REPORT FROM THE 67TH AMERICAN ACADEMY OF NEUROLOGY (AAN) ANNUAL MEETING – WASHINGTON DC, APRIL 18-25, 2015 – A number of analyses of phase III studies have shown that about one-third of patients treated with a higher efficacy disease-modifying therapy can achieve no evidence of disease activity (NEDA), defined as no relapses, no MRI activity and no EDSS progression (see Optimizing patient assessment in MS: NEDA and beyond, NeuroSens, March 12, 2015).

Moreover, preliminary data suggest that 2-year NEDA rates are prognostic of better outcomes at long-term follow-up. In the STRATA extension study (which included patients from AFFIRM), at 7.4-year follow-up the mean ARR was 0.08 in those with NEDA in the first two years of treatment and 0.13 in those who didn’t achieve NEDA (O’Connor et al. AAN 2015; abstract P7.221). The cumulative probability of EDSS progression confirmed at 6 months was 23.3% and 37.5%, respectively, for the two groups. An improvement in EDSS scores was seen in 38.7% and 26.8%, respectively, in the NEDA+ and NEDA- groups.  Read More

REPORT FROM THE 67TH AMERICAN ACADEMY OF NEUROLOGY (AAN) ANNUAL MEETING – WASHINGTON DC, APRIL 18-25, 2015 – The GLORIA non-interventional study recently reported interim results of levodopa-carbidopa intestinal gel (LCIG) in the routine management of patients with advanced Parkinson’s disease (Antonini et al. Parkinsonism Relat Disord 2015;21:231-235). Read More

REPORT FROM THE 67TH AMERICAN ACADEMY OF NEUROLOGY (AAN) ANNUAL MEETING – WASHINGTON DC, APRIL 18-25, 2015 – It is well established that the risk of progressive multifocal leukoencephalopathy (PML) is substantially increased after 24 infusions of natalizumab. What is less well known is how best to manage patients following natalizumab discontinuation, and several studies at AAN have examined different switching options.  Read More

REPORT FROM THE 67TH AMERICAN ACADEMY OF NEUROLOGY (AAN) ANNUAL MEETING – WASHINGTON DC, APRIL 18-25, 2015 – Impaired olfaction is a common observation in patients with mild cognitive impairment (MCI) and Alzheimer’s disease, and has been variously attributed to neurodegenerative changes of the olfactory bulb, amygdala, hippocampus or other structures (Thomann et al. J Alzheimers Dis 2009;17:213-21; Kjelvik et al. BMC Neurol 2014;14:168). Read More