Cerebral Venous Thrombosis

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Chapter 14 Cerebral Venous Thrombosis

Cerebral venous thrombosis (CVT) was first described by Ribes in the early 19th century on the basis of postmortem examination.1 For a long time, CVT was seen as a rare and severe illness resulting in seizures, focal deficits, and often death. Its association with sinus infections was well described,2 but other predisposing conditions were not yet recognized. However, advances in vascular neuroimaging have led to a renewed appreciation of this disorder, which is more common, more variable, and less uniformly severe than previously assumed.36

Cerebral sinus venous thrombosis is estimated to account for 0.5% of all strokes in adults,3 but its true incidence is unknown, and frequent underrecognition is suspected.7 Initially asymptomatic venous sinus thrombosis has been implicated in the etiology of idiopathic intracranial hypertension.8,9 Indeed, studies have demonstrated that the most common symptom of CVT is headache (80%–90%) and the most common sign papilledema (50%–60%).10 Other clinical signs include focal deficits and partial seizures, and alteration of consciousness. Headache may be the only clinical symptom of CVT.11,12 Approximately one quarter of all patients have completely normal examination.3

Multiple causes and risk factors for CVT have been identified.5 The list comprises genetic and acquired prothrombotic conditions (the latter most prominently including pregnancy, puerperium, and combination of hormonal contraceptives and smoking), infections (particularly sinusitis, otitis, mastoiditis, and meningitis), systemic inflammatory illnesses (such as systemic lupus erythematosus, sarcoidosis, and inflammatory bowel disease), hematological disorders (e.g., polycythemia, leukemia, thrombocythemia, paroxysmal nocturnal hemoglobinuria), systemic cancer, severe dehydration, and head trauma. The threshold for obtaining brain imaging to exclude CVT should be lower in the presence of these conditions.

Current neuroimaging techniques have greatly enhanced our ability to diagnose CVT.3,13 Magnetic resonance imaging (MRI), particularly in combination with MR venography (MRV), provides excellent diagnostic yield in cases of thrombosis of dural sinus or deep cerebral veins (Figure 14-1).13,14 It is worth reemphasizing that noninvasive imaging modalities are allowing us to learn the broad spectrum of CVT. Although once the diagnosis was only suspected after severe intracranial hypertension or venous infarctions had occurred, today the possibility of CVT must be considered in the differential diagnosis of patients with new headaches and benign intracranial hypertension. Often CVT can be timely diagnosed only by keeping a low threshold for its clinical suspicion. A delayed or missed diagnosis of CVT, unfortunately still a common occurrence in practice, cannot be justified now that we have reliable and extremely safe means to reach the diagnosis.

Although MRI/MRV is the most proved and widely used set of tests for the identification of CVT, computed tomography (CT)/CT venogram (CTV) represent a valuable alternative when MRI is contraindicated or unavailable. The main disadvantage of CTV is the requirement for administration of iodinated contrast material.

Case Vignette

A 23-year-old woman presented during her puerperium for evaluation of new severe headaches. They had developed soon after child delivery and had worsened over the previous several days. She described them as bifrontal and pulsating. They were not accompanied by nausea or vomiting, but photophobia was intense. Soon after initial evaluation, the patient experienced increasing vomiting and developed right facial weakness and double vision on right lateral gaze. She did not have any significant medical history except for several early miscarriages and heavy smoking. She had recently begun using an oral hormonal contraceptive.

On examination at the hospital, the patient was drowsy, had bilateral papilledema, right VI nerve palsy, and peripheral right facial nerve palsy. Otherwise the examination was unremarkable. She underwent MRI and MRV of the brain that demonstrated extensive thrombosis of the posterior two thirds of the superior sagittal sinus and the proximal transverse sinuses (Figure 14-2). Thrombophilia workup was negative.

The patient improved gradually after initiation of anticoagulation. Anticoagulation was continued for 1 year, and she was advised to avoid contraceptives and stop smoking.

Knowledge of the normal anatomy of the cerebral venous system and its variations is essential to interpret the vascular images effectively. Hence we begin by illustrating and summarizing basic anatomical information.

ANATOMY OF THE VENOUS SYSTEM

The cerebral venous system consists of dural venous sinuses, superficial veins, and deep veins. The dural venous sinuses are venous channels devoid of valves situated between the two layers of the dura, and thus they are not collapsible. They constitute the major draining pathways of the cerebral venous circulation. Cerebral veins are also devoid of valvular structures and have a very thin wall with no muscular tissue. They empty into the dural sinuses but may reverse their flow in cases of dural sinus occlusion. Venous anatomy is illustrated on angiographic pictures shown in Figure 14-3.

