Review Article
David S. Warner, M.D., Editor
Neuraxial Anesthesia in Parturients with Intracranial
Pathology
A Comprehensive Review and Reassessment of Risk
Lisa R. Leffert, M.D.,* Lee H. Schwamm, M.D.†
This article has been selected for the Anesthesiology CME Program. Learning objectives
and disclosure and ordering information can be found in the CME section at the front
of this issue.
ABSTRACT
Parturients with intracranial lesions are often assumed to
have increased intracranial pressure, even in the absence of
clinical and radiographic signs. The risk of herniation after
an inadvertent dural puncture is frequently cited as a con-
traindication to neuraxial anesthesia. This article reviews the
relevant literature on the use of neuraxial anesthesia in par-
turients with known intracranial pathology, and proposes a
framework and recommendations for assessing risk of neu-
rologic deterioration, with epidural analgesia or anesthe-
sia, or planned or inadvertent dural puncture. The authors
illustrate these concepts with numerous case examples and
provide guidance for the practicing anesthesiologist in deter-
mining the safety of neuraxial anesthesia.
D ESPITE the decrease in case-fatality rates for general
anesthesia for cesarean delivery from 16.8 per million
(1991–1996) to 6.5 per million (1997–2002),1 neuraxial
anesthesia remains the technique of choice for the majority
* Vice Chair, Faculty Development and Chief, Obstetric Anes-
thesia, Department of Anesthesia, Critical Care & Pain Medicine,
Massachusetts General Hospital and Assistant Professor of Anesthe-
sia, Harvard Medical School, Boston, Massachusetts. † Vice Chair,
Department of Neurology, Massachusetts General Hospital and Pro-
fessor of Neurology, Harvard Medical School.
Received from the Department of Anesthesia, Critical Care, and
Pain Medicine, Massachusetts General Hospital, Boston, Massachu-
setts. Submitted for publication October 26, 2012, Accepted for pub-
lication March 12, 2013. Corrected on February 27, 2017. Support
was provided solely from institutional and/or departmental sources.
Address correspondence to Dr. Leffert: Department of Critical
Care, Anesthesia, and Pain Medicine, Massachusetts General Hospi-
tal, GRB 444, 55 Fruit Street, Boston, Massachusetts 02114. lleffert@
partners.org. This article may be accessed for personal use at no
charge through the Journal Web site, www.anesthesiology.org.
Copyright © 2013, the American Society of Anesthesiologists, Inc. Lippincott
Williams & Wilkins. Anesthesiology 2013; 119:703–18
Anesthesiology, V 119 • No 3 703 September 2013
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of these procedures.2,3 A timely and safely administered neur-
axial technique can potentially avoid (1) instrumentation of
the parturient’s airway, (2) fetal exposure to the potentially
toxic effects of general anesthetics on the developing brain,4–7
(3) a high-risk setting for increased risk of awareness under
general anesthesia,8 and (4) the uterine relaxant effects of vol-
atile anesthetics. In addition, neuraxial anesthesia for cesarean
delivery allows the parturient and partner to experience the
birth. For postoperative analgesia, the literature supports the
use of epidural opioids for improved efficacy in comparison
with intermittent injections of IV or intramuscular opioids.2
For labor, neuraxial (epidural) analgesia has been shown to
significantly decrease parturients’ pain scores when compared
with IV meperidine9 or continuous midwifery support with
supplemental intramuscular meperidine, nitrous oxide inha-
lation, or other nonpharmacological adjuncts.10,11
Parturients with intracranial lesions are often assumed
to have increased intracranial pressure (ICP), and the risk
of herniation is frequently cited as a contraindication to
neuraxial anesthesia.11–18 To care for these parturients and
ascertain which of them can safely undergo spinal or epi-
dural analgesia or anesthesia;19–21 we must understand the
factors that contribute to clinically significant brain tissue
shifts (i.e., brain herniation), such as increased ICP, brain
edema, or hydrocephalus. Anesthesiologists can then most
effectively weigh the relative risks and benefits of neuraxial
anesthesia for these patients and engage in productive multi-
disciplinary peripartum planning.
We review the relevant intracranial anatomy and
physiology, and integrate cases from the obstetric anesthesia
and neurological literature, to clarify the risks of neuraxial
Supplemental digital content is available for this article. Di-
rect URL citations appear in the printed text and are avail-
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to the digital files are provided in the HTML text of this article
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 Neuraxial Anesthesia and Intracranial Lesions in Pregnancy

anesthesia in patients with intracranial pathology, and to

recommend strategies for decision making. We use case
examples of parturients with brain tumors, Arnold–Chiari
malformations, benign intracranial hypertension, and
intracranial vascular lesions to illustrate the inaccuracy
of some commonly held beliefs, and present a practical
approach to determine whether or not a parturient is an
appropriate candidate for spinal, epidural, or other neuraxial
analgesia or anesthesia. To identify the medical literature
representative of the anesthetic choices for these patients, we
reviewed MEDLINE articles published in English regarding

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human subjects. The search was conducted on human
subjects using the following Medical Subject Headings
terms: “Arnold–Chiari Malformation”, “Benign Intracranial
Hypertension”, “Brain”, “Brain Abscess”, “Brain Disease”
“Brain Neoplasms”, “Cerebrovascular Disorders”, “Cysts”,
“Intracranial”, “Monro–Kellie”, “Pseudotumor Cerebri”,
“Vasculitis,” and the keywords: “anesthesia”, “anaesthesia”,
“brain compliance”, “coning”, “epidural”, “herniation”,
“hydrocephalus”, “increased intracranial pressure”,
“infectious”, “inflammatory”, “lesion, “lumbar puncture”,
“malformation”, “neuraxial anesthesia”, “obstetric”,
“pregnancy”, “pregnancy complications”, “spinal”, “spinal
tap”, and “tumor”. The relevant findings from these articles
are summarized in a table provided as Supplemental Digital
Content 1, http://links.lww.com/ALN/A928.
Intracranial Anatomy and Physiology
The Three Primary Intracranial Elements
In order to estimate the association between ICP and brain
herniation, it is vital to understand intracranial compliance.
Compliance is the relationship between the ICP and the vol-
ume of the primary intracranial elements—the brain, cere-
brospinal fluid (CSF), and blood—within the rigid structure
of the cranium. Figure 1 illustrates the relative volumetric
contributions of these three components under normal cir-
cumstances. Disorders of each of these intracranial contents
and the physical laws that govern compliance are presented
here.
Brain Tissue. The brain represents approximately 1,400 cc
of volume and comprises mostly intra- and extracellular
water (fig. 1), which is relatively noncompressible. Brain tis-
sue volume can increase through abnormal growth in benign
or malignant tumor cells or via an increase in intra- or extra-
cellular water. Malignant brain tumors, one common form
of space-occupying lesion, are often associated with local-
ized edema, necrotic tissue, and hemorrhage, which further
increase brain volume. Anesthesiologists are often reluctant
to proceed with neuraxial anesthesia in patients with these
pathologies for fear of precipitating herniation or neurologic
deterioration.12–18
CSF. The intracranial volume of CSF is approximately 150 cc
(fig. 1) and is contained in the cerebral ventricles, a system
of communicating chambers that connect the intracranial
Fig. 1. Schematic illustration of the three primary intracranial
elements—the brain, cerebrospinal fluid (CSF), and blood—
and their relative volumetric contributions.
cavity with the spinal subarachnoid space and lumbar cis-
tern.22–24 CSF circulates between the two lateral ventricles,
the third ventricle, the aqueduct, and the fourth ventricle.
It then flows through the foramen magnum at the base of
the skull into the spinal subarachnoid space, which termi-
nates in the lumbar cistern. CSF is produced in the choroid
plexus within the intracranial portion of the system at a rate
of approximately 20 cc/h. Under normal circumstances, this
intracranial CSF freely communicates back and forth with
the extracranial subarachnoid space. CSF is ultimately reab-
sorbed in the arachnoid granulations, which then empty into
the intracranial venous sinuses, which are noncompressible
channels cut into the bone of the skull (fig. 2). The CSF
system plays an important role in the exchange of nutrients
in and waste removal from the central nervous system and
also acts like a compressible bladder and cushion within
and around the brain. Ordinarily, approximately 400–500
cc of new CSF is produced daily. Each of the intracranial
and spinal compartments of the CSF system typically con-
tains 150cc of CSF, and the remainder is continuously reab-
sorbed. Normal CSF pressure ranges from 13 to 20 cm H2O
when measured by manometer, or less than 10–15 mmHg
by strain gauge or fiberoptic device.
If the flow of CSF is impeded within or between
the ventricles, “noncommunicating” or “obstructive”
hydrocephalus develops (fig. 3).24 Hydrocephalus (Greek for

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Fig. 2. Schematic illustration of the cerebrospinal fluid (CSF) circulation in the sagittal plane (A) and coronal plane (B). The direc-
tion of CSF flow is indicated by black arrows, and the choroid plexus where CSF is produced is indicated by red.

“water on the brain”) is a radiological finding of increased when cerebral atrophy causes dilation of the ventricles
ventricular volume. An increased ventricular volume is not (“ventriculomegaly”) and “hydrocephalus ex-vacuo”, the ICP
always associated with increased pressure. For example, is usually normal. Hydrocephalus, which is associated with

Fig. 3. Schematic illustration in the coronal plane of a normal brain without hydrocephalus or mass effect (A), and hydrocephalus
due to obstruction at the level of the cerebral aqueduct (B). Magnetic resonance imaging shows obstruction at the level of the
3rd ventricle, as seen in the coronal T1-weighted, spoiled gradient echo (C) and axial fluid attenuated inversion recovery images
(D) of the same lesion.

