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PubMed2005

Specialization in pyramidal cell structure in the sensory-motor cortex of the Chacma baboon (Papio ursinus) with comparative notes on macaque and vervet monkeys.

The systematic study of pyramidal cell structure has revealed new insights into specialization of the phenotype in the primate cerebral cortex. Regional specialization in the neuronal phenotype may influence patterns of connectivity and the computational abilities of the circuits they compose. The comparative study of pyramidal cells in homologous cortical areas is beginning to yield data on the evolution and development of such specialized circuitry in the primate cerebral cortex. Recently, we have focused our efforts on sensory-motor cortex. Based on our intracellular injection methodology, we have demonstrated a progressive increase in the size of, the branching structure in, and the spine density of the basal dendritic trees of pyramidal cells through somatosensory areas 3b, 1, 2, 5, and 7 in the macaque and vervet monkeys. In addition, we have shown that pyramidal cells in premotor area 6 are larger, more branched, and more spinous than those in the primary motor cortex (MI or area 4) in the macaque monkey, vervet monkey, and baboon. Here we expand the basis for comparison by studying the basal dendritic trees of layer III pyramidal cells in these same sensory-motor areas in the chacma baboon. The baboon was selected because it has a larger cerebral cortex than either the macaque or vervet monkeys; motor cortex has expanded disproportionately in these three species; and motor cortex in the baboon reportedly has differentiated to include a new cortical area not present in either the macaque or vervet monkeys. We found, as in monkeys, a progressive increase in the morphological complexity of pyramidal cells through areas 3b, 5, and 7, as well as from area 4 to area 6, suggesting that areal specialization in microcircuitry was likely to be present in a common ancestor of primates. In addition, we found subtle differences in the extent of the interareal differences in pyramidal cell structure between homologous cortical areas in the three species.

Animals↗

PubMed1996

Ipsilateral cortico-cortical inhibition of the motor cortex in various neurological disorders.

We used a paired-pulse magnetic stimulation technique to study ipsilateral cortico-cortical inhibition of the motor cortex in 48 patients with various neurological disorders and in 20 normal volunteers. In the normal subjects, the first subthreshold conditioning stimulus suppressed responses to the second suprathreshold test stimulus at interstimulus intervals (ISIs) of 1-5 ms (inhibition at short intervals), and facilitated them at ISIs of 8-15 ms (facilitation at long intervals). Patients with motor neuron disease, except those in whom brain stimulation produced control responses that were generated by direct activation of corticospinal neurons (D-waves), had normal inhibition at short intervals. Facilitation at long intervals was not elicited in some patients with amyotrophic lateral sclerosis. Less inhibition at short intervals and normal facilitation at long intervals was found for all the patients with progressive myoclonic epilepsy, a condition in which the excitability of cortical inhibitory interneurons is thought to be affected. Inhibition at short intervals was disturbed, but facilitation at long intervals was intact in the patients with movement disorders (Parkinson's disease, corticobasal degeneration, and Wilson's disease). In these patients, positron emission tomography (PET) studies showed decreased regional cerebral blood flow (rCBF) in the basal ganglia in the relaxed state. However, normal suppression was elicited in the patients with Parkinson's disease with normal rCBF. In four patients with chorea, the time-course of inhibition and facilitation was normal, even though PET studies showed decreased rCBF in the basal ganglia in two of them. Normal inhibition could not be elicited in patients who had a small lesion in the basal ganglia or in the pathway from basal ganglia to the primary motor cortex; the putamen, globus pallidus, and supplementary motor cortex. In contrast, patients who had a lesion in a sensory system (sensory cortex or sensory thalamus) or in the pontine nucleus had normal suppression. We conclude that the results of ipsilateral cortico-cortical inhibition with paired magnetic stimulation reflect the excitability of inhibitory interneurons in the motor cortex and that outputs from the basal ganglia markedly affect this inhibition, but outputs from somato-sensory systems or cerebellum do not. Moreover, dysfunction of the corticospinal tract or spinal motoneurons does not affect results obtained by the paired magnetic stimulation technique when the control responses are generated by I-waves (i.e. descending volleys are produced by transsynaptic activation of the corticospinal tract neurons.

Adult↗

PubMed2004

A functional connection between inferior frontal gyrus and orofacial motor cortex in human.

