**3.3.6 Stroke details**

Few studies have reported details of the type (e.g., ischemic vs. haemorrhagic), hemisphere (left vs. right), site (e.g., frontal, temporal, etc.) or severity of the stroke. Sampson et al. (2003) reported details of the hemisphere of stroke, Sagen et al. (2009, 2010) reported whether the stroke was a cerebral infarction or a cerebral haemorrhage, whereas Bruggiman et al. (2006) and Wang et al. (2011) provided detailed information regarding the location of the stroke and neurological deficit. Moreover, these aspects of the stroke have rarely been related to PTSD symptom severity. One exception is Bruggiman et al. (2006) who reported that lesion site and neurological deficit were unrelated to PTSD symptomatology, although it should be noted that the sample included only non-severe strokes.

Psychobiological models of PTSD (Charney et al., 1993) and neuroimaging evidence (Lanius et al., 2006) suggest that the development of PTSD is related to impaired functioning of the medial prefrontal cortex which limits regulation of the amygdala. Neural networks involving these areas have been implicated in fear processing. As a result, damage to such networks may be uniquely related to anxiety disorders (Rauch, 2003). Bryant et al. (2010) reported that traumatic injury survivors who also sustained a mild traumatic brain injury (which tends to be associated with damage to frontal regions of the brain) were more likely to develop anxiety disorders, including PTSD, but not depressive disorders. Other research on stroke has noted that left hemispheric, subcortical and large lesions are associated with verbal memory deficits (Godefroy et al., 2009; Schoten et al., 2009) which, more generally, have been related to PTSD (Brewin et al., 2007; Johnsen & Asbjørnsen, 2008). Such deficits may lead to poorer processing of trauma memories thereby contributing to the development of PTSD.

Many stroke survivors are asleep or unconscious during their stroke. Whether or not PTSD symptoms can develop under such circumstances has been the subject of much debate (e.g., Harvey et al., 2003; Klein et al., 2003). For example, it has been argued that individuals who are amnesic of the trauma event, by definition, cannot meet Criterion A2 of DSM-IV for PTSD (i.e., experience feelings of intense fear, helplessness or horror in response to the trauma event) (O'Donnell et al., 2003). Studies have produced conflicting results on this issue (e.g., Bryant et al., 2009; Caspi et al., 2005; Creamer, O'Donnell, & Pattison, 2005). For example, Bryant et al. (2009) found that longer periods of post-traumatic amnesia were related to less severe intrusive memories one week post-injury, suggesting a protective effect. Thus, individuals who experience post-traumatic amnesia may have fewer or incomplete mental representations of the trauma which are less likely to be triggered by matching cues. However, post-traumatic amnesia was unrelated to the severity of PTSD symptoms at three months, suggesting that it does not protect against the development of PTSD over longer time periods. In relation to stroke, Field et al. (2008) reported that PTSD symptom severity at three months was unrelated to whether the survivor was conscious or not at the time of their stroke. There are a number of ways in which PTSD could develop following post-traumatic amnesia or impaired consciousness. First, it is possible that impaired consciousness does not last throughout the traumatic event, and that PTSD symptoms may develop in relation to those aspects of the trauma experience that individuals are able to encode (Creamer et al., 2005). Second, individuals may retrospectively reconstruct memories of the trauma experience, for example from witnesses' reports, which subsequently develop into intrusive memories or flashbacks (Bryant et al., 2009). Third, processing of the trauma experience may occur at an implicit level during periods of impaired consciousness (Bryant, 2001).

### **3.3.7 Chronic stressors**

258 Post Traumatic Stress Disorders in a Global Context

memory bias (Williams et al., 2007). Thus, intentional memory searches may be stopped prematurely at an abstract level in order to avoid retrieving potentially distressing material related to the trauma. To date, no studies have examined the relationship between

Few studies have reported details of the type (e.g., ischemic vs. haemorrhagic), hemisphere (left vs. right), site (e.g., frontal, temporal, etc.) or severity of the stroke. Sampson et al. (2003) reported details of the hemisphere of stroke, Sagen et al. (2009, 2010) reported whether the stroke was a cerebral infarction or a cerebral haemorrhage, whereas Bruggiman et al. (2006) and Wang et al. (2011) provided detailed information regarding the location of the stroke and neurological deficit. Moreover, these aspects of the stroke have rarely been related to PTSD symptom severity. One exception is Bruggiman et al. (2006) who reported that lesion site and neurological deficit were unrelated to PTSD symptomatology, although

