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Imaging in Subarachnoid
Hemorrhage
Updated: Mar 09, 2016
Author: Abner Gershon, MD; Chief Editor: Eugene C Lin, MD more...

OVERVIEW

Overview
Subarachnoid hemorrhage (SAH) is a condition in which there is bleeding into the subarachnoid space
around the brain and spinal cord, as shown in the images below. This space is normally filled with
clear, colorless cerebrospinal fluid (CSF). The most common causes of subarachnoid hemorrhage are
head trauma and rupture of an intracranial aneurysm. Atraumatic subarachnoid hemorrhage
accompanied by the sudden onset of neurologic symptoms has been termed hemorrhagic stroke.
Radiologic evaluation is essential for determining the prognosis and treatment of subarachnoid
hemorrhage. Radiologic interventional procedures have become increasingly important for the
management of this condition.

Subarachnoid hemorrhage (SAH). A nonenhanced computed tomography scan of the brain that demonstrates an extensive
SAH filling the basilar cisterns in a patient with a ruptured intracranial aneurysm.
An angiogram showing the onset of an aneurysmal rupture, with extravasation of contrast material into the subarachnoid
space from the anterosuperior aspect of a bilobed aneurysm in a posteroinferior cerebellar artery.

A late angiogram demonstrating contrast medium filling the posterior fossa subarachnoid spaces, including the ambient,
prepontine, and perimedullary cisterns.

Anatomy

Rupture of a saccular intracranial aneurysm causes approximately 80% of nontraumatic subarachnoid

hemorrhage. Intracranial aneurysms develop predominantly at vessel bifurcation or branching points.
Saccular aneurysms are acquired lesions that rarely present before the third decade of life.
Most intracranial aneurysms occur at typical locations within or near the circle of Willis. The most
common specific locations of intracranial aneurysms are at the middle cerebral artery bifurcation and
along the anterior communicating artery. These 2 locations account for approximately 60% of all
intracranial aneurysms. Other common sites of aneurysm formation in the anterior circulation are at
the origins of the posterior communicating and ophthalmic arteries. Approximately 10-20% of
aneurysms arise from the vertebral and basilar arteries.

The tip of the basilar artery is the most common location of aneurysm formation in the posterior
circulation. The origins of the posterior inferior cerebellar arteries also are common sites of aneurysm
formation. Arteriovenous malformations (AVMs) occur throughout the brain without predisposition for a
particular anatomic area.

Neuroradiologic intervention
Approximately 10-30% of patients with subarachnoid hemorrhage die before reaching medical
attention. For those reaching a hospital alive, mortality rates for nontraumatic subarachnoid
hemorrhage have been reported in the 30-60% range. [1] In-hospital mortality has been shown to be
lower at facilities with interventional neuroradiology. [2]

The endovascular treatment of intracranial aneurysms has evolved rapidly. The initial experience in
the treatment of intracranial aneurysm with catheter-based techniques relied predominantly on parent-
vessel occlusion by various mechanisms, including endovascular detachable balloons and coils. With
widespread physician acceptance and approval of the Guglielmi detachable coil (GDC) by the US
Food and Drug Administration (FDA), the emphasis of endovascular management has changed to
aneurysm occlusion with the preservation of patency of the parent vessel. [3, 4]

Although the primary indication for GDC embolization of an intracranial aneurysm is for patients with
surgically high-risk aneurysms, a growing body of evidence indicates that endovascular treatment
should be considered as a primary option for aneurysm in certain anatomic locations. Specifically,
patients with basilar tip aneurysms appear to have better outcomes with endovascular therapy than
with open craniotomy and surgical aneurysm clipping. The technical expertise and experience of the
local treating physicians may determine the optimal treatment for aneurysms at other locations.