The inferior frontal gyrus (IFG) of humans is known to play a critical role in speech production. The IFG is a highly convoluted and cytoarchitectonically diverse structure, classically forming 3 subgyri. It is reasonable to speculate that during speaking the IFG, or some portion of it, influences by corticocortical connections the orofacial representational area of primary motor cortex. To test the hypothesis that such corticocortical connections exist, electrical-stimulation tract tracing experiments were performed intraoperatively on 14 human subjects undergoing surgical treatment of medically intractable epilepsy. Bipolar electrical stimulation was applied to sites on the IFG, while the resulting evoked potentials were recorded from orofacial motor cortex, using a multichannel recording array. Stimulation of the IFG evoked polyphasic waveforms on motor cortex of both language-dominant and -nondominant hemispheres. The evoked waveforms had consistent features across subjects. The responses were seen in discrete regions on precentral cortex. Stimulation of motor cortex also evoked responses on portions of IFG. The data provide evidence for a functional connection between the human IFG and orofacial motor cortex.

Adult↗

PubMed1988

Corticospinal direct response in humans: identification of the motor cortex during intracranial surgery under general anaesthesia.

The corticospinal direct (D) response to stimulation of the motor cortex exposed for intracranial surgery was recorded in 20 cases from wire electrodes inserted into the spinal epidural space. The D response was obtained from stimulation of restricted areas of the cerebral cortex, that is, the hand, trunk and thigh areas of the motor cortex. The D response was resistant to anaesthesia and unaffected by muscle relaxants. Thus, recordings of the D response are useful for identifying the location of the motor cortex during intracranial surgery under general anaesthesia.

Anesthesia, General↗

PubMed2001

Are the after-effects of low-frequency rTMS on motor cortex excitability due to changes in the efficacy of cortical synapses?

OBJECTIVES: To investigate the mechanisms responsible for suppressing the amplitude of electromyogram (EMG) responses to a standard transcranial magnetic stimulus (TMS) after prior conditioning of the motor cortex with repetitive subthreshold TMS (rTMS) at a frequency of 1 Hz. METHODS: EMG responses from the first dorsal interosseous, abductor pollicis brevis and flexor carpi radialis (FCR) muscles were recorded after suprathreshold TMS of the motor cortex. In some experiments, H-reflexes were also obtained in the FCR. The amplitude of these responses was compared before and after applying from 150 to 1500 rTMS pulses to motor cortex at an intensity of 95% resting motor threshold through the same figure-of-8 coil. RESULTS: When tested with subjects relaxed, rTMS conditioning reduced the amplitude of motor evoked potentials (MEPs) to approximately 60% of pre-conditioning values for 2-10 min after the end of the conditioning train, depending on the number of pulses in the train. There was more suppression with 1500 rTMS pulses than with 150 pulses. There was no effect on H-reflexes. There was no effect on MEPs if the test stimuli were given during active contraction of the target muscle. CONCLUSIONS: The findings confirm previous observations that low-frequency, low-intensity rTMS to motor cortex can produce transient depression of MEP excitability. Since there was no effect on spinal H-reflexes, this is consistent with the idea that some of the suppression occurs because of an effect on the motor cortex itself. The lack of any conditioning effect on MEPs evoked in actively contracting muscle is not readily consistent with the idea that rTMS depresses transmission in synaptic connections to pyramidal cells activated by the test TMS pulse. An alternative explanation is that rTMS reduces the excitability of cortical neurones in relaxed subjects, so that responses to a given input are smaller than before conditioning. Voluntary contraction normalises excitability levels so that the effect is no longer seen.

Adult↗

PubMed2004

Modulation of motor cortex excitability induced by pinch grip repetition.

UNLABELLED: We examined the influence of right handed pinch grips and the effect of a motor training on motor cortex excitability of the left first dorsal interosseus muscle (FDI). TMS single and paired pulses were applied over the right human motor cortex (M1) during and after right handed pinch grips with low force. In another experiment, these stimulations were performed before and after a 30-minute right handed pinch grip training. RESULTS: MEP amplitudes in left FDI were reduced when TMS single pulses were applied during the pinch grip. Simultaneously, motor cortex excitability was enhanced but returned to baseline after the training period. CONCLUSION: Phasic pinch grips of the right hand exert an inhibiting effect on the corticospinal excitability of the ipsilateral motor cortex and lead to an increase of intracortical excitability. These changes are distinct and independent of each other. Motor training has an interhemispheric effect on intracortical excitability.

