Analytic Reviews

Journal of Intensive Care Medicine

1-7
Spontaneous Intracranial Hypotension ª The Author(s) 2021
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in the Critical Patient DOI: 10.1177/08850666211024886
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Mark D. Mamlouk, MD1,2 , Peter Y. Shen, MD1 ,

and Mark F. Sedrak, MD3

Abstract
Spontaneous intracranial hypotension typically manifests with orthostatic headaches and is caused by spinal dural tears, ruptured
meningeal diverticula, or CSF-venous fistulas. While most patients are diagnosed and treated in the outpatient setting, some
patients will occasionally present in the emergent ICU setting due to subdural hematomas, coma, or downward brain herniation.
In this review paper, we will discuss the diagnostic and treatment steps that intensivists can undertake to coordinate a team
approach to successfully manage these patients. A brief general overview of spontaneous intracranial hypotension will also be
discussed.

Keywords
spontaneous intracranial hypotension, critical patient, subdural hematoma, CSF-venous fistula

Background and with Valsalva maneuvers. In addition, headaches can wane

Spontaneous intracranial hypotension (SIH) is a well-
recognized and treatable cause of headaches. SIH is secondary
to spontaneous spinal CSF leaks, and there are 3 recognized
types: dural tears from calcified disc protrusions or spiculated
osteophytes, ruptured meningeal diverticula, and CSF-venous
fistulas.1,2
SIH is not typically a condition that requires urgent medical
attention. The majority of patients with SIH can be safely man-
aged and treated in an outpatient setting. Furthermore, because
SIH is sometimes difficult to diagnosis, a significant number of
patients live with the condition for months to years before
treatment. A minority of patients; however, can become acutely
obtunded or comatose,3 and SIH can even be fatal in in a small
percentage of patients.4 While most of the existing literature on
SIH focuses on the diagnostic and treatment plans, there is
relatively little discussion of the specific workflow that pertains
to the critical patient. Moreover, because SIH is prevalent
throughout small and large hospitals, not all critical patients
will be managed in a dedicated neurointensive care unit or a
center that specializes in SIH. The purpose of this paper is to
provide a clinical workflow for the critical SIH patient that can
be managed in most intensive care units, which will be based
on a literature review and the authors’ clinical experience.
General SIH Overview
Clinical Symptoms
Headaches are the most common feature in SIH and are usually
positional. Headaches can worsen in the second half of the day
with time or be absent altogether, making the diagnosis chal-
lenging. Additional symptoms can include neck pain, nausea,
tinnitus, cranial nerve palsies, and even a frontotemporal-like
dementia.5
MRI Brain Findings
In patients with clinical concern for SIH, contrast-enhanced
brain MR imaging is performed and typical findings include
brain sag, dural enhancement, venous distension, and subdural
collections.6 The brain MRI is positive in the majority of SIH
patients and has always been abnormal in the critical patient in
our experience. Subdural collections can be seen with SIH and
are invariably bilateral. In the absence of trauma, bilateral sub-
dural collections should raise suspicion for SIH.
1
Department of Radiology, The Permanente Medical Group, Kaiser
Permanente Medical Center, Santa Clara, CA, USA
2
Department of Radiology and Biomedical Imaging, University of California,
San Francisco, CA, USA
3
Department of Neurosurgery, The Permanente Medical Group, Kaiser
Permanente Medical Center, Redwood City, CA, USA
Received March 9, 2021. Received revised May 21, 2021. Accepted May
26, 2021.
Corresponding Author:
Mark D. Mamlouk, Department of Radiology, The Permanente Medical Group,
Kaiser Permanente Medical Center, Santa Clara, 700 Lawrence Expy, Santa
Clara, CA 95051, USA.
Emails: mark.d.mamlouk@kp.org; mark.mamlouk@ucsf.edu
2 Journal of Intensive Care Medicine XX(X)
Spine Imaging
The spinal imaging approach to SIH can differ depending on
the institution, and the nuances are beyond the scope of this
discussion but will be briefly described. After SIH is confirmed
clinically and on MRI brain imaging, the spine should be
imaged to evaluate the spinal leak. MR imaging of the total
spine is performed and typically includes T2 fat-suppressed
images in the sagittal and axial planes. The whole goal of
imaging is to identify a CSF leak; therefore, additional T1
sequences and contrast administration are unnecessary.7 If the
spine MRI shows an extradural collection, the leak is either
from a dural tear from a calcified disc or a ruptured meningeal
diverticulum. A dynamic CT myelogram is then performed in
either the prone position (for ventral disc-related leaks) or lat-
eral decubitus position (for ruptured meningeal diverticula) to
identify the exact leak site.7 If the spine MRI does not show an
extradural collection, a CSF-venous fistula should be sus-
