Skip Navigation LinksHome > February 2014 - Volume 20 - Issue 1, Neurology of Pregnancy > Neuroradiology in Women of Childbearing Age
CONTINUUM: Lifelong Learning in Neurology:
doi: 10.1212/01.CON.0000443835.10508.2b
Review Articles

Neuroradiology in Women of Childbearing Age

Bove, Riley M. MD; Klein, Joshua P. MD, PhD

Free Access
Article Outline
Collapse Box

Author Information

Address correspondence to Dr Joshua P. Klein, Department of Neurology, Room AB-124, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, jpklein@partners.org.

Relationship Disclosure: Dr Bove reports no disclosure. Dr Klein receives financial compensation for serving on the editorial boards of the Journal of Neuroimaging and AccessMedicine Neurology, and royalties from McGraw-Hill for Adams and Victor’s Principles of Neurology.

Unlabeled Use of Products/Investigational Use Disclosure: Drs Bove and Klein report no disclosures.

Collapse Box

Abstract

Purpose of Review

This review summarizes safety concerns associated with diagnostic neuroimaging in patients who are of childbearing age, focusing on diagnostic modalities and radiologic features of neurologic conditions encountered by pregnant women.

Recent Findings

During pregnancy, women experience a range of physiologic changes that can affect neurologic function. These include endocrine, hemodynamic, endothelial, immunologic, and coagulopathic changes that can alter susceptibility to stroke, subarachnoid hemorrhage, demyelination, venous thrombosis, and other neurologic conditions. Unique safety concerns are associated with imaging procedures performed to diagnose neurologic conditions that occur during pregnancy.

Summary

This review discusses the use of diagnostic neuroimaging, including administration of IV contrast, in pregnant women and in nonpregnant women of childbearing age.

Back to Top | Article Outline

INTRODUCTION: PREGNANCY AND NEUROLOGIC FUNCTION

During pregnancy, a range of physiologic changes occur that impact neurologic function, including hemodynamic, endocrine, immune, metabolic, and other adaptations to accommodate the needs of the fetus.1 These physiologic adaptations alter the risk of neurologic disorders during pregnancy. An appreciation of gestational physiology can aid the clinician in distinguishing between more typical pregnancy-associated changes in neurologic symptoms and concerning neurologic changes requiring further evaluation. For example, while the gradual onset of low back pain and urinary stress incontinence may be common in the later stages of pregnancy, an abrupt onset of back pain and urinary retention may warrant imaging of the spine.

Back to Top | Article Outline

SAFETY OF IMAGING PROTOCOLS

Exposure to ionizing radiation from CT and strong magnetic fields from MRI, with or without use of contrast, carry potential risks to the pregnant patient and her conceptus. The choice of diagnostic modality to evaluate neurologic disorders in the pregnant patient should aim to provide the patient with the standard of care for diagnosis and treatment while minimizing potential risks to her conceptus. The evidence-based and comprehensive practice guidelines and recommendations established by independent consensus panels of the American College of Obstetricians and Gynecologists (ACOG),2 the American College of Radiology (ACR),3 and the European Society of Urogenital Radiology (ESUR)4 for the use of these diagnostic modalities during pregnancy are largely concordant. Specific indications, risks, and benefits from any diagnostic modality should be discussed with the pregnant patient and her other caregivers (obstetrician and radiologist) whenever possible, and this discussion should be documented in the medical record. Elective imaging should be deferred to the postpartum period.

Back to Top | Article Outline
Computed Tomography

Harm to fetus. The risks of exposure to ionizing radiation associated with CT can be categorized as stochastic versus deterministic. Stochastic effects, including mutagenesis and childhood malignancies, may theoretically occur after any amount of radiation exposure. Given these effects, the “as low as reasonably achievable” paradigm encourages limitation of radiation.2 In contrast, deterministic effects (such as cataract formation and infertility) are associated with specific exposure thresholds.

Radiation threshold for conceptus injury. Three research settings—all associated with much greater radiation exposure than is used clinically today—have provided most of the guidance regarding the risk of gestational exposure. These settings include (1) observational studies of human survivors of the Hiroshima and Nagasaki atomic bombs, (2) observational studies of patients exposed to radiation before the advent of concerns about radiation safety during pregnancy, and (3) experimental studies in animals. These have shown that the effects of radiation depend on the dose of radiation absorbed, the rate of dose absorption, and fetal gestational age (Table 1-1).3,5,6

Table 1-1
Table 1-1
Image Tools

Dose considerations. Low-dose irradiation to the fetus has been linked to an increased risk of childhood cancer, particularly leukemia.7 The baseline rate of childhood leukemia, 3.6 per 10,000 children, increases to 5 per 10,000 after in utero exposures of 1 to 2 rad (unit of absorbed dose equal to 0.01 Gy; the Gy, or gray, is the International System of Units base unit for absorbed dose of ionizing radiation, in joules [J]/kg). A meta-analysis showed a 6% increase in risk of childhood cancer per 100 rad.7 Even with repeated imaging, however, such exposures would not be achieved; therefore, the attributable risk of childhood cancer from modern clinical imaging is believed to be low.

Rate of absorption. During the entire gestation, fetal exposure to background environmental radiation is estimated at 0.23 rad.6 With CT, the dose absorbed by the fetus varies based on maternal size, examination parameters, and whether it receives direct rather than indirect radiation.

Fetal exposure to indirect radiation occurs with imaging of the maternal head or cervical spine; the fetus is exposed only to attenuated scattered radiation through the mother’s body, with a dose estimated at less than 0.01 rad.6 Fetal exposure to direct radiation occurs with imaging of the maternal lumbar spine or pelvis. The fetus in this case may be exposed to direct radiation at higher doses: 0.28 rad to 2.4 rad for a lumbar spine CT and up to 3 rad for an abdomen/pelvis CT.6 Attention to patient positioning and beam collimation parameters can minimize fetal exposure to direct radiation.

Gestational age considerations. Conception to implantation (days 0 to 15) is the period of highest risk, with an all-or-nothing effect: animals exposed to radiation during this period experience either death or no consequences; atomic bomb survivors exposed before 15 days gestational age had no sequelae. An increased risk of miscarriages through week 4 is usually cited.3 During organogenesis (weeks 3 through 8), an increased risk of congenital malformations, transient growth retardation, and neonatal death is noted in animal studies. Human fetuses exposed to medical irradiation during this period also manifested malformations, but in atomic bomb survivors, only dose-dependent microcephaly was noted.8 Although malformations have not been noted in the fetal period (week 6 until birth), the risk of mental retardation associated with irradiation is increased during this period. In the most sensitive period, from 8 to 15 weeks, a 12-rad to 20-rad dose threshold (much higher than used in clinical imaging) is associated with an increased risk of mental retardation; this risk is 4 times greater than in the period from 15 to 25 weeks, beyond which the risk is negligible.3

Patient management and counseling. Whenever possible, radiologists should consider estimated radiation doses and either adjust preset parameters or dynamically reduce doses based on habitus to limit the radiation exposure in the pregnant patient. Advanced image reconstruction techniques may offer alternative sources of diagnostic images that limit the need for additional radiation exposure. Imaging parameters, including estimated dose received, should be included in all CT reports and become part of the patient’s medical record. If necessary, a radiation dosimetry expert can assist in calculating the total dose to which the fetus was or will be exposed.2 Eventually, investigations of these data may provide better information about the impact of current diagnostic imaging and fetal outcomes.

