A Depression Switch?

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A Depression Switch?

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It worked that way for other patients too. For those for whom it worked, the first surges of mood and sensation were peculiar to their natures. Patient 4, for instance, was fond of taking walks, and she had previously told Mayberg that she knew she was getting ill when whole landscapes turned dim, as if "half the pixels went dark." Her first comment when the stimulator went on was to ask what they'd done to the lights, for everything seemed much brighter. Patient 5, an elite bicycle racer before his depression, told me that a pulling that he had long felt in his legs and gut, "as if death were pulling me downward," had instantly ceased. Patient 1, who in predepression days was an avid gardener, amazed the operating room by announcing that she suddenly felt as if she were walking through a field of wildflowers. Two days after going home, she put a scarf over her shaved, stitched head, found her tools and went out to reclaim her long-neglected gardens.

Not all was light and flowers. On a purely biological level, the improvement made by D.B.S. sometimes amplified the side effects of the high doses of medication the patients had been taking. Doctors don't quite understand this phenomenon, but they see it happen in other instances too; it is as if the patient, deadened, is again made sensate. Deanna broke out in hives and felt nauseated; her hands shook. These symptoms eased when she (as several of the patients have done) reduced her meds — slowly, so as not to introduce new variables. She now takes standard doses of Effexor, an antidepressant, and Seroquel, an anti-psychotic drug.

The cure also brought challenges at home. As with other disabilities, any partner turned caretaker gets used to calling the shots, and rearranging power, dependencies and expectations after a sudden recovery can prove hard. One patient, the cyclist, faced this challenge starkly, for he had started a relationship and married while he was depressed. "Frankly," he told me, "I'm not sure we've quite finished working this out." All the patients have benefited from coordinated assistance from psychiatrists, social workers and occupational therapists who try to smooth the transition.

"That help is crucial," says Mayberg, who is now a professor of psychiatry and neurology at Emory University in Atlanta. "We're just fixing the circuit. The patient's life still needs work. It's like fixing a knee. They need that high-quality physical and supportive therapy afterward if they're really going to move around again."

This transition is not back to a former self and family but to a new one. Gary Benjamin says he sees similar things in military families. "These soldiers get sent away for six months, they come back and all they want to do is return to their old home. But their old home isn't there, because everybody's changed. It takes some tough rearranging sometimes."

For a change so profound, these seem acceptable adjustments. And the treatment so far seems remarkably free of side effects. No one has suffered significant neural complications, probably because, unlike ECT, which sends 70 to 150 volts through the entire brain, these electrodes deliver only about 4 volts to an area about the size of a pea.

But what will happen when larger groups are treated? The team is continuing to operate on depressed patients, with a goal of 20. And would the successes stay high and the side effects low in a large, placebo-controlled trial? Neither Mayberg nor any of the other collaborators cares to guess. Other treatments have started this well and fizzled. For instance, vagus nerve stimulation, which sends a low current to the brain via a major nerve with connections to various brain areas, appeared to help about half of the patients in a small, initial, uncontrolled trial, but failed its only placebo-controlled trial. (In a controversial move, the Food and Drug Administration overruled its own reviewers and approved the device as a depression treatment anyway.)

"What if you do a hundred patients," I asked Mayberg one day, "and they do no better than placebo?"

"I suppose that's possible," she said. But she doesn't think that will be the case. The several authorities I talked to agree that the high success rate so far, along with the soundness of the theoretical base and D.B.S.'s track record with Parkinson's, suggests that this isn't just a lucky run.

"This just makes so much sense," says Dr. Antonio Damasio, director of the University of Southern California's Brain and Creativity Institute and a renowned neurologist, "and the weight of the results is so sizable. I would be surprised if they had no results with a larger body of patients."

On the other hand, even if it works, no one sees this becoming the new Prozac. The procedure costs too much (around $40,000) to use on anyone who hasn't tried everything else. The appropriate candidates for D.B.S. probably number in the thousands, not the millions. Perhaps the most sensible worry is that if the thing works, doctors might use it too freely, as they tend to do with successful new treatments; witness the problematic boom in D.B.S. for Parkinson's.

In the end, the procedure's greatest clinical value may lie in inspiring less intrusive ways of tweaking key nodes — localized delivery of drug or gene therapies, or other means still to come. Such possibilities probably lie at least a decade away.

Regardless of how it pans out in the clinic, Mayberg and Lozano's D.B.S. study is already changing how neuroscientists and psychiatrists think about depression. One possibility, for instance, is that refining the networks that go awry in depression may reveal neurological subtypes of depression that can be diagnosed and treated differently. For example, Mayberg has already found that patients who respond well to Prozac usually show a change in their brain scans only a week after they start medication — even though they don't feel a difference for 3 to 10 weeks (a long and sometimes dangerous wait). She's done preliminary work suggesting she might be able to identify such Prozac-friendly patients before they even start the drug. If she or others can replicate and elaborate on this diagnostic ability, doctors might be able to characterize a patient's depression and choose a best-odds therapy — Prozac for one patient, talk therapy for a second, both for a third — at the very beginning of treatment, savings weeks or months of trial and error.

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The network model — which some scientists also call a "systems" model — also offers an organizing principle for research. Andreas Meyer-Lindenberg, a researcher with the N.I.M.H., points out that research on depression has so far followed clues left by drugs that were found to be effective only by chance. "We'd find a drug that helped depression, figure out how it works and make hypotheses from that about how the brain works," he says. The effectiveness of selective serotonin reuptake inhibitors (S.S.R.I.'s) like Prozac, for instance, inspired piles of research showing that mood regulation depends heavily on the availability of the neurotransmitter serotonin. (Neurotransmitters are chemicals that help carry messages across the spaces between neurons; S.S.R.I.'s treat depression by making more serotonin available in those spaces.)

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Last updated: 4/06

A Depression Switch?

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