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Spinal canal

The spinal canal, also known as the vertebral canal, is a continuous bony cavity formed by the stacked vertebral foramina of the , extending from the at the to the sacral at the lower end of the . This tubular structure serves as a protective enclosure for the , its , , and associated nerve roots, facilitating the safe transmission of neural signals between the and the rest of the body. Structurally, the spinal canal is delineated by the posterior aspects of the vertebral bodies anteriorly, the pedicles and laminae of the vertebral arches laterally and posteriorly, and the ligamentum flavum connecting adjacent laminae. Its cross-sectional diameter varies regionally, measuring approximately 17 mm in the cervical spine, narrowing to about 15 mm at the mid-thoracic level (the smallest dimension), and widening again to around 17.5 mm in the region, which accommodates the broader vertebral bodies and the . The itself, a cylindrical extension of the , occupies the upper two-thirds of this canal in adults, typically terminating at the between the first and second , beyond which the canal contains the bundle of lumbosacral nerve roots known as the . Enclosed within three protective layers—the , , and —the and its contents are further cushioned by , which circulates through the subarachnoid space. The spinal canal's design enables the emergence of 31 pairs of spinal nerves through intervertebral foramina, comprising eight , twelve thoracic, five , five sacral, and one coccygeal pair, which distribute sensory and motor innervation to the body's periphery. This anatomical arrangement not only shields the delicate neural elements from trauma but also supports the vertebral column's role in posture and movement, with deviations such as or herniated discs potentially compressing the canal's contents and leading to neurological deficits.

Anatomy

Gross anatomy

The spinal canal, also known as the vertebral canal, is the bony cavity within the vertebral column formed by the superposition of the vertebral foramina, extending continuously from the foramen magnum at the base of the skull to the sacral hiatus. This structure provides a protective conduit for the spinal cord along its length. The anterior boundary of the spinal canal is defined by the posterior surfaces of the vertebral bodies and intervertebral discs, reinforced by the posterior longitudinal ligament that spans the posterior aspects of these bodies. Posteriorly, the boundary is formed by the vertebral laminae and the ligamenta flava, which are elastic ligaments connecting the laminae of adjacent vertebrae. Laterally, the pedicles of the vertebrae enclose the canal, with the intervertebral foramina providing outlets for spinal nerves. These bony and ligamentous elements collectively create a tubular enclosure that maintains structural integrity throughout the column. In adults, the spinal canal measures approximately 57 cm in length on average, accommodating the , which terminates around the L1-L2 level. The anteroposterior diameter varies regionally, averaging 15-25 mm, with narrower dimensions in the mid-cervical (around 15-17 mm at ) and upper thoracic regions, and wider in the and sacral areas. The represents the outermost compartment within the spinal canal, lying between the and the surrounding bony and ligamentous walls.

Regional variations

The spinal canal exhibits distinct regional variations in dimensions and shape to accommodate the differing demands of neural structures and spinal across its length. In the region, the canal is the widest, with an average anteroposterior (AP) diameter of approximately 17-20 mm in the upper segments (C1-C3), narrowing slightly to 14-17 mm in the lower levels, reflecting the enlargement of the that supports innervation via the . The shape here is typically triangular or , providing ample space for the larger cord of up to 13 mm. In contrast, the thoracic region features the narrowest canal, with AP diameters ranging from 13-18 , smallest at mid-thoracic levels like T4 (around 15 ) and slightly wider at T12 (up to 18 ), maintaining a relatively uniform circular or oval cross-section to support postural stability and articulation. This narrower configuration aligns with the smaller thoracic diameter of about 6-10 and the absence of major enlargements. The lumbar region shows progressive widening, with AP diameters averaging 15-25 mm and transverse diameters of 26-30 mm, adopting a triangular in the lower segments to house the nerve . At L5, the canal reaches up to 17.5 mm , facilitating the increased neural volume post-spinal cord termination. In the sacral region, the canal tapers gradually, maintaining an AP diameter of about 17 mm at S1 before narrowing to fuse into the sacral canal, which ends at the sacral hiatus and contains the terminal filum and sacral nerve . The remains triangular, adapting to the fused sacral vertebrae. These variations are influenced by vertebral , such as the size and orientation of the vertebral foramina, which determine the canal's baseline dimensions; spinal curvatures like cervical and thoracic , which modulate space availability; and age-related changes, including formation and ligamentous that can progressively narrow the canal, particularly in narrower thoracic segments, elevating risk.