Dural Sinuses

The major dural sinuses are the superior and inferior sagittal sinuses; cavernous and intercavernous sinuses; superior and inferior petrosal sinuses; occipital sinus; and straight, transverse, and sigmoid sinuses.

The major superficial sinus is the superior sagittal sinus, which is located in the convex margin of the falx cerebri. It runs from the foramen cecum to the torcula Herophili, where it merges with the transverse sinuses. It receives blood from cortical parasagittal veins on the cortical surface.

The inferior sagittal sinus is much smaller and is contained in the posterior half or two thirds of the free margin of falx cerebri. It terminates at the falcotentorial apex by joining with the great cerebral vein (vein of Galen) to form straight sinus. It receives blood from the falx, corpus callosum, cingulum, and medial cerebral hemispheres. The occlusion of this sinus is rarely clinically significant.

The straight sinus is situated at the line of the junction of the falx cerebri with the tentorium cerebelli. After a descending course, it terminates at the internal occipital protuberance, usually emptying into the left transverse sinus. It receives venous blood flow from the great vein of Galen and superior cerebellar veins, thus participating in the deep venous drainage. Occlusion of this sinus usually produces venous infarcts in the deep basal ganglia.

The transverse sinuses are contained within the attachment of the tentorial leaves to the calvarium. At the posterior border of the petrous temporal bone, the transverse sinuses receive the superior petrosal sinus to become the sigmoid sinuses. Transverse sinuses receive blood from the superior sagittal sinus and straight sinus, as well as bridging veins from cerebellum, inferolateral surfaces of the temporal and occipital lobes, and tentorium. It also receives blood from the cortical vein of Labbé. In more than half of cases, the right transverse sinus is larger than the left.15,16 In up to 20% of the cases, a narrowed or atretic segment can be identified in at least one of the transverse sinuses.16

The sigmoid sinuses begin where the transverse sinus leaves the tentorial margin and drain into the jugular bulb, thus becoming the internal jugular veins. There are numerous anastomoses between sigmoid sinuses and the vertebral plexus, muscular, and scalp veins.

The superior petrosal sinuses extend from the cavernous sinus to the sigmoid sinus, running along the attachment of the tentorium to the dorsal ridge of the petrous temporal bones. They receive venous drainage from the pons and upper medulla, lateral mesencephalic vein, cerebellar veins, and veins draining the inner ear.

The inferior petrosal sinuses lie in a groove between the petrous apex and the clivus, extending posterolaterally along the petrooccipital fissure. They have multiple anatomical variations but usually terminate draining into the jugular bulb. On their way, they form multiple anastomoses with deep venous plexuses.

The cavernous sinuses lie on either side of the sphenoid body. They are formed by numerous small veins with multiple interconnections that constitute a trabeculated space. They extend from the superior orbital fissure to the petrous apex. They contain the cavernous segment of internal carotid artery and cranial nerve VI. Cranial nerves III, IV, and V1 branch of trigeminal nerve are located in the lateral wall of the sinus. This sinus receives venous drainage from superior and inferior ophthalmic veins, intercavernous sinus, and multiple deep venous plexuses. They drain into the superior and inferior petrous sinuses.

Arachnoid granulations are present along venous sinuses and often protrude into their lumen. They can be confused with areas of restricted flow on imaging studies when they are prominent (most frequently the case in the transverse and superior sagittal sinus).

Deep Cerebral Veins

Deep venous drainage is variable, although major basal veins are relatively constant. The deep venous system drains the inferior frontal lobe; most of the white matter of the frontal, temporal, and parietal lobes; basal ganglia; thalamus; corpus callosum; and upper brainstem. Small medullary veins are responsible for draining blood from the deep cerebral white matter and basal ganglia into the subependymal veins of the lateral ventricles. Those veins form the thalamostriate veins, which unite with septal veins to form the internal cerebral veins. The internal cerebral veins are the largest deep veins. They are paired and originate behind the foramen of Monro. After collecting venous drainage from deep white matter and basal ganglia, they join to form the vein of Galen.

The basal veins of Rosenthal arise deep within the Sylvian fissure. They course posteriorly around the cerebral peduncles and across the tectum to join the vein of Galen. The anterior and deep middle cerebral veins as well as veins from the insula and cerebral peduncles drain through this system.

The great cerebral vein of Galen arises under the splenium of the corpus callosum from the junction of the internal cerebral veins and basal veins of Rosenthal. It usually runs a short trajectory before joining with inferior sagittal sinus to form the straight sinus.

