Porth's Essentials of Pathophysiology, 4e

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Stress and Adaptation

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is the removal of the necessity for the individual to experience an intense emotional response at the time of the exposure. This change was made because many individuals, particularly professionals that witness horrific events, reported feeling nothing at the time of the event—instead their professional training “kicked in.” 71 With PTSD, the threat results in a constellation of symptoms that are experienced as intrusion, avoid- ance, negative alterations in cognition and mood associated with the event, and marked alterations in arousal and reactivity associated with the event. Intrusion involves the recurrent involuntary distress- ing memories or “flashbacks” during waking hours or nightmares in which the past traumatic event is relived, often in vivid and frightening detail. In children, there may be frightening dreams without recognizable con- tent. Avoidance refers to the attempt to avoid situa- tions, including people, places, activities, and objects that arouse distressing memories. At least one avoid- ance symptom must be present for definitive diagnosis of PTSD. Negative alterations in cognition and mood involve an inability to remember an important aspect of the event (i.e., dissociative amnesia) that is not the result of a head injury, alcohol, or drugs. Marked alter- ations in arousal and reactivity replace the numbing symptom in DSM-IV, and it includes inability to expe- rience positive emotions such as love, joy, pleasure, or satisfaction. In addition, distorted beliefs regard- ing blame of self or others about the causes or conse- quences of the traumatic event may occur. In addition, irritable and angry outbursts, reckless and destructive behavior, hypervigilance, problems with concentra- tion, and sleep disturbances may occur. DSM-5 no longer includes immediate fear, helplessness, or horror following the event, as it did not improve diagnostic accuracy. Diagnosis of PTSD requires that the dura- tion of disturbance persists for more than a month, causes clinically significant distress or impairment of social or other areas of functioning, and is not attrib- utable to the effects of medication, alcohol, or other medical condition. Pathophysiology. Although the pathophysiology of PTSD is not completely understood, there is increasing evidence that the disorder results from an exaggerated stress response and a failure of the stress response sys- tem to regain homeostasis. The SNS and the HPA axis are the major constituents of the body’s neuroendocrine response to physical and physiological threat and stress. Normally, the SNS response is brief, followed by an HPA axis response that serves to reinstate homeostasis and induces long-lasting adaptive changes that contrib- ute to stress recovery and resilience. This is mediated by glucocorticoids (i.e., cortisol), the product of the HPA axis. 72 Initial research focused on an exaggerated and unre- lenting extension of the normal sympathetic and HPA response to the stress associated with the traumatic event. More recent research has revealed that although persons with PTSD have been shown to have increased

levels of the SNS activity, they have decreased cortisol levels and an enhanced negative feedback inhibition of cortisol release with the dexamethasone (a synthetic glucocorticoid) suppression test. 72 Cortisol’s circadian rhythm, which is critically influenced by corticosteroid function, is altered with the progression of PTSD, sug- gesting a explanation for sleep disturbances that accom- pany the disorder. Although neuroendocrine research suggests that lower cortisol levels are implicated in the pathophysi- ology of PTSD, emerging research findings suggest this may instead reflect pretraumatic stress vulner- ability, explaining why some people develop the dis- order and others do not. It has been suggested that genetic 73,74 and previous environmental/experiential factors 65,75,76 may predispose to subsequent develop- ment of PTSD. In addition to the neuroendocrine changes that occur with PTSD, neuroanatomic studies have identified alter- ations in two brain structures (the amygdala and hip- pocampus) that occur in persons with PTSD. Positron emission tomography (PET) and functional magnetic resonance imaging (MRI) have shown increased reac- tivity of the amygdala and hippocampus and decreased reactivity of the anterior cingulate and orbitofrontal areas. These areas of the brain are involved in fear responses. The hippocampus also functions in memory processes. Differences in hippocampal function and memory processes suggest a neuroanatomic basis for the intrusive recollections and other cognitive problems that characterize PTSD. 77 Diagnosis and Treatment. Although originally con- ceptualized as a mental disorder, PTSD is becoming increasingly recognized as a highly comorbid condi- tion, much like hypertension, cardiovascular disease, chronic fatigue syndrome, fibromyalgia, and other dis- eases. For a number of reasons, including the stigma attached to mental illness, limited availability and high cost of treatment, and socioeconomic issues associ- ated with the disorder, people with PTSD frequently do not seek specialized mental health treatment until the disorder has been present for a considerable amount of  time. 78,79 Initial treatment of PTSD focuses on reducing or eliminating the symptoms and signs of PTSD and any trauma-related comorbid conditions. Next, adaptive functioning must be improved, with an emphasis on returning the person to a psychological state of safety and trust. Finally, general treatment approaches focus on limiting any generalizations of the initial trauma and protecting the person with PTSD from subse- quent relapse. Debriefing, or talking about the trau- matic event at the time it happens, often is an effective therapeutic tool. Crisis teams are often among the first people to attend to the emotional needs of those caught in catastrophic events. Some people may need continued individual or group therapy. Selective sero- tonin reuptake inhibitors (SSRIs) are considered the first-line drug treatment for PTSD. Often concurrent pharmacotherapy with antidepressant, antianxiety,