DOI: 10.1148/rg.26si055174
RadioGraphics 2006;26:S19-S41
© RSNA, 2006
Imaging of Cerebral Venous Thrombosis: Current Techniques, Spectrum of Findings, and Diagnostic Pitfalls1
James L. Leach, MD,
Robert B. Fortuna, MD,
Blaise V. Jones, MD and
Mary F. Gaskill-Shipley, MD
1 From the Department of Radiology, University of Cincinnati College of Medicine, 234 Goodman St, Cincinnati, OH 45246 (J.L.L., R.B.F., M.F.G.S.); the Neuroscience Institute, Cincinnati, Ohio (J.L.L., M.F.G.S.); and Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio (B.V.J.). Recipient of a Cum Laude award for an education exhibit at the 2004 RSNA Annual Meeting. Received September 19, 2005; revision requested January 13, 2006 and received February 17; accepted April 6. All authors have no financial relationships to disclose.
Address correspondence to J.L.L. (e-mail: james.leach{at}uc.edu).
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Abstract
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Cerebral venous thrombosis is a relatively uncommon but serious neurologic disorder that is potentially reversible with prompt diagnosis and appropriate medical care. Because the possible causal factors and clinical manifestations of this disorder are many and varied, imaging plays a primary role in the diagnosis. Magnetic resonance (MR) imaging, un-enhanced computed tomography (CT), unenhanced time-of-flight MR venography, and contrast material–enhanced MR venography and CT venography are particularly useful techniques for detecting cerebral venous and brain parenchymal changes that may be related to thrombosis. To achieve an accurate diagnosis, it is important to have a detailed knowledge of the normal venous anatomy and variants, the spectrum of findings (venous sinus thrombi and recanalization, parenchymal diffusion or perfusion changes or hemorrhage), other potentially relevant conditions (deep venous occlusion, isolated cortical venous thrombosis, idiopathic intracranial hypertension), and potential pitfalls in image interpretation.
© RSNA, 2006
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LEARNING OBJECTIVES FOR TEST 2
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After reading this article and taking the test, the reader will be able to:- Identify the anatomic components of the cerebral venous system.
- Describe the CT and MR imaging features of cerebral venous thrombosis.
- Recognize the pitfalls in image interpretation that may hinder accurate diagnosis.
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Introduction
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Cerebral venous thrombosis is a relatively uncommon disorder, with an estimated annual incidence of between two and seven cases per million in the general population (1). The incidence likely was underestimated before the advent of accurate noninvasive imaging methods. It is estimated that five to eight cases may be seen per year at a typical tertiary-care referral center (2). Accurate and prompt diagnosis of cerebral venous thrombosis is crucial, because timely and appropriate therapy can reverse the disease process and significantly reduce the risk of acute complications and long-term sequelae. Since the possible causal factors and clinical manifestations of thrombosis are many and varied, imaging plays a primary role in the diagnosis. A wide range of cross-sectional imaging methods and venographic techniques may be used to detect abnormalities in the brain parenchyma as well as the cerebral veins and venous sinuses. This article provides a survey of common findings in cerebral venous thrombosis and in several other disorders that may include a venous thrombotic process as a component. To provide a context for the discussion of abnormal findings, the normal venous anatomy and variants also are reviewed, and potential pitfalls related to image interpretation are described.
Causal Factors
More than 100 causes of venous thrombosis have been described in the literature (1). Causal factors may be classified as local (related to intrinsic or mechanical conditions of the cerebral veins and dural sinuses) or systemic (related to clinical conditions that promote thrombosis). Local processes that alter the venous flow (eg, sinus trauma, regional infection such as that in mastoiditis, and neoplastic invasion or compression) may potentiate the development of thrombosis. Systemic causes include protein S and protein C deficiencies, a peripartum state, oral contraceptive use, and hypercoagulable states secondary to malignancy. In as many as 25% of cases, no cause is identified (1).
Clinical Manifestations
The clinical manifestations of cerebral venous thrombosis vary, depending on the extent, location, and acuity of the venous thrombotic process as well as the adequacy of venous collateral circulation (2). Generalized neurologic symptoms (eg, headache, experienced by 75%–95% of patients) and focal neurologic deficits, including seizure, may result. Focal neurologic symptoms are more often seen in patients with parenchymal changes observed at imaging than in those without such changes. Because thrombosis and endogenous thrombolysis and recanalization may occur concurrently, the clinical manifestations may fluctuate in as many as 70% of patients, adding to clinical uncertainty (2). 
Intracranial hypertension occurs in 20%–40% of patients with cerebral venous thrombosis and should be excluded in patients with the specific complex of symptoms (2).
Anatomic Distribution
A review of the magnetic resonance (MR) imaging literature published in 1995–2004 (3–14) enables a general description of the anatomic distribution of thrombosed cerebral venous structures identified primarily at MR imaging (Table 1). Multiple locations of thrombosis, particularly in the contiguous transverse and sigmoid sinuses, are found in as many as 90% of patients (11). Cortical venous involvement is seen in 6% of patients but is likely to be underreported when the dominant imaging finding is dural sinus involvement.
Pathophysiology
The pathophysiology of brain parenchymal involvement in venous occlusion differs from that in arterial occlusion. Parenchymal changes may be secondary to cytotoxic edema, vasogenic edema, or intracranial hemorrhage. The primary underlying mechanism is likely to be increased venous pressure. If collateral pathways of venous drainage are insufficient, especially in the presence of cortical venous involvement, subsequent parenchymal changes may occur. If venous pressure continues to increase, with a consequent diminishment in arterial perfusion pressure, cell death may ensue. If adequate collateral pathways develop or recanalization occurs before cell death or intracranial hemorrhage, the parenchymal changes may resolve partly or completely. Vasogenic and cytotoxic edema patterns may coexist (15–17).
