Abstract
Hyperkinetic or dyskinetic disorders are characterized by excessive motor activity that interferes with normal motor control mechanism. Levodopa-induced dyskinesias (LID) are mainly associated with several molecular, biochemical, and physiological changes in the basal ganglia (BG). This chapter focuses on LID. The origin of LID in PD is mainly related to the impact on striatal physiology of nigrostriatal dopaminergic depletion and discontinuous levodopa replacement therapy. These combine to induce abnormal expression of dopamine-receptor signaling and neuropeptides, leading to deranged corticostriatal plasticity. LID generally occur in patients with motor fluctuations and can be classified into three main groups: (1) peak-dose choreic or dystonic movements, (2) diphasic dyskinesias, and (3) off -period dystonia. Avoiding pulsatile dopaminergic stimulation results in reduction in the incidence and severity of LID in the general PD population. Treatment of severe LID requires continuous dopaminergic stimulation by means of infusions. DBS of the GPi or the STN is also highly efficacious in the treatment of LID. In patients with very severe and complex LID, GPi-DBS can be a safer indication, even when pallidal surgery is not associated with a significant reduction in daily levodopa intake.
Published Version
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