Case 36 A 42-year-old woman in her 41st week of pregnancy presented in the delivery ward with a mild holocephalic headache and slightly elevated blood pressure. She was diagnosed with pre-eclampsia and labor was induced without any complications, leading to the birth of a healthy child the following day. During delivery, she suffered from a new, severe bifrontal headache. Her systolic blood pressure was 160 mm Hg. Ten minutes after delivery, she developed dysarthria and left-sided hemiplegia. Her medical history was unremarkable and a pregnancy 2 years prior was uneventful. Cranial CT showed a right-sided subcortical dorsal striatocapsular hemorrhage of maximal 30 × 25 mm extension with only mild perifocal edema (Fig. B36.1). No other pathology was identified. CT angiography (CTA) revealed no arterial or venous abnormalities. Follow-up cranial CT 24 hours later remained almost identical. Digital subtraction angiography (DSA) did not offer any clues regarding the cause of bleeding. Specifically, no intracranial angiomas, fistulas, or aneurysms were identified. There was also no evidence of cerebral vasospasm (Fig. B36.2). Pre-eclampsia with pregnancy-related intraparenchymal hemorrhage (IPH). The patient was transferred to the neurology intensive care unit. Blood pressure control was achieved with urapidil, metoprolol, and dihydralazin. She remained stable from a cardiopulmonary perspective. Mild proteinuria remitted spontaneously and mild thrombocytopenia normalized within 4 days. Plasma coagulation screening was within normal limits. On neurologic examination, she was transiently disorientated and agitated and required sedation and neuroleptic medication. Clinically, a posterior encephalopathy was assumed. A second follow-up cranial CT showed that the size of the IPH had remained the same but there was a slight increase in focal edema. B-mode and color-mode imaging revealed no atherosclerosis and no evidence of carotid or vertebral artery dissection. Doppler spectrum analysis showed normal and symmetric flow signals in all extracranial brain-supplying arteries. Increased peak systolic flow velocities with a turbulent flow pattern were detected in all intracranial arteries: M2-middle cerebral artery (MCA) (left 289 cm/s, right 223 cm/s), M1-MCA (left 198 cm/s, right 182 cm/s), A1-ACA (left 187 cm/s, right 190 cm/s), P2-posterior cerebral artery (PCA) (left 135 cm/s, right 197 cm/s), carotid siphon (left 150 cm/s, right 220 cm/s), basilar artery (BA) (251 cm/s). No poststenotic distal flow pattern was observed in any artery (Fig. B36.3, Fig. B36.4, Fig. B36.5, Fig. B36.6). For peak systolic velocities, the Lindegaard Index (LI) was 3.2 on the left side and 1.6 on the right. Multilocular intracranial stenoses >50% in both M2-MCA and A1-ACA segments, in the right P2-PCA, and in the BA, and to a lesser extent in both carotid siphons, both M1-MCA segments, and the left P2-PCA segment, though these were not hemodynamically relevant. Additionally, right hemispheric hyperperfusion with uncertainty regarding a possible generalized hyperperfusion. Fig. B36.1 CT scan, axial plane. Right-sided dorsal striatocapsular hemorrhage (30 × 25 mm) with only mild perifocal edema. Fig. B36.2 DSA, left and right common carotid artery (CCA) injection, posteroanterior view. Superimposed image to facilitate overview of bilateral circulation, showing normal caliber of all intracranial arteries on day 2. Fig. B36.3 TCCS (transtemporal approach), left-sided insonation, axial midbrain plane. Left M1-MCA segment with increased flow velocity on day 5 (flow velocity 198/104 cm/s). Fig. B36.4 TCCS (transtemporal approach), left-sided insonation, axial midbrain plane. Left M2-MCA segment with increased flow velocity on day 5 (flow velocity 289/135 cm/s). Fig. B36.5 TCCS (transtemporal approach), left-sided insonation, axial midbrain plane. Left A1-ACA segment with increased flow velocity on day 5 (flow velocity 187/105 cm/s). The Doppler spectrum is inverted. Fig. B36.6 TCCS (transtemporal approach), right-sided insonation, axial thalamic plane. Right distal P2-PCA segment with increased flow velocity on day 5 (flow velocity 197/96 cm/s). The Doppler spectrum is inverted. Fig. B36.7 3D TOF-MRA, coronal maximal intensity projection (MIP). Multiple vessel narrowing suggestive of RCVS. Pronounced narrowing in the left carotid siphon (arrow), left PCA (arrowheads), and left distal M1-MCA near its bifurcation (large arrowhead). Note the long segmental tailored BA and the large artifact caused by the parenchymal hemorrhage. Fig. B36.8 3D TOF-MRA, sagittal MIP. Multiple vessel narrowing suggestive of RCVS. Visible are multisegmental PCA narrowing (large and small arrowheads), an A2-ACA narrowing (small arrow), and a narrowing of the carotid siphon (large arrow). Cerebral MRI confirmed IPH and ruled out secondary hemorrhagic transformation of ischemic stroke. No signs of posterior reversible encephalopathy syndrome (PRES) were seen. Time-of-flight MR-angiography (TOF-MRA) was considered to show only mild vessel irregularities. Retrospectively, multiple bilateral vessel narrowing was diagnosed in the anterior and posterior circulation (Fig. B36.7 and Fig. B36.8). Peak systolic flow velocities further increased in both M1-MCAs (left 258 cm/s, right 235 cm/s) and in the right A1-ACA (234 cm/s). Flow remained stable in the left M2-MCA, in the left A1-ACA and in both carotid siphons, whereas slightly decreased flow velocities were seen in the right M2-MCA (176 cm/s), right P2-PCA (140 cm/s), and left P2-PCA (106 cm/s). Raised systolic peak flow velocities were seen for the first time in the right A2-ACA (160 cm/s). The LI increased on the left side to 4.4 and on the right side to 2.5 (Fig. B36.9, Fig. B36.10, Fig. B36.11). Persisting multilocular intracranial stenoses with only mild modifications of graduation. Probably less hyperperfusion on the right side. Intracranial flow velocities declined slowly during the following week. Elevated systolic flow velocities were still seen in both M1-MCAs (left 178 cm/s, right 180 cm/s), in the left M2-MCA (120 cm/s), in both A1-ACAs (left 128 cm/s, right 157 cm/s), in one of the A2-ACAs (159 cm/s), and in the right P2-PCA (100 cm/s). The highest LI was measured on day 8 at 4.2 on the right side and 4.5 on the left side (not shown). Partial remission of intracranial vasoconstriction and complete remission of hyperperfusion. Following the initial detection of elevated blood flow velocities, calcium channel blockers were administered. The neuropsychologic deficits disappeared within 1 week and dysarthria and hemiparesis improved substantially. At hospital discharge, only a mild facial asymmetry and a slight disturbance of fine motor skills remained. The latter symptoms subsided completely during the following months. Follow-up MRI and MRA 6 months later revealed a residual posthemorrhagic parenchymal lesion on the right side. No vessel abnormalities were seen (not shown).
Postpartum Angiopathy (Reversible Cerebral Vasoconstriction Syndrome)
Clinical Presentation
Initial Neuroradiologic Findings
Conventional Angiography (Day 2)
Suspected Diagnosis
Clinical Course (1)
Questions to Answer by Ultrasound Techniques
Initial Neurosonologic Findings (Day 5)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
Neuroradiologic Findings (Day 6)
Follow-up Neurosonologic Findings (Day 6)
Transcranial Duplex Sonography
Conclusion
Follow-up Neurosonologic Findings (Days 7–17)
Transcranial Duplex Sonography
Conclusion
Clinical Course (2)
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