Balance risks/benefits to mother/fetus. CT & MRI entail potential risk to fetus.

When scanning the mother during pregnancy: Involve pt & family, obstetrician, & radiologist in discussion, & document this. Modify MRI & CT exams under direction of radiology to be as informative as possible w/as little exposure as possible (e.g., minimize sequences, contrast exposure, etc.). Avoid all imaging in the first trimester if possible, & delay elective imaging until after the delivery. Consider alternate imaging modalities (e.g., ultrasound) or diagnostic approaches (e.g., LP). MRI generally a safer option than CT. Abd shielding during CT head is of questionable benefit for fetal protection, but may help reduce maternal anxiety. Gadolinium is a category C drug in pregnancy, & should be avoided. Iodinated contrast is a category B drug.

Head CT: No human studies for ionized radiation, but there is risk for pregnancy loss, malformations, carcinogenic effects, growth/developmental delays. Fetal radiation exposure during maternal head CT is very minimal. At that level of fetal radiation, there is no evidence for fetal malformation, development/growth delays, or pregnancy loss. Risk of CA in the fetus, controversial, but generally felt that the risk is unlikely to be greater than 1/1,000 children exposed (Obstet Gynecol 2004;104:647). Iodinated contrast can be used during pregnancy.

MRI: Safe to use, no reported harmful effects. Gadolinium: Due to long half-life & limited data, do not use unless benefit outweighs risk.

Epidemiology: Preeclampsia/eclampsia → leading cause of maternal death in the US, affecting up to 8% of pregnancies. Eclampsia in one pregnancy predicts 46% risk in subsequent pregnancy. Overall mortality is ˜9%-23%, highest early in the pregnancy.

Clinical features: HTN in pregnancy → BP ≥ 140/90 after 20 wk gestation. Proteinuria in pregnancy → 1+ protein reading on a random urine test dipstick. Preeclampsia → ↑ BP & proteinuria after the 20th wk of pregnancy. Severe preeclampsia → considered to be present w/one or more of the following criteria: BP ≥ 160/110 (on two occasions); proteinuria (3+ or more on two random urine samples); oliguria < 500 mL/24 h; pulmonary edema; diffuse peripheral edema; abnormal LFTs; thrombocytopenia; impaired fetal growth; HELLP syndrome. Eclampsia → Sz + Preeclampsia (exclude other causes of Sz → venous sinus thrombosis, stroke, & ruptured aneurysms). Relation to delivery: >70% occur prior to delivery, 25% before labor, 50% during labor, & 25% after delivery. Eclampsia before 20 wk rare, & suspicion should be high for molar pregnancy, multiple pregnancy, or noneclamptic neurologic disease. HELLP syndrome → Hemolysis, elevated liver enzymes, & low platelet counts (below 100,000 to 150,000/mm³).

Cerebral pathology: Mechanism of preeclampsia/eclampsia: unclear. Cerebral pathology due to vascular injury from ↑ BP & predisposition to coagulopathies. Entire neuroaxis subject to potential ischemia, edema, or hemorrhage.

Imaging: MRI preferable, w/similar findings to PRES.

Management: Therapeutic goals: Protecting the fetus (w/delivery if possible). Controlling HTN to w/in the normal range for the individual pt. Suppressing szs. Seizures: Magnesium sulfate mainstay of management, not traditional antiepileptics. Mechanism of action for magnesium sulfate → antivasospastic effect. If Mg fails, add antiepileptic drugs of proven efficacy: lorazepam or phenytoin. Blood pressure: HTN associated w/eclampsia often adequately controlled by stopping sz. Goal diastolic
blood pressure <110 mm Hg. Meds: Hydralazine, nicardipine, labetalol, nifedepine. Avoid ACE-I because of potential toxicity to the fetal kidneys. Avoid diuretics in eclampsia, unless indicated for maternal sx (e.g., pulmonary edema), because these pts often intravascularly depleted.

