Cairns and coworkers (1941) introduced the term "akinetic mutism" to denote a syndrome characterised by lack of responsiveness in the presence of apparently preserved vigilance. The present paper reviews clinical data as well as results of animal experimentation to outline the functional-neuroanatomic basis of this constellation. The clinical literature following the original publication of Cairns et al. (1941) reported syndromes of "akinetic mutism" in bilateral mesodiencephalic or frontal lesions of various aetiology. At least two pathomechanisms of akinetic mutism can be differentiated: (a) reduced "arousal" of cortical functions due to lesions at or rostral to the mesodiencephalic junction; (b) impaired activation of the motor system following bilateral damage to the frontal lobes. Since perceptual and cognitive functions are disturbed as well in mesodiencephalic akinetic mutism, the latter notion does not seem to be adequate. The terms "apallic syndrome" or "vegetative state" are rather more appropriate in these instances. The label "akinetic mutism" can then be restricted to a pathophysiologically distinct syndrome, i.e. reduced motor activation following bilateral frontal damage.