Acute neurologic symptoms in pregnant and postpartum women may be caused by exacerbation of a preexisting neurologic condition, the initial presentation of a non–pregnancy-related problem, or a new neurologic problem. Pregnant and postpartum patients with headache and neurologic symptoms are often diagnosed with preeclampsia or eclampsia; however, other etiologies must also be considered. A team approach with close communication between emergency physicians, neurologists, maternal–fetal medicine specialists, and radiologists is the key to obtaining best outcomes. This article reviews the clinical features and differential diagnosis of acute serious neurologic conditions in pregnancy and the puerperium, focusing on diagnosis.
Key points
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Pregnant and postpartum patients with headache and seizures are often diagnosed with preeclampsia or eclampsia because they are the most common conditions; however, other etiologies must be considered.
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Most cases of cerebral venous sinus thrombosis present in the early postpartum period.
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Although stroke and other cerebrovascular diseases are uncommon in pregnant women, the incidence is higher than in age and sex-matched nonpregnant individuals.
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Computed tomography scanning is insensitive to many of the acute neurologic conditions that affect pregnant and postpartum women.
Introduction
Acute neurologic symptoms in pregnant and postpartum women may be owing to an exacerbation of a preexisting neurologic condition (eg, multiple sclerosis or a known seizure disorder) or to the initial presentation of a non–pregnancy-related problem (eg, a new brain tumor). Alternatively, patients can present with new, acute onset neurologic conditions that are either unique to or precipitated by pregnancy.
In this review, we focus on these latter conditions. The most common diagnostic tool used in emergency medicine to evaluate many of these symptoms—noncontrast head computed tomography (CT)—is often nondiagnostic or falsely negative. Misdiagnosis can result in morbidity or mortality in young, previously healthy individuals. Therefore, if a poor outcome occurs, the medical, social, and medicolegal impact is usually high. For all of these reasons, prompt diagnosis is imperative.
The unique pathophysiologic states of pregnancy and the puerperium have been reviewed. Increasing concentrations of estrogen stimulate the production of clotting factors, increasing the risk of thromboembolism. Increases in plasma and total blood volumes increase the risk of hypertension. Elevated progesterone levels in pregnancy increase venous distensibility and, potentially, leakage from small blood vessels. The high estrogen levels decrease in the postpartum period. Combined, these hormonal changes can result in increased permeability of the blood–brain barrier and vasogenic edema.
Preeclampsia, the new onset of hypertension and proteinuria or laboratory abnormalities after 20 weeks in a previously normotensive woman, occurs in 2% to 8% of pregnancies. The incidence of preeclampsia has increased by 25% in the United States over the last 20 years, which has been attributed in part to the increase in maternal obesity and maternal age. Diagnostic criteria for preeclampsia were recently revised. Whereas previously preeclampsia was defined by systolic blood pressures of 140/90 mm Hg or greater and proteinuria of 0.3 g or greater of protein in a 24-hour urine specimen, the new criteria allow for the diagnosis of preeclampsia without proteinuria, permit the use of a spot protein/creatinine ratio or urine dip to diagnose preeclampsia, and rename what was previously called “mild preeclampsia” as “preeclampsia without severe features,” among other changes. Preeclampsia is now defined as blood pressures of 140/90 mm Hg or greater on 2 occasions at least 4 hours apart after 20 weeks of gestation in a woman with a previously normal blood pressure, plus either proteinuria, or in the absence of proteinuria, thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, or new-onset neurologic symptoms such as visual changes or headache. In practical terms, this means any woman with persistently increased blood pressure and a persistent new headache meets diagnostic criteria for preeclampsia, and the headache would confer the diagnosis of preeclampsia with severe features. However, other neurologic conditions requiring significantly different management than preeclampsia should be considered in these cases. Of note, the revised criteria state that severe range blood pressures (those ≥ 160/110 mm Hg) “can be confirmed within a short interval (minutes) to facilitate timely antihypertensive therapy,” to stress that antihypertensive therapy should not be delayed in these women to confirm a diagnosis.
