Interhemispheric and ipsilateral connections in Parkinson's disease: Relation to mirror movements

• Published in: Movement disorders 2007-04, Vol.22 (6), p.813-821
• Main Authors: Li, Jie-Yuan, Espay, Alberto J., Gunraj, Carolyn A., Pal, Pramod K., Cunic, Danny I., Lang, Anthony E., Chen, Robert
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Brain - physiopathology; Corpus Callosum - anatomy & histology; Corpus Callosum - physiopathology; cortical inhibition; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Electromyography; Female; Functional Laterality; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Humans; Male; Medical sciences; Middle Aged; mirror movements; Motor Activity - physiology; Movement Disorders - physiopathology; Nervous system (semeiology, syndromes); Neurology; Parkinson Disease - physiopathology; Parkinson's disease; Reference Values; transcallosal inhibition; transcranial magnetic stimulation
• ISSN: 0885-3185; 1531-8257
• DOI: 10.1002/mds.21386

Mirror movements (MM) occur in early, asymmetric Parkinson's disease (PD). To examine the pathophysiology of MM in PD, we studied 13 PD patients with MM (PD‐MM), 7 PD patients without MM (PD‐NM), and 14 normal subjects. Cross‐correlogram did not detect common synaptic input to motoneuron pools innervating homologous hand muscles in PD‐MM patients. Transcranial magnetic stimulation studies showed no significant difference in ipsilateral motor‐evoked potentials between PD‐MM patients and normal subjects. The MM side of PD‐MM patients showed a slower increase in ipsilateral silent period area with higher level of muscle contraction than the non‐MM side and normal subjects. There was less interhemispheric inhibition (IHI) at long interstimulus intervals of 20 to 50 ms in PD‐MM than PD‐NM. IHI reduced short interval intracortical inhibition in normal subjects and PD‐NM, but not in PD‐MM. IHI significantly increased intracortical facilitation in PD‐MM and PD‐NM patients, but not in normal subjects. Our results suggest that MM in PD is due to activation of the contralateral motor cortex. PD‐MM patients had reduced transcallosal inhibitory effects on cortical output neurons and on intracortical inhibitory circuits compared to PD‐NM patients and controls. These deficits in transcallosal inhibition may contribute to MM in PD patients. © 2007 Movement Disorder Society