Pregnant women who have been exposed to radiation or for whom imaging is planned should be counseled that no definitive association between radiation exposure of less than 5 rad (50 mGy) and an increased risk of spontaneous abortion, developmental malformations, or mental retardation has been proven. A very small association exists between radiation and childhood malignancies. Fetal-absorbed doses of 5 rad to 15 rad (50 mGy to 150 mGy) may result in a small but detectable increase in the risk of congenital defects above the baseline population risk of 5% to 10% of births.3

Safety of iodinated contrast. The use of IV iodinated contrast should be avoided during pregnancy if possible. Iodinated contrast is classified by the US Food and Drug Administration (FDA) as class B (Appendix A). Animal studies have not shown teratogenic or mutagenic outcomes from iodinated contrast exposure,9 and well-controlled studies have not been performed in humans; however, iodinated contrast instilled directly into the fetal cavity (as opposed to intravenously) has been associated with neonatal hypothyroidism. Therefore, if iodinated contrast administration cannot be deferred until after delivery, written informed consent should be obtained3 and neonatal thyroid function testing should be performed in the first week of life.10 If contrast is to be used, standard precautions pertaining to the risk of contrast-induced nephropathy should be followed. During lactation, no adverse effect on the infant of the low concentrations of iodinated contrast transmitted in breast milk has been proven.2,4 A 24-hour period of “pump and dump” interruption from breast-feeding may be preferred by the nursing mother but is not indicated.

Back to Top | Article Outline
Magnetic Resonance Imaging

Harm to fetus. To date, no conclusive evidence has shown that MRI exposure up to 3 Tesla is associated with fetal harm.3,11 Theoretical concerns include noise exposure, positioning within strong magnetic fields, and increase in body temperature caused by radiofrequency pulse energy deposition. Fetal MRI is routinely used when reliable fetal imaging cannot be obtained by ultrasonography, according to practice guidelines established by the ACR and the Society of Pediatric Radiology.3 While MRI of the mother or fetus can be safely obtained when clinically indicated, elective imaging should be deferred to the postpartum period if possible.

Safety of gadolinium-based contrast. During pregnancy, the use of gadolinium should be avoided unless it is likely to result in changes in management that would directly benefit the patient or fetus.3,4 Gadolinium contrast is classified by the FDA as class C. In animal studies, maternal exposure to concentrations of gadolinium higher than typically administered in humans has been associated with abortion and developmental abnormalities, and gadolinium can enter fetal circulation.9 When gadolinium use cannot be avoided, informed written consent, including a risk-benefit analysis, should be obtained. If gadolinium contrast is to be used, one should be aware of the possibility of nephrogenic systemic fibrosis (a rare condition that can occur in patients with underlying renal insufficiency who are exposed to gadolinium) developing in the mother.

During lactation, gadolinium is probably safe to use in the mother without concern for direct toxicity or allergic reaction to the neonate, as no adverse outcome has been documented from the very low estimated delivery of gadolinium via breast milk.4 A 24-hour period of “pump and dump” interruption from breast-feeding is suggested by the ESUR4 but not by the ACOG or ACR.2,3

Back to Top | Article Outline

RADIOGRAPHIC CHARACTERISTICS OF NEUROLOGIC CONDITIONS ASSOCIATED WITH PREGNANCY

Ischemic Stroke

Changes to the cardiovascular, hematologic, and endocrine systems, including volume expansion and estrogenic stimulation of blood-clotting factors, occur during pregnancy. Consequently, risk of ischemic stroke is increased in the peripartum and first 6 weeks postpartum periods,12,13 but interestingly, not earlier during the gestational period. Pregnancy-specific causes of ischemic stroke may include preeclampsia/eclampsia, paradoxical embolism from deep vein thrombosis through a patent foramen ovale, trophoblastic embolism, amniotic fluid embolism, air embolism, and cardioembolism from postpartum cardiomyopathy.

The imaging appearance of ischemic stroke is the same as in nonpregnant patients. On CT, the earliest changes from ischemia include loss of gray-white matter differentiation and subtle swelling of infarcting tissue, mostly due to cytotoxic edema. As an ischemic stroke evolves, hypoattenuation of infarcting tissue due to mixed cytotoxic and vasogenic edema is seen, often with mass effect on adjacent structures (ie, sulcal and ventricular effacement). During the subacute period, petechial hemorrhage (hyperattenuation) within the infarcted tissue can be seen, reflecting reperfusion of infarcted tissue after clot dissolution. Chronic infarctions appear hypodense on CT, with accompanying parenchymal volume loss.

With MRI, diffusion-weighted imaging (DWI) sequences can detect reduced diffusivity of water due to cytotoxic edema in acute infarctions within minutes of the onset of ischemia. As an infarct evolves, mixed cytotoxic and vasogenic edema appears hyperintense on T2-weighted sequences and hypointense on T1-weighted sequences. As with CT, petechial hemorrhage can be detected in subacute infarcts, often appearing hyperintense on T1-weighted sequences (due to methemoglobin) and hypointense on gradient echo and susceptibility-weighted sequences. Chronic infarctions appear hypointense on T1-weighted sequences and hyperintense on T2-weighted sequences, with accompanying parenchymal volume loss.

Amniotic fluid embolism, arising from passage of amniotic fluid, fetal cells, and other organic matter into the maternal circulation, occurs in 1 in 20,000 deliveries and can lead to cardiorespiratory collapse, anaphylaxis (anaphylactoid syndrome of pregnancy), and coagulopathy. Neurologic sequelae include focal deficits, seizures, and coma. Mortality occurs in at least one-quarter of cases and accounts for 5% to 10% of maternal mortality in the United States.14 MRI, while nonspecific, may reveal multiple foci of abnormal T2 hyperintensity and reduced diffusivity, as seen in thromboembolic infarctions.

Back to Top | Article Outline
Cerebral Venous Thrombosis

The risk of cerebral venous thrombosis (CVT) in pregnancy is increased, although pregnancy-associated CVT has a better prognosis than CVT from other etiologies. In the first trimester, the risk may be attributed to underlying thrombophilia, but the risk is most increased in the first 4 to 8 weeks postpartum.15 Contributing factors include dehydration, cesarean delivery or traumatic delivery, intracranial hypotension from dural puncture during neuraxial anesthesia, anemia, raised homocysteine levels, or other etiologies. Patients present with severe, diffuse, and constant headaches; these are typically progressive but may also present as thunderclap headaches. Other manifestations include encephalopathy, seizures, papilledema, and focal neurologic deficits. Additionally, 20% to 40% of patients with CVT have intracranial hypertension and thus can present with symptoms mimicking idiopathic intracranial hypertension.16

Infarctions may occur as a result of venous outflow obstruction with consequent increase in venous pressure relative to arterial pressure. These infarctions do not respect arterial territories and may be peripheral; in the case of CVT in the deep cerebral veins, bilateral thalamic infarctions may occur. Because of differences in mechanism, venous infarctions are often surrounded by more edema than would be expected from an arterial infarct. Parenchymal and subdural hemorrhage may also occur as a result of CVT. Clinical symptoms from CVT may fluctuate as a result of variability in collateral drainage, partial recanalization of thrombosed veins or dural sinuses, and fluctuating parenchymal changes (vasogenic and cytotoxic edema).