Neurologic prognosis: ˜10% of pts have repeated szs w/o treatment. Up to 56% of pts w/eclampsia may have transient deficits, including cortical blindness. ICH usually associated w/BP > 170/120 mm Hg, & responsible for up to 20% of eclamptic deaths. Ischemic stroke accounts for 5% of pregnancy-related maternal deaths in the United States. Range of increased perinatal mortality is 5% (for history of preeclampsia) to 45% (for abruptio placentae). Sz duration has not been associated w/increased perinatal mortality.

Ischemic stroke: Stroke in young pts due to: heart disease, substance abuse, coagulopathies, arterial dissection, early atherosclerosis. Pregnancy & the postpartum period ↑ relative stroke rate, w/up to 35% of strokes between ages 15 and 45 being related to pregnancy. Overall risk of stroke in pregnancy is generally low and largely the result of background risk factors. The postpartum period: greatest risk. The major specific risk factors are preeclampsia/eclampsia & hypercoagulability. Standard stroke imaging should be pursued under the guidelines discussed in the “Imaging in Pregnancy” section of this chapter.

Treatment: Acute arterial occlusion: Standard stroke treatment employs the use of IV tPA, not well studied in pregnancy. Potential complications include: uterine or fetal hemorrhage, pregnancy loss, hemorrhagic complications in the mother. Use of thrombolysis has largely been free of major adverse effects & fetal tPA exposure is likely very low. Consider thrombolytic therapy for potentially disabling strokes, but have OB service on alert in the event of the need for emergent delivery of the fetus. If emergent delivery needed w/in 24 h of tPA, then effects of tPA need to be reversed. IA therapy should also be considered (risk to the fetus likely minimal).

Imaging in pregnancy: U/S & MRI preferred over ionized radiation (see above).

Introduction: Young to middle aged pts (˜75% women), ˜80% of pts w/good outcome. Poor pts w/age >37 yo, male, coma, altered mental status, GCS <9, ICH on admission, DVT, CNS infection, & CA (Stroke 2004;35:664). Recurs in 2% of pts.

Etiologies: Genetic: Antithrombin III, protein C/S deficiencies, factor V Leiden, prothrombin gene mutation, homocysteinemia. Acquired: Pregnancy/puerperium, nephrotic syndrome, antiphospholipid syndrome, homocysteinemia, malignancy. Infection: Sinusitis, otitis, mastoiditis, meningitis. Rheum. Meds: OCP, hormone replacement therapy, asparaginase, tamoxifen, steroids. Trauma: Neurosurgery, IJ central line, LP.

Clinical manifestations: Highly variable; HA (90% of pts) gradual in onset usually (may be thunderclap in some cases); neurologic si/sxs develop in 50% of pts; szs in 40% of pts (half of which are focal/limited). ICH: 40% of pts, even prior to anticoagulation. Cavernous sinus thrombosis: proptosis, periorbital edema, chemosis, & CN III, IV, V palsies.

Diagnosis: Consider dx in younger pts w/no risk factors w/stroke sxs, unusual HA, ICH, intracranial HTN. MR or CT venography (angiography if CT or MR negative).

Risk factor workup: Most pts have identifiable risk factors (˜50% have multiple ones), ˜13% cause of SVT unknown (Stroke 2004;35:664). Following labs in all pts (since pts can have multiple risk factors): Antiphospholipid syndrome (including lupus anticoagulant), prothrombin G20210A gene mutation, Factor V Leiden, protein C/protein S/antithrombin III deficiencies, homocysteine. LP: If pt febrile. Look for malignancy in older pts w/o risk factors.

Treatment: Anticoagulation: Heparin (even if ICH present) goal PTT 2-2.5× baseline, bridge to warfarin for 6 mo or longer w/INR goal 2-3. Two main trials: First trial: 20 pts, long treatment delay, avg. 4 wk, stopped early due to significant benefit w/heparin (based on a SVT scale, authors argue other stroke scales do not account for all sxs of SVT) (Lancet 1991;338:597). Second trial: 59 pts, SC LMWH used, no statistical difference but trend toward better outcome w/LMWH, possible imbalance at baseline favoring placebo group (Stroke 1999;30:484). Meta-analysis of both trials: nonsignificant trend toward fewer death & dependency, anticoagulation safe w/no new ICH occurring in either trial (Cochrane 2004;(4):CD002005).

