Canadian Association of Radiologists Journal 65 (2014) 225e231

www.carjonline.org

Neuroradiology / Neuroradiologie

Pseudo-Subarachnoid Hemorrhage: A Potential Imaging Pitfall

Chun-Yu Lin, MDa, Ping-Hong Lai, MDb,c,*, Jui-Hsun Fu, MDb, Po-Chin Wang, MDb,c,
Huay-Ben Pan, MDb,c
a
Department of Medical Imaging, Taipei Medical University Hospital, Taipei Medical University, Taipei, Taiwan
b
Department of Radiology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
c
School of Medicine, National Yang-Ming University, Taipei, Taiwan

Key Words: Pseudo-subarachnoid hemorrhage; Subarachnoid hemorrhage mimics

Increased density of the basal cisterns and subarachnoid
spaces on computed tomographies (CT) is a characteristic
finding of acute subarachnoid hemorrhage (SAH) [1].
Excluding head injury, SAH leads to the performance of
angiographic studies to rule out vascular lesions. Thus, recog-
nition of the radiologic feature of pseudo-SAH on CT is
important to avoid unnecessary testing and treatment delay.
Several mimics of SAH have been reported: diffuse cerebral
oedema due to various causes, purulent meningitis, cerebral
infarction, subdural hematoma (SDH), leakage of intravenous
contrast into the subarachnoid space, status epilepticus, intra-
cranial hypotension, intrathecally administered contrast
medium, and polycythemia [2e20]. This pictorial essay pres-
ents the varied manifestation of radiologic mimics of SAH.
Diffuse Cerebral Oedema
between the parenchyma and the cistern. A mass effect of the
fourth ventricle and poor grey-white matter differentiation
may imply this situation (Figure 1) [2].
Purulent Meningitis
Infectious meningitis, especially tuberculous meningitis,
has been reported to show increased CT attenuation over
basal cistern. Toxins elaborated by the organism lead to
breakdown of the brain-blood barrier. The leak of proteina-
ceous material due to brain-blood barrier disruption and
purulent material in the subarachnoid space may lead to
increased attenuation and mimic SAH [5,6]. Clinical history,
CSF analysis, and enhancement of the basal cistern in
postcontrast CT are clues for the diagnosis (Figure 2).
Infarction

Several etiologies could result in diffuse brain oedema,
including, for example, hypoxic ischemic encephalopathy,
cardiopulmonary arrest, metabolic encephalopathy, trauma.
The cerebral cortex becomes displaced into cerebrospinal
fluid (CSF) space and veins become congested. The
increased tissue attenuation immediately deep to the dura
and superficially within the cerebral sulci results in hyper-
density on precontrast CT, which simulates the appearance
of SAH [2e4]. In addition, the decreased attenuation of
brain parenchyma due to oedema increases ‘‘contrast’’
* Address for correspondence: Ping-Hong Lai, MD, Department of Radi-
ology, Kaohsiung Veterans General Hospital, 386 Ta-Chung First Rd,
Kaohsiung, 813, Taiwan.
E-mail address: phlai@vghks.gov.tw (P.-H. Lai).
Large cerebral or cerebellar hemispheric infarction, which
may present with brain oedema, mass effect, and effacement of
basal cistern, could have a pseudo-SAH appearance (Figure 3)
[7,8]. Thunderclap headache might be the first sign of SAH,
but sometimes it is accompanied by ischemic stroke, retro-
clival hematoma, and spontaneous intracranial hypotension
[21]. Also a large amount of SAH may sometimes cause
vasospasm and result in secondary cerebral infarction; the risk
for vasospasm is usually between days 5 and 10 after SAH [9].
SDH
The pseudo-SAH appearance was secondary to the mass
effect caused by the unilateral or bilateral SDHs. These large

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226 C.-Y. Lin et al. / Canadian Association of Radiologists Journal 65 (2014) 225e231

Figure 1. A 47-year-old man with hypoxic ischemic encephalopathy. (A, B) Precontrast computed tomography, showing uncal herniation, increased attenuation
over basal cisterns and sylvian fissures, and tentorium (white arrows) and cerebrospinal fluid space (black arrows). Diffuse low attenuation over the bilateral
hemisphere with poor grey-white matter differentiation is characteristic for hypoxic ischemic encephalopathy.