Because of the potential risks of CVT to mother and fetus, adequate diagnostic workup is essential. MRI is the preferred imaging modality to identify CVT in pregnant patients for several reasons (Case 1-1). First, the use of noncontrast-based vessel imaging techniques such as time-of-flight (TOF) MR angiography allows for an assessment of the patency of the cerebral veins and dural sinuses without exposing the mother or conceptus to IV contrast. Second, MRI sequences, particularly DWI, are more sensitive than CT for detecting acute infarctions. Finally, MRI spares the conceptus exposure to ionizing radiation.

Back to Top | Article Outline
Case 1-1

Four days after cesarean delivery, a 33-year-old woman presented with left hemianesthesia followed by a generalized seizure. Anticonvulsive treatment was started. As the differential for new onset of neurologic deficits and seizures in the postpartum period included cerebral venous thrombosis, posterior reversible encephalopathy syndrome, and eclampsia potentially complicated by hemorrhage, MRI was selected as the most sensitive imaging modality of the brain parenchyma and vasculature. Sagittal and axial T1 MRI (Figure 1-1A and Figure 1-1B) performed 1 day after presentation showed focal thrombosis (T1 hyperintensity) of a cerebral vein overlying the right parietal lobe. Subtle loss of cortical gray-white matter differentiation was evident in the gyrus adjacent to the thrombosed vessel. On axial T2 fluid-attenuated inversion recovery (FLAIR) MRI (Figure 1-C), the thrombosed vessel appeared hyperintense, suggesting that the blood had degenerated into methemoglobin. Abnormal T2 hyperintensity consistent with vasogenic edema was also noted within the juxtacortical white matter of the adjacent postcentral gyrus. Gradient echo (GRE) imaging (Figure 1-1D) showed abnormal hypointensity in the thrombosed cortical vein as well as within the postcentral gyrus and sulcusthat was consistent with blood products. No diffusion abnormalities were present to suggest venous infarction. Patent arteries and veins should appear hypointense on both T1-weighted and T2-weighted sequences as a result of flow voids due to movement of molecules during image acquisition.

Figure 1-1
Figure 1-1
Image Tools

Comment. The findings of focal venous thrombosis, surrounded by edema and some hemorrhage, support the clinical picture of focal neurologic deficits and seizures, and are consistent with cerebral venous thrombosis. The risk for cerebral venous thrombosis is increased during pregnancy, particularly in the first 4 to 8 weeks postpartum. MRI is the most sensitive diagnostic modality.

Typical findings on MRI include the following16:

  • TOF venography allows for visualization of blood flow through the cerebral veins and dural venous sinuses and is typically acquired in thin slices. If interruption of flow through any of these structures occurs, a lack of flow-related signal will be evident on this sequence. Since veins and sinuses are under low pressure, reduced or absent signal on TOF does not absolutely imply thrombotic occlusion.
  • Absence of normal hypointense vascular flow voids in the cerebral veins and venous sinuses on T1-weighted and T2-weighted sequences can be associated with thrombosis or slow flow. The MRI appearance of thrombus within a cortical vein depends on its age, similar to the appearance of an evolving intraparenchymal hematoma.
  • Focal hemorrhage appears hypointense on gradient echo (GRE) and susceptibility-weighted imaging (SWI) sequences.
  • Focal ischemia appears hyperintense on DWI and hypointense on the apparent diffusion coefficient (ADC) sequence.
  • Variable signal may be present on DWI and ADC, reflecting both vasogenic (enhanced diffusivity) and cytotoxic (reduced diffusivity) edema.

If MRI cannot be used, a noncontrast head CT, while often unrevealing, may show a focal hyperdense venous sinus or cortical vein, or occasionally focal edema or parenchymal hemorrhage, diffuse cerebral edema, or subdural hemorrhage. If CT venography is used in the postpartum period,a thrombus in the superior sagittal sinus will appear hypodense relative to the surrounding hyperdense contrast-enhanced flowing blood and dura, producing the so-called empty delta sign as seen on axial and coronal images. Certain anatomic variants complicate the diagnosis of CVT on both MR venography and CT venography, such as sinus atresia/hypoplasia, asymmetric sinus drainage, and normal sinus-filling defects related to prominent arachnoid granulations or intrasinus septae.16

Back to Top | Article Outline
Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is the third leading cause of maternal death for reasons that are not related to obstetric complications. Recent reviews have suggested that, contrary to conclusions from prior studies, risk of SAH is not increased during pregnancy.17,18 Additionally, a greater proportion of SAH occurring during pregnancy may be nonaneurysmal and triggered by hypertension, disrupted cerebral autoregulation, or other etiologies. Contributing risk factors to SAH in pregnancy include advanced maternal age; advanced gestational age; underlying hypertension and disorders of coagulation; and tobacco, drug, or alcohol use.17 Patients with SAH typically present with acute onset of severe thunderclap headache and meningismus. Because rapid treatment of ruptured aneurysms improves both maternal and fetal outcomes, rapid radiologic evaluation is essential. In the acute setting, noncontrast head CT has a greater than 90% sensitivity for detecting SAH18 and can be used to monitor for expansion of the hemorrhage as well as for the presence of hydrocephalus. Whenever possible, however, three-dimensional TOF MRI should be used to identify and monitor aneurysms while limiting the conceptus’ exposure to ionizing radiation. Aneurysms are typically assessed for size, location, proximity to vessel origin, neck size (narrow versus wide neck), and orientation of the aneurysm apex in relation to its base. If MRI cannot be performed, CT angiography provides a rapid assessment. Catheter angiography is the gold standard, although risks associated with radiation, arterial puncture, contrast-induced nephropathy or allergy, and catheter tip thrombosis exist. Primary nonaneurysmal SAH remains a diagnosis of exclusion.

Back to Top | Article Outline
Preeclampsia and Eclampsia

Preeclampsia and eclampsia refer to a multisystem condition that arises in 2% to 8% of pregnancies, probably from immune-induced endothelial and vascular dysregulation triggered by the placenta in susceptible pregnant women, after week 20 (and usually after week 28) of pregnancy and continuing until 6 to 8 weeks postpartum. Contributing risk factors include prior preeclampsia, primiparity, maternal age, family history, preexisting hypertension, diabetes mellitus or renal disease, and certain autoimmune conditions, such as systemic lupus erythematosus. Clinical manifestations depend on the end organ affected. The mildest form of the condition is pregnancy-induced hypertension. Preeclampsia is diagnosed by the combination of hypertension and proteinuria; peripheral edema often accompanies these manifestations but is not necessary for diagnosis.

The hemolysis, elevated liver enzymes, and low platelet-count (HELLP) syndrome occurs in 10% to 20% of cases of severe preeclampsia. It probably results from activation of the fibrinolytic cascade and presents with malaise, epigastric pain, and nausea/vomiting. Additional manifestations may include pulmonary edema, acute renal failure, and disseminated intravascular coagulation. Neurologic signs and symptoms of preeclampsia include bilateral throbbing headaches, confusion, visual blurring and scintillating scotomata, photophobia, increased deep tendon reflexes, and paresthesias.

