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Lesions of the sensorimotor region: somatosensory evoked potentials and ultrasound guided surgery.

In 10 patients with lesions of the sensorimotor cortex cortical SEP were registered to identify the postcentral gyrus, and intra-operative ultrasound sonography served to locate the lesion. The combination of both techniques helped to find the optimal approach to the lesion. Postoperative results were considered favourable, as only one patient suffered transient postoperative deterioration, six were unchanged and in three patients the pre-operative motor deficits were improved. The combination of intra-operative ultrasound and neurophysiological identification of the sensorimotor cortex is concluded as being useful in surgery within this region.

Adult↗

Electrophysiological and morphological properties of embryonic neocortical grafts developing in different regions of the host rat brain.

Parallel morphological and electrophysiological studies of embryonic neocortical tissue (primordia of anterior parietal--presumptive sensorimotor--cortex) grafted into different regions of the host adult brain (sensori-motor cortex, caudate-putamen, septum or thalamus) were carried out to investigate to what extent the properties of transplanted embryonic neocortex--an advanced organizational form of neuronal tissue--are affected by homotopic or heterotopic surroundings. The results point to the importance of the host tissue environment as it influences both the size, the morphological and functional properties of the implanted embryonic cortical plate tissue. The cortical grafts were smaller in size when developed homo-topically in sensorimotor cortex and grew larger in heterotopic environment (caudate-putamen, septum, thalamus). The orientation of neuronal dendrites in the grafts tends to follow that seen in the surroundings. The homotopic grafts showed a better structural integration into the host brain. Differences were seen between intracortical and subcortical transplants in the spontaneous firing rate of neurons and in the ratio of units with various types of spontaneous discharge.

Animals↗

Activation of cerebellum and basal ganglia on volitional swallowing detected by functional magnetic resonance imaging.

Although regions of the sensorimotor cortex, insula, and anterior cingulate gyrus are reported to be activated during swallowing, findings concerning contributions of the cerebellum and basal ganglia have been contradictory. We investigated cerebellar and basal ganglionic activation using functional magnetic resonance imaging (fMRI). In 11 subjects, single-shot gradient-echo echoplanar image volumes sensitive to BOLD contrast were acquired in block design fashion using an oblique orientation covering both cerebrum and cerebellum. Using statistical parametric mapping, regional activation upon swallowing was observed in the sensorimotor cortex, insula, cerebellum, putamen, globus pallidus, thalamus, anterior cingulate gyrus, supplementary motor area, superior temporal gyrus, and substancia nigra. The cerebellum was activated bilaterally, especially on the left; activation of the putamen and globus pallidus was also found bilaterally. Thus, volitional swallowing involves the cerebellum and basal ganglia as well as cortical structures. The method used was well tolerated by normal subjects and should also be applicable to patients with dysphagia.

Adult↗

GABAergic intrinsic interneurons in the red nucleus of the cat demonstrated with combined immunocytochemistry and anterograde degeneration methods.

The presence of glutamic acid decarboxylase (GAD), the enzyme synthesizing gamma-aminobutyric acid (GABA), was investigated in the red nucleus by an immunocytochemical method. The ipsilateral sensorimotor cortex was ablated prior to the immunocytochemical procedures to examine whether cortical neurons make synaptic contacts with GAD-immunoreactive neurons. Small GAD-immunoreactive neurons with a major diameter of 16.1 +/- 3.2 micron (mean +/- S.D.) were observed in the red nucleus under both light and electron microscopy. They were uniformly distributed throughout the nucleus. Degenerating axon terminals were found making synaptic contact with GAD-immunoreactive neurons in the red nucleus, which suggests that there is an input from the ipsilateral sensorimotor cortex to these neurons. This observation, along with our previous findings that GABAergic axon terminals make synaptic contact with the rubrospinal neurons, provides anatomical evidence for the presence of intrinsic GABAergic interneurons which mediate cortical inhibition in cat rubrospinal neurons.