This complex anatomical composition can be simplified by knowing the major venous drainage territories. Four general pathological patterns can be identified in cases of CVT:

IMAGING CHARACTERISTICS OF CVT

Computed Tomography

Signs of Venous Thrombosis

Noncontrast CT scan may disclose the delta sign (Figure 14-4), a dense triangle that represents an acute thrombus at the end of the superior sagittal sinus or torcula. However, this sign is insensitive and lacks specificity. It is present in less than a quarter of cases of superior sagittal sinus thrombosis17 and may be mimicked by blood hyperviscosity (e.g., dehydration, erythrocytosis), sinus calcification, or adjacent subarachnoid or subdural hemorrhage.13
Contrast CT scan may demonstrate the empty delta sign (Figure 14-5), caused by lack of contrasted flow in the occluded sinus but enhancement of the sinus wall. It is slightly more sensitive than the delta sign and may be present in close to 30% of cases of superior sagittal sinus thrombosis.17 This sensitivity may be substantially greater when thin sections of helical CT scan are carefully reviewed.13 The empty delta sign is probably produced by rich dural venous collateral circulation (from meningeal venous tributaries) and a vascular mesh of cavernous spaces within the dural wall.17

Signs of Parenchymal Involvement

Venous infarctions are characterized by their tendency to develop early hemorrhagic transformation and the presence of marked perilesional edema. Hemorrhage may be observed in more than 20% of patients at the time CVT diagnosis10 and occurs in more than 30% of patients during the acute phase of the disease.13,21 Hemorrhages are typically cortical with subcortical extension, but purely subcortical hemorrhages have been described in cases of isolated cerebral vein thrombosis.22

Magnetic Resonance Imaging

Signs of Venous Thrombosis

Acute venous occlusion (0–5 days) most often appears isointense on T1-weighted and hypointense on T2-weighted sequences, making it difficult to detect without concomitant MRV. The absence of flow void in a cerebral sinus, as evidenced by the empty delta sign on the contrast T1-weighted images shown in Figure 14-6, should make one suspicious of the possibility of venous thrombosis. Conversely, gadolinium enhancement of the sinus does not exclude sinus thrombosis because slow flow through dural or intrathrombus collateral channels may mimic normal sinus flow.26
During the subacute phase (6–15 days), MRI characteristics of the clot change, becoming hyperintense on T1-weighted and shifting from iso- to hyperintense (Figure 14-7) on T2-weighted sequences as the clot ages. Hence, MRI is sensitive for the detection of the sinus thrombosis after the first week.
Diffusion-weighted imaging (DWI) may depict the intrasinus thrombus as a hyperintense signal with matching reduction of the apparent diffusion coefficient (ADC) (Figure 14-9).29 Diffusion abnormalities were noted in more than 40% of patients with sinus thrombosis, especially during the subacute stage, and correlated with lower chances of recanalization in one study,29 but the sensitivity and significance of this finding remains to be firmly validated.

Signs of Parenchymal Involvement

Acute ischemic infarction can be detected by its hyperintense signal on DWI with corresponding reduction of ADC (dark signal)3032 (Figure 14-10). Areas of infarction are often patchy, intermixed with regions of vasogenic edema (bright on DWI and ADC), which often predominate33 and do not respect arterial perfusion territories. DWI also allows timing of parenchymal lesions as diffusion restriction is present only during the first 7 to 10 days following the infarction.31 Although areas of decreased ADC almost invariably become infarcted, resolution of lesions with reduced ADC has been reported in patients with CVT.34
There is little reported experience with the use of perfusion MRI in cases of CVT.30,35 As expected, there is no evidence of hypoperfusion in areas of vasogenic edema.30 Prolongation of mean transit time in the absence of diffusion restriction or changes in cerebral blood volume may indicate reversible degrees of compromised perfusion.35

Angiographic, Magnetic Resonance, and Computed Tomography Venograms

MR Venography

Gadolinium-enhanced three-dimensional MRV affords better visualization of smaller venous channels and may also improve assessment of sinus flow compared with TOF MRV,14 which is more susceptible to artifacts from flow turbulence.37,38 Flow gaps are much less common in contrast-enhanced MRV.

CT Venography

Helical CTV provides a reliable and rapid alternative to MRV for the detection of sinus thrombosis.40 Anatomical definition is excellent, and flow gaps are seldom a problem. Its accuracy has been shown to be comparable to that of TOF MRV.41

Conventional Angiography

Conventional cerebral angiography should be strongly considered when isolated cortical venous thrombosis is suspected.42 However, even conventional angiograms often fail to provide conclusive evidence for this elusive diagnosis.