Contents

Meninges and spaces

The spinal comprise three distinct layers that envelop the , providing protection and compartmentalization within the spinal canal: the , , and . These layers are continuous with the cranial at the and extend inferiorly to enclose the and its nerve roots. The outermost layer, the , is a robust, fibrous primarily composed of dense fibers, offering tensile strength and mechanical protection to the underlying structures. In the spinal region, it functions as the sole meningeal layer, as the periosteal component of the dura ends at the , and it continues distally to form the around spinal nerves. Its thickness gradually decreases from superior to inferior, becoming thinner toward the coccygeal region. Lying internal to the is the , a thin, avascular, and translucent membrane consisting of flattened fibrocytes connected by delicate strands, which imparts a web-like appearance. It adheres closely to the due to pressure and lacks blood vessels, relying on for exchange. The innermost pia mater is a delicate, vascularized layer of flattened fibrocytes and collagen bundles that closely invests the , conforming to its irregular surface and penetrating its fissures. It gives rise to lateral extensions known as the , which anchor the to the at intervals along its length. Inferiorly, the continues as the . Between the and lies the subarachnoid space, a fluid-filled compartment spanned by fine arachnoid trabeculae that provide structural support and prevent excessive separation of the meningeal layers. These trabeculae, resembling a spiderweb, connect the arachnoid to the pia and facilitate the containment of within this space. External to the is the , a potential interval between the dural sac and the lining the vertebral canal, containing , , , and lymphatics. This space varies in volume with age and body habitus and holds clinical relevance for due to its accessibility for needle insertion. A narrow exists as a potential cleft between the and , which is normally collapsed and without contents under physiological conditions. The dural sac terminates at the level of the second sacral vertebra (S2) in adults, below the conus medullaris of the spinal cord. The filum terminale, originating from the pia mater, extends through the caudal end of the dural sac as the filum terminale externum (coccygeal ligament) to anchor at the dorsum of the coccyx, stabilizing the spinal cord's position.

Cerebrospinal fluid and vasculature

The (CSF) fills the subarachnoid space within the spinal canal, providing a buoyant medium for the enclosed neural structures. This clear, colorless fluid is primarily composed of (approximately 99%), along with electrolytes such as , and magnesium at higher concentrations than in , and lower levels of , calcium, and proteins (typically 15-45 mg/dL). Glucose levels in CSF range from 50-80 mg/dL, and cell counts are normally 0-5 cells/mm³, reflecting its role as an ultrafiltrate of produced mainly by the . In adults, the total CSF volume is approximately 150 mL, with about 30-70 mL distributed within the spinal subarachnoid space and the remainder in the cranial ventricles and cisterns. CSF dynamics involve continuous production at a rate of around 500 mL per day, circulation downward through the and into the spinal subarachnoid space via the foramina of Magendie and Luschka, and eventual reabsorption primarily through arachnoid granulations into the , supplemented by drainage via dural lymphatic vessels to . Normal CSF pressure, measured during in the lateral decubitus position, ranges from 7 to 18 cm H₂O, maintaining along the neuroaxis. The vascular elements within the spinal canal include arterial supply to the and associated structures, primarily via the and paired posterior spinal arteries. The single arises from the union of branches from the vertebral arteries and courses along the anterior median fissure, supplying the anterior two-thirds of the cord. The two posterior spinal arteries originate from the posterior inferior cerebellar arteries (or directly from the vertebral arteries) and descend along the posterolateral sulci, perfusing the posterior one-third of the cord. These longitudinal arteries receive segmental reinforcement from radicular arteries, which enter at each spinal level via the intervertebral foramina from adjacent spinal arteries; among these, the radiculomedullary arteries serve as critical feeders, with 8-10 such vessels typically contributing significantly to the anterior and posterior systems. A key radiculomedullary artery is the , which arises from the (usually on the left) between T9 and L2 levels—most commonly T9-T12—and provides the dominant blood supply to the lower thoracic, , and sacral segments of the . Venous drainage occurs through an extensive, valveless network of anterior and posterior spinal veins that converge into the internal vertebral venous plexus within the , which interconnects longitudinally and drains externally via basivertebral veins into segmental veins such as the azygos system in the thoracic region. This plexus facilitates collateral flow and eventual systemic return.

