Obsessive-Compulsive Disorder & Post-Traumatic Stress

Posttraumatic Stress Disorder

 

Posttraumatic Stress Disorder (PTSD) is reported to be the fourth most common psychiatric disorder, occurring in 10% of males and 18% of females (Breslau et al., 1998). To accurately evaluate individuals with PTSD requires exposure to some distress evoking situation that others would appraise as shocking. For example, observing harm to another person can also qualify as trauma. Following trauma, the individual is overwhelmed by invasive feelings, strong physiological reactions given cues of the prior trauma, a generalisation of the fear reaction to other stimuli, active avoidance of reminders, emotional deadening, heightened startle response and hypervigilance. Although symptoms typically develop soon after the traumatic event, in some individuals, there is a delay in the development of PTSD signs and symptoms. 

 

There have been reported differences in those with PTSD compared to other anxiety disorders. Typically, most anxiety disorders are coupled with higher levels of cortisol. Those individuals with PTSD show lower baseline levels of cortisol compared to controls, although higher levels of corticotrophin-releasing hormone, a hormone that is involved in initiating the release of cortisol, have been located in their cerebrospinal fluid (Jovanovic et al., 2010b).

 

Factors Associated with Enhanced Risk for PTSD

 

 

Evidence is presently varied with some individuals developing PTSD while others do not.  Several studies have reported that even when subjects are exposed to trauma some 80-90% of subjects are resilient and do not develop PTSD (Gillespie et al., 2009; Hoge et al., 2004; Jovanovic and Ressler, 2010). Additionally, a Swedish study reported that the type of trauma was 16.7% of the variance in determining whether PTSD would ensue after the trauma. 

 

When reviewing the various types of life-threatening events that result in PTSD, traumatic events caused by individuals are more likely to result in PTSD compared to other types.  For example, trauma such as an accident result in PTSD <10% of the time compared to rape or combat exposure which an occurrence rate between 20-60%. Loss of trust trauma because of others are associated with more frequent development of PTSD. Charuvastra and Cloitre (2008), questioned whether the loss of trust in others, is a moderator for when an event will result in PTSD. 

 

Coherent with the notion that loss of trust in others is a significant factor in PTSD development, social support during the time directly ensuing the stressor decreases the development of PTSD (Boscarino, 1995). Several studies have reported that early abuse, such as child abuse, increases risk (Charuvastra and Cloitre, 2008; Duncan et al., 1996). Ozbay and assoicates (2007) noted that repeated exposure to stressors also increases the probability of developing PTSD. Individuals’ personal characteristics also impact on whether they will develop PTSD following exposure to trauma. Having a greater predisposition to experience anxiety elevates the risk of developing PTSD after trauma.

 

Several researchers have reported that individuals who display greater skin conductance to threat and slower habituation to fear-provoking stimuli are more likely to develop PTSD following trauma (Guthrie and Bryant, 2006; Pole et al., 2009). Additionally, a study by Gilbertson et al., (2002) using firefighter subjects reported that those individuals who displayed a heightened startle response (as assessed prior to exposure to a fire) had a greater tendency of developing PTSD after a fire (Gilbertson et al., 2002). Those who experience disconnection at the time of the event are more prone to develop PTSD (Charuvastra and Cloitre, 2008).

 

The probability that those individuals with PTSD will have less emotional regulatory capacity has been examined. New et al. (2009) compared three groups: subjects with PTSD; subjects who had not been exposed to trauma, and subjects without PTSD but who had been exposed to trauma. Furthermore, subjects were requested to either suppress or amplify their response to negative images while their brains were scanned. Those subjects with PTSD exhibited less ability to alter (suppress or amplify) their responses compared to others. During the suppression directions, those with PTSD displayed less activity in the ventrolateral prefrontal cortex than subjects that were never exposed to trauma. However, the difference between those with and without PTSD who had been trauma exposed was not significant. In terms of the capacity to amplify distress, the two groups without PTSD stimulated similar regions and varied from those with PTSD. These findings by New et al., suggests that self-regulatory capacity may be impaired in those with PTSD. Coherent with this is the structural differences in the ventromedial prefrontal cortex of those with PTSD (Christianson et al., 2012), a region that can inhibit fear experience and expression, have also been acknowledged.

