The hallmark symptoms of PTSD can be attributed to both underlying emotional and cognitive processes. Furthermore, these two processes are thought to interact with one another to both explain the emergence and maintenance of the disorder. For example, Brown and Morey (2012) have proposed an emotion-cognition interaction model which is based on two networks of altered brain activation (i.e., trauma-disrupted network and a fear learning network). Evidence for deficits within these two networks could potentially explain predisposition, or susceptibility, for suicidal behavior among individuals with PTSD.

As commonly seen in the clinical presentation of the disorder, individuals with PTSD often struggle with the ability to accurately assign value to external events. This inability is reflected by struggles with re-experiencing, hyperarousal, and avoidance symptoms. Behavioral processes of fear conditioning and extinction are often used to explain how PTSD may impact the ability to accurately assign value to external stimuli. For example, several studies and reviews have found evidence for enhanced fear conditioning (Hayes et al. 2012) in individuals with PTSD. Imaging results suggest greater activation in the amygdala in PTSD (Etkin and Wager 2007; Liberzon and Sripada 2007; Shin et al. 2005, 2006; Shvil et al. 2013), which is important given that the amygdala is involved in the assessment of threat-related stimuli. Studies suggest that individuals with PTSD show greater activation in the amygdala when presented with both trauma-related stimuli and affective stimuli (Shin et al. 2006; Shvil et al. 2013). The hyperresponsivity of the amygdala likely intensifies processes associated with risk-detection, especially as it relates to hyperarousal and vigilance (Liberzon and Sripada 2007), thus making it more likely that the individual is inaccurately assessing value of external events. This initial inability to perceive the environment accurately plays an integral role in processes to follow, such as those that underlie attention, memory, and problem solving.

Across a variety of different paradigms (e.g., emotional stroop), evidence suggests that individuals with PTSD suffer from attentional biases. These biases appear to relate primarily to an individual’s inability to disengage from negative stimuli (Hayes et al. 2012) and have been found to be positively associated with intrusive symptoms (Weber 2008). Together these findings suggest a feedback loop in which difficulty disengaging from negative stimuli increases the likelihood of intrusive symptoms, which in turn facilitates continued attentional bias. These attentional biases also have direct implications for memory encoding processes, as greater resources may be directed toward encoding emotional information (Hayes et al. 2012) at the cost of neutral information.

The brain structures (e.g., amygdala, dorsal anterior cingulate cortex (ACC), insula, ventromedial PFC) thought to be implicated in the previously described deficits seen in PTSD do not completely overlap with brain areas thought to be associated with altered value attribution seen in individuals with a history of suicidal behavior (Jollant et al. 2011); however, findings do suggest similar underlying processes related to suicide risk. The hyperactivation of the amygdala, a key defining feature of the fear network, could present susceptibility of both increased negative emotions (e.g., anger) and biased perceptual processes. Due to elevation of threat perceptions in the environment with subsequent difficulty disengaging from negative stimuli, an individual with PTSD is likely to engage in disadvantaged decision making, which appears to be associated with a predisposition to suicidal behavior (Jollant et al. 2011).

The triggering of automatic negative emotions and attentional biases, especially over prolonged periods of time, likely contributes to intense and prolonged negative states. In fact, several authors suggest that the emotional and cognitive resources that are dedicated to threat perception leave fewer resources available to oversee the regulation of responses (Hayes et al. 2012; Weber 2008). Intense negative states with poor emotional and cognitive regulation could likely present greater susceptibility to suicidal behaviors, especially via processes related to hopelessness and rumination.

Neuroimaging studies have provided evidence that hyperactivity in emotion processing networks (e.g., amygdala, ventrolateral PFC, medial PFC) and hypoactivation in the dorsal executive functioning processing networks are associated with impaired maintenance of information in working memory (Hayes et al. 2012). Impaired maintenance of information within working memory due to emotional distraction likely has important implications for emotional and cognitive regulation. For example, these deficits could impact concentration ability, mental flexibility, and memory encoding, all aspects necessary to regulatory mechanisms.

