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Tela choroidea

The tela choroidea is a thin, highly vascularized membrane composed of pia mater that adheres closely to the ependyma lining the brain's ventricular system, serving as the structural foundation for the choroid plexus, which produces cerebrospinal fluid (CSF).^[1] It forms through the invagination of pia mater and ependyma along the choroidal fissures, creating a double-layered fold in certain regions that encloses vascular fringes essential for CSF secretion.^[2] In the lateral ventricles, the tela choroidea extends along the medial wall via the choroidal fissure, receiving blood supply from the anterior choroidal artery (derived from the internal carotid artery) and the medial and lateral posterior choroidal arteries (from the posterior cerebral artery), facilitating the choroid plexus's role in maintaining CSF homeostasis.^[1] Within the third ventricle, it covers the roof as a triangular fold between the lateral walls, with two longitudinal vascular fringes projecting downward to form the choroid plexus, supplied primarily by the medial posterior choroidal arteries and occasionally a superior posterior choroidal artery.^[3] In the fourth ventricle, the tela choroidea constitutes a double-layered fold in the lower half of the roof, enclosing the choroid plexus in a characteristic "T" shape with vertical and horizontal limbs that extend laterally through the foramina of Luschka, and it is vascularized by branches of the inferior cerebellar arteries.^[3]^[1] The primary function of the tela choroidea is to support the choroid plexus epithelium, which regulates CSF composition by actively transporting ions, nutrients, and waste across the blood-CSF barrier, thereby protecting the central nervous system and aiding in brain development and homeostasis.^[3] Pathologically, abnormalities in the tela choroidea can contribute to conditions such as arachnoid cysts, meningiomas, ependymomas, or disruptions in CSF production leading to hydrocephalus.^[1]

Anatomy

Location

The tela choroidea is defined as a thin, double-layered extension of the pia mater that adheres to the ependymal lining within the four ventricles of the brain, forming a vascular membrane that invaginates into the ventricular cavities.^[3] This structure is present in the lateral, third, and fourth ventricles, where it contributes to the formation of the choroid plexus along specific anatomical interfaces.^[4] In the lateral ventricles, the tela choroidea is positioned along the choroidal fissure, a narrow C-shaped cleft that follows the medial wall of each ventricle. Specifically, it lies between the fornix superiorly and the thalamus inferiorly in the body of the lateral ventricle, extending posteriorly and inferiorly to the atrium and temporal horn, where it is situated between the stria terminalis and the fimbria of the hippocampus.^[5] This C-shaped configuration allows the tela choroidea to span from the interventricular foramen to the inferior choroidal point near the uncus.^[6] Within the third ventricle, the tela choroidea constitutes the roof, forming a double fold of vascularized pia mater that extends from the habenular commissure to the interventricular foramina, with two longitudinal vascular fringes projecting downward into the ventricular cavity.^[7] In the fourth ventricle, the tela choroidea forms the inferior portion of the roof as a double-layered fold of pia mater and ependyma, enclosing the choroid plexus in a characteristic "T" shape with vertical and horizontal limbs extending laterally through the foramina of Luschka, positioned over the dorsal surface of the pons and medulla oblongata.^[8]^[9]

Structure

The tela choroidea is a thin, transparent membrane composed of a double-layered structure, with an outer layer of pia mater and an inner layer of ependyma lining the ventricular surface.^[3] This delicate architecture separates the cerebrospinal fluid (CSF)-filled ventricular space from the surrounding subarachnoid space, providing a clear demarcation that facilitates the visualization of ventricular boundaries in anatomical studies.^[10] The membrane's transparency and minimal thickness allow for the unobstructed passage of light and imaging modalities, aiding in the delineation of CSF compartments.^[3] The choroid plexus arises from the invagination of the tela choroidea at the choroid fissures, where the membrane folds inward into the ventricular lumen during embryonic development.^[4] This process begins around the seventh week of gestation, with the pia mater and ependyma approximating along the fissure lines in the roofs of the lateral, third, and fourth ventricles, forming a vascularized protrusion that constitutes the plexus.^[4] The invagination creates a continuous extension of the tela, embedding capillaries within the folded layers to support the emerging choroidal tissue.^[3] Vascular fringes, consisting of fenestrated capillaries embedded within the connective tissue core of the tela choroidea, project from the membrane and promote the development of the choroid plexus by providing a rich blood supply that protrudes into the ventricles.^[10] These fringes are particularly prominent in the third and fourth ventricles, where they hang downward as longitudinal or T-shaped structures, facilitating the architectural integration of the plexus into the ventricular walls.^[3] The tela's supportive role ensures the stability and positioning of these fringes, enabling the plexus to occupy specific ventricular regions such as the temporal horns of the lateral ventricles and the body of the third ventricle.^[4]

