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Transverse sinuses

The transverse sinuses, also known as the lateral sinuses, are a pair of major dural venous sinuses located in the posterior aspect of the cranium, responsible for draining venous blood from the cerebellum, occipital lobe, and inferior surfaces of the cerebrum.^[1] They originate at the confluence of the sinuses (torcular Herophili), where the superior sagittal, straight, and occipital sinuses converge near the internal occipital protuberance, and extend laterally in a groove along the inner surface of the occipital bone, embedded within the layers of the tentorium cerebelli.^[2]^[3] Anatomically, the right transverse sinus typically receives the majority of drainage from the superior sagittal sinus and is often larger than the left counterpart, which primarily drains the straight sinus, reflecting an asymmetry that can influence cerebral venous outflow.^[1] Each sinus courses anterolaterally for approximately 6-7 cm, following the posterolateral border of the tentorium cerebelli over the occipital, parietal, and temporal bones, before curving inferiorly to become the sigmoid sinus near the jugular foramen.^[2]^[3] The sinuses are valveless and endothelial-lined channels formed by the reflection of the dura mater, lacking venous valves, which facilitates bidirectional flow but increases susceptibility to thrombosis.^[1] The transverse sinuses receive tributaries including the superior petrosal sinus, which drains the cavernous sinus and adjacent structures, as well as the inferior anastomotic vein (vein of Labbé) on the left side more commonly, and direct veins from the cerebellum and basal brain regions.^[2]^[3] This venous network collects deoxygenated blood from the posterior fossa and delivers it to the sigmoid sinuses, which then form the jugular bulbs and continue as the internal jugular veins, ultimately returning blood to the systemic circulation via the brachiocephalic veins.^[1] The right sinus often exhibits a larger mean diameter compared to the left (with notable hypoplasia in up to 39% of cases, predominantly left-sided), contributing to efficient drainage of posterior cerebral veins.^[4] Clinically, variations in transverse sinus anatomy, such as hypoplasia (up to 39% on the left) or aplasia (about 20% on the left), can predispose to conditions like idiopathic intracranial hypertension or complicate endovascular interventions for dural venous sinus thrombosis.^[2] Intraluminal septations, present in many sinuses (average 1.75 per side), may anchor thrombi and influence thrombolysis or stent placement strategies.^[4] These structures are critical in neuroimaging evaluations, as their patency affects intracranial pressure regulation and cerebral venous return.^[3]

Anatomy

Location and course

The transverse sinuses are paired dural venous sinuses situated within the lateral walls of the posterior cranial fossa.^[4] They originate at the confluence of sinuses, known as the torcular Herophili, where the superior sagittal, straight, and occipital sinuses converge near the internal occipital protuberance.^[5] From this point, each sinus courses horizontally along the attached margin of the tentorium cerebelli, occupying the transverse sulcus—a groove formed at the junction of the squamous portion of the temporal bone and the occipital bone.^[2] This pathway positions the sinuses in the posterior aspect of the tentorium, separating the occipital lobes superiorly from the cerebellum inferiorly.^[6] The transverse sinuses extend laterally for an average length of approximately 7 cm in adults, with the left sinus typically measuring slightly longer (mean 7.4 cm) than the right (mean 6.8 cm).^[4] Slight asymmetry is common, with the right transverse sinus often dominant in size and flow, observed in a majority of individuals.^[6] As they progress laterally, the sinuses maintain a relatively straight horizontal trajectory until approaching the posterolateral aspect of the petrous temporal bone, where they curve downward to continue as the sigmoid sinuses toward the jugular foramen.^[5] Developmentally, the transverse sinuses arise from the embryonic tentorial plexus, formed by the anterior and middle dural plexuses that drain into the primary head sinus and evolve with brain growth to establish the mature venous pathways by the end of the embryonic period.^[7] This origin contributes to their consistent positioning along the tentorial margin in postnatal anatomy.^[6]

