Has anyone tried light therapy? This is just my fourth experiment with it, but I swear to goodness that it seems to work! I stumbled to bed about 10:30 PM with my usual freezing coming on. Woke about 11:30 to hit the john and thought I would struggle to the kitchen for a cracker or two. As I expected, it was doable but still a pain. I knew it would be at least three or four o'clock before it started to shift so I figured I would eat and flee back to my wonderfully horizontal bed. But while I was eating I thought what the heck and turned on the light that I had been experimenting with for the last few days.

It is now 1:00 AMand I have been fully "ON" for 45 minutes! The previous and admittedly sloppy trials had shown enough benefit that I didn't quite write it off as imagination. But this one is the most impressive yet.

I'm using a $20 wonder from Office Depot with a full spectrum type bulb (T4 12W 6400K) full in the face from about six feet away. Stay tuned.

Went on to bed shortly after the first post. Still in unusually good shape for that time of the morning. Slept through until shortly after 6 AM. Took meds and sat blearily in front of light. Came on in 30 min - half my usual!!

I shut the light off at about the 45 min point. Am coming up on the 2 hour point and feeling good. This is getting interesting.

1: Brain Res. 2008 Jun 27;1217:119-31. Epub 2008 Apr 11.

Intraocular microinjections repair experimental Parkinson's disease.

Willis GL.

The Bronowski Institute of Behavioural Neuroscience, Coliban Medical Centre,
Kyneton, Victoria, Australia. gwillbro@bigpond.com

Circadian involvement in Parkinson's disease (PD) and more specifically in
nigro-striatal dopamine (NSD) function is of increasing interest to the
neurosciences. Given that bright light therapy is of therapeutic value in PD,
possible mechanisms underlying retinal involvement in this phenomenon was
explored further by administering anti-Parkinsonian chemotherapies into the
vitreus humour directly adjacent to the retina. 2 microl of a 100 mM solution of
L-Dopa significantly improved motor function in the later stages of degeneration
and during the day while the injection of 2 microl of a 10 mM solution of the
melatonin receptor antagonist ML-23 improved motor function in the early stages
of PD and during the dark phase of the light/dark cycle. The results suggest that
the function of nigral cells is regulated by a more global system embracing
circadian physiology that extends from the retina to the pineal. Furthermore, the
induction of PD is characterised by an imbalance between melatonin and dopamine
(DA) whereby this ratio is elevated at least 6 to 1 in favour of melatonin. The
commonly observed treatment failures and side effects of DA replacement therapy
probably result from increasing endogenous DA without taking parallel melatonin
dysfunction into account. The proposed integrated function of the NSD and
circadian systems may permit therapeutic targeting at a level which is safer,
more effective and without the side effects of systemically administered regimens
of DA replacement.


PMID: 18502399 [PubMed - indexed for MEDLINE]

1: Chronobiol Int. 2007;24(3):521-37.

Primary and secondary features of Parkinson's disease improve with strategic
exposure to bright light: a case series study.

Willis GL, Turner EJ.

The Bronowski Institute of Behavioural Neuroscience, Coliban Medical Centre,
Kyneton, Victoria, Australia. gwillbro@nex.net.au

The antagonism of melatonin in models of Parkinson's disease (PD) can reduce the
severity of motor impairment associated with dopamine (DA) degeneration. In
consideration of the potent antidepressant effects of bright light therapy (LT),
that LT suppresses melatonin secretion, that depression is commonly observed in
PD, and that exposure to constant light facilitates recovery from experimental
PD, the object of the present study was to strategically administer LT to PD
patients and observe the effects on depression, insomnia, and motor performance.
Twelve patients diagnosed with PD were exposed to white fluorescent light for
1-1.5 h at an intensity of 1000 to 1500 lux once daily commencing 1 h prior to
the usual time of sleep onset, approximately 22:00 h in most patients. All
patients were assessed before LT commenced and at two weeks, five weeks, and
regular intervals thereafter. Within two weeks after commencing LT, marked
improvement in bradykinaesia and rigidity was observed in most patients. Tremor
was not affected by LT treatment; however, agitation, dyskinaesia, and
psychiatric side effects were reduced, as verified by decreased requirement for
DA replacement therapy. Elevated mood, improved sleep, decreased seborrhea,
reduced impotence, and increased appetite were observed after LT. LT permitted
the reduction of the dose of L-dopa, bromocriptine, or deprenyl in some patients
by up to 50% without loss of symptom control. Factors limiting the efficacy of LT
included multiple disease states, treatment compliance, polypharmacy, emotional
stress, advanced age, and predominance of positive symptoms. The results of this
case series study confirms previous work describing light as efficacious in the
treatment of PD and suggest that controlled trials may help to elucidate how LT
might be used strategically as an adjunct therapy to improve the morbidity of PD
patients.


