|Year : 2014 | Volume
| Issue : 3 | Page : 296-303
Cerebral venous sinus thrombosis on MRI: A case series analysis
Sanjay M Khaladkar, Dhaval K Thakkar, Dolly K Thakkar, Harshawardhan Shrotri, Vilas M Kulkarni
Department of Radio-Diagnosis, Padmashree Dr. D.Y. Patil Medical College, Hospital and Research Centre, Dr. D.Y. Patil Vidyapeeth, Pimpri, Pune, Maharashtra, India
|Date of Web Publication||18-Mar-2014|
Sanjay M Khaladkar
Flat No. 5, Plot No. 8, S. No. - 26/A, Tejas Bldg., Sahawas Society, Karve Nagar, Pune - 411 052, Maharashtra
Source of Support: None, Conflict of Interest: None
Background: Cerebral venous sinus thrombosis (CVST) is a rare form of stroke seen in young and middle aged group, especially in women due to thrombus of dural venous sinuses and can cause acute neurological deterioration with increased morbidity and mortality if not diagnosed in early stage. Neurological deficit occurs due to focal or diffuse cerebral edema and venous non-hemorrhagic or hemorrhagic infarct. Aim and Objectives: To assess/evaluate the role of Magnetic Resonance Imaging (MRI) and Magnetic Resonance Venography (MRV) as an imaging modality for early diagnosis of CVST and to study patterns of venous thrombosis, in detecting changes in brain parenchyma and residual effects of CVST using MRI. Materials and Methods: Retrospective descriptive analysis of 40 patients of CVST diagnosed on MRI brain and MRV was done. Results: 29/40 (72.5%) were males and 11/40 (27.5%) were females. Most of the patients were in the age group of 21-40 years (23/40-57.5%). Most of the patients 16/40 (40%) presented within 7 days. No definite cause of CVST was found in 24 (60%) patients in spite of detailed history. In 36/40 (90%) of cases major sinuses were involved, deep venous system were involved in 7/40 (17.5%) cases, superficial cortical vein was involved in 1/40 (2.5%) cases. Analysis of stage of thrombus (acute, subacute, chronic) was done based on its appearance on T1 and T2WI. 31/40 (77.5%) patients showed complete absence of flow on MRV, while 9/40 (22.5%) cases showed partial flow on MR venogram. Brain parenchyma was normal in 20/40 (50%) patients while 6/40 (15%) cases had non-hemorrhagic infarct and 14/40 (35%) patients presented with hemorrhagic infarct. Conclusion: Our study concluded that MRI brain with MRV is sensitive in diagnosing both direct signs (evidence of thrombus inside the affected veins) and indirect signs (parenchymal changes) of CVST and their follow up.
Keywords: Deep venous sinus thrombosis, dural venous sinus thrombosis, hemorrhagic and non-hemorrhagic infarct, isolated cortical venous sinus thrombosis, magnetic resonance imaging (MRI), magnetic resonance venography (MRV)
|How to cite this article:|
Khaladkar SM, Thakkar DK, Thakkar DK, Shrotri H, Kulkarni VM. Cerebral venous sinus thrombosis on MRI: A case series analysis. Med J DY Patil Univ 2014;7:296-303
|How to cite this URL:|
Khaladkar SM, Thakkar DK, Thakkar DK, Shrotri H, Kulkarni VM. Cerebral venous sinus thrombosis on MRI: A case series analysis. Med J DY Patil Univ [serial online] 2014 [cited 2019 Sep 20];7:296-303. Available from: http://www.mjdrdypu.org/text.asp?2014/7/3/296/128964
| Introduction|| |
One of the causes of acute neurological deterioration is cerebral venous sinus thrombosis (CVST). It is a rare form of stroke and results from thrombosis of dural venous sinus (which drain blood from brain). 
