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Intracranial Venous Thrombosis: Imaging Signs and Common

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Intracranial Venous Thrombosis: Imaging Signs and Common 1 Revista Chilena de Radiología. Vol. 16 N 4, Año 2010; 175-187. INTRACRANIAL VENOUS THROMBOSIS: IMAGING SIGNS AND COMMON PITFALLS Drs. Michael Hirsch S1, Alejandra Torres G2. 1Radiology Resident, Hospital Clínico Universidad de Chile. 2Neuroradiologist, Hospital Clínico Universidad de Chile. Corresponding Author: Michael Hirsch S. Postal Address: Av. Santos Dumont #999. Independencia, Santiago. Phone: 9789191 E-mail: [email protected] Abstract Although intracranial venous thrombosis is a relatively rare disease, it constitutes an entity that must be timely and accurately diagnosed in emergency services, given the need for prompt treatment to avoid serious complications, including neurological deficits or even death. There are several imaging signs that can be visualized on both computed tomography (CT) and magnetic resonance (MR) imaging scans that allow for this early diagnosis. On the other hand, some differential diagnoses need to be performed to prevent mistaking intracranial venous thrombosis for any other entity. 2 Key words: Cranial Sinuses; Sinus Thrombosis, Intracranial; Tomography, Spiral Computed Tomography; Magnetic Resonance Imaging; Radiology. Introduction Intracranial venous thrombosis (IVT) is a cerebrovascular condition that may affect all ages, occurring predominantly in infants and in adults around the third decade of life (1,2). It may include cerebral veins (CV) as well as dural venous sinuses (DVS). There are over a hundred causes described as etiopathogenic factor of IVT (Table I) (1), summarized in the classic “Virchow's triad” which encompasses states of hypercoagulability, vessel wall damage and disturbance of venous flow (3). However, the causal factor of IVT may be found only in 75 to 85% of patients, even though when all available examinations and laboratory tests are performed (1, 4). By reviewing the clinical presentation of IVT, a wide range of symptoms and signs, ranging from headache and intracranial hypertension to coma and even death, may be observed (Table II). Headache is the most commonly encountered symptom─seen in 75 to 95% of patients with IVT─, usually preceding by days, weeks or exceptionally months (2,5) the manifestation of other neurological disorders (70-75%). Headache has been associated with manifestations of intracranial hypertension in 20 to 40% of cases (2); it can be mild, moderate, or severe in intensity, and predominantly diffuse (2). Given the variability and nonspecificity of presenting symptoms of the IVT, an imaging diagnostic technique is essential to understand the etiology of symptoms, mainly because an early diagnosis allows the implementation of a timely anticoagulant therapy, thus reducing the rate of complications and neurological sequelae. 3 Table I. Causes and risk factors associated with intracranial venous thrombosis. Prothrombotic genetic conditions Antithrombin deficiency Protein C and S deficiency Factor V-Leiden mutation Prothrombin mutations Homocysteinemia caused by mutations in the methyltetrahydrofolate reductase gene. Acquired prothrombotic conditions Nephrotic sindrome Antiphospholipid antibodies Homocysteinemia Pregnancy Puerperium Infections Otitis, mastoiditis, sinusitis Meningitis Systemic infectious disease Inflammatory diseases Systemic lupus erythematosus Wegener’s granulomatosis Sarcoidosis Inflammatory bowel disease Behçet’s syndrome Hematologic conditions Polycythemia, primary and secondary Thrombocythemia Leukemia Anemia, including paroxysmal nocturnal hemoglobinuria Drugs Oral contraceptives Asparaginase Mechanical/ traumatic causes Head trauma Injury to sinuses or jugular vein, jugular catheterization Neurosurgical procedures Lumbar puncture Miscellaneous Dehydration, especially in children Cancer 4 Table II. Clinical features of intracranial venous thrombosis Symptoms Headache Visual disturbances Impairment of consciousness Nausea, vomiting Signs Papilledema Focal neurological deficit Cranial nerve palsies Convulsions, coma Imaging aspects There are several imaging findings that allow us to suspect or make the diagnosis of IVT, both on computed tomography and magnetic resonance imaging scannings: A) Signs of vein occlusion B) Parenchymal alterations and other changes secondary to venous stasis C) Signs of recanalization. Each of them will be discussed. A) Signs of venous occlusion 1) The Empty Delta Sign This finding was originally described on CT cuts with intravenous contrast agent; it corresponds to a triangular and hypodense filling defect associated with a hyperdense peripheral area, which is produced by contrast material enhancement in the thrombosed superior sagittal sinus (SSS) (Figure 1) (3.6). Currently, it is possible to observe