Eclampsia, referring to seizures occurring as a result of cerebral involvement, arises in 1% to 2% of severe preeclampsia cases and has an associated mortality rate of up to 14%. Seizures are usually generalized tonic-clonic and last up to 1 minute. In up to one-third of cases, neither proteinuria nor elevated blood pressure (above 140/90 mm Hg) are present before seizure onset. Symptoms may resolve in the hours after delivery of the placenta, but women are at risk of preeclampsia up to 6 to 8 weeks postpartum.19

Most women with typical preeclampsia or eclampsia do not require neuroimaging, but diagnostic imaging should be performed in the following circumstances: seizures arising before week 20 of pregnancy, postpartum eclampsia, focal neurologic deficits, persistent visual symptoms, and symptoms that are refractory to magnesium infusion and antihypertensive therapy. In these cases, posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS) should be considered, as both pregnancy-associated PRES and RCVS are likely to share an underlying pathophysiologic mechanism with preeclampsia/eclampsia. Additionally, imaging should be performed if concern exists for injuries sustained during seizure activity.

Back to Top | Article Outline
Posterior Reversible Encephalopathy Syndrome

PRES is a clinical and imaging syndrome in which, perhaps as a result of disrupted posterior cerebral autoregulation and increased vascular endothelial permeability, vasogenic edema arises diffusely but predominantly in the occipital and parietal lobes. Patients present with dull headaches, encephalopathy, cortical visual changes (eg, hallucinations, blurring, hemianopsia, diplopia, cortical blindness, and visuospatial dysfunction), and seizures that are usually generalized tonic-clonic but may have focal onset. The onset of symptoms is rapid and without a prodrome, typically over 12 to 48 hours. Additionally, patients may develop vasospasm and intracranial hemorrhage.

Most pregnancy-related PRES is likely to be a manifestation of preeclampsia/eclampsia, even in patients who are normotensive and without proteinuria.20 Hemorrhage may be exacerbated by concurrent thrombotic thrombocytopenic purpura (TTP), which is also associated with pregnancy, and presents with the pentad of fever, microangiopathic hemolytic anemia, renal insufficiency, thrombocytopenia, and neurologic dysfunction. Many patients with TTP do not manifest all these symptoms. In addition to eclampsia and TTP, other causes of PRES in nonpregnant patients include malignant hypertension, hypercalcemia, and use of drugs such as cyclosporine, tacrolimus, and other cancer chemotherapeutics.

The radiologic appearance of PRES, probably due to a shared underlying pathophysiology, is similar to eclampsia, hypertensive encephalopathy, and TTP (Case 1-2).20–22

Back to Top | Article Outline
Case 1-2

A 36-year-old woman in her third trimester of pregnancy, with no relevant medical history, developed nausea, headache, and visual disturbances. On examination in the emergency department, she was noted to be hypertensive with a blood pressure of 140/90. An urgent head CT was obtained and revealed subtle hypoattenuation posteriorly. An MRI was subsequently obtained to better characterize this finding. Axial CT and T2 fluid-attenuated inversion recovery (FLAIR) MRIs are shown in Figure 1-2. Subtle CT hypoattenuation is noted within the bilateral parietal and occipital and posterior temporal gray matter and subcortical white matter, corresponding to abnormal T2 hyperintensity seen on MRI. These findings are consistent with edema. No diffusion abnormality or evidence of hemorrhage was present.

Figure 1-2
Figure 1-2
Image Tools

Comment. The MRI findings of edema in the white and gray matter, more prominent posteriorly, without associated hemorrhage or diffusion abnormality, are consistent with posterior reversible encephalopathy syndrome (PRES). Most pregnancy-related PRES is likely to be a manifestation of preeclampsia/eclampsia; in this case, the blood pressure was only marginally elevated but concerning in a pregnant woman without a history of hypertension. The patient received supportive treatment for her headaches, as well as antihypertensive therapy. Radiologic manifestations typically normalize after clinical resolution, unless infarction or hemorrhage have occurred.

On CT, nonspecific patchy white matter hypoattenuation is noted, predominantly in the parieto-occipital lobes. Radiologic manifestations typically normalize after clinical resolution, unless infarction or hemorrhage have occurred.22

On MRI, patchy areas of T2-hyperintense and T1-hypointense edema involving cortical and subcortical structures and not strictly adhering to arterial territories are seen.20 The lesions can be distinguished from posterior cerebral artery infarctions because they often spare the medial occipital lobe and calcarine cortex. Occasionally, the lesions extend into the frontal lobes, basal ganglia, and brainstem structures. With contrast, enhancement of the lesions is variable, reflecting focal areas of blood-brain barrier disruption.20

Hemorrhage, when it occurs, can be detected on GRE and SWI sequences. Diffusion abnormalities consistent with ischemic infarction are sometimes seen. Lastly, vasospasm of medium and large cerebral arteries (particularly the basilar artery) may be observed with angiography.

Back to Top | Article Outline
Postpartum Angiopathy/Reversible Cerebral Vasoconstriction Syndrome

Postpartum angiopathy (PPA)/RCVS in pregnancy is likely to be a manifestation of the preeclampsia/eclampsia syndrome, even though patients may be normotensive and without proteinuria or other features of eclampsia. PPA (occasionally referred to as postpartum cerebral angiopathy) denotes the form of RCVS that occurs postpartum.23,24 Other triggers for RCVS (sometimes referred to as Call-Fleming syndrome) include iatrogenesis (use of ergot alkaloids, sympathomimetics, and selective serotonin reuptake inhibitors), uncontrolled hypertension, or endocrine dysregulation. Pathophysiologically, multifocal segmental constriction of large- and medium-sized cerebral arteries occurs. Patients with PPA typically present with acute onset of severe thunderclap headache, usually in the first 4 weeks postpartum. Patients may also manifest vomiting, photophobia, encephalopathy, seizures, and focal neurologic deficits. The clinical course of PPA is typically uniphasic and reversible.23,24 In the most severe cases, patients can develop subarachnoid and intraparenchymal hemorrhage as well as cerebral infarction and occasionally cervicocranial arterial dissections.

Brain MRI may reveal patchy foci of abnormal T2 hyperintensity, predominantly in the white matter and most often at the border zones between arterial territories. These lesions may show reduced diffusivity, indicating acute ischemic infarction, as well as hemorrhage. Vascular imaging should be performed; however, CT or catheter-based angiography may be replaced in the pregnant patient by TOF MRI to optimize maternal and fetal safety (Case 1-3). Imaging may be initially unremarkable; however, it is positive in 80% of patients and reveals multifocal and segmental constriction and post-stenotic dilation of large- and medium-sized intracranial arteries in a “string of beads” pattern (Figure 1-3). The constriction is reversible, even in the setting of infarction. Transcranial Doppler ultrasound measurements of arterial flow velocity can be used as a noninvasive means of monitoring the resolution of RCVS.23

Back to Top | Article Outline
Case 1-3

Eight weeks after vaginal delivery, a 28-year-old woman experienced sudden-onset right occipital headaches. She was referred to the emergency department, where she was found to be hypertensive. Because she had no history of headaches or hypertension, urgent neuroimaging was indicated. MRI was selected because of its increased sensitivity. Three-dimensional time-of-flight intracranial magnetic resonance (MR) angiogram (Figure 1-3) showed diffuse segmental arterial narrowing involving the anterior, middle, and posterior cerebral arteries. No diffusion abnormality or evidence of hemorrhage was present on MRI. A repeat MR angiogram 6 weeks later showed resolution of vasoconstriction.