Animals↗

Cytophotometric analysis of neuronal chromatin and RNA changes in oxotremorine-treated rats.

Neuronal nucleic acid responses were examined within the rat striatum and sensorimotor cortex (layer V) following single intraperitoneal injections of the central cholinergic-muscarinic agonist oxotremorine (0.1, 0.7, or 1.0 mg/kg). After stoichiometric Feulgen and azure B staining of brain sections, scanning-integrating microdensitometry was used to quantify Feulgen-deoxyribonucleic acid levels, changes in the susceptibility of chromatin to Feulgen acid hydrolysis (F-DNA yield) and azure B-ribonucleic acid (RNA) content of neurons on an individual basis. Changes in neuronal nuclear and nucleolar volumes were also determined histometrically. Within the striatum and sensorimotor cortex, oxotremorine produced marked dose-dependent elevations in both F-DNA yield and RNA content. These metabolic increases were typically paralleled by elevations in nuclear and nucleolar volumes. The data demonstrate that the oxotremorine-induced central muscarinic activation is associated with dose-related enhancements in neuronal chromatin template activity, RNA content, and protein synthetic capacity.

Animals↗

Rhythmic cortical and muscle discharge in cortical myoclonus.

Seven patients with cortical action myoclonus were studied. Six of these also had cortical reflex myoclonus. Surface and needle recordings were made from intrinsic hand muscles. Reflex and action jerks often consisted of a series of EMG bursts, some of which were polyphasic. The interval between repetitive EMG bursts was most commonly approximately 20 ms. The first EMG burst following median nerve stimulation varied in latency by a few milliseconds. Needle recordings of this reflex response showed more than one peak in half of the post-stimulus time histograms (PSTH) collected. Multiple peaks were narrow and separated by as little as 4 ms. Single trials of the EEG activity over the sensorimotor cortex were recorded during stimulation or voluntary movement of the contralateral limb in five patients. Activity typically consisted of a rhythmic series of giant positive spike-slow negative wave complexes. Intervals between spikes tended to cluster at approximately 20 ms. Frequency histograms of spike to EMG burst intervals confirmed that spikes preceded muscle discharges but they showed more than one peak. These peaks were narrow and separated by as little as 3 ms. Thus, in patients with cortical myoclonus rhythmic muscle responses are driven by the sensorimotor cortex, which has a tendency to oscillatory activity. Two types of cortical rhythmicity are present. The first determines the frequency of repetitive EEG spikes and EMG bursts. The second is of higher frequency and underlies the multiple peaks separated by short intervals in PSTHs and histograms of spike to EMG burst intervals. Both phenomena may have their correlate in normal functioning.

Adult↗

Critical stages for growth in the development of cortical neurons.

In order to study the role of efferent connectivity in the development of CNS neurons, the growth of pyramidal tract neurons within the hamster sensorimotor cortex was studied during normal development and after early postnatal lesions of the pyramidal tract. We first determined, by a combination of Nissl and retrograde HRP techniques, that within the lumbar representation of cortical layer 5B in adult animals two cell populations exist: a large-celled population (40% of the total) projecting to the spinal cord and a small-celled population (60% of the total) projecting intracortically and to targets rostral to the medulla. We could not determine whether large layer 5B cells in the infant sensorimotor cortex also represent the corticospinal population. Nevertheless, measurements of the growth in cross-sectional area of the large cells from 7 days postnatal to adulthood showed that these cells continue to grow until 51 days of age. The most rapid rate of growth occurs between 7 and 14 days, during which time the cross-sectional area of the cell bodies triples, coincident with the arrival of corticospinal axons in the lumbar cord and the beginning of target innervation (Reh and Kalil, '81). The growth of the large neurons in layer 5B was then charted after the pyramidal tract was cut ipsilaterally in the medulla at various postnatal ages. Early lesions of the tract (4-8 days postnatal) interrupt lumbar projection fibers before they establish synapses in the cord. Nevertheless, cortical cell bodies in the lumbar representation continue to grow normally after axotomy until 11 days after birth. At this time, large cells are arrested in development and their cell size remains in the 11-day stage (50% of normal adult large cell size) indefinitely. In contrast, adult lesions of the tract cause a 60% shrinkage of large cells, which in the adult represent corticospinal neurons. No evidence for cortical cell death was found after pyramidal tract lesions at any age. The results of axotomy reveal a turning point in the development of layer 5B cortical neurons. Before the age of 11 days the large cells have an independent program of cell growth that proceeds despite axotomy. After this time, the large cortical neurons appear to require intact axons for further growth and, in the absence of normal connectivity, are arrested in development.

