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PTSD is a psychiatric disorder that develops in some individuals following exposure to a severely traumatic event. It is characterised by four symptom clusters: intrusive re-experiencing of the trauma, persistent avoidance of trauma-related cues, negative alterations in cognition and mood, and marked hyperarousal. Symptoms must persist beyond one month and cause significant functional impairment.
ICD-11 defines PTSD using a narrower six-symptom model, producing lower prevalence estimates than DSM-5's 20-item criteria set, which permits diagnosis from over half a million possible symptom combinations.
How it works
At the circuit level, PTSD reflects a failure of the brain's threat-appraisal system to return to baseline after danger has passed. The amygdala, which encodes fear memories, becomes hyperreactive, generating exaggerated responses to stimuli that resemble the original trauma. Simultaneously, the medial prefrontal cortex, ordinarily responsible for top-down suppression of amygdala output, fails to provide adequate inhibitory control 25. Hippocampal volume is reduced in PTSD, impairing the contextualisation of traumatic memories and preventing accurate attribution of threat signals to the past rather than the present 25. The net effect is that the traumatic event continues to be processed as an ongoing threat.
A further layer of dysregulation occurs in the hypothalamic-pituitary-adrenal (HPA) axis. Counter to the common assumption that stress chronically elevates cortisol, PTSD is typically characterised by lower basal cortisol alongside heightened glucocorticoid receptor sensitivity, producing exaggerated negative feedback suppression. This profile distinguishes PTSD biochemically from major depression 3. Fear extinction, the process by which conditioned fear responses are inhibited through repeated exposure to feared stimuli without reinforcement, is also impaired: safety signals fail to suppress re-experiencing, and the threat circuitry remains chronically activated 35.
Example
A first responder who attended a mass-casualty incident finds, months later, that radio static triggers a racing pulse and unbidden recall of the scene. Crowds feel hostile; sleep is fractured by nightmares. They withdraw from colleagues and struggle to concentrate on routine duties, not from weakness but because their threat-detection circuitry cannot distinguish the memory from a present danger.
PTSD is not a failure to recover; it is a misfiring of a protective system that no longer recognises the danger has passed.
Why it matters
PTSD carries a burden that extends well beyond the individual. Lifetime prevalence reaches 7.8% in the general population, with women affected at approximately twice the rate of men 1. The disorder rarely presents alone: comorbid major depression, substance use disorder, chronic pain, and cardiovascular disease are common, collectively multiplying healthcare costs and reducing occupational functioning 3. Mean duration of untreated PTSD exceeds a decade in those who do not recover spontaneously 3.
Evidence-based treatments are available, though they do not work for everyone. Trauma-focused cognitive-behavioural therapy and Eye Movement Desensitisation and Reprocessing (EMDR) both produce clinically meaningful symptom reductions by facilitating fear extinction and updating the emotional valence of traumatic memories 35. Roughly one third of sufferers do not achieve adequate recovery with these approaches, and identifying neural predictors of treatment response remains an active research priority 3.
How is PTSD different from a normal stress reaction after trauma?+
Normal acute stress responses typically resolve within days to weeks as threat circuits recalibrate. PTSD is diagnosed when four distinct symptom clusters persist beyond one month and cause significant impairment. The disorder reflects a failure of fear extinction, not simply a prolonged but proportionate response to overwhelming stress.
What happens in the brain during PTSD?+
The amygdala becomes hyperreactive, generating exaggerated fear responses, while the medial prefrontal cortex loses its ability to suppress them. Hippocampal volume is also reduced, preventing the brain from attributing threat signals to the past rather than the present. The result is a threat-detection system that cannot tell memory from current danger.
What are the most effective treatments for PTSD?+
Trauma-focused cognitive-behavioural therapy and Eye Movement Desensitisation and Reprocessing (EMDR) have the strongest evidence bases, both working by facilitating fear extinction and reprocessing the emotional content of traumatic memories. Roughly one third of patients do not achieve full recovery with current treatments, and refinement of these approaches remains an active research priority.
What is Complex PTSD and how does it differ from PTSD?+
Complex PTSD, recognised in ICD-11 but not DSM-5, includes the core PTSD symptom clusters plus disturbances in self-organisation: difficulties with emotional regulation, negative self-concept, and impaired relationships. It typically follows prolonged or repeated trauma exposure rather than a single discrete event, and the additional symptom domains require distinct therapeutic attention.
