- Email: [email protected]
Postpartum headache
International Journal of Obstetric Anesthesia (2010) 19, 422–430 0959-289X/$ - see front matter c 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.ijoa.2010.07.009
REVIEW ARTICLE
www.obstetanesthesia.com
Postpartum headache A.M. Klein, E. Loder Department of Neurology, Harvard Medical School, Boston, MA, USA ABSTRACT Headache is a common puerperal complaint. A wide variety of factors can be involved, ranging from hormonal shifts, physiological changes, and peripartum procedures that may precipitate, worsen, or cause troublesome headache. The differential diagnosis of postpartum headache is broad and potentially daunting to the various clinicians caring for the postpartum patient. It often requires further neurological consultation or imaging to resolve. This review will focus on the main causes of postpartum headache, their incidence, and clinical presentation. Causes of postpartum headache that will be covered include benign primary headache disorders such as migraine and tension type headache as well as secondary headache disorders such as postdural puncture headache, stroke, and venous sinus thrombosis. A structured approach to headache evaluation in the postpartum patient will be presented to help differentiate the possible causes of headache. c 2010 Elsevier Ltd. All rights reserved.
Introduction Headache is a common puerperal complaint that can be precipitated, worsened or caused by a wide variety of factors ranging from hormonal shifts, physiological changes and peripartum procedures. The differential diagnosis of postpartum headache is broad, potentially daunting to the various clinicians providing care and often requiring further neurological consultation or imaging to resolve. This review focuses on the main causes of postpartum headache, their incidence, and clinical presentation. Causes of postpartum headache that are covered include benign primary headache disorders such as migraine and tension type headache as well as secondary headache disorders such as postdural puncture headache (PDPH), stroke, and venous sinus thrombosis.
Incidence of postpartum headache The overall incidence of postpartum headache is difficult to ascertain. Minor headaches are often not reported since they are thought to be normal for the postpartum period or overshadowed by events surrounding childbirth. Research studies on this subject are often limited by analysis from a single specialty group (e.g., anesthesiologists, neurologists, obstetricians), focused only on Accepted July 2010 Correspondence to: Autumn Klein, MD PhD, Director, Program in Women’s Neurology, Instructor, Harvard Medical School, Tower 5D, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA. E-mail address: [email protected]
inpatients in the immediate postpartum period (2–4 days on average), or lacking rigorous headache criteria. Despite these limitations, there are several recent studies that have looked robustly at the incidence of postpartum headaches (Table 1). One prospective cohort study of almost a thousand women over a three-month period in a single institution in Canada showed that 39% of women reported headache in the first week after delivery. Diagnoses were made according to the International Classification for Headache Disorders (ICHD),1 with the majority attributed to tension-type headache, 4.7% due to PDPH, and 8.1% due to undetermined causes.2 One study of women’s health after childbirth performed in France and Italy showed that physical symptoms were more common at 12 months than five months and that almost one third of women reported a headache (45.1% at 12 months versus 22.5% at 5 months).3 While this longitudinal study included different demographic populations, it was focused on socioeconomic factors related to women’s health and thus lacked information on specific headache diagnoses in the immediate postpartum period. An Italian study suggested that 5% of women developed migraine for the first time during the postpartum period.4 Finally, a prospective Italian study performed at an obstetrical clinic looking specifically for migraine showed that 34% of women had migraines recur in the first week postpartum and 55% within the first month.5 Several studies have examined postpartum headache related to the use of labor analgesia. In a general obstetric population in the UK, about 23% of women receiving epidural analgesia reported headache.6 In a later
A.M. Klein, E. Loder Table 1
423
Postpartum headache studies
Author
Population
Prevalence
Comment
General OB
Prospective >1000 patients, ICHD criteria
Saurel-Cubizolles3 General OB
39% In 1 week 75% Primary headache 1/3 Women headache
Grove6
General OB
23%
Benhamou7
Epidurals, no known dural puncture 12%
Granella4
Headache clinic – migraine
Sances5
OB clinic – migraine
Goldszmidt
2
Longitudinal interviews 5 and 12 months postpartum Excluded women with epidurals Most on postpartum day 1 or 2 Mailed survey 1200 41% response
5% First time Retrospective postpartum migraine 34% Migraine 1st week, Retrospective 55% 4th week
ICHD: International Classification for Headache Disorders.
study, 12% of women with epidural analgesia but without dural puncture reported headache at two weeks after delivery.7 Of interest, 15% of women without epidural analgesia reported headache. Due to the low number of women who did not receive epidural analgesia and the low response rate to the questionnaire, low study power limited the ability to make meaningful comparisons. These percentages may be somewhat altered by breastfeeding and other factors that affect headache. However, despite these studies being conducted in different countries with different patient populations, methods and diagnostic criteria, all concluded that postpartum headache is common. Given the high prevalence of primary headache disorders, it is not surprising that this entity was the most common headache diagnosis in these studies.
Differential diagnosis of postpartum headache The differential diagnosis of postpartum headache is extensive but can be easily focused on primary and secondary causes. Worrisome headache characteristics or ‘red flags’ are similar to those in the non-pregnant patient (Table 2). Primary headache disorders, such as migraine and tension type headache, are common in reproductive age women and are diagnosed using well-defined criteria established by the ICHD.1 The probability that a headache in a postpartum patient has a secondary cause is low, but such disorders can cause significant morbidity and mortality if missed. This Table 2
Worrisome headache features
New neurological symptoms with headache Change in character or pattern of any previously diagnosed headache type New headache, especially if fixed to one side Sudden uncontrollable vomiting Change in mental status with headache Headache not relieved by pain medications Other concerning medical issue (bleeding disorder, immunocompromised)
review focuses on stroke (ischemic, hemorrhagic, and venous), as well as PDPH, preeclampsia/eclampsia, and a few rare other diagnoses. A more complete, although not exhaustive, list of dangerous causes of postpartum headache can be found in Table 3. Certain factors, such as a history of headache, peripartum events such as epidural administration, hypertension, and the timing of onset of headache can assist in narrowing the diagnostic considerations and provide a framework for approaching the patient with a postpartum headache (Fig. 1). If a primary headache is suspected, pre-pregnancy headache characteristics as well as the pattern of headache in pregnancy and the postpartum period can be very helpful. This information, in conjunction with the ICHD criteria for primary headache types, will help determine whether imaging would be of assistance. Given the hypercoaguable state of women during the Table 3
Differential diagnosis of postpartum headache
Primary Migraine Tension-type headache Cluster Vascular Ischemic stroke Hemorrhagic stroke Subarachnoid hemorrhage Vascular malformation (aneurysm, AVM) Hypertension Venous sinus thrombosis Dissection Vasculidities Reversible cerebral vasoconstrictive syndromes Other Preeclapmsia/eclampsia Benign intracranial hypertension Sinusitis Drug use Postdural puncture headache Tumor
424
Postpartum headache Question
Possible cause
Test to confirm
Comments
Is headache postural or associated with tinnitus or hypacusia?
Low pressure headache
Empirical treatment is appropriate if no other cause of headache is apparent and diagnostic suspicion is high. Otherwise, MRI with gadolinium may show meningeal enhancement; LP may show low pressure; CT myelogram may show leak; radionuclide cisternogram may pick up slow leaks
Postural features may be subtle, particularly if headache is longstanding; case reports suggest this diagnosis is sometimes mistaken; do not discard alternative diagnoses too quickly
Is there a history of similar headaches?
A third to a half of women with a history of migraine will have postpartum headache
Assess against diagnostic criteria (see tables)
Migraine increases risk of or may co-occur with dangerous causes of headache. Consider avoiding use of vasoconstrictive migraine treatments such as triptans or ergots even if a diagnosis of migraine seems certain because of rare but serious risk of precipitating vasoconstriction
Did headache come on abruptly or gradually?
Aneurysmal subarachnoid hemorrhage, cerebral venous thrombosis, reversible cerebral vasoconstrictive syndrome
Plain CT, LP to assess for hemorrhage, if negative then MRA/MRV looking for cerebral venous thrombosis or typical bead-like appearance of vasoconstrictive syndromes
Occasionally migraine will begin suddenly, so-called ‘crash migraine’, but this is a diagnosis of exclusion.
Is headache associated with hypertension, proteinuria or seizure?
Postpartum preeclampsia or eclampsia
Assess and monitor for proteinuria, hypertension and hyperreflexia
Headache can precede other signs of preeclampsia and may mimic that of migraine; the risk of preeclampsia is elevated in women with migraine, especially migraine with aura
Has the patient received or used any vasoconstrictive medications?
Reversible cerebral vasoconstrictive syndromes
MRI/MRV looking for typical bead-like appearance of vessels seen in vasoconstrictive syndromes
Nonprescribed licit and illicit drugs should be considered, e.g. cocaine, pseudephredrine
Fig. 1 A history-driven approach to postpartum headache. LP: lumbar puncture; MRA: magnetic resonance angiography; MRV: magnetic resonance venography.
puerperium, and possible obstetrical complications associated with pregnancy and the postpartum period, the threshold for further evaluation and imaging in this population should be low. Breastfeeding is not a contraindication to imaging procedures when they are needed. Contrast and gadolinium can be administered and then the breast milk can be pumped and discarded.
