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Subdural space

The subdural space is a potential anatomical compartment located between the meningeal layer of the dura mater and the arachnoid mater, two of the three protective meninges that surround the brain and spinal cord.^[1] This space is not a distinct, fluid-filled cavity under normal physiological conditions but rather a virtual area that becomes evident only in pathological states, such as when fluid or blood accumulates due to trauma or other disruptions.^[1]^[2] In the cranial region, the subdural space lies deep to the dura mater and superficial to the arachnoid, with bridging veins traversing it to connect the cerebral hemispheres to the dural venous sinuses.^[1] Recent anatomical research has challenged the traditional view of it as a pre-existing potential space, proposing instead that it forms through the separation or tearing of neurothelial cells and collagen fibers within the arachnoid-dural interface during injury.^[3] Similarly, in the spinal cord, the subdural space exists as a latent area between the dura and arachnoid, typically absent without pathology, and is relevant in conditions involving cerebrospinal fluid dynamics or hemorrhage.^[2] Clinically, the subdural space is most notable for its role in subdural hematomas, where rupture of bridging veins—often from head trauma—leads to the gradual accumulation of venous blood, potentially causing increased intracranial pressure, neurological deficits, and anemia if significant blood loss occurs.^[3]^[4] These hematomas can progress slowly due to the low pressure of venous bleeding, distinguishing them from more acute epidural hemorrhages, and may require surgical intervention like burr hole drainage in severe cases.^[3] Additionally, the space can harbor other collections, such as subdural hygromas (fluid accumulations post-trauma), whose pathogenesis involves disrupted cerebrospinal fluid absorption and carry uncertain prognostic implications.^[5] Understanding this space is crucial for neuroimaging interpretation and neurosurgical approaches, as its involvement underscores the vulnerability of meningeal structures to mechanical stress.^[1]

Anatomy

Location and boundaries

The subdural space is defined as a potential space located between the meningeal layer of the dura mater and the arachnoid mater, which is normally collapsed with no visible separation under physiological conditions.^[1] This space is maintained by adhesions between the two layers, preventing the formation of a true cavity.^[6] In the cranial region, the subdural space lines the inner surface of the skull and extends along the dural reflections, including the falx cerebri, tentorium cerebelli, and diaphragma sellae.^[7] It surrounds the brain throughout the intracranial cavity, accommodating bridging veins that traverse from cerebral veins to dural sinuses.^[1] The space is continuous inferiorly through the foramen magnum into the spinal region, where it surrounds the spinal cord from this entry point to approximately the S2 vertebral level, following the extent of the arachnoid mater.^[8] The boundaries of the subdural space are clearly delineated: it is bounded superiorly and laterally by the meningeal layer of the dura mater (the outer boundary) and inferiorly by the arachnoid mater (the inner boundary), with lateral limits formed by dural reflections and the skull base.^[6] Unlike the adjacent subarachnoid space, the subdural space lacks trabeculae and contains only a thin layer of serous fluid, which helps maintain adhesion between the dura and arachnoid.^[9]

Microscopic structure

The dura mater, the outermost bounding layer of the subdural region, consists of dense fibrous connective tissue primarily composed of fibroblasts embedded in a matrix rich in collagen fibers and elastin, providing tensile strength and elasticity.^[10] Its inner surface features a specialized dural border cell layer formed by flattened fibroblasts with sinuous processes and minimal collagen, lacking robust cell junctions and containing scattered extracellular spaces.^[11] The arachnoid mater, the inner bounding layer, is an avascular membrane formed by a layer of arachnoid barrier cells that are tightly apposed and interconnected by numerous tight junctions, forming an effective barrier to fluids and ions; these cells are supported by a basal lamina and lack significant extracellular collagen.^[10] Deeper within the arachnoid, reticular cells with desmosomal attachments contribute to trabecular structures that extend toward the pia mater. At the interface between these layers, dural border cells interdigitate with arachnoid barrier cells, creating a seamless attachment reinforced by desmosomes and gap junctions, while meningeal fibroblasts bridge any potential gaps with minimal extracellular matrix, ensuring no true subdural space exists in the normal state.^[10] Electron microscopy confirms the absence of a distinct cleft or space at this junction, revealing only close cellular apposition; separation into a visible space occurs solely under traumatic or pathological conditions, often cleaving within the weaker dural border cell layer.^[12] Recent studies propose that the subdural space does not pre-exist as a potential compartment but forms through the cleavage of neurothelial cells and collagen fibers at the arachnoid-dural interface during injury or pathology.^[3] With aging, brain atrophy enlarges the potential subdural space by increasing the distance between the brain and the dura mater, stretching bridging veins and thereby increasing vulnerability to separation and hemorrhage in the elderly.^[13]

