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PubMed2000

Immunocytochemical and ultrastructural study of the motor cortex in patients with lower motor neuron disease.

This report conveys the results of an immunocytochemical and ultrastructural study of the motor cortices of six patients with clinically and pathologically-diagnosed lower motor neuron disease (LMND) such as progressive spinal muscular atrophy, progressive bulbar palsy, or both. These patients showed neither upper motor neuron signs nor upper motor neuron system involvement including the corticospinal tract in postmortem tissues after conventional stainings. Specimens from 12 age-matched normal individuals served as controls. All patients showed loss of brainstem motor neurons and anterior horn cells. Betz cells in LMND patients were significantly reduced in number as compared to controls (P<0.01). However, there was no significant difference in the density of phosphorylated neurofilament (PNF) (200 kDa)-positive Betz cells between LMND patients and controls. The pyramidal cells of layer III were immunostained for PNF in four of six LMND patients, but there was no significant difference in the density of PNF-positive pyramidal cells between LMND patients and controls. The number of astrocytes immunostained for glial fibrillary acidic protein increased in layer III and at the transition between white matter and motor cortex in three out of six patients and one of 12 controls. Ultrastructural examination revealed that the Betz cells of five of six LMND patients had Bunina bodies, Lewy body-like inclusions or skein-like inclusions, all of which are characteristic of amyotrophic lateral sclerosis (ALS). These findings suggest that most patients with clinically and pathologically-diagnosed LMND should be classified into the category of ALS.

Adult↗

PubMed2002

Unilateral sensorimotor cortex lesions in adult rats facilitate motor skill learning with the "unaffected" forelimb and training-induced dendritic structural plasticity in the motor cortex.

In humans and other animals, sufficient unilateral damage to the sensorimotor cortex can cause impairments in the opposite forelimb and the development of a hyper-reliance on the nonimpaired limb. This hyper-reliance is adaptive to the extent that it contributes to functional compensation for lesion-induced impairments. We have found that unilateral lesions of the forelimb region of the sensorimotor cortex (FLsmc) in rats, or callosal transections, cause neurons of the opposite motor cortex to become exceptionally responsive to changes in forelimb behavior. This enhanced responsiveness might facilitate learning of compensatory strategies with the nonimpaired forelimb after unilateral FLsmc lesions. The possibility that these lesions facilitate learning with the nonimpaired forelimb was addressed in this study. Rats were required to learn a skilled forelimb reaching task after either unilateral FLsmc lesions or sham operations. The trained limb in animals with lesions was the nonimpaired limb. Compared with shams, rats with unilateral lesions had a greater rate of acquisition and asymptotic performance level on the task, which was especially evident on more difficult trials. Quantitative measures of microtubule associated protein-2 (MAP2) immunostained dendrites indicated an enhancement of training-induced dendritic cytoskeletal changes in the motor cortex opposite lesions. Thus, unilateral FLsmc lesions facilitate learning of at least some types of motor skills using the nonimpaired forelimb as well as some of the neuronal changes associated with this learning. This facilitation could be a substrate underlying behavioral compensation for unilateral FLsmc damage and may contribute to the phenomenon of learned nonuse of the impaired limb.

Adaptation, Physiological↗

PubMed2004

Macaque ventral premotor cortex exerts powerful facilitation of motor cortex outputs to upper limb motoneurons.

The ventral premotor area (F5) is part of the cortical circuit controlling visuomotor grasp. F5 could influence hand motor function through at least two pathways: corticospinal projections and corticocortical projections to primary motor cortex (M1). We found that stimulation of macaque F5, which by itself evoked little or no detectable corticospinal output, could produce a robust modulation of motor outputs from M1. Arrays of fine microwires were implanted in F5 and M1. During terminal experiments under chloralose anesthesia, single stimuli delivered to M1 electrodes evoked direct (D) and indirect (I1,I2, and I3) corticospinal volleys. In contrast, single F5 shocks were ineffective; double shocks (3 msec separation) evoked small I waves but no D wave. However, when the test (T) M1 shock was conditioned (C) by single or double F5 shocks, there was strong facilitation of I2 and I3 waves from M1, with C-T intervals of <1 msec. Intracellular recordings from 79 arm and hand motoneurons (MNs) revealed no postsynaptic effects from single F5 shocks. In contrast, these stimuli produced a robust facilitation of I2 and I3 EPSPs evoked from M1 (60% of MNs); this was particularly marked in hand muscle MNs (92%). Muscimol injection in M1 reduced I waves from F5 and abolished the F5-induced facilitation of late I waves from M1, and of EPSPs associated with them. Thus, some motor effects evoked from F5 may be mediated by corticocortical inputs to M1 impinging on interneurons generating late corticospinal I waves. Similar mechanisms may allow F5 to modulate grasp-related outputs from M1.

