Sensorimotor Integration (sensorimotor + integration)

Distribution by Scientific Domains


Selected Abstracts


Sensorimotor integration in movement disorders

MOVEMENT DISORDERS, Issue 3 2003
Giovanni Abbruzzese MD
Abstract Although current knowledge attributes movement disorders to a dysfunction of the basal ganglia,motor cortex circuits, abnormalities in the peripheral afferent inputs or in their central processing may interfere with motor program execution. We review the abnormalities of sensorimotor integration described in the various types of movement disorders. Several observations, including those of parkinsonian patients' excessive reliance on ongoing visual information during movement tasks, suggest that proprioception is defective in Parkinson's disease (PD). The disturbance of proprioceptive regulation, possibly related to the occurrence of abnormal muscle-stretch reflexes, might be important for generating hypometric or bradykinetic movements. Studies with somatosensory evoked potentials (SEPs), prepulse inhibition, and event-related potentials support the hypothesis of central abnormalities of sensorimotor integration in PD. In Huntington's disease (HD), changes in SEPs and long-latency stretch reflexes suggest that a defective gating of peripheral afferent input to the brain might impair sensorimotor integration in cortical motor areas, thus interfering with the processing of motor programs. Defective motor programming might contribute to some features of motor impairment in HD. Sensory symptoms are frequent in focal dystonia and sensory manipulation can modify the dystonic movements. In addition, specific sensory functions (kinaesthesia, spatial,temporal discrimination) can be impaired in patients with focal hand dystonia, thus leading to a "sensory overflow." Sensory input may be abnormal and trigger focal dystonia, or defective "gating" may cause an input,output mismatch in specific motor programs. Altogether, several observations strongly support the idea that sensorimotor integration is impaired in focal dystonia. Although elemental sensation is normal in patients with tics, tics can be associated with sensory phenomena. Some neurophysiological studies suggest that an altered "gating" mechanism also underlies the development of tics. This review underlines the importance of abnormal sensorimotor integration in the pathophysiology of movement disorders. Although the physiological mechanism remains unclear, the defect is of special clinical relevance in determining the development of focal dystonia. [source]


Genetic manipulation, whole-cell recordings and functional imaging of the sensorimotor cortex of behaving mice

ACTA PHYSIOLOGICA, Issue 1 2009
C. C. H. Petersen
Abstract Sensory processing, sensorimotor integration and motor control are amongst the most basic functions of the brain and yet our understanding of how the underlying neuronal networks operate and contribute to behaviour is very limited. The relative simplicity of the mouse whisker sensorimotor system is helpful for detailed quantitative analyses of motor control and perception during active sensory processing. Recent technical advances now allow the measurement of membrane potential in awake-behaving mice, using whole-cell recordings and voltage-sensitive dye imaging. With these recording techniques, it is possible to directly correlate neuronal activity with behaviour. However, in order to obtain causal evidence for the specific contributions of different neuronal networks to behaviour, it is critical to manipulate the system in a highly controlled manner. Advances in molecular neurobiology, gene delivery and mouse genetics provide techniques capable of layer, column and cell-type specific control of gene expression in the mouse neocortex. Over the next years, we anticipate considerable advances in our understanding of brain function through measuring and manipulating neuronal activity with unprecedented precision to probe the molecular and synaptic mechanisms underlying simple forms of active sensory perception and associative learning. [source]


Clinical, neuropsychological, neurophysiologic, and genetic features of a new Italian pedigree with familial cortical myoclonic tremor with epilepsy

EPILEPSIA, Issue 5 2009
Antonio Suppa
Summary We studied the clinical, neuropsychological, neurophysiologic, and genetic features of an Italian family with familial cortical myoclonic tremor with epilepsy (FCMTE). Clinically affected members of the family had limb and voice tremor, seizures, and myoclonus involving the eyelids during blinking. Neuropsychological testing disclosed visuospatial impairment, possibly due to temporal lobe dysfunction. Neurophysiologic findings suggested increased primary motor cortex excitability with normal sensorimotor integration. Linkage analysis excluded the 8q24 locus, where patients shared a common haplotype spanning 14.5 Mb in the pericentromeric region of chromosome 2. [source]