Figure 1-3
Figure 1-3
Image Tools

Comment. The findings of diffuse segmental arterial narrowing of the intracerebral arteries in a postpartum patient presenting with hypertension and headaches is consistent with postpartum angiopathy/reversible cerebral vasoconstriction syndrome.

Back to Top | Article Outline
DEMYELINATION

Demyelinating diseases, such as multiple sclerosis (MS) and neuromyelitis optica (NMO), commonly present in young women of childbearing age. Gonadal hormones influence immunologic function; thus, the hormonal changes associated with pregnancy appear to influence disease course. This section focuses on MS, but it should be noted that the risk of relapse of NMO is likely to be increased in the postpartum period, as well.25

Back to Top | Article Outline
Multiple Sclerosis

MS affects 3 times more women than men and, with a peak onset in women at age 24 years, primarily manifests in women of childbearing age. Pregnancy (particularly the third trimester) is a time of relative quiescence for MS, with a rebound in relapses noted in the first few months postpartum.

During pregnancy, the radiologic assessment of new or evolving neurologic symptoms pertaining to demyelination should consist of brain or spine MRI without gadolinium. On MRI, demyelinating lesions appear as focal T2 hyperintensities, characteristically ovoid and periventricular or intracallosal. In addition to periventricular and juxtacortical locations, lesions may be found in the brainstem, cerebellar peduncles, optic nerves, cerebellum, and spinal cord. “Black holes,” or hypointensities seen on T1-weighted sequences, reflect axonal loss and have a similar morphology and distribution to the lesions seen on T2-weighted sequences.

The avoidance of contrast has four implications. First, it is important to compare the current lesion burden to that on a prior MRI in assessing for inflammatory activity. Second, it is not possible to confirm the diagnosis of MS by making the radiologic diagnosis of dissemination in time based on the simultaneous appearance of enhancing and nonenhancing lesions on the same MRI, per 2010 McDonald Criteria.26 Third, clinicians and radiologists should maintain a high index of suspicion for alternative diagnoses, such as progressive multifocal leukoencephalopathy in a pregnant patient previously treated with natalizumab or other immunosuppressive therapies, in a patient with MS. Finally, in select cases in which contrast is deemed essential to diagnostic imaging, a careful documentation of risks and benefits should be outlined and signed by the clinician, radiologist, and patient.

Back to Top | Article Outline
NEOPLASMS

Pregnancy-related hormonal changes have trophic effects on intracranial neoplasms—most commonly meningiomas and pituitary adenomas but also ependymomas, hemangioblastomas, and schwannomas, as well as metastases from breast cancer and melanoma.27

Back to Top | Article Outline
Meningiomas

Meningiomas, the most common primary intracranial tumor, arise from the arachnoid cap cells in the meningeal arachnoid villi, and the presence of hormonal receptors causes them to increase in size during pregnancy. Meningiomas most commonly arise from the parasellar and petroclival dura, the tentorium and falx, and the dura overlying the cerebral hemispheres. Presenting symptoms are attributable to mass effect and, depending on tumor location, may include headache and symptoms related to elevated intracranial pressure, seizures, visual impairment from optic nerve compression and atrophy, or other focal deficits.

On MRI, meningiomas most often appear as rounded lesions that arise from dura and in some cases have a dural tail. The margins of a meningioma are well defined, and meningiomas displace but do not infiltrate into surrounding brain parenchyma. On T1-weighted images, meningiomas are typically isointense to hypointense compared to cortex, and, if contrast is given, avid homogenous enhancement is seen. Hypercellular meningiomas can demonstrate reduced diffusivity on DWI. A rim of T2-hyperintense parenchymal edema may surround a meningioma and can be an indicator of the tumor’s rate of growth. Similarly, but conversely, T2-hyperintense gliosis of adjacent parenchyma with volume loss may indicate a more chronic lesion, and the effects of long-term parenchymal compression.

Back to Top | Article Outline
Gestational Trophoblastic Disease (Choriocarcinoma)

Gestational trophoblastic diseases encompass a range of malignancies, from benign hydatidiform molar pregnancy to invasive molar pregnancy and choriocarcinoma. Choriocarcinoma, a highly vascular and aggressive tumor prone to hemorrhage, is the most malignant form of these gestational trophoblastic tumors. It is characterized by markedly elevated serum β-human chorionic gonadotropic hormone (hCG) levels. Choriocarcinoma exerts local invasive effects and metastasizes to the spine, liver, lungs, and (in 15% to 20% of cases) brain.28 Intracerebral manifestations of an isolated lesion include headaches, encephalopathy, seizures, and focal neurologic deficits. In the setting of massive hemorrhage, signs of elevated intracranial pressure may be present.29

In patients with acute or catastrophic neurologic presentations, a noncontrast head CT can reveal hemorrhagic metastases with marked surrounding edema. MRI, which is the imaging modality of choice for choriocarcinoma in nonemergent situations, will reveal mass lesions with variable size, associated edema, hemorrhage, and enhancement.29 GRE and SWI sequences will reveal blood products in these lesions and can potentially detect smaller hemorrhagic metastases that are not visible on T1- and T2-weighted sequences.

Back to Top | Article Outline
PITUITARY LESIONS

Gestational hormonal changes lead to a variety of pituitary and parasellar changes. Most generally, during pregnancy the pituitary’s normally concave upper margin may become convex, mimicking pituitary hyperplasia and at times causing optic chiasm compression leading to bitemporal hemianopia. It has been estimated that the pituitary gland enlarges by 136% during pregnancy, exceeding 10 mm in height and regressing by 6 months postpartum. Other, more serious changes to the pituitary include apoplexy, pituitary tumor growth, and lymphocytic hypophysitis.30

Back to Top | Article Outline
Pituitary Apoplexy and Sheehan Syndrome

Pituitary apoplexy refers to an acute infarction of the pituitary, arising as the pituitary gland grows and outstrips its vascular supply, which leads to hemorrhagic and/or ischemic changes. Patients may develop sudden headache, nausea and vomiting, encephalopathy, and endocrine dysfunction.30 Focal visual and oculomotor deficits may arise, given the proximity of the pituitary to the optic chiasm and cranial nerves III, IV, and VI. Noncontrast head CT reveals an enlarged pituitary gland and may reveal the associated hemorrhage, best seen in sagittal or coronal reconstructed images. MRI is the diagnostic modality of choice. The intensity of blood products on T1-weighted and T2-weighted images will, as with any hemorrhage in the brain, vary according to temporal evolution.31

Sheehan syndrome refers to clinical hypopituitarism that results in deficits in lactation and postpartum resumption of menses and is precipitated by pituitary ischemia in the setting of maternal hemorrhage, shock, or other obstetric clinical event. Necrosis of the pituitary gland subsequently occurs. Initially, MRI reveals an enlarged pituitary gland without associated hemorrhage. Over time, loss of tissue volume results in an empty sella, best seen on sagittal MRI or CT.30

Back to Top | Article Outline
Pituitary Tumors

Pituitary adenomas are classified as microadenomas (ie, less than 10 mm) or macroadenomas (ie, equal to or greater than 10 mm). Clinical manifestations may include headaches and visual field abnormalities from compression of optic pathways, as well as hormonal alterations (eg, in nonpregnant patients, prolactinomas may manifest with amenorrhea and galactorrhea). Microadenomas are often slow growing with a benign course and minimal clinical manifestations. Macroadenomas can cause chiasmal compression and expand into the cavernous sinuses, surrounding and in some cases compressing the cavernous carotid arteries. During pregnancy, 1.5% of microadenomas and 26% of macroadenomas become symptomatic. The most common functioning pituitary adenomas are prolactinomas, followed by those causing acromegaly.30

On MRI, both microadenomas and macroadenomas are discrete mass lesions arising from the pituitary gland. They often cause asymmetric enlargement of the pituitary gland and are best seen in the coronal and sagittal planes. If gadolinium is given, adenomas typically enhance less avidly than surrounding pituitary tissue.

