Akinetic mutism and locked-in syndrome: the functional-anatomical basis for their differentiation

Abstract

The accurate location and extent of brainstem lesions that cause akinetic mutism (a.m.) and/or locked-in syndrome (LiS) are reviewed. We compared the data of our morphological analysis with recent neurochemical findings and speculated on the possible pathomechanism that results in the clinical state. There seems to be an anatomic correspondence between pathways of dopamine containing neurons and the lesions associated with a.m. We argue that mesocoeruleo, diencephalospinal and/or mesocorticolimbic dopaminergic systems are selectively damaged in a.m. but spared in LiS.