Psychobiological models of PTSD (Charney et al., 1993) and neuroimaging evidence (Lanius et al., 2006) suggest that the development of PTSD is related to impaired functioning of the medial prefrontal cortex which limits regulation of the amygdala. Neural networks involving these areas have been implicated in fear processing. As a result, damage to such networks may be uniquely related to anxiety disorders (Rauch, 2003). Bryant et al. (2010) reported that traumatic injury survivors who also sustained a mild traumatic brain injury (which tends to be associated with damage to frontal regions of the brain) were more likely to develop anxiety disorders, including PTSD, but not depressive disorders. Other research on stroke has noted that left hemispheric, subcortical and large lesions are associated with verbal memory deficits (Godefroy et al., 2009; Schoten et al., 2009) which, more generally, have been related to PTSD (Brewin et al., 2007; Johnsen & Asbjørnsen, 2008). Such deficits may lead to poorer processing of trauma memories thereby contributing to the development

Many stroke survivors are asleep or unconscious during their stroke. Whether or not PTSD symptoms can develop under such circumstances has been the subject of much debate (e.g., Harvey et al., 2003; Klein et al., 2003). For example, it has been argued that individuals who are amnesic of the trauma event, by definition, cannot meet Criterion A2 of DSM-IV for PTSD (i.e., experience feelings of intense fear, helplessness or horror in response to the trauma event) (O'Donnell et al., 2003). Studies have produced conflicting results on this issue (e.g., Bryant et al., 2009; Caspi et al., 2005; Creamer, O'Donnell, & Pattison, 2005). For example, Bryant et al. (2009) found that longer periods of post-traumatic amnesia were related to less severe intrusive memories one week post-injury, suggesting a protective effect. Thus, individuals who experience post-traumatic amnesia may have fewer or incomplete mental representations of the trauma which are less likely to be triggered by matching cues. However, post-traumatic amnesia was unrelated to the severity of PTSD symptoms at three months, suggesting that it does not protect against the development of PTSD over longer time periods. In relation to stroke, Field et al. (2008) reported that PTSD symptom severity at three months was unrelated to whether the survivor was conscious or not at the time of their stroke. There are a number of ways in which PTSD could develop following post-traumatic amnesia or impaired consciousness. First, it is possible that impaired consciousness does not last throughout the traumatic event, and that PTSD

overgeneral memory bias and PTSD after stroke.

it should be noted that the sample included only non-severe strokes.

**3.3.6 Stroke details** 

of PTSD.

Stroke is a leading cause of severe disability. Survivors typically experience a range of ongoing problems (e.g., weakness or paralysis, cognitive impairment, communication difficulties, problems with balance and coordination). One important question is the extent to which PTSD symptom severity reflects the impact of these ongoing stressors, rather than reactions to the stroke event itself. For example, in relation to MI, Shemesh et al. (2001) found that patients who experienced ongoing physical symptoms (e.g., angina) reported more intrusion and avoidance PTSD symptoms than those who were asymptomatic. In addition, in relation to stroke, Wang et al. (2011) reported that the level of physical disability was related to the severity of PTSD symptoms at three months post-stroke. There are a number of ways in which chronic stressors may contribute to the severity of PTSD symptoms. First, chronic stressors may erode individuals' resources, or their ability, to deal with their psychological reactions to the acute stressor (Adams & Boscarino, 2006). Second, chronic stressors may evoke reminders of the stroke which may, more directly, act as triggering cues for the reexperiencing symptoms of PTSD. Third, the experience of ongoing disability may be perceived by the individual to signify permanent negative change. Fourth, some disabilities experienced after stroke, including cognitive and language impairments, may impede the person's ability to fully process and integrate trauma memories with other autobiographical material. For example, cognitive impairment has been related to difficulties in recalling specific autobiographical memories in the elderly (Phillips & Williams, 1997) and in stroke survivors (Sampson et al., 2003). Fure et al. (2006) reported that cognitive impairment was related to elevated levels of anxiety in stroke patients; however, to date, no studies have examined the relationship between cognitive impairment and PTSD. In addition, Thomas and Lincoln (2008) reported that stroke survivors with aphasia had higher levels of emotional distress at one and six months post-stroke, with more detailed analyses revealing that this was the result of expressive, but not receptive, communication impairments. It is possible that stroke survivors with aphasia may also experience more PTSD symptoms.