Intracranial dural sinus thrombosis is potentially fatal and relatively common condition. Spontaneous thrombosis has an estimated incidence of 1 per 50,000 though the true incidence of the disorder is probably underestimated.  It usually occurs in young and middle age groups and is responsible for 1-2% of stroke in these patients.  Morbidity occurs when there is impairment of the venous drainage of the brain due to a thrombus occluding a major dural sinus or propagating into a cortical vein. This may result in focal or diffuse cerebral edema, venous hemorrhagic and non-hemorrhagic infarcts. Pathologic findings may vary with the site of the thrombosis and interval between the onset of symptoms and death. Fresh thrombus is red and rich in red blood cells, fibrin and platelets. When it is old, it is substituted by fibrous tissue, sometimes showing recanalization. Thrombus formation occurs due to various factors: venous stasis, changes in the vessel wall, increased clotting tendency, and less frequently embolization. Computed tomography (CT) scan and magnetic resonance imaging (MRI) studies have now shown that sinus thrombosis can induce edema without infarction and can even have no detectable effect on the brain. 
There may be a wide range of signs and symptoms at presentation, so in almost any cerebral syndrome, CVST could be considered. However certain clinical features provide clue to the presence of CVST. Since growth of thrombus is usually slow, and venous collateralization is extensive, the symptoms typically evolve over days or weeks, although the onset may be acute.  The severity of symptoms depends on chronicity of development and on the vessels involved. Headache is a key presenting feature and since this may be associated with papilledema, it may be confused with benign intracranial hypertension.Seizures and focal deficits resulting from infarction or venous edema may be present. An uncommon but classical presentation is superior sagittal sinus (SSS) thrombosis and parasagittal venous infarction leading to bilateral alternating deficits predominating in the legs.
Diplopia and hemianopia may result from occlusion of the transverse sinus or posterior SSS and associated cortical veins. Impairment of consciousness may occur due to thrombosis of deep cerebral venous system or transtentorial herniation, resulting from cerebral edema. A sixth nerve palsy is usually secondary to intracranial hypertension; however, it may also result from thrombus extension to the sigmoid or transverse sinus (III-VIII), petrosal sinus (V) and jugular vein (IX-XI). Although a predisposing factor in up to 80% of patients is identified, its absence should not deter the radiologist from the diagnosis of CVST. The commonest etiologies are puerperium and pregnancy, dehydration, use of oral contraceptives, adjacent infection (e.g. mastoiditis or sinusitis), trauma, compressive tumor, blood dyscrasias, malignancy and hematological disorders like polycythemia, essential thrombocytosis, paroxysmal nocturnal hemoglobinuria and collagen vascular disease. In these patients, coagulation disorders such as protein S and C deficiency, factor V Leiden mutation or antithrombin III deficiency and antiphospholipid antibody syndrome must be excluded. Dehydration and acute illness are frequently associated with CVST in neonates, and coagulopathy and infection are the commonest underlying condition in children.
In the past, the diverse clinical presentation has made CVST a difficult and often delayed diagnosis; however, with advent of MRI and MR Venography early diagnosis of CVST is possible with resultant good prognosis without serious neurological sequel. While mortality has recently been reported as low as at 5-15%, survivors often have significant morbidity. Now the standard therapy is systemic heparin anticoagulation. In severe acute cases, local infusion of the thrombolytic agent urokinase is used.  The availability of treatment for dural sinus thrombosis has increased the need for accurate and prompt diagnosis.