Animals↗

PubMed1987

Neuronal activity in the primate non-primary cortex is different from that in the primary motor cortex.

This paper describes differences in the properties of single-cell activity in the primary and non-primary motor cortex of behaving monkeys (Macaca fuscata). New findings were obtained in relation to two different behavioural paradigms. First, we found that a large number of non-primary motor cortex neurons exhibit selective or preferential relationships to either signal-triggered or self-paced movement. In the second series of experiments, monkeys were trained to press a small key with the right or left hand, or with both hands. Most primary motor cortex neurons behaved like muscles in the contralateral hand. In contrast, a number of non-primary motor cortex neurons exhibited a selective relationship to the movement (right or left key press, or bilateral key press). The differences suggest the different roles of these two areas in motor control. Studies of this sort seem to start providing answers to the old question of why the non-primary motor cortex exists.

Animals↗

PubMed1989

Magnetic stimulation of the human motor cortex: facilitation and its relationship to a visual motor task.

Transcranial magnetic stimulation of the motor cortex can evoke motor responses in small hand muscles. This response can be facilitated by a background muscle contraction of the target muscle, resulting in an enhanced compound muscle action potential (CMAP) with a shorter onset latency. A number of intracortical mechanisms may account for this facilitatory effect, including, in part, direct input from visual to motor cortex. We studied the facilitation produced by a visual-motor task and compared those results with the facilitation produced by the same task without the visual cues. No differences in facilitation of amplitude or latency were observed. This suggests that there is no direct influence exerted by the visual cortex upon those elements of the motor cortex activated by a tangential magnetic stimulus, i.e., corticocortical and corticospinal neurons and their processes. Also, the large majority of facilitation (90%) was produced by a very small background voluntary contraction (less than 5% of maximum), indicating that any mild-to-moderate contraction of the target muscles will produce a consistent response for clinical measurements.

Electromyography↗

PubMedDate not supplied

Arterial supply of the feline motor cortex.

The arterial supply of the feline motor cortex is derived from both the anterior and middle cerebral arteries. The anterior cerebral artery supplies most of cortical area 6 (premotor cortex), the intrafundal cruciate and medial postcruciate cortex, (hindlimb motor cortex), and the midline and medial portions of the sensory areas 3a-7. The middle cerebral artery supplies the lateral prorean cortex, (lateral premotor cortex), precruciate and lateral sigmoid cortex, (forelimb motor cortex), and the remainder of the coronal and Sylvian cortical areas.

Animals↗

PubMed1991

The distribution of corticocortical, thalamocortical, and callosal inputs on identified motor cortex output neurons: mechanisms for their selective recruitment.

Motor cortex neurons were identified antidromically in anesthetized cats by their axonal projections to one of six targets: (1) somatosensory cortex, (2) opposite motor cortex, (3) red nucleus, (4) lateral reticular nucleus, (5) spinal cord, and (6) ventrolateral thalamus. Three inputs to motor cortex were tested for their influences on the identified cortical efferent neurons. The tested inputs originated from ipsilateral somatosensory cortex, opposite motor cortex, and ventral thalamus. Subthreshold effects of input pathways were detected by monitoring latency variations of antidromic responses. The three afferent sources, when activated by electrical stimulation, were not equally effective on motor cortex neurons. Ipsilateral corticocortical and thalamocortical excitation were found for the majority of neurons; the influenced proportions ranged from 55% to 100%, according to the target of the output neurons. Effects from the opposite hemisphere were found for only 5% to 30% of the neurons in the same projection classes. Many neurons (36 of 81, or 44%) were excited from more than one source, but few (5 of 37, or 14%) were influenced by all three possible sources of input, even in small regions of cortex innervated by all three of the inputs. Among 19 electrode tracks where all three inputs were present, there were only 2 tracks where all the neurons shared the same combination of inputs. Even for neurons in closest anatomical proximity ("clusters"), it was unusual (only 7 of 25 clusters) for all the neurons to have the same input pattern. Among the seven clusters where all the neurons shared the same input pattern, five of the clusters projected to the same target. These variable combinations of inputs to motor cortex neurons support the conclusion that efferent neurons could be recruited selectively from separate cortical layers or from within clusters of nearby neurons, according to the target of their axonal projection.

