I am not sure why the median SNAP is normal in TOS, but the medial CMAP is abnormal.
Both signify a neurogenic process (early reinnervation). What is the best way to differentiate the two on EMG? Also, I read that a satellite potential is "time locked" which does not make sense to me since these are unstable potentials ...
I have never read any articles or books that state vitamin d deficiency could be an etiology of peripheral neuropathy. I have heard some physicians suggest this could be an etiology. Is there any data to suggest that this could ...
My understanding is that there is a decrease in amplitude AND area in conduction block, but why is there not supposed to be an increase in duration as well?
Acetazolamide has been recommended for channelopathies such as hypo and hyperkalemic periodic paralysis, but what is the MOA?
What is the role of MRI spine in prognostication of 'Clinically Isolated syndrome'?MRI brain if abnormal would suggest 85% chance of Multiple sclerosis.
Some people routinely check IgA levels prior to giving IVIG. Others think this is outdated. Can anyone post about their experience? Has anyone caught IgA deficiency doing routine IgA levels? Shouldn't screening questions for IgA deficiency be enough?
I have read that both are seen very early in axonal loss, but there have been conflicting statements as to which one is a more sensitive indicator for axonal loss.
We know that IV steroids hasten recovery, but why would oral steroids actually worsen the natural course?
Adrenoleukodystrophy is caused by defective oxidation of VLCFAs and the treatment is to give fatty acids (lorenzo's oil) -- why wouldn't giving this exacerbate the disease? I would think the patient would not be able to break down those fatty ...
Often times, frontotemporal dementia is associated with parkinsonism features such as bradykinesia and rest tremor. I wonder whether these symptoms respond to Sinemet, like a typical Parkinson's disease. Or it is more similar to atypical parkinsonism, which would not respond ...
I also read that cholinesterase inhibitors may actually worsen symptoms in Musk positive patients??
My understanding is that familial hemiplegic migraine involves the mutation of the P/Q type calcium channel, so giving a calcium channel blocker such as diltiazem has been proposed to work. But Dravet's syndrome involves the mutation of the Na channel, ...
How long (before seeing a benefit) would you need to treat CIDP with IVIG?
Steroids seem to help in other immune-mediated neuropathies, such as CIDP. So why would cause and exacerbation in MMN?
Why is there a predilection for certain muscle groups (ie finger flexors, quadriceps) in IBM? I would think there would be no difference in the muscle fibers in these muscle groups.
