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Somatosensory System (somatosensory + system)
Selected AbstractsDifferences between the effects of three plasticity inducing protocols on the organization of the human motor cortexEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2006Karin Rosenkranz Abstract Several experimental protocols induce lasting changes in the excitability of motor cortex. Some involve direct cortical stimulation, others activate the somatosensory system and some combine motor and sensory stimulation. The effects usually are measured as changes in amplitude of the motor-evoked-potential (MEP) or short-interval intracortical inhibition (SICI) elicited by a single or paired pulses of transcranial magnetic stimulation (TMS). Recent work has also tested sensorimotor organization within the motor cortex by recording MEPs and SICI during short periods of vibration applied to single intrinsic hand muscles. Here sensorimotor organization is focal: MEPs increase and SICI decreases in the vibrated muscle, whilst the opposite occurs in neighbouring muscles. In six volunteers we compared the after effects of three protocols that lead to lasting changes in cortical excitability: (i) paired associative stimulation (PAS) between a TMS pulse and an electrical stimulus to the median nerve; (ii) motor practice of rapid thumb abduction; and (iii) sensory input produced by semicontinuous muscle vibration, on MEPs and SICI at rest and on the sensorimotor organization. PAS increased MEP amplitudes, whereas vibration changed sensorimotor organization. Motor practice had a dual effect and increased MEPs as well as affecting sensorimotor organization. The implication is that different protocols target different sets of cortical circuits. We speculate that protocols that involve repeated activation of motor cortical output lead to lasting changes in efficacy of synaptic connections in output circuits, whereas protocols that emphasize sensory inputs affect the strength of sensory inputs to motor circuits. [source] Rapid functional plasticity in the primary somatomotor cortex and perceptual changes after nerve blockEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2004Thomas Weiss Abstract The mature human primary somatosensory cortex displays a striking plastic capacity to reorganize itself in response to changes in sensory input. Following the elimination of afferent return, produced by either amputation, deafferentation by dorsal rhizotomy, or nerve block, there is a well-known but little-understood ,invasion' of the deafferented region of the brain by the cortical representation zones of still-intact portions of the brain adjacent to it. We report here that within an hour of abolishing sensation from the radial and medial three-quarters of the hand by pharmacological blockade of the radial and median nerves, magnetic source imaging showed that the cortical representation of the little finger and the skin beneath the lower lip, whose intact cortical representation zones are adjacent to the deafferented region, had moved closer together, presumably because of their expansion across the deafferented area. A paired-pulse transcranial magnetic stimulation procedure revealed a motor cortex disinhibition for two muscles supplied by the unaffected ulnar nerve. In addition, two notable perceptual changes were observed: increased two-point discrimination ability near the lip and mislocalization of touch of the intact ulnar portion of the fourth finger to the neighbouring third finger whose nerve supply was blocked. We suggest that disinhibition within the somatosensory system as a functional correlate for the known enlargement of cortical representation zones might account for not only the ,invasion' phenomenon, but also for the observed behavioural correlates of the nerve block. [source] Deafferentation-induced apoptosis of neurons in thalamic somatosensory nuclei of the newborn rat: critical period and rescue from cell death by peripherally applied neurotrophinsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2000Alfonso Baldi Abstract This study shows that unilateral transection of the infraorbital nerve (ION) in newborn (P0) rats induces apoptosis in the contralateral ventrobasal thalamic (VB) complex, as evidenced by terminal transferase-mediated deoxyuridine triphosphate-biotin nick end labelling (TUNEL) and electron miscroscopy. Double-labelling experiments using retrograde transport of labelled microspheres injected into the barrel cortex, followed by TUNEL staining, show that TUNEL-positive cells are thalamocortical neurons. The number of TUNEL-positive cells had begun to increase by 24 h postlesion, increased further 48 h after nerve section, and decreased to control levels after 120 h. Lesion-induced apoptosis in the VB complex is less pronounced if ION section is performed at P4, and disappears if the lesion is performed at P7. This time course closely matches the critical period of lesion-induced plasticity in the barrel cortex. Nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF), applied on the ION stump alone or in combination, are able to partially rescue thalamic neurons from apoptosis. Total cell counts in the VB complex of P7 animals that underwent ION section at P0 confirm the rescuing effect of BDNF and NGF. Blockade of axonal transport in the ION mimics the effect of ION section. These data suggest that survival-promoting signals from the periphery, maybe neurotrophins, are required for the survival of higher-order neurons in the somatosensory system during the period of fine-tuning of neuronal connections. We also propose that anterograde transneuronal degeneration in the neonatal rat trigeminal system may represent a new animal model for studying the pathways of programmed cell death in vivo. [source] Abnormal