Magnetic resonance imaging, and recently MR venography, have increased the ability to detect CVST. MRI offers major advantage for the evaluation of patients suspected of dural sinus thrombosis because of its ability to visualize the thrombus, its sensitivity to flowing blood and being noninvasive and radiation free. MR was considered as the investigation of choice for the diagnosis of dural sinus thrombosis.  However, complex signal intensity pattern of flowing blood on MR images has made it difficult to distinguish between thrombosis and flow-related enhancement. This difficulty has led to use of MR venography in the evaluation of CVST and other abnormalities of cerebral venous system. The technique of choice for diagnostic evaluation and follow up of dural sinus thrombosis is MR venography. The MR techniques that are used for the diagnosis of cerebral venous thrombosis are: Time-of-flight (TOF), phase-contrast angiography (PCA) and contrast-enhanced MR-venography. Contrast MR venography is considered more superior to TOF venography.
| Materials and Methods|| |
A retrospective descriptive analytical study in which 40 patients of CVST who were referred to a tertiary care teaching hospital for MRI brain with MRV from June 2011 to June 2013 were included and their demographic, etiological, radiological and prognostic characteristics were evaluated. MRI was performed on SIEMENS AVANTO 1.5 Tesla MRI system. Structured case proforma was used with detailed clinical history and systemic findings and investigations. History was taken to exclude the following: Pacemaker, Implant, Clip.
A written consent was obtained from each patient. Before being transferred to MRI suite, patients were checked for any metallic devices in or on his/her body (a metallic detector was used to find out any hidden ferromagnetic substance in the body).
Sequences taken were T1WI (TR/TE-450/8.7, Matrix-320 × 320), T2WI (TR/TE-3550/93, Matrix-406 × 448) and FLAIR (TR/TE-8500/89, Matrix-228 × 320) using head coil. These were supplemented by diffusion weighted image (TR/TE-3500/103, Matrix-192 × 192), gradient (TR/TE-700/26, flip angle 30 o , Matrix-256 × 256), and MRV using 2D-TOF (TR/TE-25/7.19, Matrix-166 × 256) on 1.5 MR system. Slice thickness was 5 mm with interslice gap of 1.0 mm. FOV used was 230 mm. Sequences were taken in axial, coronal and sagittal planes. Suitable variations were made depending on the patient's condition.
| Results|| |
Sex wise distribution
Forty patients (n = 40) showed evidence of dural venous sinus thrombosis. Out of 40 patients, there were 29 males (72.5%) and 11 females (27.5%) as shown in [Table 1].
Age wise distribution
Age ranged from 9 months to 72 years. Out of 40 cases, 13 (32.5%) belonged to 21-30 years age group, 10 (25%) belonged to 31-40 years age group and 8 (20%) belonged to 41-50 years age group [Table 2].
Signs and symptoms
Headache was the most common symptom in 29/40 (72.5%), followed by seizures 16/40 (40%), neurological deficit 10/40 (25%), diminished vision in 7/40 (17.5 %) and vomiting associated with headache and trauma in 7/40 (17.5%). One patient (2.5%) had dehydration due to diarrhea as given in [Table 3].
Duration of symptoms
Most of the patients presented with more than one symptom. 16/40 (40%) patients presented with acute symptoms within seven days, 9/40 (22.5%) within 14 days, 9/40 (22.5%) within 30 days, 1/40 (2.5%) within 3 months and 5/40 (12.5%) presented late within 2 years [Table 4].
In majority of the patients 24 (60%), no predisposing factors were identified. Infections were found in 5/40 (12.5%), trauma in 3/40 (7.5%), oral contraceptive pills in 3 (7.5%). In two cases (5%), hypertension was associated with alcohol intake. One case each of postpartum, diarrhea and hypercoagulable state (due to polycythemia) were seen as shown in [Table 5].
In present study, the most common sinus involved was superior sagittal sinus [Figure 1] with almost equal involvement of transverse [Figure 2] and [Figure 3] and sigmoid sinuses [Figure 3] and [Figure 4]. The deep venous system [Figure 5] was affected in seven (17.5%) patients, and superficial venous system [Figure 6]a and b affected in 2.5% of cases. Most of the patients had involvement of more than 1 sinus. Commonest association was noticed between superior sagittal sinus and transverse or sigmoid sinuses. Thrombosis of deep venous system was least observed as given in [Table 6].