 

The academic literature has suggested that individuals with PTSD, as a group, have smaller hippocampi. The discovery of smaller hippocampal volume has been attributed to greater exposure to cortisol. That said, Pitman and associates questioned whether a reduction in hippocampus volume occurs after trauma, or whether the small hippocampus precedes the trauma and renders an individual susceptible to the development of PTSD.  To address this, Pittman and colleagues (Gilbertson et al., 2002) assessed the hippocampi of the never–trauma-exposed identical twins of Vietnam veterans with PTSD. The authors noted that hippocampi of these twins who had never been exposed to trauma were also smaller. These outcomes suggested that a small hippocampus may be a risk factor for PTSD rather than a consequence.

 

There have been several allelic variations in genes that have been identified related with PTSD. For instance, Norrholm and colleagues (2013) identified a variation in the gene for catechol-O-methyltransferase, which is an enzyme for degrading dopamine, norepinephrine, and epinephrine. Mehta et al (2011) identified a variation in the FKBP5 gene, which is involved in regulating sensitivity to cortisol. Lastly Feder and associates (2009) identified a variation in the gene for the receptor for corticotrophin-releasing hormone, which is involved in responding to stress hormones. The pituitary adenylate cyclase-activating peptide (PACAP) protein receptor is one of the latest genes to be recognised as risk factors for PTSD. In females, a single nucleotide changes in the receptor for pituitary adenylate cyclase activating polypeptide has been associated with PTSD, as has increased circulating levels of the PACAP protein. It has been acknowledged by Lehmann et al., 2013) that the PACAP system is involved in regulating corticotrophin-releasing levels. Individuals without PTSD have been appraised to establish how the PACAPR genetic risk factor effects response to threat. Several researchers have noted that females carrying the risk factor for genetic variation for PACAPR display increased amygdala activation to threat stimuli as evaluated by functional MRI (Ressler et al., 2011; Stevens et al., 2014). In conclusion, variants in proteins involved in responding to cortisol and to the stimulus for cortisol production (corticotrophin-releasing hormone) increase the risk for PTSD.

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PTSD Recovery

 

There are two suggested diverse processes that may transpire when an individual recovers from PTSD specifically extinction and learning safety cues. As previously discussed, extinction occurs through a process during which conditioned stimuli are met without being followed by the unconditioned stimulus. Importantly, extinction does not erase the original memory trace through the amygdala. Rather, the ventromedial prefrontal cortex inhibits the amygdala. 

 

The previously discussed research suggests that those with PTSD may have deficit volume for the regulation of an emotional response, a capacity pertinent for the process of extinction. Recovery from PTSD can also comprise another type of conditioning: learning safety cues. This type of learning involves relating a relaxation response to safety signals. In their daily lives, individuals with PTSD more often fail to distinguish threatening from nonthreatening environments. They are hypervigilant even in safe environments (Christianson et al., 2012; Jovanovic, Kazama et al., 2012; Jovanovic and Norrholm, 2011). Laboratory studies are consistent with this premise, that those with PTSD fail to learn safety signals. Javanovic and associates (2012) developed a procedure to demonstrate that those with PTSD have trouble learning to develop appropriate responses to safety signals. In the laboratory, fear-potentiated startle can be assessed. For most individuals, if a calming stimulus precedes a loud noise, the startle response (eye contractions) is reduced relative to when an aversive stimulus (i.e., frightening images) precedes the loud noise. In a laboratory study, Jovanovic and associates conditioned symbols to be linked with a presentation of aversive stimulus and some stimuli to signal safety. Those with PTSD startled to the same extent when soothing stimuli (safety signal) preceded the loud noise as when the disturbing stimuli preceded the loud noise. This happened even though those with PTSD were aware that the comforting stimuli were signals for relaxation (Jovanovic et al., 2010a; Jovanovic et al., 2012). Consequently, in those with PTSD, there are difficulties to both the extinction process and the learning safety-cue route to recovery. 

 

Another conceivable system that may facilitate or harm the capacity for recovery from PTSD is the immune system. Alterations in immune system function are also related with PTSD. Epigenetic variations in gene coding for proteins in the immune system have been reported. Those with PTSD display greater levels of tumour necrosis factor alpha (TNF-alpha) in plasma. They are also lower on interleukin 4 (IL-4), a cytokine that exerts an anti-inflammatory influence in the brain (Smith et al., 2011). Those with PTSD display lower heart rate variability (Minassian et al., 2014), a feature that indicates less control over inflammation.  Coherent with the effect of inflammation on reward structures, those with PTSD also display less activation in the nucleus accumbens in response to social and financial reward (Elman et al., 2009). In terms of recovery from PTSD, strengthening the regulatory capacity of the prefrontal cortex should facilitate both extinction and conditioning a relaxation response to safety cues. Activating approaches for reducing systemic inflammation offers another method for increasing recovery.

