The Long Term Effects of Trauma on Cognitive Functioning

The main causes of PTSD in the United States are from common events that can leave lasting effects. These include criminal victimization, motor vehicle accidents, and childhood maltreatment. PTSD tends to occur more in women than in men, who are twice as likely to develop symptoms of PTSD and also more likely to have their symptoms persist for longer amounts of time. The reason women are thought to be so susceptible to the development of PTSD is related to the type of trauma they experience. Women report much more accounts of severe sexual abuse and moderate physical and emotional abuse than men do, which tend to originate during childhood. Research data also suggests that PTSD is linked to several other comorbid conditions, especially for individuals who suffered traumatic childhood abuse or have a history of prior drug abuse. These comorbid disorders include social phobia, major depression, and dysthymia (Nemeroff et al., 2006). Additionally, individuals who experience lifetime PTSD symptoms with a comorbid major depressive disorder are significantly more likely to attempt suicide.

Disturbances in memory are one of the most common symptoms of PTSD. In the first six months after the trauma has occurred, the majority of PTSD patients usually experience intrusive memories, which are usually involuntary distressing and uncontrollable recollection of the prior traumatic experience (Halligan et al., 2002). Intrusive memories can take the form of flashbacks as well as dreams or nightmares of the traumatic event and tend to make the individual very upset when they occur (Nemeroff et al., 2006). These intrusive memories are exceptionally vivid in comparison to normal long-term memory recall and typically are made up of segments of episodic memory instead of the entire event. These vivid flashbacks are often triggered by perceptual cues, which closely resemble the cues present during the time the trauma occurred (Halligan et al., 2002). Intrusive memories have the potential to cause additional common symptoms such as insomnia, difficulties concentrating, irritability, hypervigilance, and being easily startled (Nemeroff et al., 2006). Symptoms less commonly experienced include avoidance, psychogenic amnesia, detachment, loss of interest, restricted affect, and a sense of a shortened future. The comprehensive effect of intrusive memories is thought to have a negative impact on an individual’s cognitive abilities.

Many researchers hypothesize that the intrusive nature of trauma-related flashbacks and goal-irrelevant environmental cues have a negative impact on an individual’s cognitive processing (Morey et al., 2009). Additionally, research suggests that it is easier to retrieve emotional memories than non-emotional memories because they are more salient and thus it is easier to encode or consolidate them. However, the types of emotions associated with a particular memory also correlate to how well it is remembered. A study by Depue, Banich, and Curran (2006) found that there was a decreased ability to recall negative information in comparison to neutral information. They concluded that cognitive control could either enhance the information presented to an individual or also reduce it depending on the type of information. Patients who have PTSD or obsessive-compulsive disorder (OCD) may lack the cognitive control mechanisms that allow for the regulation of emotional memories (Depue, Banich, & Curran, 2006). These individuals tend to show an enhanced ability to remember emotional information but also display an inability to suppress that information. In contrast to the vivid flashbacks that accompany PTSD, many individuals may simultaneously experience difficulties with their ability to intentionally recall the traumatic event (Halligan et al., 2002). Deliberate attempts at remembering the trauma often fall victim to sequential confusion about the order of events that occurred. Some individuals even have amnesia about a significant part or details of the experience.

Various neuroimaging studies about PTSD have been helpful in revealing the complex ways that PTSD can cause changes in brain function. There seem to be several cognitive-emotional interactions such as, regulation of emotions, threat processing, appraisal, social-emotional processing, and the concept of self-relatedness that are having significant implications on certain regions of the brain. One study sought to investigate the function of the hippocampus in firefighters, half of which were diagnosed with PTSD. The test subjects completed a word stem completion task consisting of three-letter word stems with deeply encoded/high recall and shallow encoded/low recall words that were encoded during a previous training session. Results from PET scans showed that the subjects with PTSD had greater regional cerebral blood flow in the hippocampi. Evidence from other studies also indicates that PTSD patients display impaired blood flow patterns specific to certain regions of the brain and suggest that it may increase the responsivity of the extended amygdala and insula areas. Another study about working memory performance in PTSD found that patients with PTSD had increased activation in bilateral inferior parietal lobules and left precentral gyrus. Additionally, the right inferior temporal gyrus, inferior medial frontal lobe, and bilateral middle frontal gyri also display a reduction in their activation (Liberzon & Martis, 2006). These deficits are consistent across the findings of many studies.

The neural circuits that are affected in PTSD are theorized to involve very complex interactions between several areas of the brain. These areas are thought to include regions such as the thalamus, which serves as a gateway for sensory inputs. The hippocampus is also involved, this area is associated with short-term memory and probably also plays a role in appraising the context of fearful events. Another region is the amygdala, which functions in the conditioning of responses to intense emotions, such as the fear associated with PTSD. In addition, regions that are involved with visuospatial processing and making assessments of threats also seem to be affected. These regions include the posterior cingulate, parietal cortex, and motor cortex. Finally, PTSD also affects the regions of the medial prefrontal cortex that are believed to extinguish more primitive subcortical responses, such as the anterior cingulate, orbitofrontal, and subcallosal gyrus (Nemeroff et al., 2005). Research also indicates that the increased levels of stress experienced by those who have experienced significant trauma or have PTSD decreased the function of the hypothalamic-pituitary-adrenal (HPA) axis (Bremner et al., 2006). In comparison, patients who have a history of chronic stress exposure have increased HPA axis reactivity following their re-exposure to stress.

