Cerebral venous sinus thrombosis medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hasnain Ali Moryani, MBBS[2]Kalsang Dolma, M.B.B.S.[3]

Overview of Medical Therapy

Medical treatment of cerebral venous sinus thrombosis (CVST) centers on therapeutic anticoagulation, which is recommended by all major guidelines even when CVST is accompanied by intracranial hemorrhage.[1][2][3][4]

Initial treatment typically uses parenteral anticoagulation with low molecular weight heparin or unfractionated heparin, followed by transition to an oral anticoagulant such as warfarin or a direct oral anticoagulant.[4][5]

Beyond anticoagulation, medical management addresses several additional priorities: control of intracranial hypertension, treatment of seizures, antimicrobial therapy for septic CVST, and population-specific considerations including pregnancy-associated CVST and vaccine-induced immune thrombocytopenia and thrombosis (VITT).[1][4]

Endovascular therapy, decompressive surgery, cerebrospinal fluid diversion, and optic nerve sheath fenestration are addressed in the surgery and procedural therapy microchapter.

Acute anticoagulation

Low molecular weight heparin (LMWH) is generally preferred for initial treatment because of predictable pharmacokinetics and a lower risk of heparin-induced thrombocytopenia. Intravenous unfractionated heparin (UFH) is appropriate when rapid reversibility may be required, severe renal impairment is present, or an urgent procedure is anticipated.[4][5]

Initial anticoagulant options
Agent Regimen from the supplied evidence Situations favoring use Monitoring and precautions
LMWH Full therapeutic, weight-based dosing; an example is enoxaparin 1 mg/kg subcutaneously every 12 hours. Preferred for most clinically stable patients. Assess renal function and platelet count. Anti-Xa measurement may be considered in pregnancy, marked obesity, or renal impairment.
UFH Intravenous bolus followed by continuous infusion, adjusted to an aPTT approximately 1.5 to 2.5 times control. Severe renal impairment, anticipated urgent procedure, or need for rapid reversal. Monitor aPTT and platelet count; assess for heparin-induced thrombocytopenia.

In patients with a history of heparin-induced thrombocytopenia unrelated to VITT, heparin products should be avoided. Non-heparin anticoagulants such as argatroban (intravenous) or fondaparinux (subcutaneous only) may be used. Argatroban is generally preferred in critically ill patients requiring intravenous anticoagulation.[6][7]

The presence of intracranial hemorrhage caused by CVST is not, by itself, a reason to withhold anticoagulation. However, the ACCP/CHEST guidelines caution that in patients with venous infarction and a large parenchymal hematoma, the risk of hemorrhage extension may be unacceptably high and the uncertain benefit of anticoagulation may not outweigh the potential for harm. The CHEST 2012 guideline used more definitive wording that the uncertain benefits did not outweigh the potential for harm, whereas the CHEST 2021 update softened this position to state that the benefits may not outweigh the potential for harm. Anticoagulation decisions in these cases require individualized assessment involving stroke neurology, hematology, and neurosurgical teams as appropriate.[2][3]

Transition to oral anticoagulation

After clinical stabilization, patients are generally transitioned from parenteral anticoagulation to either a vitamin K antagonist or a direct oral anticoagulant (DOAC). The AHA 2024 statement considers transition to either strategy reasonable after an initial parenteral phase.[4]

Vitamin K antagonists

Warfarin is titrated to an international normalized ratio of 2.0 to 3.0.[4][1]

LMWH or warfarin is generally favored over a DOAC during pregnancy and in patients with antiphospholipid syndrome or severe renal impairment. Patients with active malignancy or central nervous system infection were excluded or underrepresented in most CVST DOAC studies, and treatment should therefore be individualized.[4][5]

Direct oral anticoagulants

Evidence from randomized and observational studies supports DOACs as a reasonable alternative to warfarin in appropriately selected patients.