Age Factors↗

Modulation of cortical and pyramidal tract induced motor responses by electrical stimulation of the basal ganglia.

Two general mechanisms based on anatomical studies are possible for modulation of motor activity by the caudate nucleus and globus pallidus. These mechanisms are: (1) modulation of the output of cortical neurons that exert motor influences; and (2) modulation of subcortical neurons that exert motor influences. Differentiation between these two mechanisms was accomplished in the present study by two experimental approaches, both of which employed the conditioning-test paradigm. The first approach was an investigation of caudate nucleus or globus pallidus modulation (conditioning stimulus) of flexor responses of the anterior tibialis muscle elicited by electrical stimulation of the sensorimotor cortex (test stimulus) or pyramidal tract (test stimulus). These investigations were carried out in the intact and in decorticate cats. The second approach was an analysis of modulation or cortically induced pyramidal tract responses (direct and indirect, D-I potentials) by conditioning shock trains delivered to various loci within the caudate nucleus or globus pallidus. Both approaches were designed to determine whixh inhibitory and facilitatory motor influences of the basal ganglia occurred at a cortical or subcortical level. Simultaneous stimulation of a locus within the caudate nucleus and the sensorimotor cortex evoked either an enhancement, reduction or no alteration of the cortically induced increase in flexor responses (measured by Ia afferent activity, EMG, myogram). In contrast, no inhibitory influences occurred from caudate nucleus stimulation upon pyramidal tract induced flexor responses in either the intact or decorticate preparation. Inhibitory loci were distributed toward the rostral portion of the caudate nucleus, whereas facilitatory loci were distributed throughout; this distribution was statistically significant (chi2; P less than 0.01). Only enhancement or no influence upon cortical induced or pyramidal tract induced responses were obtained by conditioning stimuli to the globus pallidus. In the unanesthetized but immobilized cat, trains of shocks delivered to the caudate nucleus enhanced, reduced or had no influence upon the cortically evoked direct (D) and indirect (I) potentials recorded in the bulbar pyramidal tract. The distribution of facilitatory and inhibitory loci was organized in a similar fashion as in theanesthetized preparation. From these observations, a model was proposed in which the output of the caudate nucleus exerts both facilitatory or inhibitory modulation of the tonically active globus pallidus cells. The latter in turn predominantly or exclusively facilitate output of pyramidal tract neurons as well as the output of subcortical structures; both effects facilitate motor responses at the spinal level.

Animals↗

Subthalamic stimulation influences postmovement cortical somatosensory processing in Parkinson's disease.

In Parkinson's disease, poor motor performance (resulting primarily from abnormal cortical activation during movement preparation and execution) may also be due to impaired sensorimotor integration and defective cortical activity termination of the ongoing movement, thus delaying preparation of the following one. Reduced movement-related synchronization of the beta rhythm in Parkinson's disease compared to controls has been put forward as evidence for impaired postmovement cortical deactivation. We assessed the effects of subthalamic deep brain stimulation and l-dopa on beta rhythm synchronization over the premotor and primary sensorimotor cortex. Ten advanced patients performed self-paced wrist flexion in four conditions according to the presence or not of stimulation and l-dopa. Compared to without treatment, the motor score improved by approximately 60%; the beta synchronization was present over the contralateral frontocentral region and increased significantly over the contralateral central region under stimulation and under l-dopa, with a maximal effect when both treatments were associated. Our advanced patients displayed very focused and attenuated beta rhythm synchronization which, under stimulation, increased over the contralateral premotor and primary sensorimotor cortex. Stimulation and l-dopa both partly restored postmovement cortical deactivation in advanced Parkinson's disease, although the respective mechanisms probably differ. They may improve bradykinesia and cortical deactivation by reestablishing movement-related somatosensory processing at the end of the movement through the basal ganglia into the cortex.

