Cerebral Venous Sinus Thrombosis in Inflammatory Bowel Disease: A Review of Published Case Reports


Aishah Ibrahim Albakr, MD1; Noor AlMohish, MBBS1

Perm J 2021;25:21.031

E-pub: 06/02/2021

Cerebral venous sinus thrombosis (CVST) is a rare extraintestinal manifestation of inflammatory bowel disease (IBD), and the risk of poor clinical outcomes remains high in patients with delayed CVST diagnoses. This study aimed to highlight the need to recognize the critical nature of CVST complications in IBD and the challenges associated with managing concurrent conditions. We retrospectively reviewed previously reported cases of CVST in patients with IBD by searching the PubMed, Web of Science, and Google Scholar databases for articles published between 2013 and 2020. Our search identified 35 cases of IBD complicated by CVST. The mean patient age was 24.6 years (range, 31 months-47 years; men > women, ratio, 1.18:1). CVST was 3.8 times more common among patients with ulcerative colitis than among those with Crohn’s disease. Active IBD was reported in 91.4% of patients. The mean interval between IBD diagnosis and CVST occurrence was 3 years (range, 2 days-16 years). Headache was the most frequently reported symptom (85.7%), and involvement of multiple sinuses was reported in almost two-thirds of the patients. Corticosteroid therapy at the time of the CVST event was the most common prothrombotic risk factor, present in 57.14% of patients. The overall recovery rate after treatment was 77.14%; whereas the bleeding complication rate was 10%. This review provides essential information that can aid clinicians in making earlier diagnoses and promotes preventive strategies for CVST in patients with IBD. Given that CVST management can be challenging in these patients, a multidisciplinary approach is warranted.


Inflammatory bowel disease (IBD)—which includes Crohn’s disease (CD), ulcerative colitis (UC), and unclassified IBD (IBD-U)—is characterized by both local (ie, intestinal) and systemic manifestations of chronic inflammation. Recently, there have been increases in the rate of IBD in developing countries, possibly as a result of westernization of dietary habits. Moreover, the highest incidence rates of IBD have been reported in northwestern Europe and North America.1,2

Extraintestinal manifestations of IBD are apparent in 5% to 50% of patients, with 29% of these manifestations occurring approximately 15 years after the initial diagnosis.2 Venous thromboembolism (VTE) is among the most critical extraintestinal manifestations, with a reported prevalence rate of 7.5% and a 1.7-fold increased risk among patients with IBD compared with the general population.3 Although patients with IBD develop cerebral venous sinus thromboses (CVST) at a younger age than those without IBD,4 the incidence of VTE is higher among older adults with IBD than among their younger counterparts.3-6 VTE events are also more frequent in patients with UC than in those with CD, and the risk is relatively higher in patients with active disease.3-6 Figure 1 summarizes the key prothrombotic factors in IBD patients.


Figure 1. Pathogenesis of inflammatory bowel disease (IBD)-associated venous thrombosis. Information adapted from the studies by Senchenkova et al71 and Scaldaferri et al.72 APC = activated protein C; EPCR = endothelial cell protein C receptor; IL-1B = interleukin 1-β; NO = nitric oxide; PAI-1 = plasminogen activator inhibitor 1; PAI-2 = plasminogen activator inhibitor 2; TF = tissue factor; TNF = tumor necrosis factor; tPA = tissue plasminogen activator; VEGF = vascular endothelial growth factor; VWF = von Willebrand factor.

The gap in knowledge that led to this review being conducted is not clear and must be stated.3-6 We have summarized the reported cases of IBD complicated by CVST, with a focus on demographic characteristics, risk factors, clinical aspects, disease management, and prognosis.


Search Strategy and Statistical Analysis

We performed a literature search for manuscripts published between November 2012 and January 2020 using the following keywords: “inflammatory bowel disease, ulcerative colitis, and Crohn’s disease,” “cerebral venous sinus thrombosis,” “dural venous sinus thrombosis,” and “diagnosis and management of cerebral venous thrombosis.” We searched the Web of Science, PubMed, and Google Scholar databases to identify cases of IBD complicated by CVST in both adults and children. Google Translate (http://translate.google.co.uk/) was used for reports not written in English, and references were scanned using Google Electronic.