Development

Embryological formation

The embryological formation of the spinal canal begins during the third and fourth weeks of , when the induces the overlying to thicken into the , which subsequently folds and fuses to form the through primary . This process starts cranially around day 22 and progresses caudally in a zipper-like manner, completing by the end of week 4, with the serving as the precursor to the , including the . Concurrently, paraxial segments into somites along the , with the ventral portions differentiating into sclerotomes that migrate around the to form the precursors of the vertebrae. As development proceeds, the lumen of the , known as the , runs the length of the future and becomes continuous with the broader spinal canal space. The sclerotome cells proliferate and cluster into loosely packed caudal halves and densely packed cranial halves, giving rise to the vertebral bodies and neural arches that enclose the dorsally by around week 8, thus delineating the bony spinal canal. The remnants contribute to the nucleus pulposus of intervertebral discs, while sclerotomal cells form the annulus fibrosus, further supporting the structural integrity around the canal. The , including the , develop from contributions of cells and by week 8, enveloping the and establishing the protective subarachnoid space within the spinal canal. Key milestones include the formation of the by week 6, allowing continuity between the cranial and spinal regions, and the progressive leading to the sacral canal during the fetal period. By weeks 8 to 10, the achieves its definitive segmental form within the maturing canal, with spinal nerves emerging through intervertebral foramina. Disruptions in these processes can lead to congenital anomalies such as , though normal development ensures the canal's enclosure of the and .

Congenital anomalies

Congenital anomalies of the spinal canal encompass structural birth defects that arise from disruptions during early embryonic development, particularly affecting the closure and formation of the and surrounding vertebral structures. These conditions can lead to incomplete enclosure of the , abnormal attachments, or herniations that compromise the canal's integrity and function. While many are detectable prenatally through imaging, their severity varies, influencing neurological outcomes from infancy onward. Spina bifida represents a primary congenital characterized by the failure of the neural arch to close completely during fetal development, resulting in defects in the and potential exposure or malformation of the and . It is classified into several types based on severity: occulta, the mildest form, involves a small gap in the vertebral arch without protrusion or neurological involvement, often asymptomatic and discovered incidentally; meningocele features a sac of filled with protruding through the defect but without neural tissue involvement; and myelomeningocele, the most severe and open form, includes both and tissue in the protruding sac, leading to significant nerve damage, , and . Recent global estimates (as of 2024) indicate a of approximately 0.3-0.5 per 1,000 live births, with declines attributed to folic acid supplementation and programs, though rates can reach 1 to 2 per 1,000 in regions with higher among women of reproductive age, underscoring the role of periconceptional folic acid supplementation in prevention. Tethered cord syndrome occurs due to an abnormal attachment of the , typically involving a thickened or shortened —the fibrous extension anchoring the cord to the —which restricts normal upward movement of the during growth, resulting in a low-lying conus position below the L1-L2 vertebral level. This congenital condition, often associated with spinal dysraphism, can cause progressive neurological deficits such as leg weakness, bladder dysfunction, and sensory loss as the child grows, due to mechanical stretching of the cord. It frequently coexists with other anomalies like , with diagnosis relying on to visualize the low conus and filum abnormalities. Chiari malformation involves the herniation of cerebellar tissue through the into the upper spinal canal, disrupting the normal flow of and potentially compressing the or . It is categorized into types based on the extent of herniation and associated features: Type I, the most common, features downward displacement of the cerebellar tonsils without brainstem involvement, often presenting in or adulthood with headaches and ; Type II, typically linked to myelomeningocele, includes herniation of both the cerebellar vermis and , leading to more severe and syrinx formation in infancy; and Type III, a rare and severe variant, entails complete or partial herniation of the through a posterior skull defect, resulting in encephaloceles and significant neurological impairment. These malformations arise from underdevelopment of the and posterior fossa, with Type I prevalence estimated at 0.5-1% in the general population based on studies.

