The Dog Who Came Back from the War
Post-Traumatic Stress Disorder
Besides love and sympathy, animals exhibit other qualities connected with the social instincts which in us would be called moral.
One pleasant morning in the summer of 1993, Bill Doust put his dog, Elsa, in the car to get ready for a ride to the local park. A large mixed-breed pooch of around seventy pounds with a semi-long-haired, blackish-brown coat, Elsa’s most marked characteristic was her sad-looking eyes. Bill parked in the shade so that the interior would not overheat, and also rolled the windows partially down to make sure Elsa would stay cool.
A construction supervisor by trade, Bill loved all animals. To Bill, Elsa was not just a dog, but a cherished member of the Doust family. The love flowed both ways. Elsa lived for him. He practically lived for her. This kind of connection of love and loyalty can rank among the deepest emotions of human life.
Several years previously, Bill had rescued one-year-old Elsa from an abusive situation. Since that time, Elsa shadowed Bill whenever he was at home, following him from room to room. She exhibited a touch of separation anxiety whenever he was away, but the Doust household provided a warm, charming environment for all creatures within its embrace. Elsa contributed a large part to making it that way.
With the dog left behind in the car, Bill ducked back inside his house for a quick shave before driving to the park. Elsa liked waiting in the car. She understood that it meant something good was in the offing.
Standing at the bathroom mirror, his face lathered with shaving cream, Bill heard a fracas outside. There were shouts, the pounding of running feet. He went to the window. Some sort of police incident was going down. A man ran past Bill’s house. There was a clamor of “Stop, thief!” A squad car, sirens on high, wailed up to the scene.
Bill watched the action unfold. The suspect dashed down the block. A cop in uniform bolted from the cruiser and headed off in hot pursuit. As the officer sprinted past Bill’s car, Elsa jumped out of the partly open window and ran after him.
Suspect, cop, and dog tore down the block. Bill couldn’t believe his eyes. He himself raced out of his house and joined the chase. Suspect, cop, dog, dog owner.
Elsa closed in on the policeman. Fearing an attack, the cop kicked her away. The normally peaceful dog lunged back and locked her jaws onto the officer’s pant cuff, snarling and worrying her head from side to side.
Bill made it down the street and approached. “Don’t worry,” he shouted. “She’s my dog! I’ll get her!”
But the policeman drew his gun. As Bill screamed, “No! No!” the cop took aim and shot Elsa in the head.
The officer pounded off, continuing the chase, leaving Elsa’s inert, bleeding body on the sidewalk. Bill scooped her into his arms. He had seen the bullet strike her and was convinced his beloved pet was dead.
Even in his panic, Bill had the presence of mind to transport Elsa to a top-of-the-line emergency veterinary clinic. Working quickly, in triage mode, the clinic staff administered multiple blood transfusions, saving her life. Elsa got patched up. The officer’s bullet, from a .38 caliber handgun, had entered her skull just in front of her ear, permanently deafening her on that side. The bullet continued on its way down Elsa’s neck and lodged in the wall of her chest cavity. We still have the X-rays on file here at Tufts. They show a serious injury. Elsa had cheated death by centimeters.
Thanks to excellent and timely critical care, Elsa survived and recovered. But unbeknownst to Bill and the veterinarians involved, the psychological trauma of the shooting had changed her profoundly. Elsa returned home after her brush with death. She became more attached to Bill than ever, a “Velcro dog,” sticking to him like the well-known fastening material. During the day, this did not pose that much of a problem, because Bill took her along with him to work. Elsa would hover around the job site, scrutinizing his every move, until he summoned her with a wave of his hand.
At night Elsa’s separation anxiety became almost impossible to tolerate. Bill could not go to sleep without Elsa pawing at the bed for attention. This was a new behavior, which led to insomnia for both parties. Luckily for Bill, his grown son lived with him. The two of them adopted a tag team approach. Bill would sleep for three hours, his son took a three-hour shift, and together men and beast would somehow make it through the night.
In the aftermath of her injury, Elsa had become hypervigilant, never settling, always on the lookout for trouble. Any element of the shooting incident triggered a terrified reaction. She became a nervous wreck whenever she saw or heard a police car, heard a siren of any kind, saw any flashing lights, or met people in uniform. The police officer happened to have been African American, and Elsa now responded with fear when she encountered black men.