We obtained information related to patient demographics, risk factors, clinical features, IBD drugs, thrombosed veins, treatments, and outcomes. Missing data were recorded as not available. Descriptive statistics are presented in the text and tables using frequencies and means.


Demographic Data

We identified a total of 35 patients with IBD7-36 with neuroimaging-confirmed CVST (Table 1). The largest case series included 6 patients with IBD.16 Among the 35 patients identified, there were 16 women and 19 men, with a male-to-female ratio of 1.18:1. The mean age at CVST diagnosis was 24.6 years, with the youngest case having been reported in a 31-month-old boy with UC.34

Table 1. Case reports of patients with IBD who developed CVST

Study Disease IBD treatment Clinical features Thrombosed sinus Treatment Outcome
Dababneh et al (2014)7 UC, active Not mentioned Age/sex: 35 y/F DCV/SSS/TS/SS/IJV LMWH Complete recovery
Time from UC diagnosis to CVST onset: not mentioned
Presenting symptoms: altered LOC and headache
Menon et al (2013)8 UC, active Steroids, 5-aminosalicylic acid, and sulfasalazine Age/sex: 35 y/F SSS/TS LMWH followed by aspirin, AEDs Complete recovery
Time from UC diagnosis to CVST onset: 2 d
Presenting symptoms: headache and seizures
Mahmoud Reza et al (2013)9 UC, active Corticosteroid, mesalamine Age/sex: 11 y/M SSS Heparin and warfarin for 6 mo Complete recovery At the 6-mo follow-up, the patient had 2 UC exacerbations with a normal MRV
Time from CD diagnosis to CVST onset: 3 mo
Presenting symptoms: (pseudotumor cerebri) headache/photophobia, blurred vision, and repeated vomiting
Kosmidou et al (2013)10 CD, active Corticosteroids, adalimumab Age/sex: 44 y/F SSS Therapeutic dose of enoxaparin for 6 mo Complete recovery, normal MRV after 3 mo
Time from CD diagnosis to CVST onset: 5 y
Presenting symptoms: psychiatric manifestations
Jaqua et al (2013)11 UC, active Sulfasalazine, 6-mercaptopurine, and corticosteroids Age/sex: 22 y/M CVST/undetermined Enoxaparin followed by warfarin Complete recovery
Time from UC diagnosis to CVST onset: 3 y
Presenting symptoms: headache
Cojocaru et al(2014)13 UC, active Sulfasalazine, corticosteroids Age/sex: 32 y/M SSS/SS/TS LMWH, AEDs Complete recovery
Time from UC diagnosis to CVST onset: NA
Presenting symptoms: headache, generalized convulsive seizures, drowsiness, papilledema
Kwon et al (2014)14 CD, active Mercaptopurine Age/sex: 44 y/F SSS/TS/SS/IJV Heparin, local fibrinolysis, mechanical thrombectomy, warfarin Partial recovery
Time from CD diagnosis to CVST onset: NA
Presenting symptoms: headache/nausea/vomiting/photophobia
Patient course: clinical deterioration (decreased GCS)
Calcagno et al (2015)15 UC, active Corticosteroids, mesalamine Age/sex: 22 y/M Superficial vein and SS Heparin/warfarin Complete recovery
Time from UC diagnosis to CVST onset: NA
Presenting symptoms: headache and speech disturbances
DeFilippis et al (2015)16 Case series n = 6 4 UC/2 CD; all had active disease 4 patients on corticosteroids, 2 on CS and anti-TNF agents Age/sex: 3 M and 3 F; mean age: 18.7 y (10-34 y) The most common locations were SSS and SS, both occurring in 3 patients. Four patients had multiple cerebral thrombi involving both DCV and superficial veins All patients received heparin followed by warfarin for 6 mo Complete recovery: 3/6, 50%; minor deficit: 1/6, 16%; death: 2/6, 33%
Time from diagnosis to CVST onset: median duration of 3.5 y (0.5-16 y)
Presenting symptoms: headache or altered LOC
Shaikh et al (2015)12 UC, active Corticosteroid, mesalamine Age/sex: pre-teenage/M Vein of Galen and SS Combined use of Solitaire FR and Penumbra devices for EVT followed by LMWH Complete recovery
Time from UC diagnosis to CVST onset: 8 wk
Presenting symptoms: 2-d history of headache, confusion, bilateral leg weakness
Patient course: clinical deterioration (decreased GCS) over 2 d
Meher et al (2016)17 UC, remission Corticosteroid, 5-amino salicylic acid, and sulfasalazine Age/sex: 38 y/F TS/SS LMWH followed by warfarin, AED Complete recovery
The onset of CVST from CD diagnosis: 2 y
Presenting symptoms: headache/nausea/vomiting/photophobia/blurring of vision seizures altered LOC
Hashim et al. (2016)18 UC, active Corticosteroid mesalamine Age/sex: 35 y/M SSS LMWH followed by warfarin, AEDs Complete recovery
Time from UC diagnosis to CVST onset: 10 y
Presenting symptoms: headache/nausea/vomiting/seizures
Cho et al (2016)19 CD, active/ileo-colonic Infliximab Age/sex: 17 y/F Cortical veins, SSS, TS, IJV Heparin and rivaroxaban for 6 mo Resolution of the venous thrombosis with recanalization on MRV after 2 wk
