Memory and executive dysfunctions associated with acute posttraumatic stress disorder

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Abstract

Posttraumatic stress disorder (PTSD) in its chronic form has been associated with a number of neurocognitive impairments involving emotionally neutral stimuli. It remains unknown whether such impairments also characterize acute PTSD. In the present investigation, neurocognitive functions were examined in trauma exposed individuals with (n = 21) and without (n = 16) acute PTSD, as well as in a group of individuals never exposed to trauma (n = 17) using specific and standardized tasks such as the Rey Auditory Verbal Learning Test, the Aggie's Figure Learning Test, the Autobiographical Memory Interview, the D2 test, the Stroop task, the digit and visual span tasks of the Wechsler Memory Scale-III, the Trail Making Test, the Tower of London and the vocabulary subtest of the Wechsler Adult Intelligence Scale-III. A number of deficits in the cognitive domains of memory, high-level attentional resources, executive function and working memory were found in the group with a diagnosis of acute PTSD only and not among the other groups. The findings, which point to the possibility of disturbed fronto-temporal system function in trauma-exposed individuals with acute PTSD, are particularly relevant for the early clinical management of this disorder.

Introduction

Two well-established facts have emerged from the literature on neuropsychological characteristics of individuals with posttraumatic stress disorder (PTSD). Firstly, information-processing biases have been repeatedly observed, the most robust finding being attentional deficits while processing emotional stimuli (e.g. McNally et al., 1990, Paunovic et al., 2002, Vasterling and Brewin, 2005). Secondly, despite the fact that their magnitude and nature tend to vary across studies, cognitive abnormalities have also been found on neuropsychological tests involving neutral stimuli (for a review see Vasterling and Brewin, 2005). Yet, in our view, the literature would be enhanced by bringing new information on an issue of great relevance: it remains unknown whether such impairments are present at the onset of the disorder. Indeed, since most of the data comes from retrospective studies including participants who have been symptomatic for years or even decades, such as war veterans or adults survivors of child abuse, it is not yet possible to conclude whether the neuropsychological profile associated with chronic PTSD also relates to acute PTSD.

Findings related to cognitive abnormalities in individuals with chronic PTSD, as measured on standard neuropsychological tasks, are undeniable. Researchers have rather consistently observed verbal (e.g. Bremner et al., 1995, Yehuda et al., 1995, Jenkins et al., 1998, Gilbertson et al., 2001, Golier and Yehuda, 2002) or visual (Bremner et al., 1993) episodic memory dysfunctions. While others have also found dysfunctions in more complex attentional and executive resources (e.g. Vasterling et al., 1998, Koenen et al., 2001, David et al., 2002, Stein et al., 2002, Vasterling et al., 2002), it seems that basic attentional capacities tend to be preserved in individuals with chronic PTSD (Vasterling and Brewin, 2005). Another type of cognitive dysfunctions often seen in patients with chronic PTSD is the reduced specificity of autobiographical memories (Wessel et al., 2002, Dalgleish et al., 2008).

However, only three studies have focused on cognitive functioning in the early posttraumatic phase. A first study, by Harvey et al. (1998), examined the specificity of autobiographical memories in survivors of motor vehicle accidents within the week following their accident. The results showed that altered accessibility of personal memories in the acute posttraumatic phase was associated with poorer outcome 6 months later. A second investigation, by Brandes et al. (2002), found that survivors with initially high levels of PTSD symptoms had impaired attention and immediate recall of visual information, as well as lower IQ compared to those with low initial symptoms. Finally, a third study obtained neuropsychological measures within days following traumatic exposure and 6 weeks later (Bustamante et al., 2001). Negative correlations were found between baseline delayed recall, as well as retroactive interference, and PTSD at follow-up. Accordingly, the authors concluded that deficits in areas of verbal memory days after trauma exposure may represent a risk factor for PTSD.

Exploring cognitive functioning of recently traumatized individuals is relevant because the factors linked to the persistence of PTSD may differ from those related to the initial development of the disorder, from which many remit. Yet, while those three studies suggest that neuropsychological deficits associated with chronic PTSD may be present in the early stages following traumatic exposure, considering that the patients were assessed within days of trauma exposure, their findings more likely relate to acute stress disorder (ASD) rather than to acute PTSD. Indeed, an important temporal distinction exists between ASD, acute and chronic PTSD. Symptoms of ASD, which must include dissociation, are experienced during or immediately after the traumatic event, last for at least 2 days and resolve within the following 4 weeks. If the disturbance persists for more than one month after the traumatic exposure, the diagnosis should be changed for acute PTSD. Finally, if the duration of symptoms persists for more than 3 months, chronic PTSD is specified. Whereas most of the previous findings related to either chronic PTSD or acute stress disorder, the nature of neuropsychological impairments linked to acute PTSD remains unclear.

The current investigation was thus designed to further our understanding of the neuropsychological concomitants of acute PTSD. To do so, the present investigation assessed neurocognitive functioning in two groups of individuals (one with and one without PTSD) who had been exposed to a single trauma in the previous month as well as in a third group of individuals never exposed to a traumatic event. Importantly, this study design was selected because it allows for the discrimination between the effects of trauma exposure and the effects related to having acute PTSD.

We hypothesized that the trauma-exposed group with acute PTSD would display a similar pattern of neuropsychological disturbances (in cognitive areas such as memory, higher-level attention and executive function) as patients suffering from chronic PTS, that this impairment would not characterize the other two comparison groups and would, therefore, be specific to the trauma-exposed group with PTSD.

Section snippets

Participants

With the help of the treating nurse, 42 individuals presenting to the emergency room as a result of trauma exposure were recruited in an extensive imaging study (not reported here), and 39 of them took part in the neuropsychological investigation (one had no availability and two others suffered a panic attack while undergoing their imaging session and did not want to engage in any further testing). Another group of 17 individuals without a history of trauma exposure was recruited via a

Characteristics of study participants

As shown in Table 1, the three study groups were similar in terms of age, gender, type of traumatic experience and current and past psychiatric comorbidity. Current psychiatric comorbidity included two cases of drug abuse (marijuana), two cases of panic disorder with agoraphobia, two cases of major depression and one case of general anxiety in the PTSD+ group, one case of drug abuse (marijuana) and one case of anorexia in the PTSD− group, and one case of alcohol abuse in the never-exposed

Discussion

This study proposed a detailed examination of cognitive functioning during the early phase of trauma exposure and relied on a design that allowed the disentanglement of the effects related to trauma exposure vs those related to having acute PTSD.

Acknowledgements

While working on this manuscript, G.L. and A.B. held, respectively, a doctoral fellowship and a salary award from the Fonds de la Recherche en Santé du Québec (FRSQ). This work was funded by a grant from the Canadian Institute of Health Research (CIHR) to the senior author. We thank Mrs. Lauriault and the personnel of the Hôpital Charles-LeMoyne for their help in recruiting the study participants. We also thank Mr. Chagnon for his assistance in conducting the statistical analyses.

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