Post-traumatic stress disorder (PTSD) is an anxiety disorder that develops as a result of emotional or psychological trauma, or physical harm (eg, unwanted sexual act, physical injury). PTSD usually occurs after a tragic event that results in feeling fear, stress, or helplessness.1 PTSD may also develop after experiencing or learning about a life-threatening event such as a war or hurricane.
PTSD accounts for approximately 4% of US mental disorders with women being twice as likely to experience PTSD as compared with men.2,3 The occurrence of PTSD in victims of interpersonal violence and combat veterans is about 25%, and the lifetime prevalence rate ranges from 5% to 10% with a 12 month rate ranging from 2% to 5%.4,5
Intense or repeated traumatic events increase the risk of PTSD. Genetic factors may predispose a person's susceptibility to experience an episode.6 Neurobiologic changes, such as decreased hippocampus size, hypocortisolism, or a hyperactive amygdala, increases the risk.6-8 Additionally, preexisting mental disorders (eg, depression, anxiety), poor socioeconomic or educational status, and substance abuse also enhance the risk of developing PTSD.9,10
The development of PTSD may be due to a dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis.6 The HPA axis is responsible for regulating responses to stress. Dysregulation of the HPA axis causes elevated glucocorticoid negative feedback sensitivity of the HPA axis which results in hypocortisolism. Since cortisol is a glucocorticoid that reduces stress, below normal concentrations cause an elevated stress response.6,11
Several neurotransmitters play a role in the pathophysiology of PTSD. The two most common neurotransmitters are serotonin (5-HT) and norepinephrine (NE). Gamma aminobutyric acid (GABA) and dopamine (DA) may indirectly play a role as well. The primary neurotransmitters (ie, 5-HT, NE) are implicated in PTSD in the following way:
Serotonin affects sleep, motor function, impulsivity, and aggression. Patients with PTSD have decreased 5-HT concentrations and neurotransmission which may result in insomnia, abnormal motor function, and aggressive behavior.12,13
Norepinephrine may be involved in regulating fear, arousal, emotional memories, and vigilance. Alpha receptors are auto-receptors which inhibit NE release. Therefore, in PTSD a down regulation of alpha-2 receptors results in increased NE concentrations and overactivity in the noradrenergic system.13
PTSD typically occurs within 3 months after a traumatic event, yet may be deferred until after 6 months or more1 (Table 57-1). After the initial onset, patients may experience three core symptom clusters. The three clusters include reexperiencing the traumatic event, avoidance or numbing symptoms, and hyperarousal symptoms.1,5 Patients with PTSD may suffer from sleep disturbances such as insomnia.14 Additionally, patients may present with general psychiatric distress, poor physical ...