PTSD is a very difficult beast to get a grip on, all the more so because its classification as a mental health disorder has always had a problematic status. As has been pointed out, “the entire canon of diagnostic categories in DSM-IV is phenomenological and descriptive, bar post-traumatic stress disorder. Aetiology [the causes] is not included in definitions because it is invariably multifactorial. Only post-traumatic stress disorder supposes a single cause.”
Viewed as a time-limited ‘normal human response’ to extraordinary external stressors, PTSD is not pathological. Viewed as a chronic response that is limited to people with certain prior life experiences, it is. There are strong arguments to be made for drawing a distinction between the two. Read the symptoms below and make up your own mind…
Symptoms of PTSD:
* Recurring thoughts or nightmares about the traumatic event or events.
* Trouble sleeping or changes in appetite.
* Anxiety and fear, especially when exposed to events or situations reminiscent of the trauma.
* Being on edge, being easily startled or becoming overly alert.
* Depression, sadness and low energy.
* Memory problems including difficulty in remembering aspects of the trauma.
* Feeling “scattered” and unable to focus on work or daily activities.
* Difficulty making decisions.
* Irritable, easily agitated, or angry and resentful.
* Feeling emotionally “numb,” withdrawn, disconnected or different from others.
* Spontaneously crying, feeling a sense of despair and hopelessness.
* Feeling extremely protective of, or fearful for, the safety of loved ones.
* Not being able to face certain aspects of the trauma, and avoiding activities, places, or even people that remind one of the events.
Psychological trauma is at the very core of understanding personality disorders.
People who have survived early and/or repetitive trauma can suffer acute and chronic physiological changes: traumatic stress affects the catecholamine system, hypothalamic-pituitary-adrenal axis (HPA), and the hypothalamic-pituitary-gonadal axis (HPG). If the trauma is early enough in life, severe enough, lasts long enough over time, or a genetic vulnerability is present (all of which may be the case with BPD), it can cause profound neurological damage to the brain. Recent research also suggests that there may exist a specific genotypic vulnerability to this form of early environmental trauma.
If you are intimately familiar with the emotional dynamics of someone suffering from Borderline Personality Disorder, the above descriptions of PTSD symptoms will not be new to you. In fact, recent research has suggested that a dual diagnosis of BPD and PTSD is redundant. Studies comparing the symptomatology of BPD and PTSD found that a physiological reaction to abandonment scripts in patients diagnosed with BPD may be the major distinguishing difference between the two.
Many researchers consider BPD to be a form of “Chronic PTSD” or “Complex PTSD”: the long-standing, seemingly permanent result of early traumatic experiences that went unacknowledged and untreated. This is both a psychodynamic viewpoint and a neurobiological one: in a kind of life-long static feedback loop, the physiological fight-or-flight response to stress feeds upon itself, continually placing the sufferer in alternating states of hyperarousal and numbness. This begs the question of how to appropriately categorize that small percentage of BPD sufferers who self-reportedly experienced no forms of early abuse or trauma. But that discussion is for another article.
This article abstract sums up the research on developmental factors for Chronic PTSD and BPD extremely well:
Stress activates the central and peripheral components of the stress system, i.e., the hypothalamic-pituitary-adrenal (HPA) axis and the arousal/sympathetic system. The principal effectors of the stress system are corticotropin-releasing hormone (CRH), arginine vasopressin, the proopiomelanocortin-derived peptides alpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids, and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks and positive social interactions.
By contrast, inappropriate responsiveness of the stress system may impair growth and development and may account for a number of endocrine, metabolic, autoimmune and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors and the timing of the stressful event(s), given that prenatal life, infancy, childhood and adolescence are critical periods characterized by increased vulnerability to stressors.
The developing brain undergoes rapid growth and is characterized by a high turnover of neuronal connections during prenatal and early postnatal life. These processes and, hence, brain plasticity, slow down during childhood and puberty, and plateau in young adulthood. Hormonal actions in early life, and to a much lesser extent later, can be organizational, i.e., can have effects that last for long periods of time, often for the entire life of the individual. Hormones of the stress system and sex steroids have such effects, which influence the behaviour and certain physiologic functions of individuals for life.
Exposure of the developing brain to severe and/or prolonged stress may result in hyperactivity/hyperreactivity of the stress system, with resultant amygdala hyperfunction (fear reaction), decreased activity of the hippocampus (defective glucocorticoid-negative feedback, cognition), and the mesocorticolimbic dopaminergic system (dysthymia, novelty-seeking, addictive behaviours), hyperactivation of the HPA axis (hypercortisolism), suppression of reproductive, growth, thyroid and immune functions, and changes in pain perception. These changes may be accompanied by abnormal childhood, adolescent and adult behaviours, including excessive fear (‘inhibited child syndrome’) and addictive behaviours, dysthymia and/or depression, and gradual development of components of metabolic syndrome X, including visceral obesity and essential hypertension.
Prenatal stress exerted during the period of sexual differentiation may be accompanied by impairment of this process with behavioural and/or somatic sequelae. The vulnerability of individuals to develop varying degrees and/or components of the above life-long syndrome is defined by as yet unidentified genetic factors, which account for up to 60% of the variance. CRH has marked kindling and glucocorticoids have strong consolidating properties, hence both of these hormones are crucial in the development and can alone produce the above syndrome. CRH and glucocorticoids may act in synergy, as in acoustic startle, while glucocorticoids may suppress or stimulate CRH, as in the hypothalamus and amygdala, respectively. A CRH type 1 receptor antagonist, antalarmin, inhibits both the development and expression of conditioned fear in rats and has anxiolytic properties in monkeys.
Profound stressors, such as those from sexual abuse, may elicit the syndrome in older children, adolescents and adults. Most frequently, chronic dysthymia and/or depression may develop in association with gastrointestinal complaints and/or premenstrual tension syndrome. A lesser proportion of individuals may develop the classic posttraumatic stress disorder, which is characterized by hypocortisolism and intrusive and avoidance symptoms; in younger individuals, it may present as a dissociative personality disorder. – article extract by S. Karger AG
