DOI:10.2214/AJR.07.2424
AJR 2007; 189:913-921
© American Roentgen Ray Society
Hyperintensity in the Subarachnoid Space on FLAIR MRI
Stephen L. Stuckey1,
Tony D. Goh2,
Theresa Heffernan3 and
David Rowan4
1 Department of Radiology, Princess Alexandra Hospital, Ipswich Rd.,
Woolloongabba, Queensland, Australia 4102.
2 Department of Radiology, Christchurch Hospital, Christchurch, New
Zealand.
3 Department of Radiology, The Wesley Hospital, Auchenflower, Queensland,
Australia.
4 Department of Radiology, The Alfred Hospital, Prahran, Victoria,
Australia.
Received January 21, 2004;
accepted after revision May 13, 2007.
Address correspondence to S. L. Stuckey.
Abstract
OBJECTIVE. The purposes of this essay are to illustrate the causes
of FLAIR hyperintensity in the subarachnoid space and to outline the
mechanisms of the findings.
CONCLUSION. FLAIR subarachnoid space hyperintensity may be
encountered with both pathological conditions and artifacts. Knowledge of
these conditions and appearances coupled with any associated findings may
suggest the cause of the FLAIR subarachnoid space hyperintensity. A diffuse
distribution and a lack of ancillary findings often remain nonspecific and may
require clinical correlation and CSF analysis.
Keywords: brain • CSF • FLAIR • MRI • subarachnoid space
Introduction
At many institutions, the FLAIR pulse sequence has become a routine part of
MRI studies of the brain. First described by Hajnal et al.
[1] in 1992, FLAIR MRI
techniques consist of an inversion recovery pulse to null the signal from CSF
and a long echo time to produce a heavily T2-weighted sequence. The FLAIR
technique produces images highly sensitive to T2-weighted prolongation in
tissue. In addition, factors that affect the T1-weighted relaxation time of
CSF may interfere with its suppression and result in CSF hyperintensity.
Compared with conventional T2-weighted and proton density–weighted
imaging, use of the FLAIR sequence improves detection of lesions within the
subarachnoid space and brain parenchyma, particularly of lesions near the
brain–CSF interface.
When disease occurs within the subarachnoid space, the relaxation time of
CSF is altered. This change translates into lesser degrees of CSF signal
nulling and resultant hyperintensity of the CSF or subarachnoid space during
the FLAIR sequence. Such findings have been well described in a wide range of
pathologic conditions, such as subarachnoid hemorrhage (SAH), meningitis, and
leptomeningeal spread of malignant disease. Other, less common causes of
subarachnoid FLAIR hyperintensity are artifacts. With increased routine use of
the FLAIR sequence, radiologists need to be familiar with the causes of
subarachnoid FLAIR hyperintensity. Analysis of the distribution of sulcal
FLAIR hyperintensity and the associated imaging findings related to the
primary pathologic condition (e.g., the presence of an adjacent mass) can help
elucidate the cause. In many instances, however, particularly when there are
no ancillary findings and the distribution is diffuse, the finding remains
nonspecific, and clinical correlation alone or in combination with CSF
analysis may be needed. This pictorial essay illustrates the known causes of
FLAIR hyperintensity in the subarachnoid space and briefly outlines the
mechanisms for each of the findings.
Pathologic Causes of Hyperintensity
Subarachnoid Hemorrhage
The appearance of SAH on MRI has been a controversial topic
[2]. Acute SAH is notoriously
difficult to detect on conventional T1-and T2-weighted sequences, and FLAIR
has been appreciated and less challenged as being superior for detection of
SAH in the subacute phase [2,
3]. Results of both in vivo and
in vitro studies have suggested that FLAIR imaging is as sensitive as or more
sensitive than CT in the evaluation of acute SAH, but compared with the
findings at lumbar puncture, the findings on FLAIR imaging are not definitive
in excluding acute SAH
[4–6].
The FLAIR sequence is particularly useful in visualization of acute SAH in
areas where CT may be limited because of beam-hardening artifacts
[7] (Fig.