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Imaging Techniques and Findings
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Normal Venous Anatomy
The intracranial venous system may exhibit a wide range of normal variations. The use of high-spatial-resolution noninvasive venographic methods at contrast material–enhanced MR imaging and computed tomography (CT) allows the visualization of a greater number of venous structures than is possible with cross-sectional (parenchymal) imaging. Greater familiarity with the details of venous anatomy and broader knowledge of anatomic variations are important for accurate interpretation of venographic images (18). The images in this section of the article were obtained with a previously described contrast-enhanced MR venographic technique (19).
According to traditional descriptions, the cerebral venous system consists of the deep venous system, superficial venous system, and dural venous sinuses (with their superior and inferior components) (18). The dural venous sinuses are enclosed in the leaves of the dura and serve as the major drainage pathway of the cerebral veins (Fig 1). The superficial veins of the cerebrum empty into the dural sinuses and are variable in morphologic structure and location. Superiorly draining (ascending) superficial veins are named for the area of cortex that they drain (20). Inferiorly draining (descending) superficial veins include the Labbé vein and the sylvian (superficial middle cerebral) veins (Fig 2). Although the venous drainage territories of the superficial cerebral veins are variable, general drainage areas can be identified (21) (Fig 3).
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Figure 1. MIP image from contrast-enhanced MR venography, with a color overlay, demonstrates the superior dural sinuses. They include the superior sagittal sinus (green), inferior sagittal sinus (light blue), straight sinus (dark purple), confluence of the sinuses (orange), transverse sinuses (dark blue), and sigmoid sinuses (yellow). The internal jugular veins and bulbs (light purple) also are depicted.
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Figure 2. Lateral MIP image from contrast-enhanced MR venography, with editing of the deep veins to improve the visibility of the ascending veins that drain into the superior sagittal sinus from the lateral hemispheric cortex (the frontopolar [1], anterior frontal [2], and posterior frontal [3] veins; Trolard vein [superior anastomotic vein] [4]; and anterior parietal veins [5]) and the larger named veins on the lateral surface of the cerebrum (the superficial sylvian vein [superficial middle cerebral vein] [6], which typically drains into the sphenoparietal sinus or the cavernous sinus, and the Labbé vein [7], which drains into the transverse sinus). The relative luminal diameters of the Trolard vein, Labbé vein, and superficial sylvian veins are reciprocal.
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Figure 3. Axial MR image series with a color overlay represents the major superficial cortical venous drainage territories according to Meder et al (21). Most of the superior cerebrum (green) is drained primarily into the superior sagittal sinus, which also receives drainage from the parasagittal cortical regions at lower levels. The sylvian veins drain blood from the peri-insular region (yellow) into the basal dural sinuses. The transverse sinuses receive blood from the temporal, parietal, and occipital lobes (blue). The Labbé vein, if dominant, may drain much of this territory. Parenchymal abnormalities such as hemorrhage or edema in this territory may be indicative of thrombosis of the transverse sinus or Labbé vein.
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The deep system includes the vein of Galen, the internal cerebral veins, and their tributaries; the Rosenthal vein (basal vein) and its tributaries; and the medullary and subependymal veins, which drain the hemispheric white matter (Fig 4). The deep system drains the inferior frontal lobe; most of the deep white matter of the frontal, temporal, and parietal lobes; the corpus callosum; the upper brainstem; the basal ganglia; and the thalamus (21). The parenchymal alterations that occur with deep venous occlusion typically involve the thalami, probably because the primary venous pathways that drain the thalami extend directly into the internal cerebral veins (Fig 5). The basal dural sinuses are complex and are interconnected with the cavernous sinus complex. Multiple emissary channels in the skull base connect with the sigmoid sinus and jugular bulb. These structures are much more commonly seen at contrast-enhanced MR venography than at time-of-flight (TOF) MR venography (Fig 6).
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Figure 4. Lateral MIP image from contrast-enhanced MR venography shows the major components of the deep venous system: the thalamostriate vein (1), septal vein (2), internal cerebral vein (3), basal vein (Rosenthal vein) (4), and vein of Galen (5).
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Figure 5. Axial MR image with color overlay shows the drainage territory of the deep cerebral veins (internal cerebral vein, vein of Galen) (pink), in which parenchymal abnormalities due to deep venous occlusion typically are found. The deep white matter (medullary) venous drainage territory (blue) also is shown.
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Figure 6. Basal dural sinuses. Anteroposterior MIP image from contrast-enhanced MR venography, with the superficial and deep veins removed for better visualization, shows the cavernous sinus complex (1) and, connecting the lateral dural sinuses with the cavernous sinus, the superior petrosal sinuses (2), which arise from the junction of the transverse and sigmoid sinuses and extend along the petrous ridge, and the inferior petrosal sinuses (3), which arise from the distal portion of the sigmoid sinus or jugular bulb and extend along the clivus. Also visible are the superficial middle cerebral vein (sylvian vein) (4), which in this case extends into the cavernous sinus, and the emissary veins and occipital venous plexus complex (5).