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increased ICP, may be due to impaired absorption of CSF
(communicating hydrocephalus) or obstructed flow of CSF
(obstructive hydrocephalus). In general, whereas sudden or
major obstruction in intracranial CSF flow will produce
symptoms within minutes to hours, the onset of neurological
deterioration due to partial obstruction can be significantly
delayed by days or weeks. As described below, parturients
with noncommunicating hydrocephalus are typically at
greater relative risk of acute neurological deterioration than
those with communicating hydrocephalus in the setting of
an intentional or inadvertent dural puncture.
Cerebral Blood Volume. The intracranial vessels and the
blood within them serve several vital functions including
facilitating the exchange of oxygen, carbon dioxide, glu-
cose, and amino acids with the brain tissue.22,25 The nor-
mal cerebral blood volume, approximately 150 cc (fig. 1),
is influenced by a variety of factors, including the degree of
vasoconstriction or vasodilation in response to local tissue
environments, or the partial pressure of arterial carbon diox-
ide. In addition to providing a physical barrier to impede
the entry of many large molecules or harmful substances,
the blood–brain barrier regulates the flow of nutrients, ions,
and fluids to the brain. Although it is a complex, multilay-
ered membrane that is designed to support optimal neuronal
electrical activity and metabolism, it is not as impermeable as
many believe. Even under normal circumstances, the blood–
brain barrier permits the flux not only of desirable but also
undesirable molecules, such as alcohol and other illicit sub-
stances. In the presence of malignant tumors or conditions
such as eclampsia, disruption of the blood–brain barrier fre-
quently leads to vasogenic edema, which increases the extra-
cellular water content, and subsequently the tissue volume,
within the skull.26–29 Abnormalities in intracranial blood ves-
sels can also impact intracranial volume in a variety of ways.
Defects in the arterial or venous walls can produce dysplas-
tic segments or aneurysms, arteriovenous malformations, or
fistulas which can bleed, dissect, or occlude. Small bridging
dural veins, and tiny collateral arteries in obstructive vascu-
lopathies, such as Moyamoya, are frail and at high risk of
rupture. When vessel rupture occurs, it produces intracranial
hemorrhage (e.g., subdural, intracerebral, or subarachnoid
hemorrhage). Venous occlusion can also lead to secondary
intracerebral hemorrhage. Any intracranial hemorrhage or
other sudden increase in intracerebral blood volume has the
potential to increase ICP by impeding the free flow of CSF
either by exerting mass effect on the ventricular system, or by
causing thrombosis within the ventricles. Alternatively, arte-
rial or venous thrombosis can produce cytotoxic or vasogenic
edema, which can increase ICP by increasing tissue volume.
Any of these circumstances can increase the risk of neuro-
logic deterioration related to neuraxial anesthesia.
Intracranial Compliance
Within the noncompliant bony skull, the sum total of
the intracranial volume remains a constant, such that an
Anesthesiology 2013; 119:703-18 706 L. R. Leffert and L. H. Schwamm
Neuraxial Anesthesia and Intracranial Lesions in Pregnancy
increase in the volume of any one component causes a com-
pensatory decrease in the volume of another. This “zero-
sum game” of the volumes of the brain, CSF, and blood
is known as the Monro–Kellie doctrine.23,30–32 Intracranial
compliance (C) is defined as the change in volume (ΔV)
for any given change in pressure (ΔP), or C = ΔV/ΔP. The
intracranial compliance curve is derived from the summa-
tion of the compliance of each of the three intracranial ele-
ments. The brain volume contributes to the steep section
of the curve because it is composed mostly of intracellular
and extracellular water, which is inherently noncompress-
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ible. The initial slope of the intracranial compliance curve is
flattened because, under normal circumstances, an equiva-
lent volume of blood and CSF can be displaced out of the
cranium when intracranial tissue volume increases. Once
blood and CSF are unable to further translocate out of the
skull (either because of obstruction, or depletion), they
then contribute to increased pressure, just like any other
noncompressible substance within the rigid skull. Because
small, slow increases in brain volume often successfully
lead to displacement of CSF or blood into their respective
extracranial reservoirs, the intracranial compliance curve is
initially flat (fig. 4). However, once this adaptive element of
compliance in the intracranial system is exhausted, further
small increases in intracranial volume will cause a substan-
tial and steep increase in ICP (fig. 4).
The Impact of Baseline Physiologic Perturbations and the
Changes during Pregnancy and Labor. In normal subjects,
magnetic resonance imaging of the brain shows that CSF
shifts from the intracranial to the spinal subarachnoid space
during cardiac systole. This phenomenon is thought to be a
physiologic response to the corresponding increased brain-
blood volume that occurs with each systolic contraction (an
example of homeostasis based on the Monro–Kellie doc-
trine). During diastole, CSF returns to the intracranial com-
partment. Hence, physiologic alterations in cerebral blood
volume results in a transient, well-tolerated increase in ICP
followed by rapid reequilibration, which does not compro-
mise neurologic function.31,33–35 The respiratory cycle has
also been found to produce smaller, well-tolerated oscilla-
tions of CSF pressure.36,37
There have been several investigations of the effect of
pregnancy, labor, or prolonged valsalva on CSF volume and
ICP. Hogan et al.38 demonstrated that obesity and external
abdominal compression, simulating the impact of the
gravid uterus, result in decreased lumbar CSF volume. They
postulated that the mechanism of lumbar CSF displacement
was compression of the spinal subarachnoid space via the
surrounding soft tissue at the sites of intervertebral foramen in
the abdomen and thorax. In the 1960s, Marx et al.39 measured
lumbar CSF pressure in 20 normal pregnant women, at
rest and during labor, and found increased CSF pressure
with contractions only when the parturient was panting,
bearing down, or otherwise changing her respiratory muscle
function. Subsequently, using more precise information
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Fig. 4. Schematic of the potential impact of a space-occupying lesion on the three primary intracranial components—brain tis-
sue, cerebrospinal fluid (CSF), and blood—and their respective volumes. The graph to the right depicts the intracranial compli-
ance curve (i.e., the relationship between intracranial pressure [ICP] and intracranial volume). This is attenuated by the ability of
CSF and blood to move from the intracranial to the extracranial compartment (dashed arrow) as intracranial volume rises. Once
this is exhausted, the curve rises steeply due to the incompressible nature of liquids (solid arrow).

from continuous intrauterine pressure catheters, Hopkins et
al.37 were able to show that CSF pressure did increase with
contractions in a predictable fashion, with a mean rise of
2.5 mmHg. This rise corresponded to an increase in central
venous pressure, which persisted even during sleep or total
sensory blockade. These findings illustrate that ICP does
not exist in a vacuum, but is influenced by the pressures
of the adjacent compartments of the thorax and abdomen
and the fluids within them. The pressures in these other
compartments are most influential when subjects are on the
steep portion of the intracranial compliance curve.
The Impact of Lumbar Epidural Injection. Injection of
medication into the lumbar epidural space compresses the
dural sac, alters the compliance of the spinal subarachnoid
space, and displaces CSF upward toward the cranium.40,41
Pregnancy and labor have been found to increase baseline
lumbar epidural pressure, an effect that is more pronounced
than the effect of pregnancy on lumbar CSF pressure.42,43
This increase in epidural pressure occurs gradually during
pregnancy and is thought to be due to the space-occupying
effect of the increased blood volume in distended epidural
veins. In the nonpregnant population, studies in animals40
and humans41 have confirmed that subjects with baseline-
elevated ICP have more pronounced transient increases
in ICP after epidural injection, than subjects with normal
preinjection ICP. Specifically, in a patient with preinjection-
elevated ICP, a 10-cc bolus of local anesthetic given over 20–
30 s caused an average increase of 21 mmHg in ICP (from
18.8 to 39.5 mmHg) lasting for 4.5 min compared with an
average increase of 6 mmHg (from 9.3 to 15.6 mmHg) for
2.3 min in a patient with preinjection-normal ICP. Decreas-
ing the volume of injection to 5 cc in the patient with pre-
injection-elevated ICP dramatically reduced the change in
ICP to 5 mmHg for a duration of 2.8 min. In a porcine
model with elevated ICP, epidural injection was shown to
correlate with more than 90% transient reduction in cere-
bral blood flow.
Intracranial Pathology and the Risks of
Neuraxial Anesthesia and Analgesia
Under normal conditions, the total intracranial volume (i.e.,
brain, CSF, and cerebral blood) is low enough so that, despite
the routine physiologic perturbations associated with the
cardiac and respiratory cycles, as well as those in pregnancy
and vaginal delivery, the ICP fluctuates within the normal
range and no neurologic consequences occur. However,
pathologic changes in brain tissue, CSF, or cerebral blood
volume can disrupt this balance and potentially result in
substantially increased ICP, brain tissue shifts, or rupture of
intracranial vascular lesions. In this section, we will apply
the principles of intracranial compliance to case examples to
help determine when harm could result from the reduction
in lumbar CSF volume, which can occur with an intentional
spinal anesthetic, accidental dural puncture during epidural
catheter placement, or epidural catheter dosing. We will

