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Table of Contents    
Year : 2021  |  Volume : 69  |  Issue : 6  |  Page : 1794-1797

Cerebral Venous Thrombosis Presenting as a Ring-Enhancing Lesion on MR imaging: A Case Report and Critical Review

1 Department of Neurology, Hebei Yanda Hospital, Sanhe, Hebei, China
2 Department of Neurology, The 309th Hospital of Chinese PLA, Beijing, China
3 Department of Neurosurgery, The 309th Hospital of Chinese PLA, Beijing, China

Date of Submission09-Sep-2018
Date of Decision22-Jul-2019
Date of Acceptance29-Dec-2019
Date of Web Publication23-Dec-2021

Correspondence Address:
Dr. Wei Wang
Department of Neurology, Hebei Yanda Hospital, NO.6 Road, Sanhe, Hebei 065201
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.333515

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 » Abstract 

Cerebral venous thrombosis (CVT) is a rare form of venous thromboembolism. The presentation of symptoms is highly variable in this disease. The findings on MRI vary depending on the age of the thrombus within the vessel. We report a 53-year-old male patient with CVT who presented with a sudden-onset grand mal seizure and limb paralysis. Primary MRI presented long T1 long T2 signals, persistent high signals on DWI and ADC maps in the cortex of right frontal lobe. Contrast-enhanced MR detected a lesion with ring-like enhancement in right frontal lobe. His symptoms were significantly improved with anticoagulant therapy of Warfarin. Our findings represent the description of abnormal MRI contrast enhancing tumor-like masses. CVT should be added to the differential diagnosis of supratentorial ring-enhancing lesions.

Keywords: Cerebral venous thrombosis, magnetic resonance image, ring-like enhancement
Key Message: CVT may appear abnormal parenchymal ring-like enhancement by MRI and be misdignosed as tumor. Multimodal MRI is an effective and non-invasive method for CVT differential diagnoses.

How to cite this article:
Wang Z, Chen Y, Tang K, Wang W. Cerebral Venous Thrombosis Presenting as a Ring-Enhancing Lesion on MR imaging: A Case Report and Critical Review. Neurol India 2021;69:1794-7

How to cite this URL:
Wang Z, Chen Y, Tang K, Wang W. Cerebral Venous Thrombosis Presenting as a Ring-Enhancing Lesion on MR imaging: A Case Report and Critical Review. Neurol India [serial online] 2021 [cited 2022 Jan 18];69:1794-7. Available from:

Cerebral venous thrombosis (CVT), including thrombosis of cerebral veins and major dural sinuses, is an infrequent variety of venous thromboembolism. The incidence of CVT is estimated at 0.2 to 0.5 per 100000 per year.[1] The clinical manifestations of CVT can be grouped into four distinct syndromes: isolated intracranial hypertension, focal syndrome, diffuse encephalopathy, and cavernous sinus syndrome. The diagnosis of CVT is often missed or delayed because of the highly variable symptoms and clinical outcome.[2] We report a case of CVT with an unusual clinical course and MRI findings.

