fluvoxamine and Cerebral-Infarction

Antidepressants have been recommended for the treatment of post-stroke depression (PSD). The purpose of this study was to evaluate the effect of fluvoxamine maleate, a selective serotonin re-uptake inhibitor (SSRI), on depressive state, sleep disturbance, and serum melatonin levels in patients with depressive state after cerebral infarction.. Nineteen patients who were hospitalized for cerebral infarction and scored 40 points or higher on the Self Depression Scale (SDS) were enrolled in this study. Nine of the 19 patients received fluvoxamine as a treatment group and the other 10 patients were used as untreated controls. Before and after commencing the drug therapy, the patients were assessed by the SDS, Pittsburgh Sleep Quality Index (PSQI), Japan Stroke Scale for Depression (JSSD), and Japan Stroke Scale for Emotional Disturbance (JSSE), and their serum melatonin levels were measured. The control group underwent the same evaluations as the treatment group.. The SDS score improved in the treatment group at 1 week after the start of drug treatment, and in the control group at 1 and 2 weeks into the observation period. In the treatment group, the JSSD and PSQI scores improved and serum melatonin levels increased.. The administration of fluvoxamine to patients with depressive state after cerebral infarction alleviated both the depressive state and sleep disturbances. Increased melatonin levels by the administration of fluvoxamine may contribute to improvement in sleep disturbance, one of the major symptoms of depression.

Topics: Aged; Aged, 80 and over; Antidepressive Agents, Second-Generation; Cerebral Infarction; Depression; Female; Fluvoxamine; Humans; Male; Melatonin; Selective Serotonin Reuptake Inhibitors; Sleep Wake Disorders; Stroke

The sigma-1 receptor has been reported to be associated with diverse biological activities including cellular differentiation, neuroplasticity, neuroprotection, and cognitive functioning of the brain. Fluvoxamine, one of the currently known antidepressants, is a sigma-1 receptor agonist; its effectiveness in treating acute cerebral ischemia has not been reported. We studied the in-vivo effects of this compound using an animal model of focal cerebral ischemia. Forty male Sprague-Dawley rats were subjected to right middle cerebral artery occlusion and assigned to five treatment groups (n=8 each). Postischemic neurological deficits and infarct volume were determined 24 h after stroke-inducing surgery. Significant reductions in infarct volume (total and cortical) were found in group 2 (fluvoxamine 20 mg/kg given 6 h before and immediately after ischemic onset) and group 3 (fluvoxamine given immediately after ischemic onset and 2 h later) compared with controls. Fluvoxamine induced significant amelioration of sensorimotor dysfunction, as indicated by the scores of forelimb and hindlimb placing tests. Moreover, NE-100, a selective sigma-1 receptor antagonist, completely blocked the neuroprotective effect of fluvoxamine. The present findings suggest that the sigma-1 receptor agonist fluvoxamine reduces infarct volume and ameliorates neurological impairment even on postischemic treatment. From the clinical viewpoint, fluvoxamine may be a promising new therapeutic approach for cerebral infarction.

Topics: Animals; Antidepressive Agents, Second-Generation; Cerebral Infarction; Fluvoxamine; Male; Neuroprotective Agents; Psychomotor Disorders; Rats; Rats, Sprague-Dawley; Receptors, sigma; Sigma-1 Receptor

Topics: Adrenergic alpha-Agonists; Aged; Antidepressive Agents, Second-Generation; Body Temperature; Cerebral Infarction; Clonidine; Drug Interactions; Female; Fluvoxamine; Heart Rate; Humans; Male; Middle Aged; Retrospective Studies