pected, which is typically an abnormal connection between a
meningeal diverticulum and a vein that shunts out CSF fluid
and results in SIH. The actual CSF-venous fistula cannot be
seen on routine MR spine imaging, but meningeal diverticula
can be seen on the spine MRI. In this scenario, a lateral decu-
bitus CT or digital subtraction myelogram are performed to
identify the CSF-venous fistula, as the decubitus position per-
mits contrast to flow into the CSF-venous fistula on the depen-
dent side of the thecal sac via gravity.8,9 In our experience, the
laterality of the decubitus myelogram is usually predicated on
which side has a greater number of meningeal diverticula on
the spine MRI, and this side is placed down on the procedure
table. If the meningeal diverticula are approximately equal, we
typically choose to start with a right lateral decubitus myelo-
gram, as we have seen more CSF-venous fistulas on the right
side in our experience. If there is no CSF-venous fistula on the
first lateral decubitus myelogram, we bring the patient back the
next day and image the contralateral decubitus myelogram.8
During any of the various types of myelogram, an opening
pressure can be performed, and a pressure of 6 cm of water
or less is a diagnostic criterion for SIH. Nonetheless, the open-
ing pressure is normal in the majority of SIH patients, as the
pathophysiology of CSF leaks is better described as low CSF
volume rather than low pressure.2 Of note, SIH is typically
secondary to spinal CSF leaks and not skull base leaks, the
latter entity usually seen with intracranial hypertension. Thus,
imaging of the skull base is not typically warranted in patients
with SIH.10
Spinal CSF Leak Treatment
Treatment of the underlying spinal leak can vary from con-
servative to percutaneous to surgical. Conservative treatments
include bed rest to permit the CSF leak to “self-patch” on its
own. Other conservative measures include oral hydration and
caffeine administration. While some patients can certainly
improve with these conservative measures, there are limited
data on the efficacy and specific duration of bed rest. Non-
targeted epidural blood patches are the next treatment and
typically entail administering autologous blood in the lumbar
spine. The efficacy of non-targeted epidural blood patches is
variable, with a 52% success rate in one study.11 The advan-
tages of a non-targeted epidural blood patch are that it can
typically be performed at most hospitals, does not typically
need image guidance, and can be performed irrespective if
the specific leak site is identified. On the other hand, we
prefer image-guided targeted percutaneous treatments
directly at the leak site origin with either blood or fibrin
sealant, as our experience and prior literature both show that
targeted treatments can increase the chance of sealing the
leak compared to non-targeted treatments.11 In the setting
of CSF-venous fistulas, CT-guided fibrin sealants and endo-
vascular transvenous embolization have been recently shown
to be effective treatment options.12,13 Lastly, surgery is typi-
cally a last resort option but is an effective treatment for all
types of spinal leaks. Neurosurgical operations include
removing calcified discs, repair of dural tears, and coagula-
tion of CSF-venous fistulas.14-16
SIH in the Critical Patient
SIH With Small or Large Subdural Collections
and Clinically Stable
Subdural collections in SIH can vary in consistency from
CSF-filled effusions to hematomas with various ages of
hemorrhage. Given the loss of CSF volume in SIH, subdural
effusions are presumably related to compensatory enlarge-
ment and are a reflection of the Monro-Kellie doctrine.2 Sub-
dural hematomas, on the other hand, are possibly related to
tearing of the bridging veins or bleeding of enlarged veins in
the subdural space.17
Treatment of the subdural collections should be guided by
the patient’s neurological stability (Figure 1). If the patient is
clinically stable, diagnosis and treatment should focus on the
spinal leak and not drainage of the subdural collections for
multiple reasons. First, it is important to remember that the
subdural collections are an effect of SIH, not the cause. Second,
in many cases, the subdural collections are chronic and there
are no resultant neurologic deficits. Third, there are multiple
reports that state that subdural collections can recur if surgi-
cally evacuated and the underlying spinal leak is not
addressed.4,17-19 Lastly, there is some evidence that treating
the subdural hematoma in isolation of SIH may even be harm-
ful, as the craniotomy can decrease the intracranial pressure
after being exposed to atmospheric pressure.20 For these rea-
sons, subdural collection evacuation should be avoided if the
patient is not directly symptomatic from the subdural collec-
tions. Instead, identifying and treating the spinal leak should be
the focus using the steps outlined in the previous section and
can either be performed in the inpatient or outpatient setting,
depending on the clinical status of the patient and availability
to perform the workup (Figure 2).
Mamlouk et al 3