Structure and relations

The transverse sinuses are formed by invaginations or reflections of the dura mater, creating endothelial-lined channels that lack valves and smooth muscle layers, distinguishing them from typical peripheral veins.^[8] These sinuses originate at the confluence of sinuses, known as the torcular Herophili, and course laterally within the posterior cranial fossa.^[5] Histologically, the walls of the transverse sinuses consist of three primary layers: an outer periosteal (endosteal) layer of dura mater adherent to the skull, an inner meningeal layer forming the dural reflection, and a thin endothelial lining continuous with vascular endothelium.^[8] This endothelium facilitates unidirectional flow potential through collateral connections, such as with the occipital sinus, which can provide alternative drainage pathways.^[2] Anatomically, the transverse sinuses are positioned superiorly along the attached margin of the tentorium cerebelli and the transverse sulcus on the inner surface of the occipital bone.^[1] Inferiorly, they relate to the superior surface of the cerebellum and the petrous portion of the temporal bone, while laterally they groove the squamous part of the temporal bone.^[3] Their close proximity to the mastoid air cells and emissary veins, which traverse the mastoid emissary foramen, allows for potential transmission of infections from extracranial sites like the middle ear to the intracranial venous system.^[9] Variations in transverse sinus development are common, with hypoplasia (underdevelopment) or aplasia (absence) occurring more frequently on the left side; left hypoplasia is reported in approximately 39% of cases and aplasia in 20%, compared to 6% and 4% on the right, respectively.^[2] Arachnoid granulations, protrusions of arachnoid villi into the sinus walls, are often present along these structures and contribute to cerebrospinal fluid absorption into the venous circulation.^[10]

Tributaries and drainage

The transverse sinuses receive venous blood primarily from the superior petrosal sinus, which drains the petrous temporal bone region, including the cerebellum, labyrinthine veins, and portions of the cavernous sinus.^[3] Additional tributaries include occipital veins, inferior cerebral veins, and cerebellar veins from the posterior fossa, which empty directly into the transverse sinuses along their course.^[11] The inferior petrosal sinus drains independently into the internal jugular vein.^[3] Further inputs arise from the mastoid emissary veins, which connect diploic veins of the skull to the transverse or sigmoid sinuses, and the vein of Labbé, an anastomotic vein draining the temporal and inferior parietal lobes.^[2] The basal vein of Rosenthal contributes indirectly through the galenic system, joining the straight sinus before reaching the confluence of sinuses and subsequently the transverse sinuses.^[3] From the confluence of sinuses, the transverse sinuses course laterally within the tentorium cerebelli and continue as the sigmoid sinuses, which curve downward to form the jugular bulbs and drain into the internal jugular veins at the jugular foramen, integrating into the systemic venous circulation.^[1] Collateral pathways exist via the superior petrosal sinus, providing anastomoses to the cavernous sinus for alternative drainage; in obstruction, these can facilitate flow reversal to maintain cerebral venous outflow.^[3] Asymmetry is common, with the right transverse sinus often larger and dominant, primarily receiving drainage from the superior sagittal sinus, while the left transverse sinus typically handles more flow from the straight sinus.^[1]

Physiology

Venous drainage role

The transverse sinuses serve as a primary conduit for collecting and transporting deoxygenated blood from the posterior cerebral hemispheres, cerebellum, and brainstem, directing it toward the internal jugular veins via the sigmoid sinuses. This function is integral to cerebral venous return, ensuring efficient removal of metabolic waste and carbon dioxide from these regions without the presence of valves or muscular walls that could impede flow.^[12] Within the broader dural sinus system, the transverse sinuses integrate with the galenic system—via the straight sinus draining deep cerebral veins—and the petrosal systems, including the superior petrosal sinus from the cerebellum and brainstem, to equalize pressure gradients across the intracranial venous network. This connectivity at the confluence of sinuses (torcular Herophili) allows for balanced distribution of venous inflow, preventing localized pressure imbalances that could affect cerebral perfusion. Arachnoid granulations along the walls of the transverse sinuses further contribute to cerebrospinal fluid (CSF) absorption, facilitating the reabsorption of CSF into the venous bloodstream and aiding in the maintenance of intracranial pressure homeostasis.^[12]^[5] In pathological conditions such as superior sagittal sinus occlusion, the transverse sinuses can function as collateral pathways, rerouting venous drainage through alternative meningeal and cortical veins to mitigate upstream congestion and preserve overall cerebral venous outflow. Embryologically, the transverse sinuses persist from the primary head vein plexuses, particularly the anterior cerebral vein components, which are essential for establishing fetal cerebral drainage patterns that evolve into the mature dural venous architecture. This developmental origin underscores their role in maintaining a low-pressure gradient that supports cerebral autoregulation, thereby preventing brain edema by accommodating fluctuations in intracranial pressure without compromising blood-brain barrier integrity.^[12]^[13]

