Background: Levodopa‐induced dyskinesias are associated with thalamo‐cortical disinhibition and frontal area overactivation. Neuroimaging and transcranial magnetic stimulation studies have highlighted the involvement of the right inferior frontal cortex in levodopa‐induced dyskinesias. Methods: Using transcranial magnetic stimulation, we tested connectivity between the inferior frontal and contralateral motor cortex in Parkinson's disease patients with and without levodopa‐induced dyskinesias compared with age‐matched controls. Furthermore, in dyskinetic patients, connectivity between the inferior frontal and contralateral motor cortex was assessed before and after a single session of continuous theta‐burst stimulation applied over the inferior frontal cortex. Results: Dyskinetic patients showed abnormal facilitatory connectivity between the inferior frontal and motor cortex when compared with the nondyskinetic group. Continuous theta‐burst stimulation over the inferior frontal cortex eliminated such facilitatory connectivity and decreased the levodopa‐induced dyskinesias that was induced by a supramaximal dose of levodopa. Conclusion: In dyskinetic patients, a weaker inhibitory cortico‐cortical interaction between the inferior frontal and contralateral motor cortex could be involved in levodopa‐induced dyskinesias and restored by continuous theta‐burst stimulation over the inferior frontal cortex.
Altered inhibitory interaction among inferior frontal and motor cortex in l-dopa-induced dyskinesias
Benussi, Alberto;
2016-01-01
Abstract
Background: Levodopa‐induced dyskinesias are associated with thalamo‐cortical disinhibition and frontal area overactivation. Neuroimaging and transcranial magnetic stimulation studies have highlighted the involvement of the right inferior frontal cortex in levodopa‐induced dyskinesias. Methods: Using transcranial magnetic stimulation, we tested connectivity between the inferior frontal and contralateral motor cortex in Parkinson's disease patients with and without levodopa‐induced dyskinesias compared with age‐matched controls. Furthermore, in dyskinetic patients, connectivity between the inferior frontal and contralateral motor cortex was assessed before and after a single session of continuous theta‐burst stimulation applied over the inferior frontal cortex. Results: Dyskinetic patients showed abnormal facilitatory connectivity between the inferior frontal and motor cortex when compared with the nondyskinetic group. Continuous theta‐burst stimulation over the inferior frontal cortex eliminated such facilitatory connectivity and decreased the levodopa‐induced dyskinesias that was induced by a supramaximal dose of levodopa. Conclusion: In dyskinetic patients, a weaker inhibitory cortico‐cortical interaction between the inferior frontal and contralateral motor cortex could be involved in levodopa‐induced dyskinesias and restored by continuous theta‐burst stimulation over the inferior frontal cortex.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
