Postpartum Headache

Etiology

Postpartum headache is a common condition affecting individuals after childbirth due to hormonal fluctuations, fluid shifts, and the physical and emotional demands of new parenthood. Postpartum headache can be classified into primary and secondary types and further subtyped into benign and life-threatening etiologies.

Benign Etiologies of Postpartum Headache

Primary headache syndromes, musculoskeletal headaches, and postdural puncture headaches (PDPH) are prognostically benign and account for over half the presentations of severe headaches in the postpartum period.[1][2] The most common cause of a headache in the postpartum period is an exacerbation of primary headache syndromes, including migraine, cluster, and tension headaches.[1] PDPH is also common in the setting of neuraxial blockade use for labor. More than half of the patients who had an accidental dural puncture reported subsequent headaches.[3][4] PDPH is usually localized but can radiate to the neck and shoulders. The intracranial hypotension that occurs with a dural puncture causes an orthostatic headache. Nausea and dizziness may be associated with this severe type of headache. Almost 46% of secondary headaches in the postpartum period are from PDPH.[5]

Another secondary headache that may be associated with neck and shoulder pain is a musculoskeletal headache from maternal physical exertion during labor, plus the associated sleep deprivation, and is one of the most common causes of secondary postpartum headaches.[5]

Life-Threatening Etiologies of Postpartum Headache

The life-threatening causes of headaches in the puerperium are all secondary and may result from complications of anesthesia, primary intracranial pathology, or obstetric complications. The diagnosis of secondary causes of postpartum headaches is difficult and hindered because patients with primary headache disorders are at increased risk for the development of hypertensive disorders of pregnancy and intracranial vascular catastrophes, all secondary causes of postpartum headaches.[6][7][8][9] Besides the physiologic changes associated with the postpartum period, people in the puerperium are at increased risk of domestic and intimate partner violence, leading to an increased risk of traumatic intracranial pathology.[10]

Life-threatening causes of headaches in the postpartum period include preeclampsia, eclampsia, cerebral venous sinus thrombosis, posterior reversible encephalopathy, intracranial mass, meningitis, hemorrhagic stroke, and reversible cerebral vasoconstrictive syndrome (RCVS).

Reversible cerebral vasoconstrictive syndrome

RCVS, previously known as Call-Fleming syndrome or postpartum cerebral angiopathy.[5] The cerebral vasculopathy in RCVS is caused by noninflammatory, diffuse, segmental narrowing of the cerebral arteries. An estimated 21% to >50% of patients with RCVS have pregnancy as the triggering factor.[11][12] 

Intracranial masses

In pregnancy, elevated progesterone levels can promote the growth of tumors like meningiomas, as 70% of these tumors have progesterone receptors. Tumor growth may cause headaches and other associated neurological symptoms. Additionally, hemodynamic changes can contribute to meningioma growth.[5] Another tumor that can rarely spread to the brain during or after pregnancy is choriocarcinoma. It presents with headaches and signs of increased intracranial pressure.[5]

Sheehan syndrome

Sheehan syndrome or pituitary apoplexy may be a cause of postpartum headaches in patients who have hypotension and peripartum hemorrhage that results in hemorrhagic or ischemic necrosis of the enlarged pituitary gland. The acute onset of Sheehan syndrome postpartum can lead to headache, loss of consciousness, lactation failure, and symptoms of acute adrenal insufficiency, including hypotension, hypoglycemia, nausea, vomiting, and hyponatremia. Headache, hypotension, and hypoglycemia in the postpartum period should prompt consideration of pituitary failure.[13]

Preeclampsia

Preeclampsia can present with delayed onset in the postpartum timeframe but usually is seen in 7 to 10 days postpartum and frequently presents with a headache.[14] A progressive bilateral throbbing headache, worsened by exertion and unresponsive to over-the-counter medications, may indicate preeclampsia. Visual disturbances resembling a migraine aura can also occur. Preeclampsia should be considered in patients with a headache at over 20 weeks gestation or within 6 weeks postpartum, along with blood pressure elevations ≥140 mm Hg systolic or ≥90 mm Hg diastolic. Headache due to preeclampsia should resolve within a week of blood pressure treatment and normalization, according to International Headache Society criteria.[5] 