Primary causes A high index of suspicion for dangerous or secondary causes of headache is appropriate in the postpartum period. Even in this setting, though, approximately 50–75% of headaches are due to primary headache disorders, particularly migraine. Approximately one-third of childbearing age women have migraine.8 Greater than 75% of patients with primary headache disorders can expect noticeable improvement during pregnancy, although many experience a flare after delivery.4 In one study, nearly a thousand consecutive women who delivered in a single hospital were carefully evaluated and followed for the development of headaches. Primary headaches, mostly migraine, were the cause of over 75% of cases.2 In another case series of 95 women, migraine or tension-type headaches were ultimately diagnosed as the cause of postpartum headache in 47%. In one study performed at an obstetric clinic, headaches occurred within a week of delivery in 34%, and within a month in 55.3%.5 Falling estrogen levels, particularly after a long period of stability, are a potent migraine trigger, but the
sleep disturbances and emotional stress of parenthood may play a role as well. Little attention has been paid to ways of minimizing the chance of migraine flares after delivery. One study suggested that headaches were less likely in women who participated in childbirth preparation classes, and another demonstrated that the likelihood of migraine return after delivery was lessened in women who breastfed their infants.5,9 Diagnostic criteria for primary headache disorders are contained in the ICHD.1 The criteria for the most common primary headaches, migraine with and without aura, and tension-type headache, are reproduced in Tables 4 and 5. Tension-type headache is the most common headache in the general population, but usually does not come to medical attention since most sufferers self-treat with simple analgesics. Nausea, vomiting and sensitivity to light and noise are characteristic of migraine but can accompany dangerous causes of headache as well. Migraine is associated with an increased risk of some dangerous causes of headache such as postpartum stroke and preeclampsia.10,11 While primary headache disorders can appear for the first time during or after pregnancy, onset of a new type of headache during this time is worrisome. In contrast, a primary headache is more likely to be the diagnosis in a woman who is known to have a history of such headaches. One study found that most women who develop postpartum headache had a history of migraine, and most described the postpartum headaches they had as
A.M. Klein, E. Loder Table 4 Diagnostic criteria for migraine with and without aura1 Migraine without aura A. At least five attacks fulfilling criteria B–D B. Headache attacks lasting 4–72 h (untreated or unsuccessfully treated) C. Headache has at least two of the following characteristics:
Unilateral location Pulsating quality Moderate or severe intensity Aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)
D. During headache at least one of the following: Nausea and/or vomiting Photophobia and phonophobia
E. Not attributed to another disorder Typical aura with migraine headache A. At least two attacks fulfilling criteria B–D B. Aura consisting of at least one of the following, but no motor weakness: Fully reversible visual symptoms including positive features (e.g., flickering lights. spots or lines) and/or negative features (e.g., loss of vision) Fully reversible sensory symptoms including positive features (i.e., pins and needles) and/or negative features (e.g., numbness) Fully reversible dysphasic speech disturbance
C. At least two of the following: Homonymous visual symptoms and/or unilateral sensory symptoms At least one aura symptom develops gradually over P5 min and/or different aura symptoms occur in succession over P5 min Each symptom lasts P5 and 660 min
D. Headache fulfilling criteria B–D for 1.1 ‘Migraine without aura’ begins during the aura or follows aura within 60 min E. Not attributed to another disorder
Table 5
Diagnostic criteria for tension type headache1
A. At least 10 episodes fulfilling criteria B–D B. Headache lasting from 30 min to 7 days C. Headache has at least two of the following characteristics:
bilateral location pressing/tightening (non-pulsating) quality mild or moderate intensity not aggravated by routine physical activity such as walking or climbing stairs
D. Both of the following: no nausea or vomiting (anorexia may occur) no more than one of photophobia or phonophobia
Not attributed to another disorder Considered infrequent if less than 1 day per month on average; frequent if more than 1 and less than 15 days per month on average, and chronic if 15 or more days per month.;
‘‘considerably milder’’ than their usual headaches. The authors of this study also calculated that a history of headache raised the risk for postpartum headache by a factor of 1.5.12 Migraine, then, increases the risk of both dangerous and non-dangerous causes of postpartum headache. In contrast, there is no evidence that women
425 with cluster or tension-type headache are at higher than average risk of puerperal headaches.13
Secondary causes Although the majority of postpartum headaches are benign, the risk of some important secondary causes of headache is elevated in the puerperium. In most circumstances, a history of a primary headache disorder such as migraine is reassuring, but women with migraine have an increased risk of serious causes of headache including preeclampsia, stroke and even, perhaps, cerebral vasoconstrictive syndromes. The headache features of many of these disorders overlap with those of migraine, so that accurate diagnosis can be challenging.
Distinguishing primary from secondary headaches Migraine is common in women of childbearing age and the abrupt postpartum decline in estrogen levels is a potent trigger of migraine attacks. Additionally, many parturients have received epidural analgesia for delivery. Migraine and PDPH are accordingly high on the list of diagnostic possibilities in many women who complain of headache following delivery. The high prior probability of these two causes of headache, though, may paradoxically increase the likelihood of misdiagnosis if doctors fail to consider alternative causes with which they are less familiar. Because the features of many types of postpartum headache overlap, it is easy to mistake one type of headache for another. Case reports suggest that diagnoses of PDPH should be made with special caution. While there may be publication bias, a large number of case reports discuss mistaken diagnoses of PDPH in women who turned out to have cerebral venous thrombosis or, less commonly, cerebral vasoconstrictive syndromes, meningitis, postpartum preeclampsia or stroke.14–20 Patients with a history of severe primary headache disorders may also be at an elevated risk of having a serious cause of postpartum headache diagnosed as an exacerbation of the pre-existing disorder.21 An overly strong belief in the principle of diagnostic parsimony can also lead to trouble. Although uncommon, it is possible for a postpartum patient to have more than one cause of headache.15,22–24 In addition to the unusual secondary causes of headache considered above, prescribed and non-prescribed drugs (both licit and illicit) should be considered as a possible cause of postpartum headache.25
Headache attributed to low cerebrospinal fluid pressure Spinal or epidural techniques are commonly used for labor and delivery.26 Thus, in the postpartum setting,
426 headache due to low cerebrospinal fluid (CSF) pressure is usually due to unintended dural puncture. Cases have also been reported in which leakage of CSF probably occurred spontaneously during delivery without anesthetic intervention, perhaps as a result of mechanical trauma from prolonged pushing and straining.27 It is likely that some unrecognized dural tears occur that produce few, if any, symptoms and resolve spontaneously.28 In one study of 229 consecutive women who received labor epidural analgesia and were closely queried about subsequent headache, most of the headaches were reported as mild, with only three requiring treatment with an epidural blood patch.2 If the puncture does not seal spontaneously, low CSF pressure may cause traction on pain-sensitive meningeal structures and result in more severe headache that comes to medical attention; 75% of women with medically recognized PDPH reported that it limited daily activities. In most cases, inadvertent dural puncture is recognized at the time it occurs. Interestingly, in those circumstances, a prophylactic epidural blood patch or the placement of spinal catheters does not seem to prevent subsequent headache.29,30 The reported incidence of PDPH ranges from approximately 1–16% in various small case series.2,31,32 A larger study evaluated the records of over 65 000 women who had received anesthetic interventions. Postdural puncture headache was diagnosed in 404, of whom 240 had an epidural blood patch. In this series, the overall incidence of headache in women who had one anesthetic intervention was low (1.1–1.9%), but increased to 11% in women who had multiple anesthetic procedures.29 It seems unlikely that the true incidence of PDPH varies so greatly; rather, the variability probably reflects study differences in the quality, timing and thoroughness of ascertainment. A meta-analysis of individual studies suggests that the incidence is likely to be about 1.5%.33,34 Despite this, there is general agreement that the occurrence of PDPH following epidural analgesia is influenced to some degree by anesthetic technique, with atraumatic (pencil-point) and smaller sized needles, among other things, shown to reduce the risk of dural puncture.35 Low pressure headache due to CSF leak is usually mild or absent when the patient is lying down, but worsens with upright posture. In a large series of patients with PDPH, this postural effect was reported by 80% of patients.16 The worsening or improvement in headache severity usually takes place within 15 min of a change in posture and is gradual rather than abrupt. The postural quality of the headache may be subtle and may even disappear if the headache becomes chronic. Table 6 lists ICHD criteria for the diagnosis of postdural puncture and spontaneous low-pressure headache. Symptoms often overlap with those seen in other primary and secondary headaches. Tinnitus, diplopia or hypacusia, however, are uncommon symptoms
Postpartum headache Table 6 Diagnostic criteria for headaches attributed to low cerebrospinal fluid pressure1 Postdural puncture headache A. Headache that worsens within 15 min after sitting or standing and improves within 15 min after lying, with at least one of the following and fulfilling criteria C and D:
neck stiffness tinnitus hypacusia photophobia nausea
B. Dural puncture has been performed C. Headache develops within 5 days after dural puncture D. Headache resolves either: spontaneously within 1 week within 48 h after effective treatment of CSF leak (usually by epidural blood patch)
Headache attributed to spontaneous (idiopathic) low CSF pressure A. Diffuse and/or dull headache that worsens within 15 min after sitting or standing, with at least one of the following and fulfilling criterion D:
neck stiffness tinnitus hypacusia photophobia nausea
B. At least one of the following: evidence of low CSF pressure on MRI (e.g., pachymeningeal enhancement) evidence of CSF leak on conventional myelography, CT myelography or cisternography CSF opening pressure <60 mm H2O in sitting position
C. No history of dural puncture or other cause of CSF fistula D. Headache resolves within 72 h after epidural blood patch
of primary headaches and should prompt suspicion of a low-pressure headache syndrome. Shoulder and neck stiffness are surprisingly common in the postpartum period, as well as in almost half of patients with PDPH; consequently, this symptom is not especially useful in formulating or ruling out a diagnosis. If there is strong reason to suspect a low-pressure headache, such as in the case of a parturient who received epidural analgesia and has no other apparent cause of headache, confirmatory testing is probably unnecessary: the prior probability of a leak is high and its location almost certain.36 In that case, it is reasonable to treat a troublesome headache with an epidural blood patch. An alternative strategy of watchful waiting could also be considered for milder headaches, since postdural puncture headache frequently resolves spontaneously within a week and in the meantime can often be managed conservatively with bed rest, caffeine, and fluids. A watchful waiting approach is somewhat controversial, however, as studies have suggested long-term headaches may result if PDPH is not managed actively.37 For this reason, intervention with a blood patch is prudent if headaches persist beyond a week.