Long-range connectivity of mouse primary somatosensory barrel cortex

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2010
Rachel Aronoff
Abstract The primary somatosensory barrel cortex processes tactile vibrissae information, allowing rodents to actively perceive spatial and textural features of their immediate surroundings. Each whisker on the snout is individually represented in the neocortex by an anatomically identifiable ,barrel' specified by the segregated termination zones of thalamocortical axons of the ventroposterior medial nucleus, which provide the primary sensory input to the neocortex. The sensory information is subsequently processed within local synaptically connected neocortical microcircuits, which have begun to be investigated in quantitative detail. In addition to these local synaptic microcircuits, the excitatory pyramidal neurons of the barrel cortex send and receive long-range glutamatergic axonal projections to and from a wide variety of specific brain regions. Much less is known about these long-range connections and their contribution to sensory processing. Here, we review current knowledge of the long-range axonal input and output of the mouse primary somatosensory barrel cortex. Prominent reciprocal projections are found between primary somatosensory cortex and secondary somatosensory cortex, motor cortex, perirhinal cortex and thalamus. Primary somatosensory barrel cortex also projects strongly to striatum, thalamic reticular nucleus, zona incerta, anterior pretectal nucleus, superior colliculus, pons, red nucleus and spinal trigeminal brain stem nuclei. These long-range connections of the barrel cortex with other specific cortical and subcortical brain regions are likely to play a crucial role in sensorimotor integration, sensory perception and associative learning. [source]


Contingent negative variation elicited before jaw and tongue movements

JOURNAL OF ORAL REHABILITATION, Issue 12 2005
K. YOSHIDA
summary, Contingent negative variation (CNV) is a negative brain potential occurring between two successive stimuli when the first stimulus is a warning and the second stimulus requires a motor response. The CNV is interpreted as an expression of the cognitive processes in preparation for a response directed to a purpose. Using 19 electrodes we recorded CNVs for mouth opening, closing and lateral movements, tongue protrusion and hand extension in 10 healthy subjects. The aim of the study was to examine the motor control mechanism underlying jaw and tongue movements in a cognitive paradigm. The first stimulus (S1) served as a preparatory warning signal for the imperative stimulus (S2) 2 s after the S1. The subject performed the experimental tasks after the S2. The grand average CNVs for jaw and tongue movements showed a bilaterally widespread negativity with the maximum in the vertex region (Cz). The early CNV was identified about 400 ms after the S1 and its amplitude was highest at the midline-frontal area. The late CNV started approximately 1000 ms after the S1 with the maximum at Cz. The mean amplitude was significantly lower for hand extension than for the other tasks, and significantly higher for lateral movement than for mouth closing, suggesting that the CNV amplitude can be affected by the complexity of the task. The CNV recording may provide a means to study the neuronal activity necessary for the sensorimotor integration of jaw and tongue movements. [source]


The effect of cutaneous input on intracortical inhibition in focal task-specific dystonia

MOVEMENT DISORDERS, Issue 9 2007
Michelle N. McDonnell PhD
Abstract In normal subjects short interval intracortical inhibition (SICI) is topographically modulated by cutaneous input, which may be important for focusing muscle activation during tasks. In patients with writer's cramp, a task-specific focal dystonia characterized by inappropriate and excessive muscle activation of the upper limb during certain motor tasks, intracortical inhibition is reduced at rest and lacks the normal topographically-specific modulation during motor tasks. In the present study we investigated whether cutaneous input modulated SICI in a group of patients with writer's cramp and a control group of subjects. Electromyographic recordings were made from the right first dorsal interosseous (FDI), abductor pollicis brevis (APB), and abductor digiti minimi (ADM) muscles. Brief electrical stimuli were applied to either digit II or digit V with ring electrodes. SICI was investigated using a paired transcranial magnetic stimulation paradigm employing interstimulus intervals of 1,15 ms. Cutaneous input from both digit II and digit V modulated motor evoked potentials and SICI in a topographically-specific manner in control subjects. In contrast, cutaneous input failed to modulate motor evoked potentials or SICI in the focal hand dystonia patients. These results provide further evidence of abnormal sensorimotor integration in focal hand dystonia. © 2007 Movement Disorder Society [source]


Abnormalities of sensory processing and sensorimotor interactions in secondary dystonia: A neurophysiological study in two patients