Bill Doust took action and sought help for Elsa, eventually coming to me at Tufts. At the time, I dubbed her condition “PTSD-like.” Certainly it was posttraumatic. Elsa’s nervousness, avoidance of anything reminiscent of the original psychological and physical trauma, plus her nocturnal anxiety—could that stem from bad dreams?—smacked strongly of post-traumatic stress disorder.
I treated Elsa with an antidepressant, supplemented with nighttime Valium and a nonaddicting morphine-type painkiller, butorphanol. With a few ups and downs, Elsa improved. But she would never completely get over that dreadful day. Fears once learned are never forgotten, although it is possible to ease them by superimposing new learning, with or without the help of medication.
Over the ensuing years, I saw many other PTSD-like cases in dogs. In my behavior course, I began to teach PTSD to Tufts veterinary students as a bona fide canine condition. I didn’t realize I was violating the sacred principle of human exceptionalism. I simply saw a situation and attempted to address it with reason, compassion, and education.
Then came Gina.
A two-year-old German shepherd, Gina had spent six months on tour in Iraq, accompanying a unit of the US Army. Her duties there focused on searching buildings for explosives, working with troops who were “cleaning out” insurgents from their hiding places, always performing in chaotic and complex urban environments. Before entering a previously unsearched structure, Gina’s human comrades would often toss flash grenades—nonlethal charges that explode in a flash of light and a high-decibel report. Once while she was riding in a convoy, an IED, an “improvised explosive device” or roadside bomb, exploded nearby.
When Gina returned from her tour, she was fearful, disturbed, and psychologically fragile. The handler to whom she was assigned back in the States, Master Sergeant Eric Haynes, the kennel master at Peterson Air Force Base in Colorado Springs, gave an interview in which he described her condition as post-traumatic stress disorder. An army veterinarian later concurred.
The press went wild. How could a dog get PTSD? Surely PTSD was a psychiatric diagnosis reserved strictly for humans?
Here is testimony from an expert interviewed by the media at that time:
A psychologist on the faculty at Columbia University’s Mailman School of Public Health, said PTSD is a diagnosis developed for humans, not dogs. “That’s not to say that animals can’t be traumatized. It sounds like this dog was traumatized from the experience of extreme stress and fear,” he said. “That causes an alteration in the animal’s nervous system similar to an alteration of the nervous system in humans.”
The Columbia guy got it right about changes in the nervous system in response to trauma, but he could not make the logical leap and call the condition by its proper name.
The press, when it covers a breaking story such as this one, becomes something like a bloodhound. Rabid for additional sources, reporters sought out anyone who would comment on the outlandish idea that a dog could suffer from a condition heretofore reserved for humans. They turned up my name, and I agreed to an interview.
Yes, I had seen it before, I told the journalist who called. Yes, PTSD can and does occur in dogs. Yes, indeed, I teach about canine PTSD in my course to veterinary students. I would consider myself remiss if I didn’t.
While I did not examine Gina firsthand, I speculated that her experiences in Iraq were the type that could lead to post-traumatic stress. Before going to war she was a happy, playful, confident dog who loved her work. Training sessions all seemed to her like great fun. Then she was deployed to Iraq and she faced extreme, violent, and unsettling real-life situations. This was a whole different ball game. Her training could not have prepared her for it. With Gina at their side, the soldiers she was with did what they had to do, kicking down doors and throwing grenades to shock and confuse the enemy.
Check out this description of such an explosive device:
Upon detonation, stun grenades emit an intensely loud “bang” of 170–180 decibels and a blinding flash, sufficient to cause immediate flash blindness, deafness, tinnitus, and inner ear disturbance.
Troops wear goggles and ear protection to shield them from the extreme visual and auditory assault meted out by the grenades. War dogs are not similarly well-insulated from such severe sensory overload. Even beyond the sound of explosions, a war environment is one of constant sensory assault. Yelling, door-kicking, and chopper noise form a brutal soundtrack to the missions, and exhaust fumes and other unfamiliar smells abound.