1A,
1B). The hyperintense
appearance of acute SAH on FLAIR images relates to several factors and effects
on both T1-and T2-weighted relaxation times. T1-weighted shortening of bloody
CSF due to the higher protein content causes an offset in the null point of
CSF inversion times, resulting in increased signal intensity. T2-weighted
prolongation also occurs as a result of the high protein content of blood and
inflammatory products in both dilute and dense blood–CSF mixtures
[7]. Oxyhemoglobin, which is
diamagnetic and the initial product of blood degradation, may also contribute
to T2-weighted prolongation. SAH differs from intraparenchymal hemorrhage in
that the mix of blood with high-oxygen-tension CSF delays generation of
paramagnetic deoxyhemoglobin, and oxyhemoglobin remains present longer than in
intraparenchymal hemorrhage
[7]. Variability in the
appearance of SAH after 48 hours most likely relates to hemoglobin
degradation, which adds further complexity to the MRI signal intensity
[8].
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Fig. 1B —41-year-old man 3 days after traumatic subarachnoid
hemorrhage. CT scan corresponding to A shows subarachnoid hemorrhage
overlying temporal lobe is more difficult to appreciate owing to
beam-hardening artifact (arrows) from adjacent calvarium.
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Meningitis
Unenhanced FLAIR MRI has been shown to be a sensitive technique for the
detection of inflammatory meningitis (Figs.
2A and
2B)
[9]. Elevations in CSF protein
and cellular concentrations that occur in meningitis result in shortening of
the T1 relaxation time, alteration of the point at which CSF is nulled, and T2
prolongation of CSF relaxation time
[10]. Unenhanced FLAIR MRI,
although moderately sensitive, is not superior to contrast-enhanced
T1-weighted imaging in the detection of meningitis
[11]. Contrast-enhanced FLAIR
images have been shown to be superior to contrast-enhanced T1-weighted images
in visualization of inflammatory leptomeningeal disease
[12,
13]. Leptomeningeal disease
can be more easily visualized on contrast-enhanced FLAIR images than on
contrast-enhanced T1-weighted images because FLAIR imaging allows clearer
distinction between enhancing meninges and enhancing cortical veins, cortical
veins becoming less clearly enhanced on FLAIR images (found in only 9% of
cases in one series) [12,
14]
(Fig. 2C). The relatively less
prominent effect of gadolinium on venous appearance with FLAIR compared with
conventional spin-echo sequences does not appear to have been previously
explained, especially in view of the apparently incongruous greater
sensitivity of FLAIR to lower concentrations of gadolinium
[12]. The relative persistence
of flow voids with FLAIR may reflect more prominent time-of-flight effects
secondary to differences in acquisition technique (i.e., several interleaved
acquisitions are often used for FLAIR). Gadolinium enhancement of subarachnoid
pathology should result in shortening of T1-weighted values and FLAIR
hyperintensity.
Meningeal Carcinomatosis
FLAIR images may depict evidence of leptomeningeal malignancy without the
use of IV gadolinium in patients with known or suspected neoplastic disease
(Fig. 3A,
3B)
[15,
16]. Some results
[9,
16] have suggested that FLAIR
images are superior to contrast-enhanced T1-weighted images for the diagnosis
of subarachnoid space metastases. Other studies, however, have not reproduced
these results, although cases in which unenhanced FLAIR may be superior to
gadolinium-enhanced T1-weighted imaging have been described. Other studies
[17,
18] have had mixed results on
the value of contrast-enhanced FLAIR imaging versus contrast-enhanced
T1-weighted imaging. With use of the contribution of gadolinium
enhancement–mediated T1-weighted shortening to the FLAIR image,
contrast-enhanced FLAIR images may be of value in the depiction of
leptomeningeal carcinomatosis, but the relative value of this technique
remains an area of controversy. Figure
4A,
4B shows the use of
gadolinium-enhanced FLAIR in imaging of a 60-year-old man with non-Hodgkin's
lymphoma. The axial contrast-enhanced FLAIR image reveals more intense and
conspicuous bilateral enhancement of the internal auditory canals and adjacent
seventh cranial nerves within the temporal bone secondary to lymphomatous
infiltration than does the corresponding gadolinium-enhanced T1-weighted
image. The FLAIR hyperintensity of leptomeningeal carcinomatosis in the
subarachnoid space results from elevations in CSF cellular and protein
concentrations. The situation is similar to that described for inflammatory
meningitis. Gadolinium enhancement similarly results in shortening of
T1-weighted values and FLAIR hyperintensity.
