Open AccessAuditory and Lower Limb Tactile Prepulse Inhibition in Primary Restless Legs Syndrome
Author(s) -
Fidias E. León-Sarmiento,
Elizabeth Peckham,
Daniel S. Leon-Ariza,
William BaraJimenez,
Mark Hallett
Publication year - 2015
Publication title -
journal of clinical neurophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.657
H-Index - 99
eISSN - 1537-1603
pISSN - 0736-0258
DOI - 10.1097/wnp.0000000000000196
Subject(s) - prepulse inhibition , psychology , restless legs syndrome , corneal reflex , reflex , stimulation , stimulus (psychology) , audiology , sensory system , neuroscience , sensory stimulation therapy , medicine , brainstem , moro reflex , sensory gating , physical medicine and rehabilitation , gating , neurology , schizophrenia (object oriented programming) , psychiatry , psychotherapist
The resting sensory discomfort transiently relieved upon movement of the affected area in restless legs syndrome suggests that sensorimotor integration mechanisms, specifically gating, may be altered in the disease. The authors sought to determine the effects of prepulse auditory and tactile stimulation applied to lower limbs on the blink reflex of patients with restless legs syndrome and healthy subjects. Seventeen patients with restless legs syndrome and 17 age- and sex-matched healthy controls were investigated. Auditory stimuli and tactile lower limb stimulation were applied as prepulses. The R2 response of the blink reflex induced by electrical stimulation applied to the right supraorbital nerve was selected as the test stimulus. Time intervals between prepulses and response-eliciting stimuli were 40, 70, 90, 110, and 200 milliseconds. There were no differences in either the auditory or tactile prepulse conditions between patients and controls and no differences between these measures within subject groups. We concluded that the tactile lower limb and the auditory prepulse effects on the brainstem interneurons mediating the blink reflex share common neural pathways. Because forebrain interneurons mediate these prepulse effects, they are likely not involved in the disordered sensorimotor interaction of restless legs syndrome.