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Dear friends, There has been something on my mind for a while now, and I would like to share a question with you. I know that none of us are neurologists, but perhaps someone can shed some light on a very intriguing thing. As some of you may know, my Parkinsonism is the result of CO poisoning. Only the dopamine receptor cells in a structure in the basal ganglia were damaged, giving me a very atypical Parkinson's syndrome. What I would like to know is this: Why would a typical P.D.er benefit from having the signals to the pallidus blocked, such as in a pallidotomy and/or a pallidal stimulation, when that brain structure is what controls the reception of dopamine, and injury to such would leave one in my condition. I know that only a small and very specific part of the pallidus is actually frozen or de-activated by the two afore-mentioned procedures. However, the fact that P.D. can be caused by an over-active reception of dopamine confounds me. Maybe it has to do with there being less dopamine to receive, and the receptors are going haywire trying to receive dopamine that isn't there? If somebody could help me out, it might add some understanding to all of our conditions.