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MR and CT Venography
Venous thrombi can be detected with direct visualization on MR and CT parenchymal images or with various venographic techniques. The most commonly used venographic techniques currently include unenhanced TOF MR venography, contrast-enhanced MR venography, and CT venography. Phase-contrast MR venography is less often used, because of its dependence on operator-defined velocity encoding parameters.
TOF MR venography is the method most commonly used for the diagnosis of cerebral venous thrombosis. Two-dimensional TOF techniques are used to evaluate the intracranial venous system because of their excellent sensitivity to slow flow and their diminished sensitivity to signal loss from saturation effects compared with the sensitivities of three-dimensional TOF techniques (22). Because two-dimensional techniques are most sensitive to flow that is perpendicular to the plane of acquisition, the coronal plane, axial and coronal planes, or an oblique plane are often used for image acquisition. Venous flow in the plane of image acquisition may produce saturation and resultant nulling of the venous signal at TOF MR venography, a potential pitfall for image interpretation and diagnosis. A close assessment of the source images is mandatory to accurately evaluate venous morphologic features and reduce the potential for diagnostic error (Fig 7).
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Figure 7a. (a, b) Lateral MR venograms show the coronal (vertical white line in a) and axial (horizontal white line in b) planes of image data acquisition used for TOF MR venography. The distal portion of the superior sagittal sinus (arrow in a), which is located in the coronal plane, is poorly depicted on coronal TOF MR venograms. The horizontal portion of the superior sagittal sinus (straight arrows in b), the junction of the vein of Galen with the straight sinus (arrowhead in b), and the portions of the transverse sinus that are located in the axial plane (curved arrow in b) are poorly depicted on axial TOF MR venograms. Poor depiction of these areas may lead to misdiagnosis of occlusion at TOF MR venography. (c) Image from contrast-enhanced MR venography provides better depiction of all the venous structures.
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Figure 7b. (a, b) Lateral MR venograms show the coronal (vertical white line in a) and axial (horizontal white line in b) planes of image data acquisition used for TOF MR venography. The distal portion of the superior sagittal sinus (arrow in a), which is located in the coronal plane, is poorly depicted on coronal TOF MR venograms. The horizontal portion of the superior sagittal sinus (straight arrows in b), the junction of the vein of Galen with the straight sinus (arrowhead in b), and the portions of the transverse sinus that are located in the axial plane (curved arrow in b) are poorly depicted on axial TOF MR venograms. Poor depiction of these areas may lead to misdiagnosis of occlusion at TOF MR venography. (c) Image from contrast-enhanced MR venography provides better depiction of all the venous structures.
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Figure 7c. (a, b) Lateral MR venograms show the coronal (vertical white line in a) and axial (horizontal white line in b) planes of image data acquisition used for TOF MR venography. The distal portion of the superior sagittal sinus (arrow in a), which is located in the coronal plane, is poorly depicted on coronal TOF MR venograms. The horizontal portion of the superior sagittal sinus (straight arrows in b), the junction of the vein of Galen with the straight sinus (arrowhead in b), and the portions of the transverse sinus that are located in the axial plane (curved arrow in b) are poorly depicted on axial TOF MR venograms. Poor depiction of these areas may lead to misdiagnosis of occlusion at TOF MR venography. (c) Image from contrast-enhanced MR venography provides better depiction of all the venous structures.
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Contrast-enhanced MR venography with elliptic centric ordering is a more recently developed venographic method in which the paramagnetic effect of intravenous gadolinium is used to shorten T1 and provide positive intravascular contrast enhancement (19). Small-vessel visualization is improved at contrast-enhanced MR venography, compared with that at TOF MR venography (19). Depiction of the dural sinuses is also superior with contrast-enhanced MR venography because of a decrease in the effects of turbulent flow on vessel contrast (Fig 7) (19).
CT venography is a rapid, readily available, and accurate technique for detecting cerebral venous thrombosis (Fig 8) (23,24). CT venography provides a highly detailed depiction of the cerebral venous system, superior to that available with conventional TOF MR venography, and has at least equivalent accuracy for the detection of cerebral venous thrombosis (23). Drawbacks of CT venography include the difficulty of reconstructing maximum intensity projection (MIP) images from the source image data sets, a process that requires the subtraction of bone adjacent to the venous sinus; it is very difficult to subtract all of the adjacent bone without also subtracting part of the sinus (25). However, source images and multiplanar reformatted images can be displayed quickly for evaluation. Investigators in a recent study advocated the use of a matched mask bone elimination technique to improve the quality of MIP images reconstructed from CT venographic data (26).
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Figure 8. Cerebral venous thrombosis in a 5-year-old girl with mastoiditis of the right ear. MIP image from CT venography with subtraction of the calvaria shows filling defects in the right transverse sinus (arrows), findings consistent with thrombosis. A persistent falcine sinus (arrowhead) was an incidental finding.
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With the continuing development of multidetector CT, the use of CT venography probably will become more widespread. However, because the technique involves the use of ionizing radiation, CT venography may have limited use in pregnant patients and children, in whom the radiation dose may be a cause for particular concern, as well as in patients with renal failure, contrast material allergy, or another contraindication to the use of iodinated contrast material. To our knowledge, the comparative accuracies of CT venography, MR imaging, and contrast-enhanced MR venography have not yet been assessed.