 » Case Presentation Top

A 53-year-old man who was robust and had no febrile convulsion or previous noteworthy medical history presented to neurology emergency department with a sudden-onset grand mal seizure on Nov 28, 2016. He had no history of hypertension, diabetes mellitus, heart disease, encephalitis, or brain trauma. His family history was negative for symptoms possibly related to epilepsy or cerebral vascular disease. The seizure lasted for about 4-5 min and the patient recovered completely after that episode. At that time, the patient was admitted to a hospital. He was afebrile, and his neurological examination was normal, with no evidence of meningismus. The patient experienced two episodes of generalized tonic-clonic (GTC) seizures during the 24 h prior to his last admission. The GTC seizures were controlled by administering sodium phenobarbital intramuscular injection and oral carbamazepine. At the time of admission, the physical examination was normal. The laboratory data including the hematological, clinical chemistry examination, and routine biochemical test of cerebrospinal fluid (CSF) showed no abnormalities. Further laboratory tests revealed that the level of anticardiolipin antibodies, antineutrophil cytoplasmic antibodies, protein S, and protein C were normal. Cerebral CT (Nov 28, 2016) showed old ischemic lesions in basal ganglia. Cerebral magnetic resonance imaging (MRI) (Nov 29, 2016) presented long T1 long T2 signals, high signals on FLAIR, diffusion-weighted imaging (DWI), and apparent diffusion coefficient (ADC) maps in the cortex of right frontal lobe [Figure 1]a,[Figure 1]b,[Figure 1]c,[Figure 1]d,[Figure 1]e. MR venography (MRV) (Dec 01, 2016) showed no visible filling of the deep venous system and the absence of blood flow in the anterior segment of superior sagittal sinus [Figure 1]f. Susceptibility-weighted imaging (SWI) (Dec 01, 2016) showed tubular-shaped signal loss at cortical veins [Figure 1]g. Features suggested the possibility of cerebral venous thrombosis. At that time, low molecular weight heparin infusion was started. After a 2-week symptom-free period, he experienced left limb paralysis. Contrast-enhanced MR (Dec 13, 2016) showed an increment of the size of right frontal lobe lesion with ring-like enhancement, while magnetic resonance spectroscopy failed to detect the significantly elevated amplitude of the choline peak within the lesion [Figure 1]h,[Figure 1]i,[Figure 1]j. CT-guided stereotactic brain biopsy was performed on Dec 18, 2016 to exclude neoplastic disease. Intraoperatively, the frontal lobe lesion was seen as soft fatty tissue with multitortuous dilation cortical veins attached to the dura. Hematoxylin and eosin (H&E)-stained sections demonstrated the brain tissues which contained numerous gitter cells were disintegrated and necrotic [Figure 2]. Multiple dilated and enlarged veins in the subarachnoid space and superficial brain tissue were frequently observed to be congested. Immunohistochemical method CD34 expression was positive. Histological analysis confirmed the diagnosis of cortical venous thrombosis. Follow-up MRV imaging 4 weeks (Dec 26, 2016) after the oneset showed the signal void of original segment of superior sagittal sinus and its bridging vein appeared [Figure 1]k,[Figure 1]l,[Figure 1]m. After a one-month medical treatment with low molecular weight heparin, limb paralysis of the patient was improving gradually and epileptic seizure disappeared.
Figure 1: Brain magnetic resonance images. Serial MRI studies 1 day (a-e), 3 days (f-g), 15 days (h-j), and 28 days (k-m) after symptom onset. Magnetic resonance venography (MRV) images (f) show the lack of flow in the anterior segment of superior sagittal sinus and its cortical veins. MRS images (i) detect no significantly elevated amplitude of the choline peak within the cortex of right frontal lobe. Check of venous sinus by MRV images (m) shows superior sagittal sinus unobstructed after thrombolytic therapy

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Figure 2: Brain tissue biopsy (hematoxylin and eosin, ×100) reveals thrombus in dilated deep venous sinus and encephalorrhagia in right frontal lobe (arrow)

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Written informed consent and informed assent were obtained from the patient before reporting the case.

 » Disccusion Top

Cortical venous thrombosis is considered a rare disease. Clinical manifestations of CVT includes isolated intracranial hypertension, focal neurological abnormalities, seizures, and encephalopathy.[3] Herein, we describe a case of CVT who presented with grand mal seizure. Focal or generalized seizures, which may be observed in 30% to 40% of patients with CVT, are duo to focal brain injury from venous ischemia or hemorrhage, or a mix of them.[4],[5] In our case, the seizures were effectively controlled by administration of anticonvulsant agents. According to the underlying coagulation abnormalities including anticardiolipin antibodies, antineutrophil cytoplasmic antibodies, protein S, and protein C, the cause of the case of CVT was unclear.