Time from CD diagnosis to CVST onset: 4 y
Presenting symptoms: severe headache and vomiting
Taous et al. (2016)20 UC, active New onset Age/sex: 22 y/F TS/SS Anticoagulation Complete recovery
Time from UC diagnosis to CVST onset: CVST revealed UC diagnosis
Presenting symptoms: sudden-onset language dysfunction
Marusic et al (2017)21 UC, active Pulsed steroid therapy Age/sex: 15 y/M SSS/TS LMWH Complete recovery
Time from UC diagnosis to CVST onset: 2 y
Presenting symptoms: headache
Goh et al (2017)22 UC, active 6-mercaptopurine and steroids Age/sex: 47 y/M SSS Heparin and warfarin Complete recovery
Time from UC diagnosis to CVST onset: 5 mo
Presenting symptoms: seizures
Dallimore et al (2018)23 UC, active NA Age/sex: 25 y/F SSS/DCV Heparin Complete recovery
Time from UC diagnosis to CVST onset: NA
Presenting symptoms: seizures
Conners et al (2018)24 UC, active Infliximab Age/sex: 17 y/F SSS/TS/SS LMWH, AEDs Complete recovery
Time from UC diagnosis to CVST onset: NA
Presenting symptoms: headache/confusion/recurrent tonic-clonic seizures
Abdalla et al (2019)25 There are 2 references that begin with UC, active Mesalamine, 6-mercaptopurine/pulsed steroid therapy Age/sex: 27 y/M SSS Heparin and apixaban, AEDs Partial recovery/discharged to a rehabilitation facility
Time from UC diagnosis to CVST onset: NA
Presenting symptoms: acute-onset right-sided numbness and weakness/seizures/headache
Lee et al(2018)26 UC, active New onset Age/sex: 35 y/M SSS/TS Heparin and lifelong warfarin Complete recovery
Time from UC diagnosis to CVST onset: simultaneous diagnosis
Presenting symptoms: headache, decreased LOC, intermittent dystonic posture of the right arm, focal motor weakness
Mathew et al (2018)27 UC, active New onset Age/sex: 32 y/M SSS LMWH Complete recovery
Time from UC diagnosis to CVST onset: NA
Presenting symptoms: headache/seizures
Zhu et al (2019)28 CD, active, colonic disease Azathioprine Age/sex: 31 y/M SS Heparin and warfarin, AEDs Complete recovery
Time from CD diagnosis to CVST onset: 7 y
Presenting symptoms: headache/nausea/vomiting/seizures
Bouomrani et al (2019)29 CD, active ileal disease New onset Age/sex: 28 y/F TS Heparin and warfarin Complete recovery for 2 y
Time from CD diagnosis to CVST onset: simultaneous diagnosis
Presenting symptoms: headache/nausea/vomiting/blurred vision
Martín-Masot al. (2019)30 UC, postproctocolectomy Corticosteroids, azathioprine, mesalamine Age/sex: 5 y and 2 mo/M TS Heparin and warfarin, AEDs Complete recovery at the 3-y follow-up
Time from UC diagnosis to CVST onset: 3 y
Presenting symptoms: headache, monoparesis, focal and recurrent seizures
Deskur et al (2019)31 UC, active CS Age/sex: 25 y/M TS LMWH for 15 mo Complete recovery
Time from UC diagnosis to CVST onset: 2 y
Presenting symptoms: subacute headache for 2 mo, followed by severe headache associated with nausea
Stamp et al (2019)32 UC, active New onset Age/sex: 17 y/F SSS and SS LMWH (long-term), AEDs Complete recovery
Time from UC diagnosis to CVST onset: NA
Presenting symptoms: headache, seizures, altered LOC, and focal weakness
Stamp et al (2019)32 UC, active Azathioprine, infliximab Age/sex: 26 y/M SS/DVS LMWH, AEDs Bleeding per rectum after LMWH; partial recovery
Time from UC diagnosis to CVST onset: 2 mo
Presenting symptoms: seizures/altered LOC/motor weakness
Orfei et al (2019)33 IBD-U New onset Age/sex: 17 y/M TS/SS/IJV LMWH followed by warfarin, ventriculoperitoneal shunting Complete recovery
Time from IBD diagnosis to CVST onset: 18 mo
Presenting symptoms: headache, nausea, vomiting (delayed diagnosis for 3 wk)
Rivera-Suazo et al (2020)34 UC, active Corticosteroids, azathioprine, infliximab Age/sex: 2 y and 7 mo/M SSS LMWH, AEDs Active bleeding; complete recovery
Time from UC diagnosis to CVST onset: 15 mo
Presenting symptoms: seizures, motor weakness
Arsovska et al (2019)35 UC, active Sulfasalazine and azathioprine Age/sex: 19 y/F SSS LMWH for 6 mo because of melena, switched to warfarin, and then switched to rivaroxaban (lifelong), AEDs Partial recovery with mRS of 3; recurrent seizures 14 mo after CVST episode
Time from UC diagnosis to CVST onset: 1 y
Presenting symptoms: headache, motor weakness
Patient course: clinical deterioration for 3 wk (seizures, decreased GCS)
Liu et al (2020)36 UC, active New onset Age/sex: 12 y/F SSS superior mesenteric artery thrombosis LMWH, EVT followed by LMWH and warfarin Partial recovery
Time from UC diagnosis to CVST onset: simultaneous diagnosis
Presenting symptoms: seizures/left-sided weakness