Back to Top | Article Outline
Lymphocytic Hypophysitis

Lymphocytic hypophysitis refers to autoimmune lymphocytic infiltration of the adenohypophysis, neurohypophysis, or infundibulum, most commonly occurring in women during late pregnancy and the first 2 months postpartum. The lymphocytic infiltrate may cause the pituitary gland to expand, thus compressing adjacent tissue and clinically mimicking a pituitary adenoma.30

On MRI, the pituitary gland and/or the infundibulum appear enlarged, and findings can be indistinguishable from a pituitary adenoma. Contrast is often required to adequately visualize the stalk, which will enhance avidly and homogenously.

Back to Top | Article Outline
BACK PAIN

During pregnancy, physiologic changes, including increased laxity of joints and spinal ligaments and increasing uterine pressure on the lumbosacral plexus and lumbar spine, commonly result in exaggerated lordosis and lower back pain. However, in cases of more severe pain or loss of motor, sensory, and bowel/bladder function, neuroimaging should be used to evaluate specific and potentially more severe etiologies.32 MRI is the preferred imaging modality for pregnancy-related back pain, except in cases of acute trauma. CT should be used in the setting of trauma to evaluate for vertebral fracture and other blunt injuries.

Back to Top | Article Outline
Epidural Processes

Epidural abnormalities can cause effacement or displacement of the normally T1-hyperintense spinal epidural fat, narrowing of the thecal sac, and displacement of the thecal sac’s dural margin. Acute intervertebral disc herniation, which may rarely occur during pregnancy, may present with acute weakness, sensory loss, radicular and back pain, and sphincter dysfunction, and in the lumbosacral spine may progress to a cauda equina syndrome. MRI can reveal a prolapsed disc causing narrowing of the spinal canal or neural foramen.33

An epidural abscess, whether arising spontaneously or resulting from instrumentation, leads to spinal tenderness, weakness, and fever. On MRI, abnormal T2 hyperintensity may correspond to a phlegmon, which enhances diffusely and homogeneously, or to an abscess, which enhances peripherally. The epidural space may circumferentially enhance.34

Epidural hematomas may occur either spontaneously during labor or as a complication of epidural or spinal anesthesia.35 On sagittal MRI, the hematoma is most often found in the posterior epidural space with well-defined borders that taper superiorly and inferiorly. Acutely, within hours to days after onset, the hematoma will appear hypointense to isointense on T1-weighted images and with mixed signal on T2-weighted imaging. With temporal evolution, signal intensity on MRI varies.

Back to Top | Article Outline
Spinal Tumors

The growth of several spinal tumors may be accelerated during pregnancy as a consequence of hormonal signaling, causing progressive neurologic deficits. As described above, this is most commonly seen with meningiomas but can also occur in spinal hemangiomas and giant cell tumors.35,39 On MRI, spinal meningioma appears as a discrete soft-tissue mass extrinsic to the spinal cord, often with a dural tail.36 Spinal hemangiomas demonstrate elevated signal on T1-weighted and T2-weighted sequences. They may contain intralesional fat, which on fat-suppression sequences (such as short T1 inversion recovery [STIR]) will appear hypointense.37 Spinal giant cell tumors, while rare, may expand dramatically during pregnancy and present as an expansile mass with heterogeneous low to intermediate signal intensity on T2-weighted images, a curvilinear area of low signal intensity on T1-weighted and T2-weighted images, cystic changes within the mass, and heterogeneous enhancement.38 Spinal metastases from gestational trophoblastic disease may also occur.

Back to Top | Article Outline
OTHER
Back to Top | Article Outline
Epilepsy

Women with primary seizure disorders may experience hormonal modulation of seizure frequency or severity. Seizure disorders may be influenced both by hormonal changes relating to pregnancy as well as altered pharmacokinetics of antiepileptic drugs during pregnancy. In a large European registry of pregnant women with epilepsy, 63.6% of the women experienced no change in seizure activity; 17% had an increase and 16% had a decrease in frequency.39 In a systematic review, seizure freedom for at least 9 months before pregnancy was associated with a high likelihood (84% to 92%) of remaining seizure free during pregnancy.40 The main concerns regarding seizure management during pregnancy may relate to antiepileptic drug choice and dosing, given concerns of teratogenesis and altered pharmacokinetics41; and neuroimaging can often be deferred.

Neuroimaging concerns arise, however, in the workup of a pregnant patient presenting with new-onset seizures. In this population, the differential diagnosis for new-onset seizures may, in addition to usual causes, include systemic processes such as hypoglycemia, but also neurologic processes such as eclampsia, CVT, PRES, intracerebral hemorrhage, RCVS, TTP, enlarging intracranial tumors, meningitis, encephalitis, or neuroinflammation. Except in patients with typical manifestations of eclampsia, neuroimaging is often necessary. Standard radiologic evaluation for epilepsy may be performed without contrast and includes evaluation of anatomy, cortical gyral patterns, and heterotopic gray matter on thin-section volumetric T1-weighted images; and evaluation of mesial temporal, hippocampal, and other parenchymal signal abnormalities on T2-weighted sequences. However, given additional diagnostic considerations in pregnant patients, gadolinium may improve diagnostic accuracy; the advantages it provides for diagnosis and management of maternal seizures must be weighed against the potential risks to the conceptus. In suspected cases of CVT or RCVS, TOF MRI angiography may be performed, thus avoiding the use of contrast.

Back to Top | Article Outline
Intracranial Hypotension

Intracranial hypotension arising from CSF leaks results most often from spinal anesthesia or inadvertent dural puncture during epidural anesthesia. Post–dural puncture headache occurs in approximately 1% of obstetric neuraxial anesthesia cases but also after other spinal interventions, such as lumbar puncture and spinal surgery during pregnancy. Usual symptoms include acute onset of nuchal or occipital positional headache when upright that improves after lying flat for 15 minutes, and that may be accompanied by neck stiffness, tinnitus/hyperacusia, diplopia, photophobia, and nausea.42

In cases with classic symptoms that do not resolve after fluids, caffeine, and pain medications, empiric treatment with an autologous epidural blood patch may be considered, with usual resolution of symptoms within 48 hours. However, in cases where the diagnosis is delayed as a result of atypical symptoms, MRI may reveal low-lying cerebellar tonsils, “brain sag,” and convexity subdural hematoma arising from the tearing of bridging veins. If it is necessary to administer gadolinium, diffuse smooth pachymeningeal enhancement is often seen.