Adult↗

PubMed2007

Decreased thickness of primary motor cortex in primary lateral sclerosis.

BACKGROUND AND PURPOSE: Primary lateral sclerosis (PLS) is a rare form of motor neuron disease characterized by upper motor neuron dysfunction. Because pathologic examination has revealed a loss of neurons in the motor cortex of patients with PLS, we sought to confirm and extend this finding by using MR imaging to measure cortical thickness. METHODS: Seven patients with PLS and 7 age-matched neurologically normal control subjects were examined with heavily T1-weighted short-tau inversion recovery (STIR) MR imaging performed at 3T. Cortical thickness in the anterior and posterior banks of both the central and precentral sulci were measured. RESULTS: Primary motor cortex (M1) was significantly thinner in patients with PLS than M1 in healthy control subjects, measuring 2.32 +/- 0.21 mm compared with 2.79 +/- 0.18 mm (P = .0008). Cortical thickness did not differ between the 2 groups for primary sensory cortex or for the anterior or posterior banks of the precentral sulcus. Therefore, loss of gray matter was specific to motor cortex. Although this difference was modest, cortical thickness discriminated between the 2 groups; only 1 PLS case was within the range of normal measurements. CONCLUSION: Decreased thickness of M1 on the anterior bank of the precentral sulcus in patients with PLS, demonstrable by MR imaging, indicates a selective loss of upper motor neurons in this disease. Measurements of cortical thickness by MR imaging may provide a useful biomarker for diagnosis and study of upper motor neuron diseases.

Adult↗

PubMed1994

Suppression of voluntary motor activity revealed using transcranial magnetic stimulation of the motor cortex in man.

1. Suppression of voluntary muscle activity of hand and arm muscles in response to transcranial magnetic stimulation (TMS) of the motor cortex has been investigated in man. 2. Suppression could be elicited by low levels of TMS without any prior excitatory response. The latency of the suppression was 3-8 ms longer than the excitation observed at a higher stimulus intensity. The duration of the suppression ranged from 8 to 26 ms. 3. A circular stimulating coil was used to determine threshold intensity for excitation and suppression of contraction of thenar muscles in response to TMS at different locations over the motor cortex. The locations for lowest threshold excitation coincided with those for lowest threshold suppression. Suppression was elicited at a lower threshold than excitation at all locations. 4. A figure-of-eight stimulating coil was positioned over the left motor cortex at the lowest threshold point for excitation of the right thenar muscles. The orientation for the lowest threshold excitatory and inhibitory responses was the same for all subjects. That orientation induced a stimulating current travelling in an antero-medial direction. Suppression was invariably elicited at lower thresholds than excitation. 5. When antagonistic muscles (second and third dorsal interosseus) were co-contracted, TMS evoked coincident suppression of voluntary EMG in the two muscles without prior excitation of either muscle. This suggests that the suppression is not mediated via corticospinal activation of spinal interneurones. 6. Test responses to electrical stimulation of the cervical spinal cord were evoked in both relaxed and activated thenar muscles. In the relaxed muscle, prior TMS at an intensity that would suppress voluntary activity failed to influence the test responses, suggesting absence of inhibition at a spinal level. However, in the activated muscle, prior TMS could reduce the test response. This may be explained by disfacilitation of motoneurones due to inhibition of corticospinal output. 7. We propose that suppression of voluntary muscle activity by TMS is due in large part to activation of a mechanism within the motor cortex that reduces the corticospinal output to the muscle. It is concluded that TMS evokes excitation and inhibition via neuronal structures lying close to one another and having similar orientations.

Adult↗

PubMed1996

An investigation of motor function in schizophrenia using transcranial magnetic stimulation of the motor cortex.

