Literature DB >> 9074827

Electrodermal activity in patients with Parkinson's disease.

F Esen1, G Celebi, C Ertekin, Z Colakoglu.   

Abstract

Peripheral sympathetic activity was investigated in 25 Parkinson's disease (PD) patients and 27 healthy subjects by measuring the skin resistance level (SRL) and skin resistance response (SRR) at the palm of the hand during rest, auditory stimulation and patellar tendon tapping. Blood flow to the hand was also monitored. Normal responses were obtained from all the 27 healthy subjects with both stimuli. All but one of the 25 PD patients responded to sound, six patients failed to respond to patellar tendon tapping and one patient failed to respond to both stimuli. The SRRs (when detectable) of PD patients were always smaller in amplitude than those of normal subjects. It was also observed that while an electrodermal response was present, no vasomotor response could be elicited by either stimulus in some patients. The opposite was true in some other patients. When response latencies were evaluated, it was found that although the mean latency of SRRs evoked by tendon taping was shorter than the mean latency of responses to auditory stimuli in normal subjects, this was not the case in PD patients. SRR mean latency to patellar tendon tapping was significantly longer in PD patients compared with that in normal subjects. Mean latencies of responses to auditory stimuli were the same for both normal subjects and patients. The ratio of the SRR amplitude to SRL (i.e. relative change in SRL) during both types of stimulation was significantly smaller in PD patients than in normal subjects. All the above findings were also true when blood flow to the tissue was interrupted briefly. These findings support the conjecture that the abnormal peripheral sympathetic neural responses associated with PD may arise from a functional disorder in the basal ganglia that influence the efferent autonomic pathway, from impairment of the intermediolateral column of the spinal cord, and possibly from cognitive deficits.

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Year:  1997        PMID: 9074827     DOI: 10.1007/bf02267624

Source DB:  PubMed          Journal:  Clin Auton Res        ISSN: 0959-9851            Impact factor:   4.435


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