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Fig. 3A —29-year-old man with leptomeningeal metastasis of
medulloblastoma. Axial contrast-enhanced T1-weighted MR image shows widespread
leptomeningeal metastatic lesions (arrows) involving surfaces of
cerebellum and cerebral hemispheres.
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Fig. 3B —29-year-old man with leptomeningeal metastasis of
medulloblastoma. Axial FLAIR MR image shows mild subarachnoid hyperintensity
and nodularity over cerebellar and cerebral surfaces in keeping with presence
of widespread leptomeningeal metastatic lesions (arrows).
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Fig. 4A —60-year-old man with non-Hodgkin's lymphoma. Axial
contrast-enhanced MR image obtained with FLAIR sequence shows bilateral
intense enhancement (arrow) of internal auditory canals and adjacent
seventh cranial nerves within temporal bone secondary to lymphomatous
infiltration.
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Fig. 4B —60-year-old man with non-Hodgkin's lymphoma.
Contrast-enhanced axial T1-weighted MR image corresponding to A shows
less conspicuous meningeal enhancement (arrow) of internal auditory
canals.
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Leptomeningeal Melanosis
Leptomeningeal melanosis is part of the neurocutaneous melanosis congenital
phakomatosis. The leptomeningeal pathologic condition can be melanosis or
melanoma. MRI performed with FLAIR may show subarachnoid hyperintensity
similar to that of meningeal carcinomatosis. It has been speculated that the
FLAIR hyperintensity may be due not only to T2-weighted prolongation
reflecting the elevated protein content but also to the T1-weighted shortening
effects of melanin [19,
20]. For these reasons, FLAIR
hyperintensity can be seen with or without gadolinium contrast enhancement
(Fig. 5A,
5B).
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Fig. 5A —34-year-old woman with neurocutaneous melanosis and
melanocytic tumor of leptomeninges. (Courtesy of Brazier D, Sydney, Australia)
FLAIR MR image shows extensive sulcal hyperintensity.
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Fig. 5B —34-year-old woman with neurocutaneous melanosis and
melanocytic tumor of leptomeninges. (Courtesy of Brazier D, Sydney, Australia)
Contrast-enhanced T1-weighted MR image shows extensive conspicuous sulcal
hyperintensity and enhancement.
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Fat-Containing Tumors
The FLAIR imaging technique entails an inversion pulse to null the signal
intensity of CSF as these spins pass through the zero point determined by the
tissue-specific (in this case CSF) T1-weighted relaxation time. Any shortening
of the CSF T1-weighted relaxation time negates this effect. Fat-containing
tumors, such as lipoma, in the subarachnoid space that appear hyperintense on
T1-weighted images therefore appear hyperintense on FLAIR sequences (Fig.
6A,
6B). Fat droplets in the
subarachnoid space from a ruptured dermoid are similarly hyperintense on FLAIR
sequences (Fig. 7A,
7B,
7C). By a similar mechanism,
droplets of residual oil-based contrast medium (e.g., iophendylate) are a
potential cause of FLAIR hyperintensity in the subarachnoid space.
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Fig. 7B —31-year-old woman with recurrent headache after resection of
ruptured dermoid. Axial T1-weighted MR image shows high-signal-intensity fat
droplets (arrows) in subarachnoid space in keeping with dermoid
rupture.
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Acute Stroke
Vascular hyperintensity in the subarachnoid space on FLAIR images may be
produced by severe (> 90%) vascular stenosis or occlusion of major cerebral
vessels with resulting slow flow
[21]. Abnormalities in
vascular signal intensity on FLAIR images as a result of large vessel
occlusion or high-grade stenosis is reported to occur as the earliest MRI sign
of ischemia in some patients and thus may be seen before detectable
abnormalities on diffusion-weighted images
[21,
22]. Arterial hyperintensity
on FLAIR images in association with acute stroke may reflect retrograde
collateral circulation, vascular congestion, slow flow, or T1-weighted
shortening and T2-weighted prolongation of thromboembolism or stationary
blood. Compared with those obtained with conventional T2-weighted sequences,
images obtained with the FLAIR sequence clearly depict arterial occlusion as
intraarterial areas of high signal intensity against a dark CSF background
(Figs. 8A and
8B)
[23]. The area of
intraarterial signal intensity is larger than the area of abnormality on
diffusion-weighted images (Fig.
