Neurophysiological evidence of neuroplasticity at multiple levels of the somatosensory system in patients with carpal tunnel syndrome.
The human somatosensory cortex (S1) is capable of modification after partial peripheral deafferentation, but it is not known whether spinal and brainstem changes contribute to this process. We recorded spinal, brainstem and cortical somatosensory evoked potentials following ulnar nerve stimulation in patients affected by unilateral carpal tunnel syndrome with EMG evidence of chronic alterations in median nerve sensorimotor conduction at the wrist lasting at least 4 weeks, and compared them with those from the unaffected hand and with those obtained in a control group. Amplitudes of spinal N13 and brainstem P14 potentials following stimulation of the ulnar nerve ipsilateral to the deafferented median nerve were greater than those following stimulation of the contralateral ulnar nerve. Side-to-side amplitude differences in N13 and P14 were greater in patients than in the control group. Parietal N20 and P27 potentials, supposedly generated in S1, were also significantly increased. The present results suggest that a chronic pathological modification of peripheral sensorimotor inputs is associated with changes in neural activity at multiple sites of the somatosensory system. Changes in spinal and brainstem structures could contribute to the mechanisms subserving changes in the S1. Changes in synaptic strength and unmasking inputs secondary to disconnection of the normally dominant inputs to the 'median nerve' cortex may be the mechanisms underlying ulnar nerve SEP changes.[1]References
- Neurophysiological evidence of neuroplasticity at multiple levels of the somatosensory system in patients with carpal tunnel syndrome. Tinazzi, M., Zanette, G., Volpato, D., Testoni, R., Bonato, C., Manganotti, P., Miniussi, C., Fiaschi, A. Brain (1998) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