A.M. Klein, E. Loder Traditional teaching is that if an epidural blood patch is attempted, the headache should be gone within 48 h in >95% of cases. Several studies have called into question the efficacy of blood patching in obstetric patients, however, and suggested that success rates with blood patching may not be as high as previously thought.38,39 Blood patches often need to be repeated after initial success is followed by subsequent return of headache. While a second blood patch is almost always successful, it is reasonable to perform additional blood patches if the positional headaches continue. Some patients do not have headache following delivery but develop positional headache days to weeks later. Presumably these late-presenting cases result from spontaneous re-opening of a small tear that sealed over or from enlargement of a small, initially asymptomatic dural tear. In these patients, the positional component of the headache may not be dramatic, and symptoms may be more meningeal or radicular. The headaches may be diagnosed as a primary headache disorder since these often return within a few weeks of delivery. To distinguish between the two possibilities, it is useful to inquire about the orthostatic nature of the headaches and to evaluate other symptoms. An epidural blood patch should be considered in these cases when the diagnosis seems obvious, but if there is any doubt magnetic resonance imaging (MRI) of the brain with gadolinium as well as magnetic resonance angiography (MRA) and venography (MRV) should also be considered, particularly if the patient has focal symptoms or vision changes. This will help to rule out any rare secondary causes of headache such as subdural hemorrhage, subarachnoid hemorrhage, or cerebral venous sinus thrombosis. A subset of patients with positional headaches who do not have clear evidence of a dural tear might have meningeal weakness, perhaps due to an underlying connective tissue disorder. It is theorized that this may lead to pooling of CSF and symptoms consistent with low CSF pressure even in the absence of a true leak. In other cases, it is theorized that spontaneous dural tears can develop that lead to CSF leakage. These spontaneous tears or defects are often located anterior to or at nerve root sheaths. This makes localization of the tear more difficult, and blood patching is less likely to be effective. Patients with areas of dural weakness may be predisposed to recurrence of positional headaches, although the rate of recurrence has not been determined. Orthostatic symptoms in these recurrent headaches can be subtle and may be unrecognized, increasing the risk that headaches will not be appropriately treated and worsen over time to become chronic daily headaches. In suspected cases of postural headache, lumbar puncture may demonstrate a low opening pressure, but pressure can also be normal. If CSF fluid is analyzed, increased protein and a lymphocytic pleocytosis may be seen.40 MRI of the brain with gadolinium may show
427 pachymeningeal enhancement, and various studies can be used to document the location of the leak. Computed tomography (CT) myelography is probably the most sensitive test; radioisotope studies with Indium-111 are also sometimes used.41 Imaging may demonstrate ‘sagging’ of the brain with descent of the cerebellar tonsils or even thin, bilateral subdural fluid collections, all of which resolve when the leak is effectively treated.41
Reversible cerebral vasoconstrictive syndromes A large number of labels have been applied to headaches attributed to vasoconstriction of the cerebral arteries including Call-Fleming Syndrome and postpartum angiopathy, but the descriptive term reversible cerebral vasoconstrictive syndromes (RCVS) is increasingly preferred for this group of disorders.42–44 In the absence of large population-based epidemiologic studies, the prevalence of RCVS in general, during pregnancy or during the postpartum period is unknown, but it is probably more common than generally appreciated.21 Since vasoconstriction is reversible, headache may remit spontaneously, and so an accurate diagnosis is never made. As with some other secondary causes of postpartum headache, patients with migraine may be more susceptible to RCVS, and some of the vasoconstrictive drugs used to treat migraine may also increase risk. The underlying mechanism is not known,42 although in two thirds of cases, a precipitant, especially the use of vasoconstrictive substances such as bromocriptine, ergots, pseudoephedrine or SSRIs in the puerperium, is evident.45 The characteristic headache in these syndromes is severe and abrupt in onset, so-called ‘thunderclap headache’ and multiple attacks may occur in close succession. It may be associated with a variety of other symptoms including confusion, agitation or focal neurologic signs (Table 7).46 Although the headache and vasoconstriction eventually remit without treatment, usually within two months, serious complications can occur rapidly after onset.47–50 Within the first week after diagnosis in one case series of 67 patients with angiographically confirmed RCVS, subarachnoid hemorrhage occurred in 22%, intracerebral hemorrhage in 6%, seizures in 3% and posterior leukoencephalopathy in 9%. Ischemic events and infarction also occurred, but were more likely in the second week.45 Reversible cerebral vasoconstrictive syndromes must be distinguished from other causes of severe, sudden headache, so the typical workup includes a non-contrast CT scan to rule out subarachnoid hemorrhage, and if negative, a lumbar puncture to assess for CT-negative subarachnoid hemorrhage, infection or vasculitis.50,51 Formal angiography can assess for cerebral venous thrombosis and RCVS. The diagnosis of RCVS is suggested by multifocal segmental ‘bead and string’ constriction of cerebral arteries, in the absence of
428
Postpartum headache
Table 7
Headache attributed to benign or reversible CNS angiopathy
A. Diffuse, severe headache of abrupt or progressive onset, with or without focal neurological deficits and/or seizures and fulfilling criteria C and D B. ‘Strings and beads’ appearance on angiography and subarachnoid haemorrhage ruled out by appropriate investigations C. One or both of the following: headache develops simultaneously with neurological deficits and/or seizures headache leads to angiography and discovery of ‘‘strings and beads’’ appearance
D. Headache (and neurological deficits, if present) resolves spontaneously within 2 months
subarachnoid hemorrhage or abnormal CSF.42 Because the constriction begins distally and works its way proximally, serial imaging may be needed to demonstrate the characteristic pattern of vasoconstriction.
Postpartum stroke Stroke plays a major role in over 12% of maternal deaths and contributes to fetal morbidity and mortality.51 Early diagnosis of stroke is critical to the patient’s and child’s well-being. Studies of stroke in pregnancy and the puerperium have estimated an incidence from 4.3 to 210 per 100 000 women. The large range is due to variations in the populations studied, stroke classifications (ischemic, hemorrhagic, and venous), and elapsed time to followup (zero to eight weeks postpartum). Three well-designed population-based studies carried out in recent years provide the most accurate estimate of stroke in pregnancy but lack specific postpartum information.52–54 Most studies agree that strokes of any etiology occur primarily in the third trimester and postpartum period; this is likely due to the significant physiological changes at these times. Women become hypercoaguable as pregnancy progresses, with peak hypercoagulability in the immediate postpartum period.55 Rising estrogen levels cause vasodilation, which may explain why vascular malformations and aneurysms are more likely to rupture. The etiology of strokes in most studies was found to be mostly ischemic with cardioemboli, venous sinus thrombosis and preeclampsia–eclampsia as the main causes. Hemorrhagic strokes are primarily due to vascular malformations and subarachnoid hemorrhage. Strokes restricted to the intraparenchymal brain tissue often occur without associated pain. Headache from stroke results from disturbance of the pain sensitive structures of the head, which include the meninges, extracranial, and short courses of some of the major intracranial blood vessels. It has been estimated that approximately 10% of patients with stroke develop headache.56 Posterior, versus anterior, circulation strokes are more often associated with headache, but this may be related to their propensity to become hemorrhagic. Nonetheless, the most diagnostic feature of a stroke’s location is the associated neurological symptoms. Headaches from stroke occur suddenly and either coincidently or immediately following associated neurological features. By contrast, the headache of migraine
usually follows the neurological symptoms by approximately 15–30 min. If neurological symptoms last more than an hour before onset of the headache, then the diagnosis of stroke, or migrainous infarction should be considered. Neurological symptoms associated with stroke are usually negative such as the absence of speech, whereas those with migraine are usually positive (e.g., fortification spectra). Headache from stroke often remits quickly, which may present a diagnostic clue in determining the etiology.57 In cases where stroke is suspected, MRI with diffusion is diagnostic. Vascular imaging with MRA and MRV is essential in the postpartum patient and in cases of possible vascular malformation or aneurysm, formal angiogram may be considered.
Cerebral venous sinus thrombosis If trauma is not involved, central venous sinus thrombosis (CVT) is a disease that is almost always limited to peripartum women or young women using estrogencontaining contraceptives. Symptoms can begin gradually and may be confused with other primary headaches or PDPH. Presentation ranges from mild headache to coma. Hypercoaguable state, damaged endothelium from pushing in labor and relative intracranial hypotension after epidural and postpartum diuresis are all factors contributing to symptoms and headache. Imaging with MRV is critical to make the diagnosis. Seizures occur in almost two thirds of CVT cases and consequently, electroencephalograms are recommended, especially if the patient is complaining of positive or intermittent neurological symptoms.
Preeclampsia–eclampsia Preeclampsia is defined by the National High Blood Pressure Program Working Group on High Blood Pressure in Pregnancy as hypertension and proteinuria in pregnancy. Eclampsia is defined as seizures not attributable to other causes in the setting of preeclampsia.58 Preeclampsia affects 3–5% of pregnant women,59 and approximately 1 in 2000 deliveries in the United States are associated with an eclamptic seizure.60 While the cause of preeclampsia and eclampsia is not precisely known, abnormal placentation and endothelial dysfunction are leading hypotheses which in turn result in
A.M. Klein, E. Loder placental hypoperfusion, increased vascular tone, systemic hypertension, and decreased organ perfusion. Autoantibodies, inflammatory mediators and genetic predisposition are also thought to play a role in the pathogenesis. The diagnosis of preeclampsia is based on the clinical presence of hypertension and proteinuria or edema. Eclampsia is based on the findings of encephalopathy or seizures in late pregnancy or the postpartum period; CT or MRI demonstrate characteristic edema and no other brain lesions. In severe preeclampsia, patients can have headache and visual changes. Despite the prevalence of preeclampsia and eclampsia, the associated headache characteristics have not been well studied. The risk of preeclampsia is increased in women with migraine, especially if an aura is present.10 Anecdotally, headache from preeclampsia is similar to other vascular-type headaches, but patients often note that it is distinctly different from other headache types. It is usually throbbing and holocephalic, or more posteriorly located. It may have characteristics of migraine (nausea, light sensitivity), but migraineurs are known to be at increased risk of preeclampsia and eclampsia so these features are not as useful as they might otherwise be.
Conclusion A high threshold of suspicion for dangerous causes of headache is appropriate when evaluating women with postpartum headache, even those with a long prior history of benign headaches. While most headaches in the postpartum period are usually benign, primary headaches, the threshold for diagnostic testing is lower than in non-pregnant women because of the serious consequences if a dangerous secondary cause of headache is missed. Appropriate testing strategies depend upon the possible diagnoses, and evaluation should be guided by a careful history and physical examination.
References 1. Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders, 2nd ed. Cephalalgia 2004;24(Suppl 1):9–160. 2. Goldszmidt E, Kern R, Chaput A, Macarthur A. The incidence and etiology of postpartum headaches: a prospective cohort study. Can J Anesth 2005;52:971–7. 3. Saurel-Cubizolles MJ, Romito P, Lelong N, Ancel PY. Women’s health after childbirth: a longitudinal study in France and Italy. BJOG 2000;107:1202–9. 4. Granella F, Sances G, Zanferrari C, Costa A, Martignoni E, Manzoni GC. Migraine without aura and reproductive life events: a clinical epidemiological study in 1300 women. Headache 1993;33:385–9. 5. Sances G, Granella F, Nappi RE, et al. Course of migraine during pregnancy and postpartum: a prospective study. Cephalalgia 2003;23:197–205. 6. Grove LH. Backache, headache and bladder dysfunction after delivery. Br J Anaesth 1973;45:1147–9.