SDHs compressed the cerebral hemispheres and caused
diffuse effacement of the cortical sulci, with a decrease in the
size of CSF space (Figure 4). Hydrocephalus would be
expected as a result of obstruction of cerebral fluid reab-
sorption in true SAH as opposed to slit-shaped ventricles as
a result of mass effect in pseudo-SAH [10e12]. After
evacuation of the SDH, the CSF space returned to its normal
size with the disappearance of the hyperdensity [11].
Contrast Extravasation
Contrast neurotoxicity seems to be related to the chemical
or ionic properties and its hyperosmolarity, lipid solubility,
and viscosity. Contrast extravasation in the brain has been
reported as an uncommon complication of angiography and
accompanied with transient cortical blindness, confusion,
amnesia, seizure, or neurologic deficits [13,14]. Besides
angiography, including coronary, carotid, spinal, renal, and
aortography, an interventional procedure such as transjugular
intrahepatic portosystemic shunt also can cause the pseudo-
SAH appearance (Figure 5). The reduced clearance
contrast in renal failure and overdose contrast usage may be
clinical factors [13]. The majority of patients recovers
without any neurologic deficit, and follow-up CT findings
return to normal. In such situations, clinical examination and
serial neurologic imaging studies can effectively help in the
differential diagnosis.
Status Epilepticus
Transient or permanent changes may occur in the brain
after status epilepticus, including focal gyral swelling,

Figure 2. A 55-year-old man with tuberculous meningitis. (A) Precontrast computed tomography (CT), showing increased attenuation over basal cisterns (black
arrows) and along the tentorium (white arrows). (B) Postcontrast CT, showing vivid enhancement in the same regions.
 Pseudo-subarachnoid hemorrhage / Canadian Association of Radiologists Journal 65 (2014) 225e231 227

Figure 3. A 56-year-old man with a sudden onset of right-side weakness. (A) Precontrast computed tomography (CT), showing cerebrospinal fluid space
narrowing with increased attenuation along basal cistern and sylvian fissures (black arrows) and tentorium (white arrows). (B, C) Precontrast CT, showing left-
side anterior cerebral artery and middle cerebral artery infarction (star in each B and C).

signal and/or volume change of the hippocampus,
enhancement after injection of contrast agent, and, occa-
sionally, diffuse brain oedema (Figure 6) [15,22]. The
mechanism for these changes has not been well elucidated,
some researchers speculated that seizures can indeed
induce brain damage, possibly on a hypoperfusion and/or
hypoxia-ischemia basis [15].
collection [16]. Subdural fluid accumulation and slit-shaped
ventricles associated with tight basal cisterns are rare
manifestations of spontaneous intracranial hypotension
(Figure 7). It has been postulated that, in intracranial hypo-
tension, tight basal cistern and the increased attenuation
along the basilar cisterns and sylvian fissures secondary to
the brain sagging resulted in the appearance of pseudo-SAH
[16,17].

Spontaneous Intracranial Hypotension After Myelography

Spontaneous intracranial hypotension usually presents
with orthostatic headache and low CSF pressure. Typical
magnetic resonance imaging (MRI) findings include pachy-
meningeal enhancement, downward displacement of the
brain, enlargement of the sellar content, and subdural fluid
Postmyelography can mimic SAH in clinical symptoms of
headache and CT images (Figure 8) [18]. When contrast
medium is injected intrathecally, it will be distributed and
absorbed from the subarachnoid space over the hemispheres
in the following days. The onset of headache is often delayed
228 C.-Y. Lin et al. / Canadian Association of Radiologists Journal 65 (2014) 225e231

Figure 4. A 54-year-old woman had recent dizziness and left-side weakness. Noncontrast computed tomography (CT), showing increased density along the
tentorium (black arrow), with pronounced effacement of basal cistern (black star in [A]), mimic subarachnoid hemorrhage. (B) Large amount of mixed stage
right-side subdural hematoma (white star), with obvious midline shift (white arrow) noted.