AEDs = anti-epileptic drugs; CD = Crohn’s disease; CS = corticosteroid; CVST = cerebral venous sinus thrombosis; d = days; DCV = deep cerebral vein; DVS = deep vein system; EVT = endovascular treatment; F = female; GCS = Glasgow Coma Scale; IBD = inflammatory bowel disease; IBD-U = IBD-unclassified; IJV = internal jugular vein; LMWH = low-molecular weight heparin; LOC = level of consciousness; M = male; mo = months; mRS = modified Rankin score; MRV = magnetic resonance venography; NA = not available SS = sigmoid sinus; SSS = superior sagittal sinus; TNF = tumor necrosis factor; TS = transverse sinus; UC = ulcerative colitis; wk = weeks; y = years.

Possible Thrombotic Risk Factors in Patients With IBD

CVST risk factors other than IBD were reported in 23 patients (65.7%; Table 2). Anemia (hemoglobin < 12 mg/dL) was reported in 15 of 35 patients (42.8%)7-12,17-20,26,28,29,31,33-36 and represented the sole risk factor other than IBD in 5 of 15 patients (33.3%).7,8,19,20,29 Normocytic normochromic anemia was noted in 2 patients,17-29 whereas microcystic hypochromic anemia was noted in 1 patient.32 The other reports did not specify the type of anemia. Twenty patients (57.14%) were on corticosteroids at the time of the CVST event,9-13,15-18,21,22,25,28,30,31,33,34 and corticosteroid use represented the only risk factor for CVST in 6 of these patients.13,15,21,22,25-34 One patient was reported to have experienced multiple thrombotic episodes, including CVST, Budd–Chiari syndrome, and idiopathic thrombocytopenia.11 Two patients had a history of deep vein thrombosis.14-23 One patient was found to have superior mesenteric artery thrombosis during the CVST event,36 whereas another patient exhibited left radial artery occlusion.22 Two patients (5.7%) developed CVST events postoperatively: one experienced the event while on VTE prophylaxis,12 whereas the other was an adolescent who was not on prophylaxis and had multiple other risk factors (ie, homozygous methylene-tetra-hydro-folate reductase [MTHFR] gene C677T mutation, total parenteral nutrition, and immobility).30 Hormonal therapy (oral contraceptive pills16 or estradiol patches14) at the time of IBD exacerbation was reported in 2 patients with CD (5.7%).

