mainecoon

I've been curious about this for some time, and I was wondering whether or not anyone else has ever wondered the same thing. I've been taking 400 Mg. of Dilantin a day for about twenty years. For twenty years before I'd taken it off and on, much to my regret. It wasn't until a friend with seizures told me that I have to maintain a steady blood serum level for the drug to do any good that I started to take it religiously.

Anyway, I know that phenytoin works by interfering with the transmission of sodium between nerve cells, thereby reducing the likelihood of a neural storm. Some of the possible side-effects of the drug are peripheral neuropathy, ataxia, and slurred speech.

About five years ago I began to have difficulty in moving my left leg. It was preceded by a drop-foot, which I had to correct with a plastic brace. I also developed a lack of dexterity in my left hand. I now have difficulty unclenching my left hand, and can only use my middle finger when typing, since I can't move the fingers independently.

After extensive testing over a long period of time, which included MRI's, EEG's, Evoked Response tests, and Lumbar Punctures the doctors finally concluded that the results were consistent with Multiple Sclerosis. They found a lesion on the Pons area of the brain, and I presume they found oligoclonal banding in the CSF. The weakness has become progressively worse, as one would expect in Primary Progressive MS.

Yet, when I last saw my neurologist he asked me who said I had MS. I reminded him that he told me so. He found it interesting that I don't have the tingling or numbing in the extremities, nor do I have any problems with my sight

What I wonder about is whether or not any other long-term users of Dilantin have developed traits which could be mistaken as symptoms of MS?

Whether or not my severe ataxia and peripheral neuropathy are due to the progression of MS or continued Dilantin use is something of a moot point. In the final analysis the diagnosis of MS is still largely a matter of eliminating all other conditions. Lesions on the CNS are not necessarily related to MS, and oligoclonal banding may indicate the presence of the disease. Lacking this circumstantial evidence the medical community has still not settled on what can definitively show the presence of the disease.