BACKGROUND: In this first investigation of motor function in schizophrenia using transcranial magnetic stimulation (TMS), the general hypothesis tested was that this methodology could be used to investigate the disruption of corticospinal inhibitory processes suggested by cognitive and psychophysiological paradigms. METHOD: Nine drug-free DSM-IV schizophrenic patients were compared with nine age- and sex-matched normal subjects. Electromyographic (EMG) recordings were made from the thenar muscles of the dominant hand during sustained, weak voluntary contraction. TMS over a particular threshold applied to the motor cortex would elicit a compound motor evoked potential (cMEP) followed by a period of suppression of EMG. RESULTS: The latency of cMEPs following TMS was significantly shorter in the schizophrenic patients. The two groups did not differ significantly with respect to mean latency of suppression of EMG activity, or stimulus thresholds for either cMEPs or EMG suppression. CONCLUSION: These findings could be the result of a relative lack of corticospinal inhibition of motor responses; a change in the site of TMS activation; or an abnormality of peripheral nervous function in schizophrenia. Drug effects were unlikely since seven of the patients were drug-naive.

Adult↗

PubMed1990

GABAA receptor immunoreactivity in adult and developing monkey sensory-motor cortex.

The areal and laminar distribution of GABAA receptor immunoreactivity was examined in fetal, early postnatal and adult monkey sensory-motor cortex by using a monoclonal antibody to the purified GABAA receptor complex (Vitorica et al. 1988). GABAA receptor immunoreactivity was distributed throughout the neuropil, often outlining the unstained somata of pyramidal and non-pyramidal cells. In all areas of the adult sensory-motor cortex, layers I-IIIA exhibited the most intense immunostaining. In deeper layers of the four cytoarchitectonic fields of the first somatic sensory area (SI), layers IIIB and V were lightly stained and alternated with somewhat more intensely stained layers IV and VI. In deeper layers of area 4, the deeper half of layer IIIA through layer VA was lightly immunostained, but layers VB and VI were slightly more intensely immunoreactive. A variable number of nonpyramidal cell somata in the cortex and underlying white matter showed immunoreactive staining. GABAA receptor immunoreactivity was present throughout the sensory-motor cortex from the youngest fetal age examined (E121), but the pattern of immunostaining differed from that in the adult. In all areas, the densest immunoreactivity was found in a diffuse band in layers III and IV and in the subplate zone. Within the subplate zone, the presence of receptor immunoreactivity and some intensely stained neuronal somata at all fetal ages suggests the presence of a synaptic neuropil. With increasing age, gradual changes in the distribution of receptor immunoreactivity occurred, resulting in an adult-like pattern of immunostaining by postnatal day 1.5. These results show that laminar pattern of GABAA receptor distribution closely follows the major concentrations of GABA immunoreactive neurons in adults and it is suggested that laminar changes seen in development are associated with the establishment of afferent connections and inhibitory circuits in the sensory-motor cortex.

Aging↗

PubMed2002

Excitability of the ipsilateral motor cortex during phasic voluntary hand movement.

We investigated the influence of self-paced, phasic voluntary hand movement on the excitability of the ipsilateral motor cortex. Single- and paired-pulse transcranial magnetic stimulation (TMS) was applied to the right motor cortex triggered by EMG onset of self-paced movements of individual right hand fingers at intervals ranging from 13 to 2,000 ms. Motor evoked potentials (MEPs) were evaluated in several left arm muscles. Significant suppression of MEP amplitudes was observed when TMS was applied between 35 and 70 ms after EMG onset. This inhibition was diffuse, affecting "adjacent" muscles (those near the homologous muscle in the same extremity) as well as homologous muscles, but more inhibition was observed in adjacent and distal muscles than homologous and proximal muscles. Significant inhibition of ipsilateral motor cortex was produced by index finger movements (both the extensor indicis proprius and the first dorsal interosseus), but not by little finger movement (the abductor digiti minimi). Paired-pulse TMS (at 2- and 10-ms interstimulus intervals) showed a significant increase in intracortical facilitation (ICF) selectively in the homologous muscle when triggered by self-paced movement of the opposite hand, but no change was observed in intracortical inhibition. When stimulation was triggered by self-paced movements, the silent period of the homologous muscle was significantly shortened, but the F-wave and compound muscle action potential were unchanged. Our findings demonstrate that voluntary hand movement exerts an inhibitory influence on a diffuse area of the ipsilateral motor cortex. This inhibitory influence is both time and movement dependent. The inhibitory influence is nonselective, while the facilitatory influence (enhancing ICF) appears to act selectively on the homologous muscles. These effects are most likely mediated by a transcallosal pathway.

