NEW YORK (Reuters Health) - Impaired executive function is common and often permanent following stroke. However, new study findings suggest that treatment with antidepressants may help patients recover their cognitive and psychosocial capacities.

Based on previous observations that antidepressants improve stroke outcomes, Dr. Sergio Paradiso and associates at the University of Iowa Carver College of Medicine in Iowa City conducted a trial to see if antidepressant treatment improves executive dysfunction.

The participants were 47 stroke patients being admitted to a rehabilitation center. They were randomly assigned to treatment for 12 weeks with nortriptyline, titrated up to a maximum of 100 mg/day; fluoxetine, maximum dose 40 mg/day; or placebo. The patients were evaluated after the 12 weeks of treatment and again 21 months later.

The authors report the study results in the March issue of the British Journal of Psychiatry.

The patients did not significantly differ in stroke type, location or volume of lesion, or neurological deficits. The physicians observed no differences among the treatment groups in executive function at the first evaluation or in overall cognitive functioning at the 12- and 21-month evaluations.

However, at the final assessment, those given active treatment demonstrated substantial increases in executive function index scores (p = 0.001), independent of depressive symptoms, whereas all but one of the placebo-treated patients had deteriorated significantly.

In a stepwise regression analysis, "the final model predicting executive function consisted of active treatment or placebo, age, past psychiatric history, neurological impairment and total lesion volume," the team reports. Differences in levels of depression had no effect.

However, the only factor having a significant, independent effect on executive function was antidepressant treatment.

Dr. Paradiso's team proposes a couple of ways that antidepressants could affect long-term executive function.

"The mechanism of executive function recovery may be the modulation of monoaminergic nuclei exerting effects on the cortical-striato-pallido-thalamo-cortical circuits," they write. Or, the drugs may enhance neurotrophin activity and neurogenesis.