Venous Sinus Abnormalities
Thrombosis.—
The classic finding of sinus thrombosis on unenhanced CT images is a hyperattenuating thrombus in the occluded sinus (Fig 9). However, variability in the degree of thrombus attenuation makes this sign insensitive; hyperattenuation is present in only 25% of sinus thrombosis cases (27). Increased attenuation in the venous sinuses also may be seen in patients with dehydration, an elevated hematocrit level, or a subjacent subarachnoid or subdural hemorrhage. In most cases, a close comparison of sinus attenuation with arterial attenuation can help differentiate between a physiologic increase in sinus attenuation and increased attenuation due to thrombosis. Increased attenuation in the sinus may be the only finding suggestive of sinus thrombosis on unenhanced CT images, and patients with this sign should be further evaluated with contrast-enhanced CT, MR imaging, or both, in the proper clinical scenario.
A well-described finding of sinus thrombosis at contrast-enhanced imaging is the empty delta sign, a central intraluminal filling defect that represents a thrombus surrounded by contrast-enhanced dural collateral venous channels and cavernous spaces within the dural envelope (Fig 10) (27,28). The filling defect is typically seen on multiple sections in contrast-enhanced CT and MR imaging studies. Initial reports described the appearance of the empty delta sign on CT images in 29% of patients with sinus thrombosis detected at contrast-enhanced CT (27). On thin-section helical CT images and volumetric MR images, the empty delta sign could be expected to appear in an even higher percentage of cases.
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Figure 10a. (a) Contrast-enhanced CT image in a patient with superior sagittal sinus thrombosis shows a central filling defect in the superior sagittal sinus (arrow), surrounded by intensely enhanced dura mater. (b) Coronal reformatted image from contrast-enhanced MR venography in another patient shows a nonenhanced thrombus (arrows) surrounded by enhanced sinus walls and dural cavernous spaces. The thrombus extends from the superior sagittal sinus through the sinus confluence and into the right transverse sinus.
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Figure 10b. (a) Contrast-enhanced CT image in a patient with superior sagittal sinus thrombosis shows a central filling defect in the superior sagittal sinus (arrow), surrounded by intensely enhanced dura mater. (b) Coronal reformatted image from contrast-enhanced MR venography in another patient shows a nonenhanced thrombus (arrows) surrounded by enhanced sinus walls and dural cavernous spaces. The thrombus extends from the superior sagittal sinus through the sinus confluence and into the right transverse sinus.
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Unenhanced MR imaging is more sensitive for the detection of venous thrombi than is unenhanced CT. The absence of a flow void and the presence of altered signal intensity in the sinus is a primary finding of sinus thrombosis on MR images. Slow or turbulent flow also may cause a signal intensity alteration in the sinus. A close assessment with multiple pulse sequences should be made. In addition, the administration of contrast material and the application of venographic techniques often are necessary for confident diagnosis.
The signal intensity of venous thrombi on T1- and T2-weighted MR images varies according to the interval between the onset of thrombus formation and the time of imaging (Table 2) (3,9,10,29–32). The change in signal intensity is thought to be related to the paramagnetic effects of the products of hemoglobin breakdown in the thrombus (31,32).
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Table 2. Predominant Signal Intensity in Intraluminal Thrombi according to MR Imaging Technique and Time after Symptom Onset
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In the acute stage of thrombus formation (0–5 days), the signal is predominantly isointense on T1-weighted images and hypointense on T2-weighted images because of deoxyhemoglobin in red blood cells trapped in the thrombus (Fig 11). A venous thrombus in the acute stage may have a signal intensity that mimics a normal flow state, and such a finding may lead to diagnostic error (33). The signal may be very hypointense on T2-weighted images and may be mistakenly thought to indicate a flow void. According to some estimates, in 10%–30% of cases of sinus thrombosis, the thrombus at initial presentation or imaging examination is in the acute stage of formation (3,33,34). Contrast-enhanced MR venography or CT venography is usually necessary to achieve a definitive diagnosis at this stage.
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Figure 11a. Acute thrombus in a 35-year-old woman with a severe headache for 5 days. (a, b) Axial T2-weighted MR image (a) and axial T1-weighted MR image (b) show a thrombus in the left sigmoid sinus (arrows). The signal in the thrombus, compared with that in the normal brain parenchyma, is hypointense in a and iso- to hyperintense in b. (c) Frontal MIP image from coronal TOF MR venography shows a lack of flow in the distal portion of the left transverse sinus and the sigmoid sinus (arrows).
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Figure 11b. Acute thrombus in a 35-year-old woman with a severe headache for 5 days. (a, b) Axial T2-weighted MR image (a) and axial T1-weighted MR image (b) show a thrombus in the left sigmoid sinus (arrows). The signal in the thrombus, compared with that in the normal brain parenchyma, is hypointense in a and iso- to hyperintense in b. (c) Frontal MIP image from coronal TOF MR venography shows a lack of flow in the distal portion of the left transverse sinus and the sigmoid sinus (arrows).
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Figure 11c. Acute thrombus in a 35-year-old woman with a severe headache for 5 days. (a, b) Axial T2-weighted MR image (a) and axial T1-weighted MR image (b) show a thrombus in the left sigmoid sinus (arrows). The signal in the thrombus, compared with that in the normal brain parenchyma, is hypointense in a and iso- to hyperintense in b. (c) Frontal MIP image from coronal TOF MR venography shows a lack of flow in the distal portion of the left transverse sinus and the sigmoid sinus (arrows).
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In the subacute stage of thrombus development (6–15 days), the signal is predominantly hyperintense on both T1-weighted images and T2-weighted images because of methemoglobin in the thrombus (Fig 12) (30,32). Subacute-stage thrombus has been found in 55% of patients at clinical presentation with cerebral venous thrombosis (3,34). This stage of formation is the easiest stage at which to detect a thrombus on MR images, as the signal intensity of the sinus is most different from that in normal flow states. The finding of increased signal intensity on both T1-weighted images and T2-weighted images is almost always abnormal.