Selected evidence for DOACs in CVST
Study Design and sample Treatment Main finding
RE-SPECT CVT Open-label randomized trial; 120 patients Dabigatran 150 mg twice daily versus dose-adjusted warfarin No recurrent venous thromboembolism occurred in either group. One major bleeding event, which was gastrointestinal, occurred with dabigatran and two major bleeding events, both intracranial hemorrhages, occurred with warfarin; recanalization outcomes were similar.[8]
SECRET Phase II randomized feasibility trial; 53 patients Rivaroxaban 20 mg daily versus standard care No major safety concern was identified with early rivaroxaban initiation; one recurrent CVST occurred in the rivaroxaban group.[9]
CHOICE-CVT Open-label randomized trial; 89 patients Dabigatran 150 mg twice daily versus warfarin Recurrent venous thromboembolism was numerically higher with dabigatran (18.2% versus 6.7%, p=0.099), but the difference was not statistically significant. Any bleeding was less frequent with dabigatran (2.3% versus 20.0%); major bleeding was 0% in both groups.[10]
ACTION-CVT Retrospective multicenter study; 845 patients Apixaban, rivaroxaban, or dabigatran versus warfarin Recurrent venous thromboembolism was similar, while major hemorrhage was less frequent with DOAC therapy.[11]
DOAC-CVT Prospective observational cohort; 619 patients DOACs versus vitamin K antagonists The composite of recurrent venous thromboembolism and major bleeding occurred in 3% of each group, with no identified mortality difference. Complete recanalization was lower with DOACs (38%) than with vitamin K antagonists (58%, p=0.0002), although the clinical significance of this difference is uncertain.[12]

Most CVST DOAC studies used an initial LMWH phase of approximately 5 to 15 days. The minimum necessary parenteral lead-in period, preferred DOAC, and need for acute venous thromboembolism loading regimens remain uncertain.[4]

Drug selection and dosing should account for renal and hepatic function, pregnancy status, antiphospholipid syndrome, bleeding risk, and clinically important drug interactions.

Duration of anticoagulation

The optimal duration of anticoagulation remains uncertain and should be individualized according to the provoking factor, persistent thrombophilia, recurrence risk, and bleeding risk.[4][5]

Suggested duration by clinical context
Clinical context Suggested duration
CVST associated with a transient or reversible provoking factor, including oral contraceptive use, pregnancy, surgery, or infection 3 to 6 months
Unprovoked CVST or mild thrombophilia 6 to 12 months
Recurrent venous thromboembolism, severe thrombophilia, antiphospholipid syndrome, or active malignancy Consider indefinite anticoagulation after individualized assessment of thrombotic and bleeding risk

The degree of venous recanalization on follow-up imaging should not be used as the sole determinant of anticoagulation duration because its clinical role remains unresolved.[4]

The EXCOA-CVT trial was designed to compare shorter anticoagulation of 3 to 6 months with 12 months of therapy.[5]

Intracranial hypertension

  • Therapeutic anticoagulation remains the primary disease-directed treatment.
  • Patients with papilledema or visual symptoms require serial funduscopic assessment and formal visual-field monitoring.[1]
  • Acetazolamide may be considered for CVST-associated intracranial hypertension, particularly when visual function is threatened. The AHA/ASA 2011 statement considers acetazolamide reasonable (Class IIa, Level of Evidence C), although randomized trial evidence is lacking. The European Stroke Organization 2017 guideline does not recommend acetazolamide or glucocorticoids for brain swelling in CVT.[1][13]
  • Therapeutic or serial lumbar puncture may provide temporary relief in selected patients, but procedural bleeding risk and interruption of anticoagulation must be carefully managed.[1]
  • Refractory intracranial hypertension with progressive visual loss requires urgent evaluation for cerebrospinal fluid diversion or optic nerve sheath fenestration, which are discussed in the procedural therapy microchapter.