Improvements in small-vessel angioplasty balloon catheters and promising initial therapeutic results
have led to increased use of intracranial angioplasty for the treatment of subarachnoid hemorrhage–
induced vasospasm. In general, intracranial angioplasty may be performed in the internal carotid,
proximal middle or anterior cerebral, and vertebral and basilar arteries. Selective intra-arterial
papaverine infusion has also been used in the treatment of intracranial vasospasm. [5]

Preferred examination

Computed tomography (CT) scanning without intravenous contrast enhancement is the preferred
initial diagnostic study, with cerebral angiography the next procedure of choice. [5, 6, 7]

Advances are being made in the noninvasive vascular imaging modalities of CT angiography and
magnetic resonance angiography (MRA). At institutions with a high degree of expertise and
experience, these noninvasive imaging technologies may be used in addition to or even replace
catheter angiography. [5]

At most institutions in the United States, conventional angiography remains the standard for
evaluating patients with subarachnoid hemorrhage. If a CT scan of the brain is negative and a strong
clinical suggestion of subarachnoid hemorrhage exists, a CSF tap may be of value for confirming this
diagnosis. If the CSF reveals no evidence of subarachnoid hemorrhage (ie, either overt hemorrhage
or xanthochromia), cerebral angiography may not be indicated.

For SAH caused by rupture of an intracranial aneurysmal vessel or arteriovenous malformation,

emergency physicians have classically performed a noncontrast CT (NCCT), followed by a lumbar
puncture. However, as CT technology has advanced, many studies have questioned the need for
lumbar puncture and have advocated for noninvasive techniques, such as NCCT alone or NCCT with
CT angiography. [8]

Limitations of techniques
Nonenhanced CT scanning may fail to depict small subarachnoid hemorrhages, particularly if imaging
is performed several days after the onset of bleeding. Furthermore, CT scans are degraded by patient
motion. If a patient cannot cooperate because of an alteration in mental status, sedation may be
necessary to obtain satisfactory diagnostic images.

Cerebral angiography is an invasive procedure with a small but significant risk of complication.
Without the use of a special hemostasis device, at least 6 hours of bed rest is required after the
procedure to prevent bleeding at the puncture site. Additionally, because of its small false-negative
rate for aneurysm, cerebral angiography must be repeated after 1-2 weeks to further improve its
diagnostic sensitivity.

Differential diagnosis and other problems to be considered

The differential diagnosis includes cerebral aneurysm, cerebral arteriovenous malformation, and
stroke.

Traumatic subarachnoid hemorrhage must be distinguished from spontaneous subarachnoid

hemorrhage. Cerebral angiography may sometimes be avoided if it can be confidently established that
the hemorrhage is caused by trauma. This distinction can be difficult to make, because the traumatic
event may not have been witnessed and the patient may be unable to provide a reliable history. There
is often a question as to whether a spontaneous subarachnoid hemorrhage has caused a traumatic
event or the trauma caused the hemorrhage. When in doubt, it is usually best to obtain a cerebral
angiogram to exclude an underlying aneurysm or vascular malformation; such angiograms can
sometimes be limited to the location of the hemorrhage, if no pathology is detected.

Special concerns
Complete and proper written informed consent must be obtained before diagnostic and interventional
procedures are performed. [9] The informed consent form should specifically include the possibility of
stroke with diagnostic cerebral angiography and neurovascular interventional procedures. [10]

Radiography
In unresponsive or unreliable patients requiring magnetic resonance imaging (MRI), plain radiographs
of the skull and orbits may be used to exclude the presence of aneurysm clips or intraorbital foreign
bodies. Plain radiographs may also be useful for evaluating facial or cervical spinal fractures to assess
the probability of traumatic subarachnoid hemorrhage (SAH) versus spontaneous SAH.
Some neuroradiologists use skull radiographs in their routine follow-up care of patients with aneurysm
treated with coil embolization. Interval follow-up skull radiographs can be compared with baseline
studies to check for coil compaction.

The degree of confidence is high for the purposes stated above; however, plain radiography offers no
reliable findings for detecting SAH.

Guglielmi detachable coils (GDC) have been observed to shift in position during the subsequent
thrombosis of large and medium-sized aneurysms. This finding does not necessarily indicate that the
aneurysm is patent. Cerebral angiography should be performed when any change in coil position is
observed on postembolization follow-up studies.

Computed Tomography
On CT scans, subarachnoid hemorrhage (SAH) appears as a high-attenuating, amorphous substance
that fills the normally dark, CSF-filled subarachnoid spaces around the brain, as shown in the images
below. The normally black subarachnoid cisterns and sulci may appear white in acute hemorrhage.
These findings are most evident in the largest subarachnoid spaces, such as the suprasellar cistern
and Sylvian fissures.