In postpartum patients, posterior reversible encephalopathy syndrome (PRES) is linked to eclampsia/preeclampsia, and affected patients should be assessed for preeclampsia due to potentially life-threatening risks to the pregnant person. PRES involves vasogenic edema, likely resulting from impaired autoregulation in cerebral blood vessels due to increased hydrostatic pressure and endothelial dysfunction.[5]

Intracerebral hemorrhage

Pregnancy is a hypercoagulable state, and intracerebral hemorrhage can occur in the setting of stroke, rupture of a vascular malformation or aneurysm, or from hypertension, PRES, or RCVS. A thunderclap headache is a hallmark sign of intracerebral hemorrhage.[5] On the other hand, headache is rarely the primary or initial symptom of a stroke and lacks specific features. Headache occurs in about one-third of posterior circulation stroke cases, often accompanied by focal neurological symptoms or altered mental status. The risk of ischemic stroke is 3 to 9 times higher in the postpartum period compared to non-pregnant people. The strongest risk factors for stroke are preeclampsia and eclampsia, but tobacco use, preexisting hypertension, diabetes, and gestational diabetes also increase the risk.[5] Cerebral venous thrombosis is associated with a severe, throbbing headache that is paroxysmal in onset. It can be whole-head or unilateral and may have migraine-like features. Focal neurological abnormalities are frequently present.

Postpartum lymphocytic adenohypophysitis

Postpartum lymphocytic adenohypophysitis, also known as autoimmune hypophysitis, is an inflammatory pituitary gland condition. It has an association with other autoimmune conditions, especially Hashimoto thyroiditis. Headache is the most common symptom in over half of the cases. The headache occurs when the inflammation extends into the cavernous sinus. Lymphocytic hypophysitis should be included in the differential diagnosis of postpartum headache, although this is a much less common cause. History and serum laboratory studies show hyponatremia but without the history of postpartum hemorrhage that is associated with Sheehan syndrome. Adrenocorticotropin hormone (ACTH) deficiency with this condition causes hyponatremia, and when unrecognized, postpartum lymphocytic adenohypophysitis can result in death.[15]

Epidemiology

Worldwide, roughly 3 billion people have a headache disorder. Approximately 1.89 billion people have tension-type headaches, whereas 1.04 billion have migraines. For biological females, tension headaches affect an age-standardized rate of almost 31%, and 19% for migraines.

Headaches are common postpartum, affecting 30% to 40% of patients. Postpartum headaches are more common in people with a prior headache history, older age, increased parity, and a shorter second stage of labor.[1] The clinical features of secondary headaches invariably present with similar or indistinguishable symptoms from primary headache disorders.

Pathophysiology

Primary and secondary headache presentations increase sharply in the puerperium, secondary to the many social and physiologic changes that occur during this period. The postpartum period is rife with factors that may exacerbate primary headache disorders, including tension and cluster headaches, migraines, medication overuse, and trigeminal autonomic cephalgias.[16] These patients also experience sleep deprivation, increased stress levels, disordered sleep cycles, depression, and irregular nutritional intake, all of which can trigger primary headaches.[17][18] 

The dramatic fluctuations in estrogen, serotonin, and oxytocin levels associated with childbirth and breastfeeding may also exacerbate underlying primary headache disorders. The physiologic changes of the puerperium also contribute to an increased risk of secondary headache syndromes. Ischemic stroke incidence rises due to hypercoagulability in pregnancy, reaching its peak in the immediate postpartum period.[19][20] Rising estrogen and progesterone levels lead to vasodilation and increased vascular distensibility, which contribute to the higher rate of rupture of vascular malformations and intracranial hemorrhages in the puerperium.[21] During pregnancy, the pituitary gland volume increases up to 120%. Due to this, pituitary adenoma headaches and visual disturbances can occur, especially when the diameter of the adenoma is >1 cm.[5]