SINUS OCCLUSION SYNDROMES

Severe headache often associated with papilledema is the most common presentation of venous sinus thrombosis.3,5 The headache typically worsens for hours to a couple of days before reaching its maximal intensity, but thunderclap headache can also be the first manifestation of CVT.43 Cranial nerve deficits, especially abducens nerve palsy, can be accompanying signs. Complex partial seizures and focal neurological deficits may occur; they usually correlate with parenchymal lesions on brain imaging but sometimes are generated by milder degrees of swelling, which only cause subtle radiological changes. Rapid development of coma may be the presentation of deep venous thrombosis with bilateral thalamic damage.

Several characteristic clinical patterns have been recognized: (1) acute to subacute onset of focal neurological deficits and seizures; (2) isolated intracranial hypertension associated with headaches, papilledema, and unilateral or bilateral VIth nerve palsy; (3) generalized encephalopathy or coma without major focal neurological deficits, a pattern that is more common in deep vein thrombosis; and (4) acute proptosis, chemosis, and painful ophthalmoplegia in cases of cavernous sinus thrombosis.4 However, atypical presentations are not exceptional.3 The onset of clinical manifestations varies substantially; subacute onset (within a month) occurs in about 50% of the cases, acute presentation in 30%, and chronic presentation in 20%.44 Symptoms may progress or fluctuate with extension of the thrombosis, opening of collateral draining channels, and recanalization from endogenous thrombolysis.6

In the following paragraphs, we present the characteristic features and radiological examples of the most common types of CVT.

Superior Sagittal Sinus

Venous infarctions, often associated with hemorrhagic transformation, tend to occur in the parasagittal frontal lobes (Figure 14-11), resulting in paraparesis (often asymmetric), hemiparesis, and fluctuating unilateral or bilateral sensory symptoms. Progression of the thrombosis into the cortical veins or severe venous hypertension in the superficial venous system may result in aphasia.

Transverse Sinus Thrombosis

The most common presentation of transverse sinus thrombosis is headaches and papilledema, even in cases with extensive thrombosis extending into the sigmoid sinus and internal jugular vein (Figure 14-12). In our experience, some of these patients may also exhibit cognitive and behavioral changes in the absence of parenchymal changes on neuroimaging.
Venous infarctions due to transverse sinus occlusion may produce large temporal hematomas (Figure 14-13). They characteristically spare the temporal pole but risk for uncal herniation nonetheless exists.

Deep Vein Thrombosis

Bilateral thalamic edema or infarction (Figure 14-14) may cause symptoms and signs ranging from inattention, spatial neglect, and amnesia, to akinetic mutism and apathy, or even sudden coma.
High attenuation changes in thrombosed deep veins can occasionally be seen on CT scan (“chord sign”).47 Signal changes on MRI depend on the age of the clot,47 as discussed in cases of dural sinus occlusion.

Cortical Vein Thrombosis

Clinical manifestations are caused by superficial infarctions involving the cortex and subjacent white matter (Figure 14-15). They are typically hemorrhagic and do not conform to arterial territory boundaries.48
Partial seizures, with or without secondary generalization, are the most common presenting feature.48 Hemiparesis, incomplete hemianopia, and aphasia, may occur and often fluctuate over days.

MANAGEMENT AND PROGNOSIS

Imaging studies are crucial to reach the diagnosis of CVT, but they can also assist in management decisions and prognostication.

Although the level of evidence supporting the use of acute anticoagulation is not solid (the three trials examining the value of anticoagulation in CVT were small, had some methodological weaknesses, and provided results that cannot be considered conclusive),5,51 current practice guidelines and most neurologists favor administration of anticoagulant therapy.3,5,52 Anticoagulation appears to be safe, and the presence of hemorrhage on brain imaging is not regarded as a contraindication for anticoagulation. In fact, because patients with hemorrhagic lesions upon diagnosis have greater risk of poor outcome, it might be agued that such patients are precisely those who require more aggressive therapy to promote recanalization, prevent propagation of the thrombus, and avoid recurrent thromboembolic complications. We strongly advocate early anticoagulation in patients with CVT.
Endovascular therapy is feasible55 and may be extremely valuable for the most severe cases in which patients experience clinical deterioration despite anticoagulation and treatment of intracranial hypertension. Because most patients with CVT have favorable prognosis (the average rate of death and dependency is 15%),21 endovascular thrombolysis or thrombectomy should be reserved for these extraordinary situations.

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