|Figure 2: MRV showing absent fl ow in left transverse sinus suggestive of thrombosis|
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|Figure 3: MRV showing thrombosis of superior sagittal sinus and left transverse sinus|
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|Figure 4: MRV showing thrombosis of superior sagittal sinus, right transverse and right sigmoid sinus thrombosis|
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|Figure 5: MR venogram showing filling defect suggestive of thrombosis of straight sinus, both internal cerebral veins and thalamostriate veins|
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|Figure 6: MRI Brain T1W (a) and GRE (b) axial images reveal thrombosed cortical veins in bilateral high fronto-parietal region seen as loss of normal fl ow void within dilated cortical veins on T1W sequence with signal loss on GRE|
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Distribution of thrombosis
In 90% of cases, dural venous sinuses were involved. The involvement of deep venous and cortical veins was less than dural venous sinuses as given in [Table 7].
Appearance of thrombus
In this study, when MRI and MRV were done within 7 days of CVST, T1 signal of thrombus was found isointense in 8 cases (20%). When MRI was done between 7 days and 14 days, the signal was hyperintense in 20 patients (50%). In chronic cases, signal was isointense on T1 in 12 (30%) patients. This shows that the signal becomes hypointense after 15 days as shown in [Table 8].
In Acute stage (0-7 days) on T2WI, thrombus appeared hypointense in 8 (20%) cases. In subacute stage (7-14 days, total 20 patients), thrombus appeared hypointense in early subacute in 12 (30%) patients and hyperintense in 8 (20%) patients in late subacute stage. In Chronic stage (>15 days), thrombus appeared hyperintense in 12 (30%) patients as shown in [Table 8].
Changes in brain parenchyma
Brain parenchymal abnormalities in CVST are diffuse cerebral edema, non-hemorrhagic [Figure 7]a and b] and hemorrhagic infarcts [Figure 8]a-c]. In this study, 20/40 (50%) cases were normal, 6/40 (15%) had non-hemorrhagic infarct and 14/40 (35%) had hemorrhagic infarction as shown in [Table 9].
|Figure 7: MRI Brain T1W (a) and T2W (b) axial images reveal nonhemorrhagic venous infarcts in bilateral thalami, lentiform nuclei and head of caudate nuclei, which appear hypointense on T1W and hyperintense on T2W sequences|
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|Figure 8: MRI Brain T1W (a), T2W (b) and GRE (c) axial images reveal hemorrhagic infarcts in bilateral high parietal regions, which appear hyperintense on T1W, hypointense on T2W and show blooming on GRE|
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Appearance of MR venography
On MRV, absence of signal or no flow (suggestive of complete thrombosis) was seen in 31/40 (77.5%) cases, while partial flow (suggestive of partial thrombosis) was seen in 9/40 (22.5%) cases as shown in [Table 10].
Follow up imaging
Out of 40 patients, 10 were referred for follow-up imaging between one month to one year. Complete resolution of infarction was seen in three patients with equivalent number of patients showing recanalization of sinuses as shown in [Table 11].
Follow up status
21/40 patients had better outcome with resolution of symptoms after appropriate treatment due to timely diagnosis. 6/40 patients had persistent focal neurological deficit, 2/6 of them had extensive hemorrhagic infarction. One patient with deep venous sinus thrombosis expired. Follow up of 12 patients was not available as shown in [Table 12].
| Discussion|| |
In this study, 40 patients with dural sinus thrombosis were studied on the basis of MRI and MRV. Out of 40 patients of CVST, 29/40 [72.5%] were males and 11/40 [27.5%] were females. This is in contrast to the study of Jose M. Ferro et al.  They stated that women are more exposed to predisposing factors like pregnancy and peripartum state and use of OCP. Male predominance in our study is likely to be due to study conducted in industrial area.
