Post-traumatic stress disorder (PTSD) has traditionally been classified as an anxiety disorder; however, it is now considered a trauma- and stressor-related disorder under the latest diagnostic criteria. PTSD develops as a result of emotional or psychological trauma, or physical harm (eg, unwanted sexual act, physical injury). PTSD may also develop after experiencing a life-threatening event such as a war or hurricane, or learning about a traumatic event that occurred to a close family member or friend.
Intense or repeated traumatic events increase the risk of PTSD. Genetic factors may predispose a person’s susceptibility to experience an episode. Neurobiologic changes, such as decreased hippocampus size, hypocortisolism, or a hyperactive amygdala, increase the risk. Additionally, preexisting mental disorders (eg, depression, anxiety), poor socioeconomic or educational status, and substance use disorders enhance the risk of developing PTSD.
The development of PTSD may be due to a dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis. 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.
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.
NE may be involved in regulating fear, arousal, emotional memories, and vigilance. Alpha receptors are autoreceptors which inhibit NE release. Therefore, PTSD downregulation of α2 receptors results in increased NE concentrations and overactivity in the noradrenergic system.
PTSD typically occurs within 3 months after a traumatic event, but may be deferred until month 6 or beyond. After the initial onset, patients experience four core symptom clusters. The four clusters include: (1) symptoms of intrusion related to the traumatic event, (2) avoidance, (3) negative changes in cognitions and emotions in relation to the event, and (4) hyperarousal symptoms. Patients with PTSD may suffer from sleep disturbances such as insomnia. Additionally, patients may present with general psychiatric distress, poor physical health, and social dysfunction.
According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) criteria, a patient with a diagnosis of PTSD must have all of the following symptoms lasting for more than or equal to 1 month:
Exposure to traumatic event
Occurrence of intrusive symptoms related to the traumatic event: