Author Affiliations: Stroke Division, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Dr Nakagawa is now with the University of California, San Francisco.
To report the very early magnetic resonance imaging features of eclampsia.
Inpatient neurology service.
A 35-year-old woman who developed late postpartum eclampsia with cerebral edema, caudate hemorrhage, and ischemic strokes.
Main Outcome Measure
Very early magnetic resonance imaging features.
Magnetic resonance imaging with gadolinium showed posterior sulcal hyperintensity and leptomeningeal enhancement preceding the development of posterior reversible encephalopathy syndrome, hemorrhage, and ischemic strokes by days.
Magnetic resonance imaging with gadolinium shows early characteristic findings that precede the more classic clinical presentation of eclampsia.
Eclampsia is a complex hypertensive disorder of pregnancy, commonly affecting the central nervous system. Cerebrovascular involvement is the direct mechanism of death in 40% of patients.1 Typical brain magnetic resonance imaging (MRI) findings in eclampsia, including vasogenic edema with T2 hyperintensity in the posterior subcortical and deep white matter, are also characteristic of posterior reversible encephalopathy syndrome (PRES).2- 5 Less commonly, postpartum angiopathy with segmental vasoconstriction can manifest as ischemia with cytotoxic edema or hemorrhage.6- 8 Approximately 44% of late postpartum eclampsia, defined as occurring more than 48 hours but less than 4 weeks postpartum, fails to manifest the hypertension, pedal edema, and proteinuria of preeclampsia prior to convulsion,9 which makes early diagnosis difficult.
We describe the very early MRI changes of posterior sulcal hyperintensity and leptomeningeal enhancement as the first radiological sign, preceding the development of postpartum eclamptic PRES, hemorrhage, and ischemic strokes by days.
A 35-year-old woman (gravida 3, para 3) with previous migraines had an uncomplicated term vaginal delivery with spinal epidural anesthesia. Seven days postpartum, she developed severe left-sided headache accompanied by photophobia, phonophobia, nausea, and a fever. At 10 days postpartum, she was seen in the emergency department with a fever of 102.3°F and blood pressure of 160/82 mm Hg. She had no proteinuria or peripheral edema. Cerebrospinal fluid values for white blood cells were 1/mm3; red blood cells, 73/mm3; and protein, 42 mg/dL. Magnetic resonance imaging showed mild sulcal hyperintensity on fluid-attenuated inversion recovery (FLAIR) sequences and leptomeningeal enhancement on postgadolinium T1 sequences in the posterior parietal, temporal, and occipital lobes (Figure 1). There was no venous occlusion on a magnetic resonance venogram. Fourteen days postpartum, she was found unresponsive, with blood pressure of 200/100 mm Hg. Brain computed tomography (CT) and MRI showed left caudate hemorrhage with intraventricular extension and diffuse vasogenic edema in the bilateral posterior parietal, occipital, and frontal subcortical white matters (Figure 2). Computed tomography angiogram showed no evidence of vasoconstriction or vascular malformation. She developed refractory hypertension requiring intravenous magnesium sulfate and multiple antihypertensive agents. An external ventricular drain was placed, and hyperosmolar therapy was started for elevated intracranial pressure (peak intracranial pressure, 37 mm H2O). A brain CT 29 days postpartum showed hypodensities consistent with cerebral infarction in the bilateral proximal anterior cerebral artery territories that were absent 3 days prior. Repeated CT angiogram did not show any evidence of major arterial vasoconstriction or occlusion. She was disinhibited and severely inattentive and had both anterograde and retrograde amnesia. Five months later, the MRI showed evolution of the bilateral anterior cerebral artery territory infarctions and complete resolution of the subcortical vasogenic edema (Figure 3).
Magnetic resonance imaging fluid-attenuated inversion recovery on postpartum day 10 showing sulcal T2 hyperintensity in the posterior parietal, temporal, and occipital lobes (A and B). Postgadolinium T1 image showing leptomeningeal enhancement in the corresponding area (C and D).
Noncontrast head computed tomography on postpartum day 14 showing left caudate hemorrhage with intraventricular extension and bilateral frontal, parietal, and occipital lobe vasogenic edema (A and B). Magnetic resonance imaging fluid-attenuated inversion recovery on postpartum day 18 showing vasogenic edema in the corresponding area (C and D).
Magnetic resonance imaging fluid-attenuated inversion recovery after 5 months showing resolution of the vasogenic edema and evolution of the bilateral anterior cerebral artery territory infarctions.
This patient had subtle MRI findings 4 days before the appearance of more typical eclamptic PRES and intracerebral hemorrhage. The early findings were sulcal hyperintensity on the FLAIR sequence and leptomeningeal enhancement by gadolinium. There was no cerebrospinal abnormality, such as subarachnoid hemorrhage or meningitis, to account for the increased T2 signal in the subarachnoid space. Although the first MRI was obtained 10 hours after the lumbar puncture, the absence of dural enhancement makes it unlikely that the findings were the result of low pressure.10 Alteration of the regional hemodynamics from congestion, inflammation, or slow flow has been suggested as the cause of sulcal hyperintensity on FLAIR imaging.11 Furthermore, endothelial damage associated with eclamptic PRES12 may contribute to the increased blood-brain barrier permeability, thus causing leptomeningeal enhancement.
We conclude that MRI with contrast may show characteristic findings of sulcal hyperintensity and leptomeningeal enhancement in early preeclampsia that could precede the more classic clinical presentation, such as hypertension, proteinuria, brain edema, or seizure. These early imaging characteristics support the hypothesis that regional changes in cerebral hemodynamics and blood-brain barrier permeability, independent of blood pressure, may play a major role in the pathogenesis of cerebrovascular manifestation of eclampsia. Identifying these characteristic MRI findings in the appropriate clinical setting may lead to earlier recognition and prompt treatment of eclampsia.
Correspondence: Kazuma Nakagawa, MD, UCSF Neurovascular Service, 505 Parnassus Ave, San Francisco, CA 94143 (firstname.lastname@example.org).
Accepted for Publication: October 12, 2007.
Author Contributions:Study concept and design: Nakagawa and Ropper. Acquisition of data: Nakagawa and Ropper. Analysis and interpretation of data: Nakagawa, Sorond, and Ropper. Drafting of the manuscript: Nakagawa and Ropper. Critical revision of the manuscript for important intellectual content: Sorond and Ropper. Study supervision: Sorond and Ropper.
Financial Disclosure: None reported.
Thank you for submitting a comment on this article. It will be reviewed by JAMA Neurology editors. You will be notified when your comment has been published. Comments should not exceed 500 words of text and 10 references.
Do not submit personal medical questions or information that could identify a specific patient, questions about a particular case, or general inquiries to an author. Only content that has not been published, posted, or submitted elsewhere should be submitted. By submitting this Comment, you and any coauthors transfer copyright to the journal if your Comment is posted.
* = Required Field
Disclosure of Any Conflicts of Interest*
Indicate all relevant conflicts of interest of each author below, including all relevant financial interests, activities, and relationships within the past 3 years including, but not limited to, employment, affiliation, grants or funding, consultancies, honoraria or payment, speakers’ bureaus, stock ownership or options, expert testimony, royalties, donation of medical equipment, or patents planned, pending, or issued. If all authors have none, check "No potential conflicts or relevant financial interests" in the box below. Please also indicate any funding received in support of this work. The information will be posted with your response.
Some tools below are only available to our subscribers or users with an online account.
Download citation file:
Web of Science® Times Cited: 3
Customize your page view by dragging & repositioning the boxes below.
The Rational Clinical Examination: Evidence-Based Clinical Diagnosis
Original Article: Does This Patient Have a Torn Meniscus or Ligament of the Knee?
The Rational Clinical Examination: Evidence-Based Clinical Diagnosis
All results at
Enter your username and email address. We'll send you a link to reset your password.
Enter your username and email address. We'll send instructions on how to reset your password to the email address we have on record.
Athens and Shibboleth are access management services that provide single sign-on to protected resources. They replace the multiple user names and passwords necessary to access subscription-based content with a single user name and password that can be entered once per session. It operates independently of a user's location or IP address. If your institution uses Athens or Shibboleth authentication, please contact your site administrator to receive your user name and password.