Table 2. Risk factors for CVST in patients with IBD (n = 35)

Risk factor Number (%)
Corticosteroid therapy 20 (57.14)
Anemia 15 (42.8)
Previous thrombotic events 5 (14.2)
Inherited thrombophilia 4 (11.4)
High homocysteine level 2 (5.7)
Hormonal therapy 2 (5.7)
Postoperative status 2 (5.7)

CVST = cerebral venous sinus thrombosis; IBD = inflammatory bowel disease.

Inherited thrombogenic mutations were reported in 4 of 35 patients (11.4%). These included heterozygous factor V Leiden gene mutation,14 heterozygous MTHFR gene mutation,16 and homozygous MTHFR gene mutation each in 1 patient.30 One patient had multiple mutations that included a heterozygous MTHFR mutation, heterozygous factor XIII mutation, homozygous endothelial nitric oxide synthase (eNOS-786 T>C) mutation, heterozygous B-fibrinogen mutation, and heterozygous eNOS G894T and lymphotoxin A mutations.35 Laboratory investigations revealed hyperhomocysteinemia in 2 patients (5.7%).13,27 A thrombophilia screen was performed in 25 patients, revealing transient abnormalities of the coagulation system in 3 (12%)10,11,19 and persistently high antiphospholipid antibodies in 1 (4%).28

Clinical Presentation

UC was more common than CD (n = 27 vs n = 7). One patient had IBD-U.33 Active disease was present in 32 patients (91.4%), whereas 3 patients (8.5%) were in remission.17,30-33 In 20% of the patients, the CVST event had occurred at or before the time of IBD diagnosis.8,20-29,32-36 The mean interval between IBD diagnosis and a subsequent CVST event was 3 years (range, 2 days-16 years). Headache was the most common symptom (n = 30, 85.7%), followed by seizures (n = 17, 48.5%), focal neurologic disorder (n = 12, 34.2%), changes in mental status (n = 11, 31.4%), and symptoms of increased intracranial pressure, such as nausea, vomiting, and papilledema (n = 11, 31.4%). A severe symptomatic increase in intracranial pressure requiring ventriculoperitoneal shunting was reported in a 17-year-old male patient with IBD-U.33 One patient with CD exhibited agitation accompanied by anxiety attacks, thoughts of impending doom, paranoia, and insomnia in the absence of headache or other common symptoms.12

Location of the Thrombosed Sinus

The most common thrombosed sinus was the superior sagittal sinus (n = 25, 71.4%). Thromboses were observed in the transverse sinus, sigmoid sinus, and deep cerebral/cortical veins in 14 (40%), 15 (42.8%), and 5 patients (14.2%), respectively. Involvement of more than 1 sinus was reported in 23 patients (65.7%).


All patients (100%) had received anticoagulation treatment with heparin or low-molecular weight heparin (LMWH) in the acute phase of CVST. Three patients underwent endovascular treatment (EVT) via thrombolysis or mechanical thrombectomy because of progressive clinical and radiologic deterioration refractory to anticoagulation therapy.12,14,36 Maintenance heparin or LMWH was used in 12 patients (34.2%).7,10,12,13,21,23,24,27,31,32,34 LMWH treatment was followed by warfarin administration in 18 patients (58.06%).9,11,15-18,22,26,28,29,30-33,36 One patient who was initially treated with warfarin was switched to rivaroxaban because of deterioration of the international normalized ratio (INR) after eating a green salad.35 Two patients were treated with LMWH followed by novel anticoagulants (apixaban25 and rivaroxaban19), whereas 1 patient was treated with LMWH followed by aspirin.8 In 1 case report, the type of anticoagulation therapy was not specified.22 Long-term anticoagulation therapy was given to 4 of 35 patients.26,31,32,35 Complete recovery was achieved in 27 patients (77.14%), whereas partial recovery was achieved in 6.14,16,25,32,35,36 Two patients died16: 1 died as a result of severe CVST and brain edema, whereas the other had recovered from CVST but died secondary to bowel perforation.16 Active bleeding after LMWH was reported in 3 patients whose therapy had been temporarily discontinued. All 3 patients stabilized and ultimately achieved complete recovery after resumption of treatment.32,34,35 Anti-epileptic drugs were administered to 17 patients with symptomatic seizures. One patient experienced recurrent seizures after 14 months of anti-epileptic drug treatment.35 No other cases of recurrence were reported.