Adult↗

PubMed1999

Prolonged postexcitatory inhibition after transcranial magnetic stimulation of the motor cortex in patients with cerebellar ataxia.

Postexcitatory inhibition after transcranial magnetic stimulation of the motor cortex (silent period, SP) is supposed to be predominantly mediated by the activation of inhibitory cortical interneurons. Cortical excitability seems to be reduced in patients with cerebellar ataxia. Motor threshold, central motor conduction time and the duration of the silent period after a single magnetic stimulus to the motor cortex on both sides were measured in five patients with cerebellar ataxia of different origin and 18 healthy controls. Duration of SP was highly significantly prolonged in patients compared with controls (P<0.001) while motor threshold and central motor conduction times were not different. Fifteen of 18 control subjects showed late EMG responses after magnetic stimulation but none of the patients did (P<0.001). These findings support the hypothesis that cerebellar lesions activate inhibitory cortical interneurons or cause a disruption of a normally tonic cerebellar excitation to the motor cortex. Silent period measurement appears to be a sensitive diagnostic tool in the neurophysiological examination of cerebellar diseases.

Adult↗

PubMed2000

Motor cortex stimulation for chronic neuropathic pain: a preliminary study of 10 cases.

There is growing evidence to support the use of motor cortex stimulation (MCS) in the management of patients with chronic neuropathic pain. A prospective audit of ten patients using a modified staged technique for motor cortex implantation provides further evidence for the analgesic effectiveness of this technique. Ten patients suffering from phantom limb pain (n=3), post stroke pain (n=5), post traumatic neuralgia secondary to gunshot injury to the brain stem (n=1) and brachyalgia secondary to neuro-fibromatosis (n=150% pain relief) and long-term benefit in 4/5 of patients who initially responded to intermittent cortical stimulation (longest follow up 31 months after implantation). Of those patients who benefited two had post stroke pain, two phantom limb pain and one post-traumatic neuralgia. We conclude that motor cortex stimulation is an effective analgesic intervention in some patients with chronic neuropathic pain, but it is difficult if not impossible to predict those patients who may respond to treatment prior to implantation. Randomised controlled trials are now urgently needed to test the effectiveness of motor cortex stimulation under double-blind conditions.

Adult↗

PubMed1998

Neural discharge and local field potential oscillations in primate motor cortex during voluntary movements.

The role of "fast," or gamma band (20-80 Hz), local field potential (LFP) oscillations in representing neuronal activity and in encoding motor behavior was examined in motor cortex of two alert monkeys. Using chronically implanted microwires, we simultaneously recorded LFPs and single or multiple unit (MU) discharge at a group of sites in the precentral gyrus during trained finger force or reaching movements, during natural reaching and grasping, and during quiet sitting. We evaluated the coupling of oscillations with task-related firing at the same site, the timing of oscillations with respect to the execution of trained and untrained movement, and the temporal synchrony of oscillations across motor cortical sites. LFPs and neural discharge were examined from a total of 16 arm sites (7 sites in 1 monkey and 9 in the other), each showing movement-related discharge modulation and arm microstimulation effects. In the trained tasks, fast LFP and MU oscillations occurred most often during a premovement delay period, ceasing around movement onset. The decrease in oscillation roughly coincided with the appearance of firing rate modulation coupled to the motor action. During this delay, LFP oscillations exhibited either "overlapping" or "mixed" relationships with the simultaneously recorded neural discharge at that site. Overlap was characterized by coincident epochs of increased neural discharge and LFP oscillations. For the mixed pattern, episodes of LFP oscillation typically coincided with periods of diminished firing but overlap also sometimes appeared. Both patterns occurred concurrently across motor cortex during preparation; LFP suppression with motor action was ubiquitous. Fast oscillations reappeared quickly upon transition from quiet sitting to resumption of task performance, indicating an association with task engagement, rather than the general motor inaction of the delay period. In contrast to trained movements, fast oscillations often appeared along with movement during untrained reaching, but oscillations occurred erratically and were not reliably correlated with elevated neural discharge. Synchronous oscillations occurred at sites as much as 5 mm apart, suggesting widespread coupling of neurons and LFP signals in motor cortex. Widespread coupling of oscillatory signals is consistent with the concept that temporal coding processes operate in motor cortex. However, because the relationship between neuronal discharge and the appearance of fast oscillations may be altered by behavioral condition, they must reflect a global process active in conjunction with motor planning or preparatory functions, but not details of motor action encoded in neuronal firing rate.

