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illness, whether they became more pronounced over time, where in the brain they localized, whether they were related to the problems in spatial orientation and facial recognition that I and many other manic-depressives experience, and whether children who were at risk for manic-depressive illness, because one or both of their parents had the disease, would show these brain abnormalities even before they became ill. The clinical side of my mind began to mull about the visual advantages of these and other imaging findings in convincing some of my more literary and skeptical patients that (a) there is a brain, (b) their moods are related to their brains, and (c) there may be specific brain-damaging effects of going off their medications. These speculations kept me distracted for a while, as changing gears from the personal side of having manic-depressive illness to the professional role of studying and treating it often does. But, invariably, the personal interest and concerns returned.

When I got back to Johns Hopkins, where I was now teaching, I buttonholed neurology colleagues and grilled my associates who were doing the MRI studies. I scurried off to the library to read up on what was known; it is, after all, one thing to believe intellectually that this disease is in your brain; it is quite another thing to actually see it. Even the titles of some of the articles were a bit ungluing: “Basal Ganglia Volumes and White Matter Hyperintensities in Patients with Bipolar Disorder,” “Structural Brain Abnormalities in Bipolar Affective Disorder: Ventricular Enlargement and Focal Signal Hyperintensities,” “Subcortical Abnormalities Detected in Bipolar Affective Disorders, Using Magnetic Resonance Imaging”; on and on they went. I sat down to read. One study found that “Of the 32 scans of the patients with bipolar disorder, 11 (34.4%) showed hyperintensities, while only one scan (3.2%) from the normal comparison group contained such abnormalities.”

After an inward snort about “normal comparison group,” I read on and found that, as usual in new fields of clinical medicine, there were far more questions than answers, and it was unclear what any of these findings really meant: they could be due to problems in measurement, they could be explained by dietary or treatment history, they could be due to something totally unrelated to manic-depressive illness; there could be any number of other explanations. The odds were very strong, however, that the UBOs meant something. In a strange way, though, after reading through a long series of studies, I ended up more reassured and less frightened. The very fact that the science was moving so quickly had a way of generating hope, and, if the changes in the brain structure did turn out to be meaningful, I was glad that first-class researchers were studying them. Without science, there would be no such hope. No hope at all.

And, whatever else, it certainly gave new meaning to the concept of losing one’s mind.

Clinical Privileges

There is no easy way to tell other people that you have manic-depressive illness; if there is, I haven’t found it. So despite the fact that most people that I have told have been very understanding—some remarkably so—I remain haunted by those occasions when the response was unkind, condescending, or lacking in even a semblance of empathy. The thought of discussing my illness in a more public forum has been, until quite recently, almost inconceivable. Much of this reluctance has been for professional reasons, but some has resulted from the cruelty, intentional or otherwise, that I have now and again experienced from colleagues or friends that I have chosen to confide in. It is what I have come to think of, not without bitterness, as the Mouseheart factor.

Mouseheart, a former colleague of mine in Los Angeles, was also, I thought, a friend. A soft-spoken psychoanalyst, he was someone I was in the habit of getting together with for a morning coffee. Less frequently, but enjoyably, we would go out for a long lunch and talk about our work and our lives. After some