The present study combined neuropsychological and electrophysiological measures to obtain a comprehensive profile of the everyday attentional and memory dysfunction reported in PTSD. The event-related potential (ERP) literature has consistently found abnormalities in late components (N2, P3) reflecting working memory (WM) function. However, the neuropsychological profile reported in the literature has considerable variation. The present study examined ERP activity in 33 PTSD participants and matched controls during a standard two-tone auditory oddball task. Neuropsychological assessment was carried out using a task battery assessing a wide range of cognitive functions. Consistent with previous work, the PTSD group showed delayed N2 latency and reduced P3 target amplitude, together with slower and less accurate target detection. Scalp topography provided evidence of widespread abnormality during WM function, but with strongest effects broadly over the left hemisphere. Neuropsychological testing found concomitant difficulties on factorial measures of verbal memory retention/access and sustained attention but enhanced performance on measures of immediate recall. This integrative pattern of effects reflects a specific impairment in the operation of working memory systems that guide ongoing, planned behavior and that facilitate the acquisition and retention of new memories.
Posttraumatic Stress Disorder (PTSD) is characterized by symptoms of hyperarousal, avoidance and intrusive trauma-related memories and deficits in everyday memory and attention. Separate studies in PTSD have found abnormalities in electroencephalogram EEG, in event-related potential (ERP) and behavioral measures of working memory and attention. The present study seeks to determine whether these abnormalities are related and the extent to which they share this relationship with clinical symptoms. EEG data were collected during an eyes-open paradigm and a one-back working memory task. Behavioral and clinical data (CAPS) were also collected. The PTSD group showed signs of altered cortical arousal as indexed by reduced alpha power and an increased theta/alpha ratio, and clinical and physiological measures of arousal were found to be related. The normal relationship between theta power and ERP indices of working memory was not affected in PTSD, with both sets of measures reduced in the disordered group. Medication appeared to underpin a number of abnormal parameters, including P3 amplitude to targets and the accuracy, though not speed, of target detection. The present study helps to overcome a limitation of earlier studies that assess such parameters independently in different groups of patients that vary in factors such as comorbidity, medication status, gender and symptom profile. The present study begins to shed light on the relationship between these measures and suggests that abnormalities in brain working memory may be linked to underlying abnormalities in brain stability.
Studies have demonstrated ERP abnormalities related to concentration difficulties in post-traumatic stress disorder (PTSD). We used an identical-twin, case-control design to investigate whether these abnormalities reflect pre-trauma vulnerability or the acquired consequence of PTSD. Vietnam combat veterans and their non-combat-exposed, identical twins completed a three-tone oddball task. Veterans with PTSD had delayed target N2 latencies compared to veterans without PTSD. In a small non-medicated, non-smoking subsample, veterans with PTSD also had significantly diminished target P3b amplitudes. A mixed-model, random-effects analysis on the non-medicated, non-smoking subsample that included the combat-unexposed co-twins showed a significant Diagnosis × combat Exposure interaction for target P3b amplitude. Results replicate increased N2 latency and diminished P3b amplitude in PTSD and suggest that diminished P3b amplitude is an acquired condition in PTSD.
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