Subarachnoid hemorrhage (SAH). A nonenhanced computed tomography scan of the brain that demonstrates an extensive
SAH filling the basilar cisterns in a patient with a ruptured intracranial aneurysm.
A computed tomography scan obtained after angiography of a rupturing bilobed aneurysm of the posteroanterior cerebellar
artery. This image shows a subarachnoid hemorrhage and contrast medium filling the right sylvian fissure, the
interhemispheric fissure, and the lateral and third ventricles.

Over the cerebral hemispheres, SAH is exhibited by the filling in of normally low-attenuating (black)
sulci with high-attenuating (white) subarachnoid blood. SAH is most conspicuous within 2-3 days of
the onset of acute bleeding. Acute SAH is typically 50-60 Hounsfield units (HU). The protein content of
the hemoglobin molecule is predominantly responsible for the attenuating effect of blood; therefore,
the absolute measurement in HU varies somewhat with the hematocrit value.

When CT scanning is performed several days or weeks after the initial bleed, the findings are more
subtle. The initial high-attenuation of blood and clot tend to decrease, and these appear as
intermediate gray. These findings can be isointense relative to normal brain parenchyma. If the patient
presents during this subacute period, evidence of SAH includes decreased visualization of the
normally hypoattenuating fluid within the sulci and basal cisterns and enlargement of the ventricles
caused by communicating hydrocephalus.

In addition to detecting SAH, CT scanning is useful for localizing the source of bleeding. This is
particularly important in cases of multiple intracranial aneurysms, which occur in 20% of patients.
Localization of SAH on CT scans correlates with the location of the ruptured aneurysm. The presence
of blood in the anterior interhemispheric fissure or the adjacent frontal lobe suggests rupture of an
anterior communicating artery aneurysm. Sylvian fissure clot correlates with an ipsilateral middle
cerebral artery aneurysm. Blood predominantly localized in the posterior fossa suggests bleeding from
a posterior circulation aneurysm.

The ability to discern the location of an aneurysm rupture is limited by the fact that many patients with
SAH have a diffuse distribution of blood in the subarachnoid spaces and basal cisterns on CT scans.
The effect of gravity has been suggested as a possible cause for misleading patterns of blood
distribution. Published studies report a wide variation in the accuracy of CT scanning in localizing the
bleeding source.

In addition to the diagnosis of SAH and the localization of the bleeding site, CT scanning also allows
for some degree of prognostication, particularly in the probability of the development of vasospasm. In
1980, Fisher originally demonstrated that the amount of blood and the presence of localized clots in
the subarachnoid space are correlated with a higher incidence of delayed symptomatic arterial spasm;
this correlation has since been well validated. [11]

A specialized CT scanning technique involving the inhalation of xenon gas allows for the quantitative
determination of regional cerebral blood flow, which can be of value in monitoring the severity and
effect of cerebral vasospasm. [5, 12]

Degree of confidence
Nonenhanced CT scanning of the brain is the study of choice for the initial evaluation of patients with
potential SAH. The sensitivity is 93-100% in patients presenting with SAH within 24 hours of symptom
onset. Conversely, the detection of SAH on CT scanning has a 0-7% false-negative rate during this
period. As the time from the onset of the bleeding episode increases, the sensitivity of CT scanning
decreases. At 5 days, the sensitivity is approximately 85%; at 1 week, it is approximately 50%.

If a high clinical concern for SAH exists and the CT brain scan is negative, a lumbar puncture (LP) is
indicated. Although LP is considered to have a higher sensitivity than that of CT scanning, its
specificity is lower. Additionally, LP is an invasive procedure. [5]

In patients with a negative noncontrast CT and xanthochromia detected on lumbar puncture, a CT

angiography (CTA) can be performed to evaluate for a saccular aneurysm. Although some institutions
will perform catheter angiography after a negative CTA on clinical grounds, multiple studies have
reported that CTA is adequate to exclude aneurysms in cases with no visible blood on CT. [13, 14]

