Isolated Cortical Vein Thrombosis Systematic Review of Case Reports and Case Series Jonathan M. Coutinho, MD, PhD; Jorn J. Gerritsma, MSc; Susanna M. Zuurbier, MD; Jan Stam, MD, PhD Background and Purpose—Isolated cortical vein thrombosis is a distinct subtype of cerebral venous and sinus thrombosis. Because of the rarity of isolated cortical vein thrombosis, limited knowledge on its clinical and radiological manifestations is available. Methods—We performed a systematic review of published data. Isolated cortical vein thrombosis had to have been diagnosed by MRI, conventional angiography, computed tomography venography, autopsy, or surgery. Cases with concurrent thrombosis of a cerebral sinus were excluded. Results—Of 175 potentially relevant studies, 47 were included in the analysis, with a total of 116 patients. All studies were case reports and case series. Mean age was 41 years and 68% were women. The most common symptoms were headache (71%), seizures (58%), and focal neurological deficits (62%). Papilledema was not reported in any patient, and increased cerebrospinal fluid pressure was reported only in 2. Infection (19%), pregnancy or puerperium (35% of women), and oral contraceptive use (21% of women) were the most common risk factors. Most cases (73%) were diagnosed with MRI, but conventional angiography was also performed in 47%. A total of 81% had a parenchymal brain lesion and 80% were treated with anticoagulation. In-hospital mortality was 6%. Conclusions—Signs of increased intracranial pressure seem to be less common in isolated cortical vein thrombosis compared with cerebral venous and sinus thrombosis. MRI and in some cases conventional angiography are the most frequently used diagnostic modalities and anticoagulation is the most widely used therapy. (Stroke. 2014;45:1836-1838.) Key Words: review, systematic ◼ sinus thrombosis, intracranial ◼ stroke
T
hrombosis of the cerebral cortical veins is mostly seen in conjunction with thrombosis of a major cerebral sinus (cerebral venous and sinus thrombosis [CVST]). Isolated cortical vein thrombosis (ICVT) is rare and has been reported only in case reports.1 Because of the paucity of data, little is known about its clinical manifestations, treatment, and outcome. The aim of the current study was to perform a systematic review of published cases on ICVT.
Methods We searched Medline, Excerpta Medica Database (EMBASE), and Current Index to Nursing and Allied Health Literature (CINAHL) (until July 1, 2013) for publications on ICVT (adult and pediatric cases), using the terms cortical vein thrombosis and cortical venous thrombosis. In addition, we searched EMBASE and Web of Science for relevant conference abstracts and the grey literature (www.opengrey.eu). The primary search was performed by 1 author (J.J.G.). Full-length articles of potentially relevant publications were reviewed independently by 2 of the authors (J.M.C. and J.J.G.). In situations of disagreement, a third author (J.S.) made the final decision. We also screened reference lists of included articles for additional relevant studies. ICVT had to have been diagnosed by MRI, conventional angiography, computed
tomography venography, or at surgery or autopsy. Cases with concurrent thrombosis of a cerebral sinus or with isolated thrombosis of the deep venous system were excluded. Studies describing both CVST and ICVT cases were included if the required data from the patients with ICVT could be extracted. Articles written in languages other than English, French, German, Spanish, Portuguese, or Dutch were only selected if they had an English abstract with sufficient data.
Results We identified 1092 publications, of which 175 were selected for full-length review. Of these, 47 articles fulfilled the inclusion criteria. All studies were case reports or case series, describing 1 to 32 cases per publication (Table I in the online-only Data Supplement). In total, we found 116 patients with ICVT. The mean age of patients was 41 years and 68% of patients were women (Table 1). There were 3 pediatric cases (1 neonatal). The median interval from symptom onset to diagnosis was 7 days (mean, 23 days). Seventy-one percent of patients reported headache, 58% had seizures, and focal neurological deficits were present in 62%. Fundoscopy was performed in 48 patients; none of these patients had papilledema.
