This morning I went to my consultation at the "center of reference for rare neuromuscular diseases" UHC, with the department head. Today's theme: failure of botulinum toxin . After explaining the neurologist city (ie botox at the base had not much to do in my eyes), I was anxious to have a slightly more elaborate explanation. The doctor who gave me injections is an ophthalmologist specializing strabologie in, and not a butcher's apprentice who is diversifying trying botox on anything that moves. I think we could from the basis that the botulinum toxin was a real indication of what a unit is easy to verify since it did not act and that my condition is always the same oculomotor, the other is a false question because even on a normal toxin is supposed to paralyze the muscles.
Well, consulting this morning still provided a good temper those comments. Indeed, regardless of whether the toxin has been shown or not: even though it would not have been, it would still have acted. If you realize this gesture in a normal subject, he causes oculomotor palsy, even though there is initially no spasm. So for him, he joined what the optometrist said, we can deduce that the origin of my troubles is downstream from the scope of action of botulinum toxin. As it acts at the neuromuscular junction, my oculomotor disorders would be strictly myogenic , including (pseudo) nystagmus (which happily survived injection).
If this explanation is correct, he seemed to understand that the treatment was severely compromised, there is no therapeutic means to stop these activities myogenic anarchic. Botulinum toxin effect is particularly effective on spasticity of neurogenic origin, but not directed to the muscle itself. Genetic analysis
launched two months ago would bring the better the diagnosis, if positive. You just wait ... 4 years? Go
time flies.
