Abstract
The use of antipsychotic medication in treating individuals with traumatic brain injury (TBI) has been controversial. Much of the caution derives from animal studies (and limited human data) with regard to typical antipsychotics. Of note, however, is that similar assumptions have been made about the newer generation of atypical antipsychotics as well. Because these agents have different mechanisms of action as well as different neurotransmitter targets, this may very well be unwarranted. In this article, mechanisms of action of typical and atypical antipsychotics are discussed, with particular attention paid to their use in TBI. Indications and contraindications are presented, and recommendations are made for the responsible prescribing of antipsychotic medications after TBI.
THE QUESTION of whether to prescribe antipsychotics after traumatic brain injury (TBI) has always been controversial. One of the first things that physicians are taught in the management of TBI patients is to avoid prescribing antipsychotics. The rationale for this approach is derived primarily from animal studies, although some human data also exist. Animal data 1-3 have suggested that motor recovery after experimental brain injury may be negatively affected by haloperidol administration. Haloperidol administration has also been noted in animal literature to result in loss of tactile placing 4 and in inhibition of binocular vision and foot placement using a sham cliff paradigm. 5,6 Sawaguchi's work 7,8 with primates has shown that the cognitive benefits facilitated by catecholaminergic treatment are inhibited by haloperidol administration.
There is also limited human literature that highlights the potential negative effects of antipsychotics on recovery after stroke and TBI. Rao et al 9 published on the effects of haloperidol administration for agitated patients after TBI. They found that administration of the agent lengthened the duration of the patients' posttraumatic amnesia even though the eventual outcome data did not reach significance. In 1995, Goldstein 10 published his analysis of the data from the Sygen in Acute Stroke Study. His work demonstrated that patients who took certain medications had impairments of motor recovery, with haloperidol being one of those medications. In 1997, Stanislav 11 reported poorer outcomes for patients who had received neuroleptics. The conclusions that can be drawn from this last study are quite limited because of the numerous agents that were used.
The literature listed here clearly does not fully answer the question of antipsychotic use in TBI, however. Drawing definitive conclusions about the typical agents is still difficult, and the question of typical versus atypical agents has not even been addressed in the literature. This latter issue is of even greater concern, because the mechanisms of actions for these two classes of medications are very different.