Most of the patients were between the age group of 21-40 years. There were 13/40 [32.5%] in age group 21-30 years and 10 [25.0%] in 31-40 years. Thus the maximum numbers of patients were in between 21-40 years [23/40 or 57.5%]. The oldest patient in this study was 72 years old. The youngest patient was 9 months old male and other was a 7-year-old boy. The occurrence of CVST in young children is very similar to the study conducted by De Veber et al. 
In CVST, large numbers of symptoms are associated with variable presentation. Most of these may be non-specific like headache, seizures, focal neurological deficit, hemiparesis, paraparesis, diminished vision, nausea, vomiting and even decreased level of consciousness. Depending upon the availability of collateral venous pathways, it can result in significant brain involvement or may be well tolerated.  In this study, headache was the most common symptom in 29/40 patients (72.5%), followed by seizures in 16/40 patients (40%) and neurological deficit in 10/40 patients (25%). This is similar to the previous study of D. Karthikeyen et al. who stated that headache is the most presenting and non-specific symptoms seen in 70-90% of cases.  Headache in most of the cases is unilateral. Focal neurological deficits such as hemiparesis, hemisensory disturbance, seizures, impairment of level of consciousness and papilledema occur in one-third to three-quarters of cases. The onset may be acute, subacute or insidious. Patients may present with symptoms that have evolved over days or weeks.
Most of the patients 16/40 (40%) presented within 7 days.While equal number of patients 9 (22.5%) presented between 8-14 and 15-30 days. One patient (2.5%) presented within 31-90 days. Five patients (12.5%) presented late after (3 months to 2 years) after onset of symptoms. These findings are similar to the findings of Jose M. Ferro et al., who observed that median delay was 9 days (5 to 18 days) for poor countries and 7 days (3-5) for countries with good income group. 
In this study, no definite cause of the CVT found was 24 (60%) patients in spite of extensive history. This figure (60%) is higher than the study conducted by Gates et al.  They stated that in 20-30% cases, underlying predisposing factor could not be revealed. It indicates that close follow up of patients is required.
Infections in the form of pan-sinusitis, mastoiditis was predisposing cause in 5 patients (12.5%). These findings are similar to the study done by Holger Allroggen, who stated that infective causes are responsible in about 8% of cases.  In our study, one infant of age nine months had systemic infection. De Veber et al. claimed that systemic and local infections are present in higher number in children. 
In this study 3 patients were using OCP from 6 months to 14 months duration. OCP have a prothrombotic effect and this is proved in laboratory by Yandenbroucke et al.  Other control studies done by Martinelli et al. revealed an increased risk of CVT in woman of younger age group who were using OCP. 
In this study, 3 cases of trauma were found [7.5%]. Two of them had closed head injury and one had depressed skull fracture present over sagittal area. Miller et al. studied 400 cases of depressed skull fractures and concluded that cerebral venous sinus involvement was seen in 11% of cases.  They depicted that sinus lumen may get damaged or obliterated with disruption of normal flow increasing intracranial pressure and along with infection may produce CVST.
In present study, one case of polycythemia (hypercoagulable) state was seen. Desechiens et al. 82 showed the prothrombin gene mutations along with deficiencies of protein C and S and anti-thrombin III or factor V Leiden may account for hypercoagulable state.  Bruno Miranda et al. (2010) found an increased risk of CVT and other VTES in cases of polycythemia. 
One case of peripartum thrombosis was found. Lauska et al described that out of one lakh deliveries, 12 cases of peripartum and postpartum sinus thrombosis were seen.  They attributed that hypercoagulable state (anti-cardiolipin) associated with puerperium may be one of the major factors.
Hypertension associated with alcohol intake was present in two cases.
In most of the patients, multiple segments of dural venous sinuses were involved at a time. The involvement of deep venous and cortical veins are much less than venous sinuses.
