Reply To: Lack of clinical markers? What could be going on?
I’m sorry to hear the tests done so far aren’t revealing what the problem is, but that only means the right test hasn’t been done yet, or perhaps the test for what you have hasn’t yet been devised.
I’m pasting a portion of a published paper below, not because I’m hazarding a guess at what your correct diagnosis might be, but just to point out that often times people with “negative” studies, get better with IVIG treatment.
Take note that the patient below is a doctor…I have noticed in my reading of a lot of case studies that all the stops are pulled out when a physician is sick…I think the major difference is that when a physician is sick the physician is always believed, and never psychoanalyzed, and when a lay person is sick, and his doctors can’t make a quick diagnosis, the doctors start thinking the patient has a psychological problem.
I have experienced it personally, and witnessed it both professionally and as a family member of the person who is sick. It’s one of the saddest things in life when a person who is already dealing with a serious, life-altering illness is being blown off as a hypochondriac.
When some doctors reach the limit of their knowledge they begin psychoanalyzing their patients. The poorer the doctor is, the sooner he starts doing this. When a good doctor reaches the limits of his knowledge he refers you to a doctor he thinks knows more than he does about what he thinks might be your problem.
Go back to your neuro and give her another chance at bat, if she swings and misses ask her for a referral by telling her you just cannot afford to be missing work because of this thing you’ve got going on.
Case study: Efficacy of IVIg in the Absence of Conduction Blocks
SR, a 62-year-old medical practitioner, developed progressive weakness of the right upper limb over a period of 4 months. It began initially in the thumb and the fore finger and progressed to weaken all the fingers and forearm muscles, with mild wasting. At this stage, the left hand also got weaker in a similar pattern. Electrophysiology detected denervation and reinnervation of the distal upper limb muscles with milder forearm involvement. The paraspinal muscles were normal. No conduction blocks were identified on repeated detailed examinations. Anti-GM1 antibody was not detected. A provisional diagnosis of motor neuron disease was made and he underwent physiotherapy. At the end of 1 year and 4 months, he had not developed any bulbar involvement or upper motor neuron signs, and the daily activities were worsening. A trial of IVIg was given with the presumption of MMN without CB, with remarkable improvement in the weakness over 6–8 weeks. He took further courses of maintenance IVIg and remained well for the next 2 years, at which stage he succumbed to a myocardial infarction.
The case highlights the efficacy of IVIg in the absence of CB and anti-GM1 positivity.