Neural responses to emotional involuntary memories in posttraumatic stress disorder: Differences in timing and activity

Abstract

BackgroundInvoluntary memories are a hallmark symptom of posttraumatic stress disorder (PTSD), but studies of the neural basis of involuntary memory retrieval in posttraumatic stress disorder (PTSD) are sparse. The study of the neural correlates of involuntary memories of stressful events in PTSD focuses on the voluntary retrieval of memories that are sometimes recalled as intrusive involuntary memories, not on involuntary retrieval while being scanned. Involuntary memory retrieval in controls has been shown to elicit activity in the parahippocampal gyrus, precuneus, inferior parietal cortex, and posterior midline regions. However, it is unknown whether involuntary memories are supported by the same mechanisms in PTSD. Because previous work has shown that both behavioral and neural responsivity is slowed in PTSD, we examined the spatiotemporal dynamics of the neural activity underlying negative and neutral involuntary memory retrieval.MethodsTwenty-one individuals with PTSD and 21 non-PTSD, trauma-exposed controls performed an involuntary memory task, while undergoing a functional magnetic resonance imaging scan. Environmental sounds served as cues for well-associated pictures of negative and neutral scenes. We used a finite impulse response model to analyze temporal differences between groups in neural responses.ResultsCompared with controls, participants with PTSD reported more involuntary memories, which were more emotional and more vivid, but which activated a similar network of regions. However, compared to controls, individuals with PTSD showed delayed neural responsivity in this network and increased vmPFC/ACC activity for negative > neutral stimuli.ConclusionsThe similarity between PTSD and controls in neural substrates underlying involuntary memories suggests that, unlike voluntary memories, involuntary memories elicit similar activity in regions critical for memory retrieval. Further, the delayed neural responsivity for involuntary memories in PTSD suggests that factors affecting cognition in PTSD, like increased fatigue, or avoidance behaviors could do so by delaying activity in regions necessary for cognitive processing. Finally, compared to neutral memories, negative involuntary memories elicit hyperactivity in the vmPFC, whereas the vmPFC is typically shown to be hypoactive in PTSD during voluntary memory retrieval. These patterns suggest that considering both the temporal dynamics of cognitive processes as well as involuntary cognitive processes would improve existing neurobiological models of PTSD.

Deficits in Spontaneous Cognition as an Early Marker of Alzheimer’s Disease

“…Several studies on involuntary episodic memories (e.g., [77][78][79]) and intrusive memories [80,81] have provided further evidence on the role of the PCC, together with inferior parietal and MTL areas, in spontaneous stimulus-dependent retrieval processes. In those studies, while PCC was reliably involved in both voluntary and involuntary memory recall, dorsolateral PFC was active only during voluntary recall, suggesting that for voluntary recall to succeed, the additional recruitment of executive areas of PFC may be necessary [77,78].…”

An East Meets West Approach to the Understanding of Emotion Dysregulation in Depression: From Perspective to Scientific Evidence

“…A growing number of studies support this ancient theory, showing that, compared with healthy people, patients with depression associated with deficiency of the heart and spleen have lower brain activity in the left frontal cortex region (Feng et al., 2005; Xie, 2007; Wang et al., 2008b). These findings are in line with the findings from Western medicine that major depression is related to decreased activity in the left hemisphere relative to right hemisphere, and to a decline in the activity of the left frontal cortex in people suffering from depression compared to normal people.…”

“…These findings are in line with the findings from Western medicine that major depression is related to decreased activity in the left hemisphere relative to right hemisphere, and to a decline in the activity of the left frontal cortex in people suffering from depression compared to normal people. Clinical studies reported that depression is related to altered resting-state activity in the PFC, and a growing number of findings from functional and structural imaging studies show that depression is associated with volume reduction in the left subgenual PFC region (Drevets et al., 1997; Öngür et al., 1998; Botteron et al., 2002; Wang et al., 2008a; Ye et al., 2012), because the orbitofrontal cortex (OFC) is involved in cognitive processing and decision-making, and the main function of the PFC is to extract the relevant information about a cognitive experience, so as to modulate the emotion and behavior changes (Feng et al., 2005). Moreover, studies have mentioned that the body temperature in depressed people is lower than in normal healthy people (Zhe, 2004; Lin et al., 2011); this may result from autonomic response dysfunction mediated by central adrenergic activation (Hughes et al., 2006; Hamer et al., 2007; Shinba et al., 2008) (Figure 7).…”

Frontal Lobe Circuitry in Posttraumatic Stress Disorder

“… 56 – 67 The altered activity patterns observed in the vmPFC and dmPFC in PTSD during exposure to negative imagery, which include both increases and decreases in activation, suggest that medial prefrontal cortical regions are also functionally impaired. 16 , 40 , 68 – 82 Furthermore, when participants with PTSD engage in cognitive tasks in the presence of negative distractors, cognitive conflict, or attentional demands, abnormalities in functional activation of vmPFC emerge. 78 , 83 – 92 Most notably, the vmPFC is overactive in PTSD during fear conditioning 93 yet under-active during fear conditioned extinction.…”

“… 57 , 60 , 62 , 105 , 108 , 110 Functionally, altered activation of the dACC and insular cortex in PTSD occurs during exposure to negative imagery. 40 , 71 , 75 , 76 , 79 – 82 During executive task performance, participants with PTSD exhibit abnormal activity in the dACC, 85 , 88 , 89 , 94 , 111 as well as in the insula. 90 , 112 In the resting state, increased connectivity of the dACC and the insula with the amygdala has been observed in PTSD, 95 , 96 perhaps indicating an increased relay of emotionally valenced information to frontal nodes of the salience circuit.…”