Aged↗

Age effect on motor recovery in a post-acute animal stroke model.

Male Fischer 344 rats aged 3, 6, 12, 18 and 24 months were trained to walk on a narrow beam, then lesioned in the right hindlimb sensorimotor cortex by photothrombosis. Motor performance was measured daily for 60 days using a 7-point rating scale from which deficit scores were calculated. Tissue analysis included lesion volume measurement after Nissl staining. Animals aged 3 and 6 months fully recovered by day 10 and 31, respectively. Animals aged 18 months acquired significant neurological impairment that persisted greater than 60 days. Deficit scores were significantly greater than in groups aged 12, 6 and 3 months. Degenerative morbidity and mortality confounded behavioral study of animals aged 24 months. The duration of neurological impairment after photochemical sensorimotor cortex lesion increased with age. Animals aged 18 months at lesion acquired the greatest chronic impairment. This aged post-acute animal model is clinically relevant to stroke rehabilitation.

Acute Disease↗

Modulation of motor cortical excitability by electrical stimulation over the cerebellum in man.

1. We have stimulated over the cerebellum of intact human subjects by applying single electrical stimuli through electrodes placed on the back of the head, approximately at the level of the inion. The intensity of stimulation used was below that required to produce direct EMG responses in pre-activated muscles of the hand. 2. In ten subjects the effect of the stimulus over the cerebellum was to reduce the size of the EMG response in first dorsal interosseous muscle evoked by a magnetic stimulus to the cerebral cortex. In all subjects the onset of the period of suppression occurred when the test magnetic cortical shock followed the conditioning cerebellar shock by 5 ms. The duration of the suppression lasted from 3 to 7 ms. 3. The amount of suppression was related to the intensity of stimulation over the cerebellum. At 15% below the threshold for direct motor activation there was no effect; increasing suppression was evident at 10, 5 and 0% below motor threshold. 4. With a conditioning-test interval of 5-6 ms the suppression was the same whether the target muscle was relaxed or active. With longer conditioning-test intervals (12 and 15 ms) the amount of suppression was greater in active than relaxed muscles. 5. The short-latency suppression was greatest when the stimulating anode was ipsilateral to the target muscle and contralateral to the stimulated sensorimotor cortex. The later period of suppression was insensitive to the polarity of stimulation. When the stimulating electrodes were moved 2 cm caudally or cranially the short latency suppression disappeared whereas the longer latency suppression was still observed with the electrodes in the lower position. 6. Different results were obtained when the test EMG response was produced by an electrical (rather than magnetic) stimulus over the sensorimotor cortex. The short latency effect was no longer visible whereas the longer latency effect was the same as when testing with a magnetic cortical stimulus. 7. We suggest that a single electrical stimulus across the base of the skull (particularly with the anode over one cerebellar hemisphere) produces a short latency (5-6 ms) disfacilitation of the contralateral motor cortex through activation of cerebellar structures. A later (12 and 15 ms), less specific suppression which is present when testing in active muscles is thought to be mediated by a different mechanism and probably produces its effect at the level of the spinal cord.

Action Potentials↗

T1-selective diffusion weighted fMRI at 1.5T.