Because of variable clinical presentations and numerous causes, the clinical diagnosis of CVT can be difficult. The combination of MR imaging showing the thrombosed vessel and MRV demonstrating the nonvisualization of the same vessel is the best method to diagnose the CVT. Acutely, brain parenchymal lesions in CVT patients are low signal intensity on T1-weighted and high signal intensity on T2-weighted images and DW images. However, the findings on the ADC-value changes remain to be elucidated.[6] Yoshikawa et al.[7] demonstrated patients had brain lesions showing both areas with decreased and increased ADC simultaneously on the initial MR imaging within 7 days of the last epitode of CVT. In the case, 3 days after clinical onset, MR imaging identified acute infarcts in the right frontal lobe involving the cortex and subcortical white matter. T2-weighted images and FLAIR images demonstrated abnormally increased signal intensity in the right frontal lobe, while ADC was increased in hyperintense areas on DWI. Follow-up MR revealed that the increase in ADC persisted up to 4 weeks. Increased in ADC suggests that vasogenic edema develops more predominantly and occurs earlier in CVT than in arterial ischemia. The previous study demonstrated that a decrease of ADC reflected severer pathological conditions and indicate future infarction or hemorrhage.[8],[9],[10] Our data were inconsistent with the above-mentioned clinical result. Lesions with an increased ADC in right frontal lobe progressed to constantly enlarging infarction. It is conceivable that the enlargement of infarct size is associated with the clinical course of partial to complete occlusion in cortical veins. Taking the above studies into account, multimodality MR shows the great value for the early diagnosis of CVT. Gyrus lesions or flame-shaped lesions present long T1 long T2, especially high signals in DWI and ADC map in the cortex, and subcortical white matter of lobes highly indicates the existence of CVT.

SWI has recently demonstrated great clinical significance in the diagnosis of intracranial venous lesions and diseases. Based on SWI and postprocessing, deep medullary venous volume in patients with superior sagittal sinus thrombosis showed a significant decline from the acute stage at baseline to 6-month follow-up.[11] In our case, we also found tubular-shaped signal loss at cortical veins. There are two reasons for lower relative susceptibility: one is decrease in cerebral metabolic rate of oxygen consumption[12] and the other reason is cerebral microbleeds resulting from localized venous hypertension produced by the conclusion of cortical veins.[13] Therefore, SWI is useful for detecting microbleed and other cerebral diseases associated with microbleed, including cerebral amyloid angiopathy and intracranial venous system disease.

On MRS, a significantly elevated amplitude of the choline peak relative to that of creatine suggests a neoplasm. However, the typical elevated choline did not show in our case. Therefore, we performed a biopsy and the result excluded neoplastic disease. A ring-enhanced intracranial lesion, which is most commonly seen in neoplasms, abscesses, primary hematomas, and inflammatory demyelinating lesions, rarely exists in the literature for CVT. Bakshi et al.[14] presented two cases of CVT with MR findings of ring-like enhancement. Nevertheless, one case of the CVTs was hemorrhagic and exerted. It is speculated that the abnormal MR finding of ring enhancement was related to the absorption period of intracerebral hemorrhage. In our case, a thin and ring-like enhancement without apparent intracranial hemorrhage in infarct hemisphere was seen. There are two probable mechanisms for this. The first is that the disruption of blood-brain-barrier (BBB) during brain ischemia results in the increase of brain vascular permeability around the hypoperfusion area of the ischemic core[15] and further presents as ring-like enhancement in contrast-enhanced MR imaging.[16] The second possibility is aseptic inflammation caused by BBB breakdown, inflammatory cell recruitment in focal cerebral ischemia. Consequently, CVT should be added to the differential diagnosis of supratentorial ring-enhancing masses.