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specifically address several generalizations frequently cited in
the literature and in clinical practice and show under what
circumstances they do and do not apply.
The Impact of a Space-occupying Lesion
The diagnosis of a brain mass during pregnancy can be devas-
tating. Fortunately, the incidence of malignant brain tumors
during pregnancy is very low, although not well quantified.
Pregnancy is not thought to change the basic rate of develop-
ing a brain tumor.44,45 Of the intracranial tumors discovered
during pregnancy due to detection of neurologic symptoms,
gliomas represent the majority, followed by meningioma,
and acoustic neuroma. Tumors such as meningiomas and
pituitary adenomas can be hormone responsive and there-
fore, may enlarge during pregnancy.
Critical to assessing the potential for neurologic deteri-
oration from neuraxial anesthesia in the setting of a brain
tumor or other space-occupying lesion is an analysis of its
effect on intracranial compliance. Although many factors
can be considered, the most relevant lesion characteristics
are its location and size, the rapidity with which the overall
brain tissue and associated volume has increased, and the
presence of imaging evidence of preexisting fluid or tissue
shifts or obstruction to CSF pathways.
To safely perform any dural puncture, there should be
preservation of continuous flow of CSF and the absence
of a substantial pressure differential between the intra-
cranial to intraspinal compartments. If a pressure differ-
ential exists, then loss of sufficient CSF volume via the
dural puncture could force brain tissue to shift from one
compartment to another. In addition, because there will
undoubtedly be some loss of lumbar CSF after a (lumbar)
dural puncture, there should be ample remaining intra-
cranial CSF so that CSF will shift to equalize the pressure
rather than brain tissue. The ultimate decision will be the
result of balancing many factors simultaneously, as there
are often competing risks.
The following generalizations about parturients with
space-occupying intracranial lesions are not supported by
evidence:
• A space-occupying lesion is always associated with
increased ICP
• Normal ICP necessarily implies low risk of herniation
after dural puncture
• Increased ICP always implies high herniation risk after
dural puncture
• An epidural anesthetic is a safe alternative when a dural
puncture, even with a small-gauge spinal needle, is con-
sidered to be too dangerous
• A spinal anesthetic with a small-gauge needle is a safe
alternative when an inadvertent dural puncture during
epidural placement is considered to be too dangerous
• When all forms of neuraxial anesthesia pose some risk
of herniation, general anesthesia is always preferable
Anesthesiology 2013; 119:703-18 708 L. R. Leffert and L. H. Schwamm
Neuraxial Anesthesia and Intracranial Lesions in Pregnancy
• A parturient with an intracranial arterial or venous
pathology should not undergo neuraxial anesthesia due
to increased risk of vessel rupture
1. Is a space-occupying lesion always associated with an
increased ICP? If a primary brain tumor or brain metastasis
is located in a region which is remote from CSF pathways,
and is of small-to-moderate size or grows slowly over time,
it may cause little-to-no ventricular compression, and have
no impact on CSF flow. A common example would be a
small, slow-growing, and low-grade glioma in the anterior
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frontal lobe. This tumor may cause minimal mechanical dis-
tortion of brain tissue or mass effect. As described above,
there may then be little-to-no increase in ICP because the
increase in brain volume is offset by caudal displacement of
CSF or cerebral blood volume (fig. 5). A sudden loss of lum-
bar CSF volume at the time of dural puncture will cause a
transient pressure gradient across the foramen magnum. In
this scenario, CSF rather than brain tissue will be displaced
from the intracranial to the lumbar CSF compartment. In
other words, there should be no herniation of brain tissue.
Similarly, one would expect that in this patient with normal
preprocedure ICP, the transient increase in ICP associated
with epidural injection would also be well tolerated.
There are several illustrative case examples reported in
the literature in which parturients with benign or malig-
nant brain tumors have had successful epidural anesthetics
(or unspecified “neuraxial anesthetics”) for cesarean or low
valsalva vaginal deliveries.19,21,46,47 Typically, these patients
lacked clinical symptoms or signs of increased ICP (e.g.,
headache, nausea, vomiting, decreased alertness, recent sei-
zure, hemiparesis, or pupillary abnormalities) or imaging
evidence suggestive of increased ICP (table 1).
In contrast, if the intracranial lesion partially or
completely obstructs the free flow of CSF, then the risk of
brain herniation after either intentional, or unintentional
dural puncture will be increased.24,48 This is particularly
likely to happen if the lesion is located at an anatomically
narrowed segment of the ventricular system (e.g., near the
third ventricle or cerebral aqueduct) or at the foramen
magnum. As the lesion grows, it displaces intracranial CSF
caudally, or in the case of an obstruction to CSF outflow,
it causes increased ventricular volume and hydrocephalus.
Space-occupying lesions that narrow the ordinarily large
opening of the foramen magnum, or are situated in the
posterior fossa and cause a bottleneck to CSF flow, can place
the parturient at significant risk of herniation. This can
occur from benign or malignant tumors anywhere in the
posterior fossa or at the opening to the foramen magnum.
It can also occur from low-lying cerebellar tonsils, either
due to a preexisting Arnold–Chiari malformation, or due to
intracranial hypotension from a persistent CSF leak. If the
intracranial CSF has been exhausted and the lumbar CSF
pressure suddenly drops from a dural puncture, then brain
tissue itself will be displaced into the neighboring intracranial
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Fig. 5. Schematic illustration in the coronal plane of a normal brain with normal ventricular volume (A), and in the axial plane of a
brain with a tumor surrounded by edema in the left occipital pole that exerts no visualized mass effect on the ventricles and no
midline shift (B). The lesion is demonstrated on fluid attenuated inversion recovery coronal (C) and axial (D) magnetic resonance
images.

compartment (i.e., transtentorial or uncal herniation) or into
the spinal canal (tonsillar herniation).12–14,17,32,49 Significant
neurological deterioration typically ensues.
In their review on brain herniation from lumbar
puncture, the neurologist van Crevel et al.50 described
“brain shift” imaging findings “anatomically (by) tense
dura, flattened gyri, narrowed sulci, effaced cisterns,
compressed (or, in obstruction, dilated) ventricles, and
in advanced stages, herniation, i.e., displacement of brain
from one intracranial compartment into another.” Evidence
regarding the safety of diagnostic lumbar puncture in
patients suspected of having acute bacterial meningitis
also provides important lessons for the management of
parturients with intracranial pathology and increased ICP.
Lumbar puncture in this setting is usually performed with
a 20-gauge Quinke spinal needle because smaller gauge
needles do not allow for adequate drainage of viscous,
infected spinal fluid. The abrupt decrease in lumbar
CSF pressure associated with a lumbar puncture is often
implicated as contributing to the neurological deterioration
of some patients who herniate immediately after the
procedure, as well as others who manifest symptoms 12–
24 h later.50–52 Preexisting clinical signs of impending or
preexisting fatal herniation, specifically deteriorating level
of consciousness, brainstem signs (e.g., pupillary changes
or asymmetry, eye movement abnormalities, dysconjugate
gaze, facial weakness, swallowing dysfunction, irregular
respirations, or limb posturing), recent new onset seizure, or
the presence of papilledema and/or hemiparesis are thought
to be the best indicators of individuals at high risk.48,50
If signs of herniation develop, then prompt attention to
airway, breathing, cerebral, and systemic circulation are
of paramount importance. The recommended maneuvers
to rapidly lower ICP include hyperosmolar therapy (e.g.,
rapid IV infusion of mannitol 100 g or 23.4% saline 15–
30 cc), intubation, and hyperventilation (with a goal of
Paco2 of 25–30 mmHg) while emergency neurosurgical
consultation is obtained.23 If a spinal needle is in place, the
stylet should be reinserted and kept in situ until the ICP
normalizes to avoid ongoing large volume CSF leak.

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Table 1.  Features Associated with Increased ICP
Clinical features
  Pupillary changes or asymmetry
  Eye movement abnormalities
 Papilledema
 Hemiparesis
  Facial weakness
  New onset seizure
  Decreased level of consciousness
Radiologic features on CT or MRI
  Tense dura
  Flattened gyri
  Narrowed sulci
  Effaced cisterns
  Compressed (or in obstruction, dilated) ventricles
  Lateral shift of midline structures
  If advanced, displacement of brain tissue from one
compartment to another
CT = computed tomography; ICP = intracranial pressure; MRI =
magnetic resonance imaging.
2. Does normal ICP always imply low risk of herniation
after dural puncture? If expansion of an intracranial mass
happens very slowly, over weeks or months, it may cause
little-to-no symptoms associated with elevated ICP and
these pressures might be at the upper end of normal. What
is critical is that these patients have exhausted all reserves for
tolerating any pressure differential across the foramen mag-
num so that any small change in intracranial volume will
cause a shift of brain tissue rather than of blood volume or
CSF. A large right hemisphere tumor with significant sur-
rounding edema causing major mass effect and shift of brain
tissue (subfalcian herniation) is shown in figure 6. If a dural
puncture were attempted, this patient would surely be at
increased risk for herniation.
Parturients with Arnold–Chiari malformations pose an
interesting challenge for assessment of the safety of neur-
axial anesthesia. Because, by definition, the cerebellar tonsils
are descended at least 5 mm through the foramen magnum,
there can be partial or intermittent obstruction of CSF and
dynamic or static herniation of brain tissue.33,35 Parturients
with the most common form, type I, may be asymptomatic
or may manifest symptoms, including headache, ataxia and/
or sensorimotor impairments of the extremities.53,54 Patients
with type II Chiari malformations usually present in infancy,
with associated myelomeningoceles. In type II or “classic”
Chiari malformation, both cerebellar and brain stem tissue
extend into the foramen magnum, resulting in episodic apnea,
cranial nerve dysfunction, and upper extremity weakness. In
type III Chiari malformations, there is further protrusion of
the cerebellum and the brain stem into the foramen magnum
and the spinal cord, resulting in severe neurologic dysfunc-
tion. Type IV disease involves cerebellar hypoplasia. Successful
surgical correction of the Arnold–Chiari malformation with
extraarachnoidal craniocervical decompression and duraplasty
Anesthesiology 2013; 119:703-18 710 L. R. Leffert and L. H. Schwamm
Neuraxial Anesthesia and Intracranial Lesions in Pregnancy
removes the obstruction and ameliorates these abnormal phe-
nomena. However, some of the associated anomalies, such as a
tethered spinal cord, may persist and may represent important
contraindications to neuraxial anesthesia.
Multiple individual reports and a case series of 30 deliv-
eries document successful spinal and epidural analgesics and
anesthetics in a heterogeneous group of patients with Chiari
malformations. Among them are patients in whom the condi-
tion was or was not previously diagnosed, and among those
previously diagnosed, there were some who had and others
who had not gone in for surgical correction.53,55 One of the
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parturients with an uncorrected Arnold–Chiari malformation
in the published case series underwent a combined spinal–
epidural and developed a spinal headache. Fortunately, she
was successfully treated with an epidural blood patch. She was
the only parturient to have an anesthetic-related complica-
tion in that series. In a separate report, a new diagnosis of
Arnold–Chiari malformation was made in a parturient who
developed a persistent headache after a failed epidural anes-
thetic, followed by a spinal anesthetic that required multiple
attempts.56 When the headache was not responsive to an epi-
dural blood patch, a subsequent brain magnetic resonance
imaging revealed the Arnold–Chiari malformation. There are
an increasing number of published reports of patients with
persistent headache after dural puncture, wherein subsequent
brain magnetic resonance imaging shows cerebellar descent
consistent with an acquired Arnold–Chiari malformation.57
These cases confirm that large-gauge dural punctures or
persistent CSF leaks can lead to cerebellar descent, even in
patients without preexisting Chiari malformations. As such,
it may be reasonable to proceed with a spinal or epidural anal-
gesic or anesthetic in a parturient with an asymptomatic, type
I Chiari malformation with minimal initial tonsillar descent.
However, if she has an inadvertent large-gauge needle dural
puncture and/or develops a persistent headache or other neu-
rologic symptoms, a neurologic consultation and consider-
ation of early epidural blood patch is recommended.
3. Does increased ICP always mean a high rate of her-
niation after dural puncture? Idiopathic or benign intra-
cranial hypertension (also known as pseudotumor cerebri)
is a common condition, in which increased ICP does not
imply herniation risk after dural puncture. This disorder,
usually occurring in obese women of childbearing age, is
defined by increased ICP (>20 cm H2O) with normal CSF
composition and the absence of a known underlying cause
(e.g., a space-occupying or vascular lesion, mass effect, or
hydrocephalus).26,58–61 Extraventricular CSF volume and
ICP are thought to be elevated in these women, who often
experience symptoms of headache, neck stiffness, papill-
edema, and visual loss. However, there is no obstruction
to CSF flow and no baseline pressure differential between
the intracranial and spinal CSF compartments. Therefore, a
sudden drop in CSF volume during lumbar dural puncture
will be rapidly accommodated by caudal flow of CSF and
should not result in brain shift or herniation. In fact, serial
 EDUCATION