Back to Top | Article Outline
Wernicke Encephalopathy

During pregnancy, hyperemesis gravidarum as well as increased fetal metabolic demand for thiamine may lead, like chronic alcoholism and malnutrition, to thiamine deficiency. This deficiency can result in Wernicke encephalopathy due to impaired neuronal metabolism, lactic acid accumulation, impaired blood-brain barrier, and neuronal death in areas of high thiamine-dependent glucose metabolism. Only rarely do patients present with the full clinical triad of acute encephalopathy, ataxia, and ophthalmoplegia; they may occasionally present in coma.43

On MRI, abnormal T2 hyperintensities in the paramedian thalamic nuclei, in the mammillary bodies, around the third and fourth ventricles, and in the periaqueductal gray matter and superior cerebellar vermis may be noted. These lesions may enhance with gadolinium. On DWI, reduced diffusivity indicating cytotoxic edema may be noted. High-dose IV thiamine can rapidly reverse this condition if administered early, and therefore, in cases with high clinical suspicion, treatment should not await imaging confirmation. Recognition of the clinical symptoms and associated radiologic findings is essential to prompt life-saving therapy in pregnant women.

Back to Top | Article Outline
SUMMARY

Pregnancy engenders a series of physiologic changes that increase the risk of certain neurologic conditions, such as preeclampsia, stroke, hemorrhage, and back pain. These changes should be considered, along with the typical range of neurologic conditions affecting women of reproductive age, in any pregnant woman presenting with neurologic symptoms.

Pregnant women presenting with neurologic symptoms may require diagnostic imaging. When this cannot be delayed to the postpartum period, the choice of appropriate imaging modality should reflect a trade-off between the most sensitive test for the pregnant patient and the safest test for her conceptus. At this time, MRI without gadolinium is most advisable in many cases. When performed in a timely and safe fashion, diagnostic imaging can be a highly useful component of the prompt evaluation of a pregnant patient presenting with neurologic symptoms.

Back to Top | Article Outline
USEFUL WEBSITES

American College of Obstetricians and Gynecologists Guidelines for Diagnostic Imaging During Pregnancy

www.acog.org/Resources_And_Publications/Committee_Opinions/Committee_on_Obstetric_Practice/Guidelines_for_Diagnostic_Imaging_During_Pregnancy

American College of Radiology and Society for Pediatric Radiology Practice Guideline for Imaging Pregnant or Potentially Pregnant Adolescents and Women With Ionizing Radiation

www.acr.org/∼/media/ACR/Documents/PGTS/guidelines/Pregnant_Patients.pdf

American Academy of Pediatrics Committee on Drugs—Maternal Medications Usually Compatible With Breastfeeding

pediatrics.aappublications.org/content/108/3/776/T6.full

University of California, San Francisco Guidelines for the Use of CT and MRI During Pregnancy and Lactation

www.radiology.ucsf.edu/patient-care/patient-safety/ct-mri-pregnancy

Back to Top | Article Outline

KEY POINTS

  • Physiologic changes during pregnancy modulate the incidence and presentation of a number of neurologic conditions.
  • Elective imaging should, when possible, be deferred to the postpartum period. When imaging is essential for the evaluation and treatment of a pregnant patient, careful review of the indications for, risks and benefits of, and alternatives to neuroimaging should be documented.
  • During head CT examination of the mother, the fetus is exposed only to radiation that is scattered through the mother’s body. Therefore, shielding of the abdomen, such as with a lead vest, does not significantly reduce the minimal fetal radiation exposure but may help to alleviate maternal anxiety.
  • The radiologist or a radiation dosimetry expert can assist the neurologist and obstetrician in deciding on CT or MRI in the pregnant patient. Some CT and MRI examinations can be modified to provide diagnostically critical information while exposing the conceptus to as little risk as possible.
  • Iodinated contrast is US Food and Drug Administration class B. If use of iodinated contrast cannot be avoided during pregnancy, neonatal thyroid testing should be performed during the first week. During breast-feeding, administration of iodinated contrast is not contraindicated.
  • MRI is the diagnostic modality of choice during pregnancy. Nonetheless, whenever possible it should be delayed to the postpartum period.
  • Gadolinium contrast is US Food and Drug Administration class C and should be avoided during pregnancy when possible. As an alternative to contrast injection, imaging of the arterial and venous circulation can often be performed using time-of-flight sequences. When gadolinium is essential, no specific monitoring tests are required.
  • During breast-feeding, gadolinium administration is not contraindicated.
  • Pregnancy-specific causes of ischemic stroke may include preeclampsia/eclampsia, paradoxical embolism from deep vein thrombosis through a patent foramen ovale, trophoblastic embolism, amniotic fluid embolism, air embolism, and cardioembolism from postpartum cardiomyopathy.
  • Contributing factors to cerebral venous thrombosis include dehydration, cesarean delivery or traumatic delivery, intracranial hypotension from dural puncture during neuraxial anesthesia, anemia, raised homocysteine levels, or other etiologies.
  • Recent reviews have suggested that, contrary to conclusions from prior studies, risk of subarachnoid hemorrhage is not increased during pregnancy.
  • Preeclampsia and eclampsia refer to a multisystem condition that arises in 2% to 8% of pregnancies.
  • Most women with typical preeclampsia or eclampsia do not require neuroimaging, but diagnostic imaging should be performed in the following circumstances: seizures arising before week 20 of pregnancy, postpartum eclampsia, focal neurologic deficits, persistent visual symptoms, and symptoms that are refractory to magnesium infusion and antihypertensive therapy.
  • The radiologic appearance of posterior reversible encephalopathy syndrome, probably due to a shared underlying pathophysiology, is similar to eclampsia, hypertensive encephalopathy, and thrombotic thrombocytopenic purpura.
  • Postpartum angiopathy/reversible cerebral vasoconstriction syndrome in pregnancy is likely to be a manifestation of the preeclampsia/eclampsia syndrome, even though patients may be normotensive and without proteinuria or other features of eclampsia.
  • Pregnancy-related hormonal changes have trophic effects on intracranial neoplasms, most commonly meningiomas and pituitary adenomas, but also ependymomas, hemangioblastomas, and schwannomas, as well as on metastases from breast cancer and melanoma.
  • Meningiomas arise from the arachnoid cap cells in the meningeal arachnoid villi, and the presence of hormonal receptors causes them to increase in size during pregnancy.
  • It has been estimated that the pituitary gland enlarges by 136% during pregnancy, exceeding 10 mm in height and regressing by 6 months postpartum. Other, more serious changes to the pituitary include apoplexy, pituitary tumor growth, and lymphocytic hypophysitis.
  • MRI is the preferred imaging modality for pregnancy-related back pain, except in cases of acute trauma.
  • Pregnancy engenders a series of physiologic changes that increase the risk of certain neurologic conditions, such as preeclampsia, stroke, hemorrhage, and back pain. These changes should be considered, along with the typical range of neurologic conditions affecting women of reproductive age, in any pregnant woman presenting with neurologic symptoms.
Back to Top | Article Outline

REFERENCES

1. Cunningham FG, Leevno KJ, Bloom SL, Hauth JC, Rouse DJ, Spong CY. , editors. Williams obstetrics. , 23rd ed. The McGraw-Hill Companies, Inc., 2010; .

2. American College of Obstetricians and Gynecologists Committee on Obstetric Practice. ACOG Committee Opinion. Number 299, September 2004 (replaces No. 158, September 1995). Guidelines for diagnostic imaging during pregnancy. Obstet Gynecol. 2004; 104:(3): 647–651.

3. American College of Radiology Committee on Drugs and Contrast Media. ACR manual on contrast media, Version 9. www.acr.org/∼/media/ACR/Documents/PDF/QualitySafety/Resources/Contrast%20Manual/2013_Contrast_Media.pdf.

