Amantadine hydrochloride is one of the most commonly used drugs in the pharmacotherapeutic treatment of disorders of consciousness (DOCs) following traumatic brain injury (TBI). Indeed, its actions as a pro-dopaminergic drug and as an N-methyl-D-aspartate antagonist makes amantadine an interesting candidate to improve consciousness and responsiveness in individuals with DOC, including vegetative state and minimally conscious state. Giacino et al (N Engl J Med. 2012;366(9):819–826) recently reported that amantadine was able to accelerate the functional recovery course of subjects after TBI with DOC, during a 4-week treatment period. Some patients with DOC following severe TBI have been reported to have parkinsonian symptoms. Severe TBI and posttraumatic parkinsonism may share a common midbrain network dysfunction. In fact, both vegetative state and minimally conscious state following severe TBI can include features of akinetic mutism and parkinsonism. Responsiveness to pro-dopaminergic agents in some patients and to deep brain stimulation in others, might depend, respectively, on the integrity, or lack thereof, of the dopaminergic postsynaptic receptors. We are of the strong opinion that more attention should be given to parkinsonian findings in persons with DOC after severe TBI and would advocate for multicenter, randomized, controlled trials to assess risk factors for parkinsonism following severe TBI.