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Fig. 6. Schematic illustration in the coronal plane showing normal ventricles (A) and a large right-sided supratentorial mass lesion
causing midline shift and compression of the right lateral ventricle (B). T1-weighted coronal (C) and fluid attenuated inversion
recovery axial magnetic resonance (D) images of a patient with a large right-sided frontal tumor causing compression of the
lateral ventricle, subfalcian herniation, midline shift causing obstruction of the foramen of Monro and dilation of the left lateral
and temporal horns.

lumbar punctures for deliberate removal of large volumes
of CSF, coupled with weight control, diuretics, and steroids
are mainstays of therapy for the disease. Although there are
individual case reports of both increased and decreased spi-
nal anesthetic effects in these patients after deliberate spinal
fluid removal,62,63 neuraxial anesthesia has been used effec-
tively for parturients with benign intracranial hypertension
with or without shunts.20,59,63–70 Slow, incremental dosing of
epidural medication may be better tolerated in symptomatic
patients who might otherwise experience exacerbation of
their symptoms due to predelivery increase in ICP. Dosages
in the range of 5 cc every 5–7 min have been recommended.
4. Is an epidural anesthetic a safe alternative when a dural
puncture, even with a small-gauge spinal needle, is consid-
ered to be too dangerous? Alternatively, is a spinal anes-
thetic with a small-gauge needle a safe alternative when
an inadvertent dural puncture during epidural placement
is considered to be too dangerous? Because epidural place-
ment always entails the risk of a dural puncture even in the
experienced hands,71 it is never a completely safe alternative
if a spinal anesthetic is contraindicated. This is especially true
because when inadvertent dural puncture does occur during
epidural placement, it is with a much larger gauge needle.
Conversely, even a small-gauge spinal needle causes a dural
tear and potential CSF leak, so spinal anesthesia is not with-
out risk when seeking to avoid significant loss of CSF.
In vitro experimental models have indicated that dural
punctures with smaller gauge needles are correlated with a
shorter duration of CSF leak: fluid loss ceased within 5 min
in 10% of dural punctures made with a 22-gauge needle and
in 65% of those made with a 29-gauge needle.72 Pencil point
versus Quincke needle design also minimized fluid loss.72–74
Results of studies to determine the impact of the angle of
needle alignment relative to the dural fibers were inconsistent.
When the dural leaks from six 17- to 20-gauge epidural nee-
dles were compared in cadaveric tissue, the 20-gauge Tuohy
needle produced the slowest rate of fluid loss.74 Noninvasive,
in vivo measurements of CSF leak after lumbar puncture have
shown considerable variation in the amount of CSF leak,
even when the same needle is used, and that predominantly

Anesthesiology 2013; 119:703-18 711 L. R. Leffert and L. H. Schwamm


cortical, sulcal CSF is depleted.75 In summary, there is ample
evidence that the leakage of CSF can persist after dural punc-
tures with both spinal and epidural needles and that to date,
nothing including postprocedure patient positioning, pro-
phylactic blood patch, or IV medications can reliably prevent
the intracranial hypotension headache syndrome.76–78
There are reports of successful epidural or small-gauge spinal
analgesics and anesthetics in patients who have been described
as having mass effect from intracranial lesions.79,80 However,
there are two salient cases that illustrate the perils of neuraxial
anesthesia when dural puncture is considered risky. Su et al.81
described a parturient with fatal brain herniation after acci-
dental dural puncture associated with epidural analgesia for
labor and delivery. Over the course of her labor, she developed
a severe headache and systemic hypertension and ultimately,
postdelivery, deep coma. Urgent brain computed tomography
revealed a slightly hyperdense tumor in the left hemisphere,
midline shift to the right and transtentorial herniation. The
most likely explanation for this patient’s neurologic deteriora-
tion is that the increased intracranial volume, associated with
her unrecognized tumor, had exhausted her compensatory
mechanisms, and put her on the steep portion of the intra-
cranial compliance curve before her epidural procedure. The
increased intracranial volume during labor contractions and
valsalva during delivery likely pushed her ICP to dangerous
levels. This increased ICP likely resulted in the translocation
of most of the intracranial CSF into the lumbar compartment
with associated collapse of the ventricles. The inadvertent dural
puncture added ongoing loss of lumbar CSF, which created a
further pressure gradient across the tentorium. When there was
no remaining intracranial CSF to shift caudally, brain tissue
then translocated, leading to transtentorial herniation.
Another parturient with a known, extensive, frontopari-
etal tumor was induced for vaginal delivery under epidural
analgesia because of signs of increased ICP.82 Despite her
expedient, nonvalsalva delivery and lack of known dural
puncture, she suffered increasingly intense intrapartum
headaches. Urgent postpartum computed tomography
revealed substantially increased tumor volume and contra-
lateral obstructive hydrocephalus. This was due to a trapped
lateral ventricle that could not empty because its drainage,
into the rest of the ventricular system via the foramen of
Monro, was blocked. Although her tumor was urgently
decompressed, she developed progressive mass effect from
edema, and ultimately fatal brain herniation. These cases
highlight that epidural placement can be just as risky as a
spinal anesthetic in patients with poor intracranial compli-
ance. In some cases, the use of a small-gauge spinal needle
for deliberate dural puncture may be the lesser of two evils,
but all options should be explored to assess that this is the
technique with the most favorable risk/benefit ratio.
5. When neuraxial analgesia or anesthesia poses a risk
of herniation, is general anesthesia always preferable?
General anesthesia can pose significant risks for neurological
deterioration in parturients with compromised intracranial
Anesthesiology 2013; 119:703-18 712 L. R. Leffert and L. H. Schwamm
Neuraxial Anesthesia and Intracranial Lesions in Pregnancy
compliance.12–14,18 Care should be taken to minimize valsalva
during the rapid sequence induction and emergence of gen-
eral anesthesia, although blunting the airway reflexes in these
patients may further increase their pregnancy-related risk of
aspiration. Strategies to blunt the sympathetic response to
intubation include combining induction agents with opioids
(e.g., fentanyl 2–5-µg/kg bolus or remifentanil 1 µg/kg over
1 min) or labetolol in 5-mg increments.83–85 Some experts
advocate replacing succinylcholine, which can theoretically
cause a transient increase in ICP due to contraction of the
muscles of the abdomen and thorax, with a nondepolariz-
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ing muscle relaxant (e.g., rocuronium 1.2 mg/kg) for a rapid
sequence induction.13 Paradoxically, while hyperventilation
is beneficial to the mother by decreasing ICP and maximiz-
ing cerebral blood flow in patients with increased ICP, it can
be detrimental to the fetus by decreasing placental blood
flow. To balance fetal and maternal cerebral perfusion, the
recommendation is to keep maternal Paco2 at approximately
25–30 mmHg and maternal blood pressure close to baseline
values.
Whereas the risk of herniation in a parturient may limit
the desirability of a neuraxial approach, Semple et al.86
makes a compelling case for doing an epidural anesthetic
for cesarean delivery, if there are equally or more compelling
risks associated with a general anesthetic. They discuss the
management of one such parturient with a Chiari malfor-
mation who had no papilledema or other symptoms associ-
ated with raised ICP, but whose airway was characterized as
a Mallampati class III, with a high arched palate, receding
chin, and protruding incisors. The authors initially consid-
ered a general anesthetic (awake fiberoptic or elective trache-
ostomy) but in collaboration with the patient, decided to
proceed with an epidural anesthetic instead because of her
unfavorable airway. They slowly titrated 23 cc of a combina-
tion of 2% lidocaine and 0.5% bupivacaine with 50 mics
of fentanyl over 30 min, and she delivered without acute
or subacute neurologic complication. Another case report
describes a parturient with a glioblastoma with mass effect
and a “fourth ventricle narrowed but not obstructed” who
was successfully managed for cesarean delivery, with a spi-
nal anesthetic using a 24-gauge pencil-point needle.79 The
authors noted that this parturient was at particularly high
risk for aspiration due to cranial nerve dysfunction, and at
low risk for herniation because “an atraumatic small-bore,
pencil-point needle, even under slightly raised ICP, presum-
ably causes only minimal CSF leakage, if at all”. On the basis
of the evidence and rationale discussed above, the authors
may have been overly optimistic in their confidence of the
safety of a dural puncture in this patient. An alternative, and
perhaps, more prudent approach for cesarean delivery could
have been a controlled general anesthetic, thus securing her
tenuous airway, and avoiding the small but very real risk of a
persistent CSF leak from the spinal anesthetic.
In summary, there are no published randomized con-
trolled trials comparing the safety of neuraxial versus general
 EDUCATION
anesthesia in patients with intracranial lesions, nor are there
likely to be any. As with all published case reports, there is an
inherent bias in the cases that are chosen for reporting. There-
fore, for each parturient with an intracranial lesion, there
needs to be a collaborative team discussion, which includes
anesthesia, obstetric, neurologic, and neonatology experts,
and a rational exploration of the likelihood of increased ICP
and the potential for related negative effects. To make recom-
mendations on the proper anesthetic choice for any individ-
ual case, it is necessary to evaluate the relative contribution of
each of the identified risks, in both severity and likelihood,
and weigh them against the potential benefits.
6. Is it unsafe for a parturient with intracranial arterial or
venous pathology to undergo neuraxial analgesia or anes-
thesia due to increased risk of vessel rupture or mass
effect? Some authors advocate avoiding neuraxial anesthesia
in parturients with intracranial hemorrhage or derangements
of the intracranial vasculature out of concern for precipitat-
ing neurological complications.87 Because there are many
attendant risks to general anesthesia in this population and
wide variability in blood vessel fragility across patients,
knowledge of the precise details of the vascular abnormality
and its risk of rupture is key to making informed decisions
about anesthetic management. Neurological or neurosur-
gical or endovascular consultation is generally required to
undertake appropriate risk/benefit analysis. Although urgent
or elective cesarean delivery has been the predominant mode
of delivery recommended for those with serious vascular
lesions prone to hemorrhage, the degree to which pregnancy
and the mode of delivery are actually risk factors for hemor-
rhage in these cases is controversial.83,84,87–91
Historically, the reason that pregnant patients with asymp-
tomatic unruptured brain aneurysms have been counseled
to avoid expulsive efforts is the concern for the following
chain of events: the associated increase in cerebral blood and
CSF volume during prolonged valsalva can elevate ICP; this
increase in ICP can cause a compensatory increase in arterial
blood pressure to maintain constant cerebral perfusion, which
may in turn increase the transmural pressure across the already
weakened aneurysmal vessel wall and precipitate aneurysmal
rupture. In addition, intracranial hypotension due to a per-
sistent CSF leak, after a spinal anesthetic or inadvertent dural
puncture during epidural placement, could theoretically cause
a compensatory increase in cerebral blood volume. This could
trigger similar increases in transmural pressure across the vul-
nerable aneurysmal wall. To our knowledge this complication
of neuraxial anesthesia has not been reported.
Of note, in a recent retrospective review of women with
aneurysmal subarachnoid hemorrhage, Tiel Groenestege et
al.91 found that pregnancy, labor, or the puerperium did not
appear to increase the risk of aneurysmal subarachnoid hem-
orrhage. The authors concluded that there was no need to
advise women, with a previous history or family history of
aneurysmal subarachnoid hemorrhage, against pregnancy or
vaginal delivery. We recently reported that in the National
Anesthesiology 2013; 119:703-18 713 L. R. Leffert and L. H. Schwamm
Inpatient Sample, a large U.S. administrative dataset, a
significant proportion of subarachnoid hemorrhage in the
puerperium is likely nonaneurysmal in etiology.92 Whereas
the precise etiologies require further investigation, advanc-
ing age, African American race, Hispanic ethnicity, hyper-
tensive disorders, coagulopathy, tobacco, drug or alcohol
abuse, intracranial venous thrombosis, sickle cell disease,
and hypercoagulability were identified as key risk factors
for pregnancy-related subarachnoid hemorrhage. The risks
associated with neuraxial anesthesia in the setting of these
nonaneurysmal etiologies are not known.
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If a pregnant patient develops subarachnoid hemorrhage
due to aneurysmal rupture, then there is consensus that the
neurosurgical management should be the same as if she were
not pregnant.44,87,88 There are multiple reports of craniot-
omy and embolization occurring simultaneously with or in
advance of cesarean delivery.84,85 For these combined proce-
dures, general anesthesia is typically used with volatile agents
plus IV anesthetics or a total IV anesthetic technique.83 For
cesarean delivery that does not require aneurysm repair, a
neuraxial anesthetic (spinal, epidural, or combined spinal–
epidural anesthesia) can be used in a stable patient and has
the advantage of (1) avoiding the valsalva potentially associ-
ated with intubation, (2) minimizing fetal exposure to gen-
eral anesthetics, and (3) allowing the mother to be awake
and participate fully in the birth experience. Hypotension is
typically well-controlled with a prophylactic phenylephrine
infusion 25–120 µg/min or intermittent 120-µg boluses.93,94
The natural history of arteriovenous malformations dur-
ing pregnancy is also a matter of some debate, although
when arteriovenous malformations do bleed during preg-
nancy, the results can be devastating.89,95,96 In 1990, Horton
et al.90 did a retrospective review of pregnant women with
untreated, symptomatic intracerebral arteriovenous mal-
formations and found these patients to be at the same risk
of nonfatal hemorrhage as their nonpregnant counterparts.
However, because these women were retrospectively identi-
fied by referral for proton beam therapy, the ascertainment
strategy did not include those parturients with fatal bleeds or
those with previous arteriovenous malformation-related sur-
gery. In contrast, in a recently published retrospective review
of women with angiographic diagnosis of arteriovenous
malformation, Gross and Du 95found an increased risk of
hemorrhage from arteriovenous malformations during preg-
nancy. Acknowledging their small sample size, retrospective
design, and the assumption that arteriovenous malforma-
tions are congenital, the authors concluded that therapeutic
intervention is indicated ideally before pregnancy, particu-
larly if the arteriovenous malformation has previously bled.
Of particular anesthetic concern in parturients with intra-
cranial hemorrhage from ruptured arteriovenous malforma-
tions is the possibility of CSF flow obstruction or raised
ICP.96 As in patients with other space-occupying lesions, the
key to deciding whether it is safe to proceed with a neur-
axial anesthetic is to determine the likelihood of creating a