429 7. Benhamou D, Hamza J, Ducot B. Post partum headache after epidural analgesia without dural puncture. Int J Obstet Anesth 1995;4:17–20. 8. Stewart WF, Wood C, Reed ML, Roy J, Lipton RBAMPP Advisory Group. Cumulative lifetime migraine incidence in women and men. Cephalalgia 2008;28:1170–8. 9. Mehdizadeh A, Roosta F, Chaichian S, Alaghehbandan R. Evaluation of the impact of birth preparation courses on the health of the mother and the newborn. Am J Perinatol 2005;22:7–9. 10. Facchinetti F, Allais G, Nappi RE, et al. Migraine is a risk factor for hypertensive disorders in pregnancy: a prospective cohort study. Cephalalgia 2009;29:286–92. 11. Bushnell CD, Jamison M, James AH. Migraines during pregnancy linked to stroke and vascular diseases: US population based casecontrol study. BMJ 2009;338:b664. 12. Stein G, Morton J, Marsh A, et al. Headaches after childbirth. Acta Neurol Scand 1984;69:74–9. 13. Manzoni GC, Micieli G, Granella F, Martignoni E, Farina S, Nappi G. Cluster headache in women: clinical findings and relationship with reproductive life. Cephalalgia 1988;8:37–44. 14. Karci A, Boyaci F, Yaka E, Cakmur R, Men S, Elar Z. Cerebral venous thrombosis initially considered as a complication of spinal–epidural anaesthesia. J Int Med Res 2005;33:711–4. 15. Ghatge S, Uppugonduri S, Kamarzaman Z. Cerebral venous sinus thrombosis following accidental dural puncture and epidural blood patch. Int J Obstet Anesth 2008;17:267–70. 16. Jungmann V, Werner R, Bergmann J, et al. Postpartum cerebral venous sinus thrombosis after epidural anaesthesia. Anaesthesist 2009;58:268–72. 17. Barrett J, Alves E. Postpartum cerebral venous sinus thrombosis after dural puncture and epidural blood patch. J Emerg Med 2005;28:341–2. 18. Umstad MP, Ross AW, Adey FD. Headache following epidural analgesia. Aust N Z J Obstet Gynaecol 1992;32:79–80. 19. Chisholm ME, Campbell DC. Postpartum postural headache due to superior sagittal sinus thrombosis mistaken for spontaneous intracranial hypotension. Can J Anesth 2001;48:302–4. 20. Lee JJ, Parry H. Bacterial meningitis following spinal anaesthesia for caesarean section. Br J Anaesth 1991;66:383–6. 21. Modi M, Modi G. Case reports: postpartum cerebral angiopathy in a patient with chronic migraine with aura. Headache 2000;40:677–81. 22. Anand A. Post-dural puncture headache associated with cerebral venous thrombosis. Br J Anaesth 2000;85:326–7. 23. Ho CM, Chan KH. Posterior reversible encephalopathy syndrome with vasospasm in a postpartum woman after postdural puncture headache following spinal anesthesia. Anesth Analg 2007; 105:770–2. 24. Winston AW, Norman D. Late postpartum eclampsia coincident with postdural puncture headache: a case report. AANA J 2003;71:371–2. 25. Maagdenberg T, Savci S, Iffy L. Cocaine intoxication mimicking preeclampsia postpartum. Int J Gynecol Obstet 2006;92:73–4. 26. Bucklin BA, Hawkins JL, Anderson JR, Ullrich FA. Obstetric anesthesia workforce survey: twenty-year update. Anesthesiology 2005;103:645–53. 27. Mokri B. Spontaneous low cerebrospinal pressure/volume headaches. Curr Neurol Neurosci Rep 2004;4:117–24. 28. Mokri B, Atkinson JL, Piepgras DG. Absent headache despite CSF volume depletion (intracranial hypotension). Neurology 2000;55:1722–4. 29. Chan TM, Ahmed E, Yentis SM, Holdcroft A. Obstetric Anaesthetists’ Association, NOAD Steering Group. Postpartum headaches: summary report of the National Obstetric Anaesthetic Database (NOAD) 1999. Int J Obstet Anesth 2003;12:107–12. 30. Scavone BM, Wong CA, Sullivan JT, Yaghmour E, Sherwani SS, McCarthy RJ. Efficacy of a prophylactic epidural blood patch in
430
31.
32.
33.
34.
35.
36. 37. 38.
39.
40. 41. 42.
43. 44.
45.
preventing post dural puncture headache in parturients after inadvertent dural puncture. Anesthesiology 2004;101:1422–7. Stella CL, Jodicke CD, How HY, Harkness UF, Sibai BM. Postpartum headache: is your work-up complete? Am J Obstet Gynecol 2007;196:318.e1–7. Ong B, Cohen MM, Cumming M, Palahniuk RJ. Obstetrical anaesthesia at Winnipeg Women’s Hospital 1975–83: anaesthetic techniques and complications. Can J Anaesth 1987;34: 294–9. Choi PT, Galinski SE, Takeuchi L, Lucas S, Tamayo C, Jadad AR. PDPH is a common complication of neuraxial blockade in parturients: a meta-analysis of obstetrical studies. Can J Anesth 2003;50:460–9. Choi PT, Galinski SE, Lucas S, Takeuchi L, Jadad AR. Examining the evidence in anesthesia literature: a survey and evaluation of obstetrical postdural puncture headache reports. Can J Anesth 2002;49:49–56. Evron S, Sessler D, Sadan O, Boaz M, Glezerman M, Ezri T. Identification of the epidural space. Loss of resistance with air, lidocaine, or the combination of air and lidocaine. Anesth Analg 2004;99:245–50. Mokri B. Headaches caused by decreased intracranial pressure: diagnosis and management. Curr Opin Neurol 2003;16:319–26. MacArthur C, Lewis M, Knox EG. Accidental dural puncture in obstetric patients and long term symptoms. BMJ 1993;306:883–5. Williams EJ, Beaulieu P, Fawcett WJ, Jenkins JG. Efficacy of epidural blood patch in the obstetric population. Int J Obstet Anesth 1999;8:105–9. Banks S, Paech M, Gurrin L. An audit of epidural blood patch after accidental dural puncture with a Tuohy needle in obstetric patients. Int J Obstet Anesth 2001;10:173–6. Mokri B. Syndrome of cerebral spinal fluid hypovolemia: clinical and imaging features and outcome. Neurology 2001;56:1607–8. Mokri B. Cerebrospinal fluid volume depletion and its emerging clinical/imaging syndromes. Neurosurg Focus 2000;9:e6. Calabrese LH, Dodick DW, Schwedt TJ, Singhal AB. Narrative review: reversible cerebral vasoconstriction syndromes. Ann Intern Med 2007;146:34–44. Singhal AB, Bernstein RA. Postpartum angiopathy and other cerebral vasoconstriction syndromes. Neurocrit Care 2005;3:91–7. Neudecker S, Stock K, Krasnianski M. Call-Fleming postpartum angiopathy in the puerperium: a reversible cerebral vasoconstriction syndrome. Obstet Gynecol 2006;107:446–9. Ducros A, Boukobza M, Porcher R, Sarov M, Valade D, Bousser MG. The clinical and radiological spectrum of reversible cerebral
Postpartum headache
46.
47.
48.
49. 50. 51.
52. 53. 54.
55.
56. 57. 58.
59. 60.
vasoconstriction syndrome. A prospective series of 67 patients. Brain 2007;130:3091–101. Chandrashekaran S, Parikh S, Kapoor P, Subbarayan S. Postpartum reversible cerebral vasoconstriction syndrome. Am J Med Sci 2007;334:222–4. Cho AH, Lim SC, Kim BS, Yang DW, Shon YM. Atypical presentation of postpartum cerebral angiopathy shown as a small penetrating arterial territory infarct with severe peri-infarct edema. J Neuroimaging 2010;20:290–1. Sengoku R, Iguchi Y, Yaguchi H, Sato H, Inoue K. A case of postpartum cerebral angiopathy with intracranial hemorrhage and subarachnoid hemorrhage immediately after delivery. Rinsho Shinkeigaku 2005;45:376–9. Gladstone JP, Dodick DW, Evans R. The young woman with postpartum ‘‘thunderclap’’ headache. Headache 2005;45:70–4. Sharma P, Poppe AY, Eesa M, Steffenhagen N, Goyal M. Postpartum thunderclap headache. CMAJ 2008;179:1033–5. Dias MS, Sekhar LN. Intracranial hemorrhage from aneurysms and arteriovenous malformations during pregnancy and the puerperium. Neurosurgery 1990;27:855–65. Kittner SJ, Stern BJ, Feeser BR, et al. Pregnancy and the risk of stroke. N Engl J Med 1996;335:768–74. Wiebers DO, Mokri B. Internal carotid artery dissection after childbirth. Stroke 1985;16:956–9. Sharshar T, Lamy C, Mas JL. Incidence and causes of strokes associated with pregnancy and puerperium. A study in public hospitals of Ile de France. Stroke in Pregnancy Study Group. Stroke 1995;26:930–6. Wickstrom K, Edelstam G, Lowbeer CH, Hansson LO, Siegbahn A. Reference intervals for plasma levels of fibronectin, von Willebrand factor, free protein S and antithrombin during thirdtrimester pregnancy. Scand J Clin Lab Invest 2004;64: 31–40. Edmeads J. Headache in cerebrovascular disease. A common symptom of stroke. Postgrad Med 1987;81;191,193,196–8 Edmeads J. Headache as a symptom of cerebrovascular disease. Clin J Pain 1989;5:89–93. Roberts JM, Pearson G, Cutler J, Lindheimer M. NHLBI working group on research on hypertension during pregnancy. Summary of the NHLBI working group on research on hypertension during pregnancy. Hypertension 2003;41:437–45. Roberts JM, Cooper DW. Pathogenesis and genetics of preeclampsia. Lancet 2001;357:53–6. Saftlas AF, Olson DR, Franks AL, Atrash HK, Pokras R. Epidemiology of preeclampsia and eclampsia in the United States, 1979–1986. Am J Obstet Gynecol 1990;163:460–5.