MOVEMENT DISORDERS, Issue 3 2005
Stefano Tamburin MD
Abstract Experimental data suggest that abnormalities of sensory processing and sensorimotor integration may play a role in the genesis of symptoms in primary dystonia. We studied 2 patients with dystonia secondary to lesions in the somatosensory pathways. We documented sensorimotor alterations in these patients that strongly resemble those found in primary dystonia. Our data are consistent with the hypothesis that abnormalities in sensorimotor processing may contribute to the pathogenesis of dystonic conditions. © 2004 Movement Disorder Society [source]


Role of the somatosensory system in primary dystonia

MOVEMENT DISORDERS, Issue 6 2003
Michele 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]


Sensorimotor integration in movement disorders

MOVEMENT DISORDERS, Issue 3 2003
Giovanni Abbruzzese MD
Abstract Although current knowledge attributes movement disorders to a dysfunction of the basal ganglia,motor cortex circuits, abnormalities in the peripheral afferent inputs or in their central processing may interfere with motor program execution. We review the abnormalities of sensorimotor integration described in the various types of movement disorders. Several observations, including those of parkinsonian patients' excessive reliance on ongoing visual information during movement tasks, suggest that proprioception is defective in Parkinson's disease (PD). The disturbance of proprioceptive regulation, possibly related to the occurrence of abnormal muscle-stretch reflexes, might be important for generating hypometric or bradykinetic movements. Studies with somatosensory evoked potentials (SEPs), prepulse inhibition, and event-related potentials support the hypothesis of central abnormalities of sensorimotor integration in PD. In Huntington's disease (HD), changes in SEPs and long-latency stretch reflexes suggest that a defective gating of peripheral afferent input to the brain might impair sensorimotor integration in cortical motor areas, thus interfering with the processing of motor programs. Defective motor programming might contribute to some features of motor impairment in HD. Sensory symptoms are frequent in focal dystonia and sensory manipulation can modify the dystonic movements. In addition, specific sensory functions (kinaesthesia, spatial,temporal discrimination) can be impaired in patients with focal hand dystonia, thus leading to a "sensory overflow." Sensory input may be abnormal and trigger focal dystonia, or defective "gating" may cause an input,output mismatch in specific motor programs. Altogether, several observations strongly support the idea that sensorimotor integration is impaired in focal dystonia. Although elemental sensation is normal in patients with tics, tics can be associated with sensory phenomena. Some neurophysiological studies suggest that an altered "gating" mechanism also underlies the development of tics. This review underlines the importance of abnormal sensorimotor integration in the pathophysiology of movement disorders. Although the physiological mechanism remains unclear, the defect is of special clinical relevance in determining the development of focal dystonia. [source]


Encoding of whisker input by cerebellar Purkinje cells

THE JOURNAL OF PHYSIOLOGY, Issue 19 2010
Laurens W. J. Bosman
The cerebellar cortex is crucial for sensorimotor integration. Sensorimotor inputs converge on cerebellar Purkinje cells via two afferent pathways: the climbing fibre pathway triggering complex spikes, and the mossy fibre,parallel fibre pathway, modulating the simple spike activities of Purkinje cells. We used, for the first time, the mouse whisker system as a model system to study the encoding of somatosensory input by Purkinje cells. We show that most Purkinje cells in ipsilateral crus 1 and crus 2 of awake mice respond to whisker stimulation with complex spike and/or simple spike responses. Single-whisker stimulation in anaesthetised mice revealed that the receptive fields of complex spike and simple spike responses were strikingly different. Complex spike responses, which proved to be sensitive to the amplitude, speed and direction of whisker movement, were evoked by only one or a few whiskers. Simple spike responses, which were not affected by the direction of movement, could be evoked by many individual whiskers. The receptive fields of Purkinje cells were largely intermingled, and we suggest that this facilitates the rapid integration of sensory inputs from different sources. Furthermore, we describe that individual Purkinje cells, at least under anaesthesia, may be bound in two functional ensembles based on the receptive fields and the synchrony of the complex spike and simple spike responses. The ,complex spike ensembles' were oriented in the sagittal plane, following the anatomical organization of the climbing fibres, while the ,simple spike ensembles' were oriented in the transversal plane, as are the beams of parallel fibres. [source]