Our blogger discusses a recent study investigating the likelihood of head trauma in older patients leading to the onset of Parkinson disease and the implications of the findings.
Samuel Pleasure, MD, PhD
What is the function of continued adult myelination in the normal undiseased brain? A recent study sheds remarkable light on this process and its importance.
A switch to a second-line drug in a patient receiving first-line therapies likely will be effective at decreasing disease activity.
The ultimate cause is found in only about half of patients, so improved understanding of the prognostic and diagnostic features is of high priority.
The risk of progressive multifocal leukoencephalopathy in patients receiving Tysabri for MS is a concern about this otherwise extremely effective therapy.
What happens before the demyelinating lesions of MS appear? Does smoking confer protection against Parkinson disease? How is NMDA receptor-associated disease reversed? Here are 4 fine papers from 2014 that set out to answer these questions.
Patients with juvenile myoclonic epilepsy appear to have modest cognitive defects and imaging abnormalities early on that are unlikely to be associated with anti-epileptic therapy. This is a clear departure from traditional teaching.
Serum testing for NMDAR and other autoantibodies is fraught with pitfalls, and careful clinical consideration is important.
If an anti-NMDAR patient has evidence of demyelination on MRI, look for other antibodies that may complicate the picture.
What emerged is that Devic’s is a distinct syndrome that results in widespread destructive lesions in the spinal cord that are not strictly demyelinating in their onset. Interesting questions remain.