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Figure 12a. Subacute thrombus of the superior sagittal sinus. (a, b) Axial T1-weighted (a) and axial T2-weighted (b) MR images show an area of abnormal increased signal intensity in the superior sagittal sinus (arrow). (c) Sagittal source image from contrast-enhanced MR venography shows filling defects (arrows) due to a thrombus.
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Figure 12b. Subacute thrombus of the superior sagittal sinus. (a, b) Axial T1-weighted (a) and axial T2-weighted (b) MR images show an area of abnormal increased signal intensity in the superior sagittal sinus (arrow). (c) Sagittal source image from contrast-enhanced MR venography shows filling defects (arrows) due to a thrombus.
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Figure 12c. Subacute thrombus of the superior sagittal sinus. (a, b) Axial T1-weighted (a) and axial T2-weighted (b) MR images show an area of abnormal increased signal intensity in the superior sagittal sinus (arrow). (c) Sagittal source image from contrast-enhanced MR venography shows filling defects (arrows) due to a thrombus.
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Chronic thrombosis with incomplete recanalization of the sinus may present a diagnostic challenge at MR imaging (Fig 13). As many as 15% of patients in whom sinus thrombosis is diagnosed at MR imaging may have a chronic (>15-day-old) thrombus (3,34). Compared with the MR signal in normal brain parenchyma, the signal in a chronic thrombus is typically isointense or hyperintense on T2-weighted images and isointense on T1-weighted images; however, significant variability in thrombus signal intensity exists (3,9,10,29,30). The signal intensity may be similar to that of very slowly moving oxygenated blood.
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Figure 13a. Chronic thrombosis of the left transverse and sigmoid sinuses in a 69-year-old man with a chronic headache. (a, b) Axial unenhanced (a) and contrast-enhanced (b) T1-weighted images show an area of the left transverse sinus (arrow) that has isointense signal on a and intensely increased signal on b. The marked contrast enhancement in this case could easily be confused with a normal state of slow flow, which commonly occurs in the left transverse sinus. Venographic techniques therefore were necessary to evaluate sinus patency. (c) Oblique MIP image from coronal TOF MR venography shows an absence of signal in the left transverse sinus, left sigmoid sinus, and left internal jugular vein (arrows) but normal flow in the right transverse sinus, right sigmoid sinus, and right internal jugular vein (arrowheads). (d) Sagittal source image from contrast-enhanced MR venography shows multiple filling defects (arrows) in the recanalized vessels.
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Figure 13b. Chronic thrombosis of the left transverse and sigmoid sinuses in a 69-year-old man with a chronic headache. (a, b) Axial unenhanced (a) and contrast-enhanced (b) T1-weighted images show an area of the left transverse sinus (arrow) that has isointense signal on a and intensely increased signal on b. The marked contrast enhancement in this case could easily be confused with a normal state of slow flow, which commonly occurs in the left transverse sinus. Venographic techniques therefore were necessary to evaluate sinus patency. (c) Oblique MIP image from coronal TOF MR venography shows an absence of signal in the left transverse sinus, left sigmoid sinus, and left internal jugular vein (arrows) but normal flow in the right transverse sinus, right sigmoid sinus, and right internal jugular vein (arrowheads). (d) Sagittal source image from contrast-enhanced MR venography shows multiple filling defects (arrows) in the recanalized vessels.
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Figure 13c. Chronic thrombosis of the left transverse and sigmoid sinuses in a 69-year-old man with a chronic headache. (a, b) Axial unenhanced (a) and contrast-enhanced (b) T1-weighted images show an area of the left transverse sinus (arrow) that has isointense signal on a and intensely increased signal on b. The marked contrast enhancement in this case could easily be confused with a normal state of slow flow, which commonly occurs in the left transverse sinus. Venographic techniques therefore were necessary to evaluate sinus patency. (c) Oblique MIP image from coronal TOF MR venography shows an absence of signal in the left transverse sinus, left sigmoid sinus, and left internal jugular vein (arrows) but normal flow in the right transverse sinus, right sigmoid sinus, and right internal jugular vein (arrowheads). (d) Sagittal source image from contrast-enhanced MR venography shows multiple filling defects (arrows) in the recanalized vessels.
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Figure 13d. Chronic thrombosis of the left transverse and sigmoid sinuses in a 69-year-old man with a chronic headache. (a, b) Axial unenhanced (a) and contrast-enhanced (b) T1-weighted images show an area of the left transverse sinus (arrow) that has isointense signal on a and intensely increased signal on b. The marked contrast enhancement in this case could easily be confused with a normal state of slow flow, which commonly occurs in the left transverse sinus. Venographic techniques therefore were necessary to evaluate sinus patency. (c) Oblique MIP image from coronal TOF MR venography shows an absence of signal in the left transverse sinus, left sigmoid sinus, and left internal jugular vein (arrows) but normal flow in the right transverse sinus, right sigmoid sinus, and right internal jugular vein (arrowheads). (d) Sagittal source image from contrast-enhanced MR venography shows multiple filling defects (arrows) in the recanalized vessels.
