Some say it has no effect on non-motor symptoms (NMS); some say it does not always control tremor or bradykinesia very well.
In my (possibly atypical) case it has absolutely no effect on motor symptoms or NMS. But, if I reduce from one 100mg tablet 4 x daily to one tablet 3 x daily, after-3 days I become socially withdrawn. I recover completely within an hour of taking an extra tablet. I have searched the web for information and found… nothing.
Parkinsons has more than just motor symptoms- it effects your mood with many early Parkinsons patients suffering from depression- of varying severity- before ever being diagnosed and treated, If you check the literature there are many articles in the journals detailing symptoms and treatment s both pharmacological and non-pharmacological. There is also a body of research supporting the role of exercise in Parkinsons patients that improves their quality of life scores and mobility. It can also effect sleep patterns with reduced quality of restorative sleep with the knock on effect on mood. Keeping your Dopamine levels as smooth as possible over the day helps to even out effects and affects.
Thanks, Fiona. I have had to go quite deep to find descriptions of symptoms that I recognise and with a plausible (though often conjectural) explanation of the cause. I am convinced now that there are few symptoms that cannot be accounted for by a lack of dopamine. Nevertheless I do not know why I have some quite severe symptoms (eg diplopia, speech festination and slurring, bradykinesia) and yet no tremor, constipation, depression, MCI, REM sleep disturbance or dementia. I do get colitis, which can be quite severe and which I thought was not connected with PD. But I have now found a number of PwP who also have colitis and I suspect there is a connection. We know that α-synuclein is found in the colon of PwP before any other symptoms are apparent, and that Lewy Bodies can be detected too. I am speculating that maybe α-synuclein appears in different forms and that different forms have different effects and produce different symptoms. I would like to apply for a small amount of funding from Parkinson's UK to see if symptom combinations that occuroffer any support for this. What do you think?
Hi Stephen- my main area of interest is in Orthopaedics but have a personal interest in Parkinsons. I also suspect that there are many atypical presentations of the disease- but since these have such variation in presenting symptoms and response to treatment, that it may be where your research would contribute. The main focus of research/ literature is on the treatment -cause & effect & in particular decreasing response and side-effects. It would be interesting to see what other quality of life issues occur but not universally to possibly identify sub-groups within the disease and possibly target research for more selective therapy for each group?
I think we can infer that, in PD, although nearly all the symptoms can be traced to dopamine deficiency the primary source of the condition, in at least some patients, is a loss of the ability to convert (by hydroxylation) l-tyrosine to l-dopa. In many of these patients this can be corrected and some motor symptoms (notably the characteristic tremor) greatly improved by the administration of l-dopa. (We must infer that the brain retains the capacity to convert l-dopa to dopamine.) Tyrosine is supplied from the diet but is also made by hydroxylation of phenylalanine. Mutations that inactivate phenylalanine hydroxylase give rise to phenylketonuria, which is never known to be associated with PD.
The question then is "what about the patients whose motor symptoms do not respond to l-dopa?"
I was diagnosed with what I would call a "Parkinson's Spectrum Disorder" in 2010 although I had symptoms in 2008 and possibly as early as 2006. I have bradykinesia (but no tremor) diplopia, speech problems and balance problems, narcolepsy (mild) but a good sense of smell, no depression, no sleep disturbance and no dementia or MCI (yet!). None of my symptoms are improved by l-dopa although I'm much less inclined to be socially withdrawn when I take Sinemet and more motivated to do things.
The problem now is that efforts that concentrate on improving the Q o L (symptoms) of PwP will not cure PD.
It doesn't look like a mutation or defect in tyrosine hydroxylase because it would have to affect or spread to many neurons very quickly but on the other hand it's quite hard to think of something that would affect just this one stage. I feel as if there is an answer in front of us if we had just a little more information.
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