How to Treat PTSD and Alcohol Misuse

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It should be noted that while these studies assessed PTSD symptoms, the main outcomes were alcohol use outcomes. One of the most fundamental and ubiquitous forms of learning is habituation, whereby responding progressively declines with repeated stimulation (Groves & Thompson, 1970). In the context of traumatic responding, habituation refers to decreases in autonomic, behavioral, or neural responses to repeatedly presented novel, intense, or fear-relevant (unconditioned) stimuli. The failure of this type of habituation is proposed as a central contributor to the hyper-arousal cluster of PTSD symptoms (e.g., hyper-vigilance, exaggerated startle, and difficulty concentrating). For example, hyper-vigilance and exaggerated startle may be maintained in the benign post-traumatic context through persistent autonomic responding to reoccurring, and more or less irrelevant, stimuli.

Among treatment-seeking populations, high rates of comorbid PTSD and SUDs also have been consistently observed. Patients with PTSD have been shown to be up to 14 times more likely than patients without PTSD to have an SUD (Chilcoat & Menard, 2003; Ford, Russo, & Mallon, 2007). Conversely, among patients seeking treatment for SUDs, lifetime PTSD rates range between 30% and over 60% (Back et al., 2000; Brady, Back, & Coffey, 2004; Dansky, Brady, & Roberts, 1994; Jacobsen, Southwick, & Kosten, 2001; Stewart, Conrod, Samoluk, Pihl, Dongier, 2000; Triffleman, Marmar, Delucchi, & Ronfeldt, 1995).


More generally, theoretical progress on this disorder may illuminate the mechanisms of anxiety disorders, the most prevalent class of psychological disorders, with a lifetime prevalence of 28.8% in the US general population (1). The final sensitization theory reviewed herein imputes non-associative learning correlates of PTSD to the uncontrollable nature of the stressor (trauma). This theory of PTSD has received little experimental testing, which is unfortunate given the general view that uncontrollability and unpredictability are critical features of PTSD-inducing events (e.g., Foa et al., 1992; Mineka & Zinbarg, 2006; Volpicelli et al., 1999). This general view stems largely from animal data documenting behavioral consequences of uncontrollable and unpredictable threat that are analogous to many symptoms of PTSD (for a review, see Foa et al., 1992). Non-experimental evidence for this perspective derives from studies documenting inverse relations between perceptions of control and PTSD symptoms among survivors of sexual victimization (Bolstad & Zinbarg, 1997; Regehr, Cadell, & Jansen, 1999) and criminal assault (Kushner, Riggs, Foa, & Miller, 1993). Extant experimental support comes from initiatives testing the relation between clinical anxiety and threat predictability (e.g., Grillon et al., 2008), which is a characteristic of threat distinct from, but highly related to, controllability.

theories of ptsd and alcoholism

The positive inner working models serve as an internalized secure base which supports the individual in regulating emotions in a functional and relatively autonomous way, and enables him/her to explore the external world on his/her own (146). Moreover, secure attachment patterns facilitate the formation of stable and functional relationships, allowing the individual to additionally regulate emotions with the help of others (121). In contrast, internalized traumatic early experiences promote the development of corresponding negative inner working models and insecure attachment patterns that hamper the functional regulation of emotions and the formation of stable relationships (80, 145, 147, 148). A review of PTSD and alcohol abuse statistics indicate that nearly 28 percent of women diagnosed with PTSD report concerns about alcohol abuse and dependence.


Summarizing this literature can inform researchers and clinicians about effective treatments, future research directions, and may offer insight into underlying mechanisms that can be studied pre-clinically in a bench to bedside and back approach. A final line of work supporting impaired inhibition of fear in PTSD comes from studies applying a conditional discrimination paradigm (AX+/BX−) designed to assess the degree to which fear to a conditioned danger-cue is reduced when presented in tandum with a conditioned safety-cue. This reduced transfer of inhibition has recently been found to predict levels of PTSD in trauma exposed, deployed soldiers 7 months after testing (Sijbrandij, Engelhard, Lommen, Leer, and Baas, 2013), suggesting that impairments in fear inhibition may serve as a premorbid risk factor for later development of PTSD. An additional formulation of the extinction model comes from Eysenck (1979) who argues that the conditioned response (i.e., an internal state of fear) is sufficiently “nocive” or uncomfortable in those disposed toward clinical anxiety to serve as an aversive US-substitute in the absence of the genuine US. That is, extinction of fear to a CS previously paired with an aversive outcome may be slowed or prevented in those for whom anxiety reactions to the CS are sufficiently strong to function as aversive reinforcement of the CS during extinction learning.

  • A final line of work supporting impaired inhibition of fear in PTSD comes from studies applying a conditional discrimination paradigm (AX+/BX−) designed to assess the degree to which fear to a conditioned danger-cue is reduced when presented in tandum with a conditioned safety-cue.
  • Specifically, peritraumatic hyperarousal is transformed into enduring hyperarousal symptoms, and this is likely mediated by a network comprising the amygdala, its inputs, and its interconnections with PRC and brainstem.
  • The past two decades have seen substantial increases in lab-based testing of associative and non-associative learning abnormalities in PTSD.
  • By contrast, such weak situations as contextual threat may elicit fear only in individuals for whom hyper-excitability of the fear system was achieved through sensitization (e.g., PTSD patients), with all others experiencing only sub-threshold levels of fear activation.
  • The brain begins to plan for survival in the long run when danger appears life-threatening or persists for a prolonged period.

