Differential effect of dopa and subthalamic stimulation on vestibular activity in Parkinson's disease.
Identifieur interne : 000E18 ( Main/Exploration ); précédent : 000E17; suivant : 000E19Differential effect of dopa and subthalamic stimulation on vestibular activity in Parkinson's disease.
Auteurs : Monika Pötter-Nerger [Allemagne] ; Martin M. Reich ; James G. Colebatch ; G. Deuschl ; Jens VolkmannSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2012.
English descriptors
- KwdEn :
- Acoustic Stimulation, Aged, Antiparkinson Agents (therapeutic use), Cerebral Cortex (drug effects), Cerebral Cortex (physiopathology), Deep Brain Stimulation (methods), Electromyography, Evoked Potentials, Auditory (drug effects), Evoked Potentials, Auditory (physiology), Female, Humans, Levodopa (therapeutic use), Male, Middle Aged, Parkinson Disease (complications), Parkinson Disease (therapy), Reaction Time (drug effects), Subthalamic Nucleus (physiology), Vestibular Diseases (etiology), Vestibular Diseases (therapy), Vestibule, Labyrinth (drug effects), Vestibule, Labyrinth (physiopathology).
- MESH :
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- complications : Parkinson Disease.
- drug effects : Cerebral Cortex, Evoked Potentials, Auditory, Reaction Time, Vestibule, Labyrinth.
- etiology : Vestibular Diseases.
- methods : Deep Brain Stimulation.
- physiology : Evoked Potentials, Auditory, Subthalamic Nucleus.
- physiopathology : Cerebral Cortex, Vestibule, Labyrinth.
- therapy : Parkinson Disease, Vestibular Diseases.
- Acoustic Stimulation, Aged, Electromyography, Female, Humans, Male, Middle Aged.
Abstract
Postural disturbances in advanced Parkinson's disease are less responsive to therapy than other cardinal motor signs. The vestibulocollic reflex represents one brain-stem neuronal circuit involved in postural adjustments. The objective of this study was to investigate the vestibulocollic reflex in parkinsonian patients and the effects of subthalamic stimulation and dopa by recording vestibular-evoked myogenic potentials. After overnight withdrawal of medication, 20 patients with Parkinson's disease with (6 men, 4 women; mean age, 64.4 ± 2.2 years) or without (8 men, 2 women; mean age, 62.7 ± 3.9 years) implanted subthalamic electrodes in different treatment conditions were compared with 10 age-matched controls (5 men, 5 women; mean age, 59.6 ± 2.4 years). Vestibular-evoked myogenic potentials were recorded by electromyographic surface electrodes applied to both sternocleidomastoid muscles (band-pass filter, 8-1600 Hz; sampling rate, 5 kHz) and averaged in response to bilateral auditory tone bursts (120 dB SPL; sine waves, 7 ms; 1000 Hz) applied through earphones. Adjusted vestibular-evoked myogenic potential amplitudes were significantly smaller in parkinsonian patients than in controls, in particular in patients without surgery. Administration of dopa, but not subthalamic stimulation, significantly increased amplitudes. Onset latencies were similar for all groups and treatment conditions. Decreased vestibular-evoked myogenic potential amplitudes in parkinsonian patients suggest reduced vestibular nuclei excitability within the brain stem, which is modulated by dopa but not by subthalamic stimulation. This suggests different pathways for the action of both treatment modalities in Parkinson's disease and may explain clinical differences in terms of postural disturbances. © 2012 Movement Disorder Society.
