Cause of headache
Common features
Treatment in pregnancy
Treatment postpartum
Migraine
Frontal (often unilateral), prolonged, and pulsatile
Other: nausea, vomiting, and aversion to loud noise, bright light, and physical activity
Acetaminophen, antiemetics, caffeine, corticosteroids (prednisone), intravenous hydration, and opioids
Treatment in pregnancy plus NSAIDS and triptans (sumatriptan)
Tension-type
Bifrontal, bitemporal, bioccipital, or neck with squeezing and aching
Other: nausea, light, and sound sensitivity
Acetaminophen, caffeine, and opioids
Alternative therapies: relaxation techniques, biofeedback, and physical therapy
Treatment in pregnancy plus NSAIDS
Cluster
Unilateral, orbitotemporal, non-throbbing, and penetrating
Other: ptosis, conjunctival injection, or lacrimation
Oxygen, intranasal lidocaine
Treatment in pregnancy plus triptans (sumatriptan)
Prophylactic medication may be needed in the management of headache in pregnancy based on frequency, severity, and duration of headaches. Below is a list of common prophylactic medications used in pregnancy (Table 10.2). A headache diary is often helpful to monitor the clinical course, triggers, and management. The clinical benefit of prophylaxis is variable and requires a clinical trial of daily use for at least 6 weeks to determine efficacy. Consideration of coexisting conditions and potential for medication interactions should be used to guide choice of prophylactic medication. For example, the use of a beta-blocker is typically contraindicated in a pregnant woman with low blood pressure especially with symptomatic dizziness. Reevaluation of therapy is important to monitor medication efficacy, side effects, and clinical course and to rule out development of a new headache etiology, such as preeclampsia. Nonpharmacologic therapies for headache prevention include relaxation, biofeedback, and stress management [9]. Lifestyle modification including avoidance of skipped meals, sleep deprivation, and dehydration should also be stressed. Women who are treated with anticonvulsant (also known as antiepileptic drug or AED) class medications for migraine prophylaxis prior to pregnancy (such as topiramate and valproic acid) should be counseled on the risk of birth defects associated with these drugs, and whenever possible, these drugs should be discontinued. Anticonvulsants are discussed later in this chapter.
Table 10.2
Prevention therapy for headaches in pregnancy
Drug class | Example |
|---|---|
Antidepressants | Amitriptyline, nortriptyline |
Beta-blockers | Propranolol, metoprolol |
Calcium channel blockers | Nifedipine, verapamil |
NSAIDS | Low-dose aspirin |
Supplements | Magnesium, riboflavin |
Seizures in Pregnancy
Background/Definition
Seizures represent the clinical manifestation of paroxysmal, synchronous firing of neurons within the cortex of the brain—generally thought of as “electrical storms” of the brain. Seizures can have provoking factors—irritation of the cortex by blood, infection, inflammation, an abnormal structure or mass, exposure to toxins, or derangements of glucose or electrolytes, among many other causes (see Table 10.3). Seizures also occur in eclampsia, among other vascular disorders of pregnancy. When seizures occur de novo in a pregnant patient, a thorough workup is necessary to rule out these conditions. When no provoking factors are identified, seizures may be a manifestation of epilepsy, which is defined as “two or more unprovoked seizures.” An alternative definition of epilepsy is “a tendency toward unprovoked seizures”; this second definition presupposes an abnormality detected on an electroencephalogram (EEG), which may be characteristic of an underlying idiopathic epilepsy syndrome.
