Content
This kind of conditioned generalization has since been adopted as a core feature of PTSD, through which fear during a traumatic event extends to safe conditions ‘resembling’ the distressing event (American Psychiatric Association, 2013). The pathogenic contribution of conditioned generalization follows from the undue proliferation of trauma cues in the individual’s environment. That is, generalization results in the spreading of traumatic reactions to stimuli that resemble the CS, but are themselves benign. Precipitating this proliferation of trauma cues may be an underlying disposition toward reduced thresholds for threat reactivity, resulting in less danger information (i.e., less resemblance to the CS) required for activation of the fear circuit among those with, or prone toward, clinical anxiety (Lissek et al., 2010). Currently, COPE is being evaluated versus standard cognitive-behavioral relapse prevention in a randomized controlled trial among OEF/OIF Veterans.
In addition, further descriptive research on how individual differences, such as gender and the nature of the trauma (combat vs. assault), affect the mechanism by which PTSD and alcohol use disorder co-occur and impact treatment outcomes will also serve to advance this ongoing and important field of research. Theorizing about fear has been dominated by the amygdala’s contribution [see for reviews, Ref. (111, 154)], but the amygdala solely cannot account for fear. The amygdala participates ptsd and alcoholism in fear, but also in diverse other emotions (81, 231, 232, 242, 243). In addition, fear is frequently elicited in laboratory animals by inflicting pain, and the latter is also processed in the amygdala (see earlier), suggesting the operation of possible confounds. Furthermore, rodents with amygdala lesions manifest impaired fear conditioning when assessed with fear-potentiated startle or freezing, yet largely intact fear conditioning when assessed by avoidance behaviors (35, 244, 245).
5. Failure to inhibit fear
The function of rACC is interpreted as the regulation of the amygdala, but the mechanisms producing its dysfunction in PTSD are unexplained (17, 18, 21). In contrast, the current model predicts that amygdala hyperactivity drives rACC hypoactivation, and this can be investigated at several levels. At the neuroanatomical level, amygdala neuronal boutons that synapse with rACC neurons are predicted to be predominantly inhibitory, and so should mainly form symmetric rather than asymmetric synapses [cf. Amygdala–rACC projections are denser and more extensive than the reciprocal ones (130, 168, 206). Quantitative estimates of these projections may provide an index of the relative frequency of recruitment, and thus of the predominant direction of activation.
Furthermore, for most of the 20th century psychoanalysis ignored significant advances in neurobiology, leading to an increasing distance from natural science and academic psychology (73). However, this crisis of psychoanalytic theory fostered the development of the field of neuropsychoanalysis, which aimed at linking psychoanalysis with neuroscience and biological psychiatry. Furthermore, the persistence of splitting obstructs the development of a coherent identity marked by an integrated (“good” and “bad”) sense of self and others. This fosters the syndrome of identity diffusion, which is characterized by dissociated representations of the self and others into multiple segments of idealized and persecutory representations (64). The original contributions presented in the study are included in the article/supplementary material; further inquiries can be directed to the corresponding author. There are definite overlaps between them and it is likely that psychological, social, and biological factors interact in the development and maintenance of PTSD.
Research Focused on the Relationship Between Childhood Trauma, Personality, and Substance Use Disorder
Convergent support is provided by findings from neuroimaging studies that PTSD symptom severity is positively correlated with amygdala activity, as measured by PET or fMRI during exposure to trauma-related or experimental stimuli (131–135). Additional brain regions, specifically insula (BA 13), anterior parts of ACC (BAs 25, 32), and dorsomedial PFC (BAs 9, 10) https://ecosoberhouse.com/article/how-long-does-alcohol-stay-in-your-system-blood-and-urine/ may also contribute to components of hyperarousal (136, 137). The model contends that the amygdala, which processes arousal (80, 81), also produces related representations on grounded cognition principles. Correspondingly, at the severe intensity levels that characterize PTSD, peritraumatic hyperarousal is transformed into enduring hyperarousal symptoms.
All but one of the studies found that PTSD symptoms and drinking outcomes improved significantly over time. There was weak evidence to support the use of medications to treat AUD among those with comorbidity with PTSD. Findings for medications that were hypothesized to treat both disorders were also contradictory. Studies reviewed thus far report a variety of results across a multiplicity of stress-related learning mechanisms with proposed relevance to PTSD. Although no unified conceptualization of these results is readily obvious, the social psychological concept of the strong situation may provide an interpretive framework with which to deduce the beginnings of a unified account.
Learning Models of PTSD: Theoretical Accounts and Psychobiological Evidence
Non-rapid eye movement (NREM) sleep is a state of attenuated arousal, during which overall brain activity is reduced substantially, according to neuroimaging findings in healthy human subjects (155, 158, 159). After controlling for this overall decline, brainstem subregions that generate and maintain sleep, as well as the amygdala and other areas, are relatively activated compared to waking (155, 156, 159). NREM sleep recurs throughout the sleep period, in alternation with rapid eye movement (REM) sleep.
In a cue-reactivity experiment among dually diagnosed individuals, severity of PTSD predicted increased craving during exposure to personalized trauma-related and substance cues (Saladin et al., 2003). With regard to symptom severity and biopsychosocial functioning, co-occurring PTSD and alcohol use disorder have proven more detrimental than a diagnosis of PTSD or alcohol use disorder alone. In a cohort of Vietnam veterans, mortality (controlling for other medical diagnoses) was 55% higher among psychiatric patients with co-occurring substance use disorders, such as alcohol use disorder, than those who did not have a co-occurring substance use disorder (Rosen, Kuhn, Greenbaum, & Drescher, 2008). Individuals with comorbid PTSD and alcohol use disorder were more likely to have attempted suicide and to report lower quality of life (Leeies, Pagura, Sareen, & Bolton, 2010). Further, veterans exposed to traumatic war zone experiences and who also met criteria for alcohol use disorder were more likely to display pervasive, declining effects on social functioning and had lower rates of employment (Fontana & Rosenheck, 2010). The detrimental effects appeared to be reciprocal, such that poor quality of life led to a more chronic course of PTSD and alcohol use disorder.
Prolonged exposure
Sensory systems, for example, which process the perception of a feature, also mediate enduring representations of that feature, usually in higher-level subregions. That is, sensory systems are engaged in both perceptual processing and in the mediation of sensory knowledge representations. Hence, a sensory system that is active during the perception of a stimulus, is later reactivated when the corresponding memory representation is retrieved. Similar principles apply to the motor system, which is involved in both action execution processes and in the mediation of action knowledge representations.