The HPA axis plays an important role in stress responses. Stress initiates the release of corticotropin-releasing factor (CRF) from nerve terminals that originate from the paraventricular nucleus of the hypothalamus (Bremner et al., 2006). Increases in CRF are associated with an increase in symptoms of depression and anxiety (Nemeroff et al., 2006). The CRF then increases the secretion of adrenocorticotropin hormone (ACTH) from the anterior pituitary gland, which will then stimulate the release of glucocorticoids from the adrenal glands (Bremner et al., 2006). Glucocorticoids are important for normal brain maturation. They play a role in remodeling the axons and dendrites of neurons and affect the survival of the cell. Both suppressed and elevated levels of glucocorticoids have been found to impair brain development and functioning (Lupien, McEwen, Gunnar, & Helm, 2009). Research has found that stressors, especially early stressors during childhood, can cause an increase in plasma glucocorticoid levels as well as to potentiate glucocorticoid and responsiveness of CRF to subsequent stressors (Bremner et al., 2006). Additionally, there are indications that the adolescent human brain might be the most sensitive to the effects of glucocorticoid levels (Lupien et al., 2009). Studies on chronically stressed animals suggest that stress can develop an inability to terminate the glucocorticoid response to stress and deficits in feedback inhibition of the HPA axis by glucocorticoids. These deficits in the negative feedback system have an effect on dexamethasone found on the HPA axis. Some researchers theorize that these deficits could be linked to the observed decreases in glucocorticoid receptor binding occurring in the hippocampus (Bremner et al., 2006). Thus, the stress response has become associated with damage to the functionality of the hippocampus.

PTSD is also associated with an inhibited growth of neurons as well as deficits in new learning and memory. The ability to learn seems to be more impaired in elderly individuals with PTSD in comparison with younger individuals (Quireshi et al., 2011). Possible explanations for these effects include elevated levels of glucocorticoids (cortisol) that are induced from the stress and associated with glutamatergic toxicity. Other explanations involve decreases in brain-derived neurotrophic factor, direct hippocampal effects of corticotropin-releasing factor, alterations in serotonin, and elevated levels of excitatory amino acids such as glutamate (Bremner et al., 2005). Additionally, images from magnetic resonance imaging (MRI) scans have found that PTSD patients have smaller hippocampal volumes or various other abnormalities in their hippocampus (Qureshi et al., 2011). These observations are associated with deficiencies in hippocampal-based verbal declarative memory function and working memory performance (Bremner et al., 2005). A study of veterans with combat-related PTSD used neuropsychological tests, such as the ability to recall paragraphs, to probe the function of the hippocampus and compare it to healthy control subjects without PTSD. Results of the tests revealed that the combat veterans had decreased immediate and delayed recall and a lower percentage of information was retained than the control subjects. However, the IQ scores of the two groups were the same (Nemeroff et al., 2006). This suggests that PTSD has a very large impact on the function of working memory.

People with PTSD also show greater activation levels in three ventral emotion-processing regions of the brain: the amygdala, ventrolateral prefrontal cortex, and fusiform gyrus. The ventrolateral prefrontal cortex regions play a role in working memory processes by maintaining object information while simultaneously inhibiting distraction irrelevant information (Morey et al., 2009). Furthermore, individuals with PTSD also exhibit poorer attention capabilities than individuals without a history of trauma. A possible explanation for decreased levels of attentiveness might relate to the observed differences in the same regions of the brain that are also associated with the decreased performance of working memory (Qureshi et al., 2011). PTSD patients exhibit greater concomitant disruption of activation for salient and task-irrelevant environmental cues associated with their traumatic experiences in the dorsal lateral prefrontal cortex than those who have not experienced any significant trauma in their lives. Generally, disruption in this area only occurs with cues specific to threatening or dangerous situations. These disruptions have been reported to negatively interfere with the performance of working memory. However, in the study by Morey et al. (2009), findings of poorer working memory performance in those with PTSD indicate that all ‘distractor’ information is more disruptive to working memory-related activity in the dorsal regions despite whether it has any relevance to prior traumatic experiences (Morey et al., 2009). The mechanisms that allow for the cognitive control of well-encoded memories may be dysfunctional, which may make these individuals hypersensitive to traumatic or threatening stimuli (Depue, Banich, & Curran, 2006). Therefore, individuals with PTSD tend to encode this emotional information to such an extensive degree that their normal cognitive control mechanisms are rendered completely ineffective for modulating the retrieval of these memories.

References

Bremner, J., Mletzko, T., Quinn, S., Williams, C., Brummer, M., Siddiq, S., et al. (2005). Effects of phenytoin on memory, cognition and brain structure in post-traumatic stress disorder: A pilot study. Journal of Psychopharmacology, 19(2), 159-165.

Depue, B. E., Banich, M. T., & Curran, T. (2006). Suppression of emotional and nonemotional content in memory: Effects of repetition on cognitive control. Psychological Science, 17(5), 441-447.

Halligan, S., Clark, D., & Ehlers, A. (2002). Cognitive processing, memory, and the development of PTSD symptoms: two experimental analogue studies. Journal of Behavior Therapy and Experimental Psychiatry, 33(2), 73-89.

Liberzon, I., & Martis, B. (2006). Neuroimaging studies of emotional responses in PTSD. Annals of the New York Academy of Sciences, 1071(1), 87-109.

Lupien, S. J., McEwen, B. S., Gunnar, M. R., & Heim, C. (2009). Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience, 10(6), 434-445.

Morey, R., Dolcos, F., Petty, C., Cooper, D., Hayes, J., Labar, K., et al. (2009). The role of trauma-related distractors on neural systems for working memory and emotion processing in posttraumatic stress disorder. Journal of Psychiatric Research, 43(8), 809-817.

Nemeroff, C., Bremner, J., Foa, E., Mayberg, H., North, C., & Stein, M. (2006). Posttraumatic stress disorder: A state-of-the-science review. Journal of Psychiatric Research, 40(1), 1-21.