Eclampsia is defined as preeclampsia plus a generalized tonic–clonic seizure in the absence of other conditions that could account for the seizure. Eclamptic seizures occur in up to 0.6% of women with preeclampsia without severe features, and in 2% to 3% of women with preeclampsia with severe features. Of note, eclampsia rarely can present atypically, without elevated pressures or proteinuria so it should remain on the differential for women with new-onset seizures in pregnancy even if the classic criteria of hypertension and proteinuria or laboratory abnormalities are not satisfied. Maternal mortality rates for eclamptic women have been reported to be as high as 14% over the past few decades, with the highest rates in developing countries. Although the most common causes of death in eclamptic women are brain ischemia and hemorrhage, most eclampsia-related neurologic events are transient, and long-term deficits are rare in properly managed patients.
However, other conditions, which overlap with eclampsia and with each other, can present similarly. These include acute ischemic stroke (AIS), intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), and cerebral venous sinus thrombosis (CVT). Severe vasoconstriction often develops in women with preeclampsia, especially when the blood pressure is poorly controlled. This vasoconstriction can cause brain infarction and/or hemorrhage. A reversible cerebral vasoconstriction syndrome (RCVS)—also referred to as postpartum angiopathy and Call–Fleming syndrome—can develop during the puerperium without hypertension or other features of preeclampsia. Preeclampsia, eclampsia and RCVS can all be complicated by the posterior reversible encephalopathy syndrome (PRES). In fact, 8% to 39% of patients with RCVS have PRES as well. PRES is a clinical (headache, seizures, encephalopathy, and visual disturbances) and imaging (reversible vasogenic edema) syndrome that may occur in preeclampsia/eclampsia, RCVS, and other conditions. It is essential to recognize the significant overlap between these various etiologies, which can occur independently or simultaneously. Whereas eclampsia is specific to pregnancy, PRES, RCVS, and CVT also occur in nonpregnant individuals.
This review is intended to help clinicians avoid misdiagnosis in these high-risk patients. We therefore limit the review to clinical manifestations and diagnosis, because once a given diagnosis is established, specific treatments should naturally follow. We have organized the data by presenting symptoms as well as by specific diagnosis. Finally, we have created clinical algorithms based on our interpretation of the existing literature and our practice.
Introduction
Acute neurologic symptoms in pregnant and postpartum women may be owing to an exacerbation of a preexisting neurologic condition (eg, multiple sclerosis or a known seizure disorder) or to the initial presentation of a non–pregnancy-related problem (eg, a new brain tumor). Alternatively, patients can present with new, acute onset neurologic conditions that are either unique to or precipitated by pregnancy.
In this review, we focus on these latter conditions. The most common diagnostic tool used in emergency medicine to evaluate many of these symptoms—noncontrast head computed tomography (CT)—is often nondiagnostic or falsely negative. Misdiagnosis can result in morbidity or mortality in young, previously healthy individuals. Therefore, if a poor outcome occurs, the medical, social, and medicolegal impact is usually high. For all of these reasons, prompt diagnosis is imperative.
The unique pathophysiologic states of pregnancy and the puerperium have been reviewed. Increasing concentrations of estrogen stimulate the production of clotting factors, increasing the risk of thromboembolism. Increases in plasma and total blood volumes increase the risk of hypertension. Elevated progesterone levels in pregnancy increase venous distensibility and, potentially, leakage from small blood vessels. The high estrogen levels decrease in the postpartum period. Combined, these hormonal changes can result in increased permeability of the blood–brain barrier and vasogenic edema.
