Depression therapies converge in brain.

People diagnosed with major depression display many of the same brain changes when their condition improves whether in response to antidepressant drug treatment or to a type of psychotherapy, two preliminary investigations find.

If confirmed in further work, these results will highlight common brain regions through which various medications and talk therapies fight the melancholy, apathy, and hopeless feelings of major depression.

Both new reports appear in the July ARCHIVES OF GENERAL PSYCHIATRY.

"This is pioneering work," says psychiatrist Wayne C. Drevets of the National Institute of Mental Health in Bethesda, Md. "There's been little research on psychotherapy's effects on the brains of depressed people."

In Drevets' view, the new data also point to some neural differences in recipients of psychotherapy and antidepressant drugs.

The first study, led by psychiatrist Arthur L. Brody of the University of California, Los Angeles Medical School, included 24 depressed adults who hadn't previously received treatment and 16 adults with no psychiatric diagnosis. Volunteers underwent positron emission tomography upon entering the study and then 12 weeks later. These scans measured glucose use--an indirect sign of neural activity--in various brain areas.

Depressed participants chose the form of treatment that they preferred. The day after the initial brain scan, 10 depressed volunteers began treatment with an antidepressant drug, paroxetine. This medication enhances the activity of serotonin, a chemical messenger in the brain.

During the week after the first scan, the remaining 14 depressed individuals attended the first of 12 psychotherapy sessions. This therapy focused on ways to improve relationships with friends and family.

Compared with nondepressed adults, depressed individuals began the study showing increased activity in parts of three brain areas--the prefrontal cortex, the caudate, and the thalamus. Activity markedly declined in these regions following either course of depression treatment.

Earlier studies had linked antidepressants' effects to activity surges in the same prefrontal regions (SN: 5/15/99, p. 308). However, that work examined hospitalized patients whose emotional unresponsiveness and slowed movements may have greatly lowered prefrontal activity, Brody's team says.

Data in the new study also show that psychotherapy, but not medication, heralded activity increases on the left side of the insula, Drevets remarks. This brain area helps to regulate sad feelings and, when particularly revved up, dampens symptoms of depression, he notes.

The strongest evidence for a shared brain response to psychotherapy and medication was an activity decline in a part of the caudate that regulates motor activity, Drevets holds. It's unclear why caudate activity eased up as symptoms of depression lifted, he says.

The second study, led by psychiatrist Stephen D. Martin of Cherry Knowle Hospital in Sunderland, England, found activity increases in the basal ganglia--which are also involved in movement--following 6 weeks of either antidepressant use or psychotherapy. Increased activity in brain areas involved in emotion showed up after only the psychotherapy.

Martin's team had studied 28 depressed adults, most of whom the researchers had randomly assigned to a treatment. However, the study didn't include people free of psychiatric disorders.