Historical observations on functional reorganization.

Accessible online at: www.karger.com/ced Since the beginning of Neurology, plans for therapy have been recognized to rest on efforts at establishing a diagnosis and on estimating prognosis. Absent modern in vivo imaging, for almost 150 years efforts at diagnosis were based on the tacit assumption that the lesion, whatever its cause and in either of the two cerebral hemispheres, creates more or less the same syndrome. The notion of syndromes rested on the second assumption of a fairly reliable correlation between the clinical syndrome and the locus and size of the brain lesion. This structure-function correlation arose from examination of post-mortem material, the autopsy specimen often available not hours but years after the initial lesion. It was soon appreciated exceptions existed. Either the lesion size exceeded or was smaller than what was assumed to be the basis of the original syndrome. Attempts to explain the discrepancies led to assumptions that the lesion causing the initial syndrome had enlarged in the time from diagnosis to autopsy, or that the acute effects of the lesion affected a region larger than that found at autopsy, or something happened to improve outcome, perhaps subsidence of edema. The initial arguments for Broca aphasia were based on the first of these notions. The large lesion in Broca’s index case was assumed to have grown in the 10 years from onset, so clinicians were justified in focusing their attention on a smaller component of the lesion, located in the area therapy had predicted. Diaschesis was invented as the basis for the second effect, the initially functional disorganization caused by the acute lesion creating some sort of shock wave requiring time to subside, braining function back in its wake. Subsidence in edema was among the third, the subsidence occurring in a time frame explaining the improvement. Few suggested that the brain itself was capable of some sort of software reprogramming in the hyperacute phase, computer then unknown and remodeling thought unlikely. Objections to the expanding lesion were not long in coming. Byron Bramwell’s case was talking within hours, the infarction found at autopsy being rather small but situated where the Broca area infarction was presumed to create a persisting and major speech and language disorder [1] a finding echoed almost a century later by a series of focal infarcts in Broca area [2]. Interest in this insight increased when more cases in retrospect were seen to have undergone considerable improvement and in too short to be explained as a growing lesion [3]. When viewed in the perspective of a century and with fresh cases to revive long-ignored examples, it appeared that the Broca area infarction was not the cause of Broca aphasia; a far larger lesion, one encompassing the insula and operculum, was required [4]. That initial mutism occurred and rapidly faded forced consideration of some sort of shared function or zone of compensatory tissue ipsilateral or contralateral to the focus of infarction [5]. The persisting syndromes appeared to reflect an originally larger lesion, a principle that applies to other regions as well [6]. Likewise, diaschesis, the term applied to remote effects on blood flow and metabolism [7, 8] has lost some of its initial luster [9]. Imaging has shown remote deactivation from fiber systems projecting from the acute lesion zone. However, the clinical improvements in many cases are at