Physiology

Normal state

The subdural space is a potential anatomical compartment situated between the inner layer of the dura mater and the outer layer of the arachnoid mater, existing primarily as a virtual interface rather than an open cavity under normal physiological conditions.^[1] Recent anatomical studies describe this interface as a layer of dural border cells (also known as neurothelial cells) that maintain close apposition between the meningeal layers, with no pre-existing separation or fluid accumulation.^[12]^[14]^[15] This tight adhesion facilitates minimal brain displacement within the cranial vault, allowing for slight movements during everyday activities such as head rotation or posture changes while preventing direct friction between the meninges and brain tissue. The tight adhesion between the dural and arachnoid layers ensures structural integrity, contributing to the overall stability of intracranial contents.^[12]^[14] In healthy states, there is no distinct fluid in the subdural interface, as the layers are continuously adherent. Intracranial pressure (ICP), typically ranging from 7 to 15 mmHg in adults, is uniformly distributed across the meningeal interface, with no independent measurable pressure gradient.^[16] Developmentally, the subdural interface emerges during embryogenesis through the progressive differentiation of meningeal layers derived from the primary meninx, a mesenchymal structure of mesodermal and neural crest origin.^[17] By approximately week 8 of gestation (Carnegie stage 22), the meninges are discernible around the neural tube, and the arachnoid layer differentiates in close adherence to the dura, establishing the foundational architecture for later brain protection via the dural border cell layer.^[18] In postnatal life, adhesions within this interface strengthen progressively, particularly during youth, enhancing meningeal cohesion.^[19] Age-related alterations influence meningeal dynamics, with tighter adhesions predominating in younger individuals due to robust arachnoid integrity, minimizing any potential for separation.^[20] In senescence, however, arachnoid atrophy and cerebral volume loss can lead to subtle loosening of these adhesions, expanding the potential for pathological separation without implications in otherwise healthy aging brains.^[21] This gradual change reflects broader neurodegenerative processes but maintains overall physiological homeostasis under normal conditions.^[22]

Interaction with cerebrospinal fluid

The arachnoid mater functions as a selective barrier that prevents direct entry of cerebrospinal fluid (CSF) from the subarachnoid space into the subdural interface. Composed of epithelial-like cells interconnected by tight junctions, this layer restricts paracellular diffusion and maintains separation between the two compartments.^[23] The absence of trabecular connections across the arachnoid-dural interface further eliminates any structural pathway for bulk CSF flow, ensuring the subdural region remains without separation under normal conditions.^[24] Indirect interactions between the subdural interface and CSF occur primarily through the absorption mechanisms at arachnoid granulations, which project from the arachnoid into the dural venous sinuses bordering the subdural compartment. These granulations facilitate the bulk reabsorption of CSF from the subarachnoid space directly into the venous circulation, bypassing the subdural interface while occurring in close anatomical proximity to it.^[25] This process supports overall CSF homeostasis without permitting fluid crossover into the subdural region.^[26] Physiological exchanges across the arachnoid barrier are limited to minimal diffusion of small solutes, such as ions and low-molecular-weight proteins, due to the impermeability conferred by tight junctions; no bulk flow of CSF into the subdural interface takes place normally.^[27] In the normal state, intracranial pressure is equilibrated across the meningeal interface due to tight adherence, preventing any pressure gradient or fluid ingress.^[28]

Clinical significance

Associated pathologies

The subdural space is susceptible to various pathologies characterized by abnormal accumulation of blood, fluid, or pus, primarily due to its potential space between the dura and arachnoid mater, which can be disrupted by trauma or other insults.^[4] The most common condition is subdural hematoma (SDH), resulting from the tearing of bridging veins that traverse this space, leading to bleeding that accumulates and exerts mass effect on the brain.^[19] Acute SDH typically develops within hours to days following high-impact trauma, involving rapid arterial or venous hemorrhage that causes significant neurological compromise.^[4] In contrast, chronic SDH evolves over weeks to months after minor or even subclinical trauma, often in vulnerable populations such as the elderly with brain atrophy, alcoholics, or those on anticoagulation therapy, where rupture of fragile bridging veins initiates a slow venous bleed.^[19] Pathophysiologically, chronic cases involve neomembrane formation around the hematoma, promoting inflammation, fibrinolysis, and angiogenesis, which can lead to rebleeding and encapsulation of the collection.^[29] Subdural hygroma involves the accumulation of cerebrospinal fluid (CSF)-like fluid in the subdural space, often following head trauma or neurosurgical procedures, and is thought to arise from a tear in the arachnoid membrane allowing CSF leakage into the potential space.^[30] This mechanism may operate via a ball-valve effect, where the arachnoid rent permits unidirectional flow, leading to gradual expansion that is typically benign but can mimic SDH on imaging and occasionally progress to symptomatic mass effect.^[31] Risk factors include traumatic brain injury, with osmotic gradients potentially drawing additional fluid into the collection.^[32] Subdural empyema represents an infectious pathology, featuring a purulent collection in the subdural space derived from contiguous spread of bacteria, such as Streptococcus or Staphylococcus aureus, often originating from sinusitis, otitis, or mastoiditis.^[33] Hematogenous dissemination or direct extension from cranial infections can also seed the space, triggering an inflammatory response that forms an abscess-like collection between the dura and arachnoid, potentially leading to rapid neurological deterioration.^[34] Other notable conditions include spontaneous SDH, which can occur without trauma in patients with coagulopathies, such as those associated with malignancy or acquired hemostatic disorders, where vascular fragility or bleeding diatheses precipitate hemorrhage into the subdural space.^[19] In neonates, SDH frequently results from birth trauma, with subdural hemorrhage observed in over one-third of normal deliveries due to shearing forces on bridging veins during passage through the birth canal, though it is often asymptomatic and resolves spontaneously.^[35] Spinal subdural hematoma or abscess, though rarer, arises from similar mechanisms of venous rupture or infectious spread in the spinal subdural space, causing radiculopathy or cord compression via accumulation of blood or pus.^[36] Across these pathologies, the core mechanism often involves disruption of the delicate bridging veins or membranes bordering the subdural space, exacerbated by underlying vulnerabilities like atrophy or infection.^[4]

