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Transient Ischemic Attack Reported with Paroxetine Use

Training Director, Department of Psychiatry, Naval Medical Center Portsmouth, Portsmouth, VA

Steven M Wechsler, MD

Chief Resident, Department of Psychiatry, Naval Medical Center Portsmouth

Reprints: Gail H Manos MD, Department of Psychiatry, Naval Medical Center Portsmouth, Portsmouth, VA 23708-2197, fax 757/953-5272, ghmanos{at}mar.med.navy.mil

OBJECTIVE: To report the occurrence of a transient ischemic attack (TIA) temporally related to the initiation of paroxetine.

CASE SUMMARY: A 57-year-old white man with a history of intermittent atrial fibrillation and hypercholesterolemia developed slurred speech and a facial droop 3 days after starting paroxetine. He was diagnosed with a TIA, hospitalized, and given anticoagulation treatment. The presenting symptoms resolved, but recurred when paroxetine was restarted 2 days later.

DISCUSSION: Platelets secrete serotonin, which mediates vasoconstriction through stimulation of 5-HT_2a receptors. This is counterbalanced by the release of the vasodilator nitric oxide upon serotonin stimulation of endothelial 5-HT₁ receptors. In conditions such as atherosclerosis, the damage to the endothelium leads to a greater vasoconstrictive response. Paroxetine has been reported to weakly inhibit norepinephrine reuptake and nitric oxide production in addition to increasing serotonergic activity, potentially compounding the vasoconstrictive response. An objective causality assessment revealed that the TIA was probably an adverse event resulting from use of paroxetine.

CONCLUSIONS: Use of paroxetine and other selective serotonin-reuptake inhibitors may result in changes of the vasculature and subsequent ischemic events in predisposed patients.

Key Words: paroxetine, SSRIs, TIA, transient ischemic attack, vasoconstriction

Published Online, February 13, 2004. www.theannals.com, DOI 10.1345/aph.1D304