Routine corticosteroids are not recommended for CVST-related cerebral edema or parenchymal lesions (AHA/ASA 2011 Class III, Level of Evidence B).[1]

The primary ISCVT matched case-control analysis found no benefit from corticosteroids in any evaluated subgroup and found an association with worse outcomes among patients without parenchymal lesions (odds ratio 4.2, 95% confidence interval 1.6 to 11.6). The AHA/ASA 2011 guideline's summary of the same dataset, using a different analytic approach, reported 4.8-fold increased odds of death or dependence with steroid treatment among patients with parenchymal brain lesions (95% confidence interval 1.2 to 19.8). Both analyses support avoiding corticosteroids regardless of parenchymal involvement.[14][1]

A subsequent prospective cohort suggesting possible benefit from pulsed corticosteroids in severe CVST is insufficient to change standard practice without randomized confirmation.[15]

Seizure management

  • After an acute seizure with a supratentorial parenchymal lesion, early initiation of an antiseizure medication for a defined duration is recommended (AHA/ASA 2011 Class I, Level of Evidence B).[1]
  • After an acute seizure without a parenchymal lesion, initiation of an antiseizure medication is probably reasonable (Class IIa, Level of Evidence C).[1]
  • Routine prophylactic antiseizure medication in a patient who has not experienced a seizure is not recommended (Class III, Level of Evidence C).[1]
  • Levetiracetam is commonly selected because it has fewer clinically important interactions with anticoagulants.
  • Enzyme-inducing antiseizure medications such as carbamazepine and phenytoin may reduce exposure to some oral anticoagulants.
  • Valproic acid has clinically important interaction and reproductive-safety concerns.
  • No evidence-based fixed duration of antiseizure therapy has been established after an acute symptomatic seizure. Duration should be individualized according to parenchymal injury, electroclinical features, and subsequent seizure recurrence.

Late seizures occurring more than 7 days after diagnosis have a high recurrence risk and should be managed as post-CVST epilepsy.[16][17]

Septic CVST

Septic CVST, particularly cavernous sinus thrombosis arising from sinus, orbital, dental, or facial infection, requires immediate antimicrobial therapy and source control.

  • Begin broad-spectrum intravenous antibiotics promptly. A commonly used empiric regimen is vancomycin plus a third-generation cephalosporin such as ceftriaxone plus metronidazole, followed by culture-directed therapy.[18]
  • Consider antifungal treatment when fungal infection is clinically plausible, including in immunocompromised patients, patients with diabetes, or infection unresponsive to antibacterial therapy.[19]
  • Obtain urgent otolaryngology, ophthalmology, neurosurgery, or dental consultation as appropriate for drainage or debridement of the infectious source.
  • Antibiotics and surgical drainage of purulent collections are recommended for septic CVST (AHA/ASA 2011 Class I, Level of Evidence C).[1]
  • Anticoagulation for CVT in general is rated Class IIa, Level of Evidence B by the AHA/ASA 2011 guideline; no separate class of recommendation exists for septic cavernous sinus thrombosis specifically. A 2025 systematic review and individual patient data meta-analysis of septic cavernous sinus thrombosis from sinusitis found significantly lower mortality with anticoagulation (adjusted odds ratio 0.067, 95% confidence interval 0.009 to 0.475), although the evidence remains observational. Treatment should be individualized according to hemorrhage risk and planned procedures.[1][20]
  • Intravenous antimicrobial therapy is commonly continued for 3 to 6 weeks, adjusted to the organism, source control, complications, and clinical response.[21][22]

VITT-associated CVST

Suspected VITT-associated CVST requires urgent hematology involvement and a treatment pathway distinct from conventional CVST.

