The impact of ventrolateral thalamotomy on tremor and voluntary motor behavior in patients with Parkinson's disease
Identifieur interne : 000688 ( PascalFrancis/Checkpoint ); précédent : 000687; suivant : 000689The impact of ventrolateral thalamotomy on tremor and voluntary motor behavior in patients with Parkinson's disease
Auteurs : Christian Duval [Canada] ; Michel Panisset [Canada] ; Antonio P. Strafella [Canada] ; Abbas F. Sadikot [Canada]Source :
- Experimental brain research [ 0014-4819 ] ; 2006.
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- Pascal (Inist)
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- topic : Homme.
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Abstract
A preferred target for parkinsonian tremor alleviation is the ventrolateral (VL) thalamus. The goal of the present study is to determine how lesions involving the presumed cerebellar and pallidal recipient areas of the "motor" thalamus would alter the tremor and motor behavior of ten patients with Parkinson's disease (PD). Tremor amplitude, power dispersion (a measure of sharpness of the power spectrum of tremor), and power distribution were quantified using a laser displacement sensor prior to, and a week after, VL thalamotomy. As well, the impact of surgery on tremor seen during movement was quantified in a manual-tracking (MT) task. Tremor-induced noise (a measure of the amount of tremor present during movement) and ERROR (difference between subject's performance and target) were quantified. Finally, bradykinesia was assessed with a rapid alternating movement (RAM) task. Duration, range, and amplitude irregularity of wrist pronation-supination cycles were computed. Both motor tasks were quantified using a highly sensitive forearm rotational sensor. Healthy age-matched control subjects were also tested. Magnetic resonance images with an integrated atlas of thalamic nuclei were used to confirm lesion location. Results show that the lesions were centered upon the posterior portion of the ventral lateral (VLp) nucleus of the thalamus, included the posterior part of the ventral lateral anterior nucleus (VLa), and extended posteriorly to encroach upon the most rostral sector of the sensory ventral posterior nucleus (VPLa). VL thalamotomy significantly decreased tremor amplitude in all cases. Power dispersion was increased significantly so that it became similar to that of control subjects. Changes in power distribution indicate that thalamotomy selectively targeted PD tremor oscillations. Tremor detected during the MT task was also markedly decreased, becoming similar to that of controls. Patients also showed significant decrease in ERROR during MT. RAM duration and range were not significantly modified by the surgery, and patients' performance remained impaired compared to healthy control subjects. Collectively, these results suggest that lesions involving the presumed "cerebellar" and "pallidal" recipient sectors of the motor thalamus do not worsen bradykinesia, suggesting that neural circuits other than the pallido-thalamo-cortical loop may be involved in slowness of movement in PD. A review of alternate pathways is presented.
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Sadikot</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>McGill Centre for Studies on Aging, McGill University. 3801 University Street</s1><s2>H3A 2B4 Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>H3A 2B4 Montreal, Quebec</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Experimental brain research</title><title level="j" type="abbreviated">Exp. brain res.</title><idno type="ISSN">0014-4819</idno><imprint><date when="2006">2006</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Experimental brain research</title><title level="j" type="abbreviated">Exp. brain res.</title><idno type="ISSN">0014-4819</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bradykinesia</term><term>Human</term><term>Irregularity</term><term>Lateral nucleus</term><term>Magnetic resonance</term><term>Manual task</term><term>Parkinson disease</term><term>Power spectrum</term><term>Sensory nucleus</term><term>Supination</term><term>Thalamus</term><term>Tracking task</term><term>Tremor</term><term>Upper limb</term><term>Ventral nucleus</term><term>Wrist</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Thalamus</term><term>Spectre puissance</term><term>Tâche manuelle</term><term>Tâche poursuite</term><term>Irrégularité</term><term>Poignet</term><term>Supination</term><term>Membre supérieur</term><term>Tremblement</term><term>Résonance magnétique</term><term>Noyau ventral</term><term>Parkinson maladie</term><term>Noyau latéral</term><term>Noyau sensitif</term><term>Homme</term><term>Pronation</term><term>Bradykinésie</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A preferred target for parkinsonian tremor alleviation is the ventrolateral (VL) thalamus. The goal of the present study is to determine how lesions involving the presumed cerebellar and pallidal recipient areas of the "motor" thalamus would alter the tremor and motor behavior of ten patients with Parkinson's disease (PD). Tremor amplitude, power dispersion (a measure of sharpness of the power spectrum of tremor), and power distribution were quantified using a laser displacement sensor prior to, and a week after, VL thalamotomy. As well, the impact of surgery on tremor seen during movement was quantified in a manual-tracking (MT) task. Tremor-induced noise (a measure of the amount of tremor present during movement) and ERROR (difference between subject's performance and target) were quantified. Finally, bradykinesia was assessed with a rapid alternating movement (RAM) task. Duration, range, and amplitude irregularity of wrist pronation-supination cycles were computed. Both motor tasks were quantified using a highly sensitive forearm rotational sensor. Healthy age-matched control subjects were also tested. Magnetic resonance images with an integrated atlas of thalamic nuclei were used to confirm lesion location. Results show that the lesions were centered upon the posterior portion of the ventral lateral (VLp) nucleus of the thalamus, included the posterior part of the ventral lateral anterior nucleus (VLa), and extended posteriorly to encroach upon the most rostral sector of the sensory ventral posterior nucleus (VPLa). VL thalamotomy significantly decreased tremor amplitude in all cases. Power dispersion was increased significantly so that it became similar to that of control subjects. Changes in power distribution indicate that thalamotomy selectively targeted PD tremor oscillations. Tremor detected during the MT task was also markedly decreased, becoming similar to that of controls. Patients also showed significant decrease in ERROR during MT. RAM duration and range were not significantly modified by the surgery, and patients' performance remained impaired compared to healthy control subjects. Collectively, these results suggest that lesions involving the presumed "cerebellar" and "pallidal" recipient sectors of the motor thalamus do not worsen bradykinesia, suggesting that neural circuits other than the pallido-thalamo-cortical loop may be involved in slowness of movement in PD. A review of alternate pathways is presented.