pressure differential between intracranial versus intraspinal
compartments, causing brain tissue to translocate down-
ward. An additional priority of anesthetic management of a
parturient with recent intracranial hemorrhage is to provide
strict hemodynamic stability. Hypertension can occur after
aggressive treatment of neuraxial-induced hypotension or
during induction or emergence from general anesthesia, and
increase the risk of fatal hemorrhage in lesions predisposed
to bleeding. Hypotension, however, can reduce maternal
brain and fetal-placental perfusion.
In the case of an unruptured arteriovenous malformation
found during pregnancy, experts recommend case-specific
multidisciplinary discussions about the relative risks of neu-
rosurgical intervention versus cesarean delivery before neu-
rosurgical intervention.95 Spinal and epidural analgesics and
anesthetics have also been successfully used for cesarean and
vaginal deliveries in parturients with intact, partially or fully
resected arteriovenous malformations.97–99 In these cases, the
anesthetic options have been guided by the usual principles.
Moyamoya syndrome, an obliterative vasculopathy
affecting the distal internal carotid and proximal middle
and anterior cerebral arteries, invokes the same principles
of anesthetic management as those of the other cerebrovas-
cular pathologies discussed.100–107 In Moyamoya, multiple
tiny collateral arterioles develop at sites of proximal arterial
occlusion. These vessels are prone to rupture, but lowering
blood pressure can increase the risk of ischemic brain infarc-
tion by decreasing collateral flow. The anesthetic goals for
parturients with known Moyamoya syndrome are to avoid
hypertension, which can precipitate the hemorrhage and
avoid hypotension or hypocapnea that can reduce placen-
tal perfusion and the already compromised cerebral blood
flow. Most affected parturients undergo successful cesarean
deliveries under neuraxial anesthesia (spinal, epidural, or
combined spinal–epidural anesthesia), often with invasive
arterial hemodynamic monitoring.
Peripartum cerebral venous thrombosis is a rare but likely
underdiagnosed intracranial pathology that occurs most
often in the postpartum period but can present before deliv-
ery.108,109 Cerebral venous sinus thrombosis is typically asso-
ciated with severe headache, sometimes worse when lying
down, and can be accompanied by visual changes, nausea,
vomiting, seizures, or lateralizing neurologic signs. Diagno-
sis of cerebral venous sinus thrombosis is usually confirmed
by computed tomography or magnetic resonance venogra-
phy.110 Anticoagulation therapy is strongly recommended by
clinical experts, even in many patients with existing hem-
orrhagic infarction.111,112 Case reports describe the use of
both catheter-based and systemic thrombolysis in selected
patients with severe neurologic symptoms due to cerebral
venous sinus thrombosis, but there are no relevant published
randomized controlled studies. Although some brain swell-
ing has been reported to occur in up to 50% of nonpregnant
patients with this entity, osmotic therapy, with or without
decompressive surgery, is thought to be necessary in only
Anesthesiology 2013; 119:703-18 714 L. R. Leffert and L. H. Schwamm
Neuraxial Anesthesia and Intracranial Lesions in Pregnancy
20% of patients. Large volume lumbar puncture has been
recommended in selected patients to reduce the raised ICP,
which is caused by the increased blood volume associated
from impaired venous drainage. Balancing the timing of
lumbar puncture with the need for continuous anticoagula-
tion therapy remains challenging.
Successful spinal anesthesia for cesarean delivery has been
reported in at least one parturient with extensive cerebral
venous sinus thrombosis that was being treated with IV
unfractionated heparin therapy.113 Despite her mild hyper-
tension and intermittent bradycardia suggesting some degree
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of increased ICP, the authors opted to perform a spinal
anesthetic with a small-gauge, pencil-point needle. These
practitioners were depending on the presence of an ample
volume of unobstructed CSF that could flow caudally so
that downward herniation of the brain would not occur. In
their estimate, this was less risky than trying to blunt the
increased ICP related to induction and emergence of general
anesthesia. In other published reports, the symptoms of cere-
bral venous sinus thrombosis have been mistaken for post-
dural puncture headache or have occurred concomitantly
with postdural puncture headache.114,115 Interestingly, dural
puncture, itself, has been proposed as a risk factor for subse-
quent cerebral venous sinus thrombosis.
When the integrity of the blood–brain barrier is dis-
rupted, vasogenic edema may occur. This increased intra-
cranial tissue water content can cause increased ICP and
has been documented in some parturients with eclamp-
sia.28,29,116,117 Because pregnant patients are not routinely
monitored for ICP, the overall incidence of asymptomatic
or mildly symptomatic increased ICP in patients with
eclampsia is not known. Using optic nerve sheath diameter
as a noninvasive proxy for ICP, a recent pilot study con-
firmed higher ICP in preeclamptic patients compared with
healthy pregnant women. The authors were not, however,
able to demonstrate a relationship between the magnitude
of optic nerve sheath diameter enlargement and the sever-
ity of preeclampsia.116 As discussed by Rollins and Flood
in their accompanying editorial, it is important to consider
whether the increased ICP identified in this study is of any
clinical significance. Most preeclamptic patients undergo
spinal or epidural analgesics and anesthetics without neu-
rologic symptoms or other untoward events. The current
American Society of Anesthesiologists guideline encourages
the “early insertion of a spinal or epidural catheter for high-
risk parturients such as those with preeclampsia.”2 The per-
ceived advantage of doing so includes decreasing circulating
catecholamines,118 and providing an in situ catheter that can
be dosed to provide surgical anesthesia as an alternative to
general anesthesia in these parturients who are at increased
risk for cesarean delivery.
Individual Patient Assessment
As with all high-risk parturients, ensuring antepartum
anesthesia consultation and multidisciplinary planning is
 EDUCATION

Does patient have known

intracranial pathology?