Received December 5, 2013; final revision received March 16, 2014; accepted March 19, 2014. From the Department of Neurology, Academic Medical Centre, Amsterdam, The Netherlands. The online-only Data Supplement is available with this article at http://stroke.ahajournals.org/lookup/suppl/doi:10.1161/STROKEAHA. 113.004414/-/DC1. Correspondence to Jonathan M. Coutinho, MD, PhD, Department of Neurology, Academic Medical Centre, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. E-mail
[email protected] © 2014 American Heart Association, Inc. Stroke is available at http://stroke.ahajournals.org
DOI: 10.1161/STROKEAHA.113.004414
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Coutinho et al Review of Isolated Cortical Vein Thrombosis 1837 Table 1. Clinical Characteristics and Risk Factors
Table 2. Ancillary Investigations, Treatment, and Outcome n/N (%)*
Demographics
n/N (%)* Ancillary investigations
Mean age, y (SD)†
41 (17)
Sex (% of women)
55/81 (68%)
Clinical characteristics
CT scan MRI Conventional angiography
34/73 (47%) 13/62 (21%)
Median duration symptom onset, diagnosis (IQR)‡
7 days (3–16)
Lumbar puncture
Median duration admission, diagnosis (IQR)§
3 days (0–10)
Increased ICP (of patients who underwent LP)†
Headache
76/107 (71%)
Radiological findings
Papilledema
0/48 (0%)
46/106 (43%) 104/106 (98%)
2/11 (18%)
Hemorrhagic lesion‡
39/84 (46%)
Seizures
67/116 (58%)
Cerebral edema
31/84 (37%)
Focal neurological deficit
71/115 (62%)
Any parenchymal brain lesion§
68/84 (81%)
2/97 (2%)
Bilateral parenchymal lesions
Comatose Risk factors
Subarachnoid hemorrhage
Oral contraceptive use (% of women)
8/39 (21%)
2/63 (3%) 14/72 (19%)
Treatment and outcome
Pregnancy or puerperium (% of women)
15/43 (35%)
Anticoagulation
78/98 (80%)
Infection
18/95 (19%)
Antiepileptic drugs
34/66 (52%)
Genetic thrombophilia
10/107 (9%)
Endovascular thrombolysis
0/99 (0%)
Lumbar puncture
14/86 (16%)
Decompressive craniectomy
4/100 (4%)
Malignancy
5/109 (5%)
In-hospital mortality
7/110 (6%)
IQR indicates interquartile range. *Categorical variables are given as n/N, where n is the number of patients in which the variable was present and N the total number of patients for which that particular variable was reported. †Calculated from data of 81 patients. ‡Calculated from data of 41 patients. §Calculated from data of 42 patients.
CT indicates computed tomography; ICP, intracranial pressure; and LP, lum bar puncture. *Categorical variables are given as n/N, where n is the number of patients in which the variable was present and N the total number of patients for which that particular variable was reported. †In 2 patients who underwent lumbar puncture, the ICP was not measured. ‡Hemorrhagic infarct or intracerebral hemorrhage. §Defined as localized edema, hemorrhagic infarct, or intracerebral hemorrhage.
Oral contraceptive use (21% of women), pregnancy or puerperium (35% of women), infection (19%), and lumbar puncture (16%) were the most common risk factors. Almost all patients underwent MRI of the brain (Table 2). In 73% of patients, MRI established the diagnosis of ICVT. Conventional angiography was performed in 47%. Thirteen patients (21%) underwent lumbar puncture as part of the diagnostic work-up and only 2 had an increased cerebrospinal fluid (CSF) pressure. Both these patients also had large cerebral lesions with mass effect. Eighty-one percent of patients had a parenchymal brain lesion at imaging: hemorrhagic (hemorrhagic infarct or intracerebral hemorrhage) in 46% and localized edema in 37%. In 19% of patients localized subarachnoid hemorrhage was present. Most patients (80%) were treated with anticoagulation and 4% underwent decompressive craniectomy because of impending cerebral herniation (Table 2). Seven patients died during admission. Of these, 5 had an underlying infection (meningitis in 4). Only 2 of the patients who died received treatment with anticoagulation and none underwent decompressive hemicraniectomy.
