New Hope for PTSD? Brain Study Uncovers Why Traumatic Memories Hit Harder

NEW YORK — A recent study reveals that traumatic memories appear in the brain in an entirely different way than sad memories. These findings may finally provide a biological explanation for why recalling traumatic memories often manifest as intrusions that differ greatly from “regular” negative memories among PTSD patients.

Study authors from the Icahn School of Medicine at Mount Sinai and Yale University explain that this project was the first ever to examine people’s real-life personal memories as opposed to focusing on basic cognitive mechanisms in an effort to link personal experience to brain function.

“For people with PTSD, recalling traumatic memories often displays as intrusions that differ profoundly from processing of ‘regular’ negative memories, yet until now, the neurobiological reasons for this qualitative difference have been poorly understood,” says Daniela Schiller, PhD, Professor of Psychiatry, and Neuroscience, at Icahn Mount Sinai and senior author of the paper, in a media release.

“Our data show that the brain does not treat traumatic memories as regular memories, or perhaps even as memories at all. We observed that brain regions known to be involved in memory are not activated when recalling a traumatic experience. This finding provides a neural target and focuses the goals of returning traumatic memories into a brain state akin to regular memory processing.”

Prior studies have established that the brain region called the hippocampus governs the formation and retrieval of episodic memories. PTSD, meanwhile, is associated with structural abnormalities (predominantly a reduction of volume) within the hippocampus. Impairments to hippocampal processes are also considered focal to PTSD pathophysiology.

Additionally, the posterior cingulate cortex (PCC) has been shown to be heavily involved in both narrative comprehension and autobiographical processing – and in particular – emotional memory imagery. Changes in PCC function and connectivity have been deemed focal to PTSD.

To figure out if and how the hippocampus and posterior cingulate cortex differentiate traumatic memories from sad ones, a group of 28 patients diagnosed with PTSD underwent reactivation of autobiographical memory using script-driven imagery while also undergoing functional magnetic resonance imaging (fMRI).

In order to generate stimuli based on the participants’ individual memories, researchers made use of an imagery development procedure. Each person had to elaborate on three types of autobiographical memories:

• The “PTSD” condition: the traumatic memory associated with their PTSD (combat, sexual assault, domestic violence)
• The “sad” condition: a sad, meaningful, but non-traumatizing event (death of a family member or pet)
• The “calm” condition: a positive, calm event (memorable outdoor activities).

All of those very personal depictions of autobiographical memory were then systematically arranged into an audio clip roughly 120 seconds long that was narrated by a member of the research staff. Importantly, the PTSD and sad narratives were scripted to maximize their structural similarity to one another in order to control for content and arousal. Participants then listened to this novel version of their own memories for the first time while undergoing functional magnetic resonance imaging.

Initially, the research team hypothesized that across PTSD participants, semantic similarity would correspond to neural similarity. In other words, if the personal memories of two participants were semantically close, researchers expected their patterns of neural responses while listening to audio recordings of these memories to be similar as well.

If traumatic and sad memories really are just different cases of autobiographical memories, study authors expected to see semantic-to-neural correspondence across pairs of traumatic memories and pairs of sad memories alike. However, if traumatic autobiographical memories are different from sad autobiographical memories, researchers would observe the semantic-to-neural relationship only for sad, but not traumatic, memories.

Ultimately, researchers were intrigued to find that patterns in the hippocampus indeed showed a differentiation in semantic representation by narrative type. Within the hippocampus, sad scripts that were semantically similar across participants elicited similar neural representations on fMRI. Conversely, thematically similar traumatic autobiographical memories did not elicit similar representations.

Crucially, study authors also noted a positive relationship between semantic content and neural patterns of the traumatic narratives in the PCC, a brain area only recently conceptualized as a cognitive bridge between world events and representation of the self.

In summation, this project identified a neural basis for the different subjective experience tied to recalling a traumatic memory in comparison to a regular memory. The data indicates treatment targets aimed at “returning” the traumatic memory representation into a typical hippocampal representation may be an effective route.

The study is published in Nature Neuroscience.

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