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On images acquired after gadolinium administration, marked contrast enhancement may be observed that resembles the enhancement typically seen in a normal sinus (35). Sinus enhancement is presumably secondary to an organized thrombus with intrinsic vascularization (35) as well as to slow flow in dural and intrathrombus collateral channels. Contrast enhancement of the sinus on MR images does not definitively indicate patency, and venography usually is necessary for a definitive diagnosis. Although the findings on images obtained with contrast-enhanced venographic techniques reportedly have been misleading in cases of chronic sinus thrombosis (35), in our experience chronic thrombosis has been well depicted and correctly diagnosed with contrast-enhanced MR venography with elliptic centric ordering. Recanalized vessels and filling defects that represent a nonrecanalized and nonvascularized thrombus are particularly well depicted on source images (Fig 13d). However, if image acquisition is delayed at contrast-enhanced MR venography, thrombus enhancement may increase to a level that simulates patency of the sinus (19).
As gradient-recalled echo (GRE) sequences are increasingly used in MR imaging protocols to detect the presence of blood breakdown products, their usefulness in depicting intraluminal thrombi in cerebral venous thrombosis has been appreciated (29). In stages of thrombus evolution in which paramagnetic products such as deoxyhemoglobin and methemoglobin are present, the sensitivity of GRE sequences to magnetic susceptibility produces blooming artifacts in the thrombosed venous segments on GRE images (Fig 14). GRE imaging sequences may be an important diagnostic aid in acute-stage thrombosis, when the signal intensities on T1- and T2-weighted images may be more subtle (24).
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Figure 14a. Magnetic susceptibility effects on MR images in a 27-year-old postpartum woman with a severe headache for 6 days. (a) T1-weighted spin-echo image shows an area of isointense signal (arrowheads) indicative of a thrombus in the right transverse sinus. (b) GRE image shows significantly diminished signal intensity and apparent enlargement of the sinus in the same area (arrows). No flow was demonstrated at TOF MR venography.
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Figure 14b. Magnetic susceptibility effects on MR images in a 27-year-old postpartum woman with a severe headache for 6 days. (a) T1-weighted spin-echo image shows an area of isointense signal (arrowheads) indicative of a thrombus in the right transverse sinus. (b) GRE image shows significantly diminished signal intensity and apparent enlargement of the sinus in the same area (arrows). No flow was demonstrated at TOF MR venography.
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There has been recent interest in evaluating the appearance of intraluminal venous thrombi on diffusion-weighted images (3). Signal hyperintensity in thrombosed sinuses on diffusion-weighted images, with corresponding diminishment in the mean apparent diffusion coefficient (ADC) values, has been described in 41% of patients with sinus thrombosis (3). The duration of clinical symptoms was longer and complete recanalization was less frequent in patients with restricted diffusion in the thrombus (3).
Recanalization.—
An irregular appearance of the sinus, with multiple intrasinus channels and dural collateral vessels, may be seen on MR venographic images and is characteristic of incomplete recanalization (Fig 15) (28). Complete recanalization may occur more often in thrombosis of the superior sagittal sinus and straight sinus than in thrombosis of the transverse and sigmoid sinuses after anticoagulation therapy (4). In patients who undergo anticoagulation therapy for sinus thrombosis, progression of recanalization is not typical after 4 months of therapy (4). Complete recanalization is not necessary for clinical recovery, and the extent of recanalization may not correlate closely with the clinical outcome (5).
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Figure 15. Oblique MIP image from TOF MR venography in a patient with a history of extensive thrombosis of the superior sagittal sinus and left transverse sinus 2 years before. Note the irregular appearance of the superior sagittal sinus (arrows), which corresponds to incomplete recanalization of the sinus. The source images showed residual intrasinus defects, intra-sinus channels, and dural collateral channels.
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Numerous venous collateral pathways may form after sinus thrombosis (Fig 16). Collateral vessels may form in the dura that surrounds the occluded sinus, arising from cortical veins that drain to nonthrombosed sinuses or from intermediate veins (ie, diploic, emissary, meningeal). The intermediate veins may form a dominant collateral system in the presence of extensive thrombosis (27).
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Figure 16. Frontal MIP image from axial TOF MR venography in a patient with prior extensive thrombosis and variable recanalization of the superior sagittal sinus, straight sinus, and both transverse sinuses. Veins of the face and scalp were subtracted for better visualization of the irregular cortical venous collateral vessels (arrows), which drain primarily to the superficial middle cerebral veins and to the sphenoparietal, cavernous, and inferior petrosal sinuses. Tentorial collateral vessels also are visible (arrowhead).
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Parenchymal Abnormalities
Focal brain abnormalities have been identified in as many as 57% of patients with cerebral venous thrombosis (Table 3). Parenchymal lesions are better depicted and more commonly identified at MR imaging than at CT (17,30). Focal edema (without visible hemorrhage) is visible on CT images in approximately 8% of cases and on MR images in 25% of cases (6–9,13,14,17,27,32, 34,36) (Fig 17). Diffusion-weighted MR imaging techniques allow subclassification of parenchymal abnormalities as either primarily vasogenic edema (with increased ADC values presumably related to venous congestion) or primarily cytotoxic edema (with decreased ADC values related to cellular energy disruption). Hemorrhage may occur with both types of edema, and various patterns may coexist in the same region (7,8). In view of the variable nature of the parenchymal abnormalities that may occur in cerebral venous thrombosis, the use of the term venous infarct in reference to these lesions should be discouraged because that term implies irreversibility. In contrast with arterial ischemic states, many parenchymal abnormalities secondary to venous occlusion are reversible.