REVIEW ARTICLE
www.obstetanesthesia.com
Postpartum headache A.M. Klein, E. Loder Department of Neurology, Harvard Medical School, Boston, MA, USA ABSTRACT Headache is a common puerperal complaint. A wide variety of factors can be involved, ranging from hormonal shifts, physiological changes, and peripartum procedures that may precipitate, worsen, or cause troublesome headache. The differential diagnosis of postpartum headache is broad and potentially daunting to the various clinicians caring for the postpartum patient. It often requires further neurological consultation or imaging to resolve. This review will focus on the main causes of postpartum headache, their incidence, and clinical presentation. Causes of postpartum headache that will be covered include benign primary headache disorders such as migraine and tension type headache as well as secondary headache disorders such as postdural puncture headache, stroke, and venous sinus thrombosis. A structured approach to headache evaluation in the postpartum patient will be presented to help differentiate the possible causes of headache. c 2010 Elsevier Ltd. All rights reserved.
Introduction Headache is a common puerperal complaint that can be precipitated, worsened or caused by a wide variety of factors ranging from hormonal shifts, physiological changes and peripartum procedures. The differential diagnosis of postpartum headache is broad, potentially daunting to the various clinicians providing care and often requiring further neurological consultation or imaging to resolve. This review focuses on the main causes of postpartum headache, their incidence, and clinical presentation. Causes of postpartum headache that are covered include benign primary headache disorders such as migraine and tension type headache as well as secondary headache disorders such as postdural puncture headache (PDPH), stroke, and venous sinus thrombosis.
Incidence of postpartum headache The overall incidence of postpartum headache is difficult to ascertain. Minor headaches are often not reported since they are thought to be normal for the postpartum period or overshadowed by events surrounding childbirth. Research studies on this subject are often limited by analysis from a single specialty group (e.g., anesthesiologists, neurologists, obstetricians), focused only on Accepted July 2010 Correspondence to: Autumn Klein, MD PhD, Director, Program in Women’s Neurology, Instructor, Harvard Medical School, Tower 5D, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA. E-mail address: [email protected]
inpatients in the immediate postpartum period (2–4 days on average), or lacking rigorous headache criteria. Despite these limitations, there are several recent studies that have looked robustly at the incidence of postpartum headaches (Table 1). One prospective cohort study of almost a thousand women over a three-month period in a single institution in Canada showed that 39% of women reported headache in the first week after delivery. Diagnoses were made according to the International Classification for Headache Disorders (ICHD),1 with the majority attributed to tension-type headache, 4.7% due to PDPH, and 8.1% due to undetermined causes.2 One study of women’s health after childbirth performed in France and Italy showed that physical symptoms were more common at 12 months than five months and that almost one third of women reported a headache (45.1% at 12 months versus 22.5% at 5 months).3 While this longitudinal study included different demographic populations, it was focused on socioeconomic factors related to women’s health and thus lacked information on specific headache diagnoses in the immediate postpartum period. An Italian study suggested that 5% of women developed migraine for the first time during the postpartum period.4 Finally, a prospective Italian study performed at an obstetrical clinic looking specifically for migraine showed that 34% of women had migraines recur in the first week postpartum and 55% within the first month.5 Several studies have examined postpartum headache related to the use of labor analgesia. In a general obstetric population in the UK, about 23% of women receiving epidural analgesia reported headache.6 In a later
A.M. Klein, E. Loder Table 1
423
Postpartum headache studies
Author
Population
Prevalence
Comment
General OB
Prospective >1000 patients, ICHD criteria
Saurel-Cubizolles3 General OB
39% In 1 week 75% Primary headache 1/3 Women headache
Grove6
General OB
23%
Benhamou7
Epidurals, no known dural puncture 12%
Granella4
Headache clinic – migraine
Sances5
OB clinic – migraine
Goldszmidt
2
Longitudinal interviews 5 and 12 months postpartum Excluded women with epidurals Most on postpartum day 1 or 2 Mailed survey 1200 41% response
5% First time Retrospective postpartum migraine 34% Migraine 1st week, Retrospective 55% 4th week
ICHD: International Classification for Headache Disorders.
study, 12% of women with epidural analgesia but without dural puncture reported headache at two weeks after delivery.7 Of interest, 15% of women without epidural analgesia reported headache. Due to the low number of women who did not receive epidural analgesia and the low response rate to the questionnaire, low study power limited the ability to make meaningful comparisons. These percentages may be somewhat altered by breastfeeding and other factors that affect headache. However, despite these studies being conducted in different countries with different patient populations, methods and diagnostic criteria, all concluded that postpartum headache is common. Given the high prevalence of primary headache disorders, it is not surprising that this entity was the most common headache diagnosis in these studies.
Differential diagnosis of postpartum headache The differential diagnosis of postpartum headache is extensive but can be easily focused on primary and secondary causes. Worrisome headache characteristics or ‘red flags’ are similar to those in the non-pregnant patient (Table 2). Primary headache disorders, such as migraine and tension type headache, are common in reproductive age women and are diagnosed using well-defined criteria established by the ICHD.1 The probability that a headache in a postpartum patient has a secondary cause is low, but such disorders can cause significant morbidity and mortality if missed. This Table 2
Worrisome headache features
New neurological symptoms with headache Change in character or pattern of any previously diagnosed headache type New headache, especially if fixed to one side Sudden uncontrollable vomiting Change in mental status with headache Headache not relieved by pain medications Other concerning medical issue (bleeding disorder, immunocompromised)
review focuses on stroke (ischemic, hemorrhagic, and venous), as well as PDPH, preeclampsia/eclampsia, and a few rare other diagnoses. A more complete, although not exhaustive, list of dangerous causes of postpartum headache can be found in Table 3. Certain factors, such as a history of headache, peripartum events such as epidural administration, hypertension, and the timing of onset of headache can assist in narrowing the diagnostic considerations and provide a framework for approaching the patient with a postpartum headache (Fig. 1). If a primary headache is suspected, pre-pregnancy headache characteristics as well as the pattern of headache in pregnancy and the postpartum period can be very helpful. This information, in conjunction with the ICHD criteria for primary headache types, will help determine whether imaging would be of assistance. Given the hypercoaguable state of women during the Table 3
Differential diagnosis of postpartum headache
Primary Migraine Tension-type headache Cluster Vascular Ischemic stroke Hemorrhagic stroke Subarachnoid hemorrhage Vascular malformation (aneurysm, AVM) Hypertension Venous sinus thrombosis Dissection Vasculidities Reversible cerebral vasoconstrictive syndromes Other Preeclapmsia/eclampsia Benign intracranial hypertension Sinusitis Drug use Postdural puncture headache Tumor
424
Postpartum headache Question
Possible cause
Test to confirm
Comments
Is headache postural or associated with tinnitus or hypacusia?
Low pressure headache
Empirical treatment is appropriate if no other cause of headache is apparent and diagnostic suspicion is high. Otherwise, MRI with gadolinium may show meningeal enhancement; LP may show low pressure; CT myelogram may show leak; radionuclide cisternogram may pick up slow leaks
Postural features may be subtle, particularly if headache is longstanding; case reports suggest this diagnosis is sometimes mistaken; do not discard alternative diagnoses too quickly
Is there a history of similar headaches?
A third to a half of women with a history of migraine will have postpartum headache
Assess against diagnostic criteria (see tables)
Migraine increases risk of or may co-occur with dangerous causes of headache. Consider avoiding use of vasoconstrictive migraine treatments such as triptans or ergots even if a diagnosis of migraine seems certain because of rare but serious risk of precipitating vasoconstriction
Did headache come on abruptly or gradually?
Aneurysmal subarachnoid hemorrhage, cerebral venous thrombosis, reversible cerebral vasoconstrictive syndrome
Plain CT, LP to assess for hemorrhage, if negative then MRA/MRV looking for cerebral venous thrombosis or typical bead-like appearance of vasoconstrictive syndromes
Occasionally migraine will begin suddenly, so-called ‘crash migraine’, but this is a diagnosis of exclusion.
Is headache associated with hypertension, proteinuria or seizure?
Postpartum preeclampsia or eclampsia
Assess and monitor for proteinuria, hypertension and hyperreflexia
Headache can precede other signs of preeclampsia and may mimic that of migraine; the risk of preeclampsia is elevated in women with migraine, especially migraine with aura
Has the patient received or used any vasoconstrictive medications?
Reversible cerebral vasoconstrictive syndromes
MRI/MRV looking for typical bead-like appearance of vessels seen in vasoconstrictive syndromes
Nonprescribed licit and illicit drugs should be considered, e.g. cocaine, pseudephredrine
Fig. 1 A history-driven approach to postpartum headache. LP: lumbar puncture; MRA: magnetic resonance angiography; MRV: magnetic resonance venography.
puerperium, and possible obstetrical complications associated with pregnancy and the postpartum period, the threshold for further evaluation and imaging in this population should be low. Breastfeeding is not a contraindication to imaging procedures when they are needed. Contrast and gadolinium can be administered and then the breast milk can be pumped and discarded.