This review of published case reports (Table 1) demonstrates that patients with IBD experiencing CVST tend to be young males, which is consistent with previous studies.37,38 However, we observed a younger age of onset than that reported in the review by Cognat et al37 (mean, 24.6 vs 30.7 years, respectively). One Danish study reported that young patients with IBD (< 20 years old) were at increased risk for developing VTE (hazard ratio, 6) compared with age- and sex-matched individuals without IBD.39 Nylund et al40 observed that children and adolescents (5-20 year old) with IBD were also at increased risk of venous thrombosis. Our analysis suggests that male patients with IBD were more often affected with CVST than their female counterparts, although the male-to-female ratio appeared nearly equal. This discrepancy is most likely explained by a higher percentage (40%) of patients under the age of 17 years, which is in turn associated with lower rates of pregnancy and hormonal therapy. Similarly, Acikgoz et al41 reported that CVST occurs in adolescents of both sexes, with IBD at equal rates.

In the International Study on Cerebral Vein and Dural Sinus Thrombosis, the presence of more than 1 risk factor was observed in 44% of the patients with CVST. Therefore, even when 1 risk factor has been identified, a complete workup should be performed to identify other potential factors.42 In this review, almost two-thirds of the patients had possible prothrombotic risk factors other than IBD at the time of the CVST event. Overall, the distribution of prothrombotic risk factors (Table 2) is relatively similar to that reported in a previous study.38 Our review verified the high risk of thrombosis in patients with active IBD (hazard ratio, 8.4),43,44 and we observed that most patients had active disease. In fact, active disease was the only risk factor in one-third of the patients with UC and CD at nearly rates; similar findings were reported by Katsanos et al.38 The risk of CVST is particularly high in patients with IBD after surgery, which is known to increase the risk of VTE by nearly 40-fold44; therefore, VTE prophylaxis has been recommended in surgical candidates.45 However, Kosmidou et al10 reported a case of superior sagittal thrombosis that occurred while the patient was on thromboprophylaxis after surgical treatment for a perianal abscess. This report contradicts the available evidence and suggests that VTE prophylaxis should not prevent clinicians from considering a diagnosis of CVST. Table 3 summarizes the recommendations for CVST prophylaxis in patients with IBD.

Table 3. Summary of recommendations for CVST prophylaxis in patients with IBD

Consideration Recommendation
Type of thromboprophylaxis If the bleeding risk is high or active bleeding is present, mechanical thromboprophylaxis using graduated compression stockings/intermittent pneumatic compression is recommended. If the bleeding risk is decreased, prophylactic anticoagulation therapy should be considered.45
CVST prophylaxis in hospitalized patients with IBD CVST prophylaxis is recommended for all hospitalized patients with severe disease and no contraindications to thromboprophylaxis.60,73-75
Hospitalized patients with reversible prothrombotic risk factors All reversible IBD- and patient-related risk factors should be managed appropriately, which includes: treating disease activity and its complications, adequate hydration, treating infections, vitamin supplementation in case of deficiency, early mobilization, cessation of smoking and oral contraceptive use, avoiding indwelling catheters, and treating other coexisting conditions such as anemia or antiphospholipid syndrome.45
Pregnant women with a history of CVST Prophylactic use of anticoagulation is recommended for women with a history of CVST during pregnancy or the postpartum period with no contraindications to prophylaxis.76
Patients with IBD undergoing major surgery Prophylactic use of anticoagulation is recommended.45,77

CVST = cerebral venous sinus thrombosis; IBD = inflammatory bowel disease.

Because most patients in this review had active disease, corticosteroid therapy was used in a large percentage of cases. Theoretically, corticosteroids exert an anti-inflammatory effect; however, some studies have reported that steroids increase the risk of thrombosis in patients with IBD. In a 2015 retrospective study of 15,000 adult patients with IBD, corticosteroid use contributed to an almost 5-fold increase in the risk of thrombotic events.46 As reported by a recent meta-analysis, patients with IBD who used corticosteroids exhibited a high risk of thrombotic risk (hazard ratio, 2.2), whereas biological therapy decreased this risk.46,47 The exact mechanism underlying these phenomena remains unclear, although they are thought to occur secondary to steroid inhibition of prostacyclin synthesis and fibrinolysis while stimulating the coagulation cascade.46,47 Anemia has been previously recognized as the most common risk factor for CVST in patients with IBD,38 in accordance with our results.