Endovascular: Reserved for pts w/poor prognosis & worsening pts despite heparin, limited evidence. Administration of urokinase or rt-PA or mechanical disruption.

Seizures: AED in pts w/both szs & parenchymal lesions on imaging—edema, ischemic/hemorrhagic infarct → these pts have higher risk of szs (Cerebrovasc Dis 2003;15:78); Otherwise no AED; Tx for a year.

Intracranial HTN: Rare complication. LP: for pts w/worsening vision & intracranial HTN, no heparin for at least 24 h after procedure, remove enough CSF to normalize closing pressure. Consider acetazolamide 500-1,000 mg daily. Surgery: If above measures fail, VPS or fenestration of optic nerve; Other Tx to consider: Mannitol/hyperventilation.

Future pregnancy: No contraindication for future pregnancy in pts w/prior cerebral venous thrombosis (CVT). Anticoagulate during pregnancy w/h/o CVT only if prothrombotic condition or other thromboembolic event (PE, DVT), dose-adjusted heparin or LMWH (w/factor Xa monitoring) in third trimester up to 8 wks postpartum.

In pregnancy, hemorrhage is usually associated w/preeclampsia/eclampsia & AVMs.

Migraine prevalence is higher during the reproductive years & shows a variable pattern during pregnancy. As a rule of thumb, 1/3 of pts improve, 1/3 worsen, & 1/3 remain unchanged. Medication discontinuation should be attempted before conception. If not possible, then those rated as safest by the FDA should be used. Clomiphene may increase the risk of migrainous infarction & so should be avoided in any pt w/a complicated migraine history. Migraine → no increased risk of malformation in infant but ↑ risk of maternal complications during pregnancy.

Treatment: The risk of migraine therapy in pregnancy largely anecdotal & conjectural because of the absence of randomized studies.

Acute treatment for migraine: Triptans—FDA pregnancy Class C. Ergots—Absolutely contraindicated (can cause fetal growth retardation). NSAIDs—Ibuprofen is the best choice & can be used in the first trimester at a dose of 200-600 mg PO q6h
(avoid aspirin, indomethacin, & other potent prostaglandin synthesis inhibitors because of the risk of constriction or closure of the fetal ductus arteriosus). Acetaminophen—FDA pregnancy category B & an excellent choice. Narcotics—Combinations w/acetaminophen can be safely used. Magnesium sulfate—The preferred treatment when it is difficult to distinguish between pre-eclampsia & migraine or when the two overlap.

Acute treatment for associated sx (e.g., N/V): Phosphorylated carbohydrate solution 15-30 mg PO q15min (for mild cases). Metoclopramide (Pregnancy Class B); Chlorpromazine (C); Promethazine (C); Prochlorperazine (C); Prednisone (C).

Prophylactic therapy: Justified if frequency & severity of migraines are disabling. Begin w/nonpharmacologic therapy such as biofeedback & relaxation therapy. If medication is required, first line should be: Propanolol (fetal growth should be monitored for risk of intrauterine growth retardation). Folic acid supplementation (1-5 mg daily) crucial for women using valproic acid as preventive therapy. Also consider magnesium supplementation for prophylaxis in difficult cases.

Lactation: Migraine treatments that are safe for both breastfeeding & pregnancy include: triptans; acetaminophen; caffeine; opioids; propanolol; metoclopramide is highly concentrated in breast milk & should be used w/caution postpartum.

Currently, there are no evidence-based practice guidelines on clinical decision making & therapeutic choices for women w/MS who choose to become pregnant or experience an unplanned pregnancy.

No evidence that MS impairs fertility. Factors to consider: