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Subthalamic nucleus stimulation modulates afferent inhibition in Parkinson disease
Umeå universitet, Medicinska fakulteten, Institutionen för farmakologi och klinisk neurovetenskap, Klinisk neurofysiologi.
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2007 (engelsk)Inngår i: Neurology, ISSN 0028-3878, E-ISSN 1526-632X, Vol. 68, nr 5, s. 356-363Artikkel i tidsskrift (Fagfellevurdert) Published
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Abstract [en]

Background: Peripheral sensory stimulation at the wrist inhibits the motor cortex as measured by transcranial magnetic stimulation at interstimulus intervals of approximately 20 ms (short latency afferent inhibition [SAI]) and 200 ms ( long latency afferent inhibition [LAI]). Previous studies suggested that reduced SAI in Parkinson disease (PD) reflects adverse effect of dopaminergic medications and reduced LAI may be related to nondopaminergic manifestations of PD. We hypothesize that subthalamic nucleus (STN) deep brain stimulation (DBS) may correct these deficiencies.

Methods: We studied the effects of STN DBS on SAI and LAI in seven PD patients and age-matched controls. PD patients were studied in an off medication followed by an on medication session, with the stimulator switched on or off in random order in each session.

Results: In the on medication session, SAI was reduced in the stimulator off condition and was restored by STN DBS. LAI was partially normalized by STN DBS in the medication on condition.

Conclusions: Subthalamic nucleus (STN) stimulation improves short latency afferent inhibition, suggesting that it could normalize pathways that are adversely affected by dopaminergic medications. The effect of STN stimulation on long latency afferent inhibition suggests that it may influence nondopaminergic pathways involved in sensorimotor integration.

sted, utgiver, år, opplag, sider
Philadelphia: Lippincott Williams & Wilkins, 2007. Vol. 68, nr 5, s. 356-363
Emneord [en]
deep brain stimulation, transcranial magnetic stimulation, peripheral input pathways, motor cortex excitability, dopa-induced dyskinesia, median nerve, sensorimotor integration, sensory symptoms, basal ganglia, levodopa
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Identifikatorer
URN: urn:nbn:se:umu:diva-118217DOI: 10.1212/01.wnl.0000252812.95774.aaISI: 000243996700007PubMedID: 17261682OAI: oai:DiVA.org:umu-118217DiVA, id: diva2:917419
Tilgjengelig fra: 2016-04-06 Laget: 2016-03-14 Sist oppdatert: 2018-06-07bibliografisk kontrollert

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