Prozosin for the Treatment of Posttraumatic Stress Disorder-Related Nightmares in an Adolescent Male

N ightmares and other sleep disturbances are common symptoms of posttraumatic stress disorder (PTSD) that often persist for years despite continuing treatment with various psychopharmacological agents (Brkanac et al. 2003) or psychotherapy (Krakow et al. 2001). Increased central nervous system (CNS) adrenergic reactivity is hypothesized to disrupt rapid eye movement (REM) sleep in persons with PTSD and promote the emergence of trauma-related nightmares (Krystal and Davidson 2007). Prazosin is a centrally-acting α1-adrenergic antagonist that decreases adrenergic activity and has been used as a treatment for PTSD-related nightmares with civilians (Taylor et al. 2006) and military veterans (Raskind et al. 2007). The study of Raskind et al. (2007) showed that prazosin significantly reduced nightmares related to military trauma and improved sleep quality when added to ongoing PTSD treatment in veterans with chronic PTSD.

Few studies have been done to investigate the effectiveness of prazosin for PTSD-related sleep disturbances in children and adolescents. Brkanac et al. (2003) reported behavioral improvement and remission of PTSD-related nightmares in a 15-year-old adolescent girl treated with 4 mg of prazosin at bedtime. We report a second case of the suggested effectiveness of prazosin in reducing trauma-related nightmares in an adolescent.

Patient B is a 16-year-old African American male with a history of conduct disorder, who was evaluated at a juvenile detention facility for treatment of recurrent, trauma-related nightmares. Upon examination, a diagnosis of PTSD was confirmed and the nightmares were noted to be thematically and historically related to psychological trauma exposure. Specifically, the nightmares emerged after Patient B witnessed his friend's violent shooting death and his cellmate's attempt to hang himself. Patient B had no history of prior psychiatric treatment. Informed consent of the legal guardian and assent of the child were obtained.

In an attempt to improve his sleep, prazosin was started at 1 mg every night at bedtime and increased to 1.5 mg after several weeks. During the one and a half months that Patient B was on 1.5 mg of prazosin, the frequency of his nightmares dropped from 7/7 to 0/7 nights per week. Then the medication was discontinued for unknown reasons. Following the discontinuation of prazosin, Patient B's nightmares increased in both frequency (to 5/7 nights per week) and intensity, and prazosin was restarted. One month later, on follow-up assessment, Patient B reported improved sleep without the reemergence of nightmares.

In summary, this case suggests the effectiveness of prazosin, a centrally acting α1-adrenergic antagonist, in reducing the intensity and frequency of PTSD-related nightmares in an adolescent boy. When prescribing prazosin, it is important for the clinician to monitor for side effects, including orthostatic hypotension with resultant dizziness and lightheadedness upon standing. This side effect is usually seen soon after treatment is initiated and can be minimized by using a low dose and titrating slowly (Miller 2008).

Although not well documented in the adolescent psychiatric literature, these results are promising and indicate the need for future placebo-controlled trials to determine the safety and efficacy of prazosin and other centrally acting noradrenergic agents in the treatment of trauma-related nightmares and sleep disturbances.