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0014-4819</s0></fA01><fA02 i1="01"><s0>EXBRAP</s0></fA02><fA03 i2="1"><s0>Exp. brain res.</s0></fA03><fA05><s2>170</s2></fA05><fA06><s2>2</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>The impact of ventrolateral thalamotomy on tremor and voluntary motor behavior in patients with Parkinson's disease</s1></fA08><fA11 i1="01" i2="1"><s1>DUVAL (Christian)</s1></fA11><fA11 i1="02" i2="1"><s1>PANISSET (Michel)</s1></fA11><fA11 i1="03" i2="1"><s1>STRAFELLA (Antonio P.)</s1></fA11><fA11 i1="04" i2="1"><s1>SADIKOT (Abbas F.)</s1></fA11><fA14 i1="01"><s1>Faculty of Applied Health Science, Brock University</s1><s2>St. Catharines, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ></fA14><fA14 i1="02"><s1>McGill Centre for Studies on Aging, McGill University. 3801 University Street</s1><s2>H3A 2B4 Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street</s1><s2>H3A 2B4 Montreal, Quebec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></fA14><fA20><s1>160-171</s1></fA20><fA21><s1>2006</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>12535</s2><s5>354000142808880030</s5></fA43><fA44><s0>0000</s0><s1>© 2006 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.3/4</s0></fA45><fA47 i1="01" i2="1"><s0>06-0335278</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Experimental brain research</s0></fA64><fA66 i1="01"><s0>DEU</s0></fA66><fC01 i1="01" l="ENG"><s0>A preferred target for parkinsonian tremor alleviation is the ventrolateral (VL) thalamus. The goal of the present study is to determine how lesions involving the presumed cerebellar and pallidal recipient areas of the "motor" thalamus would alter the tremor and motor behavior of ten patients with Parkinson's disease (PD). Tremor amplitude, power dispersion (a measure of sharpness of the power spectrum of tremor), and power distribution were quantified using a laser displacement sensor prior to, and a week after, VL thalamotomy. As well, the impact of surgery on tremor seen during movement was quantified in a manual-tracking (MT) task. Tremor-induced noise (a measure of the amount of tremor present during movement) and ERROR (difference between subject's performance and target) were quantified. Finally, bradykinesia was assessed with a rapid alternating movement (RAM) task. Duration, range, and amplitude irregularity of wrist pronation-supination cycles were computed. Both motor tasks were quantified using a highly sensitive forearm rotational sensor. Healthy age-matched control subjects were also tested. Magnetic resonance images with an integrated atlas of thalamic nuclei were used to confirm lesion location. Results show that the lesions were centered upon the posterior portion of the ventral lateral (VLp) nucleus of the thalamus, included the posterior part of the ventral lateral anterior nucleus (VLa), and extended posteriorly to encroach upon the most rostral sector of the sensory ventral posterior nucleus (VPLa). VL thalamotomy significantly decreased tremor amplitude in all cases. Power dispersion was increased significantly so that it became similar to that of control subjects. Changes in power distribution indicate that thalamotomy selectively targeted PD tremor oscillations. Tremor detected during the MT task was also markedly decreased, becoming similar to that of controls. Patients also showed significant decrease in ERROR during MT. RAM duration and range were not significantly modified by the surgery, and patients' performance remained impaired compared to healthy control subjects. Collectively, these results suggest that lesions involving the presumed "cerebellar" and "pallidal" recipient sectors of the motor thalamus do not worsen bradykinesia, suggesting that neural circuits other than the pallido-thalamo-cortical loop may be involved in slowness of movement in PD. 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l="FRE"><s0>Trouble neurologique</s0><s5>22</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Neurological disorder</s0><s5>22</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Trastorno neurológico</s0><s5>22</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>23</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>23</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>23</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>24</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>24</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>24</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>25</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>25</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>25</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>26</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>26</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>26</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>27</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Central nervous system</s0><s5>27</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>27</s5></fC07><fN21><s1>219</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist><affiliations><list><country><li>Canada</li></country><region><li>Québec</li></region><settlement><li>Montréal</li></settlement><orgName><li>Université McGill</li></orgName></list><tree><country name="Canada"><noRegion><name sortKey="Duval, Christian" sort="Duval, Christian" uniqKey="Duval C" first="Christian" last="Duval">Christian Duval</name></noRegion><name sortKey="Duval, Christian" sort="Duval, Christian" uniqKey="Duval C" first="Christian" last="Duval">Christian Duval</name><name sortKey="Duval, Christian" sort="Duval, Christian" uniqKey="Duval C" first="Christian" last="Duval">Christian Duval</name><name sortKey="Panisset, Michel" sort="Panisset, Michel" uniqKey="Panisset M" first="Michel" last="Panisset">Michel Panisset</name><name sortKey="Panisset, Michel" sort="Panisset, Michel" uniqKey="Panisset M" first="Michel" last="Panisset">Michel Panisset</name><name sortKey="Sadikot, Abbas F" sort="Sadikot, Abbas F" uniqKey="Sadikot A" first="Abbas F." last="Sadikot">Abbas F. Sadikot</name><name sortKey="Strafella, Antonio P" sort="Strafella, Antonio P" uniqKey="Strafella A" first="Antonio P." last="Strafella">Antonio P. Strafella</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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