Are the neural substrates of memory the final common pathway in posttraumatic stress disorder (PTSD)?

Abstract

A model for the posttraumatic stress disorder (PTSD) as a disorder of memory is presented drawing both on psychological and neurobiological data. Evidence on intrusive memories and deficits in declarative memory function in PTSD-patients is reviewed in relation to three brain areas that are involved in memory functioning and the stress response: the hippocampus, amygdala, and the prefrontal cortex. Neurobiological studies have shown that the noradrenergic stress-system is involved in enhanced encoding of emotional memories, sensitization, and fear conditioning, by way of its effects on the amygdala. Chronic stress also affects the hippocampus, a brain area involved in declarative memories, suggesting that hippocampal dysfunction may partly account for the deficits in declarative memory in PTSD-patients. Deficits in the medial prefrontal cortex, a structure that normally inhibits the amygdala, may further enhance the effects of the amygdala, thereby increasing the frequency and intensity of the traumatic memories. Thus, by way of its influence on these brain structures, exposure to severe stress may simultaneously result in strong emotional reactions and in difficulties to recall the emotional event. This model is also relevant for understanding the distinction between declarative and non-declarative memoryfunctions in processing trauma-related information in PTSD. Implications of our model are reviewed.

Extracellular Hippocampal Acetylcholine Level Controls Amygdala Function and Promotes Adaptive Conditioned Emotional Response

“…It must be emphasized that alterations in this hippocampal cholinergic control of the amygdala are sufficient to produce a subjective appraisal of emotionally laden stimuli that does not match their predictive values for aversive events. In particular, the intensification of emotional memory for an arousing simple stimulus and the concomitant weakening of context learning after intrahippocampal scopolamine infusions is reminiscent of the paradoxical coupling of memory intensification (for a simple trauma-related stimulus) and amnesia (for traumatic contextual cues) observed in human posttraumatic stress disorder (Elzinga and Bremner, 2002;Layton and Krikorian, 2002). Hence, such findings might highlight the neural dysfunction involved in pathological memories based on maladaptive processing of relevant emotional information.…”

The Basolateral Amygdala Interacts with the Medial Prefrontal Cortex in Regulating Glucocorticoid Effects on Working Memory Impairment

“…In support of this hypothesis, high doses of norepinephrine infused into the mPFC, known to impair working memory, have been reported to induce enhancement of long-term memory consolidation when administered after a training experience (Liang, 2001). Moreover, acutely administered corticosterone increases the expression of neural cell adhesion molecules in the mPFC, molecules that have been implicated in the stabilization of synaptic contacts and long-term memory consolidation (Sandi and Loscertales, 1999); however, prolonged or uncontrolled activation of this brain state such as that found in patients with hypercortisolemia and several neuropsychiatric disorders may be associated with cognitive impairment (Semple et al, 2000;Elzinga and Bremner, 2002).…”

Trauma-related memories in PTSD after interpersonal violence: an ambulatory assessment study

“…There is also the possibility that repeated assessments may trigger intrusive memories (Pfaltz, Michael, Grossman, Margraf, & Wilhelm, 2010). While frequent assessments had only little impact on pain ratings in patients with chronic pain (Stone et al, 2003), intrusive memories related to PTSD are easily triggered by external cues (Elzinga & Bremner, 2002) and might therefore be influenced by frequent assessment. Furthermore, Chun (2016) hypothesized that the settings in which intrusive memories are assessed may also influence the data.…”