Functional brain imaging and neurological recovery

It is unwise to prophesy either death or recovery in acute diseases. (Hippocrates: Aphorisms II-19 c. 500 BC) Neurological recovery occurs commonly, and is mediated by many mechanisms from cells to systems. Research is currently trying to clarify which neural mechanisms of recovery are behaviorally significant. It is a common observation on neurology wards that most patients improve after a stroke or a traumatic brain injury. About 80-90% of all stroke patients have motor deficits (or hemiparesis) at onset, while only 40-60% of them have a persistent deficit at 6 months to 1 year (Dobkin, 2005). Similar degrees of recovery occur for language and visuospatial perception (Sarno & Levita, 1971; Stone et al., 1993). Whereas early (1-3 days) recovery may be explained by vascular changes, such as early canalization of an obstructed vessel or reduction in the amount of edema surrounding an ischemic area, recovery that occurs in the weeks and months following the stroke must be explained by different mechanisms. The central nervous system reacts to injuries (stroke, trauma) through changes that occur at the level of brain networks, areas, neurons, connections, molecules and even genes (Carmichael, 2003a; Nudo, 1999; Weiller, 1998). Many of these changes represent "house-keeping" operations unrelated to behavioral recovery. For instance, in the area of ischemic damage an inflammatory reaction is mounted within 24-48 hours that leads to the elimination of vascular and cellular debris. At the level of brain networks, damage to one area may lead to a decrement of synaptic activity downstream in a connected area, which will in turn downregulate its metabolic demands (diaschisis) (Baron et al., 1980).