Hemodynamic characteristics

The transverse sinuses function within a low-pressure venous system, with mean pressures typically ranging from 10 to 15 mmHg in the proximal segments, substantially lower than systemic arterial pressures of 80-120 mmHg; this gradient is maintained by the sinuses' enclosure in the rigid dural layers, which limits distensibility, and the lack of valves, allowing passive drainage reliant on upstream intracranial pressure and downstream central venous pressure.^[14] These pressures decrease progressively from the superior sagittal sinus confluence toward the sigmoid junction, ensuring efficient cerebral venous outflow without active propulsion. Blood flow through the transverse sinuses is unidirectional, progressing from the medial confluence of sinuses laterally along the tentorium cerebelli to the sigmoid sinuses, with directionality reinforced by anatomical channeling and, in the upright posture, augmented by gravitational assistance that promotes downward drainage toward the jugular veins.^[3] Flow velocities average 10-20 cm/s, characterized by low pulsatility (systolic peaks around 16-19 cm/s and diastolic minima 11-13 cm/s), and exhibit phasic variations synchronized with the cardiac cycle; these parameters are reliably quantified noninvasively via transcranial Doppler ultrasound, which corrects for insonation angles to capture accurate forward flow profiles.^[15] At the distal narrowing where the transverse sinus transitions to the sigmoid sinus, flow velocity accelerates due to the reduced cross-sectional area, as described by the Bernoulli principle—in which energy conservation results in inverse relationships between velocity and static pressure in streamlined flow—thereby optimizing momentum transfer without inducing turbulence in healthy states.^[16] Anatomical asymmetry frequently results in the right transverse sinus being dominant, handling up to 60% of total bilateral drainage volume (approximately 4-5 mL/s on the right versus 3 mL/s on the left), a pattern observed in over 50% of individuals and attributable to variations in confluence drainage allocation.^[17] Phase-contrast magnetic resonance imaging (MRI) corroborates these dynamics by visualizing predominantly laminar flow patterns in the transverse sinuses, with streamlines parallel to the vessel walls and minimal vorticity, offering quantitative validation of velocity fields and flow partitioning in vivo.^[17]

Clinical aspects

Thrombosis and occlusion

Thrombosis of the transverse sinuses represents a significant subtype of cerebral venous sinus thrombosis (CVST), commonly involving these structures either unilaterally or bilaterally, with involvement reported in 40-70% of CVST cases across various studies.^[18]^[19] Isolated transverse sinus thrombosis occurs less frequently but can present without multi-sinus involvement, while bilateral cases, which can exacerbate hemodynamic compromise due to disrupted bilateral venous outflow.^[20] The overall incidence of CVST, including transverse sinus involvement, is estimated at approximately 10-15 cases per million population annually according to recent studies, with a higher prevalence among women of childbearing age, where rates can increase to 12 cases per 100,000 deliveries during pregnancy or the puerperium.^[21]^[22]^[23] Risk factors for transverse sinus thrombosis mirror those of broader CVST and include acquired prothrombotic conditions such as dehydration, which promotes blood stasis, and hypercoagulable states like factor V Leiden mutation.^[22] Hormonal influences, particularly pregnancy and oral contraceptive use, elevate risk by 5-20-fold in susceptible women, while local infections such as mastoiditis can propagate thrombi via emissary veins connecting the transverse sinus to extracranial structures.^[24]^[25] More recently, COVID-19 infection and, in rare cases, vaccination with certain COVID-19 vaccines have emerged as additional risk factors.^[22] Other contributors include systemic diseases like malignancy or inflammatory conditions that induce endothelial damage, aligning with Virchow's triad of stasis, hypercoagulability, and vessel injury.^[23] Pathophysiologically, thrombosis initiates with venous stasis in the transverse sinuses, leading to clot formation that obstructs drainage from the temporal and occipital lobes, resulting in venous hypertension and subsequent cytotoxic edema.^[24] This elevated pressure impairs cerebral perfusion, potentially causing hemorrhagic or ischemic infarction in the affected cortical regions, with cytotoxic mechanisms driven by disrupted blood-brain barrier integrity and cellular swelling.^[22] If untreated, progression can lead to increased intracranial pressure and herniation.^[26] Clinical presentation often begins with headache, reported in 70-90% of cases, typically progressive and severe due to dural stretching from venous congestion.^[27] Additional symptoms include seizures (in 30-50% of patients), papilledema from transmitted pressure to the optic nerve, and focal neurological deficits; without intervention, deterioration to altered consciousness or coma may occur in severe cases.^[28]^[29] Historically, transverse sinus thrombosis as part of CVST was first detailed in 1825 by French physician François Ribes in a case of dural sinus occlusion confirmed at autopsy, with John Abercrombie providing the initial description of puerperal-related cases in 1828; modern diagnostic recognition advanced in the 1990s with the advent of magnetic resonance venography (MRV), enabling non-invasive visualization of thrombi.^[30]^[31]

