Neurology News Network for the week ending August 31, 2019.
This week, Neurology News Network covered the FDA approval of Kyowa Kirin’s istradefylline for the use as an add-on therapy to levodopa/carbidopa in the treatment of Parkinson disease, as well as the agency’s approval of rimabotulinumtoxinB (Myobloc, US WorldMeds) for the treatment of chronic sialorrhea. Additionally, the network covered the findings of a recent trial of the pathway of dementia in those with chronic traumatic encephalopathy (transcript below).
Welcome to Neurology News Network. I’m Matt Hoffman. Let’s get into the news from this week.
The FDA has given the go-ahead to Kyowa Kirin for its istradefylline (Nourianz) tablets as an add-on therapy to levodopa/carbidopa in adults with Parkinson disease who are experiencing off episodes. Ultimately, the selective adenosine A 2A receptor antagonist’s approval was based on its success in 4 clinical studies which lasted 12 weeks and included more than 1100 participants in which statistically significant decreases from baseline in daily off time compared to placebo were observed.
The FDA also approved a supplemental BLA for rimabotulinumtoxinB injection, or Myobloc, in the treatment of chronic sialorrhea in adults. This adds to its existing approval for the treatment of cervical dystonia, which it received in 2000. The US WorldMeds agent is the first and only approved botulinum toxin type B. In clinical trials, it showed significant decreases in sialorrhea symptoms with a single treatment as soon as the first week, lasting up to 3 months.
Recent study findings suggest that in individuals who have played football with chronic traumatic encephalopathy, dementia is a result of neuropathologic alterations caused by repeated head impacts. These changes include worse white matter rarefaction and phosphorylated tau, and even non-head trauma like arteriolosclerosis. The study, which consisted of 180 deceased men over the age of 40 years with CTE, also found that the number of years of football played was associated with worse white matter rarefaction and greater dorsolateral frontal cortex neurofibrillary tangles.
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