No wonder Gina became unnerved. Anxiety overwhelmed her. She became terrified of people. After returning from Iraq, she could no longer perform her duties during training sessions. She balked at entering homes when directed, stiffening her legs and pulling back at the threshold. When forced to go inside, she would slink and cower, often immediately taking shelter under the nearest piece of furniture.
In the wake of trauma, Gina also became hypervigilant, always on the lookout for trouble. Her handlers said she suffered the “full range” of PTSD symptoms, which would also include sleep disturbances like Elsa. Gina had developed what Sigmund Freud labeled “war neurosis,” which later became known as “shell shock.”
Like Elsa, Gina recovered after spending some months of treatment in a safe environment. She went back into training and managed to handle it without balking. The US Army is a stern taskmaster in the normal course of events, and often sends soldiers suffering from PTSD back into war zones. The army had great hopes for Gina going back into service, but I doubted that she would ever be satisfactorily rehabilitated. The memories of what went on before would forever haunt her. Gina’s condition might not count as a reason for honorable discharge, but I think that it should.
Let’s consider the human condition of PTSD. According to the DSM,I PTSD occurs after a person has been exposed to a traumatic event, such as witnessing or experiencing events that threaten death or serious injury to self or others. To be classified as PTSD, the response of the victim must involve intense fear, helplessness, or horror, which sounds similar to what Elsa and Gina went through. People with PTSD also have dreams and flashbacks, which we cannot verify in a nonverbal species, but recurrent dreams of the event may explain nocturnal agitation in dogs. Clearly apparent for both Elsa and Gina were symptoms straight out of the DSM, including “intense psychological and physiological distress on exposure to external cues that symbolize or resemble the traumatic event.” They also avoided stimuli associated with the trauma, another basis for the diagnosis of PTSD in people, as well as difficulty falling or staying asleep, difficulty concentrating, and hypervigilance. Finally, they seemed detached and disinterested in life after their trauma.
To qualify for a PTSD diagnosis, the duration of the disturbance must be greater than one month. During this period, the condition must cause clinically significant (that is, measurable) distress or impairment in interactions with others. Gina and Elsa both qualified in duration and degree of distress. On almost all counts, dogs with PTSD display syndromes comparable to those of affected people. And we can establish this even without the benefit of actually speaking with the subject.
Although Gina was a dog of war with a classic history of “battle fatigue,” Elsa had never been to war. People don’t need to go war to develop PTSD, either. Any traumatic events can trigger the condition. Street violence and other forms of “violent personal assault” (such as Elsa experienced) are also well-established causes of PTSD. Incarceration as a prisoner of war, confinement in a jail or concentration camp, abusive relationships in childhood and adulthood—all can trigger the disorder. We don’t have to search too far to find a parallel in dogs and other animals. Brood bitches in puppy mills, for instance, suffer PTSD as a result of their long isolation in pens and forced breeding.
Automobile accidents can cause PTSD in both people and pets. A serious accident of any kind necessitates treatment in an intensive care unit, which itself could create unpleasant memories. A stay in the ICU, especially one that involves distressing experiences, such as being intubated, paralyzed, and ventilated, can trigger or compound PTSD in people and in pets.
At Tufts we treated a dog, Star, who had developed an extreme panic reaction to visiting veterinary hospitals following a painful treatment for a grievous injury. The upshot: Star wouldn’t even get out of the car a hundred yards from the entrance to the vet hospital. The location itself triggered her distress. The dog’s regular vet made house calls for a while, to avoid causing the dog the anxiety of office visits, but the owner wanted to cure Star of her fear of clinics.
To me, it was clear that Star had PTSD and my approach was similar to the human treatment for PTSD. I prescribed a short-acting, as-needed medication, clonidine, to assuage Star’s strong fear reaction. And I also suggested a long series of desensitizing retraining actions, in which the owner would gently reintroduce the dog to the experience of hospital care in stages. She should not force Star into the situation, as this would only aggravate her condition. The dog’s owner dutifully took on the task, emailing us every week with the latest news. Progress occurred gradually over the course of a year, and Star will now walk into the vet’s office, tail wagging, and will take treats from the staff.