Accessed December 5, 2013.


4. Webb JA, Thomsen HS, Morcos SK . The use of iodinated and gadolinium contrast media during pregnancy and lactation. Eur Radiol. 2005; 15:(6): 1234–1240.

5. Hall EJ, Giaccia AJ . Radiobiology for the Radiologist. Philadelphia, PA: Lippincott, Williams, and Wilkins, 2006; .

6. Osei EK, Faulkner K . Fetal doses from radiological examinations. Br J Radiol. 1999; 72:(860): 773–780.

7. Wakeford R, Little MP . Risk coefficients for childhood cancer after intrauterine irradiation: a review. Int J Radiat Biol. 2003; 79:(5): 293–309.

8. Yamazaki JN, Schull WJ . Perinatal loss and neurological abnormalities among children of the atomic bomb. Nagasaki and Hiroshima revisited, 1949 to 1989. JAMA. 1990; 264:(5): 605–609.

9. Nelson JA, Livingston GK, Moon RG . Mutagenic evaluation of radiographic contrast media. Invest Radiol. 1982; 17:(2): 183–185.

10. Gruters A, Krude H . Detection and treatment of congenital hypothyroidism. Nat Rev Endocrinol. 2011; 8:(2): 104–113.

11. Kanal E, Shellock FG, Talagala L . Safety considerations in MR imaging. Radiology. 1990; 176:(3): 593–606.

12. Salonen Ros H, Lichtenstein P, Bellocco R, et al. Increased risks of circulatory diseases in late pregnancy and puerperium. Epidemiology. 2001; 12:(4): 456–460.

13. Wilterdink JL, Easton JD . Cerebral ischemia in pregnancy. Adv Neurol. 2002; 90: 51–62.

14. Gilbert WM, Danielsen B . Amniotic fluid embolism: decreased mortality in a population-based study. Obstet Gynecol. 1999; 93:(6): 973–977.

15. Coutinho JM, Ferro JM, Canhao P, et al. Cerebral venous and sinus thrombosis in women. Stroke. 2009; 40:(7): 2356–2361.

16. Saposnik G, Barinagarrementeria F, Brown RD Jr, et al. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011; 42:(4): 1158–1192.

17. Bateman BT, Olbrecht VA, Berman MF, et al. Peripartum subarachnoid hemorrhage: nationwide data and institutional experience. Anesthesiology. 2012; 116:(2): 324–333.

18. Kotsenas AL, Roth TC, Hershey BL, Yi JK . Imaging neurologic complications of pregnancy and the puerperium. Acad Radiol. 1999; 6:(4): 243–252.

19. Steegers EA, von Dadelszen P, Duvekot JJ, Pijnenborg R . Pre-eclampsia. Lancet. 2010; 376:(9741): 631–644.

20. Roth C, Ferbert A . The posterior reversible encephalopathy syndrome: what’s certain, what’s new? Pract Neurol. 2011; 11:(3): 136–144.

21. Bakshi R, Shaikh ZA, Bates VE, Kinkel PR . Thrombotic thrombocytopenic purpura: brain CT and MRI findings in 12 patients. Neurology. 1999; 52:(6): 1285–1288.

22. Bartynski WS . Posterior reversible encephalopathy syndrome, part 1: fundamental imaging and clinical features. AJNR Am J Neuroradiol. 2008; 29:(6): 1036–1042.

23. Ducros A . Reversible cerebral vasoconstriction syndrome. Lancet Neurol. 2012; 11:(10): 906–917.

24. Fugate JE, Ameriso SF, Ortiz G, et al. Variable presentations of postpartum angiopathy. Stroke. 2012; 43:(3): 670–676.

25. Bourre B, Marignier R, Zephir H, et al. Neuromyelitis optica and pregnancy. Neurology. 2012; 78:(12): 875–879.

26. Polman CH, Reingold SC, Banwell B, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol. 2011; 69:(2): 292–302.

27. Doyle S, Messiou C, Rutherford JM, Dineen RA . Cancer presenting during pregnancy: radiological perspectives. Clin Radiol. 2009; 64:(9): 857–871.

28. Smith HO, Kohorn E, Cole LA . Choriocarcinoma and gestational trophoblastic disease. Obstet Gynecol Clin North Am. 2005; 32:(4): 661–684.

29. Mamelak AN, Withers GJ, Wang X . Choriocarcinoma brain metastasis in a patient with viable intrauterine pregnancy. Case report. J Neurosurg. 2002; 97:(2): 477–481.

30. Motivala S, Gologorsky Y, Kostandinov J, Post KD . Pituitary disorders during pregnancy. Endocrinol Metab Clin North Am. 2011; 40:(4): 827–836.

31. Turgut M, Ozsunar Y, Basak S, Guney E, Kir E, Meteoglu I . Pituitary apoplexy: an overview of 186 cases published during the last century. Acta Neurochir (Wien). 2010; 152:(5): 749–761.

32. Han IH . Pregnancy and spinal problems. Curr Opin Obstet Gynecol. 2010; 22:(6): 477–481.

33. Del Grande F, Maus TP, Carrino JA . Imaging the intervertebral disk: age-related changes, herniations, and radicular pain. Radiol Clin North Am. 2012; 50:(4): 629–649.

34. Sandhu FS, Dillon WP . Spinal epidural abscess: evaluation with contrast-enhanced MR imaging. AJNR Am J Neuroradiol. 1991; 12:(6): 1087–1093.

35. Wang P, Xin XT, Lan H, et al. Spontaneous cervical epidural hematoma during pregnancy: case report and literature review. Eur Spine J. 2011; 20:(suppl 2): S176–S179.

36. Gezen F, Kahraman S, Canakci Z, Beduk A . Review of 36 cases of spinal cord meningioma. Spine (Phila Pa 1976). 2000; 25:(6): 727–731.

37. Vijay K, Shetty AP, Rajasekaran S . Symptomatic vertebral hemangioma in pregnancy treated antepartum. A case report with review of literature. Eur Spine J. 2008; 17:(suppl 2): S299–S303.

38. Kwon JW, Chung HW, Cho EY, et al. MRI findings of giant cell tumors of the spine. AJR Am J Roentgenol. 2007; 189:(1): 246–250.

39. EURAP Study Group. Seizure control and treatment in pregnancy: observations from the EURAP epilepsy pregnancy registry. Neurology. 2006; 66:(3): 354–360.

40. Harden CL, Hopp J, Ting TY, et al. Management issues for women with epilepsy-Focus on pregnancy (an evidence-based review): I. Obstetrical complications and change in seizure frequency: Report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Epilepsia. 2009; 50:(5): 1229–1236.

41. Tomson T, Landmark CJ, Battino D . Antiepileptic drug treatment in pregnancy: Changes in drug disposition and their clinical implications. Epilepsia. 2013; 54:(3): 405–414.

42. Chang LY, Carabuena JM, Camann W . Neurologic issues and obstetric anesthesia. Semin Neurol. 2011; 31:(4): 374–384.

43. Chiossi G, Neri I, Cavazzuti M, Basso G, Facchinetti F . Hyperemesis gravidarum complicated by Wernicke encephalopathy: background, case report, and review of the literature. Obstet Gynecol Surv. 2006; 61:(4): 255–268.

Copyright © 2014 by the American Academy of Neurology.

Login