Table of Contents  
CASE REPORT
Year : 2014  |  Volume : 7  |  Issue : 2  |  Page : 218-221  

High diagnostic value of gradient echo sequence in isolated cortical vein thrombosis


Department of Radio-Diagnosis, Padmashree Dr D Y Patil Medical College, Hospital and Research Centre, Dr D Y Patil Vidyapeeth, Pimpri, Pune, India

Date of Web Publication4-Feb-2014

Correspondence Address:
Sanjay M Khaladkar
Flat No.5, plot no.8, S.No. - 26/A, Tejas Bldg., Sahawas Society, Karve Nagar, Pune 411052
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.126352

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  Abstract 

Isolated cortical vein thrombosis is quite less common than dural venous sinus thrombosis. Its diagnosis is difficult and needs high index of suspicion clinically and on magnetic resonance imaging (MRI). A 38-year-old man presented with the history of three episodes of generalized seizures and weakness and sensory loss in the both upper limbs with headache. MRI brain with magnetic resonance venography (MRV) was performed. MRI brain showed hemorrhagic infarcts in bilateral frontoparietal region. Gradient echo sequence showed hypo-intense signal within thrombosed cortical veins. MRV showed paucity of cortical veins in involved areas suggestive of cortical vein thrombosis.

Keywords: Gradient echo sequence (T2 FNx01 ), hemorrhagic infarct, isolated cortical vein thrombosis, magnetic resonance venogram


How to cite this article:
Khaladkar SM, Thakkar DK, Kulkarni VM. High diagnostic value of gradient echo sequence in isolated cortical vein thrombosis. Med J DY Patil Univ 2014;7:218-21

How to cite this URL:
Khaladkar SM, Thakkar DK, Kulkarni VM. High diagnostic value of gradient echo sequence in isolated cortical vein thrombosis. Med J DY Patil Univ [serial online] 2014 [cited 2019 Dec 9];7:218-21. Available from: http://www.mjdrdypu.org/text.asp?2014/7/2/218/126352


  Introduction Top


Isolated cortical vein thrombosis (ICoVT) is a distinct cerebrovascular disorder affecting mostly young adults and is rare in comparison with the more frequently occurring dural venous sinus thrombosis. [1] The predicament of the physician encountering these cases is compounded by multiple factors; their rarity, the non-specificity of neurologic symptoms that could be caused by a multitude of vascular events and lastly, a difficult radiological diagnosis. Detection of (ICoVT) on sectional imaging involves visualization of the thrombosed vein itself, as well as associated findings of hemorrhage or venous infarction. [1],[2]


  Case Report Top


A 38-year-old man presented with the history of three episodes of generalized seizures and weakness and sensory loss in the both upper limbs. This was associated with headache and the interval between the seizures was 2 and 3 days and weakness was increasing with every episode of seizure. Headache was temporarily relieved by analgesics.

No fever, photophobia vomiting or nausea was complained. Patient was conscious, normal looking and normotensive. Routine lab tests were unremarkable. Brain magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) was performed and T1, T2 and gradient echoes (GREs) were observed.

Based on MRI scan a large area of hemorrhagic infarction was seen in left posterior high parietal region and centrum semiovale region appearing hyperintense on T1WI [Figure 1] and hypointense on T2WI [Figure 2]. A small hemorrhagic infarction was also seen in right high frontal region [Figure 3]. On T1WI, multiple tortuous and dilated cortical veins were seen in high parietal region on either side with the loss of normal flow void [Figure 4]. On GRE sequence, blooming was seen in areas of hemorrhagic infarct [Figure 5], signal loss in cortical veins with hemorrhagic infarct was seen in bilateral high fronto-parietal region suggestive of cortical vein thrombosis [Figure 6] and signal loss in cortical veins in bilateral high fronto-parietal region [Figure 7]. On MRV, loss of signal and paucity of cortical veins were seen in bilateral high fronto-parietal region. Left transverse and sigmoid sinus were hypoplastic. Other dural venous sinuses were patent [Figure 8].
Figure 1: Hemorrhagic infarct in left high parietal region which is hyperintense on T1WI

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Figure 2: Hemorrhagic infarct in left high parietal region which is hypointense on T2WI

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Figure 3: Hemorrhagic infarct in right high frontal region, appearing hyperintense on T1WI

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Figure 4: Tortous, dilated cortical veins with the loss of normal flow void on T1WI

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Figure 5: Hemorrhagic infarct showing blooming in left high parietal region on gradient echo sequence

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Figure 6: Signal loss in cortical veins in bilateral high fronto-parietal region on gradient echo

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Figure 7: Signal loss in cortical veins on gradient echo

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Figure 8: Absent flow and paucity of cortical veins in bilateral high fronto-parietal region. Left transverse and sigmoid sinus are hypoplastic

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  Discussion Top


ICoVT indicates thrombosis of cortical vein without dural sinus involvement. Its occurrence is rare and is reported as isolated case reports or in small series. It is less commonly encountered than dural sinus thrombosis. It is difficult to diagnose both clinically and radiologically and needs high index of suspicion. [1]

Its detection on computed tomography (CT) or MRI depends on visualizing the thrombosed vein (direct sign) and detection of venous infarction and hemorrhage (indirect sign) which may be non-specific. [1],[3] ICoVT is difficult to diagnose on MRI in the acute stage of thrombosis when the clot is isointense to brain on T1WI and hypointense on T2WI when it mimics a flow void. Many a times associated indirect signs are absent in the acute stage.