plasticity of the sensorimotor cortex to slow repetitive transcranial magnetic stimulation in patients with writer's crampMOVEMENT DISORDERS, Issue 1 2007Tobias Bäumer MD Abstract Previous studies demonstrated functional abnormalities in the somatosensory system, including a distorted functional organization of the somatosensory cortex (S1) in patients with writer's cramp. We tested the hypothesis that these functional alterations render S1 of these patients more susceptible to the "inhibitory" effects of subthreshold 1 Hz repetitive transcranial magnetic stimulation (rTMS) given to S1. Seven patients with writer's cramp and eight healthy subjects were studied. Patients also received rTMS to the motor cortex hand area (M1). As an outcome measure, short-latency afferent inhibition (SAI) was tested. SAI was studied in the relaxed first dorsal interosseous muscle using conditioning electrical stimulation of the index finger and TMS pulses over the contralateral M1. Baseline SAI did not differ between groups. S1 but not M1 rTMS reduced SAI in patients. rTMS had no effects on SAI in healthy subjects. Because SAI is mediated predominantly at a cortical level in the sensorimotor cortex, we conclude that there is an abnormal responsiveness of this area to 1 Hz rTMS in writer's cramp, which may represent a trait toward maladaptive plasticity in the sensorimotor system in these patients. © 2006 Movement Disorder Society [source] Role of the somatosensory system in primary dystoniaMOVEMENT DISORDERS, Issue 6 2003Michele Tinazzi MD Abstract The pathophysiology of dystonia is still not fully understood, but it is widely held that a dysfunction of the corticostriatal,thalamocortical motor circuits plays a major role in the pathophysiology of this syndrome. Although the most dramatic symptoms in dystonia seem to be motor in nature, marked somatosensory perceptual deficits are also present in this disease. In addition, several lines of evidence, including neurophysiological, neuroimaging and experimental findings, suggest that both motor and somatosensory functions may be defective in dystonia. Consequently, abnormal processing of the somatosensory input in the central nervous system may lead to inefficient sensorimotor integration, thus contributing substantially to the generation of dystonic movements. Whether somatosensory abnormalities are capable of triggering dystonia is an issue warranting further study. Although it seems unlikely that abnormal somatosensory input is the only drive to dystonia, it might be more correlated to the development of focal hand than generalized dystonia because local somesthetic factors are more selectively involved in the former than in the latter where, instead it seems to be a widespread deficit in processing sensory stimuli of different modality. Because basal ganglia and motor areas are heavily connected not only with somatosensory areas, but also with visual and acoustic areas, it is possible that abnormalities of other sensory modalities, such as visual and acoustic, may also be implicated in the pathophysiology of more severe forms of primary dystonia. Further studies have to be addressed to the assessment of the role of sensory modalities and their interaction on the pathophysiology of different forms of primary dystonia. © 2003 Movement Disorder Society [source] Somatosensory disinhibition in dystoniaMOVEMENT DISORDERS, Issue 4 2001Emma Frasson MD Abstract Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease. © 2001 Movement Disorder Society. [source] Unmyelinated tactile afferents underpin detection of low-force monofilamentsMUSCLE AND NERVE, Issue 1 2006Jonathan Cole MD Abstract Human hairy but not glabrous skin has unmyelinated (C) tactile (CT) afferents that project to insular cortex. We studied two subjects with the rare sensory neuronopathy syndrome who lack A-beta fibers but have relatively preserved C-fiber function. Weak monofilaments were detected on hairy skin alone. Hence, the ability to detect light touch does not depend entirely on the A-beta somatosensory system; CT afferents may contribute to the detection of weak monofilaments. Muscle Nerve, 2006 [source] Anatomically based guidelines for systematic investigation of the central somatosensory system and their application to a spinocerebellar ataxia type 2 (SCA2) patientNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2003U. Rüb Dysfunctions of the somatosensory system are among the clinical signs that characterize a variety of polyglutamine or CAG-repeat diseases. Deficits within this system may hinder the perception of potential threats, be detrimental to somatomotor functions, and result in uncoordinated movements, ataxia, and falls. Despite the considerable clinical relevance of such deficits, however, no systematic pathoanatomical studies of the central somatosensory system in polyglutamine diseases are currently available. The present paper has two goals: (1) re-commendation of an economical tissue sampling method and optimized histological processing of this tissue to allow rapid and reliable evaluation of the structural integrity of all known relay stations and interconnecting fibre tracts within this complex system, and (2) the proposal of guidelines for a rapid and detailed pathoanatomical investigative procedure of the human central somatosensory system. In so doing, we draw on the current state of neuroanatomic research and apply the methods and guidelines proposed here to a 25-year-old female patient with spinocerebellar ataxia type 2 (SCA2). The use of 100 µm serial sections through the SCA2 patient's central somatosensory components showed that obvious neuronal loss occurred in nearly all of the relay stations of this system (Clarke's column; cuneate, external cuneate and gracile nuclei; spinal, principal and mesencephalic