patient with ICVT, compared with 28% of patients with CVST. Headache was also less common in ICVT (71% versus 89%), although still present in most cases. The almost invariable presence of headache in CVST is partly explained by intracranial hypertension. Because in ICVT the venous outflow through the large sinuses is not affected, intracranial hypertension is less likely to occur. The absence of papilledema in these cases and the lower frequency of headache would support this hypothesis. Furthermore, although increased CSF pressure is a common finding in patients with CVST,3 only 2 of 11 patients with ICVT had increased CSF pressure. Both these patients had a large venous infarct, which might explain the increased CSF pressure. Unfortunately, the large amount of missing data on papilledema and CSF pressure makes it difficult to draw definitive conclusions on the frequency of intracranial hypertension in ICVT. A parenchymal brain lesion (localized edema, hemorrhagic infarct, or intracerebral hemorrhage) was present in the majority of patients with ICVT, more often than in patients with CVST in the ISCVT study (81% versus 63%).2 This is in agreement with the hypothesis that venous infarcts are caused by thrombosis of cortical veins because not all patients with CVST have thrombosis of a cortical vein.4 However, the high frequency of venous infarcts in ICVT could also be the result of selection bias because case reports tend to describe more severe cases. Also, without such infarcts the diagnosis of ICVT is even more difficult. Patients without visible brain lesions and thus with less severe neurological symptoms may be misdiagnosed more often or even be missed altogether.
Discussion This is the first systematic review of the literature on ICVT. Comparison of our data with the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT) shows that the clinical manifestations of ICVT largely coincide with those of CVST.2 However, papilledema was not reported in any
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1838 Stroke June 2014 MRI was the most frequently used imaging method, especially in contemporary studies. Although we lacked data to determine whether computed tomography venography is insufficient to diagnose ICVT, this imaging technique was used rarely. When MRI is performed, a T2*-gradient echo sequence should be included because this is the most sensitive technique to demonstrate the presence of a thrombus in a cortical vein.1 In difficult cases, however, even MRI can be nondiagnostic, and conventional angiography may still be required. It seems prudent to extrapolate the guidelines on the treatment of CVST to patients with ICVT.5 Anticoagulation with therapeutic doses of heparin therefore seems to be the standard of care, as was used in most patients. In rare cases where impending herniation occurs, decompressive craniectomy should be performed, similar to CVST.6 Endovascular thrombolysis does not seem to be an option because the cortical veins cannot be reached with a microcatheter without a high-risk perforation. The in-hospital mortality of 6% in the published cases is similar to the mortality in CVST (4.3% in the ISCVT study). Death most often occurred in patients with an infection of the central nervous system, which is also an established risk factor for poor outcome in CVST.2 An important limitation of our study is that we only identified case reports and case series. As a result, publication bias is a probable confounder and the data must be interpreted with caution. For instance, 16% of the patients developed ICVT after lumbar puncture, mostly after epidural anesthesia. Although lumbar puncture is a known risk factor for CVST or ICVT, it is improbable that this percentage is an accurate estimate. Instead, it is much more likely that these patients are over-represented in the literature because neurological complications are among the most-feared complication of epidural anesthesia. In conclusion, our systematic review suggests that signs of increased intracranial pressure are less common in ICVT
compared with CVST, whereas localized cerebral edema or hemorrhagic lesions are more frequent in ICVT. MRI and conventional angiography are the most frequently used diagnostic modalities, and anticoagulation is the most widely used therapy.
Sources of Funding Dr Coutinho has received research grants from The Netherlands Organisation for Scientific Research, The Thrombosis Foundation Holland, The Dutch Heart Foundation, and The Netherlands Brain Foundation.
Disclosures None.
References 1. Boukobza M, Crassard I, Bousser MG, Chabriat H. MR imaging features of isolated cortical vein thrombosis: diagnosis and follow-up. Am J Neuroradiol. 2009;30:344–348. 2. Ferro JM, Canhão P, Stam J, Bousser MG, Barinagarrementeria F; ISCVT Investigators. Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke. 2004;35:664–670. 3. Bansal BC, Gupta RR, Prakash C. Stroke during pregnancy and puerperium in young females below the age of 40 years as a result of cerebral venous/venous sinus thrombosis. Jpn Heart J. 1980;21:171–183. 4. Bergui M, Bradac GB, Daniele D. Brain lesions due to cerebral venous thrombosis do not correlate with sinus involvement. Neuroradiology. 1999;41:419–424. 5. Saposnik G, Barinagarrementeria F, Brown RD Jr, Bushnell CD, Cucchiara B, Cushman M, et al; American Heart Association Stroke Council and the Council on Epidemiology and Prevention. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42:1158–1192. 6. Ferro JM, Crassard I, Coutinho JM, Canhão P, Barinagarrementeria F, Cucchiara B, et al; Second International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT 2) Investigators. Decompressive surgery in cerebrovenous thrombosis: a multicenter registry and a systematic review of individual patient data. Stroke. 2011;42:2825–2831.
