Q J Med 2002; 95: 137-142
© 2002 Association of Physicians
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Cerebral venous sinus thrombosis
From the Wessex Neurological Centre, Southampton General Hospital, Southampton, UK
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Introduction |
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Cerebral (dural) venous sinus thrombosis is an uncommon condition, but its clinical presentation is varied and often dramatic. It often affects young-to-middle-aged patients, and more commonly women. Although recognized for more than 100 years,1 it has only in recent years come to be diagnosed frequently ante-mortem. This is partly due to greater awareness among physicians and neurologists, and partly to improved non-invasive imaging techniques.
We have no reliable data on its incidence, nor on geographical or racial differences in susceptibility. According to British death certification data from 1952 to 1961, the average mortality from venous sinus thrombosis was 0.4/106/year over this period.3 Assuming a mortality rate of 10–20% over this period produces an incidence figure of 4–8/106/year, which is likely to be an underestimate.
Data from a US study in 1993–4 estimated that dural sinus thrombosis might complicate 11.6/100 000 deliveries, although mortality in this survey was zero. They were unable to identify a significant effect of race or income following multivariate analysis, but increasing maternal age was a risk factor.64
From the body of literature on intracranial venous thrombosis, there appears to have been an increasing trend in recent decades away from reported cases related to infection, and toward cases in which prothrombotic states are causal.
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Anatomy |
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Venous blood from the brain flows via the superficial (cortical) and the deep cerebral veins into the venous (dural) sinuses. There are numerous connections between the cortical veins and dural sinuses, and also with the venous system of the meninges, scalp and nasal sinuses. This facilitates the spread of thrombus or infection between these vessels, but also may allow the opening of collateral draining vessels in the event of an occlusion.
The superior sagittal and lateral sinuses are commonly (70%) individually involved by thrombosis. In 30%, both are affected, in addition to cortical and cerebellar veins.2
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Aetiology |
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More than 100 causes of cerebral venous sinus thrombosis have been recorded in the scientific literature.1 However, even with extensive investigation, no cause is identified in 20–25% of cases.2 The more common causes are listed in Table 1
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Infective causes related to the middle ear, facial skin infection or penetrating head trauma probably occur less commonly with modern aggressive antibiotic treatments, and may now only account for <10% of cases.2
Largely inherited prothrombotic tendencies such as factor V Leiden mutations, protein S and C and antithrombin III deficiencies are an important cause, accounting for perhaps 10–15% of cases.32
Various drugs have been implicated, including androgens, ecstasy, HRT and the oral contraceptive pill.
Pregnancy and the puerperium have long been recognized as periods of increased susceptibility.10,11 A recent survey in the US based on data from the 1993–4 Healthcare Cost and Utilization project64 identified a number of independent risk factors for intracerebral venous thrombosis. Interestingly, most occurred in the peripartum period. Significant increased risk was associated with caesarian delivery (odds ratio 3.1), increasing maternal age (odds ratio 2.5) and the presence of several co-morbid conditions including hyperemesis (odds ratio 14.2), intercurrent infection (odds ratio 3.45) and maternal hypertension (odds ratio 1.9). This last association of hypertension is suprising, since there has been no other reported association of raised BP with venous sinus thrombosis. The authors of the study suggest that the small increased risk might be due to a higher rate of casesarian section in women with hypertension. There may be a cumulative effect of resistance to activated protein C during pregnancy together with decreased protein C levels following surgery.65,66
A reliable systematic case-control study from the Dutch Venous Sinus Thrombosis group prospectively compared a series of cases with cerebral sinus thrombosis with age-controlled population data.33 They found 85% of women with a cerebral sinus thrombosis used oral contraceptives, compared to 45% of control women (age-adjusted odds ratio 13). Nineteen percent had a prothrombotic tendency, which in the majority was a factor V Leiden mutation, compared to 7% expected in the population (age-adjusted odds ratio 3.2). In women using the Pill and harbouring a prothrombotic defect, the odds ratio for cerebral sinus thrombosis was 30, compared to women without either risk factor.
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Clinical presentation |
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Clinical presentation can be extremely varied, and symptoms can evolve over hours to a few weeks. In a recent Dutch-European study34 the most frequent symptoms and signs were headache (95%), focal seizures with or without secondary generalization (47%), paresis (uni- or bilateral) (43%) and papilloedema (41%). Fifteen percent were comatose and a further 39% had some impairment of consciousness at presentation. Twenty percent presented with a isolated intracranial hypertension (BIH) type picture (headache, visual disturbance and papilloedema).
