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Somatosensory Pathway (somatosensory + pathway)

Distribution by Scientific Domains

Medical Sciences	57%

Selected Abstracts

Neural substrates of tactile object recognition: An fMRI study

HUMAN BRAIN MAPPING, Issue 4 2004
Catherine L. Reed
Abstract A functional magnetic resonance imaging (fMRI) study was conducted during which seven subjects carried out naturalistic tactile object recognition (TOR) of real objects. Activation maps, conjunctions across subjects, were compared between tasks involving TOR of common real objects, palpation of "nonsense" objects, and rest. The tactile tasks involved similar motor and sensory stimulation, allowing higher tactile recognition processes to be isolated. Compared to nonsense object palpation, the most prominent activation evoked by TOR was in secondary somatosensory areas in the parietal operculum (SII) and insula, confirming a modality-specific path for TOR. Prominent activation was also present in medial and lateral secondary motor cortices, but not in primary motor areas, supporting the high level of sensory and motor integration characteristic of object recognition in the tactile modality. Activation in a lateral occipitotemporal area associated previously with visual object recognition may support cross-modal collateral activation. Finally, activation in medial temporal and prefrontal areas may reflect a common final pathway of modality-independent object recognition. This study suggests that TOR involves a complex network including parietal and insular somatosensory association cortices, as well as occipitotemporal visual areas, prefrontal, and medial temporal supramodal areas, and medial and lateral secondary motor cortices. It confirms the involvement of somatosensory association areas in the recognition component of TOR, and the existence of a ventrolateral somatosensory pathway for TOR in intact subjects. It challenges the results of previous studies that emphasize the role of visual cortex rather than somatosensory association cortices in higher-level somatosensory cognition. Hum. Brain Mapping 21:236,246, 2004. © 2004 Wiley-Liss, Inc. [source]

Functional MRI of the rodent somatosensory pathway using multislice echo planar imaging,

MAGNETIC RESONANCE IN MEDICINE, Issue 1 2004
Shella D. Keilholz
Abstract A multislice EPI sequence was used to obtain functional MR images of the entire rat brain with BOLD contrast at 11.7 T. Ten to 11 slices covering the rat brain, with an in-plane resolution of 300 ,m, provided enough sensitivity to detect activation in brain regions known to be involved in the somatosensory pathway during stimulation of the forelimbs. These regions were identified by warping a digitized rat brain atlas to each set of images. Data analysis was constrained to four major areas of the somatosensory pathway: primary and secondary somatosensory cortices, thalamus, and cerebellum. Incidence maps were generated. Electrical stimulation at 3 Hz led to significant activation in the primary sensory cortex in all rats. Activation in the secondary sensory cortex and cerebellum was observed in 70% of the studies, while thalamic activation was observed in 40%. The amplitude of activation was measured for each area, and average response time courses were calculated. Finally, the frequency dependence of the response to forepaw stimulation was measured in each of the activated areas. Optimal activation occurred in all areas at 3 Hz. These results demonstrate that whole-brain fMRI can be performed on rodents at 11.7 T to probe a well-defined neural network. Magn Reson Med 52:89,99, 2004. Published 2004 Wiley-Liss, Inc. [source]

Effects of essential hypertension on short latency human somatosensory-evoked potentials

PSYCHOPHYSIOLOGY, Issue 2 2010
Louisa Edwards
Abstract Reduced perception of somatosensory stimulation in patients with essential hypertension may be due to deficits in the ascending somatosensory pathway. Function in the ascending somatosensory pathway was assessed by measuring N9, N13, and N20 somatosensory-evoked potentials in 14 unmedicated essential hypertensives and 22 normotensives. N9 amplitudes were smaller and N13 amplitudes marginally smaller in hypertensives than normotensives. N9 amplitudes were inversely associated with blood pressure. N20 amplitudes and N9, N13, and N20 latencies did not differ between groups. In addition, plexus-to-cord, cord-to-cortex, and plexus-to-cortex conduction times were not different between groups. These data suggest that hypertension affects the peripheral nervous system by reducing the number of active sensory nerve fibers without affecting myelination. However, hypertension does not seem to affect the afferent somatosensory pathway within the brain. [source]

Electrophysiological evidence for altered early cerebral somatosensory signal processing in schizophrenia

PSYCHOPHYSIOLOGY, Issue 3 2004
Till D. Waberski
Abstract Various studies have indicated an impairment of sensory signal processing in schizophrenic patients. Anatomical and functional imaging studies have indicated morphological and metabolic abnormalities in the thalamus in schizophrenia. Other results give evidence for an additional role of cortical dysfunction in sensory processing in schizophrenia. Advanced analysis of human median nerve somatosensory evoked potentials (SEPs) reveals a brief oscillatory burst of low-amplitude and high-frequency activity (,600 Hz), the so-called high frequency oscillations (HFOs). The present study explores the behavior of HFOs in a cohort of schizophrenic patients in comparison to a group of controls. HFOs in the group of patients appeared with a delayed latency. In the low-frequency part of the SEPs an increase in amplitude was found. These results are interpreted to reflect a lack of somatosensory inhibition in the somatosensory pathway, either at a thalamic or a cortical level. [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]

Dystonia: A disorder of motor programming or motor execution?

MOVEMENT DISORDERS, Issue 6 2002
Petr Ka, ovský MD
Abstract For some time, dystonia has been seen as purely a motor disorder. Relatively novel concepts published approximately 10 years ago also presumed that in the development of dystonic dyskinesias, only motor behaviour was abnormal. Neurophysiological observations of various types of dystonic disorders, which were performed using sophisticated electromyography, polymyography, H-reflex examination, long-latency reflex, etc., as well as new insights into the behaviour of dystonia, have urged the inclusion of sensory (particularly somatosensory) mechanisms into the pathophysiological background of dystonia. The major role has been considered to be played by abnormal proprioceptive input by means of the Ia proprioceptive afferents, with the source of this abnormality found in the abnormal processing of muscle spindle afferent information. However, neurophysiological investigations have also provided evidence that the abnormality in the central nervous system is located not only at the spinal and subcortical level, but also at the cortical level; specifically, the cortical excitability and intracortical inhibition have been revealed as abnormal. This evidence was revealed by SEP recordings, paired transcranial magnetic stimulation recordings, and BP and CNV recordings. The current concept of dystonic movement connects the abnormal function of somatosensory pathways and somatosensory analysers with the dystonic performance of motor action, which is based on the abnormality of sensorimotor integration. © 2002 Movement Disorder Society [source]