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DOI:10.2214/AJR.07.7038
AJR 2007; 189:S76-S78
© American Roentgen Ray Society

Radiologic Diagnosis of Cerebral Venous Thrombosis: Self-Assessment Module

Colin S. Poon1,2 and Felix S. Chew3

1 Department of Diagnostic Radiology, State University of New York Upstate Medical University, Syracuse, NY.
2 Department of Diagnostic Radiology, Yale University School of Medicine, New Haven, CT.
3 Department of Radiology, University of Washington, Box 354755, 4245 Roosevelt Way NE, Seattle, WA 98105.

Received August 30, 2007; accepted after revision August 30, 2007.

 
Address correspondence to F. S. Chew (fchew{at}u.washington.edu).


Abstract
Top
Abstract
INTRODUCTION
EDUCATIONAL OBJECTIVES
REQUIRED READING (available at...
INSTRUCTIONS
References
 
The educational objectives of this self-assessment module are for the participant to exercise, self-assess, and improve his or her understanding of the radiologic diagnosis of cerebral venous thrombosis.

Keywords: brain imaging • cerebral venous thrombosis • CT • MRI • neuroradiology


INTRODUCTION
Top
Abstract
INTRODUCTION
EDUCATIONAL OBJECTIVES
REQUIRED READING (available at...
INSTRUCTIONS
References
 
This self-assessment module on the radiologic diagnosis of cerebral venous thrombosis has an educational component and a self-assessment component. The educational component consists of two required articles that the participant should read. The self-assessment component consists of six multiple-choice questions with solutions. All these materials are available via the ARRS Web site at www.arrs.org. To claim CME and SAM credit, each participant must enter his or her responses to the questions online.


EDUCATIONAL OBJECTIVES
Top
Abstract
INTRODUCTION
EDUCATIONAL OBJECTIVES
REQUIRED READING (available at...
INSTRUCTIONS
References
 
By completing this activity, the participant will:

  1. Exercise, self-assess, and improve his or her understanding of the radiologic diagnosis of cerebral venous thrombosis, accurately identify the condition, and distinguish it from other entities.
  2. Exercise, self-assess, and improve his or her ability to diagnose cerebral venous thrombosis accurately, using the optimal imaging tools to achieve this goal.


REQUIRED READING (available at www.arrs.org)
Top
Abstract
INTRODUCTION
EDUCATIONAL OBJECTIVES
REQUIRED READING (available at...
INSTRUCTIONS
References
 

  1. Poon CS, Chang JK, Swarnkar A, Johnson MH, Wasenko J. Radiologic diagnosis of cerebral venous thrombosis: pictorial review. AJR 2007; 189[suppl]:S64–S75
  2. Leach JL, Fortuna RB, Jones BV, Gaskill-Shipley MF. Imaging of cerebral venous thrombosis: current techniques, spectrum of findings, and diagnostic pitfalls. RadioGraphics 2006; 26[suppl 1]:S19–S41; discussion S42–S43


INSTRUCTIONS
Top
Abstract
INTRODUCTION
EDUCATIONAL OBJECTIVES
REQUIRED READING (available at...
INSTRUCTIONS
References
 

  1. Complete the required reading.
  2. Visit www.arrs.org and go to the left-hand menu bar under Publications/Journals/SAM articles.
  3. Using your member login, order the online SAM as directed.
  4. Follow the online instructions for entering your responses to the self-assessment questions and complete the test by answering the questions online.Go


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Solution to Question 1
Infection contributes to fewer than 10% of cerebral venous thrombosis (CVT) cases in adults [1, 2]. Option A is not the best response. CVT occurs more often in puerperium than during the pregnancy. Option B is not the best response. Although pregnancy-related CVT occurs more often in older women, aging per se is not a risk factor. Option C is not the best response. In 20–35% of cases, the cause remains unknown, so one should remain suspicious even in the absence of known risk factors [13]. Option D is the best response. The pathogenesis of CVT is complex and is poorly understood.

Solution to Question 2
Common presentations include headache, focal neurologic deficits, seizures, and altered consciousness. Options A, B, and D are not the best responses. A syndrome of intracranial hypertension (headache and papilledema) accounts for 40% of cases in a series, so CVT needs to be excluded in patients considered for the diagnosis of benign intracranial hypertension [1]. Although subdural hemorrhage has not been associated with CVT, cases of subarachnoid hemorrhage as a rare presentation of CVT have been reported [1, 4]. Option C is the best response. There is also a wide distribution in the mode of onset of symptoms, with approximately 28% acute (< 48 hours), 42% subacute (between 48 hours and 30 days), and 30% chronic (> 30 days) presentation [1]. Option A, which is true, is not the best response. The teaching point is that CVT may present with an atypical presentation or even an absence of clinical symptoms.

Solution to Question 3
An infarction not conforming to a major arterial vascular territory, such as the presence of multiple isolated lesions, involvement of the subcortical region with sparing of the cortex, or extension over more than one arterial distribution, is highly suspicious for a venous cause. The infarction may be hemorrhagic or nonhemorrhagic. Option A is not the best response. The empty delta sign may be seen on contrast-enhanced CT and represents a filling defect (thrombus) in the dural sinus, with peripheral enhancement possibly secondary to the development of collaterals. The empty delta sign may be seen 5 days to 2 months from onset [5]. Option B is the best response. Indirect evidence of CVT may be seen as contrast enhancement of the falx and tentorium, secondary to venous stasis and hyperemia of the dura mater. This is seen in approximately 20% of cases. Option C is not the best response. The "dense clot sign" and the dense cord sign represent direct visualization of the thrombosed cortical vein or the venous sinus in short and long axes, respectively, but are seen in only one third of cases. Option D is not the best response.