Figure 1. SIH algorithm in the critical patient. The algorithm begins with identifying a patient with positive clinical and neuroimaging findings of
SIH. The patient is first assessed if clinically stable (a). If yes (b), then diagnosis and treatment of the spinal leak should be performed. If the patient
is not clinically stable (c), then the patient is assessed for physical exam findings suggestive of elevated intracranial pressure. If yes, and there are
subdural collections (d), then subdural evacuation should be performed, followed by addressing the spinal leak. If there is no elevated intracranial
pressure (e), then the patient should be placed in the Trendelenburg position. Clinical and imaging assessment should be made if there are other
worrisome neurologic signs besides coma (f). If no (g), then the spinal leak should be addressed. If there is additional clinical concern, and there is
severe central downward herniation (h), then intrathecal saline infusion and/or non-targeted blood patching should be performed, followed by
addressing the spinal leak.

SIH With Large Subdural Collections and Clinically
Unstable
One major difficulty in this group of patients is determining if
the patient is clinically unstable from the large subdural collec-
tions or from downward herniation related to SIH. As described
in the previous section, many subdural collections can be
managed without drainage and by addressing the spinal leak
(Figure 3). There are reports that state subdural evacuation
should be performed in the setting of uncal herniation and loss
of consciousness21; however, both of these features can be seen
with severe SIH resulting in central herniation and brainstem
compression and are discussed in the subsequent sections. Thus,
we propose that subdural evacuation should solely be performed
if there are distinct physical exam signs of increased intracranial
pressure that are directly attributed to the subdural collections.
In the event that subdural evacuation is done, we have empiri-
cally placed a drain in the subdural space and maintained a
negative pressure using a subdural evacuating port system. This
negative pressure can be obtained using standard materials, such
as Jackson-Pratt or Blake bulbs. In our experience, ventricular
drains at gravity provide insufficient negative force for these
circumstances. Also, keeping the patient supine or even in inter-
mittent Trendelenburg positions while draining can be benefi-
cial. We generally maintain this negative pressure drainage
while the patient is undergoing targeted or non-targeted percu-
taneous treatment for the spinal leak. Finally, unlike other sub-
dural evacuations, a clamp and reimage trial of the brain can be
entertained prior to removal of the drain.
SIH With Coma and/or Central Herniation
This subset of patients is the most life threatening and challen-
ging to clinically address. Clinically, patients can present with
lethargy, confusion, coma, fixed pupils, Cheyne-Stokes breath-
ing, and decerebrate posturing. Coma is an uncommon clinical
presentation in patients with SIH and is invariably seen with
brain sagging although not all patients with brain sagging man-
ifest with coma.3 A recent study that evaluated brainstem
lesions found the left pontine tegmentum to be the potential
anatomic location to induce coma if affected.22 In SIH patients
with brain sag, the pons is flattened and this could potentially
4 Journal of Intensive Care Medicine XX(X)