History and Physical

Clinical History

Clinical features help distinguish benign from life-threatening headache presentations in the postpartum period. Essential historical points to elicit include: 

• Timing of headache onset
• Vaginal versus cesarean delivery
• Complications of the pregnancy, eg, preeclampsia or gestational hypertension
• Delivery complications, including bleeding and intrapartum fevers
• Use of epidural anesthesia
• New medications
• Illicit drug use
• Personal or family history of hypercoagulability or bleeding syndromes
• Shortness of breath
• Chest pain
• "Thunderclap" onset

The clinical characteristics commonly linked to migraines include unilateral or throbbing headaches, sensitivity to light, and nausea. Cluster headaches often present with symptoms including tearing in 1 eye, nasal congestion, and a runny nose. In contrast, tension-type headaches are typically described as a dull, pressure-like sensation without additional associated symptoms.[22]

A thunderclap headache is characterized by a sudden onset of severe head pain that reaches its maximum intensity within 1 minute. This type of headache is often described as the "worst headache of my life" and can be indicative of several serious underlying conditions, the most common of which is subarachnoid hemorrhage.[23][24] Simply asking if a headache started suddenly may not be enough to determine if it had a true thunderclap onset. Therefore, clarifying whether the pain escalated from none to extreme within seconds or up to a minute is more effective. Using a hand gesture, like a clap, can also help emphasize that "sudden" refers to an immediate, severe onset rather than a gradual increase over several minutes or hours.[22]

Physical Examination

Physical examination findings that raise suspicion for a life-threatening secondary cause of a headache in the puerperium include: 

• Severe hypertension
• Decreased urination
• Visual changes
• Abnormalities on neurological examination, including hyperreflexia

Evaluation

Diagnostic Laboratory Studies

The diagnosis of primary headache disorders and PDPH is clinical; no additional laboratory or imaging studies are typically necessary. However, laboratory workup for secondary headache syndromes in the puerperium includes a urinalysis, a spot urinary protein to creatinine ratio, complete blood count, comprehensive metabolic panel, and lactate dehydrogenase. A lumbar puncture with fluid analysis is necessary if meningitis is suspected.

Diagnostic Imaging Studies

The imaging modality of choice differs based on the most likely suspected headache etiology. Brain magnetic resonance imaging (MRI) is preferred when evaluating intracranial or neurovascular secondary causes of headaches. A noncontrast head computed tomography (CT) is rapid and may be used to exclude intracranial blood from spontaneous or traumatic intracranial hemorrhage and identify skull fractures.[22] However, CT is inferior to MRI when assessing the cerebrovasculature and is not sensitive to early ischemic strokes and sinus venous thrombosis.[25][26] CT venography is as sensitive as MR venography and is more readily available.[26] MRI is most sensitive for early ischemic strokes. Rarely, postpartum headaches may indicate cerebrovascular disease, a mass lesion, or postpartum cerebral arterial dissections. Correct diagnosis thus relies on imaging, and MRI is often preferred.[27][28] An urgent magnetic resonance angiogram (MRA) or computed tomography angiography (CTA) can detect vascular abnormalities, and prompt surgical or endovascular intervention should be initiated as needed.[5]

The risk of venous thromboembolism is significantly elevated in pregnancy and even higher during the postpartum period.[29] When imaging is necessary, particularly for patients experiencing sudden, severe headaches or those described as the "worst headache of my life", a noncontrast head CT is the preferred modality due to its speed and sensitivity in detecting critical conditions such as hemorrhage, herniation, mass effect, and hydrocephalus. However, imaging is not necessary for patients with new headaches that align with classic migraines or tension-type headaches if they have a normal neurologic examination.

Treatment / Management

The underlying etiology of the headache guides the management of postpartum headaches. Management of primary headache exacerbations includes analgesia and counseling regarding the importance of consistent nutrition and sleep. The treatment of choice for PDPH is bed rest, analgesia, intravenous hydration, and caffeine supplementation. Patients not responding to this treatment within 48 hours may require a blood patch. Please see StatPearls' companion resource, "Epidural Blood Patch", for further information on this procedure. 