False positives/negatives

Various normally attenuating extra-axial structures may be misinterpreted as SAH, and these can lead
to false-positive results. The falx cerebri, tentorium cerebelli, and intracranial blood can be confused
for small amounts of SAH. Streak artifacts from bone at the skull base and partial volume-averaging
artifacts may also lead to a false diagnosis of SAH. False-negative studies may occur from errors in
interpretation or from failure of the technology itself. Perceptual errors aside, several conditions may
lead to the inability of CT scanning to detect a SAH. [5]

An interval of days to weeks between the bleeding episode and the CT scan allows for the breakdown
and resorption of some or all of the hemoglobin from the subarachnoid space, decreasing the contrast
between the SAH and CSF. Similarly, small amounts of SAH may be masked by dilution by the CSF
and/or CT volume averaging with CSF. Motion artifacts occurring in the scans of agitated or confused
patients can lead to either false-positive or false-negative SAH diagnoses.

"Pseudosubarachnoid hemorrhage" can occur when high-density areas are seen in the cisterns and
cortical sulci in the setting of severe brain edema. Although the mechanism is not clear, it may be
related to a combination of decreased attenuation of the brain parenchyma and distention of the
superficial vessels secondary to elevated intracranial pressure. Yuzawa et al suggested that
"pseudosubarachnoid hemorrhage" can be differentiated from true subarachnoid hemorrhage by a
lower attenuation (pseudosubarachnoid hemorrhage is < 43 HU) and an absence of intraventricular
high attenuation (patients with subarachnoid hemorrhage, however, may not have intraventricular
blood). [15]

In a study of patients with aneurysmal SAH, CT evidence of SAH was present but went unrecognized
in 4% (18 of 452 cases), according to the final radiology report in cases of presumed CT-negative
aSAH. [16]
Magnetic Resonance Imaging
Fluid-attenuated inversion recovery (FLAIR) is the most sensitive MRI pulse sequence for the
detection of subarachnoid hemorrhage (SAH). On FLAIR images, SAH appears as high signal-
intensity (white) in normally low signal-intensity (black) CSF spaces. In cases of SAH, FLAIR and CT
scanning have similar findings. T2- and T2*-weighted images can potentially demonstrate SAH as low
signal-intensity in normally high signal-intensity subarachnoid spaces. On T1-weighted images, acute
SAH may appear as intermediate-intensity or high-intensity signal in the subarachnoid space. [17]

MRA may be useful for evaluating aneurysms and other vascular lesions that cause SAH. The low
sensitivity for aneurysms smaller than 5 mm, the inability to evaluate small aneurysm contour
irregularities, and difficulty in obtaining high-quality images in patients who are agitated or confused
limits the utility of MRI in the diagnosis of acute SAH. [5]

A study of 49 patients with aneurysmal SAH found that T2* was highly predictive of the location of the
initial hemorrhage (positive predictive value, 95%), especially in the Sylvian cisterns (positive
predictive value, 100%) and the anterior interhemispheric fissure (positive predictive value, 90%). [18]

Degree of confidence
In vivo and in vitro studies suggest that FLAIR MRI is as sensitive as or more sensitive than CT
scanning in the evaluation of acute SAH; however, compared with lumbar puncture, FLAIR MRI
cannot exclude SAH. [17] Relative to CT scanning, MRI is often more valuable in the subacute phase
of SAH, in which the density of hemorrhage on CT scans decreases. In patients with equivocal
findings on CT scanning or angiography or in those patients who cannot undergo CT scanning or
conventional angiography, MRI and/or MRA may provide clinically useful information.

False positives/negatives

Magnetic field inhomogeneity can lead to artifactual increase in signal intensity in sulci over the
cerebral convexities on FLAIR images, which can mimic SAH. CSF flow artifacts can mimic the
appearance of SAH on either T1- or T2-weighted images. Intracranial thrombus can appear similar in
signal to flowing blood on time-of-flight (TOF) gradient-echo (GRE) MRA. In uncooperative patients,
motion artifacts may produce images that can lead to either false-positive or false-negative
interpretations.