Other rarer presentations include thunderclap headache mimicking subarachnoid haemorrhage.35
Cortical vein involvement alone without extension to the dural sinuses, and therefore lacking features of raised CSF pressure, is rare and may present with a ‘stroke-like’ episode.61 Thrombosis of the deep cerebral veins is usually accompanied by impairment of consciousness and occasionally abnormalities of eye movements or pupillary reaction.62 Occasionally, cerebellar veins may be involved, usually related to middle-ear infection, and may lead to a slowly evolving syndrome of vertigo, vomiting and ataxia, often with headache and coma.63
Involvement of the cavernous sinus is commonly the result of sepsis from the paranasal sinuses or facial cellulitis, and produces a localized syndrome of proptosis, cheimosis, painful external ophthalmoplegia, papilloedema and involvement of the ophthalmic and maxillary divisions of the trigeminal nerve.
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Complications |
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Increasing venous congestion results in raised dural venous sinus and CSF pressure if collateral venous drainage is insufficient.58 Parenchymal oedema with venous infarction and haemorrhage complicate up to 50% of venous sinus thromboses.2
Pulmonary embolism from a dural sinus thrombosis is uncommon but often carries a poor prognosis. A review of the literature between 1942 and 1990 revealed that in 11.3% of cases, venous sinus thrombosis was associated with pulmonary emboli, and in these cases the overall mortality rate was 95.6%, far higher than in those without embolism.42
Hypopituitarism may result from cavernous sinus thrombosis.40
Dural venous sinus thrombosis has been cited by several authors as an aetiological association of dural arteriovenous fistulas, although it may be difficult in some cases to ascertain if the thrombosis was a primary or secondary event.41
Focal seizures with or without secondary generalization may persist following dural sinus thrombosis, requiring continuing anti-epileptic therapy.
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Diagnosis |
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The confirmation of a diagnosis of dural venous sinus thrombosis is reliant on demonstration of the thrombus by neuroimaging. Non-invasive imaging by magnetic resonance venography is used in preference to cerebral angiography,44 although CT contrast venography remains popular in some centres, and may be a superior technique in certain cases.43 The ‘typical’ empty delta sign seen on contrast CT scanning is present, however, only in 20% of cases.2 This is seen on axial CT images, and represents enhancement with i.v contrast of the wall of the posterior sagittal sinus, outlining the clot within the lumen anteriorly. In most centres however, MRI/V is usually the investigation of choice for demonstrating dural sinus thrombosis, as it may exclude significant alternative diagnoses and will also demonstrate cerebral venous infarction complicating cerebral venous occlusion. Difficulties in diagnosis arise due to unusual normal anatomical variants and cases where there is near-occlusion of the venous sinus.45
Lumbar puncture is usually not helpful in establishing the diagnosis of dural sinus thrombosis, although abnormalities are commonly found. It may show raised pressure, pleocytosis, increased red cells or elevated CSF protein.46 Conversely, LP may be required in severely-ill patients with venous sinus thrombosis to exclude other treatable diagnoses within relevant clinical settings such as subarachnoid haemorrhage and bacterial meningitis. Also, in patients with an isolated intracranial hypertension (BIH) presentation, an abnormal LP may suggest the diagnosis.
Appropriate investigation towards possible aetiogenesis in each case should also be conducted.
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Therapy |
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Anticoagulation with heparin was first advocated for venous sinus thrombosis 50 years ago10 and has been widely adopted. There have been many open,2,48 but only a single randomized trial of i.v heparin vs, placebo.47 The trial was halted following recruitment of only 10 patients in each arm of the study, as there was a significant difference in outcome: eight of the heparin-treated group recovered compared to one in the placebo. Similarly there were no deaths in the heparin group, compared to three in the placebo group. The same trialists went on to report retrospectively 102 cases treated with heparin, and found no significant increase in cerebral haemorrhage even in those with pre-existing bleeds at presentation.47
In most studies and indeed in clinical practice, the dose of heparin used results in an APTT of twice the baseline figure (but >120 s) and is followed by empirical warfarin for 3–6 months.
A more recent trial comparing low-molecular-weight heparin (LMWH) and placebo for 3 weeks failed to demonstrate any benefit within the treatment arm of the trial.49 The study confirmed that there was no significant increased risk of haemorrhage with heparin. The reasons for the discrepancy between the two trials is uncertain.1 One possibility reflects the good outcome within the placebo arm of the LMWH trial, and indeed there were more ‘BIH’ type patients randomized to this arm of the study than to active treatment. Another possibility reflects earlier treatment in the LMWH trial compared to the i.v heparin trial (10 vs. 30 days), implying that less severely affected patients in the LMWH trial may have benefited less,1 and this is supported by the overall differences in mortality within the placebo arm of each trial (30% vs. 14%).