Figure 2. Subdural collections in a clinically stable 33-year-old woman who had abrupt orthostatic headaches after kickboxing class. (A) Axial
noncontrast CT head shows a left frontoparietal convexity subdural collection with acute (arrow) and chronic (arrowhead) hemorrhage. (B)
Sagittal CT image of a dynamic myelogram in the prone position shows normal intrathecal contrast (arrow) and a ventral extradural CSF leak
(arrowhead) at the T1-T2 level, which was secondary to a calcified disc (C, arrow). (D) CT-guided epidural blood patch was performed with
circumferential contrast-enhanced blood in the epidural space (arrows), which cured the patient. Air is also noted in the epidural space from the
prior epidurogram (not shown) that was performed to confirm the epidural space prior to injection of blood.

Figure 3. Large subdural hematomas in a 64-year-old man that was clinically stable and endorsed orthostatic headaches. A, Axial noncontrast
CT head shows bilateral holohemispheric subacute subdural hematomas (arrows), left greater than right. Subdural evacuation was not
performed, as there were no physical exam findings to suggest elevated intracranial pressure. B, Right lateral decubitus CT myelogram was
performed after a normal spine MRI (not shown) and reveals a right T9-T10 CSF-venous fistula with a paravertebral course (arrows). C,
CT-guided fibrin glue occlusion was performed with contrast-enhanced glue injected in the neural foramen and epidural space (arrow). D,
Post-treatment right lateral decubitus CT myelogram 1.5 months later shows resolution of the CSF-venous fistula. The patient’s symptoms also
clinically resolved, including a frontotemporal-like dementia.

result in disruption of the pontine tegmentum. While coma is an The first step in treatment is to place the patient in the Tren-
alarming feature in the SIH patient, it is typically reversible if delenburg position, which is the exact opposite positioning for
the underlying spinal leak is treated. central herniation not related to SIH and could be life-saving.4
Mamlouk et al 5

Figure 4. Coma in a 57-year-old man with a CSF-venous fistula. A, Sagittal T1-weighted imaging of the brain shows midbrain sag (arrow) that is
in keeping with SIH. B, Axial T2-weighted image at the vertex shows small subdural effusions (arrows) without significant mass effect. C, Axial
T2-weighted image at the base of the brain shows bilateral uncal herniation (arrows). There is still some CSF present in the left ambient cistern
(arrowhead), suggesting incomplete central herniation. Steroids were administered, and the patient regained normal consciousness. D, Right
lateral decubitus CT myelogram in the coronal plane performed the next day shows an irregular meningeal diverticulum (arrow) at the right
T11-T12 level that communicates with a vein (arrowhead), which is compatible with a CSF-venous fistula. This patient was treated with fibrin
glue occlusion (not shown), similar to the previous figure, and was cured.

Figure 5. Fatal case of SIH in a 35-year-old woman with severe central herniation. A, Axial noncontrast CT head shows hyperdensity along the
bilateral middle cerebral arteries (arrows) and tentorium cerebelli (arrowheads), which is compatible with pseudo-subarachnoid hemorrhage. B,
Sagittal T1-weighted image of the brain shows severe sagging of the cerebellar tonsils (arrow) and midbrain (arrowhead). C, Axial T2-weighted
image shows bilateral uncal herniation (arrows) and complete CSF effacement of the basal cisterns (arrowheads). In addition, the gray matter is
diffusely hyperintense and the sulci are effaced, which are consistent with cerebral edema. D, Apparent diffusion coefficient image of the brain
shows hypointense signal in the bilateral posterior cerebral artery distributions (arrows) that is compatible with acute infarction secondary to
narrowing of the posterior cerebral arteries (not shown). This patient was declared brain dead shortly after, despite intrathecal saline infusion.
An undiagnosed CSF-venous fistula was likely the cause of the SIH.