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Supplemental material Table I: study characteristics
First author Ishiwata
1 2
Milandre 3
Yokota
DiNubile
4
Year of
Nr. of
publication
patients*
Mode of diagnosis
Selection of specific patients
1985
1
DSA
None
1989
1
DSA
None
1990
1
DSA
None
1990
9
DSA, autopsy or
Sepsis related
surgery 5
Chang
Vuillier
6
Jacobs
7
Derdeyn Rudolf
8
9
10
Park
11
Minadeo 12
Stocks Ahn
13 14
Chang
1995
1
DSA
None
1996
1
DSA
Genetic thrombophilia
1996
4
DSA
None
1998
1
DSA
Ulcerative colitis
1999
1
Surgery
None
1999
1
DSA
None
1999
1
MRI
None
2000
1
MRI
Pregnancy and epidural anesthesia
2003
1
MRI
None
2004
3
MRI
Subarachnoid hemorrhage present
Cakmak
15
2004
2
MRI
None
Duncan
16
2005
1
DSA
None
2005
1
MRI
None
2005
4
MRI or DSA
None
2006
32
MRI
None
2007
1
MRI
Spontaneous intracranial hypotension
2007
1
CT-venography
Pregnancy and epidural anesthesia
2007
1
MRI
Spontaneous intracranial hypotension
2007
1
DSA
Spontaneous intracranial hypotension
2008
1
MRI
None
2009
1
MRI
None
Rubí
17
Urban
18
Sagduyu Lai
19
20
Katzin
21
Richard Wang
22
23
Chakraborty Sharma
24
25
Boukobza
26
2009
8
MRI
None
Albayram
27
2009
1
MRI
Epidural anesthesia
Thamburaj
28
2009
1
MRI
Leukemia
Sasidharan
29
2009
1
MRI
None
Bittencourt
30
2009
1
MRI
Subarachnoid hemorrhage present
Rodrigues
31
2009
3
MRI
None
Martins
2009
1
CT-venography
None
Sinha
33
2010
1
MRI
After lumbar puncture
Yildiz
34
2010
3
MRI
Epidural anesthesia
2010
1
DSA
Subarachnoid hemorrhage present
2010
3
MRI
None
2011
3
MRI or DSA
Subarachnoid hemorrhage present
2011
5
MRI or DSA
None
2012
1
MRI
Pregnancy and epidural anesthesia
40
2012
1
MRI
None
41
2012
1
MRI
Pregnancy and epidural anesthesia
2013
1
MRI
None
2013
3
MRI
None
2013
1
MRI
Pregnancy and epidural anesthesia
2013
1
MRI
None
2013
1
DSA
Sickle cell disease
2013
1
MRI
After lumbar puncture
32
Morris Linn
36
Oda
37
35
Rathakrishnan Fiala
39
Martinez
Machado Lavan Xue
42
43
Laverse
44
Khosravi
45
Hamamoto Adatia
47
46
38
*Only the number of patients with ICVT is provided. The original publication may describe additional patients. DSA = digital substraction angiography
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(26) 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;30:344-348. (27) Albayram S, Kara B, Ipek H, Ozbayrak M, Kantarci F. Isolated cortical venous thrombosis associated with intracranial hypotension syndrome. Headache. 2009;49:916-919. (28) Thamburaj K, Choudhary A. Hyperintense vessel sign: isolated cortical venous thrombosis after L-asparaginase therapy. Pediatr Radiol. 2009;39:757. (29) Sasidharan PK, Mohamed A. Cortical venous thrombosis due to acquired hyperhomocysteinaemia. Natl Med J India. 2009;22:300-301. (30) Bittencourt LK, Palma-Filho F, Domingues RC, Gasparetto EL. Subarachnoid hemorrhage in isolated cortical vein thrombosis: are presentation of an unusual condition. Arq Neuropsiquiatr. 2009;67:1106-1108. (31) Rodrigues AM, Mariz JA, Fernandes J, Ribeiro M, Ferreira C, Rocha J, et al. Isolated cortical vein thrombosis - Clinical and imaging findings. Cerebrovasc Dis. 2009;27:186.