Blood supply

The tela choroidea, as the vascularized membrane forming the choroid plexus in the brain's ventricles, receives its arterial blood supply from branches of major cerebral arteries, tailored to each ventricular location to support the dense capillary network essential for nutrient delivery and secretory functions.^[11] In the lateral ventricles, the tela choroidea is primarily supplied by the anterior choroidal artery, a branch of the internal carotid artery, along with contributions from the posterior choroidal arteries arising from the posterior cerebral artery; these vessels anastomose to form an intricate capillary bed within the choroid plexus.^[11]^[12] For the third ventricle, the blood supply originates from the medial posterior choroidal arteries, also branches of the posterior cerebral artery, ensuring targeted perfusion to the midline structure.^[11]^[12] The tela choroidea of the fourth ventricle draws its arterial supply mainly from the posterior inferior cerebellar artery (PICA), a branch of the vertebrobasilar system, with occasional supplementary branches from the anterior inferior cerebellar artery (AICA), facilitating vascular integration into the choroid plexus for efficient nutrient transport and support of cerebrospinal fluid dynamics.^[11]^[8]^[12] This segmental arterial pattern reflects the tela choroidea's role in embedding a fenestrated capillary network that permeates the pial and ependymal layers, optimizing exchange between blood and ventricular fluid without unique venous drainage adaptations beyond general dural sinus outflow.^[11]

Function

Cerebrospinal fluid production

The tela choroidea contains the choroid plexus, a specialized epithelial structure responsible for the production of cerebrospinal fluid (CSF), which cushions and nourishes the central nervous system. CSF secretion occurs primarily through a combination of ultrafiltration across fenestrated capillaries in the choroid plexus stroma and active transport mechanisms in the overlying epithelial cells, drawing from blood plasma while selectively modifying its composition.^[13] This process involves ion transporters, such as the Na⁺/K⁺-ATPase and Na⁺-K⁺-2Cl⁻ cotransporter (NKCC1), which establish electrochemical gradients to drive water movement via aquaporin-1 channels, independent of simple osmotic filtration.^[14]^[15] In adults, the choroid plexus produces approximately 500 mL of CSF per day, equivalent to a turnover of about three to four times the total ventricular volume.^[13]^[14] The resulting CSF has a distinct composition compared to plasma, featuring low protein concentrations (typically 15–45 mg/dL versus 6,000–8,000 mg/dL in plasma) to minimize neuronal interference, and elevated chloride levels (around 120–130 mEq/L versus 98–106 mEq/L in plasma) that support its electrolyte balance.^[16] These characteristics arise from the active secretion process, which filters out large molecules while concentrating specific ions.^[13] Once produced, CSF circulation within the ventricular system is initiated and propelled by the coordinated beating of ependymal cilia lining the ventricular walls, which generate directional flow toward the subarachnoid space.^[14] These ependymal cells possess multiple primary cilia per cell, contributing to flow sensing and regulation alongside motile cilia.^[15] This ciliary activity, combined with pressure gradients from ongoing secretion, ensures efficient CSF distribution.^[13]

Cellular and vascular components

The tela choroidea, as part of the choroid plexus, consists primarily of specialized epithelial cells that form a single layer of cuboidal morphology, connected by tight junctions such as those formed by claudin proteins, which establish the blood-cerebrospinal fluid (CSF) barrier to regulate solute passage.^[11] These choroid plexus epithelial cells exhibit microvilli on their apical surfaces facing the ventricular lumen, enhancing surface area for secretion, while their basolateral surfaces interface with underlying connective tissue.^[12] Adjacent to this epithelium are ependymal cells, which are ciliated glial cells that contribute to CSF circulation through coordinated ciliary motility, aiding in the flow within the ventricular system.^[11] Vascular components within the tela choroidea include a dense network of fenestrated capillaries embedded in a loose stroma of connective tissue, which facilitates the filtration of plasma ultrafiltrate by allowing the passage of water and small solutes across the endothelial gaps.^[12] These capillaries are surrounded by pericytes and fibroblasts, supporting structural integrity, and their fenestrations contrast with the non-fenestrated vessels elsewhere in the brain, enabling efficient nutrient and ion exchange for epithelial function.^[11] The interaction between cellular and vascular elements is critical for CSF homeostasis, as choroid plexus epithelial cells actively transport ions such as Na⁺ and Cl⁻ from the blood via basolateral uptake mechanisms (e.g., Na⁺/H⁺ exchangers and Na⁺-K⁺-2Cl⁻ cotransporters) and apical extrusion driven by Na⁺/K⁺-ATPase, creating an osmotic gradient that draws water into the CSF space.^[17] This process integrates with the fenestrated capillaries to supply plasma-derived ions, supporting the overall production of CSF, though the detailed secretion dynamics are addressed elsewhere.^[17]