ICoVT is difficult to diagnose on MRI using T1WI, T2WI and MRV imaging as - cortical veins are variable in location, size and number. Thrombosed small cortical veins are difficult to identify using routine MR sequences and MRV. Only occluded large cortical veins are detectable on MRV as missing cortical veins. [2]

Addition of T2* gradient echo (T2*GE) sequence is extremely useful in detecting ICoVT in the acute stage when T1WI and T2WI fail to diagnose the same. Conventional T2 * GE sequence has higher sensitivity for ICoVT than other sequences as it shows thrombus material as hypointense signal in the acute stage when it is not hyperintense yet on T1WI (blooming artifact). It exhibits higher sensitivity to susceptibility difference and shows hypointense signal from symptom onset up to 1 year for a long time. It is important to assess signal intensity of adjacent cortical vein when evaluating a focal cortical area of edema or hemorrhage when these findings occur in atypical arterial vascular distribution. Hypointense signal on T2 * GE is due to magnetic susceptibility effect, the signal being similar to intracranial hemorrhage. [2],[4],[5],[6]

A hypointense signal on T2 * GE image is present in 90% of sites of cerebral venous thrombosis (CVT) on the first MRI scan while a hyperintense signal is detected on T1WI in 84% of sites. This excellent sensitivity of T2 * GE sequence is extremely useful in 1 st 3 days (acute stage) when frequency of hypointense signal on T2 * GE is higher than 90% and that of hyperintense signal on T1WI is only 70%. The detection rate of ICoVT in the absence of visible occlusion on MRV on T2 * GE is 97%, on T1WI is 78%, fluid attenuated inversion recovery (FLAIR) is <40%. Hence T2 * GE is of utmost importance in detecting ICoVT as T1, T2, FLAIR sequences are not sensitive enough. [7]

MRV shows asymmetric absence of flow signal (missing cortical vein) or diminished enhancement in thrombosed cortical vein. [4]

The appearance of thrombus varies depending up to the duration after onset. Acute stage thrombus (in 1 st 7 days after onset) is due to deoxyhemoglobin within trapped red blood cells within the thrombus and is isointense on T1WI and hypointense on T2WI. This stage is often missed on MRI as it mimics flow void. T2 * GE shows hypointense signal at this stage. [3],[4]

Subacute phase (7-14 days) is divided into early and late subacute phase. Early subacute phase is due to intracellular meth-hemoglobin in which thrombus appears hyperintense on T1WI and hypointense on T2WI and appears hypointense on T2 * GE. Late subacute phase is due to extracellular meth-hemoglobin in which thrombus is hyperintense on T1WI and T2WI and hypointense on T2 * GE. On CT, it is seen as "cord sign." [8] MR equivalent is "hyperintense vein sign" appearing hyperintense on T1WI seen only in subacute stage. [4],[8] Chronic phase (>15 days), signal intensity is isointense on T1WI and hyperintense on T2WI and is probably related to the vascularized connective tissue of chronic thrombus.

Parenchymal findings (indirect signs) are areas of focal edema and hemorrhage, which are non-specific. Edema appears as hypointense signal on T1WI, hyperintense on T2WI and FLAIR. Hemorrhagic areas show variable appearance on MR sequence depending upon acute, subacute and chronic stage.

Addition of diffusion-weighted imaging (DWI) in imaging of CVT is of recent interest. Signal hyperintensity in thrombosed sinuses on DWI with corresponding diminished in the mean apparent diffusion coefficient values is seen in 41% of patients with sinus thrombosis and is associated with the absence of recanalization. Complete recanalization was less frequent with longer duration of clinical symptoms in patients with restricted diffusion in thrombus. [3],[4]

This addition of T2 * GE and DWI sequences in imaging of ICoVT is of utmost importance in early diagnosis and prognosis respectively in addition to routine sequences (T1WI, T2WI, fluid-attenuated inversion recovery). [6]

 
  References Top

1.Duncan IC, Fourie PA. Imaging of cerebral isolated cortical vein thrombosis. AJR Am J Roentgenol 2005;184:1317-9.  Back to cited text no. 1
    
2.Boukobza M, Crassard I, Bousser MG, Chabriat H. MR imaging features of isolated cortical vein thrombosis: Diagnosis and follow-up. AJNR Am J Neuroradiol 2009;30:344-8.  Back to cited text no. 2
    
3.Chiewvit P, Piyapittayanan S, Poungvarin N. Cerebral venous thrombosis: Diagnosis dilemma. Neurol Int 2011;3:e13.  Back to cited text no. 3
    
4.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:S19-41.  Back to cited text no. 4
    
5.Cakmak S, Hermier M, Montavont A, Derex L, Mauguière F, Trouillas P, et al. T2*-weighted MRI in cortical venous thrombosis. Neurology 2004;63:1698.  Back to cited text no. 5
    
6.Fellner FA, Fellner C, Aichner FT, Mölzer G. Importance of T2*-weighted gradient-echo MRI for diagnosis of cortical vein thrombosis. Eur J Radiol 2005;56:235-9.  Back to cited text no. 6
    
7.Linn J, Michl S, Katja B, Pfefferkorn T, Wiesmann M, Hartz S, et al. Cortical vein thrombosis: The diagnostic value of different imaging modalities. Neuroradiology 2010;52:899-911.  Back to cited text no. 7
    
8.Sharma VK, Teoh HL. Isolated cortical vein thrombosis - The cord sign. J Radiol Case Rep 2009;3:21-4.  Back to cited text no. 8
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

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