Afferent Pathways↗

PubMedDate not supplied

Mechanisms of LTP induction in rat motor cortex in vitro.

The motor cortex displays remarkable plasticity in response to changes in sensory and motor experience; however, the synaptic mechanisms underlying functional plasticity are not known. It is believed that synaptic processes that alter the strength of neuronal connections, such as long-term potentiation (LTP), are mechanisms by which synaptic circuits are modified by experience, resulting in functional adaptations. In the present study, we examined the mechanisms of LTP of synaptic responses in layers II/III to vertical (stimulation in layers V/VI) and horizontal (stimulation in layers II/III) inputs, in slices from rat motor cortex. Tetanic stimulation in layers V/VI or II/III induced LTP in 60% of the field potentials (n = 20) and in 73% of the intracellularly recorded postsynaptic potentials (n = 33). LTP was induced in cells with firing patterns characteristic of regular-spiking, fast-spiking, or bursting cells. LTP was expressed, for the most part, in kainate/AMPA receptor-mediated responses; however, potentiation of NMDA receptor-mediated components was also observed. Induction of LTP was prevented when either NMDA receptors or dihydropyridine-sensitive Ca2+ channels (DSCCs) were blocked, although blockade of DSCCs was less effective in preventing LTP induction. Based on the present data and previous LTP studies, we suggest that in many forms of LTP more than one mechanism participates in the induction process. The present findings may be relevant to the synaptic mechanisms underlying functional plasticity in motor cortex.

Animals↗

PubMed2005

Early adaptations in somatosensory cortex after focal ischemic injury to motor cortex.

In response to a lesion, intact regions of cortex in both hemispheres undergo adaptive changes in network function. For example, changes in excitability and intracortical inhibition in primary motor cortex (M1) were reported after lesioning contralateral or ipsilateral brain regions. Close interactions exist between M1 and primary somatosensory cortex (S1) within one hemisphere. Therefore, we hypothesized that lasting modifications would occur in S1 excitability after lesioning ipsilateral M1. Imaging of intrinsic optical signals (IOS, at 570 nm) was used to investigate the evolution of the somatosensory cortical response evoked by contralateral median nerve stimulation during the first hour after a photothrombotic lesion to M1 (caudal motor cortex) of the rat (n=10). Control rats (n=6) received no lesion. Perfusion was monitored by Laser speckle imaging and the extent of the resulting lesion was determined histologically. Control animals did not show evidence for reduced perfusion, infarction, or changes in IOS. M1 infarction led to a significant increase in evoked response amplitude, duration, and area of activation, and a shortening of latencies. These parameters reached a plateau around 50 min after ischemia. These results indicate S1 hyperexcitability after M1 injury. Whether these adaptations contribute to functional deficits or play a role in recovery, remains to be determined.

Adaptation, Physiological↗

PubMed2006

Motor training induces experience-specific patterns of plasticity across motor cortex and spinal cord.

The motor cortex and spinal cord possess the remarkable ability to alter structure and function in response to differential motor training. Here we review the evidence that the corticospinal system is not only plastic but that the nature and locus of this plasticity is dictated by the specifics of the motor experience. Skill training induces synaptogenesis, synaptic potentiation, and reorganization of movement representations within motor cortex. Endurance training induces angiogenesis in motor cortex, but it does not alter motor map organization or synapse number. Strength training alters spinal motoneuron excitability and induces synaptogenesis within spinal cord, but it does not alter motor map organization. All three training experiences induce changes in spinal reflexes that are dependent on the specific behavioral demands of the task. These results demonstrate that the acquisition of skilled movement induces a reorganization of neural circuitry within motor cortex that supports the production and refinement of skilled movement sequences. We present data that suggest increases in strength may be mediated by an increased capacity for activation and/or recruitment of spinal motoneurons while the increased metabolic demands associated with endurance training induce cortical angiogenesis. Together these results show the robust pattern of anatomic and physiological plasticity that occurs within the corticospinal system in response to differential motor experience. The consequences of such distributed, experience-specific plasticity for the encoding of motor experience by the motor system are discussed.

Action Potentials↗

PubMed2000

Magnetic stimulation of the human motor cortex evokes skin sympathetic nerve activity.