Apparent diffusion coefficients (ADC) of protons contributing to the functional signal can be determined from diffusion weighted functional magnetic resonance imaging (MRI) studies. An earlier study indicated that ADCs calculated from the functional signal of an activated primary sensorimotor cortex are large, and consistent with a CSF or intravascular contribution to the functional signal. We have added inversion recovery pulses to isotropic diffusion weighted imaging to null CSF protons selectively within the imaging slice, or to null the outer volume blood flowing into the imaging slice. With the use of gradient recalled diffusion weighted echo-planar imaging at low gradient b factors, and without the use of inversion pulses, the ADCs x 10(3) in mm2/s (+/- SD) from the functional signal were 6.81 +/- 1.19. These ADCs were significantly higher than resting primary sensorimotor cortex ADCs of 2.26 +/- 1.49, measured at the same b factors. When CSF nulling was applied, the functional signal ADCs remained high. Application of inflow nulling decreased the functional signal to such a small value, that ADCs estimated from these functional signals were not assessed. The results are consistent with an intravascular contribution to the functional signal and to its large ADC.

Adult↗

[Reactions of red-nucleus neurons in the alert cat to cutaneous stimulation].

Responses of the red nucleus (RN) neurones to cutaneous stimulation were studied in unanaesthetized chronic cats by means of microelectrode technique. It was revealed that the reactions were predominantly excitatory and the RN neurons had larger receptive fields covering one half of the body or all the limbs of the animal. The somatotopic principle of the cutaneous representation in RN was shown. The destruction of the cerebellar nuclei and sensorimotor cortex caused the lowering of the background activity of the RN neurones, changed their responses to cutaneous stimulation, as well as the narrowing and redistribution of the peripheral receptive fields. With all the changes described, the somatotopic character of the cutaneous representation in RN as preserved, though a large majority of RN neurones (52,8%) did not show this somatotopic distribution. The cerebellum is the main collector in transferring the cutaneous impulsation to the RN. In awake cats there were predominantly involved spinocerebellar pathways, activated by the flexor reflex afferents. The participation of the sensorimotor cortex in the reaction under study is revealed by the phenomenon of sprouting of the corticorubral axon terminals from the dendritic portions to the neuronal somata of RN.

Animals↗

[Effect of epicortical stimulation on depolarization of primary afferents in rats during early postnatal ontogenesis].

Studies have been made on the parameters cord dorsum potentials (CDP) during stimulation of sensorimotor cortex in rats during first month of their postnatal life. First CDP were recorded from the 10th day, their latency being equal to about 80 msec, amplitude--65-70 microV, duration--more than 200 msec. During postnatal life of rats, the latent period decreases twice, the amplitude increases more than 3-fold, whereas the duration remains almost unchanged. These data indicate maturation of the descending pathways to the spinal cord, the increase in the propagation rate along these pathways and formation of segmentary mechanisms responsible for the generation of CDP. The effect of stimulation of the sensorimotor cortex on depolarization of primary afferent was also investigated. It was found that from the 2nd week of postnatal, life, formation of supraspinal control of afferent impulsation takes place.

Action Potentials↗

Epileptic negative myoclonus.

Five patients with partial epilepsy of diverse etiology insidiously developed action-activated jerks. The disorder was limited to one arm in two patients and to the legs in another, and was multifocal in the remaining two. Each jerk was related to an EMG silent period lasting 100 to 400 msec, causing a lapse followed by resumption of posture. Simultaneous EEG-EMG recording showed each postural lapse to be time-locked with a sharp or spike and slow-wave transient over the contralateral sensorimotor cortex, where almost continuous paroxysmal activity occurred. The three patients who were able to cooperate during neurologic evaluation also exhibited motor neglect in the most affected body segment and decreased awareness of the disorder. In three patients, the phenomenon was medically resistant, and in two of them it was continuous and could be defined as epilepsia partialis continua. In the other two, medical treatment induced remission of EEG, motor, and neuropsychological abnormalities. This disabling movement disorder can be classified as "epileptic negative myoclonus" and may result from focal-discharge-related transient disruption of cortical function in the sensorimotor cortex.

Adolescent↗

Three types of reticular neurons involved in the spino-bulbo-spinal reflex of cats.