PTSD in people can be triggered by seemingly harmless situations that are reminiscent of the initial trauma. I’ve encountered a similar trigger for canine PTSD. For instance, the smell of cooking lamb triggers terror in some dogs. Dogs that are frightened by the scent of lamb chops on the stove may be reliving some traumatic event that occurred. Perhaps they burned their noses while investigating the source of the formerly delectable odor. One trainer amusingly suggested that the condition may be restricted to sheep dogs distressed by the smell of the sheep they protect and herd being cooked.
Not every person or every dog exposed to psychological or physical trauma will develop PTSD. Some soldiers and some military dogs return unscathed after multiple tours of duty. Others seem primed to acquire this debilitating psychological condition. The reason for this may be something to do with genetic predisposition, which in conjunction with environmental events, may affect a person’s (or a dog’s) response.
Resilience has been the subject of extensive psychological testing, and researchers have determined that people with a positive outlook on life bounce back more quickly in the face of multiple life, medical, and psychological challenges. This suggests the inviting possibility that there might be a “resilience gene” lurking somewhere on the human genome. If we could find the genetic basis for resilience, we would have new avenues to treat any particular behavior causing distress by tweaking the resilience system.
As exciting as this is, much of the relevant research in lab animals on PTSD has already been accomplished. But it has simply not been taken up by the medical community as a whole. Attention must be paid.
Genes expressed in the central nervous system make proteins that activate neural pathways. If we knew what genes were involved in the response to trauma, we could predict PTSD susceptibility and explore ways of preventing—and treating—PTSD in man and animals.
For example, in traumatic situations, animals release large amounts of stress hormones and neurotransmitters. Adrenaline, the fight-or-flight neurotransmitter, enhances memory of highly emotive events. This makes evolutionary sense. When an animal acutely remembers a place or situation that is dangerous, and avoids it in the future, it is more likely to survive than a counterpart whose memory of those events is less sharp. The latter remain more likely to stumble into the same dangerous situation again. The next time could be the last time.
But in treating cases of PTSD, we seek to reverse such fear-based learning. If fight-or-flight brain chemicals enhance memory, then blocking their effects with a so-called beta-blocker, such as propranolol, should prevent acute and lasting memory acquisition.
This turns out to be the case. Propranolol prevented the imprinting of stress-induced learning in rats. Beta-blockers do the same in people. The brain region central to high-stress learning is called the amygdala. Activation of the amygdala enhances fear-induced effects, so tamping down the “vigilance” of the amygdala reduces anxiety throughout the brain.
At one time it was thought that taking a beta-blocker before a predicted trauma was the only way to avert stress-induced imprinting. That conclusion was drawn from studies of rodents and clearly was not convenient for a military application. But it has now been shown that treatment with beta-blockers after the fact can also prevent the brutal “flashback” aspects of post-traumatic stress. This finding renders beta-blocker treatment all the more compelling, as it points out a way of addressing PTSD in people and in animals.
So soldiers in battle need not take a beta-blocker three times a day, “just in case.” They could take a pill within a few hours of fighting or being involved in a horrific event to ward off PTSD. Beta-blockers can prevent the experience of trauma from leaving a deep psychological wound. Prevention—even slightly after the fact—is better than a cure.
Since the recent conflicts in Iraq and Afghanistan, we in the United States find ourselves with an abundant supply of PTSD subjects: both our human veterans from the armed forces and their canine support troops. We simply need sponsors for studies of war dogs to help us better understand the condition in humans and canines. If only we could get funding to heal the traumas of war as easily as the Army is able to secure funding to make war.
It would be much more enlightening to study PTSD in war dogs than in lab rodents. Because dogs develop the condition after being in similar situations to those that traumatize soldiers, they would provide a more accurate, real-life study. We could study which dogs were more susceptible and why and explore the genetics and neurobiology of that susceptibility. And we could develop new and better treatments—for dogs and people.
Clearly, the adrenaline system is “switched on” in PTSD when an animal or person is exposed to a traumatic event. Subjects experiencing the same traumatic event can have widely different responses. One might develop PTSD while another does not. This implies that a factor in the genetic makeup of the affected subjects may render them vulnerable to the disorder. And that, in turn, points the way to a genetic-based treatment. If we can find a gene that figures into the process of PTSD, we can figure out who is vulnerable and treat them accordingly.