In about 90% of cases, dural venous sinuses were involved. Deep venous system was found affected in 17.5% of cases. These findings are similar to the findings of Bousser et al., who stated that thrombosis of deep cerebral venous system is rare and difficult to diagnose.  In present study, the most common sinus involved was superior sagittal sinus with almost equal involvement of transverse sinus and sigmoid sinus. The deep venous system was involved in 7 patients (17.5%) and superficial venous system in 2.5% of cases. Commonest association was noticed between superior sagittal and transverse or sigmoid sinus. These findings are similar to the findings of Greiner et al.  They concluded that in veno-occlusive stroke, the superior sagittal sinus followed by transverse, sigmoid, and straight were generally involved.
Acute stage thrombus was seen in 8 (20%) cases, early subacute stage thrombus was seen in 12 (30%) cases, while late subacute stage thrombus was seen in 8 (20%) cases and chronic stage thrombus was seen in 12 (30%) cases. The appearance of thrombus on MRI is variable according to the stage of thrombus as described in results. ,, Dormont et al. showed that signal varies with degree of turbulence and force of flow and the signal intensity vary with the age of clot. 
In this study, brain parenchyma was normal in 20/40 (50%) patients, while the infarction was non-hemorrhagic in 6/40 (15% cases), and 14 (35%) patients presented with hemorrhagic infarction. Tasi Fy et al. described spectrum of MR imaging and narrated that in initial stages there is mild increase in dural venous pressure, and only sinuses are affected without parenchymal abnormalities.  With further increase in intracranial pressure, focal neurological deficit takes place and affected brain region show edema or infarction with or without hemorrhage in 10 to 50% of cases. This finding was similar in present study.
In this study, 21 patients had good recovery after appropriate treatment and good nursing care. Persistent focal neurological deficit was seen in 6 patients who had hemorrhagic infarction. One patient expired and follow up of 12 patients was not available. Malvinchiu claimed in their study that mortality rate in CVT is as high as 3%-5%.  In this study, mortality rate was 2.5% may be due to early diagnosis and appropriate treatment. Intractable seizures, coma, hemorrhagic infarction, old age are some of the factors associated with poor prognosis. F. Dentali showed in his study that most of the patients have benign prognosis due to recanalization of thrombus and vessels. 
Follow-up imaging was done in 10 patients. Resolution of infarction was seen in 3 patients. Complete recanalization was noticed in three cases and partial recanalization in two cases was noted. Gliosis was seen in one old aged patient.
| Conclusion|| |
The result of present study shows that MRI and MRV are efficacious in detecting cerebral venous sinus thrombosis and brain parenchymal abnormalities due to CVST. Deep venous system involvement and isolated cortical vein thrombosis can be detected. These help in early detection and management of CVST to avoid neurological deficit. MRV is useful for demonstrating recanalization of thrombosed venous sinuses.
| References|| |
|1.||Stam J. Thrombosis of the cerebral veins and sinuses. N Engl J Med 2005;352:1791-8 |
|2.||Adams WM, Laitt RD, Beards SC, Kassner A, Jackson A. Use of single-slice thick slab phase-contrast angiography for the diagnosis of dural venous sinus thrombosis. Eur Radiol 1999;9:1614-9. |
|3.||Bogousslavsky J, Pierre P. Ischemicstroke in patientsunder age 45. Neurol Clin 1992;10:113-24. |