Hence there remains some uncertainty as to the relative efficacy of heparin and LMWH in dural sinus thrombosis. A meta-analysis of the two trials shows a relative risk reduction with heparin of 70% in death and 56% for death or dependency, but the confidence intervals are wide.
Use of systemic thrombolysis for dural sinus thrombosis was first reported 30 years ago using urokinase.51 There followed a series of open case studies using local infusions either via a frontal burrhole,52 or more usually, selective venous catheterization.53 These report benefit in terms of recovery in most cases, although with no comparable data on controls, the true therapeutic benefit remains unknown. There appeared to be no documented increase in symptomatic haemorrhages.
Recombinant tissue plasminogen activator (rtPA) has theoretical advantages in mechanism of action over urokinase.1 Two series (totalling 21 patients)54,55 have been reported in the literature of its use in dural sinus thrombosis, administered via a jugular catheter. Both used post-infusion heparin and warfarin. In most cases, outcome was good, with the larger study reporting complete recovery in 7/12 patients.55 The authors stressed this may have been due to more rapid recannalization of the vein than with heparin alone, although the correlation between outcome and vein patency on angiography is far from clear.1 The development of venous collaterals may also be instrumental in recovery. Local rtPA carries an undoubted risk of increased symptomatic haemorrhage.54,55
The value of neurosurgical intervention in dural sinus thrombosis remains unproven. It may be worth considering decompressive craniotomy in patients with coma and significantly raised intracranial pressure, although outcomes are commonly poor.59
In conclusion, therefore, in patients presenting with dural sinus thrombosis, heparin therapy should be instigated, even in those with pre-existing haemorrhage. Failure to respond to therapy, usually suggested by deepening coma or CNS deficits despite adequate heparinization and exclusion of seizure activity or pulmonary embolus, should result in local thrombolysis with rtPA via appropriate considiration of selective catheterization of the cerebral veins. Further studies of thrombolysis are required and are currently in progress.68
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Outcome |
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It may be helpful in the acute stage to identify those patients who are likely to have a poor outcome, as this provides useful prognostic information for relatives and possibly influence the use of more invasive treatment.
In early series of cerebral venous thrombosis (largely diagnosed by angiography) and largely related to sepsis, mortality was 30–50%.1 Recent studies have shown a mortality rate closer to 10%.34
A recent study by the Dutch Venous Sinus Thrombosis study group looked at prognostic factors in a series of 59 cases.34 Poor outcome at 12 weeks (death or Oxford handicap score >3) was associated with patients presenting with papilloedema, coma or altered consciousness, age >33, diagnostic delay >10 days, intracerebral haemorrhage and involvement of the straight sinus. Good outcome was associated with an isolated intracranial hypertension presentation and a delta sign on CT (perhaps because this led to early diagnosis). Other studies have suggested poor outcome with these and other parameters including involvement of the cerebellar veins, uncontrolled seizures, pulmonary embolism, infectious or malignant aetiology.50 However, even in those surviving ‘intact’, a further paper from the Dutch group looking 1 year later found 35% had cognitive impairments, 6% were dependent, 40% had symptoms that led to restrictions in lifestyle, and 40% could not resume their previous level of economic activity.56 This suggests there may be more morbidity after sinus thrombosis than reported previously, and interestingly, there was no significant effect of treatment on this later outcome data.
Little is known about the long-term outcome or risk of recurrence of cerebral venous sinus thrombosis, although one study reports as high a risk as 12%.57 Patients also have an increased risk (14%) of venous thrombosis elsewhere (DVT, PE).
Studies following recanalization of the venous sinuses have shown it may be incomplete in some cases.67 Raised intracranial pressure may also persist following the acute presentation of the thrombus.58 Although one study had suggested this results in no significant cognitive or visual morbidity,69 patients with persistent papilloedema and therefore raised intracranial pressure should have serial visual field assessment and be considered for a CSF shunting procedure.
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Conclusions |
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Dural venous sinus thrombosis may present to the physician in a number of guises. Diagnosis can be confirmed by MR imaging in most cases. Early recognition of the condition and instigation of appropriate therapy probably reduces mortality and morbidity. The initial treatment should be intravenous heparin, with thrombolysis reserved for cases undergoing secondary deterioration.
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Notes |
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Address correspondence to Dr J. Kimber, Wessex Neurological Centre, Southampton General Hospital, Tremona Road, Southampton SO16 6YD. e-mail: jeffkimber{at}doctors.org.uk
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References |
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