PMID: 17612949 [PubMed - indexed for MEDLINE]

I seem to be making better use of the medications and getting longer on times. I also find it noticeably helps to come on in a shorter time. Today in the early afternoon I began to slip toward off and a week ago might have lost half a day. Thirty minutes of computer time with the light peeking over my laptop screen sent things back the other way. It is now 10:40 PM and I have had no meds since 4:00 PM and am fully on. I did an hour of light therapy (LT) from about 8:30 to 9:30. A week ago it would have been a struggle to get to bed at this time but I seem fine.

No dyskenisias today and only minor freezing in the early afternoon. Big improvement for me over last week.

There is little research beyond what I have posted. Just one other report from a Russian researcher in 1996 that I will add tomorrow. If this gets past the placebo stage for me (and I think it will handily) then I nominate it as a classic case of the drawback to allowing profits and patentability to guide research.

1: Zh Nevrol Psikhiatr Im S S Korsakova. 1996;96(3):63-6.

[The phototherapy of parkinsonism patients]

[Article in Russian]

Artemenko AR, Levin IaI.

40 patients with idiopathic parkinsonism were treated by artificial white light
(intensity--3300 lux) together with total or partial "drugs holidays". The
patients with newly made diagnosis "parkinsonism" were treated too. Both before
and after light therapy (LT) (10 light exposures) we performed estimation of the
main clinical manifestations of the disease (in rating scales), psychological
assessment (Back's depression rating scale), examination of motility (authors'
own special computer program "Hand's Movement Test for Windows"). It was observed
that LT resulted in a decrease of the severity of either rigidity or bradykinesia
(but not the tremor) as well as it also decreased the depression gravity and
improved the motor functions. LT facilitated the patients' capacity to tolerate
"the drugs holidays". LT permitted to combine it with drug therapy as well as LT
decreased the complications of DOPA-containing drugs (on-off-effects and dystonic
hyperkinesias). LT may be used as monotherapy in patients with initial
manifestations of the disease. LT didn't cause any complications and was quite
simple in carrying out. The conclusion is made about the perspectivity of LT
application in parkinsonism treatment as important non-drug therapy.


PMID: 8992840 [PubMed - indexed for MEDLINE]

Rick, my daughter, a pediatrician, sent me a high-intensity light box powered by hundreds of LEDs for my birthday in June. I used it a time or two then, but was not looking for any significant effects on PD motor symptoms, but for prevention of depression, and decided that I got plenty of light therapy from my outdoor time, so I stopped using it.

I think I will do some experiments with this apparatus and see if I can make small decreases in sinemet intake and maintain the same symptom relief. I will report my results at about this time next week.
Do you suppose she knew something about this melatonin/dopamine ratio stuff but didn't tell me?

Robert
btw, Dr. Marcie practices not far from you. She is in Murfreesboro, TN.

Robert-

This is both quite interesting and unexpected. I had no problem with thinking of it as a way of synchronizing circadian cycles. But this is something more immediate - as though it stimulates the release of something (or inhibits it).

I seem to be settling into a pattern of 30 to 60 minutes before bed and upon first arising - "dead" zones anyway. I try to remove my glasses at least part of the time but am not sure that is needed.

Stayed up until midnight to see if it was a "miracle cure". Was not. Hobbled to bed but happy since I had had no meds for over six hours which was about double of previous state.

Woke at 6 AM in better than average condition and meds kicked in in half an hour (about half the usual time). It is now 7:20 and I seem to be fully on.

I have to read up on it a bit, but if I remember correctly, the optic nerve stimulates the pineal gland which then starts up everything else in the endocrine system as morning comes on.

does it have similar benifits??

One would be looking right at it. Also. it rather thoughtlessly is not around when one needs it. That is not saying, however, that this is the only way that light may be important in PD. Consider the blue light effect, for example.

Thus far, I suspect that I am using a strong light as a tool to adjust some unknown force in my endocrine system or neurotransmitters. I am watching for a potential problem if raw material runs low for, say, dopamine due to forcing its production or something. No reason to expect it, but just possible.

Given the that the pineal gland is still mysterious, anything could be happening. It might even be that it is not working via the eyes at all, but through receptors in the skin of the forehead connected to the pineal. A couple of years ago they discovered similar receptors in the skin back of the knee which acted to relieve jet lag. Why not?