MRI picture of subarachnoid hemorrhage
May 23rd, 2013 by Administrator

The author: Professor Yasser Metwally


May 23, 2013 — The pathophysiology of subarachnoid hemorrhage and the physical principles of CT explain the change in sensitivity of CT in detecting subarachnoid hemorrhage with time from ictus. X Ray techniques including CT produce tissue contrast because of the proportion of the incident X ray beam that is stopped (attenuated) by the tissue. This relies on two factors: the amount of tissue traversed by the beam and the attenuation coefficient of the tissue. The attenuation coefficient bears a direct relation to the electron density of the tissue. Fresh haemorrhage has the same electron density as brain and other soft tissues and so hyperacute (within 2 hours of ictus) subarachnoid hemorrhage may not be seen directly on CT. As reabsorption of serum from a haematoma progresses the local packed cell volume, and hence electron density, increases making acute subarachnoid hemorrhage visible as a high attenuating “white” area. With the passage of further time subarachnoid hemorrhage becomes less visible on CT principally because of two processes. Firstly, CSF circulation redistributes focal subarachnoid hemorrhage into other parts of the subarachnoid space and ventricular system. The resulting dilution reduces the conspicuity on CT. Secondly, reabsorption of serum is followed by reabsorption of the protein component, which also leads to reduced conspicuity. Consequently the sensitivity of CT to subarachnoid hemorrhage falls drastically over the first 14 days from ictus. [4]

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Magnetic resonance imaging does not directly rely on the electron density of substances for its contrast resolution. The MR signal principally relies on proton (hydrogen nuclei) density, and T1 and T2* (which includes the T2 component) relaxation times. The different physical and chemical states of iron within haemorrhage have profound effects on the MR signal. [14] Standard spin echo MR sequences are considered to be insensitive in detecting acute haemorrhage; however, MR imaging offers two possibilities for improved detection of subarachnoid hemorrhage, both of which depend on the appearance of haemoglobin and its breakdown products.

The protein component produces high T2 signal which is swamped by the bright T2 signal from CSF on a conventional T2 weighted image. FLAIR sequences suppress the CSF signal and allow the signal from globin and its breakdown products to be seen. FLAIR has been reported to be a sensitive test for subarachnoid hemorrhage in the subacute phase. [7]

Iron in the form of Fe3+ or Fe2+ is paramagnetic. The presence of paramagnetic species in the CSF leads to localised perturbations in the magnetic field “seen” by the MR visible hydrogen nuclei. This leads to an increase in the precession rate in the immediate vicinity of Fe ions on the atomic scale and hence a faster dephasing and loss of T2* signal. Gradient echo sequences with significant T2* weighting are particularly sensitive to this localised change and are thus suited to detecting subarachnoid hemorrhage, even in the acute stage.

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Figure 1. MRI T1 image showing a precontrast hyperintensity in the right parieto-occipital region and in the 4th ventricle due to the presence of methemoglobin in the subarachnoid spaces secondary to subarachnoid hemorrhage

The combination of lumbar puncture and CT is sensitive and specific for acute subarachnoid hemorrhage. CT suffers from a loss of sensitivity to subarachnoid hemorrhage in the subacute phase. MRI, particularly FLAIR and T2*, may be able to supplement CT in this situation. Both FLAIR and T2* can be performed on standard MR scanners.

Appropriately selected MR sequences are sensitive and specific in the detection of subarachnoid hemorrhage. This is by contrast with the widespread view in the clinical neuroscience literature, although some reports [7] show the value of FLAIR in detecting subarachnoid hemorrhage. one practical point of view in this chapter is that MR using FLAIR and T2* sequences together is a valuable tool in the detection of subarachnoid hemorrhage.

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Figure 2. An acute subarachnoid hemorrhage. Brain CT was performed on the day of the haemorrhage; MR scans were taken 48 hours later. (A) CT shows blood in the interhemispheric fissure which is not seen on a comparable MR cut with (B) a T1 weighting sequence or (C) a fast spin echo T2 weighting sequence. (D) subarachnoid hemorrhage is seen on the gradient echo T2* image as an area of low signal. Lower cuts on the same patient show interhemispheric, sylvian, and cisternal blood on (E) CT and (F) T2* MR.

  • Conclusions

Sensitivity to subarachnoid hemorrhage varied among the five MR sequences studied from 50% to 94% in acute subarachnoid hemorrhage and from 33% to 100% in subacute subarachnoid hemorrhage. The most sensitive sequences were FLAIR and T2* with T2* performing slightly better than FLAIR. The sensitivity of T2* was 94% under 4 days from the ictus and 100% between 4 and 14 days.

Fluid-attenuated inversion recovery (FLAIR) is the most sensitive MRI pulse sequence for the detection of subarachnoid hemorrhage (subarachnoid hemorrhage). On FLAIR images, subarachnoid hemorrhage appears as high signal-intensity (white) in normally low signal-intensity (black) CSF spaces. In cases of subarachnoid hemorrhage, FLAIR and CT scanning have similar findings. T2- and T2*-weighted images can potentially demonstrate subarachnoid hemorrhage as low signal-intensity in normally high signal-intensity subarachnoid spaces. On T1-weighted images, acute subarachnoid hemorrhage may appear as intermediate-intensity or high-intensity signal in the subarachnoid space.

MRA may be useful for evaluating aneurysms and other vascular lesions that cause subarachnoid hemorrhage. 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 subarachnoid hemorrhage.

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Figure 3. A subtle subacute subarachnoid hemorrhage. (A) Brain CT was done 7 days after the haemorrhage and shows abnormal isointense material in the suprasellar cistern and along the path of the left middle cerebral artery towards the sylvian fissure. (B) A comparable slice of FLAIR MR imaging done 24 hours after the CT. It shows the abnormality more clearly as high signal material in the left side of the suprasellar cistern and left sylvian fissure (arrows) in keeping with subacute subarachnoid hemorrhage. (C) The same area shows as low signal on T2* MR imaging (arrow). (D) One slice down from C illustrates a problem with the T2* images. The low signal arising from the boundary between tissues of differing susceptibility—in this case the surface of the right lesser sphenoid wing (arrow)—obscures any additional low signal due to blood in the sylvian fissure and could be misinterpreted as blood. This is one reason why we regard the FLAIR and T2* sequences as complementary rather than alternatives.

Degree of confidence of FLAIR images

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 subarachnoid hemorrhage; however, compared with lumbar puncture, FLAIR MRI cannot exclude subarachnoid hemorrhage. Relative to CT scanning, MRI is often more valuable in the subacute phase of subarachnoid hemorrhage, 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.

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Figure 4. A CT negative subarachnoid hemorrhage as confirmed by lumbar puncture. (A) Brain CT taken 4 days after the onset of headache is normal. The MR scans were done within 1 hour of the CT. (B) The T2* image closest to the slice of A. It shows an area of low signal (arrow). (C) The corresponding FLAIR image shows high signal from the same area (arrow). Note the different angulation used for CT and MR images.

False positives/negatives of Flair images

Magnetic field inhomogeneity can lead to artifactual increase in signal intensity in sulci over the cerebral convexities on FLAIR images, which can mimic subarachnoid hemorrhage. CSF flow artifacts can mimic the appearance of subarachnoid hemorrhage 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. 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 without renal failure and without abnormalities known to disrupt the blood-brain barrier. Substantial increases in subarachnoid FLAIR signal have also been reported in patients receiving 100% supplemental oxygen.


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