Hyperintensity in the subarachnoid space on FLAIR images can also be secondary to other
pathologies, such as meningitis or meningeal carcinomatosis. [17] It is important to know whether
recent contrast-enhanced MRIs have been performed, as delayed leakage of gadolinium into the
subarachnoid space can result in hyperintense signal on FLAIR images. This has been reported to
result from contrast studies performed 24-48 hours before MRI scanning in patients with intact renal
function and an intact blood-brain barrier. However, this is typically associated with abnormalities that
can alter perfusion and disrupt the blood-brain barrier (eg, acute ischemic stroke and after carotid
artery and balloon stenting), as well as found in patients with renal failure or who are receiving high
doses of gadolinium . [19] Substantial increases in subarachnoid FLAIR signal have also been reported
in patients receiving 100% supplemental oxygen. [17]
Ultrasonography
Echoencephalography is useful for diagnosing germinal matrix and intraventricular hemorrhage in the
newborn; however, ultrasonography has no direct role in the diagnosis of subarachnoid hemorrhage
(SAH) in the adult patient. Conversely, transcranial Doppler ultrasonography has become increasingly
used in the diagnosis and management of vasospasm in patients with SAH.

Serial transcranial Doppler ultrasonographic examinations accurately detect the presence of

vasospasm and allow for the maximization of medical therapy for vasospasm before the patient
becomes symptomatic. Increases in flow velocity correspond to cross-sectional diameter decreases in
vessel lumen resulting from vasospasm. The more severe the vasospasm, the higher the flow velocity.

Flow is most easily measured in the middle cerebral arteries, which have been found to have flow
velocities normally in the 30-80 cm/s range. Elevation to 120 cm/s indicates moderate vasospasm,
and elevation to 200 cm/s indicates severe vasospasm. Single abnormal measurements are much
less reliable then serial examinations that performed to establish patient baseline velocities before the
development of vasospasm.

The sensitivity of transcranial Doppler ultrasonographic imaging for the detection of vasospasm has
been reported to be 85-90%. Because not all vasospasm is necessarily symptomatic, the finding must
be correlated with a clinical neurologic examination to determine the appropriate therapy.

Elevated intracranial vascular flow from an arteriovenous malformation or fistula may cause high flow
velocities in the absence of vasospasm. Similarly, elevation of cardiac output from any cause
generally leads to a systemic increase in flow velocities. Doppler ultrasonographic measurements are
highly dependent on technical factors. Inaccuracy in the angle of insonation may result in artifactual
elevation or reduction in the reported velocity measurements.

Nuclear Imaging
Like ultrasonography, nuclear medicine studies are not useful in the initial diagnosis of subarachnoid
hemorrhage (SAH), but they can play a role in the diagnosis of related vasospasm. The nuclear
medicine study technique that is most used for this purpose is single-photon emission computed
tomography (SPECT) scanning with the radiopharmaceutical technetium-99m (99m Tc)
hexamethylpropyleneamine oxime (HMPAO).

SPECT scanning allows for the evaluation of qualitative or semiquantitative regional blood flow. The
information provided is complementary to the transcranial Doppler ultrasonographic findings. SPECT
scanning demonstrates perfusion of the brain tissue, whereas transcranial Doppler ultrasonography
provides information about the flow in medium and large intracranial arteries. These 2 data sets are
independent variables.

Perfusion of brain tissue can be maintained through collateral circulation and autoregulation despite
the presence of severe vasospasm in a proximal artery. Conversely, perfusion can be persistently
diminished in areas of infarction or small vessel ischemia despite the successful angioplasty of a
proximal intracranial artery. [20]

The results of 99mTc HMPAO SPECT scanning are semiquantitative and qualitative in that the
cerebellum is generally considered as a control value for normal perfusion. Generalized cerebral
hypoperfusion may go unrecognized, but this pattern is not typical of vasospasm. Because early
vasospasm is frequently asymptomatic, correlation with serial clinical examination is crucial to
establish the appropriate therapy. Clinical use of this study is hampered by the qualitative nature of the
results. Absolute negative results are uncommon, and positive results may not be clinically relevant.

Space-occupying lesions such as cerebral hematoma can cause perfusion defects on SPECT
perfusion imaging. These should be obvious when correlated with conventional CT scan images.
Hydrocephalus can lead to a global decrease in cerebral perfusion which, because of the lack of
absolute quantification of the cerebral blood flow, could go unrecognized.