the empty delta sign not only in the SSS, but also in the transverse (TS) and sigmoid sinuses (SS) on multiplanar 5 reconstructions from multidetector CT, as well as on contrast-enhanced MR imaging studies. Figure 1. Contrast enhanced CT sequence (a, b) where empty delta sign in superior sagittal sinus at various levels is identified in the same patient DVS exhibit an elongated and triangular shape in cross section; they are valveless structures with a plexus of adjacent venous channels that act as a collateral pathway for drainage in the event of thrombosis (Figure 2) (7). Numerous hypotheses intended to explain the appearance of this sign have been formulated, including: . Recanalization of the thrombus within the venous sinus . Organization of the blood clot . Blood-brain barrier breakdown 6 . Dilatation of collateral peridural and dural venous channels. Seemingly, the latter would be the most likely explanation since contrast- enhancement of dural venous collateral circulation─primarily consisting of lateral lacunae, vascular mesh (dural cavernous spaces), and meningeal venous tributaries─would produce the empty delta sign in the thrombosed sinus (3, 6, 7). In up to 90% of cases the location of thrombosis involves more than one sinus, particularly the ST and SS, collectively termed as lateral sinus. (Table III) (4, 8, 9). Figure 2. Coronal sections of an anatomical preparation. a) Identifies the superior sagittal sinus (S) formed by the divergence of the periosteal and meningeal layers of the dura mater. The latter converge at the falx cerebri (H). Around the sinus there is a collateral venous plexus (asterisks). b) In the transverse sinus (TS) the meningeal layers of the dura mater converge at the tentorium (T), also giving it a triangular appearance. Calotte (C), cerebellum (Ce). 7 Table III. % Thrombus location Superior sagittal sinus 62.0 Left lateral sinus 44.7 Right lateral sinus 41.2 Straight sinus 18.0 Cortical veins 17.1 Deep venous system 10.9 Cerebellar veins 0.3 Late-phase contrast-enhanced CT scans have proved to be a reliable method to investigate the cerebral venous structures (especially by multiplanar reformatting), with a sensitivity of 95% when compared with angiography, as reported in several publications (10). This capability allows a high performance, thus avoiding the inherent risks of the interventional procedure. The empty delta sign is observed in 25 to 75% of cases of DVS thrombosis, depending on the different techniques applied. Ideally, it has to be detected by means of multiplanar reformation at different spatial planes, especially in the SSS and TS horizontal portions (Figure 3) by using wider window settings than those normally used for brain parenchyma, with a window width of 260 HU and a level of 130 HU (Figure 4) (5). It should be noted that the empty delta sign may disappear in the chronic stages due to enhancement of organized clot (5). 8 Figure 3. Coronal plane reformation Contrast-enhanced CT. The empty delta sign in the right transverse sinus is identified; to compare with contralateral sinus. 9 Figure 4. Contrast-enhanced CT. A small thrombus in the superior sagittal sinus can be observed only by changing window width and window level. 2) The hyperdense sinus sign and the cord sign In 20% of cases the clot can be seen in its early stages at the level of the DVS (6) as a hyperdense image on non-contrast-enhanced CT scans (Figure 5, 6a, 7a), since the thrombus retracts and its water content decreases while the concentration of hemoglobin increases, thus achieving an attenuation value of 50-80 HU, which normalizes within 1-2 weeks’ time (11). The tentorium and beam hardening artifacts caused by bones may obscure this finding or it may be confused with a subarachnoid hemorrhage, an underlying subdural hematoma, or it can be caused by a high hematocrit (11). The cord sign corresponds to the same principle as that of the hyperdense sinus, but applied to cortical veins (Figure 7a), which are rarely involved in isolation in IVT (4). 3) Absence of flow void and hyperintense vein sign On non-contrast MR images, vessels are usually hypointense on all sequences due to its flow; this is called flow void sign, also known as "flow void." When this flow-void is absent, vessels become hyperintense, which may be indicative of thrombosis (Figures 6c, 8a); nevertheless, a slow or turbulent flow can cause changes in DVS signal intensity, thus leading to misdiagnosis (4). Moreover, the various states of hemoglobin degradation may alter the appearance of the thrombus and make it less obvious, mimicking the typically observed absence of flow void signal (12,13). For example, deoxyhemoglobin will cause the acute thrombus to appear as a very hypointense area on T2-weighted sequences (Figure 9), mimicking the normal flow void, and isointense on T1-weighted sequences, resembling
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