Abstract

Reversible cerebral vasoconstriction syndromes (RCVS) are a group of disorders characterized by prolonged but reversible vasoconstriction of the cerebral arteries, usually associated with acute-onset, severe, recurrent headaches, with or without additional neurologic signs and symptoms [1]. These syndromes are known to occur secondarily to the use of drugs such as cannabis, cocaine, ecstasy, amphetamine, selective serotonin-reuptake inhibitors (SSRIs) and nasal decongestants, or during pregnancy or the puerperal period itself [2]. RCVS which presents at puerperium is known as postpartum cerebral angiopathy (PCA) and is associated with the concomitant use of vasospastic drugs such as bromocriptine [3]. However, RCVS induced by bromocriptine beyond the puerperal period has not so far been reported. We describe here a case of bromocriptineinduced RCVS with ischemic stroke arising 1 year after the birth of second baby. A 32-year-old woman presented with an episode of transient left-sided weakness and dysarthria that lasted approximately 15 min, and a progressively worsening headache over several days. She had given birth to a second healthy baby 1 year before the present admission and it was uncomplicated as was her first pregnancy. Sixteen days before admission she had started on a course of 2.5 mg oral bromocriptine mesylate twice a day for 7 days to suppress lactation. After 7 days use of the bromocriptine, she was admitted to an outside hospital because of severe headache, transient left-sided weakness and dysarthria. At that time her vital signs were stable, including blood pressure of 130/85 mmHg and neurologic examination was unremarkable. Diffusion and fluid attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) revealed focal high-signal areas in the right frontal lobe (Fig. 1a, b) and magnetic resonance angiography (MRA) showed up severe stenosis in both middle cerebral arteries (Fig. 2a). A transcranial Doppler (TCD) disclosed abnormally high flow velocities in both middle cerebral arteries, and a CSF examination was normal. Low-dose acetylsalicylic acid (100 mg once a day) was initiated on a suspicion of transient ischemic attack with right middle cerebral artery stenosis. The patient was referred to our hospital 9 days after the onset of her symptoms due to recurrent severe headache. Upon arrival, vital signs were stable including a blood pressure of 125/80 mmHg. The patient had severe headache without any abnormalities of neurologic examination. Laboratory examinations including renal function, urinalysis, international normalized ratio, partial thromboplastin time, thrombin time, antithrombin III, protein C, protein S, D-dimer, and fibrin monomers were unremarkable. In addition, tests for antinuclear and anticardiolipin antibodies, and complement indices were normal. On the second day in our hospital, her headache worsened with newly developed left-sided weakness and dysarthria. At that time, diffusion and FLAIR images demonstrated extended highsignal areas in the bilateral fronto-parietal area (Fig. 1c, d). Y. S. Kim W. Baek J. Kim H. Y. Kim Department of Neurology, College of Medicine, Hanyang University, Seoul, Republic of Korea

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