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Why Does PTSD Make Trauma Unforgettable but Hard To Recall?

A soldier sitting on a couch with his head in his hands.
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Researchers from ATR Computational Neuroscience Laboratories and the University of Tokyo have discovered a novel mechanism that explains how fear memories change over time. Their study, published in Nature Communications, offers new insights that could reshape our understanding of post-traumatic stress disorder (PTSD) and point to potential novel interventions.

The contradictory effects of PTSD

PTSD is a mental health condition triggered by experiencing or witnessing a traumatic event. It often affects individuals who have faced life-threatening situations such as military combat, natural disasters or serious accidents, and can lead to intense, disturbing thoughts and feelings long after the event has ended. The condition affects ~3.9% of the population worldwide. Symptoms can include flashbacks, nightmares and severe anxiety. PTSD can be extremely debilitating for sufferers, impacting their daily lives.

 

Researchers remain puzzled by the contradictory nature of fear memories in individuals with PTSD. While those affected often experience frequent, vivid flashbacks of the traumatic event, they may also struggle with recalling key details of the same memories. Studies have found trauma can both strengthen episodic aspects of memories, yet, also weaken them. This paradox complicates the understanding of how trauma is processed and stored in the brain.

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Fear memories require the integration of multiple brain regions

To understand the contradictory effects of PTSD, the team used functional magnetic resonance imaging (fMRI) and machine learning to track brain activity as participants experienced simulated threatening events. The participants watched semi-animated traffic videos from a driver’s perspective, with some trials featuring a truck crashing into the car, while others involved the truck passing by. Different sound sequences were played during the waiting period, some associated with the crash, others not. Participants rated the likelihood of a crash on select trials. They completed three sessions: 

  1. Acquisition Session: This was the initial learning phase. Participants experienced both truck crash trials and non-crash trials. The sound sequences during this session helped condition participants to associate specific sequences with the crash and others with no crash.
  2. Immediate Test Session: Conducted shortly after the Acquisition session on the same day, this session tested what participants had learned. However, no truck crash occurred during these trials, only sound sequences and likelihood ratings.
  3. Long-Term Test Session: This was a follow-up test conducted on the next day. Before the test, participants experienced a "fear reinstatement" where they watched unsignaled crashes to revive their fear. The test itself was similar to the Immediate test, with no crash trials but included sound sequences and likelihood ratings to assess long-term memory of the conditioned fear response.

Immediately after the fear-inducing event, the team found the brain relied on associative memories. Their fear response was broad and generalized and they learned to fear a specific sound or cue that was directly associated with the crash. However, after 24 hours, the participant's responses became more selective; instead of just reacting to one cue, they started recognizing and responding to the sequence of cues leading up to the crash. Their fear memory became more detailed and precise, allowing them to anticipate the crash based on the order of events, not just a single trigger.

 

The fMRI scans highlighted a change in communication between brain regions between sessions. Initially, the hippocampus prioritized the final threat cue, but in the long-term test sessions, the dorsolateral prefrontal cortex took over to encode full cue sequences, influencing the fear circuit. This shift highlights the different roles of the hippocampus and dorsolateral prefrontal cortex in fear memory regulation.

 

Participants with higher trait anxiety failed to show the normal rebalancing between the two brain regions, which might explain persistent fear memories and disorganized episodic recall in PTSD.

A potential intervention window for PTSD

"This time-dependent rebalancing between brain regions may explain why some individuals develop PTSD while others don't," said corresponding author Dr. Ai Koizumi, a researcher from Sony Computer Science Laboratories, Inc.

 

Understanding this time-dependent memory mechanism suggests the potential for a novel time window to target temporal re-organization processes to rescue incoherent episodic memories in PTSD.

 

"Our findings reveal a previously unknown phenomenon in how the brain prioritizes and processes fear memories", said lead author Dr. Aurelio Cortese, a group leader from the Advanced Telecommunications Research Institute (ATR).

 

Reference: Cortese A, Ohata R, Alemany-González M, Kitagawa N, Imamizu H, Koizumi A. Time-dependent neural arbitration between cue associative and episodic fear memories. Nat Comm. 2024;15(1):8706. doi: 10.1038/s41467-024-52733-4


This article is a rework of a press release issued by ATR Brain Information Communication Research Laboratory Group. Material has been edited for length and content.