The prevalence of genetic mutations is similar in patients with IBD and the general population, and does not vary based on the presence of VTE.48,49 However, the presence of hereditary factors seems to increase the risk of VTE. In this review, only 11% of patients had hereditary thrombophilia. Although factor V Leiden mutations are well recognized as the most common hereditary forms of thrombophilia,48,49 MTHFR mutations were most frequent among the cases reviewed in the present study.

Routine screening for thrombophilia and autoimmune diseases is not recommended,50,51 because the findings of these examinations are nonspecific, especially in the acute phase of CVST, and have not been shown to influence the disease outcome.4,45,50 Our findings are consistent with those of previous studies, because only 1 of 25 patients who underwent thrombophilia screening exhibited persistent increases in antiphospholipid antibodies, leading to a diagnosis of antiphospholipid syndrome concurrent with IBD.26 Considering the systemic thrombotic effects of IBD, multiple potential sites should be considered in patients with CVST.11,22,36 Although hyperhomocysteinemia is not uncommon in patients with IBD, the association between hyperhomocysteinemia and thrombosis is yet to be fully established.52,53 In our literature review, we identified 2 cases in which hyperhomocysteinemia was the only risk factor other than IBD.13,27

In accordance with our findings, a previous study noted that the distribution of CVST symptoms appears to be similar in patients with and without IBD.37 The diagnosis may be easier when neurologic symptoms are associated with headaches, whereas the presence of isolated symptoms can result in delayed diagnosis. Kosmidou et al10 reported the case of a 44-year-old woman with CD who had psychiatric manifestations in the absence of headaches, which delayed the diagnosis by 3 weeks. Although the distribution of the thrombosed sinus in our review was similar to that noted in previous analyses,49 the rate of multisinus involvement was higher in our review than in previous reports (65% vs 50%, respectively).37,38

The presumed safety of heparin in patients with IBD experiencing CVST events is indirectly based on previous studies that have suggested that heparin exerts immunomodulatory and anti-inflammatory effects that can be beneficial in steroid-resistant IBD.54,55 Katsanos et al38 stated that heparin treatment for CVST leads to good neurologic outcomes and low mortality rates in patients with IBD. In a 2012 review of 54 studies, Cognat et al37 documented complete recovery and good outcomes in 84% (47/54) of the patients with IBD who had undergone full anticoagulation therapy. The most common treatment strategies in these cases included intravenous or subcutaneous LMWH followed by oral anticoagulant treatment (warfarin), with the goal of achieving an INR of 2 to 3 when the patient was relatively stable. Table 4 summarizes the management of CVST in patients with IBD.

Table 4. Summary of recommendations for CVST management in patients with IBD

Consideration Recommendation
Confirmed CVST diagnosis on CTV or MRV Start anticoagulation immediately with heparin at the therapeutic dosage, even in patients with ICH at baseline.38,51
Duration of anticoagulation therapy Oral anticoagulants (warfarin) for 6-12 mo are recommended to prevent the recurrence of CVST and other VTE events.38,51
In patients with active disease who have CVST, anticoagulation therapy is recommended for at least 3 mo after IBD remission.45
Patients with recurrent VTE or irreversible prothrombotic conditions may require lifelong anticoagulation therapy.38,51
EVT If the clinical condition deteriorates or ICP continues to increase despite anticoagulation, EVT is recommended.51
Managing seizures If the patient develops seizures, anti-epileptic drugs are recommended to prevent recurrent episodes.51
Patients with IBD experiencing CVST during pregnancy or the postpartum period Subcutaneous LMWH is recommended in patients with acute CVT.51
CVST in the pediatric age group (> 28 d old) Therapeutic anticoagulation followed by maintenance treatment (LMWHs/warfarin) for 3-6 mo.50

CTV = computed tomography venography; CVST = cerebral venous sinus thrombosis; CVT = cerebral venous thrombosis; EVT = endovascular treatment; IBD = inflammatory bowel disease; ICH = intracerebral hemorrhage; ICP = intracranial pressure; LMWH = low-molecular weight heparin; MRV = magnetic resonance venography; VTE = venous thromboembolism.

