According to the Brain Injury Society, a premier resource for those wanting to know more about the human brain, 14.8 million American adults will suffer yearly from a major depressive disorder. This works out to about 6.7 percent of the U.S. population over the age of 18, in 2005 figures.
The incidence, in 2016, is roughly 21.7 million people. This is four times as many as are expected to experience their first heart attack, or die of cancer.
Depending on the cause, some victims of depression will recover, thanks to pharmaceuticals and/or cognitive therapy. Where depression is the result of changes in brain chemistry – like hormone levels or emerging medical problems – the likelihood of recovery (or, at least, stability) is very high.
Where the cause of depression is genetic, the likelihood of achieving emotional stability is also high, as it is with external depressive influences like grief, stress, or loss. The secret is consistency (in taking medication) and supervision – by a medical professional, for as long as the depression persists.
When the roots of depression lie in the brain’s own, unique physiology, the probabilities change.
Depression and Brain Injury
Over 40 percent of individuals who experience a concussion – traumatic brain injury, or TBI – will develop depression during the next 12 to 15 months. In fact, the ratio may be even higher. The Mayo Clinic suggests that the risk may be five times higher than for the population at large.
Because a TBI is exogenous (occurring from outside the brain) rather than endogenous (caused from within), treating brain-injury depression may follow an entirely different path than that of major depressive disorders. The reasons why lie in brain chemistry.
Macrophages, Microglia, Oh My
The human brain is a physical entity within a larger entity. The so-called “blood-brain barrier” is an example of this more or less peaceful coexistence. Though this barrier has proven to be more permeable than first thought, there is no doubt that the brain is the most carefully shielded organ in the human body.
The brain even has its own immune system, comprised of macrophages, microglia, and other inflammatory cells that go to work removing dangerous substances. These specialized fighting cells can be seen via neuroimaging, notably of a translocator protein (TSPO) that transports cholesterol into the mitochondria.
Cholesterol is the brain’s “food”, and the TSPO in question is the peripheral benzodiazepine receptor. Benzodiazepine is a tranquilizer used to treat anxiety and depression.
When a person sustains a head injury, these microglia and macrophages are overstimulated and forced to work hard enough that some may die. This puts more strain on remaining immune system cells. Either state – overwork or underperformance – can lead to depression.
Common Symptoms of Depression (per the Mayo Clinic):
Changes in appetite
Difficulty concentrating
Feelings of worthlessness or guilt
Frequent tearfulness, anger, irritability, or frustration
Loss of interest or pleasure in activities a person usually enjoys
Persistent feelings of sadness, emptiness, or hopelessness
Problems with thinking and memory
Significant fatigue or lack of energy
Sleep problems
Identifying symptoms of depression in someone who has a TBI can be tricky, because some depression symptoms may be mistaken for symptoms caused by the brain injury.
Treating TBI Depression
The nature, extent, and severity of TBIs vary from person to person. So, too, do treatment regimens, as TBI-depression victims experience what can be a long history of cognitive or mental symptoms, including confusion, difficulty with reasoning or learning, frequent mood changes, and memory loss.
When depression is diagnosed along with a traumatic brain injury, notes the Mayo Clinic, treatment may be two-pronged, using both antidepressant medication and behavioral therapy. This is the same as treatment for depressed individuals who have not experienced a TBI, with one significant difference: the TBI individual will have his or her care carefully integrated into a TBI treatment plan aimed at alleviating symptoms like headaches, dizziness, fatigue, irritability, anxiety, insomnia, loss of memory and concentration, and noise and light sensitivity. This insures that recovery from the brain injury and depression can move forward together.
Future directions
Tomorrow, or next year, TBI depression may include the use of anti-inflammatory agents, infusion therapy, ketamine-like drugs, and medication choices based on individual neuroimaging. Beyond that, treatment for TBI depression may evolve to what one psychiatrist describes as:
“…radically different, non-pharmacological treatments for depression following brain injury. A barrier to these advances is the fundamental resistance on the part of psychiatrists to look at the organ they are treating and to open their eyes to possible alternative explanations for the depression the patient describes to them.”