Function

Protective mechanisms

The spinal canal serves as a primary protective for the , formed by the , which consists of stacked vertebrae creating a bony tunnel that shields neural elements from external . This bony structure absorbs and distributes mechanical forces across the vertebral bodies and arches, preventing direct impact on the during everyday movements or minor injuries. The intervertebral discs, positioned between vertebrae, further enhance this protection by acting as shock absorbers, with their gel-like nuclei distributing compressive loads and maintaining spacing within the canal. The meninges provide an additional layer of mechanical safeguarding, with the dura mater and arachnoid mater forming tough, fibrous coverings that offer tensile strength to resist deformation and tearing under traumatic forces. The dura mater, the outermost meningeal layer, exhibits high longitudinal stiffness and tensile properties, enabling it to withstand stretching and compression that could otherwise transmit harmful stresses to the underlying spinal cord. Similarly, the arachnoid mater contributes to this barrier function, helping to compartmentalize pressure and limit the propagation of injury forces within the spinal canal. Cerebrospinal fluid (CSF) within the subarachnoid space acts as a dynamic , providing buoyant support that reduces the effective weight of the by approximately 95% and dampens vibrational forces from impacts. This fluid-filled cushioning minimizes direct contact between the and surrounding bony or meningeal structures, distributing mechanical stresses evenly and protecting neural tissue from concussive damage. The CSF's viscoelastic properties further aid in dissipating energy during rapid movements, maintaining neural integrity. Ligamentous structures enhance overall stability to prevent excessive motion that could compromise the spinal canal's protective environment, with the playing a key role in limiting vertebral separation and buckling. These elastic ligaments, composed largely of , connect adjacent laminae and resist hyperflexion or extension, thereby preserving the canal's dimensions and avoiding compression of the . Other ligaments, such as the extending from the , anchor the laterally, providing tensile support to counteract displacement forces during spinal motion.

Physiological support

The spinal canal supports spinal cord homeostasis through the circulation of cerebrospinal fluid (CSF) within the subarachnoid space, which bathes the neural tissue and contributes to nutrient delivery and waste removal, supplementing the primary vascular supply. Glucose and oxygen are transported to the mainly through vessels, with facilitating additional exchange via driven by arterial pulsations and respiratory movements that propel caudally and cranially along the canal. This dynamic circulation also facilitates waste removal, as metabolic byproducts and proteins are cleared through bulk flow and the glymphatic pathway, where enters perivascular spaces to mix with interstitial fluid and promote solute efflux, particularly during when glymphatic efficiency peaks. These processes collectively prevent accumulation of neurotoxic substances, sustaining neuronal function throughout the . Epidural fat, distributed along the extradural space of the spinal canal, contributes to physiological stability by providing mechanical buffering and insulation. This cushions the dural sac against compressive forces and facilitates its smooth gliding over the vertebral during flexion, extension, and rotation, thereby minimizing on the . Vascular integrity within the spinal canal is upheld by the blood-spinal cord barrier (BSCB), a selective endothelial interface analogous to the blood-brain barrier, which regulates solute exchange to protect neural while permitting essential nutrient ingress. Autoregulation of anterior and posterior spinal artery flow maintains consistent to the cord, adjusting in response to systemic variations between 60 and 150 mmHg to avert ischemia or hyperemia. The lumbar cistern, a dilated segment of the spinal canal from L1 to S2 devoid of the , ensures CSF pressure equilibrium by accommodating fluid volume changes and serving as the primary site for pressure monitoring through . This procedure measures opening pressure (typically 70-180 mm H₂O in lateral recumbency) to assess overall CSF dynamics, reflecting the canal's role in balancing intracranial and intraspinal .