Single-pulse magnetic coil stimulation (Cadwell MES 10) over the cranium induces without pain an electric pulse in the underlying cerebral cortex. Stimulation over the motor cortex can elicit a muscle twitch. In 10 subjects, we tested whether motor cortical stimulation could also elicit skin sympathetic nerve activity (SSNA; n = 8) and muscle sympathetic nerve activity (MSNA; n = 5) in the peroneal nerve. Focal motor cortical stimulation predictably elicited bursts of SSNA but not MSNA; with successive stimuli, the SSNA responses did not readily extinguish (94% of discharges to the motor cortex evoked SSNA responses) and had predictable latencies [739 +/- 33 (SE) to 895 +/- 13 ms]. The SSNA responses were similar after stimulation of dominant and nondominant sides. Focal stimulation posterior to the motor cortex elicited extinguishable SSNA responses. In three of six subjects, anterior cortical stimulation evoked SSNA responses similar to those seen with motor cortex stimulation but without detectable movement; in the other subjects, anterior stimulation evoked less SSNA discharge than that seen with motor cortex stimulation. Contrasting with motor cortical stimulation, evoked SSNA responses were more readily extinguished with 1) peripheral stimulation that directly elicited forearm muscle activation accompanied by electromyograms similar to those with motor cortical stimulation; 2) auditory stimulation by the click of the energized coil when off the head; and 3) in preliminary experiments, finger afferent stimulation sufficient to cause tingling. Our findings are consistent with the hypothesis that motor cortex stimulation can cause activation of both alpha-motoneurons and SSNA.

Acoustic Stimulation↗

PubMed2002

Driving plasticity in human adult motor cortex is associated with improved motor function after brain injury.

Changes in somatosensory input can remodel human cortical motor organization, yet the input characteristics that promote reorganization and their functional significance have not been explored. Here we show with transcranial magnetic stimulation that sensory-driven reorganization of human motor cortex is highly dependent upon the frequency, intensity, and duration of stimulus applied. Those patterns of input associated with enhanced excitability (5 Hz, 75% maximal tolerated intensity for 10 min) induce stronger cortical activation to fMRI. When applied to acutely dysphagic stroke patients, swallowing corticobulbar excitability is increased mainly in the undamaged hemisphere, being strongly correlated with an improvement in swallowing function. Thus, input to the human adult brain can be programmed to promote beneficial changes in neuroplasticity and function after cerebral injury.

Adult↗

PubMed1991

Patterns of connectivity in the cat sensory-motor cortex: a light and electron microscope analysis of the projection arising from area 3a.

Through its complex network of interconnections, each of the functionally specialized subdivisions in the cat primary somatosensory cortex may provide the motor cortex with different input and thus play a unique role in motor behavior. Areas 2 and 3a receive separate peripheral information. Cells in both regions project directly to the cat motor cortex but are thought to target different populations of neurons. In this study the morphology and distribution patterns of the area 3a projection to the motor cortex were compared to previous findings on the projection from area 2. Also, details of the projection from area 3a to area 2 were studied. Injections of Phaseolus vulgaris leucoagglutinin were made into area 3a and fixed brain tissue was processed for immunohistochemical staining of this anterograde tracer. Tissue was examined with the light microscope to determine the patterns of the 3a projections to area 2 and motor cortex, area 4. Axons arising from cells in area 3a terminated in multiple column-like clusters in both motor cortex and area 2. The small number of cells labeled at the injection sites suggested that multiple foci of the 3a fibers are formed by collateral axonal branches of the same neurons. The topography of the projection from area 3a to the motor cortex was more clearly defined than that from area 3a to area 2. Electron microscope analysis determined the laminar distribution and types of synapses formed between area 3a efferents and their target neurons. A high proportion of synapses was found in layer III in both target regions. However, unlike in area 4, labeled terminals were sparse in laminae I and II of area 2. Axospinous synapses were slightly more numerous than axodendritic synapses, but both were distributed similarly throughout the thickness of the cortex. In area 2 the axospinous synapses accounted for 63% of synapses and in area 4 for 57% of synapses. No axosomatic synapses were detected.

Animals↗

PubMed1983

Evidence for an amygdaloid projection to premotor cortex but not to motor cortex in the monkey.