In addition to deficits in working memory, individuals with PTSD consistently show bias for both episodic and autobiographical memories (Weber 2008). For example, individuals with PTSD show greater memory bias for traumatic information, and studies have found that individuals with PTSD perform worse when asked to recall personal memories compared to individuals without PTSD (Hayes et al. 2012). Findings suggest that recall often lacks detailed information and shows consistent “gist-like” performance across both traumatic memories and neutral/positive events (Hayes et al. 2012). Implications for this type of biased memory could facilitate reduced problem-solving abilities, especially given the deficit in memory for autobiographical events. As discussed by Jollant et al. (2011), poor recall, or biased recall, for autobiographical events, likely creates even greater difficulty when attempting to generate solutions for emotional regulation based on prior experience.

The hypoactivation of the mPFC may be a large contributor to difficulties in emotional and cognitive regulation. In addition to providing inhibitory control over the amygdala, the mPFC is believed to play a role in the contextualizing of stimuli, which helps guide the selection of appropriate responses based on environmental factors (Liberzon and Sripada 2007). Diminished functioning of the mPFC, which is tasked with regulation of affect and integration of emotional and cognitive information, then, is likely less effective in larger executive control processes, especially when affective content is triggered (Brown and Morey 2012). Furthermore, deficits in the mPFC are likely associated with diminished habituation of amygdala responses (Shin et al. 2005). Together, the lack of inhibitory control, poorer extinction/habituation processes, and overall diminished functioning of the mPFC, contribute to greater demands on the fear network. These greater demands tax emotional and cognitive regulatory abilities, especially when activated within an emotional context and could prolong the negative emotional state and reduce problem-solving abilities, both factors that may contribute to suicide risk.

The ability to engage in complex goal-directed behavior requires the synthesis of many of the aforementioned processes, especially those involving attention, working memory, flexibility, and planning. Given that many of these processes are impacted when PTSD is present, overall executive control of behavior is likely challenged. Poor regulation of attention and responses to stimuli likely play a large role in the development of potentially maladaptive coping mechanisms (Aupperle et al. 2012). Regardless of whether these coping mechanisms are either directly or indirectly associated with suicidal behaviors, the presence of maladaptive coping mechanisms, especially due to underlying difficulties with response inhibition, could present another view of neurobiological susceptibility for suicidal behaviors.

Several researchers have suggested a possible functional relationship between the amygdala and mPFC (Hayes et al. 2012; Shin et al. 2005, 2006). This functional relationship may help to conceptualize how the aforementioned areas of susceptibility for risk interact with one another to facilitate additional suicidal risk. Neuroimaging studies suggest that there may be a functional exchange between hyperactivation of prefrontal areas and the hypoactivation of inhibition areas (Aupperle et al. 2012). Hyperactivation promotes biased perception of increased negativity, while hypoactivation leads to the inability to manage incoming information within the context of competing contextual stimuli. For example, studies using several paradigms (e.g., continuous performance tasks, Go/No-go, attention network tasks) consistently find that individuals with PTSD have difficulty with the inhibition of automatic responses (Aupperle et al. 2012). Additional findings suggest that individuals with PTSD also have difficulty disengaging from emotional stimuli, which as previously described effects memory and working memory, but also overall executive function. If unable to disengage from emotional stimuli, behavioral responses (including those aimed at regulatory function) could likely be characterized by more emotional valence (Etkin and Wager 2007). Furthermore, inability to disengage or inhibit responses to a stimulus that is emotionally taxing promotes avoidance behavior, which further reinforces the pattern of maladaptive coping. Heightened emotional coping and/or avoidance are key factors that maintain PTSD symptoms. These same behaviors, however, could also serve as catalysts to more severe forms of inadequate coping, such as suicidal behaviors.

Focal injuries to the frontal and temporal lobes are common after a TBI (Bigler 2001). As a result, those with moderate to severe injury often present with dysexecutive, behavioral, affective, and cognitive problems (Bigler 2001; Zappala et al. 2012; Stuss 2011). In turn, those with a history of TBI can have a dramatic change in personality, impulse control problems, lack of social awareness, disinhibition, and attention modulation deficits. Each of these areas of deficit is likely to interact with one another to facilitate increased risk for suicidal behavior. Moreover, they correspond with aspects of the Jollant et al. (2011) model.

While value attribution as defined by Jollant et al. (2011) has not been directly studied in TBI, many related topics have been, such as the executive dysfunction seen in rumination. This has a strong relationship with hopelessness, depression, and impaired problem-solving ability as well as with SI and suicidal behavior (Morrison and O’Connor 2008). Increased rumination may impact the ability to accurately assign value to external and internal events. Rumination has been localized to the anterior and posterior medial PFC, areas known to be frequently damaged in TBI (Bigler 2001). Disruption of these areas by TBI may lead to problems in regulating the amount of rumination occurring in those with SI.

