Cerebral Venous Thrombosis 

  • Author: W Alvin McElveen, MD; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Nov 14, 2011
 

Background

Thrombosis of the venous channels in the brain is an uncommon cause of cerebral infarction relative to arterial disease but is an important consideration because of its potential morbidity. Venous thrombosis may occur with headache and cranial nerve palsies. Newer imaging procedures have led to easier recognition of venous sinus thrombosis (see the images below), offering the opportunity for early therapeutic measures. Venous thrombosis also may be associated with other medical complications that require therapeutic intervention.

Case 2: CT scan demonstrates a left posterior tempCase 2: CT scan demonstrates a left posterior temporal hematoma in a 38-year-old woman on oral contraceptives (the only identified risk factor). Case 2: Contrast-enhanced MRI showing lack of fillCase 2: Contrast-enhanced MRI showing lack of filling of left transverse sinus. Case 2: Axial view of MR venogram demonstrating laCase 2: Axial view of MR venogram demonstrating lack of flow in transverse sinus. Case 2: Coronal view of MR venogram demonstrating Case 2: Coronal view of MR venogram demonstrating lack of flow in the left transverse and sigmoid sinuses.
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Pathophysiology

Knowledge of the anatomy of the venous system is essential in evaluating patients with venous thrombosis, since symptoms associated with the condition are related to the area of thrombosis. Cerebral infarction may occur with cortical vein or sagittal sinus thrombosis secondary to tissue congestion with obstruction. Lateral sinus thrombosis may be associated with headache and a pseudotumor cerebri–like picture. Extension into the jugular bulb may cause jugular foramen syndrome; cranial nerve palsies may be seen in cavernous sinus thrombosis as a compressive phenomenon. Cerebral hemorrhage also may be a presenting feature in patients with venous sinus thrombosis.

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Epidemiology

Frequency

International

Incidence of cerebral venous thrombosis (CVT) is difficult to determine. Generally, it is believed to be an uncommon cause of stroke. However, with the advent of newer imaging techniques, the reported incidence is likely to increase as less severe cases are found. In 1973, Towbin reported CVT in 9% of 182 autopsies.[1] In 1995, Daif reported a frequency in Saudi Arabia of 7 cases per 100,000 hospital patients.[2] The ratio of venous to arterial strokes has been found to be 1:62.5.

Mortality/Morbidity

Mortality in untreated cases of venous thrombosis has been reported to range from 13.8-48%; this high mortality rate may be a reflection of clinical severity at entrance into the study. Between 25% and 30% of patients have full recovery.

More recently, a Portuguese study group prospectively analyzed 91 consecutively admitted patients from 1995 to 1998 over a mean 1-year follow-up interval.[3] Of the patients analyzed, 7% died in the acute phase, 1% died during the one year follow-up, 82% recovered completely, and 1% were dependent; 59% developed thrombotic events during the follow-up, 10% had seizures, 11% complained of severe headaches, and 1 patient experienced severe visual loss.

In 2003, Buccino et al found a good overall outcome in their reinvestigation of a series of 34 patients with confirmed cerebral venous thrombosis.[4] However, 10 patients (30%) had episodic headaches, 3 patients (8.8%) had seizures, 4 patients (11.7%) had pyramidal signs, and 2 (5.9%) had visual deficits. Mild nonfluent aphasia was seen in 3 patients. Working memory deficit and depression of mood were seen in 6 patients (17.6%).

Race

No racial predilection has been observed.

Sex

Cerebral venous thrombosis is believed to be more common in women than men. In a series of 110 cases, Ameri and Bousser found a female-to-male ratio of 1.29:1.[5]

Age

In 1992, Ameri and Bousser reported a uniform age distribution in men with cerebral venous thrombosis, while 61% of women with CVT were aged 20-35 years.[5] This may be related to pregnancy or the use of oral contraceptives.[6]

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Contributor Information and Disclosures
Author

W Alvin McElveen, MD  Director, Stroke Unit, Lakewood Ranch Medical Center; Neurologist, Manatee Memorial Hospital

W Alvin McElveen, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Society of Neuroimaging, American Stroke Association, and Southern Clinical Neurological Society

Disclosure: Nothing to disclose.

Coauthor(s)

Ralph F Gonzalez, MD  Private Practice, Bradenton Neurology, Inc; Consulting Staff, Department of Neurology, Blake Hospital, Lakewood Ranch Medical Center, Manatee Memorial Hospital

Ralph F Gonzalez, MD is a member of the following medical societies: American Academy of Neurology and Florida Medical Association

Disclosure: Nothing to disclose.

Andrew P Keegan, MD  Private Practice, Bradenton Neurology, Inc; Consulting Staff, Department of Neurology, Manatee Memorial Hospital, Lakewood Ranch Medical Center, Blake Medical Center

Andrew P Keegan, MD is a member of the following medical societies: American Academy of Neurology and American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Norman C Reynolds Jr, MD  Neurologist, Veterans Affairs Medical Center of Milwaukee; Clinical Professor, Medical College of Wisconsin

Norman C Reynolds Jr, MD is a member of the following medical societies: American Academy of Neurology, Association of Military Surgeons of the US, Movement Disorders Society, Sigma Xi, and Society for Neuroscience

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Howard S Kirshner, MD  Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD  Professor, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

References

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Case 1: Left lateral sinus thrombosis demonstrated on MR venography. This 42-year-old woman presented with sudden onset of headache. Physical examination revealed no neurological abnormalities.
Case 1: One week after treatment with heparin, the MR venogram displayed increased flow in the left lateral sinus consistent with early recanalization of the sinus; headache had resolved at this point.
Magnetic resonance venogram - axial view; A = lateral (transverse) sinus; B = sigmoid sinus; C = confluence of sinuses; and D = superior sagittal sinus.
Magnetic resonance venogram - sagittal view; A = lateral (transverse) sinus; C = confluence of sinuses; D = superior sagittal sinus; and E = straight sinus.
Case 2: CT scan demonstrates a left posterior temporal hematoma in a 38-year-old woman on oral contraceptives (the only identified risk factor).
Case 2: Contrast-enhanced MRI showing lack of filling of left transverse sinus.
Case 2: Axial view of MR venogram demonstrating lack of flow in transverse sinus.
Case 2: Coronal view of MR venogram demonstrating lack of flow in the left transverse and sigmoid sinuses.
Table. Patients With Cerebral Venous Thrombosis Treated With Heparin and Local Infusion of Urokinase vs Nontreated Group
Treated Group, % (n = 12)Nontreated Group, % (n = 21)
Full recovery62.529
Mild disability12.513
Severe disability12.59.6
Fatal outcome12.548
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