By Crina Frincu-Mallos, PhD
BALTIMORE, Md -- October 14, 2009 -- The use of nortriptyline and paroxetine in the treatment of depression does not affect cognitive functioning in patients with Parkinson's disease (PD); however, the higher the baseline performance on measures of executive functioning, speed of processing, and verbal memory, the better the response to antidepressant treatment, according to results presented here at the American Neurological Association (ANA) 134th Annual Meeting.
"This is one of the few studies to examine the impact of antidepressant treatment on cognition in PD patients with depression," said Roseanne D. Dobkin, PhD, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey.
More than 1 million people are affected by PD in the United States alone. It is the second most common neurodegenerative disease in the country, said Dr. Dobkin on October 10.
"Depression is one of the most common nonmotor symptoms of PD, affecting as many as half of these patients," she added.
The investigators evaluated the effect on cognition of antidepressant treatment administered for 8 weeks (acute phase) versus 24 weeks (extension phase) in this patient population. They were also interested in determining any cognitive predictors of response to antidepressant treatment.
The analysis included data from 52 PD patients aged 35-80 years (27 men) who participated in the randomised, placebo-controlled, double-blind clinical trial of nortriptyline and paroxetine. Time since diagnosis of PD averaged 6.6 years. All patients received treatment for major depression or dysthymia with either nortriptyline 25- to 75-mg tablets, paroxetine 12.5- to 37.5-mg tablets, or 1-3 placebo tablets.
During the acute phase, 15 patients responded to treatment. Response was defined as >50% reduction on the Hamilton Depression Rating Scale between baseline and week 8, according to protocol.
"Treatment responders had significantly higher baseline scores on measures of processing speed, executive functioning, and memory," indicated Dr. Dobkin. The Stroop composite value was t(50) = 2.80 (P = .007), and the memory composite score was t(50) = 2.05 (P = .018).
"However, executive function and speed of processing, but not memory, were found to be neuropsychological predictors of acute treatment response," remarked Dr. Dobkin, adding that in this phase, responders did not demonstrate greater improvement in cognition than nonresponders.
Regardless of responder status, patients who agreed to remain blinded to study therapy and had scored between 1 and 3 on the Clinical Global Impression Improvement scale were eligible to continue with the extension phase.
Over the course of the study, the 20 patients in the extension phase demonstrated significant improvement in verbal memory (F[2,17] = 7.93; P = .004) and on a test of language (F[2,16] = 6.37; P = .009). Interestingly, the antidepressant drug had no effect on cognition in the extension phase either, noted Dr. Dobkin.
"Overall, our findings suggest that higher baseline performance on measures of executive functioning, speed of processing, and verbal memory was associated with antidepressant treatment response in PD," said Dr. Dobkin.
The researchers warned that the language improvements observed during the extension phase need to be interpreted carefully, given the absence of a comparison condition. They acknowledged the need for further research in a larger population sample to replicate and better explain these findings.
Funding for this study was provided by the National Institute of Neurological Disorders and Stroke, National Institutes of Health.
[Presentation title: The Impact of Antidepressant Treatment on Cognitive Functioning in Depressed Patients With Parkinson's Disease. Abstract CD-6]
E-Mail this DGDispatch to a colleague