There are several important considerations when managing CVST in patients with IBD. First, commonly used regimens for IBD flare-ups have been associated with drug or food interactions. For example, steroid therapy is known to interact with warfarin. In 2 retrospective studies, steroids were found to increase the mean INR by 1.24 in patients on warfarin.56,57 The INR should be monitored closely, and the warfarin dose should be adjusted accordingly.58 Although there are no recommendations for the use of direct oral anticoagulants (DOACs) in patients with CVST,51 they have been used off-label by physicians to avoid food interactions with warfarin.59 In this review, CVST occurred in 3 patients with IBD who had been treated with DOACs as a result of difficulty in achieving the target INR.19,25,35 A second major consideration is active gastrointestinal bleeding. Hematochezia may occur at the time of the CVST event11 or after anticoagulation therapy, as previously noted in 3 cases.32,34,35 The treatment plan should be individualized, taking into consideration the clinical status and episode severity of each patient, and it often requires a multidisciplinary approach.60 Third, patients should be carefully monitored for active intracranial bleeding. Given the high mortality rate of untreated CVST and venous hemorrhages, continuation of anticoagulation therapy has been recommended.50,51 Finally, clinicians should monitor patients for warfarin resistance. Multiple bowel resections are not uncommon in patients with CD, and such resections may influence warfarin absorption because of loss of effective surface area. A higher dose of warfarin may be required because of possible short gut syndrome in patients with multiple resections.14

EVT should be considered when the patient’s clinical condition deteriorates despite anticoagulation therapy or when intracranial pressure continues to increase despite optimal management. Possible EVT approaches include direct thrombolytic therapy, mechanical thrombectomy, balloon angioplasty, and stenting.52,53 Despite reports of favorable clinical outcomes, no large-scale randomized controlled trials have provided evidence supporting the use of EVT in patients with CVST.61,62,63 EVT and on-site thrombolysis for the treatment of CVST have been documented in 7 patients with IBD,12,14,36,64-66 5 of whom achieved complete recovery with no reported mortality or bleeding-related complications.12,64-66 Thrombolytic agents are thought to be safer and more effective than heparin, because they are more rapidly metabolized and carry a lower risk of bleeding. Moreover, thrombolytics play an important role in improving venous flow and inhibiting thrombus progression.67,68

In this review, complete recovery was noted in most patients who had received treatment. This phenomenon may partly be due to improvements in diagnostic methods and CVST therapies since the publication of previous studies.69,70 The rate of complete recovery was comparable to that in the review by Katsanos et al.38 Despite major concerns regarding bleeding in patients with IBD, bleeding complications were observed in only 3 of the reviewed cases, and the events were controlled without complications in all patients.32,34,35 Other treatment options, including DOACs, aspirin, thrombolysis, and EVT have been associated with relatively promising results; however, because of the small number of reported cases, their safety and efficacy are yet to be definitively concluded.


Thrombosis is a well-recognized feature of IBD that can be related to the pathogenesis of the disease as well as the presence of prothrombotic risk factors. However, CVST events can be prevented, and awareness of IBD-related risk factors is essential for avoiding future occurrences. Future studies and trials should aim to investigate issues concerning CVST prophylaxis, including the need to extend thromboprophylaxis postdischarge, especially in ambulatory patients with IBD flare-ups. CVST should be suspected in all patients with IBD presenting with neurologic symptoms. Furthermore, the critical nature of CVST complications in IBD and the challenges associated with managing the concurrent conditions must be recognized. Given that anticoagulation therapy is both safe and effective, it is considered the mainstay treatment for CVST in patients with IBD. However, further studies are required to validate the safety and efficacy of DOACs and EVT in these patients.

Disclosure Statement

The author(s) have no conflicts of interest to disclose.


No source of funding.

Author Affiliations

1Department of Neurology, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia

Corresponding Author

Aishah Ibrahim Albakr, (abakr@iau.edu.sa)

Author Contributions

Aishah Ibrahim Albakr conceptualized the content and participated in the literature search, manuscript editing, and manuscript review. Noor AlMohish participated in the literature search and manuscript preparation.


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Keywords: cerebral veins, inflammatory bowel disease, venous thrombosis


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