Preeclampsia, the new onset of hypertension and proteinuria or laboratory abnormalities after 20 weeks in a previously normotensive woman, occurs in 2% to 8% of pregnancies. The incidence of preeclampsia has increased by 25% in the United States over the last 20 years, which has been attributed in part to the increase in maternal obesity and maternal age. Diagnostic criteria for preeclampsia were recently revised. Whereas previously preeclampsia was defined by systolic blood pressures of 140/90 mm Hg or greater and proteinuria of 0.3 g or greater of protein in a 24-hour urine specimen, the new criteria allow for the diagnosis of preeclampsia without proteinuria, permit the use of a spot protein/creatinine ratio or urine dip to diagnose preeclampsia, and rename what was previously called “mild preeclampsia” as “preeclampsia without severe features,” among other changes. Preeclampsia is now defined as blood pressures of 140/90 mm Hg or greater on 2 occasions at least 4 hours apart after 20 weeks of gestation in a woman with a previously normal blood pressure, plus either proteinuria, or in the absence of proteinuria, thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, or new-onset neurologic symptoms such as visual changes or headache. In practical terms, this means any woman with persistently increased blood pressure and a persistent new headache meets diagnostic criteria for preeclampsia, and the headache would confer the diagnosis of preeclampsia with severe features. However, other neurologic conditions requiring significantly different management than preeclampsia should be considered in these cases. Of note, the revised criteria state that severe range blood pressures (those ≥ 160/110 mm Hg) “can be confirmed within a short interval (minutes) to facilitate timely antihypertensive therapy,” to stress that antihypertensive therapy should not be delayed in these women to confirm a diagnosis.
Eclampsia is defined as preeclampsia plus a generalized tonic–clonic seizure in the absence of other conditions that could account for the seizure. Eclamptic seizures occur in up to 0.6% of women with preeclampsia without severe features, and in 2% to 3% of women with preeclampsia with severe features. Of note, eclampsia rarely can present atypically, without elevated pressures or proteinuria so it should remain on the differential for women with new-onset seizures in pregnancy even if the classic criteria of hypertension and proteinuria or laboratory abnormalities are not satisfied. Maternal mortality rates for eclamptic women have been reported to be as high as 14% over the past few decades, with the highest rates in developing countries. Although the most common causes of death in eclamptic women are brain ischemia and hemorrhage, most eclampsia-related neurologic events are transient, and long-term deficits are rare in properly managed patients.
However, other conditions, which overlap with eclampsia and with each other, can present similarly. These include acute ischemic stroke (AIS), intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), and cerebral venous sinus thrombosis (CVT). Severe vasoconstriction often develops in women with preeclampsia, especially when the blood pressure is poorly controlled. This vasoconstriction can cause brain infarction and/or hemorrhage. A reversible cerebral vasoconstriction syndrome (RCVS)—also referred to as postpartum angiopathy and Call–Fleming syndrome—can develop during the puerperium without hypertension or other features of preeclampsia. Preeclampsia, eclampsia and RCVS can all be complicated by the posterior reversible encephalopathy syndrome (PRES). In fact, 8% to 39% of patients with RCVS have PRES as well. PRES is a clinical (headache, seizures, encephalopathy, and visual disturbances) and imaging (reversible vasogenic edema) syndrome that may occur in preeclampsia/eclampsia, RCVS, and other conditions. It is essential to recognize the significant overlap between these various etiologies, which can occur independently or simultaneously. Whereas eclampsia is specific to pregnancy, PRES, RCVS, and CVT also occur in nonpregnant individuals.
This review is intended to help clinicians avoid misdiagnosis in these high-risk patients. We therefore limit the review to clinical manifestations and diagnosis, because once a given diagnosis is established, specific treatments should naturally follow. We have organized the data by presenting symptoms as well as by specific diagnosis. Finally, we have created clinical algorithms based on our interpretation of the existing literature and our practice.
Headache
Roughly 40% of postpartum women have headaches, often during the first week. Primary headache disorders—tension type and migraine—are the most common causes in both pregnant and postpartum women. This can paradoxically make correct diagnosis more difficult unless physicians pay careful attention to “red flags” that suggest a secondary cause ( Fig. 1 B ). In 1 series, among 95 patients with severe postpartum headache, one-half had tension type (39%) or migraine (11%), followed by preeclampsia/eclampsia (24%) and postdural puncture headache (PDPH; 16%). Pituitary hemorrhage, mass lesions, and CVT each accounted for another 3%. This study was skewed toward sicker, hospitalized patients whose headaches were “resistant to usual therapy.”