Primary causes A high index of suspicion for dangerous or secondary causes of headache is appropriate in the postpartum period. Even in this setting, though, approximately 50–75% of headaches are due to primary headache disorders, particularly migraine. Approximately one-third of childbearing age women have migraine.8 Greater than 75% of patients with primary headache disorders can expect noticeable improvement during pregnancy, although many experience a flare after delivery.4 In one study, nearly a thousand consecutive women who delivered in a single hospital were carefully evaluated and followed for the development of headaches. Primary headaches, mostly migraine, were the cause of over 75% of cases.2 In another case series of 95 women, migraine or tension-type headaches were ultimately diagnosed as the cause of postpartum headache in 47%. In one study performed at an obstetric clinic, headaches occurred within a week of delivery in 34%, and within a month in 55.3%.5 Falling estrogen levels, particularly after a long period of stability, are a potent migraine trigger, but the
sleep disturbances and emotional stress of parenthood may play a role as well. Little attention has been paid to ways of minimizing the chance of migraine flares after delivery. One study suggested that headaches were less likely in women who participated in childbirth preparation classes, and another demonstrated that the likelihood of migraine return after delivery was lessened in women who breastfed their infants.5,9 Diagnostic criteria for primary headache disorders are contained in the ICHD.1 The criteria for the most common primary headaches, migraine with and without aura, and tension-type headache, are reproduced in Tables 4 and 5. Tension-type headache is the most common headache in the general population, but usually does not come to medical attention since most sufferers self-treat with simple analgesics. Nausea, vomiting and sensitivity to light and noise are characteristic of migraine but can accompany dangerous causes of headache as well. Migraine is associated with an increased risk of some dangerous causes of headache such as postpartum stroke and preeclampsia.10,11 While primary headache disorders can appear for the first time during or after pregnancy, onset of a new type of headache during this time is worrisome. In contrast, a primary headache is more likely to be the diagnosis in a woman who is known to have a history of such headaches. One study found that most women who develop postpartum headache had a history of migraine, and most described the postpartum headaches they had as
A.M. Klein, E. Loder Table 4 Diagnostic criteria for migraine with and without aura1 Migraine without aura A. At least five attacks fulfilling criteria B–D B. Headache attacks lasting 4–72 h (untreated or unsuccessfully treated) C. Headache has at least two of the following characteristics:
Unilateral location Pulsating quality Moderate or severe intensity Aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)
D. During headache at least one of the following: Nausea and/or vomiting Photophobia and phonophobia
E. Not attributed to another disorder Typical aura with migraine headache A. At least two attacks fulfilling criteria B–D B. Aura consisting of at least one of the following, but no motor weakness: Fully reversible visual symptoms including positive features (e.g., flickering lights. spots or lines) and/or negative features (e.g., loss of vision) Fully reversible sensory symptoms including positive features (i.e., pins and needles) and/or negative features (e.g., numbness) Fully reversible dysphasic speech disturbance
C. At least two of the following: Homonymous visual symptoms and/or unilateral sensory symptoms At least one aura symptom develops gradually over P5 min and/or different aura symptoms occur in succession over P5 min Each symptom lasts P5 and 660 min
D. Headache fulfilling criteria B–D for 1.1 ‘Migraine without aura’ begins during the aura or follows aura within 60 min E. Not attributed to another disorder
Table 5
Diagnostic criteria for tension type headache1
A. At least 10 episodes fulfilling criteria B–D B. Headache lasting from 30 min to 7 days C. Headache has at least two of the following characteristics:
bilateral location pressing/tightening (non-pulsating) quality mild or moderate intensity not aggravated by routine physical activity such as walking or climbing stairs
D. Both of the following: no nausea or vomiting (anorexia may occur) no more than one of photophobia or phonophobia
Not attributed to another disorder Considered infrequent if less than 1 day per month on average; frequent if more than 1 and less than 15 days per month on average, and chronic if 15 or more days per month.;
‘‘considerably milder’’ than their usual headaches. The authors of this study also calculated that a history of headache raised the risk for postpartum headache by a factor of 1.5.12 Migraine, then, increases the risk of both dangerous and non-dangerous causes of postpartum headache. In contrast, there is no evidence that women
425 with cluster or tension-type headache are at higher than average risk of puerperal headaches.13
Secondary causes Although the majority of postpartum headaches are benign, the risk of some important secondary causes of headache is elevated in the puerperium. In most circumstances, a history of a primary headache disorder such as migraine is reassuring, but women with migraine have an increased risk of serious causes of headache including preeclampsia, stroke and even, perhaps, cerebral vasoconstrictive syndromes. The headache features of many of these disorders overlap with those of migraine, so that accurate diagnosis can be challenging.
Distinguishing primary from secondary headaches Migraine is common in women of childbearing age and the abrupt postpartum decline in estrogen levels is a potent trigger of migraine attacks. Additionally, many parturients have received epidural analgesia for delivery. Migraine and PDPH are accordingly high on the list of diagnostic possibilities in many women who complain of headache following delivery. The high prior probability of these two causes of headache, though, may paradoxically increase the likelihood of misdiagnosis if doctors fail to consider alternative causes with which they are less familiar. Because the features of many types of postpartum headache overlap, it is easy to mistake one type of headache for another. Case reports suggest that diagnoses of PDPH should be made with special caution. While there may be publication bias, a large number of case reports discuss mistaken diagnoses of PDPH in women who turned out to have cerebral venous thrombosis or, less commonly, cerebral vasoconstrictive syndromes, meningitis, postpartum preeclampsia or stroke.14–20 Patients with a history of severe primary headache disorders may also be at an elevated risk of having a serious cause of postpartum headache diagnosed as an exacerbation of the pre-existing disorder.21 An overly strong belief in the principle of diagnostic parsimony can also lead to trouble. Although uncommon, it is possible for a postpartum patient to have more than one cause of headache.15,22–24 In addition to the unusual secondary causes of headache considered above, prescribed and non-prescribed drugs (both licit and illicit) should be considered as a possible cause of postpartum headache.25
Headache attributed to low cerebrospinal fluid pressure Spinal or epidural techniques are commonly used for labor and delivery.26 Thus, in the postpartum setting,
426 headache due to low cerebrospinal fluid (CSF) pressure is usually due to unintended dural puncture. Cases have also been reported in which leakage of CSF probably occurred spontaneously during delivery without anesthetic intervention, perhaps as a result of mechanical trauma from prolonged pushing and straining.27 It is likely that some unrecognized dural tears occur that produce few, if any, symptoms and resolve spontaneously.28 In one study of 229 consecutive women who received labor epidural analgesia and were closely queried about subsequent headache, most of the headaches were reported as mild, with only three requiring treatment with an epidural blood patch.2 If the puncture does not seal spontaneously, low CSF pressure may cause traction on pain-sensitive meningeal structures and result in more severe headache that comes to medical attention; 75% of women with medically recognized PDPH reported that it limited daily activities. In most cases, inadvertent dural puncture is recognized at the time it occurs. Interestingly, in those circumstances, a prophylactic epidural blood patch or the placement of spinal catheters does not seem to prevent subsequent headache.29,30 The reported incidence of PDPH ranges from approximately 1–16% in various small case series.2,31,32 A larger study evaluated the records of over 65 000 women who had received anesthetic interventions. Postdural puncture headache was diagnosed in 404, of whom 240 had an epidural blood patch. In this series, the overall incidence of headache in women who had one anesthetic intervention was low (1.1–1.9%), but increased to 11% in women who had multiple anesthetic procedures.29 It seems unlikely that the true incidence of PDPH varies so greatly; rather, the variability probably reflects study differences in the quality, timing and thoroughness of ascertainment. A meta-analysis of individual studies suggests that the incidence is likely to be about 1.5%.33,34 Despite this, there is general agreement that the occurrence of PDPH following epidural analgesia is influenced to some degree by anesthetic technique, with atraumatic (pencil-point) and smaller sized needles, among other things, shown to reduce the risk of dural puncture.35 Low pressure headache due to CSF leak is usually mild or absent when the patient is lying down, but worsens with upright posture. In a large series of patients with PDPH, this postural effect was reported by 80% of patients.16 The worsening or improvement in headache severity usually takes place within 15 min of a change in posture and is gradual rather than abrupt. The postural quality of the headache may be subtle and may even disappear if the headache becomes chronic. Table 6 lists ICHD criteria for the diagnosis of postdural puncture and spontaneous low-pressure headache. Symptoms often overlap with those seen in other primary and secondary headaches. Tinnitus, diplopia or hypacusia, however, are uncommon symptoms
Postpartum headache Table 6 Diagnostic criteria for headaches attributed to low cerebrospinal fluid pressure1 Postdural puncture headache A. Headache that worsens within 15 min after sitting or standing and improves within 15 min after lying, with at least one of the following and fulfilling criteria C and D:
neck stiffness tinnitus hypacusia photophobia nausea
B. Dural puncture has been performed C. Headache develops within 5 days after dural puncture D. Headache resolves either: spontaneously within 1 week within 48 h after effective treatment of CSF leak (usually by epidural blood patch)
Headache attributed to spontaneous (idiopathic) low CSF pressure A. Diffuse and/or dull headache that worsens within 15 min after sitting or standing, with at least one of the following and fulfilling criterion D:
neck stiffness tinnitus hypacusia photophobia nausea
B. At least one of the following: evidence of low CSF pressure on MRI (e.g., pachymeningeal enhancement) evidence of CSF leak on conventional myelography, CT myelography or cisternography CSF opening pressure <60 mm H2O in sitting position
C. No history of dural puncture or other cause of CSF fistula D. Headache resolves within 72 h after epidural blood patch
of primary headaches and should prompt suspicion of a low-pressure headache syndrome. Shoulder and neck stiffness are surprisingly common in the postpartum period, as well as in almost half of patients with PDPH; consequently, this symptom is not especially useful in formulating or ruling out a diagnosis. If there is strong reason to suspect a low-pressure headache, such as in the case of a parturient who received epidural analgesia and has no other apparent cause of headache, confirmatory testing is probably unnecessary: the prior probability of a leak is high and its location almost certain.36 In that case, it is reasonable to treat a troublesome headache with an epidural blood patch. An alternative strategy of watchful waiting could also be considered for milder headaches, since postdural puncture headache frequently resolves spontaneously within a week and in the meantime can often be managed conservatively with bed rest, caffeine, and fluids. A watchful waiting approach is somewhat controversial, however, as studies have suggested long-term headaches may result if PDPH is not managed actively.37 For this reason, intervention with a blood patch is prudent if headaches persist beyond a week.