Yes

Are there new neurologic symptoms

(e.g., worsening headache, visual Repeat neuroimaging,
changes, seizure, or decreased level of preferably magnetic
level of consciousness) or a known Is there resonance imaging
Yes No
lesion that is likely to grow or change recent (MRI)
during pregnancy? imaging?

No
Yes

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Is there imaging evidence of an
intracranial space-occupying DO NOT PROCEED
Yes Patient is likely at high risk of
lesion (e.g., tumor, hematoma, Is there imaging evidence of
edema, or intracranial cyst)? Yes significant mass effect with herniation from dural puncture.
or without midline shift?
No
No
No Is there minimal or Yes DO NOT PROCEED
Is there imaging evidence subtle mass effect? WITHOUT
of hydrocephalus?
NEUROLOGICAL
Yes
Is there obstruction to CONSULTATION
Yes Patient is likely at mild-to-
No CSF flow at or above the
Yes foramen magnum? moderate risk of
Do the clinical or herniation from dural
imaging findings No puncture.
suggest increased
intracranial
pressure?
MAY BE REASONABLE TO PROCEED
WITH NEURAXIAL ANESTHESIA
Patient is likely at minimal-to-no risk of herniation
No from dural puncture

Fig. 7. Decision tree summarizing the critical elements for assessing the risks of neurological deterioration from neuraxial anes-
thesia in patients with intracranial space-occupying lesions. CSF = cerebrospinal fluid.

of paramount importance for pregnant patients with intra-
cranial pathology. Decisions regarding the mode of delivery
are, by their nature, linked to the anesthetic plan. As such,
timely assessment of whether the parturient is a candidate
for a neuraxial anesthetic is necessary. Using the basic ana-
tomic, physiologic, and radiologic principles described,
anesthesiologists can work collaboratively with their neu-
rologic colleagues to evaluate a parturient’s appropriate-
ness for neuraxial anesthesia. The decision tree (fig. 7) that
accompanies this chapter synthesizes the critical elements
to be considered, when assessing the risks of neuraxial
anesthesia in parturients with space-occupying lesions, and
helps to provide the framework for informed consultative
questions. This requires the availability of a brain scan (usu-
ally magnetic resonance imaging) that accurately reflects
the current pathology and an individual with neurologic
or neuroradiologic expertise to interpret it. Unless the par-
turient has neurologic symptoms, or a tumor that is likely
to be hormone responsive as described above, then repeat
imaging is often not necessary. Ultimately, decisions about
which kind of imaging is most appropriate and whether
or not repeat imaging is necessary for optimal predelivery
planning is best made by a provider with neurologic exper-
tise. In light of the lack of evidence of fetal harm due to
performance of maternal brain magnetic resonance imag-
ing, this diagnostic test should not be withheld during
pregnancy if needed.119
To summarize, in the absence of unrelated contrain-
dications to neuraxial anesthesia, parturients with space-
occupying lesions that have no mass effect, hydrocephalus,
or clinical or imaging findings suggestive of increased ICP
are likely to have minimal to no increased risk of herniation
from a dural puncture. Parturients at high risk of herniation
from a dural puncture are those with lesions that compress
normal brain tissue and cause it to shift across the midline
(i.e., “midline shift”) or downward, with or without obstruc-
tion to the flow of CSF. Understanding a parturient’s risk
of neurological deterioration not only allows appropriate
low-risk candidates to reap the potential benefits of neur-
axial anesthesia, but also allows proper preparation for a
ICP-controlled general anesthetic for high-risk parturients
when needed.
The authors acknowledge the following individuals for their
careful review of the article and helpful suggestions: Brian Bate-
man, M.D., Department of Critical Care, Anesthesia, and Pain
Medicine, Massachusetts General Hospital, Assistant Professor of
Anesthesia, Harvard Medical School, Boston, Massachusetts, and
Ala Nozari, M.D., Team Leader, Neuroanesthesia, Department of

