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Mirror movements may result from a primary motor efferent system dysfunction with secondary motor reorganisation. A profound dysfunction of the motor pathways has been reported in Parkinson’s disease (PD) during execution of motor tasks.1,2 Recent PET studies have demonstrated overactivation of ipsilateral motor areas in hemiparkinsonian patients.3,4 However, the clinical expression of ipsilateral cortical activation was not specifically investigated in previous reports. In this study, we explored the presence of mirror movements (MM) during standardised unilateral hand tasks in a series of 21 hemiparkinsonian patients.
Patients were divided into two groups: de novo patients (n=11), age 53.2 (7.5) years (mean (SD)), duration of evolution 1.8 years (range: 1–5 years), UPDRS III motor score 12 (5.7), affected side: left n=5, right n=6; and treated patients (n=10), age 59.8 (7.6) years, duration of evolution 3.7 (1.8) years (range: 2–7 years), UPDRS III motor score 14 (7.5), affected side: left n=4, right n=6, mean daily dose of levodopa: 450 mg (range: 300–900 mg), improvement of motor disability >40% (range: 40%–80%). Evaluation was performed as follows: for de novo patients, before treatment; for the treated patients, in the “off” condition after at least 12 hours withdrawal of antiparkinsonian treatment (levodopa). Patients were not tested in the “on” condition, to avoid confusion between dyskinesia and MM. They were compared with 21 age matched normal subjects, age 56.4 (10.8) years.
Subjects were told to hold their hands in the air with the elbows flexed and to perform a voluntary movement with one hand while the other hand was relaxed. Each hand was tested separately in the following four tasks performed 10 times as rapidly as possible with the widest amplitude: (1) pronosupination movements, (2) opening and closing of the hand, (3) finger tapping (thumb and index finger), (4) flexion-extension movements of the wrist. Tasks 1 to 3 correspond to items 23 to 25 of the UPDRS III, respectively.
Each task was scores as follows: 0= no MM, 1=MM (that is, the presence of repetitive unintentional contralateral movements that mimic totally or partially the intended movement. The “MM score” was the combined score for the task, for each side (maximum 4). Statistical analysis was performed using the non-parametric Spearman test, for a correlation analysis between the “MM score” and the UPDRS motor score.
In 80% of the de novo patients and 90% of the already treated and more severely affected patients, tested in the “off” condition, MM were observed in the relaxed hand while voluntary movements were being performed with the other hand. The most remarkable finding was that MM were never observed when voluntary movements were performed with the non-affected hand, whereas they were almost constant when voluntary movements were performed with the affected hand. They were observed both in the de novo group and the treated group. There were more often observed for alternate movements or repetitive flexion/extension movements of the wrist than for finger tapping. None of the control subjects displayed MM.
In the de novo patients, there was a significant correlation (r=0.60; p=0.0475) between the severity of motor impairment, as defined by the UPDRS III motor score, and the occurrence of MM as indicated by the “MM score”. No such correlation existed in the treated group.
Mirror movements could reflect the higher than normal level of cerebral activation in response to complex movements reported both in normal subjects2 and in PD patients.1–3 However, none of the controls displayed MM and the four tasks were not complex as patients performed them without difficulty, albeit more slowly.
Alternatively, extended recruitment of cortical motor areas could reflect an overflow of commands into the contralateral hemisphere in unilaterally affected patients. In line with recent experimental results in a unilateral rodent model of Parkinson’s disease,5 and in patients,2,3 we suggest that MM observed in the non-involved hand during movements of the akinetic hand reflect ipsilateral activation of the primary motor cortex.3,4 In the absence of sensorimotor activation controlateral to the affected akinetic (right) hand, the ipsilateral diffusion of activation may be considered as a compensatory mechanism.3 This ipsilateral activation could be explained in two different ways. Firstly, a corticocortical spread as the two hemispheres are connected via the corpus callosum and corticocortical pathways. Secondly, bilateral basal ganglia projections as several anatomical observations have shown that the basal ganglia are reciprocally and directly connected to the contralateral cortex.6 Thus, the activation of the ipsilateral motor cortex could result from the activation of one or both of these pathways. The precise role of the ipsilateral activation of the primary cortex in the pathophysiology of Parkinson’s disease is still unknown but it could be suggested that this phenomenon is a compensatory mechanism.
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