At Emory University in Atlanta, Georgia, a team investigating PTSD focused on just such a genetic approach to the problem. Unlike the folks involved in the kerfuffle over Gina’s PTSD, the Emory research team members have no issue with animals having the disorder. And they willingly extrapolate from animals to humans. Testing on animal subjects and extending the findings to humans pretty much describes how biological research science is normally conducted, and that kind of back and forth sums up One Medicine in a nutshell.
The Emory team used mice in their study, the tried-and-true subjects that have spurred so many scientific advances. They stressed the mice by immobilizing them so they couldn’t seek cover or hide, which made them afraid. Researchers then released them into a maze through which they had to find their way. Mice that had been stressed by immobilization had trouble finding their way out of the maze, indicating long-term memory impairment, which is also found in cases of human PTSD.
In order to find the pathways underlying the fear response in the amygdala, the Emory team focused on a specific gene. Going by the technical name of Oprl1, the gene influences numerous brain activities, particularly instinctive and emotional behaviors. The researchers basically showed the physical pathway that fear takes and what it does to the brain. This is what real science can do today, penetrate deeply into areas heretofore unavailable to research. We aren’t limited to cells or even genes anymore. We deal in molecules.
The discovery at Emory suggests that effective treatment can be developed to heal the specific pathway of fear. The endgame, of course, is to come up with effective treatments for PTSD-afflicted service personnel, and for war dogs such as Gina and traumatized animals such as Elsa.
The Emory researchers also looked at the Oprl1 gene in humans, both PTSD and anxiety sufferers. In research studies where subjects viewed pictures of fearful faces, the amygdala lit up more brightly in PTSD-susceptible people, as determined by changes in the Oprl1. So changes in this specific gene may increase the likelihood of developing PTSD. This suggests that measures taken to limit those genetic changes might be beneficial.
The new discoveries have determined the reason why some animals and people are susceptible to developing PTSD. The Emory scientists nailed down the gene and neural pathway that promotes it, yielding promising new opportunities for effective, genetic-based treatment. Gene therapy delivers therapeutic substances directly into a patient’s cells to treat a disease—or, in this case, to treat a vulnerability to a disorder.
The next step is to confirm these findings and try such a genetic-based approach in a group of war dogs. Again, it would be the right thing to do for the Department of Defense to step up.
Recently I attended a meeting of the American College of Veterinary Behaviorists. One of the talks was given by my colleague Dr. Walter Burghardt, a war dog specialist. A veterinary behaviorist like me, he has served as chief of behavioral medicine at the Daniel E. Holland Military Working Dog Hospital at Lackland Air Force Base in Texas and is responsible for the behavioral care of more than 1,500 military working dogs around the world. He is considered an authority on what he refers to as C-PTSD (canine PTSD), which he defines narrowly. The added C in the acronym is designed to calm the kind of uproar that developed over Gina’s condition by a name some people thought should be exclusively reserved for Homo sapiens.
Dr. Burghardt describes himself as an “extreme behaviorist,” meaning he observes but does not interpret behavior. To be diagnosed with C-PTSD, dogs have to have a history of deployment in a combat environment. Second, they have to have been present at a “combat event.” Dr. Burghardt’s clinical signs of the condition include: hypervigilance to environmental events, escape/avoidance reactions when faced with certain challenges, generally skittish behavior (tail down, acting scared all the time), changes in social rapport (increased dependence on the military handler), and disruption of task performance.
The onset of these behaviors would have to occur during or after a combat event and persist long afterward for the diagnosis to be confirmed. He found that the prevalence of C-PTSD was 5–10 percent of deployed dogs, making it a serious concern for the military. Curiously, Labrador retrievers were the breed most affected.
Dr. Burghardt’s assessment of canine PTSD is essentially similar to mine, although his definition is a little more narrow. He deals with war dogs and has little cause to be concerned with what the military calls civvy street. I consider the Army’s approach to treating C-PTSD to be a tad conservative and only somewhat effective. We could better serve afflicted dogs by funding an array of research into optimal therapies. We could also confirm the genetic cause for susceptibility, thus allowing the military in the future to choose dogs for military service that were almost literally “bomb proof.”
Perhaps some of these future research findings would translate into new possibilities for human war fighters, too, opening up better training, deployment selection, and treatment options. And isn’t that the bottom line?