PTSD (Post-Traumatic Stress Disorder) is both neurological and psychological – it is a psychiatric condition with clear, measurable changes in brain structure and function. The most accurate way to describe it is as a neuropsychiatric disorder, meaning it involves the interplay between psychological experience and lasting biological (neurological) changes in the brain.

Psychologically, PTSD is classified in the DSM-5-TR and ICD-11 as a trauma- and stressor-related disorder. It develops after exposure to actual or threatened death, serious injury, or sexual violence, and is characterized by symptoms in four clusters: intrusion (flashbacks, nightmares), avoidance, negative alterations in cognition and mood, and hyperarousal (hypervigilance, exaggerated startle).

Neurologically, decades of neuroimaging research (MRI, fMRI, PET scans) have shown consistent abnormalities in people with PTSD:

• Hyperactive amygdala (fear center) → exaggerated fear responses
• Hypoactive prefrontal cortex (especially ventromedial PFC) → reduced ability to regulate fear and suppress intrusive memories
• Smaller hippocampal volume → difficulties with context-dependent memory and distinguishing safe from dangerous situations
• Dysregulated HPA (hypothalamic-pituitary-adrenal) axis → abnormal cortisol levels and stress response
• Altered connectivity in the default mode network, salience network, and fear circuitry

These brain changes are not just correlates; longitudinal studies show that some (e.g., smaller hippocampus) can predate trauma and increase risk, while others (e.g., reduced PFC activation) develop after trauma and can partially reverse with successful treatment (CBT, EMDR, SSRIs).

In short: PTSD begins with a psychological trauma, but the brain adapts in a maladaptive, biological way that becomes “wired” for danger long after the threat is gone. This is why evidence-based treatments target both mind (psychotherapy) and brain (medication, neuromodulation techniques such as TMS).