  • Send an anti-platelet factor 4 antibody enzyme-linked immunosorbent assay when VITT is suspected.[4]
  • Avoid heparin products, including heparin-containing line flushes.[4][23]
  • Administer intravenous immunoglobulin 1 g/kg daily for 2 days.[24]
  • Short-course corticosteroids, such as dexamethasone, have also been advised as part of the initial VITT treatment regimen in the AHA 2024 statement, although supporting evidence is limited and based largely on expert consensus.[4]
  • Use a non-heparin anticoagulant such as argatroban or fondaparinux for initial therapy, followed by a DOAC after platelet recovery when clinically appropriate.[4][23]
  • Avoid routine platelet transfusion because it may intensify thrombosis.[4]
  • Plasma exchange has been used as rescue therapy in severe or refractory VITT, but supporting evidence is observational.[23]

Pregnancy and puerperium

  • Full-dose LMWH is the treatment of choice during pregnancy. Treatment with full-dose LMWH rather than UFH is considered reasonable (AHA/ASA 2011 Class IIa, Level of Evidence C).[4][1]
  • Warfarin is avoided during pregnancy because of fetal toxicity and bleeding risk.
  • DOACs should not be used during pregnancy or lactation.[4]
  • After delivery, anticoagulation may be continued with LMWH or transitioned to warfarin with a target INR of 2.0 to 3.0.
  • The AHA/ASA 2014 Women's Stroke Prevention guideline recommends at least 6 weeks of postpartum anticoagulation and a total minimum treatment duration of 6 months (Class I, Level of Evidence C), consistent with the ACCP recommendation referenced in the AHA/ASA 2011 CVT guideline.[25][1] The AHA 2024 Scientific Statement recommends oral anticoagulation for 3 to 12 months depending on the underlying cause, without specifying a separate pregnancy-specific minimum; this general recommendation may represent a shift from the explicit 6-month minimum for pregnancy-associated CVT stated in the 2011 and 2014 guidelines, though the 2024 document does not directly address this difference.[4][1][25]
  • LMWH dose and monitoring should be reassessed as maternal weight and renal function change during pregnancy.

Future-pregnancy prophylaxis and long-term recurrence prevention are addressed in the primary and secondary prevention microchapters.

Supportive care and monitoring

  • Maintain euvolemia and avoid dehydration.
  • Admission to a stroke unit is reasonable for treatment and prevention of clinical complications (AHA/ASA 2011 Class IIa, Level of Evidence C).[1]
  • Provide appropriate analgesia without delaying neurologic reassessment.
  • Treat the underlying provoking condition, including infection or medication exposure, when identified.
  • Monitor neurologic status, visual function, platelet count, renal function, bleeding, and anticoagulant-specific laboratory parameters.
  • Escalate urgently for clinical deterioration, impending herniation, progressive visual loss, or thrombus propagation despite adequate anticoagulation. Procedural options are covered separately.

Key practice points

  • Therapeutic anticoagulation is the principal medical treatment for CVST.
  • Venous intracranial hemorrhage is not, by itself, a contraindication to anticoagulation.
  • Exercise caution in patients with large parenchymal hematomas, where the risk-benefit balance is less certain.
  • Prefer LMWH for most clinically stable patients; use UFH when severe renal impairment, urgent intervention, or a need for rapid reversal makes it advantageous.
  • A DOAC or warfarin is reasonable after initial parenteral treatment in an appropriately selected patient.
  • Do not prescribe routine prophylactic antiseizure medication to patients without seizures.
  • Do not use corticosteroids routinely for conventional CVST-related edema or parenchymal lesions; corticosteroids may be advised as part of the distinct VITT treatment pathway.
  • In suspected VITT, avoid heparin, administer intravenous immunoglobulin, and use a non-heparin anticoagulant.
  • During pregnancy, use therapeutic LMWH and avoid DOACs.