Clinical significance

Common disorders

The spinal canal is susceptible to several common disorders that can compromise its structural integrity and neural contents, leading to significant neurological impairment. Among these, represents a prevalent condition characterized by the narrowing of the spinal canal, which can be congenital or, more commonly, acquired through degenerative processes such as . This narrowing exerts pressure on the or nerve roots, resulting in symptoms like , cramping, or weakness in the legs exacerbated by walking and relieved by rest—and, in severe cases, manifesting as disturbances, , or upper extremity weakness. Degenerative affects approximately 8-11% of individuals over 60 years old, with involvement being most frequent due to age-related disc degeneration and . Trauma to the spinal canal often arises from fractures or dislocations of the vertebrae, which directly compress the canal and may cause (SCI). High-energy impacts, such as those from accidents or falls, account for a substantial portion of cases, with and thoracolumbar regions particularly vulnerable due to their biomechanical alignment and the canal's narrower dimensions in these areas. Resulting SCI is classified using the American Spinal Injury Association () Impairment Scale, which grades severity from A (complete injury with no sensory or motor function below the level) to E (normal function), guiding prognosis and management. Globally, traumatic SCI incidence ranges from 8 to 55 cases per million population annually, with long-term complications including and autonomic dysfunction. Tumors within or adjacent to the spinal canal constitute another major category, broadly divided into intradural (within the dura mater) and extradural (outside the dura) types. Intradural tumors, such as meningiomas and schwannomas, are typically benign and slow-growing, originating from arachnoid cells or nerve sheaths, respectively, and often present with radicular pain or sensory deficits due to root compression. Extradural tumors, including metastases from primary cancers like breast or lung, are more aggressive and account for about 70% of spinal tumors in adults, frequently causing cord compression with symptoms of back pain, weakness, and bowel/bladder dysfunction. Overall, spinal tumors represent roughly 10-15% of central nervous system neoplasms, with extradural metastases being the most common subtype in oncology patients. Infections affecting the spinal canal, such as epidural abscess and , pose acute risks through inflammatory compression or direct tissue invasion. Epidural abscesses, often bacterial (e.g., ), form pus collections in the and can rapidly progress to cord compression, presenting with fever, severe , and neurological deficits like if untreated. Discitis involves of the , frequently secondary to hematogenous spread, and may extend to involve the canal via . Risk factors include diabetes mellitus, intravenous drug use, and , with incidence rates estimated at 2-5 cases per 10,000 hospital admissions for spinal infections. Early intervention is critical to prevent permanent deficits, as delays can lead to high morbidity.

Diagnostic approaches

Diagnostic approaches to spinal canal abnormalities rely on a combination of imaging modalities, endoscopic techniques, electrophysiological testing, and standardized clinical scales to identify structural and functional impairments. These methods help detect conditions such as or compression that may affect the , nerve roots, or dynamics. plays a central role in evaluation, with (MRI) established as the gold standard for assessing soft tissues, including the and surrounding . T1-weighted sequences provide anatomical detail of the cord and vertebral structures, while T2-weighted sequences highlight (CSF) as hyperintense, allowing visualization of through reduced CSF space or altered flow patterns. Computed (CT) excels in delineating bony details, such as osteophytes, facet , or fractures that narrow the canal, offering superior resolution for calcified or osseous abnormalities compared to MRI. When MRI is contraindicated, such as in patients with pacemakers, CT involves intrathecal contrast injection to enhance visualization of the , nerve roots, and canal patency, providing dynamic insights into compressions. Endoscopy of the spinal canal, or epiduroscopy, offers direct optical access to the via a flexible fiberoptic inserted through a caudal or interlaminar approach, enabling real-time identification of adhesions, inflammation, or scar tissue in cases of chronic back pain. Electrophysiological assessments, particularly somatosensory evoked potentials (SSEPs), evaluate integrity by stimulating peripheral nerves and recording cortical responses, with prolonged latencies indicating conduction deficits due to or ischemia. Clinical grading scales, such as the Nurick , quantify severity on a 0-5 scale based on disturbance and status, where 0 denotes no cord involvement and 5 indicates inability to walk, aiding in and decisions.