In general, migraine improves during pregnancy and returns postpartum as estrogen levels decrease. Pregnant patients with new, worsening headaches, positional headaches, or headaches that have changed in character suggest the possibility of secondary causes. Although new migraines can develop during pregnancy, migraine should be considered a diagnosis of exclusion. Implicit in the diagnosis of migraine and tension-type headache is the presence of multiple episodes (≥5 episodes for migraine and ≥10 for tension-type headache). Therefore, one cannot definitively diagnose a first new headache that develops during pregnancy or the puerperium—or in any other patient for that matter—as a manifestation of a primary headache disorder.
Preeclamptic patients often have bilateral throbbing headaches accompanied by blurred vision and scintillating scotomata. Pregnant women with new headaches must be screened carefully for preeclampsia. Hypertension, epigastric or right upper quadrant abdominal pain, edema, increased deep tendon reflexes, proteinuria, and occasionally agitation or restlessness may accompany the headache. Laboratory findings that increase the concern for preeclampsia include thrombocytopenia, hemoconcentration, transaminitis, elevated creatinine, and elevated uric acid. Unfortunately, despite considerable research and progress, there is no current routinely available biomarker to definitively diagnose preeclampsia.
Patients with abrupt onset of a severe, unusual headache (“thunderclap headache”) require urgent investigation. Large studies evaluating the possible increased incidence of SAH in pregnant and postpartum patients report mixed results, possibly owing to varying methods of case acquisition, as well as the fact that some instances of SAH in these patients are nonaneurysmal. Hormonal changes affecting cerebral blood vessels and surges in blood pressure from pushing during labor are 2 potential mechanisms for an increased incidence of aneurysmal SAH. All patients presenting with a thunderclap headache require a thorough evaluation to exclude SAH, usually a head CT scan followed by lumbar puncture if the CT scan is nondiagnostic.
However, if the workup for SAH is negative, disorders such as PRES, CVT, RCVS, and cervicocranial arterial dissections must be considered in pregnant and postpartum patients who present with thunderclap headache ( Fig. 1 ). Because CT and lumbar puncture may both be negative in these latter conditions, physicians should strongly consider following up a nondiagnostic CT and lumbar puncture with MRI sequences including diffusion-weighted images as well as vascular studies of the arteries (MR angiogram) and veins (MR venogram). If arterial dissection is suspected, acquisition of T1 fat-saturated images should be considered to increase the sensitivity for detecting a thrombus within a dissection flap.
In patients who have had a spinal or epidural anesthetic, PDPH is an important consideration, and has been estimated to occur in 0.5% to 1.5% of these patients. Caused by low intracranial pressure owing to a cerebrospinal fluid leak, headaches, often nuchal and occipital, typically begin 1 to 7 days postpartum, rapidly worsen upon standing, and resolve upon lying flat over 10 to 15 minutes. Tinnitus, diplopia, and hypacusia may occur. Symptoms usually resolve within 48 hours of a blood patch. Patients who have not had a spinal or epidural anesthetic may also develop postpartum low-pressure headaches, presumably owing to dural tears from labor-related pushing.
Rare complications of PDPH include subdural hematoma, PRES, and CVT. Low intracranial pressure can cause subdural hematoma from the tearing of bridging veins that become taut as the brain sags. Clues to this complication include loss of the postural component of headache (owing to the offsetting effects of low intracranial pressure from the dural puncture and elevated pressure from the subdural hematoma) and lack of response to a blood patch.
Most serious causes of headache are more common postpartum than during pregnancy. Therefore, if migraine or PDPH is not likely based on the history and neurologic examination, physicians must consider these other etiologies.