Antimicrobial Regimen

  • Cavernous sinus thrombosis is considered a medical emergency.
  • Duration of therapy is usually a total of 3-4 weeks. More prolonged administration of antimicrobial therapy (total of 6-8 weeks) may be indicated among patients who are suspected to have developed complications (e.g. suppurative intracranial disease).
  • ENT surgery must be consulted to evaluate the need of surgical drainage (e.g. sphenoidotomy if sphenoid sinus infection is the primary cause).
  • Septic thrombosis of cavernous or dural venous sinus
Note (1): If risk of MRSA is high, Vancomycin should be administered instead of either nafcillin or oxacillin
Note (2): The optimal duration of therapy remains unclear
  • 2. Specific anatomic considerations
  • 2.1 Cavernous sinus
Note: Daptomycin 8–12 mg/kg IV q24h OR Linezolid 600 mg IV q12h could be considered for patients unable to tolerate vancomycin
  • 2.2 Lateral sinus
  • 2.3 Superior sagittal sinus
  • Preferred regimen: Ceftriaxone 2 g IV q12h for 3-4 weeks AND Vancomycin 15–20 mg/kg for 3-4 weeks AND Dexamethasone 10 mg IV q6h continued until symptomatic improvement and tailed gradually over several weeks
  • Alternative regimen: Meropenem 1–2 g IV q8h for 3-4 weeks AND Vancomycin 15–20 mg/kg for 3-4 weeks AND Dexamethasone 10 mg IV q6h continued until symptomatic improvement and tailed gradually over several weeks
  • 3. Pathogen-directed antimicrobial therapy
  • Staphylococcus aureus, methicillin-resistant (MRSA)[30]
  • Preferred regimen: Vancomycin 15–20 mg/kg/dose IV q8–12h for 4–6 weeks
  • Alternative regimen: Linezolid 600 mg PO/IV q12h for 4–6 weeks OR TMP-SMX 5 mg/kg/dose PO/IV q8–12h for 4–6 weeks
  • Pediatric dose: Vancomycin 15 mg/kg/dose IV q6h 4–6 weeks OR Linezolid 10 mg/kg/dose PO/IV q8h 4–6 weeks
  • Note (1): Surgical evaluation for incision and drainage of contiguous sites of infection or abscess is recommended whenever possible
  • Note (2): Consider the addition of Rifampin 600 mg qd or 300–450 mg bid to vancomycin