Figure 5. A 54-year-old woman with a seizure attack after transjugular intrahepatic portosystemic shunt. (A, B) Precontrast computed tomography (CT),
showing bilateral, mutifoci ill defined and subtle high densities in the subarachnoid space and/or brain cortical regions (arrows) with brain swelling. (C, D) Her
seizure subsided 3 days later. Precontrast CT, showing resolution of prior high-density lesions.

for 24-48 hours, usually lasts for 1 or 2 days, and is Polycythemia

frequently severe enough to immobilize the patient [19].
Tracing the clinical history after myelography is the clue for Polycythemia may mimic intravascular enhancement and
the diagnosis. SAH on noncontrast CT, which is associated with an increase
 Pseudo-subarachnoid hemorrhage / Canadian Association of Radiologists Journal 65 (2014) 225e231 229

Figure 6. A 19-month-old boy had status epilepticus after the flu-like symptoms. (A-C) Precontrast computed tomography (CT), showing hyperdensity over the
basal cisterns (black arrows) and along the tentorium (white arrows), with pronounced effacement of basilar cisterns. Diffuse low density over bilateral basal
ganglia (white stars [C]), with diffuse brain swelling (black stars [B]) and uncal herniation, which suggests that this acute encephalopathy presumably was
induced by viral infection and status epilepticus, probably associated with hypoxia.

Figure 7. A 35-year-old woman with spontaneous intracranial hypotension. (A, B) Precontrast computed tomography, showing tight basal cistern and increased
attenuation along the basilar cisterns and sylvian fissures (black arrows) in addition to subdural hematoma (white arrowheads [A and B]).
230 C.-Y. Lin et al. / Canadian Association of Radiologists Journal 65 (2014) 225e231

Figure 8. A 55-year-old man with severe headache and vomiting after a myelography. (A, B) Precontrast computed tomography, showing increased density
along cerebrospinal fluid space (arrows [A and B]). The patient got relief of symptoms 2 days later.

Figure 9. A 3-year-old man with secondary polycythemia (hematocrit level, 65%) due to congenital heart disease of transposition of the great vessels. (A)
Precontrast computed tomography (CT), showing diffuse intravascular hyperdensity in the branches of the circle of Willis, along tentorium cerebelli and
sigmoid sinuses. (B, C) Precontrast CT, showing diffuse hyperdensity in the deep veins, dural venous sinuses, and small vasculature of cerebral parenchyma.
 Pseudo-subarachnoid hemorrhage / Canadian Association of Radiologists Journal 65 (2014) 225e231
in circulating red cell mass [20,23]. Characteristic image
finding is symmetrical, diffuse hyperdensity that affects the
cerebral vasculature, including the circle of Willis, the dural
sinuses, and other vessels in the subarachnoid space (Figure 9).
Hemoglobin and hematocrit levels help in the diagnosis of
a patient with hyperdense vessels on noncontrast CT [20,23]. A
hallmark of polycythemia is an elevated hematocrit level, with
a hematocrit level >55% seen in 83% of cases [24].
Conclusion
This pictorial essay illustrates the mimics of SAH.
Awareness of the various manifestations of pseudo-SAH is
important for patient counseling and treatment. All radiolo-
gists should be familiar with these potential mimics of SAH.
Acknowledgements
This study was supported in part by grants from National
Science Council NSC97-2314-B-075B-010-MY3 and NSC
100-2314-B-075B-001 (P.H.L.), Veterans General Hospital
Kaohsiung VGHKS100-075 and VGHKS101-011 (P.H.L.).
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