Acute neurologic symptoms and deficits
Pregnant or postpartum patients who present with acute motor, sensory, or visual findings (with or without headache) may have more serious causes and require urgent, thorough evaluation (see Fig. 1 ). Pregnant patients with acute neurologic deficits most often have migraine with aura, even in the absence of headache (ie, acephalgic migraine). Two studies using different methods both found that of pregnant patients referred for transient motor, sensory or visual symptoms, the vast majority could be ultimately attributed to migraine with aura.
Historical clues for a migrainous etiology include gradual onset of the neurologic symptoms and positive phenomenon (such as brightness or shimmering) as opposed to negative ones (blackness or loss of vision). The gradual onset and slow progression over 15 to 30 minutes differentiates migrainous symptoms from those attributable to cerebral ischemia, which are typically maximal at onset, and seizure, which spread more rapidly (ie, over seconds). Another clue that may help to differentiate migraine from vascular thromboembolic disease is the pathophysiologic process of cortical spreading depression that is believed to cause migrainous neurologic deficits often crosses vascular territories. Migrainous positive phenomena (brightness or sparkling in vision, tingling or prickling feelings in the limbs or body) often leave in their wake transient loss of function (scotoma or numbness). Symptoms affecting 1 modality (eg, vision) may clear and then involve another modality (eg, sensation).
Because visual symptoms are common with preeclampsia, one must be cautious not to make that diagnosis without considering other possibilities such as PRES, pituitary apoplexy or tumor growth, and strokes affecting the visual pathways. Because pituitary adenomas (micro or macro) may grow during pregnancy, any woman with a known pituitary tumor and new onset of headache with or without diplopia and a bitemporal field cut should undergo emergent pituitary imaging. Another consideration is orbital hemorrhage, which presents as acute diplopia, proptosis, and eye pain, and can occur during the first trimester (from hyperemesis) or during labor (from pushing).
Overall, stroke in pregnant and postpartum women is rare; however, the risk is increased compared with nonpregnant age-matched controls, especially in late pregnancy and the early puerperium. Recent evidence suggests that the rate of pregnancy- and postpartum-associated strokes is increasing. This epidemiologic trend is true for patients with and without pregnancy-related hypertensive disorders. The event rates per 100,000 deliveries range from 4 to 11 (AIS), 3.7 to 9 (ICH), 2.4 to 7 (SAH), and 0.7 to 24 (CVT). These epidemiologic studies varied in their methodology ( Table 1 ). The wide range for CVT likely reflects variability in the case-finding definitions and radiologic modalities. Moreover, the extremely low stroke rate in the most recent study is likely owing to the fact that postpartum patients (the period of highest risk) were not included.
| Study, Year Published | AIS | ICH | SAH | CVT | Eclampsia | Comments (Methods, Total Deliveries, Years of Analysis) |
|---|---|---|---|---|---|---|
| Sharshar et al, 1995 | 4.3 | 4.6 | — | — | 47% of AIS 44% of ICH | Population-based regional French study 348,295 deliveries 1989–1991 |
| Kittner et al, 1996 | 11 | 9 | Excluded | — | 25% of AIS 15% of ICH | Population-based regional US study 141,243 deliveries 1988–1991 |
| Jaigobin & Silver, 2000 | 11.1 | 3.7 | 4.3 | 6.9 | 23% of AIS 38% of CVT 17% of ICH 0% of SAH | Referral single-center Canadian study 50,700 deliveries 1980–1997 |
| Lanska & Kryscio, 2000 b | 13 a | a | a | 12.1 | Not reported | US national inpatient database 1,408,015 deliveries 1993–1994 |
| Salonen Ros et al, 2001 | 4.0 | 3.8 | 2.4 | — | Not reported | Population-based national Swedish study 1,003,489 deliveries 1987–1995 |
| James et al, 2005 b | 9.2 | 8.6 | — | 0.7 | 15.7 c | US national inpatient database 8,322,799 deliveries 2000–2001 |
| Kuklina et al, 2011 b | 11 | 7 | 7 | 24 | Not reported | US national inpatient database 8,786,475 deliveries 2006–2007 |
| Scott et al, 2012 Note: included prenatal events only; see text | 0.9 d | 0.4 e | — | — | 11% of AIS 33% of ICH (preeclampsia and eclampsia) | United Kingdom national population-based cohort and nested case-control study 1,958,203 deliveries 2007–2010 |
a The 13 includes AIS, ICH and SAH in this study.