(32) Martins J. Santos G, Casimiro C, Marnoto D. The role of ct-venography imaging on the diagnosis of an isolated cortical vein thrombosis case. Neuroradiology. 2009;51:S118.
(33) Sinha A, Petkov S, Meldrum D. Unrecognised dural puncture resulting in subdural hygroma and cortical vein thrombosis. Anaesthesia. 2010;65:70-73. (34) Yildiz OK, Balaban H, Cil G, Oztoprak I, Bolayir E, Topaktas S. Isolated cortical vein thrombosis after epidural anesthesia: report of three cases. Int J Neurosci. 2010;120:447-450. (35) Morris JG, Fisher M, Carandang RA. Cortical Vein Thrombosis as a Mimic for Isolated Cortical Subarachnoid Hemorrhage and Transient Ischemic Attack. Case Rep Neurol. 2010;2:63-68. (36) 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. (37) Oda S, Shimoda M, Hoshikawa K, Osada T, Yoshiyama M, Matsumae M. Cortical subarachnoid hemorrhage caused by cerebral venous thrombosis. Neurol Med Chir (Tokyo). 2011;51:30-36.
(38) Rathakrishnan R, Sharma VK, Luen TH, Chan BP. The clinico-radiological spectrum of isolated cortical vein thrombosis. J Clin Neurosci. 2011;18:1408-1411. (39) Fiala A, Furgler G, Baumgartner E, Paal P. Delayed subdural haematoma complicated by abducens nerve palsy and cortical vein thrombosis after obstetric epidural anaesthesia. Br J Anaesth. 2012;108:705-706. (40) Martinez PM, Rodriguez G, Langendorf F. Convexity Subarachnoid Hemorrhage Heralding an Isolated Cortical Vein Thrombosis. Cerebrovasc Dis. 2012;34:2-3.
(41) Machado Olano F. Freire L, Armand R, Gracia C, Ortells P. Cerebral venous thrombosis after accidental dural puncture and blood patch. Eur J Anaesthesiol. 2012;29:163.
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(43) Xue SF, Ma QF, Ma X, Jia JP. Isolated cortical vein thrombosis: a widely variable clinicoradiological spectrum. Eur Neurol. 2013;69:331-335. (44) Laverse E, Cader S, de Silva R, Chawda S, Kapoor S, Thompson O. Peripartum isolated cortical vein thrombosis in a mother with postdural puncture headache treated with an epidural blood patch. Case Rep Med. 2013;2013:701264. (45) Khosravi M, Hill CS, Kitchen N. Cord sign: cortical venous thrombosis evolving to a ring enhancing lesion. Br J Neurosurg. 2013;27:139-140. (46) Hamamoto Filho PT, Gabarra RC, Braga GP, Ruiz E Resende LS, Bazan R, Zanini MA. Isolated cortical vein thrombosis in a patient with sickle cell disease: treatment with decompressive craniotomy and anticoagulation and literature review. Neurol India. 2013;61:173-175. (47) Adatia SP, Nambiar VK. Isolated cortical vein thrombosis from lumbar puncture: high suspicion yields high diagnostic yield. Neurol India. 2013;61:181-183.
Isolated Cortical Vein Thrombosis: Systematic Review of Case Reports and Case Series Jonathan M. Coutinho, Jorn J. Gerritsma, Susanna M. Zuurbier and Jan Stam Stroke. 2014;45:1836-1838; originally published online April 17, 2014; doi: 10.1161/STROKEAHA.113.004414 Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2014 American Heart Association, Inc. All rights reserved. Print ISSN: 0039-2499. Online ISSN: 1524-4628
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Data Supplement (unedited) at: http://stroke.ahajournals.org/content/suppl/2014/04/17/STROKEAHA.113.004414.DC1.html
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