History

Early descriptions

The earliest known references to the spinal canal appear in medical texts, particularly in the context of and vertebral injuries. (c. 460–377 BCE), often regarded as the father of , provided the first descriptions of the vertebral canal in discussions of spinal fractures and dislocations, noting how such injuries could lead to neurological deficits due to compression within the bony enclosure. He emphasized the canal's role in housing the spinal marrow, linking traumatic deformities like to disruptions in this structure, as detailed in his work On Articulations. Building on Hippocratic ideas, the Roman physician (c. 129–216 CE) advanced anatomical understanding through animal dissections, as human cadaver study was limited. In his extensive writings on anatomy, Galen described the spinal canal as a protective bony tube containing the dural sac, which he identified as the outermost meningeal layer encasing the . He detailed the canal's formation by successive vertebral arches and noted the dura mater's role in safeguarding the neural contents, contributing to early concepts of spinal protection despite inaccuracies from non-human models. During the , renewed interest in direct human dissection led to more precise observations. In 1542, French physician Jean Fernel provided one of the first explicit anatomical descriptions of the spinal canal in his Universa medicina, highlighting its role as a continuous enclosure for the and its membranes. This marked a shift toward systematic physiological terminology. Shortly thereafter, (1514–1564) offered groundbreaking visual and descriptive insights in his seminal 1543 work De humani corporis fabrica. Through meticulous human dissections, Vesalius illustrated the spinal canal's boundaries, depicting the vertebral foramina forming a protective archway and detailing access methods like transverse sectioning through intervertebral discs to reveal the dural tube and . His woodcut plates provided the first accurate representations of the canal's segmental structure, correcting Galenic errors and establishing a foundational model for modern spinal .

Modern advancements

In the early 19th century, François Magendie advanced understanding of the spinal canal's meningeal spaces through his studies on (CSF) circulation, demonstrating in 1825 that CSF is secreted by the choroid plexuses and flows through the foramen of Magendie into the spinal subarachnoid space, clarifying the fluid dynamics within the canal's protective layers. Concurrently, the Bell-Magendie law, established in the 1820s by and Magendie, delineated the functional separation of roots—dorsal roots for sensory input and ventral roots for motor output—providing foundational insights into the neural interfaces bordering the spinal canal, though initial credit disputes arose due to Bell's prior observations. By the mid-19th century, Rudolf Virchow's cellular framework linked degenerative processes to spinal canal narrowing, describing in the 1850s how protrusions and ligamentous contribute to by compressing the canal's contents, marking a shift toward histopathological explanations of canal-related disorders. The brought diagnostic innovations, with Jean Sicard inventing in 1921 by injecting iodized oil into the subarachnoid space to visualize spinal canal obstructions via , enabling precise localization of tumors and herniations that previously required invasive exploration. This technique dominated until the 1970s, when (MRI) emerged, with and Peter Mansfield's developments producing the first clinical spinal images by the late 1970s, revolutionizing non-invasive assessment of canal anatomy, soft tissue , and neural compression without radiation or contrast risks. Surgical progress accelerated in the 1990s with endoscopic techniques, pioneered by figures like Parvis Kambin, who defined a "safe zone" for transforaminal access in 1990, allowing minimally invasive decompression of the spinal canal for herniated discs and stenosis via small incisions and real-time visualization, reducing recovery times and complication rates compared to open laminectomy. Into the 21st century, genetic research uncovered links between folate metabolism disruptions and congenital spinal canal anomalies, such as neural tube defects including spina bifida; studies in the 2000s identified variants in genes like MTHFR that impair folate processing, elevating risks by altering neural closure during embryogenesis and emphasizing periconceptional supplementation for prevention.

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