DOI: 10.1002/mds.25061
PubMed: 22693156
Affiliations:
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Reich</name></author><author><name sortKey="Colebatch, James G" sort="Colebatch, James G" uniqKey="Colebatch J" first="James G" last="Colebatch">James G. Colebatch</name></author><author><name sortKey="Deuschl, G" sort="Deuschl, G" uniqKey="Deuschl G" first="G" last="Deuschl">G. Deuschl</name></author><author><name sortKey="Volkmann, Jens" sort="Volkmann, Jens" uniqKey="Volkmann J" first="Jens" last="Volkmann">Jens Volkmann</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acoustic Stimulation</term><term>Aged</term><term>Antiparkinson Agents (therapeutic use)</term><term>Cerebral Cortex (drug effects)</term><term>Cerebral Cortex (physiopathology)</term><term>Deep Brain Stimulation (methods)</term><term>Electromyography</term><term>Evoked Potentials, Auditory (drug effects)</term><term>Evoked Potentials, Auditory (physiology)</term><term>Female</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (therapy)</term><term>Reaction Time (drug effects)</term><term>Subthalamic Nucleus (physiology)</term><term>Vestibular Diseases (etiology)</term><term>Vestibular Diseases (therapy)</term><term>Vestibule, Labyrinth (drug effects)</term><term>Vestibule, Labyrinth (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cerebral Cortex</term><term>Evoked Potentials, Auditory</term><term>Reaction Time</term><term>Vestibule, Labyrinth</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Vestibular Diseases</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Evoked Potentials, Auditory</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebral Cortex</term><term>Vestibule, Labyrinth</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term><term>Vestibular Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acoustic Stimulation</term><term>Aged</term><term>Electromyography</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Postural disturbances in advanced Parkinson's disease are less responsive to therapy than other cardinal motor signs. The vestibulocollic reflex represents one brain-stem neuronal circuit involved in postural adjustments. The objective of this study was to investigate the vestibulocollic reflex in parkinsonian patients and the effects of subthalamic stimulation and dopa by recording vestibular-evoked myogenic potentials. After overnight withdrawal of medication, 20 patients with Parkinson's disease with (6 men, 4 women; mean age, 64.4 ± 2.2 years) or without (8 men, 2 women; mean age, 62.7 ± 3.9 years) implanted subthalamic electrodes in different treatment conditions were compared with 10 age-matched controls (5 men, 5 women; mean age, 59.6 ± 2.4 years). Vestibular-evoked myogenic potentials were recorded by electromyographic surface electrodes applied to both sternocleidomastoid muscles (band-pass filter, 8-1600 Hz; sampling rate, 5 kHz) and averaged in response to bilateral auditory tone bursts (120 dB SPL; sine waves, 7 ms; 1000 Hz) applied through earphones. Adjusted vestibular-evoked myogenic potential amplitudes were significantly smaller in parkinsonian patients than in controls, in particular in patients without surgery. Administration of dopa, but not subthalamic stimulation, significantly increased amplitudes. Onset latencies were similar for all groups and treatment conditions. Decreased vestibular-evoked myogenic potential amplitudes in parkinsonian patients suggest reduced vestibular nuclei excitability within the brain stem, which is modulated by dopa but not by subthalamic stimulation. This suggests different pathways for the action of both treatment modalities in Parkinson's disease and may explain clinical differences in terms of postural disturbances. © 2012 Movement Disorder Society.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>Schleswig-Holstein</li></region><settlement><li>Kiel</li></settlement></list><tree><noCountry><name sortKey="Colebatch, James G" sort="Colebatch, James G" uniqKey="Colebatch J" first="James G" last="Colebatch">James G. Colebatch</name><name sortKey="Deuschl, G" sort="Deuschl, G" uniqKey="Deuschl G" first="G" last="Deuschl">G. Deuschl</name><name sortKey="Reich, Martin M" sort="Reich, Martin M" uniqKey="Reich M" first="Martin M" last="Reich">Martin M. Reich</name><name sortKey="Volkmann, Jens" sort="Volkmann, Jens" uniqKey="Volkmann J" first="Jens" last="Volkmann">Jens Volkmann</name></noCountry><country name="Allemagne"><region name="Schleswig-Holstein"><name sortKey="Potter Nerger, Monika" sort="Potter Nerger, Monika" uniqKey="Potter Nerger M" first="Monika" last="Pötter-Nerger">Monika Pötter-Nerger</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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