Angiography
Cerebral angiography is considered the standard imaging technique for the detection of intracranial
aneurysms, arteriovenous malformations (AVMs), and fistulae, as shown in the images below.
Aneurysms are detected as focal areas of outpouching or dilatation of the arterial wall. These
frequently occur at arterial branching points in characteristic locations within or near the circle of Willis.

Cerebral angiography should include anteroposterior (AP), lateral, and one or more oblique views of
both carotid and vertebral artery contrast injection studies. A submentovertical view is sometimes
useful in demonstrating the neck of a middle cerebral artery bifurcation aneurysm or anterior
communicating artery aneurysm.

An angiogram showing a bilobed aneurysm of a posteroinferior cerebellar artery immediately before rupturing.
An angiogram showing the onset of an aneurysmal rupture, with extravasation of contrast material into the subarachnoid
space from the anterosuperior aspect of a bilobed aneurysm in a posteroinferior cerebellar artery.

A later-phase angiogram of a rupturing bilobed aneurysm of a posteroinferior cerebellar artery shows progressive
opacification of the subarachnoid space in the posterior fossa.
A late angiogram demonstrating contrast medium filling the posterior fossa subarachnoid spaces, including the ambient,
prepontine, and perimedullary cisterns.

Compression of the contralateral carotid artery should be performed during carotid cerebral
angiography to demonstrate the anterior communicating artery if it does not fill spontaneously during
one of the internal carotid artery injections. Carotid artery compression should be done on a segment
of the common carotid artery without atherosclerotic plaque, if possible. One vertebral arteriogram is
occasionally omitted by some angiographers if there is abundant reflux proximal to the origin of the
posterior inferior cerebellar artery of that vertebral artery when the contralateral vertebral artery is
injected with contrast medium. This technique does not, however, depict all aneurysms. The most
reliable method of aneurysm detection is the invariable selective injection of contrast medium into both
common or internal carotid arteries and both vertebral arteries.

Cerebral angiography reliably demonstrates the presence or absence of an intracranial aneurysm or

an AVM, and it establishes the number and locations of aneurysms. Morphologic information, such as
aneurysm size and shape, helps to determine which aneurysm has bled in a patient with multiple
aneurysms. Specifically, the presence of a lobulation, tit, or a daughter aneurysm is highly suggestive
that the aneurysm is the one that has bled. In the absence of any distinguishing aneurysm shape
features or hemorrhage localization by a CT scan, the largest aneurysm is the most likely to have
bled. Features such as aneurysm location, shape, neck size, and neck-to-maximal diameter ratio are
crucial in determining whether the aneurysm is better treated with open craniotomy or with an
endovascular technique. [5]

Degree of confidence
Cerebral angiography provides a high degree of accuracy. A small false-negative rate does occur,
probably in the range of 1-2%. A repeat cerebral arteriogram at 10-14 days is indicated if the initial
angiogram does not demonstrate the cause of a subarachnoid hemorrhage (SAH). In a small number
of patients, a follow-up angiogram will detect an aneurysm that was not demonstrated on the initial
study.
Bilateral selective external and internal carotid artery angiograms can be performed to exclude a dural
arteriovenous fistula, which is a rare cause of SAH. Bilateral vertebral arteriograms of the neck (and, if
necessary, selective thyrocervical trunk and/or careful injections of the right superior intercostal artery)
demonstrate the arterial and venous circulation of the cervical spinal cord. In rare cases, they show a
spinal vascular malformation or neoplasm, such as hemangioblastoma, as the cause of SAH.

Cervical spinal MRI and/or MRA may indicate the necessity of an additional arteriographic study. If
thorough arteriographic studies do not demonstrate a specific cause for an SAH, a presumptive
diagnosis of idiopathic perimesencephalic hemorrhage is sometimes made. [5]

False positives/negatives
The reason that some aneurysms are not initially diagnosed by angiography and are only detected on
subsequent follow-up angiograms is not always evident. Vasospasm is believed to be the most
common cause. Arteriographic double densities simulating aneurysm or apparent areas of vessel wall
bulge or outpouching may be caused by arterial tortuosity and atherosclerosis or overlap of adjacent
arteries on standard angiogram views. This can usually be determined by comparing all angiographic
views and, if necessary, obtaining additional oblique arteriographic views.

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