The current issue of Brain contains four papers that illuminate different aspects of inflammatory demyelinating disease, especially multiple sclerosis (Black et al ., 2006; Coman et al ., 2006; Howell et al ., 2006; Patrikios et al ., 2006). One paper focuses on axonal protection, while the others describe aspects of spontaneous remyelination in the disease. Promoting remyelination is a major therapeutic goal in multiple sclerosis, but some observations from the current papers raise the possibility that remyelination may transiently render axons vulnerable to degeneration before long-term protection is achieved, as discussed below. In recent years the identification of strategies to protect axons from degeneration in multiple sclerosis has emerged as a major research priority. This emphasis is in response to the realisation that axonal degeneration is substantial in the disease (Trapp et al ., 1998; Ganter et al ., 1999), and that it is a major cause of permanent neurological deficit (De Stefano et al ., 1998). The mechanisms responsible for the axonal degeneration are not certain, but inflammation and demyelination appear to be major risk factors (Raine and Cross, 1989; Ferguson et al ., 1997; Trapp et al ., 1998). This observation has prompted a new therapeutic approach based on the partial blockade of sodium channels (reviewed in Bechtold and Smith, 2005), and the potential value of this approach is explored in the current paper by Black et al . (2006) (see below). However, in addition to drug based approaches to axonal protection, there is widespread agreement amongst multiple sclerosis researchers that repair of the demyelinated axons by remyelination should also provide a good strategy for protection (Kornek et al ., 2000; Stangel and Hartung, 2002; Dubois-Dalcq et al ., 2005). Unfortunately, promoting remyelination in patients has proven to be …