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| Diagnostic criteria The diagnostic criteria for PTSD, according to Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV), are stressors listed from A to F. The current diagnostic criteria for the PTSD published in the Diagnostic and Statistical Manual of Mental Disorders may be found DSM-IV-TR here. Notably, the stressor criterion A is divided into two parts. The first (A1) requires that "the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others." The second (A2) requires that "the person’s response involved intense fear, helplessness, or horror." The DSM-IV A criterion differs substantially from the previous DSM-III-R stressor criterion, which specified the traumatic event should be of a type that would cause "significant symptoms of distress in almost anyone," and that the event was "outside the range of usual human experience." Since the introduction of DSM-IV, the number of possible PTSD-traumas has increased, and one study suggests that the increase is around 50% (Breslau & Kessler 2001). Symptoms and their possible explainations Symptoms can include general restlessness, insomnia, aggressiveness, depression, dissociation, emotional detachment, or nightmares. A potential symptom is the memory loss about an aspect of the traumatic event. Amplification of other underlying psychological conditions may also occur. Young children suffering from PTSD will often enact aspects of the trauma through their play, and may often have nightmares that lack any recognizable content. One patho-psychological way of explaining PTSD is by viewing the condition as secondary to deficient emotional or cognitive processing of a trauma (Cordova 2001). This view also helps to explain the three symptom clusters of the disorder (Shalev 2001): Intrusion: Since the sufferer cannot process difficult emotions in a normal way, they are plagued by recurrent nightmares, or daytime flashbacks, while realistically re-experiences the trauma. These re-experiences are characterized by high anxiety levels, and make up one part of the PTSD symptom cluster triad called intrusive symptoms. Hyperarousal: PTSD is also characterized by a state of nervousness with the organism being prepared for "fight or flight". The typical hyperactive startle reaction, characterized by "jumpiness" in connection with high sounds or fast motions, is typical for another part of the PTSD cluster called hyperarousal symptoms, and could also be secondary to an incomplete processing. Avoidance: The hyperarousal and the intrusive symptoms are eventually so distressing that the individual strives to avoid contact with everything, and everyone, even to their own thoughts, that can arouse memories of the trauma and thus cause the intrusive and hyperarousal states to go on. The sufferer isolates themselves, becoming detached in their feelings with a restricted range of emotional response, and can experience so-called emotional detachment ("numbing"). This avoidance behavior is the third and most important part of the symptom triad that makes up the PTSD criteria. Dissociation: Dissociation is another "defense" that includes a variety symptoms including feelings of depersonalization and derealization, disconnection between memory and affect so that the person is "in another world," and, in extreme forms can involve multiple personalities and acting without any memory ("losing time"). Biology of PTSD Neurochemistry PTSD displays biochemical changes in the brain and body, which are different from other psychiatric disorders such as major depression. In PTSD patients, the dexamethasone cortisol suppression is strong, while it is weak in patients with major depression. In most PTSD patients the urine secretion of cortisol is low, at the same time as the catecholamine secretion is high, and the norepinephrine/cortisol ratio is increased. Brain catecholamine levels are low, and corticotropin-releasing factor (CRF) concentrations are high. There is also an increased sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis, with a strong negative feedback of cortisol, due to a generally increased sensitivity of cortisol receptors (Yehuda, 2001). The response to stress in PTSD is abnormal with long-term high levels of norepinephrine, at the same time as cortisol levels are low, a pattern associated with facilitated learning in animals. Translating this reaction to human conditions gives a pathophysiological explanation for PTSD by a maladaptive learning pathway to fear response (Yehuda 2002). With this deduction follows that the clinical picture of hyperreactivity and hyperresponsiveness in PTSD is consistent with the sensitive HPA-axis. Swedish United Nations soldiers serving in Bosnia with low pre-service salivary cortisol levels had a higher risk of reacting with PTSD symptoms, following war trauma, than soldiers with normal pre-service levels (Aardal-Eriksson 2001). Another possible factor in PTSD is that a persistence of depressive symptoms may be caused by an underlying biochemical disorder, associated with insulin resistance (dysglycemia), that can be treated by a hypoglycemic diet. Neuroanatomy In animal research as well as human studies, the amygdala has been shown to be strongly involved in the formation of emotional memories, especially fear-related memories. Neuroimaging studies in humans have revealed both morphological and functional aspects of PTSD. The amygdalocentric model of PTSD proposes that it is associated with hyperarousal of the amygdala and insufficient top-down control by the medial prefrontal cortex and the hippocampus. Further animal and clinical research into the amygdala and fear conditioning may suggest additional treatments for the condition. |