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Questions posted in the
Neurology and Neurosurgery Forum have been answered by doctors from The Cleveland Clinic Foundation.
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Subject: Re: new treatments HI, MY MOTHER WAS DIAGNOSED WITH P ARKINSONS IN 1989 AND JUST BEFORE SHE PASSED AWAY IN 1993 WE DISCOVERED THAT IT ACTUALLY WAS MSA. ALL WE KNEW AT THAT TIME WAS THAT IT WAS RARE AND HAD NO KNOWN CAUSE OR CURE. FROM MY RESEARCH ON THE NET I HAVE SEEN THAT THE MIS-DIAGNOSIS WITH PARKINSONS IS QUITE COMMON. MY QUESTION IS: I HAVE SEEN PROGRAMS ON T.V SHOWING VERY PROMISING RESULTS FOR PARKINSONS WHEN PATIENTS HAD FETAL PIG CELLS IMPLANTED INTO THIER BRAINS. IS THIS AN OPTION FOR SHY DRAGER AND OTHER RELATED DISEASES? ALSO, WHAT IS THE CONTROVERSY ABOUT THIS KIND OF TREATMENT? I CAN'T FATHOM WHY ANYONE WOULD OBJECT TO RESEARCH THAT MAY LEAD TO THE CURE FOR THESE HORRIBLE, DEVASTATING DISEASES. THANKS FOR YOUR REPLY = You are quite correct that MSA is often misdiagnosed as Parkinson's disease, and sometimes the diagnosis persists for quite a long time. At early stages, even experienced movement disorders specialists can have a difficult time distinguishing them (as well as a related disorder called PSP). Fetal tissue implants have been in a research phase for maybe 15 years, and as you know have not reached a stage where the FDA is ready to approve them for general use. The intrinsic pathology of PD and MSA is quite different. In PD, the degeneration is in a specific region called the substantia nigra, a collection of cells which makes dopamine and sends it to another region of the brain called the striatum (part of a larger collection of structures called the basal ganglia). In MSA, degeneration involves multiple systems (hence the name). There is nigral degeneration, but also striatal degeneration, and loss of cells in the cerebellum and inferior olivary complex (in the lower brainstem), as well as in autonomic nervous system structures. Further, the brains look different under the microscope. Parkinson's disease is characterized by Lewy bodies; MSA by oligodendroglial inclusion bodies. I expect these terms are just so much gibberish: the point is that they are different diseases, involving different distributions of brain structures, and with different fundamental processes going on (hence the different appearance under the microscope). The implication for treatment is this: in PD, the strategy is to re-introduce dopamine to a striatum that is starving for it. Hence, the use of levodopa (Sinemet) and dopamine agonists (Parlodel, Permax, Mirapex, Requip, etc). Fetal grafts of dopamine-producing cells are supposed to grow into the striatum and provide near-physiologic release of dopamine rather than the pulsatile, widely varying blood levels made available by taking pills. As you probably experienced, just adding dopamine to people with MSA isn't such a satisfactory solution. Some people with MSA do get somem benefit from Sinemet, but it generall doesn't work as well as with PD. Likewise, you would expect the same difference in response (PD vs MSA) with fetal grafts. Now, we find that it's a good idea to try Sinemet anyway because it's what we've got. When we know more about how grafts help PD patients, we may develop the same philosophy about treating MSA patients with grafts. I personally have no experience with graft treatment. I am not aware of any center attempting to use grafts for MSA - anyone trying to prove something works and get it approved by the FDA usually attacks the "easier" diseases first. So you'll probably have to wait some years to hear more about this. My bet is that the most productive treatment will be neuroprotective (for PD, MSA, PSP, and all other degenerative diseases). Right now, there is a great deal of interest in mechanisms of neuronal degeneration and therefore in strategies for neuroprotection. Unfortunately, there isn't anything really promising yet. But research is unpredictable. Keep your eyes on it. I hope this helps. Sorry about the rambling response. CCF MD mdf. |
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