Development

Embryonic origins

The tela choroidea originates from the roof plate of the neural tube during early human embryogenesis, specifically around the fourth to fifth weeks of gestation, as the neural tube undergoes primary neurulation and closes. This thin epithelial layer forms the dorsal midline of the developing central nervous system, serving as the primordial tissue that later contributes to the choroid plexuses in the brain ventricles. The roof plate emerges from the neuroectoderm following induction by signals from the overlying non-neural ectoderm, establishing the dorsal identity of the neural tube.^[18] In the initial formation, the diencephalic region plays a key role in specifying the roof plate that gives rise to the tela choroidea of the third ventricle, while the mesencephalic region contributes to the dorsal midline structures influencing adjacent ventricular development. These regions differentiate as the prosencephalon and mesencephalon vesicles form by the end of the fourth week, with the roof plate thinning and vascularizing to create the foundational tela choroidea. The process involves coordinated expansion of the neural tube lumen, setting the stage for later invagination without yet forming distinct ventricular boundaries.^[19] Genetic and signaling pathways are critical for roof plate specification and subsequent tela choroidea development, particularly the bone morphogenetic protein (BMP) and Sonic hedgehog (Shh) pathways. BMP signaling, emanating from the roof plate and non-neural ectoderm, is essential for inducing dorsal telencephalic midline fates, including choroid plexus precursors; disruption of BMP receptor 1a (Bmpr1a) leads to failure in choroid plexus differentiation while preserving other dorsal structures. Conversely, Shh signaling from ventral sources maintains a balance to prevent excessive roof plate expansion; over-expression expands the roof plate domain at the expense of choroid plexus formation, whereas reduced Shh results in loss of choroid plexus markers like transthyretin. These pathways interact to specify the epithelial progenitors of the tela choroidea, ensuring proper dorsal patterning by embryonic day 10.5 in mouse models, analogous to weeks 4-5 in humans.00900-5)^[20]

Ventricular formation

The development of the tela choroidea involves the invagination of vascularized mesenchymal tissue from the roof of the neural tube into the forming ventricles, beginning around the sixth week of gestation at the sites of the choroid fissures. This process starts with the protrusion of pia mater through these fissures, allowing the formation of the choroid plexuses as specialized extensions of the tela choroidea. By the seventh to eighth week, mesenchymal cells invaginate more prominently, establishing the foundational vascular network that will support cerebrospinal fluid production.^[21]^[22] Ventricle-specific assembly of the tela choroidea reflects the underlying brain vesicle derivations. In the lateral ventricles, derived from telencephalic evaginations, the tela choroidea invaginates bilaterally through the telencephalic roof, forming frond-like plexuses that extend from the temporal horn to the body by the end of the first trimester. The third ventricle's tela choroidea arises from the diencephalic roof, appearing later but connecting via foramina to the lateral plexuses, with invagination completing around weeks 8 to 10. In the fourth ventricle, originating from the rhombencephalon, the tela choroidea develops earliest, with signs of plexus formation evident by the sixth week as bilateral folds in the hindbrain roof, maturing into a single midline structure.^[12]^[23]^[24] Maturation of the tela choroidea and its plexuses involves progressive vascularization and epithelial differentiation, with the ependymal lining of the ventricles integrating seamlessly around the invaginated structures. Vascularization begins around the 10th week, as choroid plexus vessels become detectable via color flow imaging, and continues to densify throughout gestation, ensuring robust perfusion by birth. The epithelial cells of the plexuses transition from pseudostratified to cuboidal morphology, developing microvilli and tight junctions that complete the blood-cerebrospinal fluid barrier by term. This process aligns with the overall ventricular expansion, resulting in fully functional plexuses at birth.^[25]^[26]^[23]