Treating secondary causes of headaches in the postpartum period often requires collaboration with consulting services for acute management and risk factor modification. Headaches caused by preeclampsia may be managed with pain medications while initiating preeclampsia treatment, including magnesium sulfate, antihypertensive medications, and admission to an obstetrics service for monitoring.[30] Please see StatPearls' companion resource, "Hypertension in Pregnancy", for further information on preeclampsia management. An ischemic stroke should undergo management with the aid of a neurologist for consideration of the initiation of thrombolytics or endovascular intervention. Spontaneous and traumatic intracranial hemorrhages may require neurosurgical intervention. Sinus venous thrombosis treatment is with systemic anticoagulation.[31] RCVS is frequently treated with the calcium channel blockers nimodipine and verapamil.[11] Please see StatPearls' companion resource, "Reversible Cerebral Vasoconstriction Syndromes", for further information on management.(A1)

The treatment for lymphocytic hypophysitis is high-dose corticosteroids, which effectively reduce pituitary size and improve the associated endocrine insufficiencies in 75% of cases. This condition has good outcomes with early recognition and treatment. Transsphenoidal resection may be required only in refractory cases.[15]

Differential Diagnosis

Differential diagnoses that should be considered when evaluating a patient with postpartum headache include:

• Cerebral infarction 
• Cluster headaches
• Medication overuse
• Trigeminal autonomic cephalgias
• Musculoskeletal headaches
• Reversible cerebral vasoconstrictive syndrome (RCVS)
• Cortical vein thrombosis
• Meningitis
• Migraine 
• Posterior reversible encephalopathy syndrome (PRES)
• Tension headache
• Post-dural puncture headache 
• Pituitary adenoma
• Preeclampsia/eclampsia
• Ischemic stroke
• Choriocarcinoma or other brain tumors
• Sinusitis
• Subarachnoid hemorrhage 
• Sheehan syndrome (pituitary apoplexy)
• Postpartum lymphocytic hypophysitis
• Traumatic intracranial pathology
• Rupture of a vascular malformation or aneurysm

Prognosis

The prognosis of exacerbations of primary headache disorders and PDPH is excellent as neither of these diseases is life-threatening. However, both conditions can lead to a delayed return to function, economic hardship, and additional emotional turmoil during an already stressful life change. Healthcare practitioners should consider these non-mortality-centered issues when counseling patients, giving discharge instructions, and arranging follow-up care.

The prognosis for other causes of secondary headaches depends on the primary disease. Patients with postpartum courses complicated by preeclampsia have a mortality rate of 6.4 per 10,000 cases.[32] Multiple studies have shown African American women to be at greater risk than the general population for the development of postpartum preeclampsia, progression to eclampsia, and morbidity and mortality from hypertensive diseases of pregnancy and the puerperium.[33][32]

Meningitis in the postpartum period has approximately a 20% mortality, resulting primarily from a delay in diagnosis rather than significant antibiotic resistance in this patient group.[34][35] Strokes in the postpartum period carry a 5% mortality rate, with hemorrhagic strokes having greater mortality than ischemic strokes and resulting in greater deficits, leading to permanent functional decline.[7] Patients with hypertensive disease of pregnancy have a higher risk of complications, including the need for mechanical ventilation and prolonged hospital stay.[7][36] 

RCVS is usually self-limited, with the resolution of bothrial abnormalities and headaches seen in 1 to 3 months for 90% of patients. However, timely diagnosis results in better clinical outcomes.

Complications

Prompt diagnosis and treatment initiation is imperative in secondary headache syndromes as delay can result in loss of life or permanent disability. The diagnosis of the life and limb-threatening disease is particularly crucial, as it represents an opportunity for acute intervention that accounts for a significant increase in both morbidity and mortality from postpartum headaches. The diagnosis of the life and limb-threatening underlying etiologies of postpartum headache also can have substantial social and medicolegal consequences for cases of missed or delayed diagnosis.