Lack of effects of pramipexole on REM sleep behavior disorder in Parkinson disease.

PARKINSON DISEASE (PD) IS A NEURODEGENERATIVE DISORDER ASSOCIATED WITH LOSS OF THE DOPAMINERGIC CELLS IN THE SUBSTANTIA NIGRA resulting in bradykinesia, tremor, and rigidity. These classical motor symptoms are responsive to dopaminergic agents. In PD, the degenerative process also involves non-dopaminergic neuronal areas beyond the substantia nigra such as the lower brainstem, the amygdala, and the cortex. Impairment of these brain areas in PD account for the occurrence of several non-motor symptoms, including dysautonomia and dementia, which do not respond to dopamine replacement therapy.1 REM sleep behavior disorder (RBD) is a frequent feature of PD that is characterized by dream-enacting behaviors, unpleasant dreams, and loss of muscle atonia during REM sleep.2,3 It is unknown if RBD in PD results from dopaminergic deficiency. To assess whether dopaminergic dysfunction plays a major role in the pathogenesis of RBD in PD, we prospectively examined the therapeutic effect of pramipexole, a D2-D3 dopamine receptor agonist, on RBD features in patients with PD.