Reticular neuron activity was recorded in 28 chloralosed cats in order to analyze the reflex arc of the spino-bulbo-spinal (SBS) reflex. Three types of reticular neurons, types I (input), II(output) and III (relay), were identified by unit discharges in response to stimulation of the sural nerve. (1) Type I (input) neurons received spinal ascending volleys monosynaptically and responded to stimulation of the sural nerve with spikes of low amplitude and short latency. Unit spikes, however, were not produced by stimulation of the superficial radial nerve and the sensorimotor cortex. These input neurons were located in the dorsocaudal part of the medial bulbar reticular formation. (2) Type II (output) neurons were part of the reticulospinal tract, which sends axons to the spinal cord, since these neurons exhibited antidromic spikes following stimulation of the ventrolateral funiculus of the spinal cord. Unit spikes were evoked by stimulation either to the sural or superficial radial nerves. These neurons were located in the ventrocaudal part of the medial bulbar reticular formation. (3) Type III neurons included relay neurons. Unit spikes were evoked by stimulation of the sural nerve, superficial radial nerve and sensorimotor cortex. However, unit discharges were not obtained by antidromic stimulation to the reticulospinal tract. These neurons were distributed widely in the brain stem, both in the bulb and pons. (4) Latency difference of unit discharges between input and output neurons was 3.5--5 msec, indicating the presence of interneurons (relays) between input and output neurons. Spikes of output neurons with 3.8--4.2 msec latency were observed following stimulation of the region where input neuron activity was found. We may conclude that three kinds of reticular neurons, input, relay and output, were involved in pathways of the SBS reflex.

Afferent Pathways↗

Induction of long-term depression is associated with decreased dendritic length and spine density in layers III and V of sensorimotor neocortex.

Long-term potentiation (LTP) and long-term depression (LTD) are currently the most widely investigated models of the synaptic mechanisms underlying learning and memory. Previous research has shown that induction of LTP increases measures of pyramidal cell dendritic morphology in the hippocampus and layers III and V of the neocortex. However, to date there are no reports on the direct effects of LTD induction on dendritic morphology. Here, we investigated the effects of LTD induction on sensorimotor pyramidal cell dendritic morphology. Rats carried a stimulating electrode in the corpus callosum (midline) and a recording electrode in the right sensorimotor cortex. Each rat received low-frequency stimulation composed of 900 pulses at 1 Hz or handling daily for a total 15 days. Evoked potentials (EPs) of the transcallosal pathway were recorded in the right hemisphere before and after the 15 days of stimulation or handling. The rats were then perfused with saline and the brains were immediately processed for Golgi-Cox staining. Our results show that LTD induction is related to decreases in dendritic length and spine density both in layers III and V as well as a decrease in dendritic branch complexity in layer V of the sensorimotor cortex. Thus, neuronal alterations following modifications in neocortical synaptic efficacy may provide a general mechanism for the physical instantiation of learning and memory.

Animals↗

The modulation of sensory transmission through the medullary dorsal horn during cortically driven mastication.

During mastication, reflexes are modulated and sensory transmission is altered in interneurons and ascending pathways of the rostral trigeminal sensory complex. The current experiment examines the modulation of sensory transmission through the most caudal part of the trigeminal sensory system, the medullary dorsal horn, during fictive mastication produced by cortical stimulation. Extracellular single unit activity was recorded from the medullary dorsal horn, and multiple unit activity was recorded from the trigeminal motor nucleus in anesthetized, paralyzed rabbits. The masticatory area of sensorimotor cortex was stimulated to produce rhythmic activity in the trigeminal motor nucleus (fictive mastication). Activity in the dorsal horn was compared in the presence and absence of cortical stimulation. Fifty-two percent of neurons classified as low threshold and 83% of neurons receiving noxious inputs were influenced by cortical stimulation. The cortical effects were mainly inhibitory, but 21% of wide dynamic range and 6% of low threshold cells were excited by cortical stimulation. The modulation produced by cortical stimulation, whether inhibitory or excitatory, was not phasically related to the masticatory cycle. It is likely that, when masticatory movements are commanded by the sensorimotor cortex, the program includes tonic changes in sensory transmission through the medullary dorsal horn.

Animals↗