Dural Puncture Headache, Postpartum Angiopathy, Pre-Eclampsia and Cortical Vein Thrombosis After an Uncomplicated Pregnancy

A 37-year-old gravida 2, para 2 woman developed a severe bi-frontal non-throbbing postural headache a few minutes after receiving epidural anaesthesia for labour. Her pregnancy was uncomplicated. There was no prior history of migraine, clotting disorders, or exposure to vasoactive drugs. The headaches persisted and she was treated with an epidural blood-patch on day 1 post-delivery for a presumptive diagnosis of low-pressure headache. The character of her headache changed from dull aching to constant throbbing. It now involved her entire head, was accompanied by nausea and vomiting, and did not have obvious precipitating or relieving factors. A non-contrast CT scan on day 4, performed at an outside hospital, was reportedly normal. Over the next 2 days she developed horizontal diplopia and right leg weakness. On day 6, a repeat non-contrast head CT scan showed a new small left posterior frontal hyperdensity, and she was transferred to our hospital. On admission she was afebrile, her blood pressure was 141/63 mmHg (different from her baseline of 120 mmHg systolic), and she had mild nonpitting leg oedema. Her neurological exam showed a right partial sixth nerve paresis, proprioceptive loss in the right lower extremity, and a wide-based gait with inability to tandem walk. Complete blood count and erythrocyte sedimentation rate were normal. Serum chemistries were notable for potassium 2.6 mmol/l, magnesium 1.4 mEq/l, and albumin 2.8 g/dL. Urine proteins were elevated at 2290 mg/l (normal, 0–135 mg/l). Repeat head CT with CT-angiography and CT-venography findings were consistent with a left posterior parietal infarction with an adjacent cortical vein thrombosis affecting the vein of Trolard (reported as a left frontal hyperdensity on the prior CT scan). In addition there was segmental narrowing and dilatation (‘beading’) of the bilateral middle, anterior and posterior cerebral arteries and their branches (Figure 1). Brain MRI showed similar findings: diffusion-weighted images showed a subacute infarct involving the left post-central gyrus; susceptibility images showed cortical vein thrombosis, and MRA showed beading in the proximal circle of Willis arteries (Figure 1). On fluid-attenuated inversion recovery (FLAIR) images, cortical vessels appeared hyper-intense, suggesting slow flow within segments of abnormally dilated vessels overlying the cortical surface as previously described in patients with cerebral vasoconstriction syndromes (1). Hypercoagulation panel tests (protein C, protein S, and antithrombin III levels, activated protein C resistance test, homocysteine, plasminogen, prothrombin gene mutation 20210 A, alpha 2 antiplasmin, tissue plasminogen activator inhibitor, and antiphospholipid antibody levels) were negative. Antinuclear antibodies were positive (1:320, speckled pattern); however, other tests for vasculitis were negative. On day 9, a repeat urinalysis showed no abnormality (urine protein level now 120 mg/l, Bence Jones proteins negative). The patient was treated with anticoagulation for cortical vein thrombosis (intravenous heparin transitioned to warfarin for 3 months). Her leg weakness resolved, the headache resolved gradually, and she was discharged on postpartum day 10. One week later, a repeat CT-angiogram and CT-venogram showed resolution of the cortical vein thrombosis and the postpartum angiopathy. When seen in follow-up (day 40 after delivery), her sixthnerve paresis and right leg proprioceptive deficits had resolved completely. doi:10.1111/j.1468-2982.2007. 01285.x