A.M. Klein, E. Loder Traditional teaching is that if an epidural blood patch is attempted, the headache should be gone within 48 h in >95% of cases. Several studies have called into question the efficacy of blood patching in obstetric patients, however, and suggested that success rates with blood patching may not be as high as previously thought.38,39 Blood patches often need to be repeated after initial success is followed by subsequent return of headache. While a second blood patch is almost always successful, it is reasonable to perform additional blood patches if the positional headaches continue. Some patients do not have headache following delivery but develop positional headache days to weeks later. Presumably these late-presenting cases result from spontaneous re-opening of a small tear that sealed over or from enlargement of a small, initially asymptomatic dural tear. In these patients, the positional component of the headache may not be dramatic, and symptoms may be more meningeal or radicular. The headaches may be diagnosed as a primary headache disorder since these often return within a few weeks of delivery. To distinguish between the two possibilities, it is useful to inquire about the orthostatic nature of the headaches and to evaluate other symptoms. An epidural blood patch should be considered in these cases when the diagnosis seems obvious, but if there is any doubt magnetic resonance imaging (MRI) of the brain with gadolinium as well as magnetic resonance angiography (MRA) and venography (MRV) should also be considered, particularly if the patient has focal symptoms or vision changes. This will help to rule out any rare secondary causes of headache such as subdural hemorrhage, subarachnoid hemorrhage, or cerebral venous sinus thrombosis. A subset of patients with positional headaches who do not have clear evidence of a dural tear might have meningeal weakness, perhaps due to an underlying connective tissue disorder. It is theorized that this may lead to pooling of CSF and symptoms consistent with low CSF pressure even in the absence of a true leak. In other cases, it is theorized that spontaneous dural tears can develop that lead to CSF leakage. These spontaneous tears or defects are often located anterior to or at nerve root sheaths. This makes localization of the tear more difficult, and blood patching is less likely to be effective. Patients with areas of dural weakness may be predisposed to recurrence of positional headaches, although the rate of recurrence has not been determined. Orthostatic symptoms in these recurrent headaches can be subtle and may be unrecognized, increasing the risk that headaches will not be appropriately treated and worsen over time to become chronic daily headaches. In suspected cases of postural headache, lumbar puncture may demonstrate a low opening pressure, but pressure can also be normal. If CSF fluid is analyzed, increased protein and a lymphocytic pleocytosis may be seen.40 MRI of the brain with gadolinium may show
427 pachymeningeal enhancement, and various studies can be used to document the location of the leak. Computed tomography (CT) myelography is probably the most sensitive test; radioisotope studies with Indium-111 are also sometimes used.41 Imaging may demonstrate ‘sagging’ of the brain with descent of the cerebellar tonsils or even thin, bilateral subdural fluid collections, all of which resolve when the leak is effectively treated.41
Reversible cerebral vasoconstrictive syndromes A large number of labels have been applied to headaches attributed to vasoconstriction of the cerebral arteries including Call-Fleming Syndrome and postpartum angiopathy, but the descriptive term reversible cerebral vasoconstrictive syndromes (RCVS) is increasingly preferred for this group of disorders.42–44 In the absence of large population-based epidemiologic studies, the prevalence of RCVS in general, during pregnancy or during the postpartum period is unknown, but it is probably more common than generally appreciated.21 Since vasoconstriction is reversible, headache may remit spontaneously, and so an accurate diagnosis is never made. As with some other secondary causes of postpartum headache, patients with migraine may be more susceptible to RCVS, and some of the vasoconstrictive drugs used to treat migraine may also increase risk. The underlying mechanism is not known,42 although in two thirds of cases, a precipitant, especially the use of vasoconstrictive substances such as bromocriptine, ergots, pseudoephedrine or SSRIs in the puerperium, is evident.45 The characteristic headache in these syndromes is severe and abrupt in onset, so-called ‘thunderclap headache’ and multiple attacks may occur in close succession. It may be associated with a variety of other symptoms including confusion, agitation or focal neurologic signs (Table 7).46 Although the headache and vasoconstriction eventually remit without treatment, usually within two months, serious complications can occur rapidly after onset.47–50 Within the first week after diagnosis in one case series of 67 patients with angiographically confirmed RCVS, subarachnoid hemorrhage occurred in 22%, intracerebral hemorrhage in 6%, seizures in 3% and posterior leukoencephalopathy in 9%. Ischemic events and infarction also occurred, but were more likely in the second week.45 Reversible cerebral vasoconstrictive syndromes must be distinguished from other causes of severe, sudden headache, so the typical workup includes a non-contrast CT scan to rule out subarachnoid hemorrhage, and if negative, a lumbar puncture to assess for CT-negative subarachnoid hemorrhage, infection or vasculitis.50,51 Formal angiography can assess for cerebral venous thrombosis and RCVS. The diagnosis of RCVS is suggested by multifocal segmental ‘bead and string’ constriction of cerebral arteries, in the absence of
428
Postpartum headache
Table 7
Headache attributed to benign or reversible CNS angiopathy
A. Diffuse, severe headache of abrupt or progressive onset, with or without focal neurological deficits and/or seizures and fulfilling criteria C and D B. ‘Strings and beads’ appearance on angiography and subarachnoid haemorrhage ruled out by appropriate investigations C. One or both of the following: headache develops simultaneously with neurological deficits and/or seizures headache leads to angiography and discovery of ‘‘strings and beads’’ appearance
D. Headache (and neurological deficits, if present) resolves spontaneously within 2 months
subarachnoid hemorrhage or abnormal CSF.42 Because the constriction begins distally and works its way proximally, serial imaging may be needed to demonstrate the characteristic pattern of vasoconstriction.
Postpartum stroke Stroke plays a major role in over 12% of maternal deaths and contributes to fetal morbidity and mortality.51 Early diagnosis of stroke is critical to the patient’s and child’s well-being. Studies of stroke in pregnancy and the puerperium have estimated an incidence from 4.3 to 210 per 100 000 women. The large range is due to variations in the populations studied, stroke classifications (ischemic, hemorrhagic, and venous), and elapsed time to followup (zero to eight weeks postpartum). Three well-designed population-based studies carried out in recent years provide the most accurate estimate of stroke in pregnancy but lack specific postpartum information.52–54 Most studies agree that strokes of any etiology occur primarily in the third trimester and postpartum period; this is likely due to the significant physiological changes at these times. Women become hypercoaguable as pregnancy progresses, with peak hypercoagulability in the immediate postpartum period.55 Rising estrogen levels cause vasodilation, which may explain why vascular malformations and aneurysms are more likely to rupture. The etiology of strokes in most studies was found to be mostly ischemic with cardioemboli, venous sinus thrombosis and preeclampsia–eclampsia as the main causes. Hemorrhagic strokes are primarily due to vascular malformations and subarachnoid hemorrhage. Strokes restricted to the intraparenchymal brain tissue often occur without associated pain. Headache from stroke results from disturbance of the pain sensitive structures of the head, which include the meninges, extracranial, and short courses of some of the major intracranial blood vessels. It has been estimated that approximately 10% of patients with stroke develop headache.56 Posterior, versus anterior, circulation strokes are more often associated with headache, but this may be related to their propensity to become hemorrhagic. Nonetheless, the most diagnostic feature of a stroke’s location is the associated neurological symptoms. Headaches from stroke occur suddenly and either coincidently or immediately following associated neurological features. By contrast, the headache of migraine
usually follows the neurological symptoms by approximately 15–30 min. If neurological symptoms last more than an hour before onset of the headache, then the diagnosis of stroke, or migrainous infarction should be considered. Neurological symptoms associated with stroke are usually negative such as the absence of speech, whereas those with migraine are usually positive (e.g., fortification spectra). Headache from stroke often remits quickly, which may present a diagnostic clue in determining the etiology.57 In cases where stroke is suspected, MRI with diffusion is diagnostic. Vascular imaging with MRA and MRV is essential in the postpartum patient and in cases of possible vascular malformation or aneurysm, formal angiogram may be considered.
Cerebral venous sinus thrombosis If trauma is not involved, central venous sinus thrombosis (CVT) is a disease that is almost always limited to peripartum women or young women using estrogencontaining contraceptives. Symptoms can begin gradually and may be confused with other primary headaches or PDPH. Presentation ranges from mild headache to coma. Hypercoaguable state, damaged endothelium from pushing in labor and relative intracranial hypotension after epidural and postpartum diuresis are all factors contributing to symptoms and headache. Imaging with MRV is critical to make the diagnosis. Seizures occur in almost two thirds of CVT cases and consequently, electroencephalograms are recommended, especially if the patient is complaining of positive or intermittent neurological symptoms.
Preeclampsia–eclampsia Preeclampsia is defined by the National High Blood Pressure Program Working Group on High Blood Pressure in Pregnancy as hypertension and proteinuria in pregnancy. Eclampsia is defined as seizures not attributable to other causes in the setting of preeclampsia.58 Preeclampsia affects 3–5% of pregnant women,59 and approximately 1 in 2000 deliveries in the United States are associated with an eclamptic seizure.60 While the cause of preeclampsia and eclampsia is not precisely known, abnormal placentation and endothelial dysfunction are leading hypotheses which in turn result in
A.M. Klein, E. Loder placental hypoperfusion, increased vascular tone, systemic hypertension, and decreased organ perfusion. Autoantibodies, inflammatory mediators and genetic predisposition are also thought to play a role in the pathogenesis. The diagnosis of preeclampsia is based on the clinical presence of hypertension and proteinuria or edema. Eclampsia is based on the findings of encephalopathy or seizures in late pregnancy or the postpartum period; CT or MRI demonstrate characteristic edema and no other brain lesions. In severe preeclampsia, patients can have headache and visual changes. Despite the prevalence of preeclampsia and eclampsia, the associated headache characteristics have not been well studied. The risk of preeclampsia is increased in women with migraine, especially if an aura is present.10 Anecdotally, headache from preeclampsia is similar to other vascular-type headaches, but patients often note that it is distinctly different from other headache types. It is usually throbbing and holocephalic, or more posteriorly located. It may have characteristics of migraine (nausea, light sensitivity), but migraineurs are known to be at increased risk of preeclampsia and eclampsia so these features are not as useful as they might otherwise be.
Conclusion A high threshold of suspicion for dangerous causes of headache is appropriate when evaluating women with postpartum headache, even those with a long prior history of benign headaches. While most headaches in the postpartum period are usually benign, primary headaches, the threshold for diagnostic testing is lower than in non-pregnant women because of the serious consequences if a dangerous secondary cause of headache is missed. Appropriate testing strategies depend upon the possible diagnoses, and evaluation should be guided by a careful history and physical examination.
References 1. Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders, 2nd ed. Cephalalgia 2004;24(Suppl 1):9–160. 2. Goldszmidt E, Kern R, Chaput A, Macarthur A. The incidence and etiology of postpartum headaches: a prospective cohort study. Can J Anesth 2005;52:971–7. 3. Saurel-Cubizolles MJ, Romito P, Lelong N, Ancel PY. Women’s health after childbirth: a longitudinal study in France and Italy. BJOG 2000;107:1202–9. 4. Granella F, Sances G, Zanferrari C, Costa A, Martignoni E, Manzoni GC. Migraine without aura and reproductive life events: a clinical epidemiological study in 1300 women. Headache 1993;33:385–9. 5. Sances G, Granella F, Nappi RE, et al. Course of migraine during pregnancy and postpartum: a prospective study. Cephalalgia 2003;23:197–205. 6. Grove LH. Backache, headache and bladder dysfunction after delivery. Br J Anaesth 1973;45:1147–9.