Solution to Question 4
An infarction not conforming to a major arterial vascular territory strongly suggests CVT. The location of an infarction with respect to the expected course of venous drainage may provide a clue to the venous structure involved [6]. Thrombosis in the sagittal sinus often leads to impaired venous drainage and, therefore, parenchymal change in the parasagittal region. Options A and B are not the best responses. Thrombosis in Labbé's vein should lead to infarction in the temporal lobe. Option C is not the best response. Bilateral or unilateral infarction in the thalami, basal ganglia, and internal capsule is typically seen in deep venous thrombosis. Option D is the best response.

Solution to Question 5
Venous thrombus may be directly visualized on MRI [7]. On conventional MRI sequences, patent dural sinuses are often seen as flow voids; thus, the absence of signal in the dural sinuses is an indication that CVT is absent. Option C is the best response because it is not a sign of CVT. The thrombus may manifest as absence of a flow void, which is often best seen on FLAIR and T2-weighted spin-echo images. The abnormal signal intensity follows the signal characteristics of intracranial hemorrhage and may evolve through the stages of oxyhemoglobin, deoxyhemoglobin, methemoglobin, and hemosiderin [8]. On T1-weighted images, thrombus with methemoglobin is seen as hyperintensity replacing the normal flow void. Option A is not the best response. Thrombus with deoxyhemoglobin is seen as an isointense or slightly hypointense signal replacing the normal flow void. Option B is not the best response. On T2*-weighted gradient-echo images, exaggerated signal loss (very hypointense) is often seen as a result of the increased susceptibility effect of deoxyhemoglobin, methemoglobin, or hemosiderin. Option D is not the best response.

Solution to Question 6
Normal hyperdense blood is commonly seen in newborns or infants and, at times, may be difficult to differentiate from true dural venous thrombosis. However, imaging features such as symmetry, homogeneity, and involvement of virtually all visualized dural venous sinuses and major venous structures would argue against true venous thrombosis. Option A is not the best response. Subarachnoid hemorrhage can be a presentation of dural venous thrombosis [4]. Therefore, cases in which subarachnoid hemorrhage is found should be carefully reviewed for direct and indirect signs of underlying dural sinus thrombosis. Option B is not the best response. Arachnoid granulations (also known as pacchionian granulations) may simulate dural sinus filling defects when found in or adjacent to a venous sinus. Arachnoid granulation may show central and inhomogeneous contrast enhancement [9]. The true diagnosis is suggested by the presence of normal patent flow immediately proximal and distal to the filling defects, the continuity of the defects with the dural surface, a localized round or lobulated appearance, and central enhancement. Option C is not the best response. The cord sign represents direct visualization of a thrombosed cortical vein, seen as linear hyperdensity, and is therefore not a pitfall in diagnosis. Option D is the best response. A hypoplastic dural sinus may be misleading if interpreted in isolation [10]. The significant change in blood flow dynamics in stenotic or hypoplastic dural venous sinuses can give rise to a loss of flow signal, suggesting occlusion by thrombus. Lack of visualization of the thrombus on conventional MRI, a small jugular foramen on the ipsilateral side, and the visualization of diffuse smooth narrowing of the sinus on enhanced CT, enhanced MRI, CT venography, or MR venography should lead one to the correct diagnosis. Option E is not the best response.


References
Top
Abstract
INTRODUCTION
EDUCATIONAL OBJECTIVES
REQUIRED READING (available at...
INSTRUCTIONS
References
 

  1. Ameri A, Bousser MG. Cerebral venous thrombosis. Neurol Clin 1992; 10:87 –111[Medline]
  2. van Gijn J. Cerebral venous thrombosis: pathogenesis, presentation and prognosis. J R Soc Med 2000;93 : 230–233[Free Full Text]
  3. gBousser MG. Cerebral venous thrombosis: diagnosis and management. J Neurol 2000;247 : 252–258[CrossRef][Medline]
  4. Oppenheim C, Domigo V, Gauvrit JY, et al. Subarachnoid hemorrhage as the initial presentation of dural sinus thrombosis. AJNR 2005; 26:614 –617[Abstract/Free Full Text]
  5. Virapongse C, Cazenave C, Quisling R, Sarwar M, Hunter S. The empty delta sign: frequency and significance in 76 cases of dural sinus thrombosis. Radiology 1987;162 : 779–785[Abstract/Free Full Text]
  6. Leach JL, Fortuna RB, Jones BV, Gaskill-Shipley MF. Imaging of cerebral venous thrombosis: current techniques, spectrum of findings, and diagnostic pitfalls. RadioGraphics 2006;26 [suppl 1]:S19 –S41; discussion S42–43[Abstract/Free Full Text]
  7. Wasenko JJ, Holsapple JW, Winfield JA. Cerebral venous thrombosis. Demonstration with magnetic resonance angiography. Clin Imaging 1995; 19:153 –161[CrossRef][Medline]
  8. Zimmerman RD, Ernst RJ. Neuroimaging of cerebral venous thrombosis. Neuroimaging Clin North Am 1992;2 : 463–485
  9. Mamourian AC, Towfighi J. MR of giant arachnoid granulation: a normal variant presenting as a mass within the dural venous sinus. AJNR 1995; 16:901 –904[Abstract]
  10. Provenzale JM, Joseph GJ, Barboriak DP. Dural sinus thrombosis: findings on CT and MR imaging and diagnostic pitfalls. AJR 1998; 170:777 –783[Free Full Text]

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This Article
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