Diagnosis and management

Diagnosis of abnormalities in the subdural space, such as subdural hematomas (SDH), typically begins with clinical evaluation. Patients often present with symptoms including headache, altered level of consciousness, confusion, nausea, vomiting, and focal neurological deficits like hemiparesis or aphasia, depending on the hematoma's size and location.^[4]^[37] In severe cases, significant mass effect can cause midline shift, a radiological marker of intracranial pressure elevation where the brain structures deviate from the midline by more than 5 mm, correlating with poorer outcomes and urgency for intervention.^[4]^[38] For neonates or infants, clinical signs may include irritability, bulging fontanelle, or seizures, prompting earlier suspicion.^[39] Imaging is essential for confirmation and characterization. Non-contrast computed tomography (CT) scan serves as the first-line diagnostic tool due to its availability and speed, revealing hyperdense collections in acute SDH (within hours to days), isodense in subacute (days to weeks), and hypodense in chronic SDH (beyond 3 weeks).^[40]^[39] Magnetic resonance imaging (MRI) provides superior soft tissue detail, using T1- and T2-weighted sequences to delineate membranes, septations, and chronic stages where collections appear hyperintense on T1 due to methemoglobin.^[41]^[42] Ultrasound is particularly useful in neonates for detecting subdural collections through the open fontanelle, appearing as echogenic or hypoechoic areas.^[39] Midline shift and hematoma thickness are measured on imaging to assess severity, with shifts greater than 5 mm often indicating surgical need.^[43] Management strategies vary by the type and severity of the subdural collection. Conservative approaches are suitable for small, asymptomatic collections (thickness less than 10 mm) or those without significant midline shift, involving observation, reversal of coagulopathy with agents like vitamin K or prothrombin complex concentrate, and serial imaging.^[44]^[43] Surgical intervention is indicated for symptomatic or large acute/chronic SDH, typically starting with burr hole evacuation under local anesthesia for liquefied chronic collections, achieving drainage through one or two 14-mm holes placed over the maximum thickness.^[45]^[46] For acute SDH with solid clots, thick membranes, or failure of burr hole drainage, craniotomy or decompressive craniectomy is preferred to allow thorough evacuation and hemostasis.^[47] In cases of subdural empyema, a purulent infection in the space, prompt surgical drainage via burr holes or craniotomy is combined with broad-spectrum intravenous antibiotics (e.g., vancomycin plus a third-generation cephalosporin and metronidazole) for 3-6 weeks, guided by culture results.^[48]^[49] Prognosis depends on factors such as hematoma thickness (symptomatic if >10 mm), patient age (worse in elderly), comorbidities like anticoagulation use, and midline shift extent.^[44]^[38] Recurrence rates after surgery range from 10-20%, higher in bilateral or septated hematomas, often necessitating reoperation within 3-6 months.^[50]^[51] One-year mortality is approximately 14-15%, influenced by neurological status at presentation.^[52] Emerging techniques aim to reduce recurrence and invasiveness. Middle meningeal artery embolization (MMAE), an endovascular procedure targeting vascular sources in the dura, is increasingly used as an adjunct to surgery or standalone for chronic SDH, with randomized trials in 2024 showing reduced reoperation rates (from 20% to under 10%) and promising safety.^[53]^[54] Neuroendoscopy-assisted evacuation, introduced in recent studies, enhances visualization of septations during burr hole procedures, improving complete removal and lowering recurrence to around 5-10% in select cases as of 2025.^[55]^[56] These minimally invasive options are particularly beneficial for high-risk patients, though long-term data are still accumulating.^[57]

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