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  In this Article
 »  Abstract
 »  Introduction
 »  Ischemic Stroke
 »  Cerebral Venous ...
 »  Vascular Malform...
 »  Vasculopathy
 »  Conclusion
 »  References
 »  Article Figures

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TOPIC OF THE ISSUE: REVIEW ARTICLE
Year : 2010  |  Volume : 58  |  Issue : 4  |  Page : 602-607

Clinical utility of susceptibility-weighted imaging in vascular diseases of the brain


Department of Imaging Sciences and Interventional Radiology, SCTIMST, Trivandrum, India

Date of Acceptance28-Jul-2010
Date of Web Publication24-Aug-2010

Correspondence Address:
Chandrasekhran Kesavadas
Department of Imaging Sciences and Interventional Radiology, SCTIMST, Trivandrum - 695011
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.68667

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 » Abstract 

Susceptibility-weighted imaging (SWI) is a rapidly evolving technique that utilizes both the magnitude and phase information to obtain valuable information about susceptibility changes between tissues. SWI is very sensitive to the paramagnetic effects of deoxyhemoglobin. SWI plays an important role in the diagnostic evaluation and management of acute stroke. In addition, it also plays an important role in the imaging of patients with chronic arterial occlusion and in understanding the effects of chronic infarction, like incomplete infarction and cortical laminar necrosis. The hemodynamic status and oxygen extraction fraction can also be evaluated. SWI is useful in evaluating cerebral venous sinus thrombosis by demonstrating the hemorrhagic venous infarction and thrombus in the sinus and the cortical veins, as well as secondary phenomena like venous stasis in the form of engorged cortical and transmedullary veins and collateral slow flow. Low-flow vascular malformations that are not visualized well on conventional sequences are depicted in exquisite detail along with the venous components on SWI. SWI is used for evaluating cavernomas, developmental venous anomalies, telangiactasias, dural arteriovenous fistulas and the various components of arteriovenous malformations. It has also evolved as a noninvasive technique for evaluating various anomalies of the venous system without administering contrast. Vasculopathies and vasculitis are associated with cerebral microbleeds which are detected on SWI. On the basis of the additional information provided by SWI, it can be included in the routine brain imaging protocol.


Keywords: Cerebral venous sinus thrombosis, stroke, susceptibility-weighted imaging, vascular malformations, vasculopathy


How to cite this article:
Hingwala D, Kesavadas C, Thomas B, Kapilamoorthy TR. Clinical utility of susceptibility-weighted imaging in vascular diseases of the brain. Neurol India 2010;58:602-7

How to cite this URL:
Hingwala D, Kesavadas C, Thomas B, Kapilamoorthy TR. Clinical utility of susceptibility-weighted imaging in vascular diseases of the brain. Neurol India [serial online] 2010 [cited 2019 Aug 24];58:602-7. Available from: http://www.neurologyindia.com/text.asp?2010/58/4/602/68667



 » Introduction Top


Susceptibility-weighted imaging (SWI) is rapidly evolving as a method that enhances the visualization of small vessels in the human brain. [1] Both magnitude and phase information are used to obtain valuable information about susceptibility changes between tissues. [2],[3],[4] SWI is particularly suited for imaging venous blood because it is very sensitive to the paramagnetic effects of deoxyhemoglobin. [5] It is also useful in evaluating intracranial hemorrhage of various causes. Increased concentrations of deoxyhemoglobin within veins can induce susceptibility changes, resulting in increased conspicuity in SWI. In this article, we review the clinical applications of SWI in various vascular diseases of brain.


 » Ischemic Stroke Top


Reduction of arterial supply to the brain due to embolism or atherothrombosis may lead to ischemia or infarction with or without hemorrhage. SWI plays a pivotal role in the diagnostic evaluation and management of acute stroke. In addition, it also plays an important role in the imaging of patients with chronic arterial occlusion and in understanding the effects of chronic infarction.