Because of the acuity of the condition, the authors suggest to
only proceed with the spinal imaging diagnostic workup if the
patient is clinically stable. If the patient is clinically unstable
with additional neurologic symptoms besides coma, and there
is severe central herniation with complete CSF effacement of
the basilar cisterns on brain imaging, maneuvers to raise intra-
cranial pressure and volume are preferred. This can be done
by an intrathecal saline infusion via a lumbar drain placement.
One group has administered large boluses up to 163 cc of
saline,23 while another group had a constant infusion rate of
20 cc/hour.24 Both groups used simultaneous intracranial pres-
sure monitoring to gauge the effectiveness of the saline infu-
sion. Alternatively, a non-targeted large volume epidural blood
patch can also be performed. No studies have compared the
2 techniques in this specific population but both have likely
similar effectiveness. In addition, both techniques could also
theoretically be performed at the same time as well. There may
be some concerns of performing a lumbar puncture for intrathe-
cal saline administration or the myelogram in the setting of
brain sagging, with particular concern for worsening the hernia-
tion; however, a spinal leak is already present and the CSF
pressure is generally low. In one study, no reports of clinical
or radiologic worsening were seen after the lumbar puncture in
patients with coma.3 The authors’ experiences also coincide
with this as well. Lastly, it is important to note that when per-
forming a lumbar puncture to ensure the needle is in the sub-
arachnoid space prior to intrathecal saline administration or
contrast injection for a myelogram, CSF return may be limited
6 Journal of Intensive Care Medicine XX(X)
or absent altogether due to the low pressure and volume in these
patients and make it challenging to ensure correct needle place-
ment. Image guidance can help mitigate this potential obstacle
in these cases.
Urgent CT or MR imaging of the brain should be performed
to determine if there is central downward herniation character-
ized by medial displacement of the uncus beyond the tentorial
incisura. If a CT scan of the head is performed, pseudo-
subarachnoid hemorrhage is a potential imaging feature and
manifests as increased attenuation in the basilar cisterns and
vessels, the tentorium cerebelli, or along the falx cerebri,
mimicking subarachnoid hemorrhage.25 Pseudo-subarachnoid
hemorrhage is often seen in patients with cerebral edema and is
likely secondary to vascular engorgement. Identification of
other features seen in SIH, such as sagging of the brainstem
or cerebellar tonsils and subdural collections, should direct the
provider to the diagnosis of pseudo-subarachnoid hemorrhage.
Many of the SIH patients with this severe complication of
the condition have subdural collections that are often small and
disproportionate to the degree of central herniation and the
aforementioned clinical signs. Subdural evacuation should
be avoided in this group of patients, and if performed, the
subdural collections can recur or even worsen the degree of
herniation.4,18,20
Steroids may be another helpful treatment to stabilize the
patient in this precarious situation. In one reported patient with
central herniation and coma, intravenous dexamethasone was
administered and decreased the brain herniation and the patient
regained consciousness.26 The authors also have witnessed a
similar experience with steroid treatment (Figure 4); however,
further studies are needed to validate these findings.
If the central herniation progresses without or with the
aforementioned stopgap treatments, the prognosis is very poor
and often fatal. Surgical options are limited, and the herniation
can result in acute infarction in the posterior cerebral artery
distribution or brainstem and death (Figure 5).4
Conclusion
Spontaneous intracranial hypotension can occasionally neces-
sitate urgent medical attention and manifest with various clin-
ical and imaging signs. In many of these settings, first
identifying and treating the spinal leak is paramount. Subdural
collections are a common manifestation in this group of
patients but evacuation is often unnecessary and care should
be made when considering subdural treatment in isolation of
the SIH syndrome.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, author-
ship, and/or publication of this article.
ORCID iDs
Mark D. Mamlouk, MD https://orcid.org/0000-0002-6689-8912
Peter Y. Shen, MD https://orcid.org/0000-0002-7657-7186
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