To conclude, multimode MRI scan has become a useful method for investigating the pathogenesis of CVT. Careful investigation of the MRI appearance of the cerebral venous structure is valuable for uncovering CVT.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initial will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Natural Science Foundation of Hainan Province (819MS111) and Foundation of the 309th Hospital of Chinese PLA (2016ZD-007)

Conflicts of interest

There are no conflicts of interest.

 » References Top

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Silvis SM, de Sousa DA, Ferro JM, Coutinho JM. Cerebral venous thrombosis. Nat Rev Neurol 2017;13:555-65.  Back to cited text no. 2
Piazza G. Cerebral venous thrombosis. Circulation 2012;125:1704-9.  Back to cited text no. 3
Tanislav C, Siekmann R, Sieweke N, Allendorfer J, Pabst W, Kaps M, et al. Cerebral vein thrombosis: Clinical manifestation and diagnosis. BMC Neurol 2011;11:69.  Back to cited text no. 4
Ferro JM, Canhao P, Bousser MG, Stam J, Barinagarrementeria F, ISCVT investigators. Early seizures in cerebral vein and dural sinus thrombosis: Risk factors and role of antiepileptics. Stroke 2008;39:1152-8.  Back to cited text no. 5
Wasay M, Bakshi R, Bobustuc G, Dubey N, Cheema Z, Dai A. Diffusion -weighted magnetic resonance imaging in superior sagittal sinus thrombosis. J Neuroimaging 2002;12:267-9.  Back to cited text no. 6
Yoshikawa T, Abe O, Tsuchiya K, Okubo T, Tobe K, Masumoto T, et al. Diffusion-weighted magnetic resonance imaging of dural sinus thrombosis. Neuroradiology 2002;44:481-8.  Back to cited text no. 7
Mullins ME, Grant PE, Wang B, Gonzalez RG, Schaefer PW. Parenchymal abnormalities associated with cerebral venous sinus thrombosis: Assessment with diffusion-weighted MR imaging. AJNR Am J Neuroradiol 2004;25:1666-75.  Back to cited text no. 8
Rottger C, Trittmacher S, Gerriets T, Blaes F, Kaps M, Stolz E. Reversible MR imaging abnormalities following cerebral venous thrombosis. AJNR Am J Neuroradiol 2005;26:607-13.  Back to cited text no. 9
Boukobza M, Crassard I, Bousser MG, Chariat 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. 10
Hsu CC, Kwan GNC, Hapugoda S, Craigie M, Watkins TW, Haacke EM. Susceptibility weighted imaging in acute cerebral ischemia: Review of emerging technical concepts and clinical applications. Neuroradiol J 2017;30:109-19.  Back to cited text no. 11
Harris NG, Mironova YA, Chen SF, Richards HK, Pickard JD. Preventing flow-metabolism uncoupling acutely reduces axonal injury after traumatic brain injury. J Neurotrauma 2012;29:1469-82.  Back to cited text no. 12
Alvis-Miranda HR, Milena Castellar-Leones S, Alcala-Cerra G, Rafael Moscote-Salazar L. Cerebral sinus venous thrombosis. J Neurosci Rural Pract 2013;4:427-38.  Back to cited text no. 13
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Bakshi R, Lindsay BD, Bates VE, Kinkel PR, Mechtler LL, Kinkel WR. Cerebral venous infarctions presenting as enhancing space-occupying lesions: MRI findings. J Neuroimaging 1998;8:210-5.  Back to cited text no. 14
Ding G, Yan T, Chen J, Chopp M, Li L, Li Q, et al. Persistent cerebrovascular damage after stroke in type two diabetic rats measured by magnetic resonance imaging. Stroke 2015;46:507-12.  Back to cited text no. 15
Nakagawa M, Matsumoto K, Higashi H, Furuta T, Ohmoto T. Acute effects of interstitial hyperthermia on normal monkey brain-magnetic resonance imaging appearance and effects on blood-brain barrier. Neurol Med Chir (Tokyo) 1994;34:668-75.  Back to cited text no. 16


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