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Available Treatments For PTSD

 

Talking Therapies

 

A key method to treating anxiety disorders is behavioural treatments. Importantly, for PTSD and various phobias, individuals are exposed to stimuli related with their fear without incidence of genuine harm. For people with OCD, are exposed to stimuli that provoke compulsive behaviour and are not allowed to perform their behavioural customs. For individuals with panic attacks, producing bodily alterations with lactic acid infusion brings on the fear, which is then allowed to extinguish. These treatments have been reported to yield effect sizes in the range of 0.79 to 1.38 (Deacon and Abramowitz, 2004) with post treatment, evidence of brain alterations. For example, Straube and colleagues (2006) noted that following exposure treatment, subjects with phobias displayed less activity in the insula and anterior cingulate cortex when viewing the feared object. Those with OCD, post treatment, presented decreases in the activity of basal ganglia (Schwartz et al., 1996).

 

Because generalised anxiety disorder (GAD) is not related with fear-eliciting stimuli, exposure and response prevention are not suitable. Specific versions of cognitive behavioural therapy have been developed for treating GAD. Management and treatment involve cognitive restructuring, relaxation, and self-monitoring

to relieve anxiety symptoms. Progressive muscle relaxation and guidance in self-monitoring are employed so that relaxation can be applied at specific periods. Learning to counter harmful thinking is also focussed on (Deacon and Abramowitz, 2004). For panic attacks, learning methods of breathing control offers an additional tool. Cognitive behavioural therapy is successful in the treatment of generalised anxiety. A study by Maslowsky et al., (2010) with youths with GAD compared the effects of cognitive behavioural therapy to SSRIs at two weeks after post treatment. Both groups had improved on measures of daily anxiety and treatment groups exhibited improved levels of right ventrolateral prefrontal cortex activation when viewing images of angry faces compared to the non-treatment group. As the ventrolateral prefrontal cortex is understood to be an area of emotional regulation, the imaging results affirmed the efficacy of both procedures.

 

Medications for Anxiety

 

Benzodiazepines are often prescribed to treat acute anxiety and for sleep. Importantly, selection among the various benzodiazepines is typically founded on their half-lives. Those with shorter half-lives include Halcion (triazolam) and Restoril (temazepam). Although Halcion is less prone to result in morning sedation, it can cause agitation and psychosis. All benzodiazepines can result in blackouts, such that individuals fail to remember what happened while they were under the drug’s influence. Benzodiazepines also impair individuals driving ability. Tolerance to these drugs have also been noted by Trevor and Way (2013) to develop after 2 to 3 weeks’ use. After use for prolonged periods, benzodiazepine discontinuation is correlated with withdrawal symptoms, including anxiety, agitation, and possible seizures. Withdrawal symptoms can be fatal and have also been associated with increased risk for Alzheimer’s disease (Billioti de Gage et al., 2014; Roy et al., 2014).

 

Moreover, there is disquiet that medicating individuals with anxiety will reduce the effectiveness of exposure therapy. Extinction during exposure therapy involves making new connections such that a individual learns that in a given situation, the unconditioned stimulus will not occur. To learn new associations during exposure therapy, the anxiety response needs to be evoked. Part of the anxiety response involves sensations from the body. However, if an individual is medicated during the exposure training, internal anxiety will not be produced. Hypothetically, there will be insufficient anxiety for the extinction process to take place. When the drugs are discontinued, then any apparent gains of exposure training will disappear. Clinical outcomes are coherent with this rational (Otto et al., 2006; Rothbaum et al., 2014).

 

Selective serotonin reuptake inhibitors (SSRI) are also prescribed in the treatment of anxiety disorders. However, approximately 20 and 33% of individuals fail to respond to the SSRIs. Response to SSRI is typically delayed for about 2 to 6 weeks (Farach et al., 2012). A meta-analysis, including all included studies provided to the Food and Drug Administration (FDA) on paroxetine for anxiety, found that paroxetine reduced scores on the Hamilton Rating Scale for Anxiety (HRSA) by merely 2.3 more points compared to placebo (note there are 56 possible points on the HRSA.) The difference in change between placebo and drug was significant, but the effect sizes were small. There was some deviation in effectiveness across types of anxiety disorders. Treatment effects were a slightly higher for panic disorder than for GAD. Unlike the effectiveness of SSRIs, which differ as a function of severity of depression, treatment efficacy did not vary for those with mild, moderate, and extreme anxiety levels. As with studies on depression, much of the variation in baseline scores may be attributed to placebo effects (Sugarman et al, 2014).