Assessment of acute stroke

While computed tomography (CT) is considered as the gold standard for detecting hemorrhage in stroke patients, magnetic resonance imaging (MRI) is emerging as a reliable tool for the detection of bleeding. Susceptibility-weighted imaging (SWI) is exquisitely sensitive in detecting hemorrhage [6],[7] and thus helps to distinguish between ischemic and hemorrhagic strokes. SWI-MRI is reported to be as accurate as CT in the detection of hyperacute hemorrhage and is superior to CT for detecting chronic hemorrhages. [8] While traditionally, MRI was not considered to be very sensitive for the detection of subarachnoid hemorrhage (SAH), SWI can detect acute SAH [9] and is extremely sensitive for subacute or chronic hemorrhage that may not be revealed on CT or Fluid-attenuated inversion recovery sequence (FLAIR) sequence of MRI. [7]

The detection of hemorrhagic transformation of an ischemic infarct is important, especially in patients in whom revascularization procedure is being planned. Conventional sequences often fail to detect minor bleeds in patients with acute ischemic stroke. SWI can detect tiny bleeds within the infarct due to exquisite sensitivity to magnetic field inhomogeneity. The bleeds are even more conspicuous on SWI than on T2*-weighted Gradient-recalled echo (GRE) sequence. [10] However, the clinical significance of detection of microbleeds is not known at this point of time. [6] In addition, prominence of the transcerebral veins is a predictor for increased risk of hemorrhagic transformation in patients receiving thrombolytic therapy. [11] SWI can also be used to detect early hemorrhagic transformation after intra- arterial thrombolysis as CT evaluation in these cases may be difficult because of extravasation of angiographic contrast. [6]

SWI can also help to detect the presence of an intra-arterial thrombus and its exact location based on the 'susceptibility sign.' [10] It has been defined by Rovira and colleagues as hypointensity within the intracranial artery with the diameter of the hypointense artery exceeding that of the contralateral artery due to the blooming artifact. [12] Compared to MR angiography, SWI also has the advantage of being able to detect distally located clots. [6] The minimum intensity projection of SWI and the hyperintensity of oxygenated blood proximal to the thromboembolism can be used to distinguish intra-arterial thrombus from subarachnoid hemorrhage. [13] Due to its ability to detect hemorrhagic complications and the presence of an intra-arterial thrombus, SWI plays an important role in decision-making in revascularization therapies.

Tamura et al. used dynamic-susceptibility contrast-enhanced MR (DSC-MR) imaging to demonstrate that T2*-sensitive MR imaging can detect local hypointensity in the vascular territory of the occluded cerebral artery in patients with acute ischemic stroke. [14] The hypointensity may result from increased deoxygenation of hemoglobin in blood, indicating increased oxygen extraction fraction (OEF) or misery perfusion and tissue at risk for infarction. The area with prominent veins may correspond to the penumbra. SWI can be utilized instead of DSC-MR for getting similar information [Figure 1]. The OEF obtained using MRI is in good agreement with the values reported in the positron emission tomography literature. It is also possible to get diffusion and perfusion MRI along with oxygen metabolic maps. [15] The utility of the information obtained from such maps has to be further validated for routine clinical practice. Thus it appears that SWI can offer some information regarding the four P's of acute stroke, including parenchyma, pipes, perfusion and penumbra. [16]
Figure 1 : Evaluation of acute stroke: FLAIR axial image (a) shows hyperintense signal involving corona radiata and periventricular white matter on right side. Diffusion-weighted images (b and c) show restriction (with low apparent diffusion coefficient (ADC) values, not shown) in the above-mentioned areas and posterior limb of internal capsule and subcortical white matter in the frontal and parietal lobes. These features are suggestive of an acute infarct in the right middle cerebral artery (MCA) territory. T1-weighted images after administration of contrast (d) show no significant enhancement. SWI images (e and f) show prominence of transmedullary (white arrow) and cortical veins in the right cerebral hemisphere, suggesting increased oxygen extraction fraction

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Evaluation of a patient with chronic arterial occlusion