429 7. Benhamou D, Hamza J, Ducot B. Post partum headache after epidural analgesia without dural puncture. Int J Obstet Anesth 1995;4:17–20. 8. Stewart WF, Wood C, Reed ML, Roy J, Lipton RBAMPP Advisory Group. Cumulative lifetime migraine incidence in women and men. Cephalalgia 2008;28:1170–8. 9. Mehdizadeh A, Roosta F, Chaichian S, Alaghehbandan R. Evaluation of the impact of birth preparation courses on the health of the mother and the newborn. Am J Perinatol 2005;22:7–9. 10. Facchinetti F, Allais G, Nappi RE, et al. Migraine is a risk factor for hypertensive disorders in pregnancy: a prospective cohort study. Cephalalgia 2009;29:286–92. 11. Bushnell CD, Jamison M, James AH. Migraines during pregnancy linked to stroke and vascular diseases: US population based casecontrol study. BMJ 2009;338:b664. 12. Stein G, Morton J, Marsh A, et al. Headaches after childbirth. Acta Neurol Scand 1984;69:74–9. 13. Manzoni GC, Micieli G, Granella F, Martignoni E, Farina S, Nappi G. Cluster headache in women: clinical findings and relationship with reproductive life. Cephalalgia 1988;8:37–44. 14. Karci A, Boyaci F, Yaka E, Cakmur R, Men S, Elar Z. Cerebral venous thrombosis initially considered as a complication of spinal–epidural anaesthesia. J Int Med Res 2005;33:711–4. 15. Ghatge S, Uppugonduri S, Kamarzaman Z. Cerebral venous sinus thrombosis following accidental dural puncture and epidural blood patch. Int J Obstet Anesth 2008;17:267–70. 16. Jungmann V, Werner R, Bergmann J, et al. Postpartum cerebral venous sinus thrombosis after epidural anaesthesia. Anaesthesist 2009;58:268–72. 17. Barrett J, Alves E. Postpartum cerebral venous sinus thrombosis after dural puncture and epidural blood patch. J Emerg Med 2005;28:341–2. 18. Umstad MP, Ross AW, Adey FD. Headache following epidural analgesia. Aust N Z J Obstet Gynaecol 1992;32:79–80. 19. Chisholm ME, Campbell DC. Postpartum postural headache due to superior sagittal sinus thrombosis mistaken for spontaneous intracranial hypotension. Can J Anesth 2001;48:302–4. 20. Lee JJ, Parry H. Bacterial meningitis following spinal anaesthesia for caesarean section. Br J Anaesth 1991;66:383–6. 21. Modi M, Modi G. Case reports: postpartum cerebral angiopathy in a patient with chronic migraine with aura. Headache 2000;40:677–81. 22. Anand A. Post-dural puncture headache associated with cerebral venous thrombosis. Br J Anaesth 2000;85:326–7. 23. Ho CM, Chan KH. Posterior reversible encephalopathy syndrome with vasospasm in a postpartum woman after postdural puncture headache following spinal anesthesia. Anesth Analg 2007; 105:770–2. 24. Winston AW, Norman D. Late postpartum eclampsia coincident with postdural puncture headache: a case report. AANA J 2003;71:371–2. 25. Maagdenberg T, Savci S, Iffy L. Cocaine intoxication mimicking preeclampsia postpartum. Int J Gynecol Obstet 2006;92:73–4. 26. Bucklin BA, Hawkins JL, Anderson JR, Ullrich FA. Obstetric anesthesia workforce survey: twenty-year update. Anesthesiology 2005;103:645–53. 27. Mokri B. Spontaneous low cerebrospinal pressure/volume headaches. Curr Neurol Neurosci Rep 2004;4:117–24. 28. Mokri B, Atkinson JL, Piepgras DG. Absent headache despite CSF volume depletion (intracranial hypotension). Neurology 2000;55:1722–4. 29. Chan TM, Ahmed E, Yentis SM, Holdcroft A. Obstetric Anaesthetists’ Association, NOAD Steering Group. Postpartum headaches: summary report of the National Obstetric Anaesthetic Database (NOAD) 1999. Int J Obstet Anesth 2003;12:107–12. 30. Scavone BM, Wong CA, Sullivan JT, Yaghmour E, Sherwani SS, McCarthy RJ. Efficacy of a prophylactic epidural blood patch in
430
31.
32.
33.
34.
35.
36. 37. 38.
39.
40. 41. 42.
43. 44.
45.
preventing post dural puncture headache in parturients after inadvertent dural puncture. Anesthesiology 2004;101:1422–7. Stella CL, Jodicke CD, How HY, Harkness UF, Sibai BM. Postpartum headache: is your work-up complete? Am J Obstet Gynecol 2007;196:318.e1–7. Ong B, Cohen MM, Cumming M, Palahniuk RJ. Obstetrical anaesthesia at Winnipeg Women’s Hospital 1975–83: anaesthetic techniques and complications. Can J Anaesth 1987;34: 294–9. Choi PT, Galinski SE, Takeuchi L, Lucas S, Tamayo C, Jadad AR. PDPH is a common complication of neuraxial blockade in parturients: a meta-analysis of obstetrical studies. Can J Anesth 2003;50:460–9. Choi PT, Galinski SE, Lucas S, Takeuchi L, Jadad AR. Examining the evidence in anesthesia literature: a survey and evaluation of obstetrical postdural puncture headache reports. Can J Anesth 2002;49:49–56. Evron S, Sessler D, Sadan O, Boaz M, Glezerman M, Ezri T. Identification of the epidural space. Loss of resistance with air, lidocaine, or the combination of air and lidocaine. Anesth Analg 2004;99:245–50. Mokri B. Headaches caused by decreased intracranial pressure: diagnosis and management. Curr Opin Neurol 2003;16:319–26. MacArthur C, Lewis M, Knox EG. Accidental dural puncture in obstetric patients and long term symptoms. BMJ 1993;306:883–5. Williams EJ, Beaulieu P, Fawcett WJ, Jenkins JG. Efficacy of epidural blood patch in the obstetric population. Int J Obstet Anesth 1999;8:105–9. Banks S, Paech M, Gurrin L. An audit of epidural blood patch after accidental dural puncture with a Tuohy needle in obstetric patients. Int J Obstet Anesth 2001;10:173–6. Mokri B. Syndrome of cerebral spinal fluid hypovolemia: clinical and imaging features and outcome. Neurology 2001;56:1607–8. Mokri B. Cerebrospinal fluid volume depletion and its emerging clinical/imaging syndromes. Neurosurg Focus 2000;9:e6. Calabrese LH, Dodick DW, Schwedt TJ, Singhal AB. Narrative review: reversible cerebral vasoconstriction syndromes. Ann Intern Med 2007;146:34–44. Singhal AB, Bernstein RA. Postpartum angiopathy and other cerebral vasoconstriction syndromes. Neurocrit Care 2005;3:91–7. Neudecker S, Stock K, Krasnianski M. Call-Fleming postpartum angiopathy in the puerperium: a reversible cerebral vasoconstriction syndrome. Obstet Gynecol 2006;107:446–9. Ducros A, Boukobza M, Porcher R, Sarov M, Valade D, Bousser MG. The clinical and radiological spectrum of reversible cerebral
Postpartum headache
46.
47.
48.
49. 50. 51.
52. 53. 54.
55.
56. 57. 58.
59. 60.
vasoconstriction syndrome. A prospective series of 67 patients. Brain 2007;130:3091–101. Chandrashekaran S, Parikh S, Kapoor P, Subbarayan S. Postpartum reversible cerebral vasoconstriction syndrome. Am J Med Sci 2007;334:222–4. Cho AH, Lim SC, Kim BS, Yang DW, Shon YM. Atypical presentation of postpartum cerebral angiopathy shown as a small penetrating arterial territory infarct with severe peri-infarct edema. J Neuroimaging 2010;20:290–1. Sengoku R, Iguchi Y, Yaguchi H, Sato H, Inoue K. A case of postpartum cerebral angiopathy with intracranial hemorrhage and subarachnoid hemorrhage immediately after delivery. Rinsho Shinkeigaku 2005;45:376–9. Gladstone JP, Dodick DW, Evans R. The young woman with postpartum ‘‘thunderclap’’ headache. Headache 2005;45:70–4. Sharma P, Poppe AY, Eesa M, Steffenhagen N, Goyal M. Postpartum thunderclap headache. CMAJ 2008;179:1033–5. Dias MS, Sekhar LN. Intracranial hemorrhage from aneurysms and arteriovenous malformations during pregnancy and the puerperium. Neurosurgery 1990;27:855–65. Kittner SJ, Stern BJ, Feeser BR, et al. Pregnancy and the risk of stroke. N Engl J Med 1996;335:768–74. Wiebers DO, Mokri B. Internal carotid artery dissection after childbirth. Stroke 1985;16:956–9. Sharshar T, Lamy C, Mas JL. Incidence and causes of strokes associated with pregnancy and puerperium. A study in public hospitals of Ile de France. Stroke in Pregnancy Study Group. Stroke 1995;26:930–6. Wickstrom K, Edelstam G, Lowbeer CH, Hansson LO, Siegbahn A. Reference intervals for plasma levels of fibronectin, von Willebrand factor, free protein S and antithrombin during thirdtrimester pregnancy. Scand J Clin Lab Invest 2004;64: 31–40. Edmeads J. Headache in cerebrovascular disease. A common symptom of stroke. Postgrad Med 1987;81;191,193,196–8 Edmeads J. Headache as a symptom of cerebrovascular disease. Clin J Pain 1989;5:89–93. Roberts JM, Pearson G, Cutler J, Lindheimer M. NHLBI working group on research on hypertension during pregnancy. Summary of the NHLBI working group on research on hypertension during pregnancy. Hypertension 2003;41:437–45. Roberts JM, Cooper DW. Pathogenesis and genetics of preeclampsia. Lancet 2001;357:53–6. Saftlas AF, Olson DR, Franks AL, Atrash HK, Pokras R. Epidemiology of preeclampsia and eclampsia in the United States, 1979–1986. Am J Obstet Gynecol 1990;163:460–5.