This approach is significantly influenced by the findings of Affective Neuroscience (AN), decisively developed by Jaak Panksepp (76), who emphasized an evolutionary perspective and affective cross-species similarities. His fusion of psychoanalysis and AN, labeled as neuropsychoanalysis, proposes a monistic relationship between mind and brain, which is expressed in the term BrainMind (77). The BrainMind is conceptualized as an interdependent and multi-layered dynamic structure comprised of primary, secondary and tertiary processes (see Figure 1) (77, 79). In correspondence to this, it is important to note that the Lacanian-framework proposes three different clinical structures which determine the function of the psychoactive substance for the addicted subject. Thereby, Lacan (33) differentiates between the (1) neurotic, (2) perverse, and (3) psychotic clinical structure, which is distinguished by their predominant mode of defense against the symbolic castration.

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In addition, fear-related conditioning in rats can be severely impaired by infusing into the amygdala pharmacological agents that block LTP and other processes in the consolidation cascade (110, 113–115). Moreover, destruction of parts of the amygdala well after fear conditioning training has been completed, abolishes that fear-related conditioning (116–118). Sensory property knowledge (e.g., object color knowledge) is represented in corresponding sensory systems (color perception system), and this is evidenced by diverse neuroimaging findings. In a neuroimaging study using functional magnetic resonance imaging (fMRI), healthy subjects were scanned while they performed a color perception task (Farnsworth–Munsell 100 hue test) and a color knowledge task (a property verification task). The findings were that partially overlapping subregions of the color processing system mediated color perception and color knowledge representation (32). In correspondence to this, our second study (118) was able to gather new insights regarding the relationship between attachment security, personality organization, and primary emotion functioning.

theories of ptsd and alcoholism

This is supported by abundant evidence from neuroimaging, neuropsychological, behavioral, and animal studies (35, 36, 177–179). The primate amygdala interconnects with approximately 90% of cerebral cortical areas (153), and numerous subcortical areas (92, 130). It is suggested amygdala hyperactivity modulates the activity of diverse interconnected brain regions, and thereby drives the development of further DSM-5 PTSD symptoms, which are generally markedly different in nature from hyperarousal. Until recently, the influence of other primary emotion systems in the emergence of SUD cycles has been largely neglected in AN-theory and research.

PTSD and alcoholism

Additional findings of amygdala hyper-excitability to neutral faces in those with versus without PTSD, indicate that the effect may not be restricted to ‘fearful’ faces (Brunetti et al., 2010). It should be noted that the increased amygdala reactivity in PTSD may reflect a premorbid risk factor rather than abnormal stress sensitization of this circuit; prospective research on amygdala responses to faces in PTSD is needed to clarify this issue. Several studies have also found stronger SCR to these same acoustic stimuli in PTSD (e.g., Shalev et al., 1992, 1997), though somewhat less robustly than HR elevations (for a review, see Pole, 2007). Because these psychophysiological results were largely found in trauma exposed individuals with versus without PTSD, such findings represent viable support for stronger, trauma-related sensitization of the autonomic nervous system as a non-associative learning correlate of PTSD. In fact, many people struggling with post traumatic stress disorder can turn to unhealthy coping skills like substance abuse or self-harm in an attempt to minimize or escape from their emotional distress.

theories of ptsd and alcoholism

Moreover, she discusses applications of these findings to the assessment and treatment of people exposed to trauma who abuse alcohol. Finally, the author outlines novel methods for testing theoretical hypotheses and makes suggestions for methodological improvements in future research. CBTs for AUD focus on the identification and modification of maladaptive cognitions and behaviors that contribute ptsd and alcoholism to alcohol misuse.21 Behavioral treatments for people with AUD also target motivation for change and improvement of specific skills to reduce the risk for relapse. Studies that compare other outcomes related to treatment retention and symptom improvement, such as sleep, mood symptoms, somatic medical conditions, and safety profiles (including violence and suicidality), would also be helpful.

Abnormal Fear Memory as a Model for Posttraumatic Stress Disorder

Collectively, there is abundant evidence that amygdala activity can enhance hippocampal consolidation, and these brain regions likely participate also in stress-induced impairment of emotional memory retrieval. The evidence generally suggests the amygdala may drive hippocampal dysfunction to produce the PTSD symptom of impaired memory for important aspects of the traumatic event, although further studies are needed. Nevertheless, the amygdala may also impair memory retrieval processes in the hippocampus, and these effects have many parallels with the memory enhancement effects; that is, participation of stress hormones, common neurotransmitters, and restriction to emotionally arousing memories (177, 179).

  • More rigorous research has been conducted with Seeking Safety (SS), a non exposure-based, manualized cognitive behavioral intervention for comorbid PTSD and SUDs (e.g., Najavits, 1998; Hien et al., 2004; 2008; additional studies summarized in Table 2).
  • The present overview aims at developing and empirically validating a neuroscientifically informed psychodynamic framework regarding the etiology of SUD.
  • In correspondence to the proposed relation between SUDs, decreased SEEKING, and increased PANIC/GRIEF, the AN-framework sheds new light on the link between depression and SUD, already emphasized by Rado (11, 23).