Chronic effects of dopaminergic replacement on cognitive function in Parkinson's disease: A two-year follow-up study of previously untreated patients

Citation
J. Kulisevsky et al., Chronic effects of dopaminergic replacement on cognitive function in Parkinson's disease: A two-year follow-up study of previously untreated patients, MOVEMENT D, 15(4), 2000, pp. 613-626
Citations number
92
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
MOVEMENT DISORDERS
ISSN journal
08853185 → ACNP
Volume
15
Issue
4
Year of publication
2000
Pages
613 - 626
Database
ISI
SICI code
0885-3185(200007)15:4<613:CEODRO>2.0.ZU;2-C
Abstract
BACKGROUND: The cognitive effects of dopaminergic treatment in Parkinson's disease (PD) are still controversial. OBJECTIVE: To evaluate, in previously untreated patients with PD, whether c hronic dopaminergic stimulation produces significant cognitive changes; whe ther they are sustained beyond the period of a few months; and whether the cognitive status of two motor-comparable groups is differently affected by levodopa and pergolide. DESIGN AND SUBJECTS: Parallel, randomized open study with blind neuropsycho logic evaluation of 20 consecutive de novo patients with PD before and 3, 6 , 12, 18, and 24 months after monotherapy with levodopa (n = 10) or pergoli de (n = 10; 6-month monotherapy; pergolide + levodopa thereafter). RESULTS: Both treatments were associated with a significant improvement in motor scores and in tests assessing learning and long-term verbal and visua l memory, visuospatial abilities, and various frontal tasks. While improvem ent in motor scores persisted, improvement in activities of daily living an d in semantic fluency, Luria's rhythm and motor and long-term memory tests was not sustained at the 24-month examination. Further, performance on atte ntional, short-term memory, and the Stroop tests did not change over the co urse of the study. CONCLUSIONS: Both treatments were associated with incomplete but long-lasti ng (18 mos) improvement in many cognitive tasks which declined thereafter, suggesting that dopaminergic replacement is not enough to compensate for al l cognitive deficits of PD.