Ritalin May Improve Parkinson's Symptoms, OHSU Study Says
ScienceDaily (May 7, 2004) — PORTLAND, Ore. – A well-known drug used to treat 
hyperactive children boosts the potency of another drug that reduces 
Parkinson's disease symptoms, an Oregon Health & Science University study has 
found.

 Scientists at the OHSU Parkinson Center of Oregon found that methylphenidate, 
known commercially as Ritalin, bolsters the effects of levodopa, a drug 
converted in the brain to dopamine. Methylphenidate inhibits the reabsorption 
of dopamine into nerve cells, increasing the neurotransmitter's potency. 
Parkinson's disease is caused by a deficiency of nerve cells that produce 
dopamine. 
A parallel study by Parkinson center researchers found that paroxetine, a 
popular antidepressant best known under the brand name Paxil, doesn't augment 
the effects of levodopa and has little benefit in reducing physical symptoms 
of Parkinson's disease. 
Paroxetine is a selective serotonin reuptake inhibitor, or SSRI, a class of 
antidepressants that block the reabsorption of another neurotransmitter, 
serotonin, into nerve cells. Researchers studied it because laboratory 
evidence has suggested the serotonin transporter, the system through which 
serotonin is reabsorbed into nerve cells, may take up dopamine as well. 
"Both studies looked at the effects of these drugs on Parkinson's disease," 
said John "Jay" G. Nutt, M.D., professor of neurology, and physiology and 
pharmacology, OHSU School of Medicine, and director of the Parkinson center. 
He also is director of the Parkinson's Disease Research, Education, and 
Clinical Center (PADRECC) at the Portland Veterans Affairs Medical Center. 
The studies were presented last week at the 56th annual meeting of the 
American Academy of Neurology in San Francisco. 
Ritalin, the drug used in the methylphenidate study, "increases the effects of 
levodopa," Nutt said, while paroxetine didn't affect Parkinson's disease 
symptoms. However, paroxetine, when taken without levodopa, did increase the 
walking speed of Parkinson's patients. 
"There was no evidence that (paroxetine) made Parkinson's disease worse, as 
some clinicians have suggested," Nutt said. "If that occurred, it probably 
wasn't by negatively impacting dopamine's effects." 
In the Ritalin study, 14 Parkinson's disease patients with fluctuating 
responses to levodopa were examined. All received two-hour levodopa infusions 
at either minimum or maximum doses for four consecutive days, but some also 
received oral doses of Ritalin. Participants were then tested for symptoms of 
Parkinsonism, including tapping and walking speeds; dyskinesia or involuntary 
movements such as twitching, nodding and jerking; mood, anxiety and fatigue; 
and sitting blood pressure. 
Ritalin amplified the effects of levodopa, particularly for those given 
minimum doses of levodopa. It increased, from 36 percent to 86 percent, the 
number of patients responding to levodopa, and it boosted the duration of 
levodopa response as measured by tapping and walking tests. But the severity 
of dyskinesia, a side effect of levodopa therapy, did not rise. 
In addition, Ritalin decreased another levodopa side effect – hypotension, or 
low blood pressure – and it enhanced improvements levodopa made in mood and 
decreased fatigue. Adverse effects, in general, were minimal, and the drug 
had no effect when given alone to Parkinson's disease patients. 
The study's findings do more than show that Ritalin improves patients' 
responses to levodopa, Nutt said. They confirm the importance of the dopamine 
transporter, the system through which dopamine is reabsorbed into nerve 
cells, and shows that the transporter may be a target for other 
levodopa-boosting drugs. 
"It may be that by blocking the dopamine transporter with one drug or another, 
we can augment the effects of levodopa and get better control of Parkinson's 
disease," he said. 
Pharmaceutical companies already are looking at other drugs that may block the 
transporter, Nutt added. And the OHSU Parkinson Center will continue to study 
Ritalin, including whether more doses promotes levodopa response throughout 
the day. 
"The first study is proof of principle – blocking the dopamine transporter," 
Nutt said. "Now the question is, would Ritalin be the drug to do that? That's 
not clear." 
The paroxetine study was conducted on 14 people with varying severity of 
Parkinson's disease. Each was given two-hour levodopa infusions; some also 
received paroxetine for two weeks while the rest were given a placebo. The 
subjects were then scored for tapping rate, tremor and dyskinesia, as well as 
walking speed. 
Paroxetine, when given with levodopa, didn't affect tapping, dyskinesia or 
tremor, according to the findings. In fact, six people reported worse balance 
while on paroxetine. 
Nutt's Ritalin study collaborators were Julie H. Carter, R.N., A.N.P., 
associate professor of neurology, OHSU School of Medicine, and associate 
director of the Parkinson center; and Gary J. Sexton, Ph.D., associate 
professor of public health and preventive medicine, OHSU School of Medicine. 
Paroxetine study collaborators were Kathryn A. Chung, M.D., assistant 
professor of neurology, OHSU School of Medicine and the Parkinson center, and 
PADRECC, Portland VA Medical Center. 
 Both studies were supported by the National Institute of Neurological 
Disorders and Stroke, National Institutes of Health; PADRECC; and the 
National Parkinson Foundation.

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