Anesthesiology 2013; 119:703-18 715 L. R. Leffert and L. H. Schwamm


Critical Care, Anesthesia, and Pain Medicine, Massachusetts General
Hospital, Assistant Professor of Anesthesia, Harvard Medical School.
References
1. Hawkins JL, Chang J, Palmer SK, Gibbs CP, Callaghan WM:
Anesthesia-related maternal mortality in the United States:
1979–2002. Obstet Gynecol 2011; 117:69–74
2. Practice guidelines for obstetric anesthesia: An updated
report by the American Society of Anesthesiologists Task
Force on Obstetric Anesthesia. Anesthesiology 2007;
106:843–63
3. Bloom SL, Spong CY, Weiner SJ, Landon MB, Rouse DJ, Varner
MW, Moawad AH, Caritis SN, Harper M, Wapner RJ, Sorokin
Y, Miodovnik M, O’Sullivan MJ, Sibai B, Langer O, Gabbe SG;
National Institute of Child Health and Human Development
Maternal-Fetal Medicine Units Network: Complications of anes-
thesia for cesarean delivery. Obstet Gynecol 2005; 106:281–7
4. Briner A, De Roo M, Dayer A, Muller D, Habre W, Vutskits L:
Volatile anesthetics rapidly increase dendritic spine density
in the rat medial prefrontal cortex during synaptogenesis.
Anesthesiology 2010; 112:546–56
5. Davidson AJ: Anesthesia and neurotoxicity to the develop-
ing brain: The clinical relevance. Paediatr Anaesth 2011;
21:716–21
6. Jevtovic-Todorovic V, Hartman RE, Izumi Y, Benshoff ND,
Dikranian K, Zorumski CF, Olney JW, Wozniak DF: Early
exposure to common anesthetic agents causes widespread
neurodegeneration in the developing rat brain and persistent
learning deficits. J Neurosci 2003; 23:876–82
7. Loepke AW, Soriano SG: An assessment of the effects of gen-
eral anesthetics on developing brain structure and neurocog-
nitive function. Anesth Analg 2008; 106:1681–707
8. Robins K, Lyons G: Intraoperative awareness during general
anesthesia for cesarean delivery. Anesth Analg 2009; 109:886–90
9. Sharma SK, McIntire DD, Wiley J, Leveno KJ: Labor analgesia
and cesarean delivery: An individual patient meta-analysis of
nulliparous women. Anesthesiology 2004; 100:142–8; discus-
sion 6A
10. Dickinson JE, Paech MJ, McDonald SJ, Evans SF: Maternal
satisfaction with childbirth and intrapartum analgesia in nul-
liparous labour. Aust N Z J Obstet Gynaecol 2003; 43:463–8
11. Hawkins JL: Epidural analgesia for labor and delivery. N Engl
J Med 2010; 362:1503–10
12. Beni-Adani L, Pomeranz S, Flores I, Shoshan Y, Ginosar
Y, Ben-Shachar I: Huge acoustic neurinomas presenting
in the late stage of pregnancy. Treatment options and
review of literature. Acta Obstet Gynecol Scand 2001;
80:179–84
13. Boker A, Ong BY: Anesthesia for Cesarean section and pos-
terior fossa craniotomy in a patient with von Hippel-Lindau
disease. Can J Anaesth 2001; 48:387–90
14. French JL, McCullough J, Bachra P, Bedforth NM: Transversus
abdominis plane block for analgesia after caesarean section
in a patient with an intracranial lesion. Int J Obstet Anesth
2009; 18:52–4
15. Smith IF, Skelton V: An unusual intracranial tumour present-
ing in pregnancy. Int J Obstet Anesth 2007; 16:82–5
16. Kuczkowski KM: Labor analgesia for the parturient with neu-
rological disease: What does an obstetrician need to know?
Arch Gynecol Obstet 2006; 274:41–6
17. Tewari KS, Cappuccini F, Asrat T, Flamm BL, Carpenter SE,
Disaia PJ, Quilligan EJ: Obstetric emergencies precipitated
by malignant brain tumors. Am J Obstet Gynecol 2000;
182:1215–21
18. Bharti N, Kashyap L, Mohan VK: Anesthetic management of
a parturient with cerebellopontine-angle meningioma. Int J
Obstet Anesth 2002; 11:219–21
Anesthesiology 2013; 119:703-18 716 L. R. Leffert and L. H. Schwamm
Neuraxial Anesthesia and Intracranial Lesions in Pregnancy
19. May AE, Fombon FN, Francis S: UK registry of high-risk
obstetric anaesthesia: Report on neurological disease. Int J
Obstet Anesth 2008; 17:31–6
20. Abouleish E, Ali V, Tang RA: Benign intracranial hyperten-
sion and anesthesia for cesarean section. Anesthesiology
1985; 63:705–7
21. Finfer SR: Management of labour and delivery in patients
with intracranial neoplasms. Br J Anaesth 1991; 67:784–7
22. Waxman S: Correlative Neuroanatomy, 23rd edition. Stamford,
CT, Appleton & Lange, 1996
23. Dunn LT: Raised intracranial pressure. J Neurol Neurosurg
Psychiatry 2002; 73(suppl 1):i23–7
24. Weerakkody RA, Czosnyka M, Schuhmann MU, Schmidt
Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/119/3/703/262530/20130900_0-00033.pdf by guest on 18 September 2020
E, Keong N, Santarius T, Pickard JD, Czosnyka Z: Clinical
assessment of cerebrospinal fluid dynamics in hydrocepha-
lus. Guide to interpretation based on observational study.
Acta Neurol Scand 2011; 124:85–98
25. Abbott NJ, Rönnbäck L, Hansson E: Astrocyte-endothelial
interactions at the blood-brain barrier. Nat Rev Neurosci
2006; 7:41–53
26. Fox MW, Harms RW, Davis DH: Selected neurologic compli-
cations of pregnancy. Mayo Clin Proc 1990; 65:1595–618
27. Crosby ET, Preston R: Obstetrical anaesthesia for a parturi-
ent with preeclampsia, HELLP syndrome and acute cortical
blindness. Can J Anaesth 1998; 45(5 Pt 1):452–9
28. Schwartz RB, Feske SK, Polak JF, DeGirolami U, Iaia A,
Beckner KM, Bravo SM, Klufas RA, Chai RY, Repke JT:
Preeclampsia-eclampsia: Clinical and neuroradiographic cor-
relates and insights into the pathogenesis of hypertensive
encephalopathy. Radiology 2000; 217:371–6
29. Apollon KM, Robinson JN, Schwartz RB, Norwitz ER: Cortical
blindness in severe preeclampsia: Computed tomography,
magnetic resonance imaging, and single-photon-emission
computed tomography findings. Obstet Gynecol 2000; 95(6
Pt 2):1017–9
30. Mokri B: The Monro-Kellie hypothesis: Applications in CSF
volume depletion. Neurology 2001; 56:1746–8
31. Alperin NJ, Lee SH, Loth F, Raksin PB, Lichtor T:
MR-Intracranial pressure (ICP): A method to measure intra-
cranial elastance and pressure noninvasively by means of
MR imaging: Baboon and human study. Radiology 2000;
217:877–85
32. Citerio G, Andrews PJ: Intracranial pressure. Part two:
Clinical applications and technology. Intensive Care Med
2004; 30:1882–5
33. Heiss JD, Patronas N, DeVroom HL, Shawker T, Ennis
R, Kammerer W, Eidsath A, Talbot T, Morris J, Eskioglu E,
Oldfield EH: Elucidating the pathophysiology of syringomy-
elia. J Neurosurg 1999; 91:553–62
34. Linninger AA, Xenos M, Zhu DC, Somayaji MR, Kondapalli
S, Penn RD: Cerebrospinal fluid flow in the normal and
hydrocephalic human brain. IEEE Trans Biomed Eng 2007;
54:291–302
35. Oldfield EH, Muraszko K, Shawker TH, Patronas NJ:
Pathophysiology of syringomyelia associated with Chiari I
malformation of the cerebellar tonsils. Implications for diag-
nosis and treatment. J Neurosurg 1994; 80:3–15
36. Friese S, Hamhaber U, Erb M, Klose U: B-waves in cerebral
and spinal cerebrospinal fluid pulsation measurement by
magnetic resonance imaging. J Comput Assist Tomogr 2004;
28:255–62
37. Hopkins EL, Hendricks CH, Cibils LA: Cerebrospinal fluid
pressure in labor. Am J Obstet Gynecol 1965; 93:907–16
38. Hogan QH, Prost R, Kulier A, Taylor ML, Liu S, Mark L:
Magnetic resonance imaging of cerebrospinal fluid volume
and the influence of body habitus and abdominal pressure.
Anesthesiology 1996; 84:1341–9
 EDUCATION
39. Marx GF, Zemaitis MT, Orkin LR: Cerebrospinal fluid pres-
sures during labor and obstetrical anesthesia. Anesthesiology
1961; 22:348–54
40. Grocott HP, Mutch WA: Epidural anesthesia and acutely
increased intracranial pressure. Lumbar epidural space
hydrodynamics in a porcine model. Anesthesiology 1996;
85:1086–91
41. Hilt H, Gramm HJ, Link J: Changes in intracranial pressure
associated with extradural anaesthesia. Br J Anaesth 1986;
58:676–80
42. BROMAGE PR: Continuous lumbar epidural analgesia for
obstetrics. Can Med Assoc J 1961; 85:1136–40
43. Galbert MW, Marx GF: Extradural pressures in the parturient
patient. Anesthesiology 1974; 40:499–502
44. Qaiser R, Black P: Neurosurgery in pregnancy. Semin Neurol
2007; 27:476–81
45. Stevenson CB, Thompson RC: The clinical management of
intracranial neoplasms in pregnancy. Clin Obstet Gynecol
2005; 48:24–37
46. Terauchi M, Kubota T, Aso T, Maehara T: Dysembryoplastic
neuroepithelial tumor in pregnancy. Obstet Gynecol 2006;
108(3 Pt 2):730–2
47. Chang LY, Carabuena JM, Camann W: Neurologic issues and
obstetric anesthesia. Semin Neurol 2011; 31:374–84
48. Gower DJ, Baker AL, Bell WO, Ball MR: Contraindications to
lumbar puncture as defined by computed cranial tomogra-
phy. J Neurol Neurosurg Psychiatry 1987; 50:1071–4
49. Mamelak AN, Withers GJ, Wang X: Choriocarcinoma brain
metastasis in a patient with viable intrauterine pregnancy.
Case report. J Neurosurg 2002; 97:477–81
50. van Crevel H, Hijdra A, de Gans J: Lumbar puncture and
the risk of herniation: When should we first perform CT? J
Neurol 2002; 249:129–37
51. Joffe AR: Lumbar puncture and brain herniation in acute
bacterial meningitis: A review. J Intensive Care Med 2007;
22:194–207
52. Hasbun R, Abrahams J, Jekel J, Quagliarello VJ: Computed
tomography of the head before lumbar puncture in adults
with suspected meningitis. N Engl J Med 2001; 345:1727–33
53. Landau R, Giraud R, Delrue V, Kern C: Spinal anesthesia for
cesarean delivery in a woman with a surgically corrected
type I Arnold Chiari malformation. Anesth Analg 2003;
97:253–5
54. Sicuranza GB, Steinberg P, Figueroa R: Arnold-Chiari malfor-
mation in a pregnant woman. Obstet Gynecol 2003; 102(5 Pt
2):1191–4
55. Chantigian RC, Koehn MA, Ramin KD, Warner MA: Chiari I
malformation in parturients. J Clin Anesth 2002; 14:201–5
56. Hullander RM, Bogard TD, Leivers D, Moran D, Dewan DM:
Chiari I malformation presenting as recurrent spinal head-
ache. Anesth Analg 1992; 75:1025–6
57. Sathi S, Stieg PE: “Acquired” Chiari I malformation after mul-
tiple lumbar punctures: Case report. Neurosurgery 1993;
32:306–9; discussion 309
58. Bagga R, Jain V, Das CP, Gupta KR, Gopalan S, Malhotra S:
Choice of therapy and mode of delivery in idiopathic intra-
cranial hypertension during pregnancy. MedGenMed 2005;
7:42
59. Karmaniolou I, Petropoulos G, Theodoraki K: Management
of idiopathic intracranial hypertension in parturients:
Anesthetic considerations. Can J Anaesth 2011; 58:650–7
60. Tang RA, Dorotheo EU, Schiffman JS, Bahrani HM: Medical
and surgical management of idiopathic intracranial hyper-
tension in pregnancy. Curr Neurol Neurosci Rep 2004;
4:398–409
61. Alperin N, Ranganathan S, Bagci AM, Adams DJ, Ertl-Wagner
B, Saraf-Lavi E, Sklar EM, Lam BL: MRI evidence of impaired
Anesthesiology 2013; 119:703-18 717 L. R. Leffert and L. H. Schwamm
CSF homeostasis in obesity-associated idiopathic intracranial
hypertension. AJNR Am J Neuroradiol 2013; 34:29–34
62. Aly EE, Lawther BK: Anaesthetic management of uncon-
trolled idiopathic intracranial hypertension during labour
and delivery using an intrathecal catheter. Anaesthesia 2007;
62:178–81
63. Kaul B, Vallejo MC, Ramanathan S, Mandell GL, Krohner RG:
Accidental spinal analgesia in the presence of a lumboperi-
toneal shunt in an obese parturient receiving enoxaparin
therapy. Anesth Analg 2002; 95:441–3
64. Heckathorn J, Cata JP, Barsoum S: Intrathecal anesthesia for
cesarean delivery via a subarachnoid drain in a woman with
benign intracranial hypertension. Int J Obstet Anesth 2010;
19:109–11
Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/119/3/703/262530/20130900_0-00033.pdf by guest on 18 September 2020
65. Bedson CR, Plaat F: Benign intracranial hypertension and
anaesthesia for caesarean section. Int J Obstet Anesth 1999;
8:288–90
66. Bédard JM, Richardson MG, Wissler RN: Epidural anesthesia
in a parturient with a lumboperitoneal shunt. Anesthesiology
1999; 90:621–3
67. Kim K, Orbegozo M: Epidural anesthesia for cesarean section
in a parturient with pseudotumor cerebri and lumboperito-
neal shunt. J Clin Anesth 2000; 12:213–5
68. Bradley NK, Liakos AM, McAllister JP II, Magram G, Kinsman
S, Bradley MK: Maternal shunt dependency: Implications for
obstetric care, neurosurgical management, and pregnancy
outcomes and a review of selected literature. Neurosurgery
1998; 43:448–60; discussion 460–1
69. Palop R, Choed-Amphai E, Miller R: Epidural anesthesia for
delivery complicated by benign intracranial hypertension.
Anesthesiology 1979; 50:159–60
70. Worrell J, Lane S: Impact of pseudotumor cerebri (idiopathic
intracranial hypertension) in pregnancy: A case report.
AANA J 2007; 75:199–204
71. Hollister N, Todd C, Ball S, Thorp-Jones D, Coghill J:
Minimising the risk of accidental dural puncture with epi-
dural analgesia for labour: A retrospective review of risk fac-
tors. Int J Obstet Anesth 2012; 21:236–41
72. Cruickshank RH, Hopkinson JM: Fluid flow through dural
puncture sites. An in vitro comparison of needle point types.
Anaesthesia 1989; 44:415–8
73. Ready LB, Cuplin S, Haschke RH, Nessly M: Spinal needle
determinants of rate of transdural fluid leak. Anesth Analg
1989; 69:457–60
74. Angle PJ, Kronberg JE, Thompson DE, Ackerley C, Szalai
JP, Duffin J, Faure P: Dural tissue trauma and cerebrospinal
fluid leak after epidural needle puncture: Effect of needle
design, angle, and bevel orientation. Anesthesiology 2003;
99:1376–82
75. Grant R, Condon B, Hart I, Teasdale GM: Changes in intracra-
nial CSF volume after lumbar puncture and their relationship
to post-LP headache. J Neurol Neurosurg Psychiatry 1991;
54:440–2
76. Carbaat PA, van Crevel H: Lumbar puncture headache:
Controlled study on the preventive effect of 24 hours’ bed
rest. Lancet 1981; 2:1133–5
77. Hilton-Jones D, Harrad RA, Gill MW, Warlow CP: Failure of
postural manoeuvres to prevent lumbar puncture headache.
J Neurol Neurosurg Psychiatry 1982; 45:743–6
78. Warwick WI, Neal JM: Beyond spinal headache: Prophylaxis
and treatment of low-pressure headache syndromes. Reg
Anesth Pain Med 2007; 32:455–61
79. Atanassoff PG, Alon E, Weiss BM, Lauper U: Spinal anaesthe-
sia for caesarean section in a patient with brain neoplasma.
Can J Anaesth 1994; 41:163–4
80. Innamaa A, Deering P, Powell MC: Advanced lung cancer
presenting with a generalized seizure in pregnancy. Acta
Obstet Gynecol Scand 2006; 85:1148–9

