If you have a broken leg, you can tell people you have a fracture in your left tibia. If you have a bad heart you can let people know you have a weak aortic valve. But what do you say if you have a mood disorder? Most of us settle for the explanation that we have a chemical imbalance, which is about as satisfactory as your mechanic handing you a bill with this one item: "Engine Imbalance."
Then there is the matter of collateral damage. We know depression can stop the brain it its tracks while mania runs it off the rails, with corresponding deficits in our ability to think and reason, but we are led to believe these are only temporary occurrences, right? Maybe not.
If only a mood disorder were just a mood disorder. A lengthy review article by Carrie Bearden PhD et al of the University of Pennsylvania published in Bipolar Disorders cites "findings of persistent neuropsychological deficits" in long-term bipolar patients, even when tested in symptom-free states. The relationship between these deficits and length of illness led the authors to suggest that "episodes of depression and mania may exact damage to learning and memory systems."
An article by FC Murphy PhD and BJ Sahakian PhD of Cambridge University in the British Journal of Psychiatry draws a similar conclusion: "The balance of evidence ... supports a hypothesis of residual cognitive impairments."
Father Time appears to be a major factor. Dr Bearden et al cite a study that found that chronic, multiple-episode patients exhibited more severe cognitive impairment than younger patients or patients who remit, and that these impairments were not restricted to their affective episodes. The same study found 40 percent of the patients were rapid-cyclers. Another study found that of 25 patients initially hospitalized with mania with no signs of cognitive impairment, one third showed significant cognitive impairment five to seven years later.
There is always the possibility that the meds are responsible. One long-term study found lithium users (one-third who had a university degree) to be in the low average range on functions of attention and memory. Nevertheless, the authors believe that while medication may cause some degree of cognitive slowing, our pills are not the main culprit.
Bearden et al's review of what could be wrong with the brain reads like a neurologist's laundry list from hell: ventricular enlargements, cortical atrophy, cerebellar vermal atrophy, white matter hypertensities (especially in the frontal cortex and basal ganglia structures), greater left temporal lobe volume, increased amygdala volume, enlarged right hippocampal volume, hypoplasmia of the medial temporal lobe, and more. Then there's the matter of those chemical imbalances, such as glucose metabolism and phospholipid metabolism.
Say all that in rap time and you have the sound of our brains breaking down, no longer capable of processing information the way it is supposed to. It is possible that these studies did not adequately account for the normal aging process, as Dr Bearden was ready to acknowledge to this writer, but she also added that it is "likely that there is an interaction between the disease process and normal aging processes, such that people affected with bipolar illness are somehow more vulnerable to the effects of aging."
Lest we cause a panic, Dr Bearden wants to remind readers that "while these brain differences are there, they are subtle. They are certainly not present in all people with bipolar illness, nor do we really know what there functional significance may be in any given individual. And most likely if a radiologist were to take a glance at a brain scan of a person with bipolar disorder, it would look normal - it's just when you actually measure things quantitatively that you find differences. I realize that sometimes these research findings can sound really horrific, and I don't want to cause anyone undue concern."
Also, it appears that our current bipolar medications actually repair and protect brain cells, which is one of the better arguments for staying compliant. Further research in this area may produce new drugs with enhanced neuroprotective properties.
One day, perhaps, brain doctors will be able to open up the hood and do a valve job. Researchers at the Salk Institute of Biological Studies isolated stem cells from the hippocampus of adult rats and modified the gene to produce glowing proteins, which were cloned and took on the properties of adult neurons as they matured, including the ability in some to make synaptic connections with other neurons. Alzheimer's and Parkinson's come most immediately to mind in the context of this type of research, but a mood application can't be far beyond that, assuming they can get the technology to work in humans, which is a very big if. In the meantime, there is hope, which we may have to suffice for the next decade or two.