8C). In combination, the two sequences can be useful for
predicting whether an area of cerebral tissue is at risk of infarction (the
ischemic penumbra). There may be important implications in the management of
hyperacute cerebral ischemia
[23]. The areas of
intravascular signal intensity on FLAIR images appear to correlate with the
perfusion abnormality
[23].
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Fig. 8A —57-year-old woman with right cerebral infarct. Axial FLAIR MR
image obtained soon after onset of neurologic symptoms shows hyperintensity
(arrow) due to thrombotic occlusion or slow flow in right middle
cerebral artery.
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Fig. 8C —57-year-old woman with right cerebral infarct. Axial
diffusion-weighted MR image shows acute right lenticulostriate infarct
(arrow) in perforator territory but no established infarct in rest of
right middle cerebral artery territory. Perfusion imaging was not performed.
Further ischemia-related diffusion abnormality is evident in left
periventricular white matter.
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Moyamoya Disease
In 1995, Ohta et al. [24]
reported diffuse leptomeningeal enhancement on contrast-enhanced T1-weighted
images of children with moyamoya disease. Those authors named this finding the
ivy sign because it resembled ivy creeping on stones. In a more recent report
[25], high signal intensity in
the subarachnoid space on FLAIR images in a patient with moyamoya disease also
was termed the ivy sign. Retrograde slow flow of engorged pial arteries
through leptomeningeal anastomoses has been proposed as the most likely
mechanism of this finding [25]
(Fig. 9). Sturge-Weber
syndrome can have a similar appearance but in a more limited distribution.
Elevated Blood Pool to CSF Ratio
Taoka et al. [26]
postulated that an increased blood pool to CSF ratio within a sulcus can be a
cause of sulcal hyperintensity on FLAIR images. The relatively small volume
and oxygenation status of the blood in vascular structures within the sulcus
normally has a minimal effect on the local magnetic field and signal intensity
of CSF protons. The blood pool effect can theoretically increase when the
relative volume ratio of CSF to blood in a voxel is decreased. Taoka et al.
suggested that this phenomenon may explain the hyperintensity of the
subarachnoid space on FLAIR images in instances of reduced CSF space or
relative increase in intravascular volume, such as that caused by mass effect
due to hydrocephalus or vascular disease such as cortical vein or dural sinus
thrombosis. Taoka et al. also suggested that assessment of the FLAIR
distribution of sulcal hyperintensity may provide a clue to causation,
vascular causes being more likely to be associated with a diffuse sulcal FLAIR
hyperintensity and the mass effect being more likely to be focal sulcal FLAIR
hyperintensity. In their series, however, Taoka et al. found the distinction
not statistically significant.
Contrast Media
Mamourian et al. [27] found
that IV contrast material can cause sulcal FLAIR hyperintensity in healthy
dogs and that this effect was most marked on triple-dose delayed imaging. In
three patients with renal impairment, Lev and Schaefer
[28] found diffuse CSF FLAIR
hyperintensity due to delayed leakage of gadolinium into the subarachnoid
space, mimicking the appearance of SAH and other pathologic conditions. In a
larger series of 33 patients, Bozzao et al.
[29] concluded that when FLAIR
images were acquired 2–24 hours after IV administration of gadolinium
contrast material to patients with pathologic conditions characterized by an
altered blood–brain barrier or neovascularization near the subarachnoid
space or ventricles (e.g., stroke, neoplasm, and surgery), CSF signal change
is likely and should not be confused with hemorrhage.
Artifact-Related Causes of Hyperintensity
Supplemental Oxygen
Abnormalities in CSF signal intensity on FLAIR images have been found in
patients undergoing MRI examinations while receiving supplemental oxygen
[30,
31]. An approximately 4-to
5.3-fold increase in signal intensity with 100% supplemental oxygen has been
found [32]. Other studies have
shown these effects with 100% oxygen but no increase in signal intensity with
50% oxygen mixtures [33]. The
weakly paramagnetic effect of supplemental oxygen results in reduction of CSF
T1-weighted relaxation time and subsequent high signal intensity on FLAIR
images [32]
(Fig. 10).
