eMedicine Specialties > Radiology > Brain/Spine

Brain, Venous Sinus Thrombosis

Author: Mahesh R Patel, MD, Chief of MRI, Department of Radiology, Santa Clara Valley Medical Center
Contributor Information and Disclosures

Updated: Oct 16, 2008

Introduction

Background

Cerebral venous thrombosis (venous sinus thrombosis) is an elusive diagnosis because of its nonspecific presentation and its numerous predisposing causes. It is more common than previously thought. Imaging plays a key role in the diagnosis.

Cerebral venous thrombosis often presents with hemorrhagic infarction in areas atypical for arterial vascular distribution. Magnetic resonance venography (MRV) in conjunction with conventional MRI can accurately diagnose cerebral venous thrombosis. With careful interpretation and a high degree of clinical suspicion, CT also may lead to the diagnosis.1,2,3,4,5,6,7,8,9,10,11

Related eMedicine topics:
Cavernous Sinus Thrombosis
Cerebral Venous Thrombosis

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Pathophysiology

Cerebral venous thrombosis results from occlusion of a venous sinus and/or cortical vein and usually is caused by a partial thrombus or an extrinsic compression that subsequently progresses to complete occlusion. Once the vein is occluded, the thrombus may extend to veins draining into the sinus. This results in cortical venous infarction with petechial or overt hemorrhagic perivascular venous infarction.12

Multiple pathophysiologic mechanisms and predisposing factors exist, including the following13,14 :

  • A hypercoagulable state
  • Extrinsic compression or local invasion of a venous sinus by tumor or an adjacent infectious process (eg, mastoiditis)
  • A low-flow state within the venous sinus
  • Dehydration
  • Pregnancy and the postpartum state

As many as 25% of patients present with no predisposing risk factor; however, in some patients, an etiologic factor is discovered subsequently.

When occlusion of a venous sinus occurs, the resulting venous congestion can lead to regional ischemia and infarction. Venous infarctions frequently are hemorrhagic and commonly occur within the white matter or at the gray-white matter junction. Involvement of the deep cerebral veins (eg, basal vein of Rosenthal) can progress to bilateral thrombosis of the internal cerebral veins with thalamic hemorrhagic infarction.

Frequency

United States

A range of occurrence of 1-9% has been suggested based on a limited autopsy series. The higher percentage may apply to older patients with concordant debilitating disease. Venous sinus thrombosis (cerebral venous thrombosis) is believed to be less common than arterial occlusive disease.

International

No current data are available. Venous sinus thrombosis (cerebral venous thrombosis) is likely to be underdiagnosed since the availability of MR in developing countries is limited, and patients are not studied often by cerebral arteriography.

Mortality/Morbidity

  • A mortality range of 10-80% has been reported for venous sinus thrombosis (cerebral venous thrombosis), although the higher rate is based on older data.
  • Studies estimate a morbidity range of 6-20%, including residual focal neurologic deficits and blindness secondary to optic nerve atrophy.
  • The prognosis for return of function is believed to be somewhat better than for arterial stroke.

Age

  • Elderly or debilitated patients (eg, those with an underlying illness) are more likely to have spontaneous cerebral venous thrombosis (venous sinus thrombosis).
  • Neonates and infants suffering from dehydration may develop cerebral venous thrombosis.10

Presentation

The signs and symptoms of cerebral venous thrombosis (venous sinus thrombosis) occasionally are nonspecific and protean, making the clinical diagnosis difficult.

  • Patients may have generalized or focal neurologic symptoms and signs.
    • Headache  
    • Nausea
    • Vomiting
    • Possible seizures
    • Occasionally venous thrombosis may be mistaken for a psychiatric disorder (neurosis, hysteria, depression)
  • Physical examination findings may include the following:
    • Papilledema may be seen.
    • Forehead skin and eyelid edema, ocular chemosis, proptosis, and cranial nerve III, IV, and VI compromise can result from cavernous sinus thrombosis.
    • An isolated cortical venous thrombosis can result in focal neurologic symptoms and signs (related to the anatomic location of the thrombosis).
  • Predisposing factors include the following:
    • Hypercoagulable states, including the use of oral contraceptives
    • Pregnancy and the postpartum period
    • Local or distant infection, including mastoiditis, otitis media, paranasal sinus infection, generalized sepsis, and facial or scalp cellulitis
    • Circulatory low-flow states resulting from blood volume depletion, dehydration, and/or cardiac disease
    • Behçet syndrome15
    • Antiphospholipid antibody syndrome
    • Factor V Leiden genetic mutation and other hereditary thrombotic conditions
    • Arteriovenous malformation posttreatment
    • Direct trauma
    • Invasion of dural sinuses by adjacent tumor
    • Numerous chronic illnesses with sepsis, dehydration
    • In neonates and infants - Sepsis, dehydration, birth trauma, shock, and L-asparaginase therapy
    • Dural arteriovenous fistulas - May develop after dural sinus thrombosis
    • Intracranial hypotension - May occur in patients with extended thrombosis of the dural sinuses.