Chronic cerebral hypoperfusion due to arterial occlusion can lead to the activation of various physiologic autoregulatory mechanisms such as dilatation of the cerebral arterioles. When the maximum autoregulation is inadequate to meet the oxygen demands, there is increase in the oxygen extraction fraction (misery perfusion). [17],[18] Hemodynamic status of cerebral circulation in vivo can be indirectly assessed using many imaging techniques, like PET, [19] MR perfusion and blood oxygen level dependent (BOLD) Functional magnetic resonance imaging (FMRI). [20] The contrast mechanism in SWI is primarily associated with the magnetic susceptibility difference between oxygenated and deoxygenated hemoglobin, leading to a phase difference between regions containing deoxygenated blood and surrounding tissues. SWI BOLD cerebrovascular reactivity studies are also based on the paramagnetic effects of deoxyhemoglobin. [21] We have described the presence of asymmetric, numerous, and large vessels over the ipsilateral cerebral hemisphere in patients with carotid occlusion but not in those with carotid stenosis. [21] The increased susceptibility arising out of elevated deoxyhemoglobin-to-oxyhemoglobin ratio leads to visualization of prominent veins over the affected cerebral hemisphere on SWI. [21]

Visualization of hyperintensities on T1-weighted magnetic resonance imaging (MRI) in the setting of brain ischemia is usually considered to indicate hemorrhagic transformation. Such changes can also be seen due to "incomplete infarction" with selective neuronal loss. SWI can differentiate hemorrhagic infarct from a non-hemorrhagic "incomplete infarct." [22] Another cause of hyperintensity in the T1-weighted image along the cortex is cortical laminar necrosis (CLN). This can occur as an end result of hypoxia or infarction. The pathophysiology behind CLN can be better understood using SWI. CLN due to hypoxic ischemic encephalopathy displays linear gyral hypointensities and basal ganglia hypointensities that are identifiable in SWI and may represent mineralization due to iron transport across the surviving neurons from the basal ganglia to the cortex. These findings are not usually seen in cortex that has undergone complete infarction. [23]


 » Cerebral Venous Sinus Thrombosis Top


Cerebral venous sinus thrombosis (CVST) is often a devastating pathology with nonspecific presenting features that are difficult to diagnose unless the clinical suspicion is high. [25] SWI is useful in evaluating CVST by demonstrating secondary phenomena like venous stasis in the form of engorged cortical and transmedullary veins and collateral slow flow. [25] Venous hypertension can be detected at an early stage of CVST before infarction or hemorrhage occurs. [24] These findings help to draw attention to the correct diagnosis even if primary findings like the 'empty delta sign' and 'cord sign' are missed. SWI also plays an important role in the follow-up imaging of these patients. With successful treatment, there is reduction in the prominence of the cortical and transmedullary veins [26] [Figure 2]. In addition, SWI phase image can also be useful to diagnose venous thrombosis based on the phase changes, as described in our recent case report. [27]
Figure 2 : Venous sinus thrombosis: T1-weighted axial image (a) shows a hyperintense area in the left temporal lobe. SWI images (b and c) confirm the presence of hemorrhage and also show prominence of the cortical and transmedullary veins bilaterally. Contrast-enhanced MR venogram (d and e) shows filling defects in the superior sagittal and right transverse sinus. Follow-up scan after 3 months of anticoagulation therapy shows resolution of the hematoma on T1-weighted axial image (f). The cortical and transmedullary veins are less prominent on SWI (g and h). There is significant improvement in the filling of the sinuses on contrast-enhanced MR venogram (i and j)

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 » Vascular Malformations Top


While high-flow vascular malformations are well visualized on conventional MR sequences as flow voids, low-flow vascular malformations may be missed on these sequences. [28] Even without administration of contrast agent, SWI can visualize abnormal deep venous structures with a high contrast ratio and unparalleled detail, showing extensive abnormalities not reported by other imaging techniques [24],[29] [Figure 3]. The phase image of SWI helps identify vascular structures that are not seen on conventional imaging. The magnitude images of the SWI help in differentiating different components of arteriovenous malformations (AVMs) and also in differentiating nidus from hemorrhage and calcification. [30] The magnitude image of SWI can also be used to quantify the arteriovenous shunt component of vascular malformations. The authors have noted that with a high-flow fistula, there is decreased deoxyhemoglobin in the veins; thus they have bright signal. SWI is also superior to time-of-flight MR angiogram in delineating the venous drainage patterns and small AVMs that may be difficult to diagnose by other MR methods. [13] Cavernomas are angiographically occult malformations that present with seizures or focal neurological deficits due to hemorrhage. Familial cavernomas are more prone to bleeding and to having multiplicity. [31] SWI has been found to be more accurate than T2*GRE imaging in detecting cavernomas. [5],[32]
Figure 3 : Developmental venous anomaly: SWI (a) shows the converging cortical veins draining into enlarged transmedullary veins (black arrows) at the frontal and occipital horns of left lateral ventricle. These are hardly appreciated on the contrast-enhanced T1-weighted axial image (b)