Table 10.3
Possible causes of seizure in pregnancy
Vascular causes – Eclampsia – Stroke, including hemorrhagic stroke, ischemic stroke due to arterial or venous occlusion, and cerebral venous sinus thrombosis – Hypertensive encephalopathy – Reversible posterior leukoencephalopathy syndrome – Primary central nervous system vasculitis |
Thrombotic thrombocytopenic purpura (TTP) |
Mass lesions (neoplasm, abscess) |
Infection (meningitis and encephalitis) |
Metabolic disorders (hypoglycemia, hyperglycemia, hyponatremia, hypocalcemia, hypomagnesemia, uremia, hyperammonemia, and liver failure, pyridoxine deficiency, thyrotoxicosis, and porphyria) |
Hypoxic-ischemic cerebral injury |
Drug exposure (amphetamines, cocaine, tricyclic antidepressants, theophylline, and lidocaine) |
Withdrawal syndromes (including withdrawal from antiepileptic drugs, benzodiazepine, alcohol, and barbiturates) |
Idiopathic epilepsy |
Preexisting epilepsy is the most common reason for seizures during pregnancy. Among patients known to have a seizure tendency—or epilepsy—prior to the pregnancy, special challenges arise. Seizures themselves can be harmful to the developing fetus, but all antiepileptic drugs (AEDs) used to treat the disorder are felt to be teratogenic to varying degrees. Seizures can change during pregnancy, in part due to circulating hormones and in part due to fluctuating levels of AEDs in response to physiologic changes of pregnancy. These changes will be discussed below.
Epidemiology
Epilepsy affects an estimated one in one hundred people, half of whom are female. About 0.5–1.3 million women with epilepsy in the United States are of childbearing age [10], and the prevalence of epilepsy in pregnant women is 0.3–0.7 % [11]. Approximately 1 % of pregnancies are thought to be complicated by seizures.
Pathobiology
The pathophysiology of seizures during pregnancy is strongly based on the etiology of the seizures. For example, eclamptic seizures are thought to result from neuronal irritation in the context of cerebral vascular dysregulation and resultant cerebral edema—although the specific cause of this process is yet unknown. Similar, hypoxic, or ischemic damage to cerebral tissue, acute blood products, cerebral edema of other etiologies—structural and otherwise—and exposure to toxic-metabolic or infectious processes (Table 10.3) can cause neuronal misfiring and resultant seizures. Epilepsy, in contrast, is considered idiopathic by nature and may be attributed to any number of causes of abnormal neuronal signaling. Some epilepsy syndromes are genetic, while for the vast majority, the cause is unidentified.
Normal Physiologic Changes
The importance of hormones in epilepsy and seizure control is well known; approximately one third of nonpregnant women with epilepsy commonly note an increase in seizures during a predictable point in their menstrual cycles, and up to 40 % of women with epilepsy note worsening seizures around menopause. Both estrogen and progesterone receptors are present in structures of the brain; experimentally, estrogen has pro-convulsant properties, while progesterone (experimentally and clinically) has anticonvulsant properties.
Effect of Pregnancy on the Disease
As both estrogen and progesterone rise during pregnancy, the clinical effect on epileptic seizures can vary among women. Among epileptic women, approximately 20–33 % experience an increase in seizures, 7–25 % experience a decrease in seizures, and 50–83 % experience no significant change [12]. While the majority of women with epilepsy maintain seizure control during pregnancy, the strongest predictor of a seizure-free pregnancy is a 9-month period of seizure freedom prior to conception [10].
Normal physiologic changes of pregnancy can also influence the metabolism of the drugs used to treat epilepsy. These changes include increases in total body water and extracellular fluid, fat stores, cardiac output, renal blood flow and glomerular filtration rate, hormone-dependent metabolic pathways such as glucuronidation, sex hormone binding, and decreases in maternal albumin. The result for many antiepileptic drugs—whether renally excreted or hepatically metabolized—is a net reduction in blood levels of the drugs through the pregnancy; this can potentially lead to breakthrough seizures for the patient. Drugs that are extensively metabolized through glucuronidation include lamotrigine and oxcarbazepine. Consequently, levels of these AEDs may fall by approximately 50 % in the first trimester, and early blood monitoring for patients taking these two drugs can be helpful. Levetiracetam, in contrast, is renally excreted, and a marked drop (over twofold) can occur in the third trimester due to increased plasma clearance. In the postpartum period, the levels of drugs can be even less predictable. Close monitoring of drug levels during pregnancy and during the postpartum period is warranted.
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