During World War I, doctors diagnosed soldiers suffering from headaches, fatigue, memory loss, and anxiety with “shell shock” – thought to result from exposure to artillery explosions that jostled the brain. Here, a shell-shocked American soldier (left) receives assistance at a first aid station in Courboin, France. Reeve Photograph Collection, National Museum of Health and Medicine, Otis Historical Archives, CC BY 2.0

Our understanding of the emotional toll of war is likely as old as war itself. What we now know as PTSD has gone by many names over the last four centuries, but its recognition as an official diagnosis in 1980 changed how we think of trauma.

What’s in a Name?

In William Shakespeare’s Henry IV, Part 1, Hotspur returns from battle a changed man. His wife, Lady Percy, inquires in a well-known soliloquy: “In thy faint slumbers I by thee have watched, / And heard thee murmur tales of iron wars.” Shakespeare described a constellation of symptoms that would go by many names over the next 400 years — soldier’s heart, shell shock, battle fatigue. Its formalization into a psychiatric diagnosis — post-traumatic stress disorder — in 1980 was a watershed moment for our understanding of trauma, affirming that traumatic experiences could have enduring consequences for brain function and mental health.

Between 1968 and 1980, American psychiatrists didn’t have an official diagnosis for trauma-related disorders. Soldiers returning from the Vietnam War advocated for a diagnosis that recognized the debilitating and enduring effects of combat on mental health. Here, American soldiers assist an injured comrade in Vietnam. Hansen Slides, National Museum of Health and Medicine, Otis Historical Archives

“The challenge … for military medicine was how to explain how a soldier could be totally incapacitated when there was no blood, no broken bones, no fever, no obvious sign of any physical problem,” says Matthew Friedman, former executive director of the National Center for PTSD.

Recognizing the need for a common language to diagnose and treat mental disorders, the American Psychiatric Association published the Diagnostic and Statistical Manual of Mental Disorders in 1952. It included a diagnosis called gross stress reaction, an overwhelming fear response brought on by the extreme emotional or physical stress of combat or a natural disaster.

For reasons that aren’t clear, the term was omitted from the second edition of the DSM in 1968.

This proved consequential as soldiers returning from Vietnam organized and clamored for a diagnosis recognizing the psychological impact of war. At the same time, clinicians realized stressful experiences like natural disasters and domestic abuse could similarly affect mental health. The DSM-III, published in 1980, introduced a term encapsulating all these experiences: post-traumatic stress disorder.

Unraveling the Neurobiology

The introduction of the PTSD diagnosis in 1980 was controversial. The impetus came not from scientists and clinicians but from activists, many of them Vietnam veterans. Here, protestors demonstrate for full Veterans Administration benefits for veterans on July 5, 1974. Jerry Engel/New York Post Archives/NYP Holdings, Inc./Getty Images

The PTSD diagnosis fundamentally changed our understanding of trauma. It recognized “that a psychological event can produce profound if not enduring alterations in brain function, behavior, emotional regulation, and cognition,” Friedman says. According to the DSM-III, anything “outside the range of usual human experience” — such as combat, rape, assault, torture, natural disasters, and accidents — qualified as a traumatic experience. The definition also recognized that symptoms could be chronic and that preexisting mental health problems increased someone’s odds of developing PTSD — a departure from earlier criteria for gross stress reaction that specified symptoms were short-lived and occurred only in previously normal individuals.

The term was also controversial. Whereas other diagnoses were based on clinicians’ observations and reports, “a major impetus for PTSD came from activists,” Friedman says. Findings from brain imaging technologies in the 1990s revealed the underlying neurobiology of PTSD and dispelled any doubts about the legitimacy of the diagnosis.

Brain imaging studies have revealed the underlying neurobiology of PTSD. Compared to healthy individuals, people with PTSD typically display heightened activity (yellow) in emotion-processing regions of the brain, including the amygdala (AMY), and less activity (blue) in the medial prefrontal cortex (vmPFC), which normally tempers emotional responses. Adapted from Hayes et al., 2012. CC BY 2.0

Intrusive recollections of a traumatic event — like flashbacks and nightmares — are a hallmark of PTSD. Some people are unable to recall details of the event, and they may have problems with memory and concentration in their daily lives. Several studies attribute this to shrinkage of the hippocampus, the region of the brain that directs the creation and storage of memories.

Fear is a learned response involving the amygdala, the brain’s emotional center that evaluates potential threats. In people with PTSD, this region is hyperreactive to reminders of the traumatic event and emotional stimuli like pictures of frightened faces. The degree of hyperactivity correlates with anxiety and symptom severity. The medial prefrontal cortex, a region in the front of the brain that acts like a braking system, normally tempers excessive activity in the amygdala. It helps us unlearn, or extinguish, fears when new information indicates we’re not in danger. But PTSD cuts the brakes: the medial prefrontal cortex is smaller, less active, and less able to restrain the amygdala’s fear response.

More Than Fear

For most people with PTSD, reminders of the trauma put their bodies on high alert. Their hearts race, and they feel anxious and afraid. A significant minority of patients don’t experience this. Instead, they experience dissociative states, where they feel detached from their emotions and perceive their surroundings are unreal. And, their brain activity is the inverse of the pattern typically seen in PTSD: they have an overactive prefrontal cortex and an underactive amygdala.

This suggested to neuroscientists that there were two distinct subtypes of PTSD — the classical presentation marked by flashbacks and intense fear, and the dissociative subtype where patients experience distortions in consciousness and perception. The DSM-5, published in 2013, makes this distinct by adding a dissociative subtype of PTSD.

PTSD is more than a maladaptive fear response. In a meta-analysis of imaging studies, researchers found that only people with PTSD — and not those with anxiety disorders — have decreased activity in the medial prefrontal cortex, a region of the brain that restrains emotional responses. The results suggest PTSD is distinct from fear and anxiety disorders. Dr. Amit Etkin

The DSM-5 also moved PTSD from the anxiety disorders to the newly created category of trauma and stressor related disorder. “I think we’ve really moved beyond fear and embraced the complexity of emotional response to trauma,” says Ruth Lanius, a psychiatrist and neuroscientist who studies PTSD. Her research in the early 2000s revealed the neural signature of dissociative PTSD and paved the way for its recognition as a distinct subtype.

Identifying and understanding all the subtypes of PTSD will help scientists and doctors tailor treatment to individuals.

Some scientists criticized the PTSD criteria in the DSM-5 for being overly complex — it includes 20 symptoms spread out across four symptom clusters. But, Friedman, who led the working group that revised the PTSD criteria for the DSM-5, believes “the reason we have all these symptoms is because we’re trying to cover a spectrum disorder with one diagnosis.”

When the first edition of the DSM was published in 1952, it included two subtypes of depression. The current edition of the DSM recognizes eight different kinds of depression. “I think PTSD is no different,” Friedman says. “We’re just starting a little later.”

This content was created with support from the Stanley Center for Psychiatric Research at Broad Institute.

About the Author Alexis Wnuk Alexis is the science writer and editor for BrainFacts.org. She graduated from the University of Pittsburgh in 2012 with degrees in neuroscience and English.

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