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Figure 17a. Parenchymal edema. Axial T2-weighted images obtained at the initial presentation (a) and 2 months later, after anticoagulation therapy (b), in a patient with segmental thrombosis of the superior sagittal sinus at MR venography. In a, note the focal signal abnormality in the right frontal lobe; the extensive signal abnormality in the white matter extending along the subcortex, consistent with vasogenic edema (arrows); and the high-signal-intensity thrombus in the anterior part of the superior sagittal sinus (arrowhead). In b, only a small zone of encephalomalacia remains, and the white matter edema has resolved. A small zone of hypointense T2 signal (arrowhead in b) consistent with hemorrhage also is visible.
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Figure 17b. Parenchymal edema. Axial T2-weighted images obtained at the initial presentation (a) and 2 months later, after anticoagulation therapy (b), in a patient with segmental thrombosis of the superior sagittal sinus at MR venography. In a, note the focal signal abnormality in the right frontal lobe; the extensive signal abnormality in the white matter extending along the subcortex, consistent with vasogenic edema (arrows); and the high-signal-intensity thrombus in the anterior part of the superior sagittal sinus (arrowhead). In b, only a small zone of encephalomalacia remains, and the white matter edema has resolved. A small zone of hypointense T2 signal (arrowhead in b) consistent with hemorrhage also is visible.
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Although parenchymal changes may occur in areas of the brain that are directly drained by the occluded venous sinus, in some patients the parenchymal changes may not closely correlate with the location of venous occlusion (6,9).
Parenchymal swelling without abnormalities in attenuation or signal intensity on images may occur in as many as 42% of patients with cerebral venous thrombosis (17). Sulcal effacement, diminished cistern visibility, and a reduction in ventricular size may occur. Patients with brain swelling and without parenchymal signal intensity changes tend to have intrasinus pressures in the intermediate range (20–25 mm Hg); however, intrasinus pressures also may be markedly elevated (6). Such patients typically have more prominent clinical symptoms than would be expected on the basis of imaging findings (6).
Diffusion Change.—
Although diffusion-weighted imaging may provide important information in the evaluation of patients with cerebral venous thrombosis, research involving the use of diffusion-weighted imaging to assess cerebral venous thrombosis has been limited. In approximately half of all patients who have lesions with increased T2 signal intensity associated with cerebral venous thrombosis (excluding those with hemorrhage), diffusion-weighted images show regions with diminished ADC values (Fig 18) (7,37,38). Information from diffusion-weighted imaging in these patients is consistent with edema related to combined vasogenic and cytotoxic processes. Patients with diminished ADC values more often have parenchymal sequelae, while those with normal or increased ADC values usually do not (7,37,38). Areas without diminishment in ADC may primarily represent vasogenic edema from venous hypertension. Complete or nearly complete resolution of edema in patients with cerebral venous thrombosis and diminished ADC values also has been reported (38).
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Figure 18a. Superior sagittal sinus thrombosis and parenchymal changes in the right parietal lobe. (a, b) Diffusion-weighted image (a) and T2-weighted image (b) obtained at presentation show an area of increased signal intensity consistent with diffusion restriction along the cortex of the right parietal lobe (arrow in a) and corresponding T2 signal abnormality (arrowheads in b). Also visible is a high-signal-intensity thrombus in the superior sagittal sinus (arrow in b). (c) T2-weighted image obtained 7 months later shows minimal atrophy in the zone of previous diffusion restriction (arrowhead) and resolution of the thrombus (arrow).
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Figure 18b. Superior sagittal sinus thrombosis and parenchymal changes in the right parietal lobe. (a, b) Diffusion-weighted image (a) and T2-weighted image (b) obtained at presentation show an area of increased signal intensity consistent with diffusion restriction along the cortex of the right parietal lobe (arrow in a) and corresponding T2 signal abnormality (arrowheads in b). Also visible is a high-signal-intensity thrombus in the superior sagittal sinus (arrow in b). (c) T2-weighted image obtained 7 months later shows minimal atrophy in the zone of previous diffusion restriction (arrowhead) and resolution of the thrombus (arrow).
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Figure 18c. Superior sagittal sinus thrombosis and parenchymal changes in the right parietal lobe. (a, b) Diffusion-weighted image (a) and T2-weighted image (b) obtained at presentation show an area of increased signal intensity consistent with diffusion restriction along the cortex of the right parietal lobe (arrow in a) and corresponding T2 signal abnormality (arrowheads in b). Also visible is a high-signal-intensity thrombus in the superior sagittal sinus (arrow in b). (c) T2-weighted image obtained 7 months later shows minimal atrophy in the zone of previous diffusion restriction (arrowhead) and resolution of the thrombus (arrow).
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Contrast Enhancement.—
Parenchymal enhancement in 1%–29% of cases of cerebral venous thrombosis has been reported (17,27,39). The enhancement is typically gyral in location and may extend into the white matter (Fig 19). Parenchymal enhancement, which indicates disruption of the blood-brain barrier, may be seen in areas of cytotoxic or vasogenic edema and in the presence of either irreversible or reversible brain abnormalities. Increased tentorial enhancement (likely related to dural venous collaterals), adjacent leptomeningeal enhancement, and prominent cortical venous enhancement (secondary to venous congestion) also may be visible after the administration of contrast material.
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Figure 19. Occlusion of the anterior superior sagittal sinus. Coronal contrast-enhanced T1-weighted image shows patchy areas of varied enhancement in both frontal lobes (arrows), findings that correspond to zones of diffusion restriction noted on diffusion-weighted images (not shown).