b Intrinsic to the studies using the US national database is a sampling of approximately 20% of patients. Therefore, the reported number of deliveries is an extrapolated number.
c The authors do not directly state which strokes are eclampsia-related but do include an International Classification of Disease, 9th edition (ICD-9) code for “pregnancy-related cerebrovascular events” separate from the ICD-9 codes for AIS, ICH, or CVT.
Preeclampsia/eclampsia plays an etiologic role in 25% to 50% of pregnant and postpartum patients with strokes: highest with ICH, lower in AIS, and lowest with CVT. Other stroke risk factors in these women include older age, African American race, congenital and valvular heart disease, hypertension, caesarian delivery, migraine, thrombophilia, systemic lupus erythematosus, sickle cell disease, and thrombocytopenia. In an analysis of 347 cases of fatal pregnancy-related strokes over a 30-year period in the United Kingdom, these patients accounted for 1 in 7 maternal deaths. Themes that emerged from analysis of these 347 fatal cases were failure to recognize and treat hypertension, delays in imaging owing to concerns about radiation exposure, delays in senior physician involvement, and diagnostic anchoring of “hysteria” or drug-seeking behavior.
Thrombocytopenia also suggests the HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) and thrombotic thrombocytopenic purpura (TTP), whose incidence is elevated in pregnancy and which can present with strokelike symptoms. These 2 conditions have very different clinical courses and management, so maternal–fetal medicine and hematology experts should be involved immediately in the evaluation, particularly if TTP is on the differential. One study of 1166 deliveries found 12 cases of HELLP syndrome of which 8 had neurologic complications—namely, seizures (4 patients), focal deficits (2 patients), and encephalopathy (2 patients). On imaging, 6 patients had PRES (3 with associated hemorrhages) and 2 had isolated ICH.
Another unusual cause of stroke in pregnant and postpartum women is cervicocranial arterial dissection. There may be an increasing frequency in pregnant and postpartum women, although comprehensive epidemiologic data are lacking. Patients with cervicocranial arterial dissections often present with isolated headache and/or neck pain without neurologic deficit, but they can also present with focal deficits owing to embolic strokes. There may be a predisposition for multiple vessel dissections. In the largest series of 8 postpartum cases, the only differences between postpartum cases and those occurring in nonpregnant/postpartum women were that simultaneous PRES, RCVS, and SAH were more often seen in the postpartum cases, again emphasizing the theme of overlapping clinical syndromes in these patients. The vast majority of these dissections occur postpartum.
Data from a small case series suggests that women with a prior cervical artery dissection without an underlying connective tissue disorder may not be at significantly increased risk for subsequent pregnancy-related dissections. Still, this series included only 11 women with completed pregnancies after the index event, only 1 of 11 had the initial event in the peripartum period, and 7 subsequent pregnancies were delivered by cesarean, suggesting possible confounding by indication, so the data must be interpreted with caution.
In patients with ICH and SAH, underlying structural lesions such as vascular malformations and aneurysms are relatively common. SAH that occurs around the circle of Willis suggests an aneurysm, whereas convexal SAH suggests RCVS or CVT (with or without an associated cortical vein thrombosis). Brain infarction and hemorrhage can result from many of the vasculopathies, including RCVS and preeclampsia. Finally, TTP, pituitary apoplexy, choriocarcinoma, amniotic fluid embolism, air embolism, and cardioembolism from postpartum cardiomyopathy are rare causes of stroke in this population. Sufficient diagnostic testing including vascular imaging must be performed in these patients to identify specific treatable causes.
