Functionally active regions were confined to the cortical ribbon and followed the gyral anatomy closely. These findings indicate that FMRI is capable of generating somatotopic maps of the primary motor cortex in individual subjects.

Adult↗

PubMed1999

Intracortical inhibition of the motor cortex is normal in chorea.

Intracortical inhibition of the motor cortex was investigated using a paired pulse magnetic stimulation method in 14 patients with chorea caused by various aetiologies (six patients with Huntington's disease, one with chorea acanthocytosis, a patient with systemic lupus erythematosus with a vascular lesion in the caudate, three with senile chorea and three with chorea of unknown aetiology). The time course and amount of inhibition was the same in the patients as in normal subjects, suggesting that the inhibitory mechanisms of the motor cortex studied with this method are intact in chorea. This is in striking contrast with the abnormal inhibition seen in patients with Parkinson's disease or focal hand dystonia, or those with a lesion in the putamen or globus pallidus. It is concluded that the pathophysiological mechanisms responsible for chorea are different from those producing other involuntary movements.

Adult↗

PubMed1986

Maternal ethanol consumption: lack of effect on synaptogenesis in layer I of the motor cortex in 19-day-old rat offspring.

Previous studies showed that in utero exposure to ethanol has an adverse effect on development of the central nervous system. Included among those abnormalities is the evidence that in utero exposure to ethanol alters the development of the cerebral cortex in terms of the arborization of pyramidal dendrites and the concentration of neurotransmitters and neurotransmitter receptors. However, limited information is available about the influence of in utero exposure to ethanol on synaptogenesis in the cortex. We examined the influence of chronic maternal ethanol consumption, prior to parturition, on synaptogenesis in layer I of the motor cortex of 19-day-old-rat offspring. Layer I (the molecular layer) was chosen because of the early timing of its development. The motor cortex was chosen because of the evidence of motor problems in children afflicted with the fetal alcohol syndrome. The results of these studies demonstrated that the 19-day-old offspring of rats that were pair-fed, using control or 6.6% (v/v) ethanol-containing liquid diets on a chronic basis prior to parturition, had a comparable density of synapses and distribution of paramembranous density lengths in layer I of the motor cortex as well as a comparable thickness of cortical layer I. Thus, evidence by this and other laboratories, of cortical neurotransmitter and dendritic abnormalities are not reflected in synaptic changes in layer I of the motor cortex at 19 days. It is possible that synaptogenesis is affected at another age or in other regions of the cerebral cortex.

Animals↗

PubMed2004

Motor cortex dysfunction revealed by cortical excitability studies in Parkinson's disease: influence of antiparkinsonian treatment and cortical stimulation.

Single or paired pulse paradigms of transcranial magnetic stimulation (TMS) provide several parameters to test motor cortex excitability, such as motor threshold (MT), motor evoked potential (MEP) amplitude, electromyographic silent period to cortical stimulation (CSP) and intracortical facilitation (ICF) or inhibition (ICI). Various changes in TMS parameters, revealing motor cortex dysfunction, were found in patients with Parkinson's disease (PD). For instance, low MT and increased MEP size disclosed an enhanced corticospinal motor output at rest, while reduced ICF and failure of MEP size increase during contraction suggested defective facilitatory cortical inputs, particularly for movement execution. Inhibitory cortical pathways were also found less excitable at rest (reduced ICI) and sometimes during contraction (shortened CSP). By restoring cortical inhibition, dopaminergic drugs and deep brain stimulation probably overcome the difficulty to focus neuronal activity onto the appropriate network required for a specific motor task. The application of repetitive TMS trains over motor cortical areas also showed some effect on cortical excitability, opening perspectives to consider the motor cortex as a target for therapeutic neuromodulation in PD. However, systematic studies of cortical excitability remained to be performed in large series of patients with PD, taking into account disease stage, clinical symptoms and medication influence.

Antiparkinson Agents↗