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While contrast-enhanced MRI demonstrates cortical atrophy, leptomeningeal angiomatosis and enlarged choroid plexus in patients with  Sturge- Weber syndrome More Details More Details (SWS), it is relatively insensitive to the presence of calcification. SWI is superior to contrast-enhanced MRI in demonstrating the abnormal transmedullary draining veins and gyriform calcification. [33] In addition, SWI may also play a role in functional imaging of patients having SWS with stasis and anoxia who present with reversible neurological deficits and stroke-like symptoms. [34]

Dural AV fistulas (DAVFs) are abnormal connections between the arteries and dural sinuses or adjacent veins, which may be congenital or due to chronic venous sinus thrombosis. On conventional imaging, multiple flow voids are seen near the venous sinuses. [35] However, they may not always be visualized. In these cases, due to the associated venous hypertension and increased oxygen extraction fraction from functional obstruction of venous drainage, there is prominence of the transmedullary and cortical veins, which can suggest the diagnosis that may otherwise be missed. [36] Another finding of DAVFs on SWI is, abnormally increased signal intensity in the venous structures due to high flow and rapid shunting of oxygenated blood. [13]


 » Vasculopathy Top


Vasculopathies are pathological conditions affecting the walls of the intracranial arteries. Many of these disorders are associated with cerebral microbleeds. Cerebral microbleeds are visualized as hypointense foci less than 5 mm in maximum diameter. The presence of these microbleeds along with white matter signal-intensity changes helps reach the imaging diagnosis. One of the most common causes for cerebral microbleeds is chronic hypertension. Many of these patients have small-vessel arteriosclerotic disease (Binswanger's disease). The microbleeds in these patients are located predominantly in the periventricular region, deep gray matter (putamen and thalamus) and in the brainstem [7],[37],[38] [Figure 4]. Patients with amyloid angiopathy have multiple lobar hemorrhages predominantly in frontal, parietal and temporal lobes. Brainstem, basal ganglia and cerebellum are only rarely involved. Patients with cerebral autosomal dominant arteriopathy, subacute infarcts, and leukoencephalopathy (CADASIL) may show microbleeds along with typical white matter involvement of temporal lobes and external capsule.
Figure 4 : Hypertensive microbleeds: FLAIR axial image (a) shows hyperintense signal in the periventricular white matter and the corona radiata, suggestive of small-vessel ischemic disease. Many more lesions (microbleeds) are visualized on SWI (b) which are not seen on FLAIR

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Patients with vasculitis have inflammatory stenoses of cerebral blood vessels. This group of vasculopathies is an important cause of cerebral ischemia in younger patients. The inflammation could be due to infective causes such as infective endocarditis. Granulomatous infection of the vessel wall can be secondary to fungal or tuberculous infection. Kuker, in a recent review article, has described various other causes for inflammatory vasculitis. [39] Cerebral microbleeds can be detected in the SWI images of many of these patients. Though the T2 hyperintensities of these patients decrease or disappear on steroid treatment, the microbleeds in SWI remain [Figure 5].
Figure 5 : Vasculitis: FLAIR axial images (a and b) show hyperintense signal involving corona radiata, external capsule bilaterally and right frontal subcortical white matter. SWI (c) shows multiple foci of blooming, suggestive of hemorrhage. Contrast-enhanced T1-weighted axial image (d) shows patchy enhancement. After treatment with steroids, follow-up imaging, FLAIR and post-contrast images show an almost complete disappearance of white matter hyperintensities and enhancement (e and f). Patient showed significant clinical improvement

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 » Conclusion Top


This article briefly outlines the usefulness of SWI in the diagnostic evaluation of various vascular diseases of the brain. The role of this technique in acute stroke is being increasingly recognized. This sequence has contributed to our understanding of the pathophysiology of some of the vascular diseases of the brain. It has also evolved as a noninvasive technique for evaluating various anomalies of the venous system without administering contrast. Because of the potential of SWI to provide additional information, we have included it in our routine brain-imaging protocol.

 
 » References Top

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

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Online since 20th March '04
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