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Background: Rasagiline, an MAO-B inhibitor, is indicated for the treatment of Parkinson's disease (PD). In this post hoc analysis, the efficacy, safety and tolerability of rasagiline as an adjunct to levodopa were compared with placebo in elderly (≥70 years) and younger (<70 years) patients with PD., Methods: Data were pooled from the Parkinson's Rasagiline: Efficacy and Safety on the Treatment of 'OFF' and Lasting effect in Adjunct therapy with Rasagiline Given Once daily randomized, double-blind, placebo-controlled trials with the primary efficacy end-point being the reduction from baseline in daily OFF time. Secondary efficacy end-points included scores for Clinical Global Improvement (CGI)-Examiner during ON time, Unified Parkinson's Disease Rating Scale (UPDRS)-ADL during OFF time, UPDRS-Motor during ON time and total daily ON time with and without troublesome dyskinesia. Tolerability was evaluated from adverse events (AEs) in the two age groups., Results: Rasagiline decreased daily OFF time versus placebo (P<0.01) and improved CGI-Examiner score (P=0.001) and UPDRS-Motor ON score (P<0.05). Changes in UPDRS-ADL OFF score and total daily ON time without dyskinesia also favoured rasagiline but were not significant. Between-group comparisons (≥70 vs. <70 years) showed that efficacy was unaffected by age for all end-points (P>0.1), and rasagiline was well tolerated amongst both groups of patients with a comparable incidence of total and dopaminergic AEs (P>0.1)., Conclusions: Adjunct rasagiline is efficacious and well tolerated in elderly non-demented patients (≥70 years) with moderate to advanced PD. Confirmation of the efficacy and safety of rasagiline in the elderly patient subgroup is especially relevant because of the increasing number of elderly patients with PD., (© 2011 The Author(s). European Journal of Neurology © 2011 EFNS.)

Although Parkinson's disease is considered a movement disorder, it has a wide range and high prevalence of affective, psychotic, cognitive, behavioral and sleep-related features. To treat such features, agents including antidepressants, anxiolytics, antipsychotics and cognition-enhancing agents are commonly prescribed, although the targeted syndromes are often incompletely understood and controlled studies demonstrating a treatment's efficacy and tolerability in Parkinson's disease patients are often lacking. Nevertheless, the available information does suggest the outlines of management methods, pending expanded research to identify optimal strategies specific to Parkinson's disease.

Dopaminergic therapy is increasingly recognized as a cause of excessive daytime sleepiness in patients with PD. This adverse effect may be a dose-related phenomenon that is somewhat more likely to occur with dopamine agonists than with levodopa, although all dopaminergic drugs can be sedating. However, medication effect is only one of several causes of somnolence in PD. Other factors include age-related changes in sleep quality, nocturnal motor disturbances, primary sleep disorders such as sleep apnea, medication-induced sleep disruption, and concurrent medical illnesses. There is also increasing evidence that the disease process itself may affect the control of the sleep-wake cycle. Although we have characterized the sleep disturbances in PD, further investigation is needed to define their prevalence and etiology, particularly with respect to the role of dopamine and dopaminergic agents. Clinicians should be alert to the complaint of excessive sleepiness in their patients and should attempt to identify and treat the underlying causes.

Decreased olfactory function is among the first signs of idiopathic Parkinson's disease (PD). Whether such dysfunction is present to the same degree on both sides of the nose, however, is unknown. Furthermore, whether the deficit results from or is influenced by anti-Parkinsonian medications has not been definitely established. Odour identification ability was evaluated on the left and right sides of the nose in 20 early-stage untreated PD patients, 20 early-stage treated PD patients, and 20 controls. In all cases, the PD related olfactory dysfunction was bilateral and no difference was observed between the test scores of patients taking or not taking drugs for PD. Although asymmetries of unsystematic direction were present in the test scores of some PD patients, similar asymmetries were observed in the controls and the asymmetries were not related to the side of the major motor dysfunction. As in earlier work, no relation was present between the olfactory test scores and the degree of tremor, rigidity, bradykinesia, or gait disturbance at the time of testing. These findings indicate that the olfactory dysfunction of early stage PD is robust, typically of the same general magnitude on both sides of the nose, and uninfluenced by anti-Parkinsonian medications.