DEPRESSION  [ back to Brain Injury 101 ]
Depression is extremely common following a TBI. It can, and often does, have an organic and psychogenic component. The organic component would include such things as physical damage to the left hemisphere of the brain; depletion of any of the monamine neurotransmitters (serotonin, dopamine or norepinephrine); insomnia with sleep debt and fatigue; lower output of of thyroid hormone; and overproduction of the stress hormone cortisol. Studies of stroke patients has revealed that damage to the left side of the brain is far more likely to trigger depression than damage to the right side. A 1988 study identified at least one factor behind this difference. The right side of the brain tends to keep serotonin at optimal levels in the brain following a brain attack, whereas the left side is less able to do so. Depletion of serotonin in non-brain damaged patients is associated with depression, irritability and increases in inter-personal violence or suicide, so this makes sense.

Neuropsychologists have observed the same response in TBI patients. People with TBI are under stress for a variety of reasons. They need to concentrate much harder to take in and remember new information, to shut out distractions and keep on task. They must also expend a great deal of extra energy to appear, or pass, as "normal." They don't sleep well which raises their level of stress hormones and blocks replenishment of "feel good" brain substances. They are understandably anxious about losing their spouse, friends, job and home. These and other "stressors" raises the level of cortisol in the bloodstream. This contributes to depression and poor memory by atrophy of the hippocampus. Older studies of war veterans with PTSD show hippocampal shrinkage. Much more recently, neurobiologists Barry Jaccobs, Henriettte van Praag and Fred Gage published a study in the July 2000 issue of the American Scientist in which they report that the dentate gyrus in the human hippocampus gives birth to 100s, possibly 1000s, of new "baby" neurons every day, which helps explain how humans can have a continuous, uninterrupted memory of their entire lives, when old hippocampal and other brain cells get retired every day - about 50,000 or so. They believe that hippocampal damage or suppression of hippocampal birthing of new cells explains poor memory and the depression which is so frequently linked to poor memory. There is some corroboration in reports of vigorous physical exercise stimulating birth of new brain cells in the rat hippocampus and improving the ability to rats to run mazes and remember the routes they took.

The psychogenic aspect refers to perceiving oneself as being impaired or disabled in the functions of everyday life, and then experiencing such negative emotional responses as shame, guilt, worry, fear, anxiety or dread. The American Medical Association's "Essential Guide to Depression," states that any random event which takes away a person's sense of having control over their life can precipitate depression, including not just a death in the family or loss of a job, but traumatic injury as well. Because of their obvious suffering, sadness, crankiness and impaired ability to function smoothly in social situations, TBI people are sometimes abandoned by friends, and this social isolation can compound the depression.To the extent depression drives a wedge between the person with the TBI and his spouse or children, the depression is also likely to worsen, as recognized in the AMA Guide.

Research shows that beginning about 3 months post-TBI, many patients who are then suffering from depression do not have identifiable structural damage to the left brain hemisphere damage, which means that  depression so long after the TBI has a  psychogenic component. Is psychogenic depression malingering? No. The depression is real and has real consequences, such as poor sleep, fatigue, over or under eating with significant weight loss or weight gain,  losing motivation, and dropping out of or curtailing vocational, social, sexual  and recreational activities. When depressed people respond well to anti-depressant medication and start sleeping well, their cognitive performance on testing goes up and they show improved brain metabolism in their frontal lobes on PET scans, as established by Dr. Helen Mayberg of the University of Texas Health Science Center in San Antonio. Litigation doctors who work for insurance companies like to separate out "organic brain problems" from "psychological troubles" arising from the mind, because this is way of linking the plaintiff's distress to something other than a TBI. Is this a fair distinction resting on contemporary neuroscientific knowledge?

Not really, because the brain that was violently shaken during the head trauma is the same brain which gives rise to and which "feels" the depression. As noted in a recent book on Functional Brain Imaging by Andrew Papanicolaou,  there is "not a single thought, decision, feeling, attitude or trait which does not depend on the brain." If depression following head trauma was faked for litigation, or resulted from the stress of litigation, one would expect the depression to show up only in head trauma patients who filed a lawsuit and to last only as long as the lawsuit . However, research shows that this type of depression strikes whether or not the person with the TBI has filed a lawsuit for damages, and that it long outlasts the monetary settlement of lawsuits. One such study appears at Journal of Psychiatry 1999; 156(3)374-378.

It is most unfortunate that in litigation for damages, the psychiatrists and psychologists who work for the insurance companies separate depression out from traumatic brain injury and phrase the debate in either/or terms, saying the plaintiff's problem is either TBI or depression, and for x reasons, the expert is convinced it is depression. This is a distortion of the medical literature which serves an economic purpose. PET scans of the brains of depressed vs. non-depressed persons are different. Depressed people (like schizophrenics) show decreased frontal lobe activation, whether the source of the depression is lifelong disorder or the recent consequence of a TBI. This result is not subject to voluntary control and cannot be faked. Autopsies of depressed suicide patients have shown structural abnormalities in serotonin receptors. See, Ernsberger's article at  Archives of Gen. Psychiatry (1990) 47:1038-1047. 

Depression tends to build on itself and worsen if not treated aggressively. Treatments include anti-depressant drugs, psychotherapy and behavior therapy (to change behaviors which may re-enforce depression). It is common for depression to become a bigger obstacle to recovery of employment and decent social functioning in the realm of marriage and family than cognitive deficits. There is no single bio-chemical cause of depression in all people, which is why some people respond well and some do not respond at all to the same anti-depressant, and why a psychiatrist may need to "try out" a patient on a variety of different anti-depressants until he hits the jackpot and gets good remission of the depression. Common anti-depressants include Elavil, Prozac,  Zoloft, Paxil   and Effexor, but there are many others. There are certain ways to predict whether a patient will respond or will not respond to anti-depressants. If the patient's depression is briefly relieved by alcohol he is likely to benefit from anti-depressants, because each drug activates the same neural circuitry. Using the PET scanner, Dr. Helen Mayberg has shown that a good clinical response to anti-depressant medication tends to occur only in patients who prior to treatment showed active  metabolism in part of the limbic system called the rostral anterior cingulate. She believes that the rostral anterior cingulate must be placed temporarily in a state of hypermetabolism to restore normal mood in a depressed patients, and that non-responders to anti-depressants are people who had weak metabolism in that part of their brain before and after the trial of medication.

Finally ATTITUDE matters. Clinical research shows that TBI survivors who engage in negative thinking all day long (e.g. blaming themselves for their injury, worrying about the future and wishing things were different) tend to be much more anxious and depressed than patients who focus on strategies of problem solving and positive outlook. See, Journal of Head Trauma Rehab. 15(6) 1256-1274) Dec. 2000 A good place to learn coping strategies that work is in a well run TBI support group.