Previous studies in the cat have demonstrated a direct projection from the amygdaloid complex to motor and premotor regions of the neocortex. In the present study both anterograde and retrograde tracer techniques have been used to determine whether a similar projection exists in the monkey brain. We have found that the dorsal, magnocellular division of the basal nucleus of the amygdaloid complex gives rise to a projection to the premotor cortex (Area 6), which terminates principally in layers I and II, and to a lesser extent in layer VI. No component of the amygdaloid complex has been found to project to the motor cortex (Area 4). The amygdaloid projection to Area 6 in the monkey appears to be substantially weaker than other rostrally directed projections from the basal amygdaloid nucleus to orbitofrontal and medial frontal areas, and also relatively weaker than the projection that has been described in the cat.

Afferent Pathways↗

PubMed1996

[Functional MRI: imaging of motor cortex function].

OBJECTIVE: To image the motor cortex with functional MRI (fMRI), and locate the activated area with the proportional grid of Talairach. DESIGN: Descriptive. SETTING: St. Radboud Academic Hospital Nijmegen. METHODS: In ten volunteers functional images of the motor cortex were made during execution of a motor task (finger movements). From the functional images the positions of activated areas were calculated using the 3D Talairach grid system. RESULTS: fMRI of the motor cortex was possible using a 1.5 T MRI scanner. Task activation of the motor cortex gave a signal increase in Brodmann's area 4, the precentral gyrus. CONCLUSION: Imaging of the active motor cortex with fMRI is feasible. The use of the 3D Talairach proportional grid system for the calculation of the position of an activated area in the motor cortex is possible with adequate accuracy.

Adult↗

PubMed2006

Modulation of excitability as an early change leading to structural adaptation in the motor cortex.

The excitability of the motor cortex is a function of single cell excitability, synaptic strength, and the balance between excitatory cells and inhibitory cells. Sustained periods of sensory stimulation enhance the excitability in the motor cortex. This adaptation, which represents an early change in cortical network function effective in motor learning and recovery from a motor deficit, is followed by longer-lasting changes, such as modifications in cortical somatotopy, and by structural plasticity. Interventions aiming at increasing excitability also positively affect learning processes. Recent studies highlight that the cerebellum, especially the interpositus nucleus, plays a key function in the adaptation of the motor cortex to repeated trains of peripheral stimulation. Interpositus neurons, which receive inputs from the sensorimotor cortex and the spinal cord, are involved in somesthetic reflex behaviors and assist the cerebral cortex in transforming sensory signals to motor-oriented commands by acting via the cerebello-thalamo-cortical projections. Moreover, climbing fibers originating in the inferior olivary complex and innervating the nucleus interpositus mediate highly integrated sensorimotor information derived from spinal modules. The intermediate cerebellum allows the motor cortex to tune the gain of polysynaptic responses originating from the spinal cord after repetitive trains of peripheral stimulation, allowing an online calibration of cutaneo-muscular responses.

Adaptation, Physiological↗

PubMed1987

The interpretation of electromyographic responses to electrical stimulation of the motor cortex in diseases of the upper motor neurone.

The complexities of interpreting results of electrical stimulation of the motor cortex in pathological states are discussed and illustrated by reference to results from a variety of patients with diseases affecting the upper motor neurone (multiple sclerosis, cervical spondylosis and myelopathy, motor neurone disease, hemiparesis due to cerebral infarction, and hereditary spastic paraplegia). The abnormalities of the electromyographic (EMG) responses after anodal cortical stimulation consisted of delay in the latency to onset, dispersion or reduction in response size or even absence of EMG responses. These changes were not confined to any specific condition or pathology. Previous work has suggested that the sequence of events that follow anodal cortical stimulation involves repetitive excitatory inputs to spinal motoneurones and transmission across at least one central synapse. Accordingly, delayed latencies may not exclusively indicate slowing of motor conduction, while the absence of any response may not indicate complete failure of conduction in corticomotoneurone pathways.

Adult↗

PubMed2003

Synchrony between neurons with similar muscle fields in monkey motor cortex.

Synchronous firing of motor cortex cells exhibiting postspike facilitation (PSF) or suppression (PSS) of hand muscle EMG was examined to investigate the relationship between synchrony and output connectivity. Recordings were made in macaque monkeys performing a precision grip task. Synchronization was assessed with cross-correlation histograms of the activity from 144 pairs of simultaneously recorded neurons, while spike-triggered averages of EMG defined the muscle field for each cell. Cell pairs with similar muscle fields showed greater synchronization than pairs with nonoverlapping fields. Furthermore, cells with opposing effects in the same muscles exhibited negative synchronization. We conclude that synchrony in motor cortex engages networks of neurons directly controlling the same muscle set, while inhibitory connections exist between neuronal populations with opposing output effects.

Action Potentials↗