Akinetic mutism (AM) is a behavioral disorder characterized by impossibility to move or speak in awake patients. lt has been typically described as a transient disorder following posterior fossa tumour resection. Besides, AM may also appear after recurrent shunt failures in hydrocephalic patients, with no tendency towards improvement, either spontaneously or with shunt revisions. However successful treatment of this second type of AM has been achieved with bromocriptine. We present a patient who developed AM after a posterior fossa surgery complicated by ventriculitis and multiple hydrocephalic events. AM only improved with bromocriptine. We review AM pathophysiology. Although not well known, it appears to be quite different, depending on its cerebellar or hydrocephalic origin. Damage to dentate nucleus or its efferents (mainly of glutamate) should promote AM of cerebellar origin, while damage to paraventricular monoaminergic pathways could explain AM related to repeated shunt failures which has successful response to bromocriptine treatment. However, a more complete study of this disorder is required to ascertain its aetiology.