Seizures
Pregnant or postpartum women with seizures can be grouped into 3 categories. The most common are patients with an established seizure disorder before pregnancy. Of note, again demonstrating the frequency of overlapping clinical syndromes, women with epilepsy before pregnancy have an increased likelihood of developing preeclampsia, and of progressing to eclampsia. The second group includes patients with a new non–pregnancy-related seizure disorder, such as a new seizure from an undiagnosed brain tumor or hypoglycemia. These pregnant and postpartum patients require the same systematic approach to a new seizure as in all seizure patients, but are not the focus of this review.
The third group has new seizures that are pregnancy related. Important causes include eclampsia, ICH, CVT, RCVS, PRES, and TTP. Seizures are very common in PRES and usually occur at presentation in the absence of prodromal symptoms, whereas in CVT seizures usually occur later and nearly always after headache. Head CT scans can be normal in each of these conditions. Seizures are much less common in RCVS.
Data are lacking to direct the initial workup in these patients. However, because of this wide differential diagnosis and lack of sensitivity of CT scanning, we believe that pregnant and postpartum patients with new-onset seizures, even those who have returned to baseline and are neurologically intact, should undergo sufficient workup, which usually includes MRI, to establish the cause of the seizure. Postpartum women, even those who are breastfeeding, should undergo the same neuroimaging study that would be done in any other patient for the same indication. For antepartum patients whose optimal neuroimaging would normally involve gadolinium, maternal–fetal medicine should be consulted to discuss the risks versus benefits of gadolinium administration in this setting.
Individual conditions
The clinical presentations of the specific conditions have considerable overlap and can coexist. However, the details (eg, characteristics of headache, evolution of symptoms over time, and frequency of some symptoms such as seizures or visual problems) can often help to distinguish among them ( Table 2 ).
| PRES | RCVS | CVT | Eclampsia | |
|---|---|---|---|---|
| Mode of onset | Rapid (over hours), usually postpartum | Abrupt, usually postpartum | Third trimester or postpartum. Symptoms often progress over days. | Antepartum, intrapartum or postpartum (10%–50%) |
| Prominent findings | Early prominent seizures Usually seizures plus at least other symptoms (stupor, visual loss, visual hallucinations) HA dull and throbbing, not thunderclap | Thunderclap HA, multiple episodes Seizures occur but much less so than in PRES Transient focal deficits (may become permanent in cases with ICH or infarction) | HA nearly universal at onset, generally progressive and diffuse, thunderclap in small minority Seizures occur in ∼40% Focal signs may develop later | Seizure, frequent visual symptoms and abdominal pain, hyperreflexia, hypertension, proteinuria |
| Evolution over time | Symptoms resolve over days to a week if blood pressure controlled | Dynamic process over time; as a general rule, HAs are common during first week, ICH during the second week and ischemic complications during the third week | Evolves over several days; nonarterial territorial infarcts and hemorrhages may develop | Can evolve (from preeclampsia) gradually or abruptly |
| CSF findings | Usually normal, may have slightly elevated protein | Often normal (unless complicated by SAH) but 50% will have slight pleocytosis and protein elevations | Opening pressure elevated ∼80% of cases ∼35%-50% will have slight elevations of protein or cells | Usually normal unless complicated by hemorrhage |
| Imaging aspects | CT positive in ∼50% of cases MR prominent T2-weighted and FLAIR abnormalities nearly always in the parietooccipital lobes but can involve other parts of the brain ICH in ∼15% of patients | CT usually normal (if no SAH) MR – 20% with localized convexal SAH CTA, MRA usually shows typical “string of beads” constriction of cerebral arteries DSA is more sensitive May have associated cervical arterial dissection Initial arteriogram may be negative | CT often negative MR may show nonarterial territorial infarcts Hemorrhage common MRV shows intraluminal clot flow voids Although MRV is preferred, CTV is also sensitive | Same as for PRES Some patients may have coincident AIS or ICH |
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