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 Saposnik G, Barinagarrementeria F, Brown RD; et al. (2011). "Diagnosis and Management of Cerebral Venous Thrombosis: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 42 (4): 1158–1192. doi:10.1161/STR.0b013e31820a8364.
  2. ↑ 2.0 2.1 Lansberg MG, O'Donnell MJ, Khatri P; et al. (2012). "Antithrombotic and Thrombolytic Therapy for Ischemic Stroke: Antithrombotic Therapy and Prevention of Thrombosis, 9th Ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines". Chest. 141 (2 Suppl): e601S–e636S. doi:10.1378/chest.11-2302.
  3. ↑ 3.0 3.1 Stevens SM, Woller SC, Kreuziger LB; et al. (2021). "Antithrombotic Therapy for VTE Disease: Second Update of the CHEST Guideline and Expert Panel Report". Chest. 160 (6): e545–e608. doi:10.1016/j.chest.2021.07.055.
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 4.17 Saposnik G, Bushnell C, Coutinho JM; et al. (2024). "Diagnosis and Management of Cerebral Venous Thrombosis: A Scientific Statement From the American Heart Association". Stroke. 55 (3): e77–e90. doi:10.1161/STR.0000000000000456.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 Field TS, Fragata I (2026). "Current Management of Cerebral Venous Thrombosis". Stroke. 57 (7): 2228–2236. doi:10.1161/STROKEAHA.125.051340.
  6. ↑ Greinacher A (2015). "Heparin-Induced Thrombocytopenia". The New England Journal of Medicine. 373 (3): 252–261. doi:10.1056/NEJMcp1411910.
  7. ↑ Linkins LA, Dans AL, Moores LK; et al. (2012). "Treatment and Prevention of Heparin-Induced Thrombocytopenia: Antithrombotic Therapy and Prevention of Thrombosis, 9th Ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines". Chest. 141 (2 Suppl): e495S–e530S. doi:10.1378/chest.11-2303.
  8. ↑ Ferro JM, Coutinho JM, Dentali F; et al. (2019). "Safety and Efficacy of Dabigatran Etexilate vs Dose-Adjusted Warfarin in Patients With Cerebral Venous Thrombosis: A Randomized Clinical Trial". JAMA Neurology. 76 (12): 1457–1465. doi:10.1001/jamaneurol.2019.2764.
  9. ↑ Field TS, Dizonno V, Almekhlafi MA; et al. (2023). "Study of Rivaroxaban for Cerebral Venous Thrombosis: A Randomized Controlled Feasibility Trial Comparing Anticoagulation With Rivaroxaban to Standard-of-Care in Symptomatic Cerebral Venous Thrombosis". Stroke. 54 (11): 2724–2736. doi:10.1161/STROKEAHA.123.044113.
  10. ↑ Ma H, Gu Y, Bian T; et al. (2024). "Dabigatran Etexilate Versus Warfarin in Cerebral Venous Thrombosis in Chinese Patients (CHOICE-CVT): An Open-Label, Randomized Controlled Trial". International Journal of Stroke. 19 (6): 635–644. doi:10.1177/17474930241234749.
  11. ↑ Yaghi S, Shu L, Bakradze E; et al. (2022). "Direct Oral Anticoagulants Versus Warfarin in the Treatment of Cerebral Venous Thrombosis (ACTION-CVT): A Multicenter International Study". Stroke. 53 (3): 728–738. doi:10.1161/STROKEAHA.121.037541.
  12. ↑ van de Munckhof A, van Kammen MS, Tatlisumak T; et al. (2025). "Direct Oral Anticoagulants Versus Vitamin K Antagonists for Cerebral Venous Thrombosis (DOAC-CVT): An International, Prospective, Observational Cohort Study". The Lancet Neurology. 24 (3): 199–207. doi:10.1016/S1474-4422(24)00519-2.
  13. ↑ Ropper AH, Klein JP (2021). "Cerebral Venous Thrombosis". The New England Journal of Medicine. 385 (1): 59–64. doi:10.1056/NEJMra2106545.
  14. ↑ Canhao P, Cortesao A, Cabral M; et al. (2008). "Are Steroids Useful to Treat Cerebral Venous Thrombosis?". Stroke. 39 (1): 105–110. doi:10.1161/STROKEAHA.107.484089.
  15. ↑ Hu S, Gu Y, Zhao T; et al. (2025). "Steroids Combined With Anticoagulant in Acute/Subacute Severe Cerebral Venous Thrombosis". Chinese Medical Journal. doi:10.1097/CM9.0000000000003502.
  16. ↑ Sanchez van Kammen M, Lindgren E, Silvis SM; et al. (2020). "Late Seizures in Cerebral Venous Thrombosis". Neurology. 95 (12): e1716–e1723. doi:10.1212/WNL.0000000000010576.