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Fig. 10 —36-year-old intubated man with meningioma undergoing
follow-up imaging. Axial FLAIR MR image shows diffuse hyperintensity
(arrows) in subarachnoid space thought to be caused by supplemental
oxygen.
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CSF Pulsation
CSF flow artifact can produce artifactual FLAIR hyperintensity in the
subarachnoid space. Intense CSF pulsation results in inflow of CSF and thus
protons, which have potentially not undergone the inversion pulse, into the
imaging plane. Such artifacts tend to occur in the basal, prepontine, and
cerebellopontine angle cisterns (Fig.
11) and in sections containing foramina of the ventricular system.
These artifacts are less common and less intense over the convexities of the
cerebral hemispheres, where CSF flow is diminished
[34]. Mechanisms such as
k-space reordering by inversion time at each slice position, tailored
radiofrequency pulses, increasing the number of interleaving acquisitions, and
adiabatic inversion pulses have been used to reduce or eliminate CSF pulsation
artifacts
[35–38].
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Fig. 11 —55-year-old man with left sensorineural hearing loss. Axial
FLAIR MR image shows focal increased signal intensity (arrow) due to
CSF flow artifact in right aspect of prepontine cistern.
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Vascular Pulsation
Vascular pulsation, because the motion is potentially periodic as a
function of k-space location, produces artifacts on FLAIR images that
reproduce the size, shape, and alignment of the responsible vessel along the
phase-encoding direction of the image
(Fig. 12). Such ghosting
artifacts produced by periodic motion in which there is synchrony between the
phase-encoding steps and the motion are commonly seen on MR images. These
artifacts may display components with alternating high and low signal
intensities and in rare instances can be mistaken for hyperintensity in the
subarachnoid space on FLAIR images. Similar phase-encoding ghosting artifacts
from eyeball motion can project over the subarachnoid space
(Fig. 13).
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Fig. 12 —39-year-old man with right sensorineural hearing loss. Axial
FLAIR MR image shows vascular pulsation artifact (arrow) from left
transverse sinus that can be mistaken for hyperintensity in subarachnoid
space. Phase-encoding direction is anteroposterior, whereas in most FLAIR
examinations phase encoding is left to right.
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Fig. 13 —33-year-old woman with left sensorineural hearing loss. Axial
FLAIR MR image shows hyperintensity (arrow) close to subarachnoid
space (in phase-encoding direction) due to ghosting artifact from eye
movement. Phase-encoding direction is anteroposterior, whereas in most FLAIR
examinations phase encoding is left to right.
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Magnetic Susceptibility Artifact
Magnetic susceptibility artifact can result in artifactual increased FLAIR
signal intensity in the subarachnoid space. At tissue interfaces where the
magnitude of local magnetic field inhomogeneities is pronounced, incomplete
nulling of CSF by the slice-selection inversion pulse can occur.
Susceptibility artifacts and resultant FLAIR subarachnoid hyperintensity most
commonly occur in the presence of metal (Fig.
14A,
14B), but more subtle local
incomplete nulling of CSF can be caused by air in the paranasal sinuses and
the temporal bones.
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Fig. 14A —44-year-old man after resection of cavernous hemangioma.
FLAIR MR image shows magnetic susceptibility artifact due to metallic clips
(arrow) from craniotomy performed 2 years earlier.
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Fig. 14B —44-year-old man after resection of cavernous hemangioma.
FLAIR MR image shows subtle artifactual hyperintensity (arrow) in
subarachnoid space overlying superior aspect of right temporal lobe.
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Motion Artifact
Marked head motion can simulate the appearance on FLAIR images of
pathologic changes in the subarachnoid space. Comparison of several slices
usually confirms the marked head motion and inconsistency in FLAIR sulcal
hyperintensity (Fig. 15). This
problem occurs because CSF in the imaging plane does not undergo the inversion
pulse.
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Abstract
Introduction
