6533b7d1fe1ef96bd125c311
RESEARCH PRODUCT
Cerebellar magnetic stimulation decreases levodopa-induced dyskinesias in Parkinson disease
Giacomo KochE Lo GerfoMassimiliano OliveriCarlo CaltagironeLivia BrusaPablo MirPaolo StanzioneFátima CarrilloSara Torrierosubject
Dyskinesia Drug-InducedLevodopaCerebellummedicine.medical_treatmentCTBStmSeverity of Illness IndexrehabilitationNOLevodopaNeural PathwaySeverity of Illness Index; Analysis of Variance; Levodopa; Dyskinesia Drug-Induced; Humans; Cerebellum; Aged; Neural Inhibition; Thalamus; Motor Cortex; Parkinson Disease; Evoked Potentials Motor; Neural Pathways; Middle Aged; Neuronal Plasticity; Transcranial Magnetic StimulationThalamusCerebellumNeural PathwaysBasal gangliamedicineHumansEvoked PotentialsThalamuAgedAnalysis of VarianceNeuronal PlasticityDyskinesiaMotor CortexNeural InhibitionParkinson DiseaseMiddle AgedEvoked Potentials MotorTranscranial Magnetic StimulationAged; Analysis of Variance; Cerebellum; Drug-Induced Dyskinesia; Evoked Potentials; Motor; Humans; Levodopa; Middle Aged; Motor Cortex; Neural Inhibition; Neural Pathways; Neuronal Plasticity; Parkinson Disease; Severity of Illness Index; Thalamus; Transcranial Magnetic StimulationTranscranial magnetic stimulationmedicine.anatomical_structureMotorDyskinesiaDrug-Inducedparkinson's diseaseSettore MED/26 - NeurologiaDrug-Induced DyskinesiaNeurology (clinical)Primary motor cortexmedicine.symptomPsychologyNeuroscienceHumanMotor cortexmedicine.drugdescription
BACKGROUND: The neural mechanisms and the circuitry involved in levodopa-induced dyskinesia (LID) are still partially obscure. LID can be considered the consequence of an abnormal pattern or code of activity that originates and is conveyed from the basal ganglia to the thalamus and the cortical motor areas. However, not only striatothalamocortical motor circuits but also other interconnected pathways could be implicated in its pathogenesis. METHODS: In a series of experiments, we applied repetitive transcranial magnetic stimulation (rTMS) over the lateral cerebellum in a group of patients with advanced Parkinson disease, to investigate whether modulation of cerebellothalamocortical circuits by means of rTMS may result in a modification of a dyskinetic state induced by levodopa ingestion. RESULTS: We found that a single session of cerebellar continuous theta burst stimulation (cTBS) was capable of transiently reducing LID. In the same patients, we observed that cerebellar cTBS changed the profile of activation of intracortical circuits in the contralateral primary motor cortex. Cerebellar cTBS reduced short intracortical inhibition and increased long intracortical inhibition, inducing a cortical reorganization that is associated with a reduction of LID. Furthermore, in another experiment, we observed that a 2-week course of bilateral cerebellar cTBS induced persistent clinical beneficial effects, reducing peak-dose LID for up to 4 weeks after the end of the daily stimulation period. CONCLUSIONS: Our study demonstrates that cerebellar continuous theta burst stimulation has an antidyskinetic effect in Parkinson disease patients with levodopa-induced dyskinesia, possibly due to modulation of cerebellothalamocortical pathways. © 2009 AAN Enterprises, Inc.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2009-01-01 | Neurology |