Impaired regulation of emotional and cognitive responses is one of the hallmarks of TBI, including emotional instability or lability, depression, and dysphoria. Problems with emotional regulation have an impact on cognitive flexibility and the ability to problem solve, both executive functions that have been implicated in suicide risk by other authors (Homaifar et al. 2012b). One such executive function, emotional regulation, is thought to predominately occur in the ACC (Bush et al. 2000), an area frequently damaged in TBI due to its location. Coding of negative moral feelings including guilt, embarrassment, and shame also take place in the medial prefrontal cortex (Takahashi et al. 2004). Without the ability to regulate emotional and cognitive responses after a TBI, individuals are left more vulnerable to suicidal thoughts and behaviors.

In addition to having problems with regulating emotion, working memory is also affected in TBI. These working memory difficulties and need for more brain area to accomplish tasks may also place larger demands on emotional and cognitive regulation leading to greater prolonged negative emotional states. fMRI has shown blood flow abnormalities in the frontal lobes in those with moderate and severe TBI when compared to normal subjects, suggesting greater quantity of brain areas are required for completing the same working memory task (Christodoulou et al. 2001). This need for increased activation when completing tasks has been seen in mTBI as well (Jantzen et al. 2004). This working memory difficulty may contribute to the increased problems with rumination previously discussed. With both increased rumination and difficulty regulating emotional and cognitive responses, having poor working memory likely contributes to worsening of these problems, possibly increasing the magnitude of each and contributing to the increased risk for suicidal thoughts and behaviors in TBI.

In addition to the more medial problems discussed above in the frontal lobe as a result of TBI, dysexecutive syndromes can also occur with damage more laterally to the frontal lobe, specifically to the dorsolateral and ventrolateral PFC. Organization, planning, reasoning, set-shifting, and monitoring can all be affected in this syndrome. Impulsivity and decision-making problems have been found in those with TBI on the Immediate and Delayed Memory Task (Dougherty et al. 2004) and the Iowa Gambling Test (Bechara et al. 1994), respectively. One study investigating executive dysfunction found that individuals with SAs had more perseverative errors on the Wisconsin Card Sort Test (Heaton et al. 1993) than individuals without SAs (Homaifar et al. 2012a). This suggests that the executive dysfunction in TBI may play a role in being unable to cease perseveration over suicidal thoughts and may impede attending to goal-directed behavior. This ‘cognitive rigidity’ has been seen in suicide attempters with reduced problem-solving ability and likely contributes to the increased suicide risk in TBI. Unfortunately, many of these studies are small and do not adequately take into account comorbidities known to occur in TBI, such as depression, pointing to the need for further research in this area.

Besides problems with emotional regulation, TBI is also characterized by disinhibition and impulsivity. For example, behavioral syndromes are characterized by aggressive or abusive behavior, selfishness, lability, impulsivity, environmental dependency, and a lack of empathy and can be best understood as a problem with impulse control and an inability to integrate feedback into one’s behavior in a meaningful way. This syndrome results from damage to the orbitofrontal region, which mediates comportment and social intelligence. Certainly, disinhibition and impulsiveness contribute to Jollant et al. (2011) characterization of facilitation of acts in an emotional context as the final step in the model. This disinhibition can result in violence toward self or others. Studies have supported claims of increased aggression toward others in those with a history of TBI compared to those with other injuries (Tateno et al. 2003). In addition, other observational studies showed that those with frontal injury had higher rates of aggression compared to those with injury in other locations (Tateno et al. 2003). Other studies have shown that those with a history of TBI have a diminished capacity for empathy (Wood and Williams 2008). Many other factors play into future violence after TBI, such as premorbid conditions, but as stated by Wortzel et al. (2013), injury to the orbitofrontal cortex may lower the individual’s ability to inhibit such behaviors. SDV, such as suicide, may follow the same pattern of a lowered ability to inhibit behavior due to alterations in impulse control, increased aggression, and increased disinhibition. This area of the brain is also activated by social exclusion as well as other situations involving self-blame and social rejection, emphasizing a possible interplay with the previously described deficits in value attribution and emotional regulation (Eisenberger et al. 2003). This diminished ability to inhibit SDV may enable a suicidal act in an individual who may already have a tendency toward increased perseveration about the external environment or other triggers.