Preferred Examination

  • MRI with MRV is preferred for diagnosis of cerebral venous thrombosis (venous sinus thrombosis). Clinical manifestations and physical findings may be nonspecific.
  • The diagnosis may be made or suggested by CT brain scan before and after intravenous contrast medium injection.

Limitations of Techniques

Two-dimensional time-of-flight (2D TOF) MRV is performed in the coronal plane; however, in-plane signal loss that mimics thrombosis may occur with this technique. Thus, a review of source data and conventional MRI brain scan is necessary. Phase-contrast MRV techniques may help, since small cortical venous infarcts may not be observed on 2D TOF MRV.16

Differential Diagnoses

Brain, Capillary Telangiectasia
Brain, Stroke
Brain, Contusion
Brain, Venous Vascular Malformations
Brain, Hypertensive Hemorrhage
Brain, Metastases
Brain, MRI Appearance of Hemorrhage

Other Problems to Be Considered

Brain, vasculitis

More on Brain, Venous Sinus Thrombosis

Overview: Brain, Venous Sinus Thrombosis
Imaging: Brain, Venous Sinus Thrombosis
Follow-up: Brain, Venous Sinus Thrombosis
Multimedia: Brain, Venous Sinus Thrombosis
References
Further Reading
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References

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  13. Milhaud D, Heroum C, Charif M. Dural puncture and corticotherapy as risks factors for cerebral venous sinus thrombosis. Eur J Neurol. Jan 2000;7(1):123-4. [Medline].

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Further Reading

EFNS guideline on the treatment of cerebral venous and sinus thrombosis.
European Federation of Neurological Societies.  2006 Jun.  7 pages.  NGC:005483
 
Thromboprophylaxis during pregnancy, labour and after vaginal delivery.
Royal College of Obstetricians and Gynaecologists.  2004 Jan.  13 pages.  NGC:004482
 
Antithrombotic and thrombolytic therapy for ischemic stroke: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy.
American College of Chest Physicians.  2001 Jan (revised 2004 Sep).  28 pages.  NGC:003882

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Keywords

venous sinus thrombosis, cerebrovenous thrombosis, sinus thrombosis, venous infarcts, cerebral venous thrombosis, deep vein thrombosis, deep venous thrombosis, deep-vein thrombosis, deep-venous thrombosis, phlebothrombosis

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Contributor Information and Disclosures

Author

Mahesh R Patel, MD, Chief of MRI, Department of Radiology, Santa Clara Valley Medical Center
Mahesh R Patel, MD is a member of the following medical societies: American Roentgen Ray Society, American Society of Neuroradiology, and Radiological Society of North America
Disclosure: Nothing to disclose.

Medical Editor

Hugh J F Robertson, MD, DMR, FRCPC, FRCR, FACR, Professor Emeritus of Radiology, Professor of Clinical Radiology, Louisiana State University Health Sciences Center, New Orleans; Clinical Professor of Radiology, Tulane University School of Medicine; Active Staff, Department of Radiology, University Hospital
Hugh J F Robertson, MD, DMR, FRCPC, FRCR, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Neuroradiology, American Society of Spine Radiology, Louisiana State Medical Society, Orleans Parish Medical Society, Radiological Society of North America, Royal College of Physicians and Surgeons of Canada, Royal College of Radiologists, and Royal Society of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

James G Smirniotopoulos, MD, Professor of Radiology, Neurology, and Biomedical Informatics, Chairman, Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences
James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

 
 
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