Espiritualidade, Religiosidade e Psicoterapia
9 de janeiro de 2018
Espiritualidade e Saúde Mental
9 de janeiro de 2018

PTSD and CHRONIC PAIN

Introduction

Exposure to traumatic stressors and psychological trauma is widespread, with a wide range of cognitive and behavioral responses/outcomes among trauma survivors [1]. The association of traumatic exposures with posttraumatic stress disorder (PTSD) and other mental health conditions is well known [2]. Although traumatic events are associated with PTSD in the literature, traumatized people do not meet DSM-IV (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition) criteria for PTSD in many cases and often present a range of psychoform or somatoform symptoms [3]. Considerable overlap in symptoms and disease comorbidity has been noted for medically unexplained symptoms in the primary care setting, such as chronic fatigue syndrome, low back pain,

irritable bowel syndrome, primary headaches, fibromyalgia (FM), temporomandibular joint disorder, major depression, panic attacks, and PTSD [4]. It is not unusual for patients presenting with chronic pain to describe significant levels of distress, including PTSD symptomatology. One of the first studies in this field was conducted in the past decade and investigated chronic pain patterns in Vietnam veterans with PTSD. Those reporting chronic pain showed significantly higher somatization than the others [5].

Epidemiologic surveys increasingly point to a relation between exposure to traumatic events and more health care utilization, adverse health outcomes, onset of specific diseases, and premature death. Certain characteristics of traumas, particularly peritraumatic cognitive response and related cognitions, appear to heighten the risk for PTSD [6]. Data from a cross-sectional survey of 3982 twins showed that comorbidity among nine conditions (chronic fatigue syndrome, low back pain, irritable bowel syndrome, chronic tension headache, FM, temporomandibular joint disorder, major depression, panic attacks, and PTSD) far exceeded chance expectations, suggesting that these medically unexplained conditions share a common etiology [7].

How people process stressors may be critical in determining whether or not trauma will be experienced, as well as the different constellation of symptoms if traumatization is characterized. More understanding of patterns of comorbidity may help clinicians care for challenging traumatized patients. This article attempts to clarify possible correlations between psychological trauma and two nosologically distinct types of chronic pain: FM and headache.

PTSD: A Single Disorder With Many Different Facets

PTSD is characterized by the emergence of three sets of symptoms after exposure to a single or several traumatic events: re-experiencing trauma (nightmares, traumatic memories, intrusive thoughts); emotional avoidance/numbness (affective

distance, emotional anesthesia); and autonomous hyperstimulation (irritability, insomnia, hyperarousal). It is estimated that 51.2% of women and 60.7% of men have experienced at least one potentially traumatic event during their lifetimes [8]. Intense or overwhelming experiences may trigger different responses, and studies have shown interindividual variability in the processing of life events and basic emotions [9]. The characterization of an event as traumatic also depends on the individual’s perceptual processing, which is significantly influenced by subjectivity. Rather than simply passively registering reality, acquisition of information is conceived as an intrinsically active dynamic process of deconstruction and reconstruction of the external world on the basis of patterns of stimulations exciting the sensory receptors [10].

Two Independent Pathways for PTSD Development

In life-threatening situations, mammals tend to react in two ways: “fight or flight” or “freezing”. In light of adaptive evolutionary theory, both types of responses lead to adaptive gains for survivors. The defensive cascade animal model shows that several animals flee from or confront other predators, whereas others pretend to be dead when captured [11]. More than 100 studies have pointed to a distinction between simple and complex PTSD; therefore, some researchers have sought to include the dissociative subtype in the DSM-V [12]. Although based on recent literature, “freeze, flight, fight, fright, faint” provides a more comprehensive description of the human acute stress response sequence than current descriptions [13]. Two main biobehavioral systems are involved in PTSD: 1) hyperstimulation of sympathetic reactivity with expressive activity of the adrenergic system typically involved in fight or flight responses, and 2) dissociation with parasympathetic reactivity involved in freeze responses [14]. Supporting these two PTSD subtypes is a model of risk factors for PTSD developed after a study with a group of acutely burned people. Two pathways to PTSD were discerned: 1) from the size of the burn and level of pain following the acute anxiety, and then to PTSD; and 2) from the size of the burn to the level of acute dissociation following the burn, and then to PTSD. Together these pathways accounted for almost 60% of variance in PTSD symptoms and constituted a model with excellent fit indices. These findings support a model of complex etiology for childhood PTSD in which two independent pathways may be mediated by different biobehavioral systems [15]. Similar results were found in a different sample of sexually abused children. Independent pathways—anxiety/arousal and dissociation—through which sexually abused children are likely to develop later PTSD symptoms, accounted for about 57% of variance in PTSD symptoms [16]. The finding that high levels of dissociative symptoms may be related to suppression of autonomic physiological responses to stress supports Bremner’s conceptualization of dissociative symptoms as comprising one of two subtypes of the acute stress response, differing physiologically as well as subjectively from a predominantly

hyperarousal or intrusive symptom response. The dissociative subtype may be seen in adults with a history of sexual abuse during childhood who present a consistent picture of dissociative amnesia, which occurs more often in victims of interpersonal violence during childhood than in combat soldiers and accident victims (who do not present hyperarousal symptoms).

Neuroimaging studies found distinct neural reciprocities for the two types of responses. The first pattern of sympathetic excitability involved attenuation of medial-prefrontal cortex activity and heightened amygdala activity leading to continuous autonomic arousal and state of alert [17]. The second pattern (dissociative) showed heightened activity of the medial-prefrontal cortex resulting in inhibition of amygdala activity, blunting the sympathetic response and leading to emotional numbing [18].

Subtype I

In a situation of unknown risk, heart and visceral alterations point to autonomous nervous system hyperactivity, whereas a subjective state of arousal potentiates an immediate search for syntheses and parameters for generating behavior. Peripheral and metabolic alterations (eg, tachycardia, mydriasis) reflect hyperactivity of the sympathetic nervous system and the hypothalamus-hypophysis-adrenal (HPA) axis leading to an immediate self-preservation response [19•]. Neurofunctional studies with hyperarousal PTSD patients using symptom provocation paradigms (in most cases, the retrieval of traumatic memories) suggest that the difficulty of synthesizing, classifying, and integrating a traumatic memory in narrative form may be related to the decreased activity of the prefrontal cortex involved in reducing negative feedback from the activity of the amygdala [17]. Studies have implicated the HPA and the sympathetic-adrenal-medullar stress axes as key components of this pathogenic process [20]. The relationship between anxiety level and performance is no longer advantageous after a certain point. Self-generated information flooding into sensory pathways affects the perceptual processing of data from surroundings, thus hampering the ability to formulate new hypotheses and syntheses.

Trauma-related studies involving epinephrine (E), norepinephrine (NE), and serotonin (5-HT) suggested that alterations in NE, E, and 5-HT may have relevance for symptoms commonly seen in survivors with PTSD, including hypervigilance, exaggerated startle, irritability, impulsivity, aggression, and intrusive memories [21]. Studies related to the role of NE in arousal, orienting to novel stimuli, selective attention, and vigilance demonstrated heightened noradrenergic neuronal reactivity, increased -2 receptor sensitivity and exaggerated arousal in organisms that have been exposed to chronic uncontrollable stress. The way an individual cognitively processes a traumatic event may trigger an anxious/arousal or a dissociative reaction. In subtype I, hyperactivity of the autonomic nervous system is observed, as in headache patients.

Subtype II