Clinical significance

Associated pathologies

The tela choroidea, through its derived choroid plexus, is implicated in several pathologies, primarily tumors, cysts, and infectious processes affecting cerebrospinal fluid (CSF) dynamics. Choroid plexus papillomas are benign tumors (WHO grade 1) arising from the epithelial cells of the choroid plexus, which overproduce CSF leading to hydrocephalus as a common symptom; these tumors are rare, accounting for approximately 0.4-0.6% of all intracranial tumors, with a pediatric predominance (about 80% of cases occurring in children under 5 years).^[27]^[28] Choroid plexus carcinomas, the malignant counterpart (WHO grade 3), also originate from choroid plexus epithelium but exhibit aggressive invasion and metastasis, similarly causing hydrocephalus alongside neurological deficits; they are even rarer, comprising less than 1% of pediatric brain tumors and showing a strong pediatric bias (median age around 2 years).^[29] Choroid plexus cysts are benign, fluid-filled formations within the choroid plexus that often appear incidentally on fetal ultrasound between 14-24 weeks gestation and typically resolve spontaneously by the third trimester.^[30] These cysts are found in about 1-2% of pregnancies and are usually isolated and asymptomatic, but when multiple or associated with other anomalies, they carry a higher risk (up to 4%) of trisomy 18, a chromosomal disorder.^[31]^[32] Other pathologies directly involving the tela choroidea include arachnoid cysts of the velum interpositum, which are rare benign entities originating from the tela choroidea and typically presenting as incidental findings or causing obstructive hydrocephalus.^[33] Intraventricular meningiomas may arise from arachnoid cap cells trapped within the stroma of the choroid plexus or the tela choroidea, accounting for a small subset of meningiomas and often occurring in the lateral or third ventricles.^[34] Ependymomas, which arise from ependymal cells lining the ventricles, can involve the tela choroidea-ependyma interface, particularly in the fourth ventricle, leading to CSF flow obstruction.^[10] In infectious contexts, the choroid plexus within the tela choroidea serves as a critical interface for pathogen entry into the CSF, facilitating the spread of meningitis via the blood-CSF barrier.^[35] Bacterial pathogens like Neisseria meningitidis can adhere to and traverse the choroid plexus epithelium, leading to leptomeningitis and ventriculitis, while the structure's vascularity and immune cell trafficking role exacerbate inflammatory responses in the CSF pathways.^[36]^[37] This involvement can disrupt normal CSF production, contributing to complications like hydrocephalus in severe cases.^[38]

Diagnostic and surgical aspects

The tela choroidea, as the origin of the choroid plexus, is primarily visualized through imaging of the associated plexus structures within the ventricular system, particularly for detecting tumors or cysts. On computed tomography (CT), choroid plexus tumors exhibit isodense or hyperdense lobulated masses with avid contrast enhancement due to the vascularity of the underlying tela choroidea.^[39] Magnetic resonance imaging (MRI) further delineates these lesions as intraventricular papillary or cauliflower-like formations, appearing isointense on T1- and T2-weighted sequences with heterogeneous or strong gadolinium enhancement, aiding in differentiation from surrounding cerebrospinal fluid (CSF).^[40] For cysts or subtle abnormalities, MRI sequences like T2-weighted fluid-attenuated inversion recovery (FLAIR) highlight the thin, avascular extensions of the tela choroidea by suppressing CSF signal.^[41] Ventriculography, often performed via CT or MRI with intrathecal contrast, assesses dynamic CSF flow dynamics around the tela choroidea-derived plexus, revealing obstructions or abnormal filling in cases of hydrocephalus or mass effect from tumors.^[42] This modality is particularly useful for evaluating subtle flow voids or pooling near the roof of the third or fourth ventricles where the tela choroidea resides.^[3] Surgical access to the tela choroidea typically involves neuroendoscopic techniques for hydrocephalus management, such as endoscopic third ventriculostomy (ETV) combined with choroid plexus coagulation (CPC). In ETV/CPC, a rigid endoscope is inserted through a burr hole to fenestrate the floor of the third ventricle, bypassing obstructions, while bipolar coagulation targets the choroid plexus fronds arising from the tela choroidea to reduce CSF production.^[43] This approach is effective in infants with communicating hydrocephalus, achieving success rates of 60-80% in avoiding shunts, as coagulation disrupts vascular tufts within the thin tela choroidea without requiring open resection.^[44] The tela choroidea's delicate, highly vascular composition poses significant procedural challenges, including intraoperative bleeding from fragile vessels during coagulation and postoperative CSF leaks due to incomplete sealing of ventricular entry sites.^[45] Bipolar diathermy mitigates bleeding risks by precise vessel cauterization, but persistent leaks occur in up to 5% of cases, often managed with fibrin glue or lumbar drainage to prevent meningitis.^[46] Overall complication rates for these endoscopic procedures remain low at 10-20%, emphasizing the need for preoperative MRI to map vascular anatomy.^[47]

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