Imaging and diagnosis

Magnetic resonance venography (MRV) serves as the primary imaging modality for evaluating the transverse sinuses, particularly in suspected thrombosis, utilizing time-of-flight (TOF) or contrast-enhanced sequences to detect flow voids indicative of absent venous flow.^[32] TOF MRV relies on the absence of flow-related signal in the affected sinus, while contrast-enhanced MRV improves visualization by highlighting filling defects, offering high sensitivity for subacute and chronic thrombi.^[22] These techniques are preferred due to their non-invasive nature and ability to assess parenchymal involvement simultaneously via MRI.^[33] Computed tomography venography (CTV) acts as an alternative, especially in acute settings where rapid acquisition is needed, revealing filling defects within the opacified transverse sinus.^[34] CTV demonstrates a sensitivity of approximately 90-95% for detecting transverse sinus thrombosis when compared to digital subtraction angiography as the reference standard.^[35] It is particularly useful in emergency departments for confirming hyperdense thrombus on non-contrast CT followed by contrast enhancement to delineate the extent of occlusion.^[36] Transcranial Doppler (TCD) ultrasound provides a non-invasive method for assessing flow velocity in the transverse sinuses, measuring parameters such as mean and peak systolic velocities to identify hemodynamic alterations suggestive of thrombosis.^[37] However, its utility is limited by the acoustic shadowing from the temporal bone, which restricts insonation windows and reduces reliability for deep venous structures like the transverse sinuses.^[38] Conventional catheter angiography remains the gold standard for complex cases, such as when non-invasive imaging is equivocal, allowing direct visualization of thrombus and collateral venous recruitment.^[39] It provides detailed angiographic filling defects and dynamic flow assessment but is reserved for situations requiring endovascular intervention due to its invasive risks.^[40] Normal anatomical variants, such as transverse sinus hypoplasia, frequently mimic thrombosis on single-plane imaging by showing apparent flow absence, necessitating multiplanar reconstructions or source images to confirm the congenital narrowing rather than acute pathology.^[41] Hypoplasia, often asymmetric and more common on the left side, can be differentiated by the absence of thrombus signal intensity on MRI and continuity with adjacent structures on reformatted views.^[42] Diagnostic criteria for transverse sinus thrombosis include absent flow signal on MRV, corroborated by the empty delta sign on contrast-enhanced CT, where a triangular filling defect is outlined by enhancing dural margins.^[22] This combination enhances specificity, as isolated flow voids may represent slow flow or variants, while the delta sign directly indicates intraluminal thrombus in the transverse segment.^[43]

Surgical and therapeutic considerations

Anticoagulation serves as the first-line treatment for transverse sinus thrombosis, typically initiated with intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin to prevent thrombus propagation and promote recanalization, followed by oral vitamin K antagonists such as warfarin for 3 to 6 months in provoked cases.^[22] This approach has significantly reduced mortality rates from historical levels of approximately 50% without treatment to around 10% with early intervention.^[40] Therapeutic monitoring targets an international normalized ratio of 2.0 to 3.0 during the oral phase.^[22] For cases refractory to anticoagulation, endovascular thrombolysis using catheter-directed tissue plasminogen activator (tPA) is employed to dissolve extensive thrombi and alleviate clinical deterioration, though it carries a 17% risk of intracranial hemorrhage.^[22] Surgical decompression via craniotomy is indicated for patients with significant mass effect, such as large venous infarcts or abscesses leading to herniation risk, yielding favorable outcomes in over 50% of severe cases despite a mortality rate of about 20%.^[22] Additionally, sinus stenting addresses transverse sinus stenosis contributing to thrombosis or associated conditions like idiopathic intracranial hypertension, effectively reducing pressure gradients (≥10 mm Hg) and improving symptoms in refractory patients.^[44] Prophylaxis against transverse sinus thrombosis is essential in neurosurgical contexts, particularly for posterior fossa tumor resections near dural sinuses, where mechanical methods such as intermittent pneumatic compression are routinely used, supplemented by pharmacologic agents like low-molecular-weight heparin when bleeding risk is low.^[45] Early treatment overall leads to full recovery in approximately 80% of patients, with complications including hemorrhage occurring in about 5%.^[40] Emerging therapies include direct oral anticoagulants (DOACs), such as rivaroxaban and dabigatran, introduced in the 2010s, which demonstrate non-inferiority to vitamin K antagonists in trials like RE-SPECT CVT, offering reduced hemorrhage risk and simplified dosing for long-term management.^[22]

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