•Reversible cerebral vasoconstriction syndrome (RCVS) is an important cause of postpartum thunderclap headache with transient focal neurologic deficits

•RCVS is an acute angiopathy characterized by multifocal vasoconstriction with segmental arterial “beading” on imaging and risk of ischemic or hemorrhagic complications

•Risk factors include; female sex, puerperium, pre-eclampsia.

31Y G2P1, IVF pregnancy, GHTN (labetalol BID from 36/40),  CD at 37+5. At ~24 hours PP, she developed; sudden thunderclap headache followed by; decreased consciousness and focal neurologic deficits (L side weakness + R facial droop), complete resolution within 1 hour, normotensive throughout (102/48, 122/57). CTA ~90 min after symptom onset: mild diffuse intracranial arterial “beading” (Fig.1) consistent with RCVS, no hemorrhage/infarction. PPD3-5: Recurrent headaches/brief focal deficits; follow-up CTAs → dynamic vasospasm, including interval worsening with irregular narrowing of both PCAs and right ACA, followed by slight progression in ACA narrowing. PPD4; elevated PCR confirmed pre-eclampsia. Labetalol was stopped and verapamil (40 mg TID) and low-dose aspirin were started with a permissive systolic BP target of 120-150mmHg. Multimodal analgesia was used to control headache and minimize sympathetic BP surges.

Discussion points

Clinical features: thunderclap headache, transient neurological deficits. Imaging is critical for diagnosis of RCVS. No guideline consensus for management of RCVS. MDT vital. Early Ca2+ channel antagonists (nimodipine, nifedipine, or verapamil). The challenge of balancing competing hemodynamic goals if pre-eclampsia co-exists. RCVS outcomes are positive: A retrospective study (of all ages) with RCVS demonstrated over 90% of patients have a good outcome, with 97.5% of patients functionally independent at follow up.

What to avoid; hypotensive episodes, glucocorticoid use (worse outcomes), SSRI's/triptans (associated with worsening vasospasm/new neurological deficits (but not worse outcomes)).