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Perfusion Changes.—
Little has been published about MR perfusion imaging in patients with cerebral venous thrombosis. In a study performed in patients with normal ADC values, the most common finding was prolongation of the mean transit time with normal relative cerebral blood volume in areas of the brain that were drained by the thrombosed sinus (40). Alterations in mean transit time were seen in areas of the brain with and without parenchymal signal intensity alterations or hemorrhage. In patients who underwent follow-up MR perfusion imaging after treatment and sinus recanalization, the perfusion abnormalities had resolved by the time of follow-up. In an additional case of deep venous occlusion, Keller et al found an increase in relative cerebral blood volume with a prolonged time to peak enhancement in the thalami; areas involved with extensive vasogenic edema; and elevated ADC measurements (41).
Perfusion changes in patients with cerebral venous thrombosis may reflect both venous congestion and diminishment of cerebral blood flow, which may be reversible before permanent brain parenchymal damage occurs (40).
MR Spectroscopic Findings.—
Little information exists regarding MR spectroscopic findings in cerebral venous thrombosis. In one patient with deep venous occlusion and extensive thalamic edema, proton MR spectroscopic findings included a very mild lactate peak with preserved N-acetylaspartate levels (42). Arterial infarction generally produces a more pronounced diminishment in neuronal metabolites and a pronounced elevation of lactate levels. Very early arterial infarction may have a similar appearance, with an elevated lactate level and variably preserved N-acetylaspartate levels (43). To our knowledge, the use of MR spectroscopy to differentiate between venous infarction and arterial infarction has not been assessed.
Hemorrhage.—
Parenchymal hemorrhage can be seen in one-third of cases of cerebral venous thrombosis (6–9,13,14,32,34,36) (Fig 20). Flame-shaped irregular zones of lobar hemorrhage in the parasagittal frontal and parietal lobes are typical findings in patients with superior sagittal sinus thrombosis and should prompt additional imaging evaluations (eg, with MR venography or CT venography). Hemorrhage in the temporal or occipital lobes is more typical of transverse sinus occlusion. Hemorrhage in cerebral venous thrombosis is typically cortical with subcortical extension. Smaller zones of isolated subcortical hemorrhage also may be seen (44) and may be accompanied by minimal edema. MR imaging with GRE sequences is sensitive in the depiction of these zones of parenchymal hemorrhage.
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Figure 20a. Axial CT images from three patients with sinus thrombosis. (a) Typical irregularly shaped right frontal lobe hemorrhage (arrows) in a patient with superior sagittal sinus thrombosis. (b) Right temporal lobe hemorrhage with extensive edema (arrow) in a patient with right transverse sinus thrombosis. (c) Small subcortical hemorrhages (arrows) in the left frontal and parietal lobes in a patient with superior sagittal sinus thrombosis.
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Figure 20b. Axial CT images from three patients with sinus thrombosis. (a) Typical irregularly shaped right frontal lobe hemorrhage (arrows) in a patient with superior sagittal sinus thrombosis. (b) Right temporal lobe hemorrhage with extensive edema (arrow) in a patient with right transverse sinus thrombosis. (c) Small subcortical hemorrhages (arrows) in the left frontal and parietal lobes in a patient with superior sagittal sinus thrombosis.
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Figure 20c. Axial CT images from three patients with sinus thrombosis. (a) Typical irregularly shaped right frontal lobe hemorrhage (arrows) in a patient with superior sagittal sinus thrombosis. (b) Right temporal lobe hemorrhage with extensive edema (arrow) in a patient with right transverse sinus thrombosis. (c) Small subcortical hemorrhages (arrows) in the left frontal and parietal lobes in a patient with superior sagittal sinus thrombosis.
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The mechanism of hemorrhage in cerebral venous thrombosis is multifactorial. Hemorrhage may be precipitated by continued arterial perfusion in areas of cell death, as can be seen at reperfusion in arterial ischemia. Elevation of venous pressure beyond the limit of the venous wall also is likely operative. In one study, hemorrhage was noted in patients with intrasinus pressures higher than 42 mm Hg but not in those with lower pressures (6).
Deep Venous Occlusion
Thrombosis of the internal cerebral veins, vein of Galen, or straight sinus has been observed in approximately 16% of patients with cerebral venous thrombosis (3–14). Most such patients present with symptoms of elevated intracranial pressure that may rapidly escalate to a coma (45,46). The manifestations may mimic those of encephalitis. Prompt and accurate diagnosis and treatment are critical.
Thalamic edema is the imaging hallmark of this condition, and it may extend into the caudate regions and deep white matter (Fig 21).
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Figure 21a. Thrombosis of the straight sinus, vein of Galen, and internal cerebral veins. (a) Axial intermediate-weighted image shows extensive signal abnormalities within both thalami and extending into the caudate nuclei (arrows). (b) Sagittal two-dimensional phase-contrast MR venogram demonstrates a portion of the deep venous system with no signal (arrows), a finding consistent with occlusion.
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Figure 21b. Thrombosis of the straight sinus, vein of Galen, and internal cerebral veins. (a) Axial intermediate-weighted image shows extensive signal abnormalities within both thalami and extending into the caudate nuclei (arrows). (b) Sagittal two-dimensional phase-contrast MR venogram demonstrates a portion of the deep venous system with no signal (arrows), a finding consistent with occlusion.
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Thalamic edema may be seen in as 
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Abstract
LEARNING OBJECTIVES FOR TEST...