Animals↗

PubMed1999

Motor cortex activation in Parkinson's disease: dissociation of electrocortical and peripheral measures of response generation.

This study investigated characteristics of motor cortex activation and response generation in Parkinson's disease with measures of electrocortical activity (lateralized readiness potential [LRP]), electromyographic activity (EMG), and isometric force in a noise-compatibility task. When presented with stimuli consisting of incompatible target and distractor elements asking for responses of opposite hands, patients were less able than control subjects to suppress activation of the motor cortex controlling the wrong response hand. This was manifested in the pattern of reaction times and in an incorrect lateralization of the LRP. Onset latency and rise time of the LRP did not differ between patients and control subjects, but EMG and response force developed more slowly in patients. Moreover, in patients but not in control subjects, the rate of development of EMG and response force decreased as reaction time increased. We hypothesize that this dissociation between electrocortical activity and peripheral measures in Parkinson's disease is the result of changes in motor cortex function that alter the relation between signal-related and movement-related neural activity in the motor cortex. In the LRP, this altered balance may obscure an abnormal development of movement-related neural activity.

Aged↗

PubMed2000

Intracortical inhibition of the motor cortex in movement disorders.

We have studied the function of inhibitory interneurons within the motor cortex in several movement disorders using a paired-pulse magnetic stimulation technique. Their function was disturbed in patients with dystonia or focal lesions of the basal ganglia. On the other hand, the inhibition was normal in patients with chorea or essential tremor. The inhibitory circuit in the motor cortex must be functionally involved in some movement disorders probably because of changes of the inputs from basal ganglia to motor cortices, but not involved in the others. This difference in the functional involvement of inhibitory interneurons of the motor cortex may reflect different pathogenesis of these movement disorders.

Adult↗

PubMed1995

Shared neural substrates controlling hand movements in human motor cortex.

Voluntary hand movements in humans involve the primary motor cortex (M1). A functional magnetic resonance imaging method that measures relative cerebral blood flow was used to identify a distributed, overlapping pattern of hand movement representation within the posterior precentral gyrus, which contains M1. The observed pattern resembles those reported in nonhuman primates and differs from a somatotopically organized plan typically used to portray human motor cortex organization. Finger and wrist movements activated a wide expanse of the posterior precentral gyrus, and representations for different finger movements overlapped each other and the wrist representation. Multiple sites of activation occurred in the precentral gyrus for all movements. The overlapping representations may mediate motor and cognitive functions requiring coordinated neural processing for finger and wrist actions rather than discrete control implied by somatotopic maps.

Brain Mapping↗

PubMed2005

A unilateral section of the corticospinal tract at cervical level in primate does not lead to measurable cell loss in motor cortex.

The effects of a unilateral interruption of the dorsolateral funiculus at cervical level on the survival of neurons in the motor cortex were investigated in macaque monkeys. The lesion was made on the left side at the transition region between the 7(th) and 8(th) cervical segments, above the motoneurons controlling hand muscles. As a result, the homolateral hand became paretic, although an incomplete recovery of manual dexterity took place during 2 months post-lesion. A quantitative anatomical assessment of pyramidal neurons in layer V was performed in the hindlimb area of the primary motor cortex and in the supplementary motor area (SMA proper). The pyramidal neurons were visualized using the marker SMI-32 and thus included the subpopulation of corticospinal neurons. These quantitative data demonstrated that the vast majority of the axotomized corticospinal (CS) neurons did not degenerate. Rather, their somata shrank, compared to the opposite hemisphere or to intact monkeys. This conclusion is in contrast to some previous studies in monkeys that argued for a substantial degeneration of motor cortex neurons as a result of transection of the corticospinal tract; yet in agreement with others that concluded the survival of most CS neurons. The survival of the majority of CS axotomized neurons is also consistent with the observation of numerous CS axons 1 mm above the cervical hemisection.

Animals↗