|4.||Bergui M, Bradac GB, Daniele D. Brain lesions due to cerebral venous thrombosis do not correlate with sinus involvement. Neuroradiology 1999;41:419-24. |
|5.||Van Gijn J. Cerebral venous thrombosis: Pathogenesis, presentation and prognosis. J R Soc Med 2000;93:230-3. |
|6.||Einhäupl KM, Villringer A, Meister W, Mehraein S, Garner C, Pellkofer M,et al. Heparintreatment in sinusvenous thrombosis. Lancet 1991;338:597-600. |
|7.||McMurdo SK Jr, Brant-Zawadzki M, Bradley WG Jr, Chang GY, Berg BO. Dural sinus thrombosis: Study using intermediate field strength MR imaging. Radiology 1986;161:83-6. |
|8.||deVeber G, Andrew M, Adams C, Bjornson B, Booth F, Buckley DJ, et al. Canadian Pediatric Ischemic Stroke Study Group. Cerebralsinovenousthrombosis in children. N Engl J Med 2001;345:417-23. |
|9.||Allroggen H, Abbott RJ. Cerebral venous sinus thrombosis.Postgrad Med J 2000;76:12-5. |
|10.||Karthikeyan D, Vijay S, Kumar T, Kanth L. Cerebral venous thrombosis-spectrum of CT findings. Ind J Radiol 2004;14:129-37. |
|11.||Ferro JM, Canhão P. Cerebral venous and dural sinus thrombosis. Pract Neurol 2003;3:214-9. |
|12.||Gates PC. Cerebralvenous thrombosis. A retrospective review. Aust N Z J Med 1986;16:766-70. |
|13.||Vandenbroucke JP, Rosing J, Bloemenkamp KW, Middeldorp S, Helmerhorst FM, Bouma BN, et al. Oral contraceptives and the risk of venous thrombosis. N Engl J Med 2001;344:1527-35. |
|14.||Martinelli I, Sacchi E, Landi G, Taioli E, Duca F, Mannucci PM. High risk of cerebral-vein thrombosis in carriers of a prothrombin-gene mutation and in users of oral contraceptives. N Engl J Med1998;338:1793-7. |
|15.||Uzan M, Ciplak N, Dashti SG, Bozkus H, Erdinçler P, Akman C. Depressed skull fracture overlying the superior sagittal sinus as a cause of benign intracranial hypertension. Case report. J Neurosurg 1998;88:598-600. |
|16.||Deschiens MA, Conard J, Horellou MH, Ameri A, Preter M, Chedru F, et al. Coagulation studies, factor V Leiden, and anticardiolipin antibodies in 40 cases of cerebral venous thrombosis. Stroke1996;27:1724-30. |
|17.||Miranda B, Ferro JM, Canhão P, Stam J, Bousser MG, Barinagarrementeria F, et al.ISCVT Investigators.Venousthromboemboliceventsaftercerebral veinthrombosis. Stroke 2010;41:1901-6. |
|18.||Lanska DJ, Kryscio RJ. Risk factors for peripartum and postpartumstroke and intracranialvenous thrombosis. Stroke 2000;31:1274-82. |
|19.||Bousser MG, Russell RR. Cerebral venous thrombosis.Philadelphia. WB Saunders;1997. p. 385-9. |
|20.||Greiner FG, Takhtani D. Neuroradiologycase of the day.Superior sagittal sinus thrombosis and infarcts. Radiographics 1999;19:1098-101. |
|21.||Sharma VK, Teoh HL. Isolated cortical vein thrombosis - the cord sign. J Radiol Case Rep 2009;3:21-4. |
|22.||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:S19-41. |
|23.||Chiewvit P, Piyapittayanan S, Poungvarin N. Cerebralvenous thrombosis: Diagnosisdilemma. Neurol Int 2011;3:e13. |
|24.||Dormont D, Anxionnat R, Evrard S, Louaille C, Chiras J, Marsault C. MRI in cerebral venous thrombosis. J Neuroradiol 1994;21:81-99. |
|25.||Tsai FY, Wang AM, Matovich VB, Lavin M, Berberian B, Simonson TM, et al. MR staging of acute dural sinus thrombosis: Correlation with venous pressure measurements and implications for treatment and prognosis. AJNR Am J Neuroradiol 1995;16:1021-9. |
|26.||Chiu M, Basiratmand S, Cader R. Cerebral Vein Thrombosis Presenting as Headache. Proc UCLA Healthcare 2002;6:7-9. |
|27.||Dentali F, Gianni M, Crowther MA, Ageno W. Natural history of cerebral veinthrombosis: Asystematic review. Blood 2006;108:1129-34. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11], [Table 12]