81. Su TM, Lan CM, Yang LC, Lee TC, Wang KW, Hung KS: Brain
tumor presenting with fatal herniation following delivery
under epidural anesthesia. Anesthesiology 2002; 96:508–9
82. Goroszeniuk T, Howard RS, Wright JT: The management
of labour using continuous lumbar epidural analgesia in a
patient with a malignant cerebral tumour. Anaesthesia 1986;
41:1128–9
83. Wang LP, Paech MJ: Neuroanesthesia for the pregnant
woman. Anesth Analg 2008; 107:193–200
84. D’Haese J, Christiaens F, D’Haens J, Camu F: Combined
cesarean section and clipping of a ruptured cerebral aneu-
rysm: A case report. J Neurosurg Anesthesiol 1997; 9:341–5
85. Whitburn RH, Laishley RS, Jewkes DA: Anaesthesia for
simultaneous caesarean section and clipping of intracerebral
aneurysm. Br J Anaesth 1990; 64:642–5
86. Semple DA, McClure JH: Arnold-Chiari malformation in preg-
nancy. Anaesthesia 1996; 51:580–2
87. Davie CA, O’Brien P: Stroke and pregnancy. J Neurol
Neurosurg Psychiatry 2008; 79:240–5
88. Stoodley MA, Macdonald RL, Weir BK: Pregnancy and intra-
cranial aneurysms. Neurosurg Clin N Am 1998; 9:549–56
89. Dias MS, Sekhar LN: Intracranial hemorrhage from aneu-
rysms and arteriovenous malformations during pregnancy
and the puerperium. Neurosurgery 1990; 27:855–65; discus-
sion 865–6
90. Horton JC, Chambers WA, Lyons SL, Adams RD, Kjellberg
RN: Pregnancy and the risk of hemorrhage from cerebral
arteriovenous malformations. Neurosurgery 1990; 27:867–71;
discussion 871–2
91. Tiel Groenestege AT, Rinkel GJ, van der Bom JG, Algra A,
Klijn CJ: The risk of aneurysmal subarachnoid hemorrhage
during pregnancy, delivery, and the puerperium in the
Utrecht population: Case-crossover study and standardized
incidence ratio estimation. Stroke 2009; 40:1148–51
92. Bateman BT, Olbrecht VA, Berman MF, Minehart RD,
Schwamm LH, Leffert LR: Peripartum subarachnoid hem-
orrhage: Nationwide data and institutional experience.
Anesthesiology 2012; 116:324–33
93. Doherty A, Ohashi Y, Downey K, Carvalho JC: Phenylephrine
infusion versus bolus regimens during cesarean delivery
under spinal anesthesia: A double-blind randomized clini-
cal trial to assess hemodynamic changes. Anesth Analg 2012;
115:1343–50
94. Habib AS: A review of the impact of phenylephrine adminis-
tration on maternal hemodynamics and maternal and neona-
tal outcomes in women undergoing cesarean delivery under
spinal anesthesia. Anesth Analg 2012; 114:377–90
  95. Gross BA, Du R: Hemorrhage from arteriovenous malfor-
mations during pregnancy. Neurosurgery 2012; 71:349–55;
discussion 355–6
  96. Le LT, Wendling A: Anesthetic management for cesarean
section in a patient with rupture of a cerebellar arteriove-
nous malformation. J Clin Anesth 2009; 21:143–8
  97. Elias M, Abouleish E, Bhandari A: Arteriovenous malforma-
tion during pregnancy and labor—Case review and man-
agement. Middle East J Anesthesiol 2001; 16:231–7 98. Benhamou D, Mercier FJ, Geeraerts T: Optic nerve sheath
Viscomi CM, Wilson J, Bernstein I: Anesthetic management
of a parturient with an incompletely resected cerebral arte-
riovenous malformation. Reg Anesth 1997; 22:192–7 99. pilot study. Anesthesiology 2012; 116:1066–71
Sharma SK, Herrera ER, Sidawi JE, Leveno KJ: The preg-
nant patient with an intracranial arteriovenous malforma-
tion. Cesarean or vaginal delivery using regional or general
anesthesia? Reg Anesth 1995; 20:455–8
100. Komiyama M, Yasui T, Kitano S, Sakamoto H, Fujitani K,
Matsuo S: Moyamoya disease and pregnancy: Case report
and review of the literature. Neurosurgery 1998; 43:360–8;
discussion 368–9
101. Kato R, Terui K, Yokota K, Nakagawa C, Uchida J, Miyao H:
Anesthetic management for cesarean section in moyamoya
Anesthesiology 2013; 119:703-18 718 L. R. Leffert and L. H. Schwamm
Neuraxial Anesthesia and Intracranial Lesions in Pregnancy
disease: A report of five consecutive cases and a mini-
review. Int J Obstet Anesth 2006; 15:152–8
102. Sharma SK, Wallace DH, Gajraj NM, Willis C, Sidawi E:
Epidural anesthesia for a patient with moyamoya dis-
ease presenting for cesarean section. Anesth Analg 1994;
79:183–5
103. Ngan Kee WD, Gomersall CD: Extradural anaesthesia for
caesarean section in a patient with moyamoya disease. Br J
Anaesth 1996; 77:550–2
104. O’Connor K, Rees SG: Anaesthetic management for caesar-
ean section in moyamoya disease. Int J Obstet Anesth 2007;
16:94
105. Dutta B, Dehran M, Sinha R: Anaesthetic management of a
parturient with moyamoya disease. Singapore Med J 2011;
Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/119/3/703/262530/20130900_0-00033.pdf by guest on 18 September 2020
52:e108–10
106. Abouleish E, Wiggins M, Ali V: Combined spinal and
epidural anesthesia for cesarean section in a parturient
with moyamoya disease. Acta Anaesthesiol Scand 1998;
42:1120–3
107. Sharma SK, Wallace DH, Sidaiwi JE, Gambling DR: Obstetric
anaesthesia and moyamoya disease. Can J Anaesth 1994;
41:756–7
108. Lockhart EM, Baysinger CL: Intracranial venous thrombo-
sis in the parturient. Anesthesiology 2007; 107:652–8; quiz
687–8
109. Cantú C, Barinagarrementeria F: Cerebral venous thrombo-
sis associated with pregnancy and puerperium. Review of
67 cases. Stroke 1993; 24:1880–4
110. Brass SD, Copen WA: Neurological disorders in pregnancy
from a neuroimaging perspective. Semin Neurol 2007;
27:411–24
111. Einhäupl K, Stam J, Bousser MG, De Bruijn SF, Ferro JM,
Martinelli I, Masuhr F; European Federation of Neurological
Societies: EFNS guideline on the treatment of cerebral
venous and sinus thrombosis in adult patients. Eur J Neurol
2010; 17:1229–35
112. Saposnik G, Barinagarrementeria F, Brown RD Jr, Bushnell
CD, Cucchiara B, Cushman M, deVeber G, Ferro JM, Tsai FY;
American Heart Association Stroke Council and the Council
on Epidemiology and Prevention: Diagnosis and manage-
ment of cerebral venous thrombosis: A statement for health-
care professionals from the American Heart Association/
American Stroke Association. Stroke 2011; 42:1158–92
113. Month RC, Vaida SJ: Spinal anesthesia for Cesarean delivery
in a patient with cerebral venous sinus thrombosis. Can J
Anaesth 2008; 55:658–9
114. Todorov L, Laurito CE, Schwartz DE: Postural headache in
the presence of cerebral venous sinus thrombosis. Anesth
Analg 2005; 101:1499–500
115. Wilder-Smith E, Kothbauer-Margreiter I, Lämmle B,
Sturzenegger M, Ozdoba C, Hauser SP: Dural puncture
and activated protein C resistance: Risk factors for cerebral
venous sinus thrombosis. J Neurol Neurosurg Psychiatry
1997; 63:351–6
116. Dubost C, Le Gouez A, Jouffroy V, Roger-Christoph S,
diameter used as ultrasonographic assessment of the inci-
dence of raised intracranial pressure in preeclampsia: A
117. Murthy BV, Fogarty DJ, Fitzpatrick K, Brady MM: Headache
during epidural top-ups in labour—A sign of reduced
intracranial compliance. Anaesth Intensive Care 1995; 23:
744–6
118. Abboud TK, Sarkis F, Hung TT, Khoo SS, Varakian L,
Henriksen E, Noueihed R, Goebelsmann U: Effects of epi-
dural anesthesia during labor on maternal plasma beta-
endorphin levels. Anesthesiology 1983; 59:1–5
119. Klein JP, Hsu L: Neuroimaging during pregnancy. Semin
Neurol 2011; 31:361–73