trigeminal nuclei; ventral posterior lateral and ventral posterior medial nuclei of the thalamus), whereas the majority of interconnecting fibre tracts (dorsal spinocerebellar tract; cuneate and gracile fascicles; medial lemniscus; spinal trigeminal tract, trigeminal nerve and mesencephalic trigeminal tract) displayed signs of atrophy accompanied by demyelinization. These pathological findings suffice to explain the patient's impaired senses of vibration, position and temperature. Moreover, together with the lesions seen in the motor cerebellothalamocortical feedback loop (pontine nuclei, deep cerebellar nuclei and cerebellar cortex, ventral lateral nucleus of the thalamus), they also account for the somatomotor deficits that were observed in the young woman (gait, stance, and limb ataxia, falls, and impaired writing). In proposing these new guidelines, we hope to enable others to study the hitherto unknown morphological counterparts of somatosensory dysfunctions in additional CAG-repeat disease patients. [source] Cortical processing of near-threshold tactile stimuli: An MEG studyPSYCHOPHYSIOLOGY, Issue 3 2010Anja Wühle Abstract In the present study we tested the applicability of a paired-stimulus paradigm for the investigation of near-threshold (NT) stimulus processing in the somatosensory system using magnetoencephalography. Cortical processing of the NT stimuli was studied indirectly by investigating the impact of NT stimuli on the source activity of succeeding suprathreshold test stimuli. We hypothesized that cortical responses evoked by test stimuli are reduced due to the preactivation of the same finger representation by the preceding NT stimulus. We observed attenuation of the magnetic responses in the secondary somatosensory (SII) cortex, with stronger decreases for perceived than for missed NT stimuli. Our data suggest that processing in the primary somatosensory cortex including recovery lasts for <200 ms. Conversely, the occupancy of SII lasts ,500 ms, which points to its role in temporal integration and conscious perception of sensory input. [source] Mal de Debarquement and Posture: Reduced Reliance on Vestibular and Visual CuesTHE LARYNGOSCOPE, Issue 3 2004Zohar Nachum MD Abstract Objective The neural mismatch theory assumes that the intersensory conflicts leading to motion sickness are resolved by changes in the relative weighting of the various senses that contribute to orientation. If this sensory rearrangement persists after disembarkment, it might result in mal de debarquement (MD): ataxia and a rocking sensation sometimes felt after landing. The objective of the present study was to examine possible changes in sensory organization in naval crew members with differing susceptibility to MD with computerized dynamic posturography (CDP). Study Design Cross-sectional parallel-group design. Methods Seventeen subjects susceptible to MD (SMD) and 17 subjects nonsusceptible to MD (NSMD) (healthy male volunteers aged 18,22) participated in the study. CDP was performed twice with each subject, before and immediately after sailing, using the EquiTest system (NeuroCom, Inc., Clackamas, OR). Results The SMD group showed a significant reduction in their scores on sensory organization tests 3, 4, and 5 after sailing. Sensory pattern analysis revealed reduced use of inputs from the vestibular and visual systems to maintain balance. Prolonged latencies of the motor responses to unexpected pitch perturbations were also recorded in the postsailing CDP of the SMD group. Reduced performance on the presailing CDP task, which presents the greatest challenge to the vestibular system, was found to control for the presence of MD postsailing. Conclusions The results show that MD is associated with postural instability, slower motor reflexes, and larger sways in response to abrupt changes in the body's center of gravity. These findings may be explained by under reliance on vestibular and visual inputs and increased dependence on the somatosensory system for the maintenance of balance. [source] Voxel-based morphometry depicts central compensation after vestibular neuritisANNALS OF NEUROLOGY, Issue 2 2010Peter zu Eulenburg MD Objective Patients who have had vestibular neuritis (VN) show a remarkable clinical improvement especially in gait and posture >6 months after disease onset. Methods Voxel-based morphometry was used to detect the VN-induced changes in gray and white matter by means of structural magnetic resonance imaging. Twenty-two patients were compared an average 2.5 years after onset of VN to a healthy sex-and age-matched control group. Results Our analysis revealed that all patients had signal intensity increases for gray matter in the medial vestibular nuclei and the right gracile nucleus and for white matter in the area of the pontine commissural vestibular fibers. A relative atrophy was observed in the left posterior hippocampus and the right superior temporal gyrus. Patients with a residual canal paresis also showed an increase of gray matter in middle temporal (MT)/V5 bilaterally. Interpretation These findings indicate that the processes of central compensation after VN seem to occur in 3 different sensory systems. First of all, the vestibular system itself showed a white matter increase in the commissural fibers as a direct consequence of an increased internuclei vestibular crosstalk of the medial vestibular nuclei. Second, to regain postural stability, there was a shift to the somatosensory system due to an elevated processing of proprioceptive information in the right gracile nucleus. Third, there was a bilateral increase in the area of MT/V5 in VN patients with a residual peripheral vestibular hypofunction. This seems to be the result of an increased importance of visual motion processing. ANN NEUROL 2010;68:241,249 [source] | ||||||||||