Brief Report
Bright light therapy in Parkinson's disease: A pilot study

Sebastian Paus, MD 1 *, Tanja Schmitz-Hübsch, MD 1, Ullrich Wüllner, MD 1, Antje Vogel, MD 2, Thomas Klockgether, MD 1, Michael Abele, MD 1
1Department of Neurology, University of Bonn, Bonn, Germany

Movement Disorders
Volume 22 Issue 10, Pages 1495 - 1498

Published Online: 21 May 2007

Abstract

Several observations suggest a beneficial effect of melatonin antagonism for Parkinson's disease (PD). Although bright light therapy (BLT) suppresses melatonin release and is an established treatment for depression and sleep disturbances, it has not been evaluated in PD.

We examined effects of BLT on motor symptoms, depression, and sleep in PD in a randomized placebo-controlled double-blind study in 36 PD patients, using Parkinson's Disease Rating Scale (UPDRS) I-IV, Beck's Depression Inventory, and Epworth Sleepiness Scale.

All patients received BLT for 15 days in the morning, 30 min daily. Illuminance was 7.500 lux in the active treatment group and 950 lux in the placebo group. Although group differences were small, BLT led to significant improvement of tremor, UPDRS I, II, and IV, and depression in the active treatment group but not in the placebo group. It was very well tolerated. Follow up studies in more advanced patient populations employing longer treatment durations are warranted. © 2007 Movement Disorder Society

http://www3.interscience.wiley.com/j...65653/abstract

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Drug News Perspect 2005, 18(7): 437
ISSN 0214-0934
Copyright 2005 Prous Science
CCC: 0214-0934


Recent preclinical and clinical work has reliably demonstrated that melatonin may be without therapeutic efficacy in Parkinson's disease and may even worsen the condition.

The Role of ML-23 and Other Melatonin Analogues in the Treatment and Management of Parkinson�s Disease

by Gregory L. Willis

Summary

Contemporary theory regarding the cause and treatment of neuropsychiatric disease strongly suggests that as the human body ages it gradually loses the intrinsic safeguards that protect it from oxidative damage. Melatonin is one hormone that serves this function in that it possesses antioxidative properties in the mammalian body and brain.

Melatonin has been shown to prevent the progressive degeneration produced by neurotoxins employed in experimental models to mimic the degenerative events in various neuropsychiatric disease states. There are an abundance of models for numerous disease states demonstrating that melatonin can inhibit oxidative stress and by such a mechanism it is presumed to exert a therapeutic effect.

While a similar scenario has been revealed with in vitro work relating specifically to Parkinson�s disease, clinical work with melatonin in this disorder demonstrates that it is devoid of any remarkable therapeutic effects. More recent preclinical and clinical work has reliably demonstrated that melatonin in fact may be without therapeutic efficacy and may even worsen the condition.

On this pretense, attempts to reduce the bioavailability of melatonin using a melatonin receptor antagonist have been found to completely restore behavioral and regulatory function in the presence of chronically reduced levels of dopamine, without producing side effects commonly seen with traditional dopamine replacement therapy.

The unavoidable conclusion from this work suggests that within the dynamic framework of the mammalian brain, hormones may play a duel, and possibly ambivalent, role in homeostasis and in the etiology of disease.

Such a position requires a reevaluation of the etiology, the role of dopamine, the neurochemical characteristics of Parkinson's disease and the validity of the models employed to study this and other neuropsychiatric disorders. © 2005 Prous Science. All rights reserved.

http://journals.prous.com/journals/s...=2836&p_IsPs=Y