  17. ↑ Lindgren E, Shu L, Simaan N; et al. (2024). "Development and Validation of a Clinical Score to Predict Epilepsy After Cerebral Venous Thrombosis". JAMA Neurology. 81 (12): 1274–1283. doi:10.1001/jamaneurol.2024.3481.
  18. ↑ Long B, Field SM, Singh M, Koyfman A (2024). "High Risk and Low Prevalence Diseases: Cavernous Sinus Thrombosis". The American Journal of Emergency Medicine. 83: 47–53. doi:10.1016/j.ajem.2024.06.024.
  19. ↑ Smith DM, Vossough A, Vorona GA; et al. (2015). "Pediatric Cavernous Sinus Thrombosis: A Case Series and Review of the Literature". Neurology. 85 (9): 763–769. doi:10.1212/WNL.0000000000001886.
  20. ↑ Akarapas C, Wiwatkunupakarn N, Sithirungson S, Chaiyasate S (2025). "Anticoagulation for Cavernous Sinus Thrombosis: A Systematic Review and Individual Patient Data Meta-Analysis". European Archives of Oto-Rhino-Laryngology. 282 (3): 1127–1134. doi:10.1007/s00405-024-08992-4.
  21. ↑ Kim TH, Bae SY (2023). "Posterior Nasal Septal Abscess Detected During Evaluation of Cavernous Sinus Thrombosis". The Journal of Craniofacial Surgery. 34 (8): e749–e752. doi:10.1097/SCS.0000000000009617.
  22. ↑ Branson SV, McClintic E, Yeatts RP (2019). "Septic Cavernous Sinus Thrombosis Associated With Orbital Cellulitis: A Report of 6 Cases and Review of Literature". Ophthalmic Plastic and Reconstructive Surgery. 35 (3): 272–280. doi:10.1097/IOP.0000000000001231.
  23. ↑ 23.0 23.1 23.2 Pavord S, Scully M, Hunt BJ; et al. (2021). "Clinical Features of Vaccine-Induced Immune Thrombocytopenia and Thrombosis". The New England Journal of Medicine. 385 (18): 1680–1689. doi:10.1056/NEJMoa2109908.
  24. ↑ Scutelnic A, Krzywicka K, Mbroh J; et al. (2022). "Management of Cerebral Venous Thrombosis Due to Adenoviral COVID-19 Vaccination". Annals of Neurology. 92 (4): 562–573. doi:10.1002/ana.26431.
  25. ↑ 25.0 25.1 Bushnell C, McCullough LD, Awad IA; et al. (2014). "Guidelines for the Prevention of Stroke in Women: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke. 45 (5): 1545–1588. doi:10.1161/01.str.0000442009.06663.48.
  26. ↑ Saposnik, Gustavo; Barinagarrementeria, Fernando; Brown, Robert D.; Bushnell, Cheryl D.; Cucchiara, Brett; Cushman, Mary; deVeber, Gabrielle; Ferro, Jose M.; Tsai, Fong Y.; American Heart Association Stroke Council and the Council on Epidemiology and Prevention (2011-04). "Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association". Stroke; a Journal of Cerebral Circulation. 42 (4): 1158–1192. doi:10.1161/STR.0b013e31820a8364. ISSN 1524-4628. PMID 21293023. Check date values in: |date= (help)
  27. ↑ Ebright, J. R.; Pace, M. T.; Niazi, A. F. (2001-12-10). "Septic thrombosis of the cavernous sinuses". Archives of Internal Medicine. 161 (22): 2671–2676. ISSN 0003-9926. PMID 11732931.
  28. ↑ Singh, B. (1993-09). "The management of lateral sinus thrombosis". The Journal of Laryngology and Otology. 107 (9): 803–808. ISSN 0022-2151. PMID 8228594. Check date values in: |date= (help)
  29. ↑ Southwick, F. S.; Richardson, E. P.; Swartz, M. N. (1986-03). "Septic thrombosis of the dural venous sinuses". Medicine. 65 (2): 82–106. ISSN 0025-7974. PMID 3512953. Check date values in: |date= (help)
  30. ↑ Liu, Catherine; Bayer, Arnold; Cosgrove, Sara E.; Daum, Robert S.; Fridkin, Scott K.; Gorwitz, Rachel J.; Kaplan, Sheldon L.; Karchmer, Adolf W.; Levine, Donald P.; Murray, Barbara E.; J Rybak, Michael; Talan, David A.; Chambers, Henry F.; Infectious Diseases Society of America (2011-02-01). "Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children". Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America. 52 (3): –18-55. doi:10.1093/cid/ciq146. ISSN 1537-6591. PMID 21208910.
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