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

<quote>
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.

<end quote>

You know, that's about as close to excitement as a researcher gets in print. :-)

ZF, any chance that you have the full text of that? Email or PM me if you do. Thanks.

PS- Does anyone have a comparative figure for "lux" as a unit of measure? Say a standard 100w incandescent bulb?

G.L. Willis has published work going back 30 years and thinks outside the box. The link below is to a listing of his works and is worth a look to those so inclines. In particular, his theory regarding PD as the result of amines accumulating at the synapses makes one look at dopamine replacement with new caution.

http://www.nextbio.com/b/literature/...thor=GL+Willis

There seems to be pineal dysfunction in PD...

Increased pineal Fdopa uptake is related to severity of Parkinson's disease - A PET study:

http://pt.wkhealth.com/pt/re/jpin/ab...195628!8091!-1

Serotonin metabolism is regulated by pineal melatonin, and the secretory activity of the pineal gland may be diminished in PD.

Bright light therapy suppresses pineal melatonin synthesis and secretion. It probably affects serotonin metabolism.

http://www.sciencedirect.com/science...d2dd180473a46c

Dopamine and retinal function

Paul Witkovsky

Abstract

This review summarizes the experimental evidence in support of dopamine''s role as a chemical messenger for light adaptation. Dopamine is released by a unique set of amacrine cells and activates D1 and D2 dopamine receptors distributed throughout the retina. Multiple dopamine-dependent physiological mechanisms result in an increased signal flow through cone circuits and a diminution of signal flow through rod circuits.

Dopamine also has multiple trophic roles in retinal function related to circadian rhythmicity, cell survival and eye growth. In a reciprocal way, the health of the dopaminergic neurons depends on their receiving light-driven synaptic inputs.

Dopamine neurons appear early in development, become functional in advance of the animal''s onset of vision and begin to die in aging animals.

Some diseases affecting photoreceptor function also diminish day/night differences in dopamine release and turnover.

A reduction in retinal dopamine, as occurs in Parkinsonian patients, results in reduced visual contrast sensitivity

http://www.springerlink.com/content/m42806m205730464/

Neuroscience Letters
Volume 360, Issue 3, 29 April 2004

Retinal illumination phase shifts the circadian rhythm of serotonin N-acetyltransferase activity in the chicken pineal gland

Jolanta B. Zawilska

Abstract

The pineal gland of birds, in contrast to its mammalian counterpart, is a directly photosensitive organ. It has recently been demonstrated that light also acting via the retina acutely suppresses melatonin synthesis in the chicken pineal gland.

The present study was aimed to investigate whether retinal illumination alone was capable of resetting the biological oscillator generating the circadian rhythm of pineal serotonin N-acetyltransferase (AA-NAT) activity in the chicken.

Ocular exposure of chickens to 6 h low intensity white light (4 lux) potently suppressed AA-NAT activity (the penultimate and key regulatory enzyme in the melatonin biosynthetic pathway) in the pineal gland. In addition, this light pulse produced phase-dependent shifts in the circadian AA-NAT rhythm.

Exposure to light early in the subjective night (circadian time (CT) 12–18) caused a phase delay in the circadian rhythm of pineal AA-NAT activity by 3.5±0.4 h compared to non-exposed controls. When the light pulse was applied during the second half of the subjective night (CT18–24), it produced a large phase advance of the circadian rhythm of pineal AA-NAT activity by 10.9±0.4 h.

The advancing effect of light was more pronounced than the phase-delaying effect.

Our results suggest that in the chicken retinally perceived light provides a powerful and important signal for synchronization of circadian rhythmicity in the pineal gland.

are very little help in providing useful data. I have to confess that, after only four days of doing the bright light therapy thing, I got distracted, lazy, or whaterver, and failed to continue.
I think one thing that weakened my resolve was the sense that I really did not want to risk possible negative consequences of decreasing meds. For the few days of use, I failed to detect any (at least subjective )changes.
Robert

Robert, sometimes no data is data. I found your notes about being averse to risking negative effects from med manipulation uncomfortably close to home. Although lord knows I do take that risk, it does make me uneasy at times.

For me it ties in to that damned sense of fragility that seems to go with this mess. Whether from PD or meds I don't know, but there is a sense of the edge of the abyss nearby at all times.

I will keep on with the morning exposure for a while and report from time to time.

Ah! Perhaps an explanation, or at least a theory that can explain why I look down at my feet in daylight and see that I am sporting one navy sock and the other black. I wondered if there was a connection to the PD.

This info is so inspiring I can' be more thrilled. That's straight talk without irony or sarcasm, nor my sometimes wry comments that are only intended to provide humor, but sometimes do not translate.

Shake 'Em Up

I came across a paper on Blue Light, melatonin/dopamine recently. After looking around for more info, I came across this old thread. Is anyone using light therapy for PD and how do they think they are doing? My problem is that I fall asleep easily but then wake up several times every night. I am no getting enough sleep. The article I read suggests that there is too much melatonin vs dopamine in PWP and that using bright light before bedtime reduces melatonin.
I have access to an Apollo blue light box but am hesitant to experiment.
Any thoughts?
Light at Night? How many minutes? Any noticeable effects? Sleep better?
Ashley