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Filum terminale

The filum terminale is a slender, fibrous filament of connective tissue that extends inferiorly from the apex of the conus medullaris—the tapered, terminal end of the spinal cord located at the level of the L1-L2 vertebrae—to the periosteum of the coccyx, serving as a non-neural extension that anchors the spinal cord within the vertebral canal.^[1]^[2]^[3] Approximately 20 cm in length, it consists primarily of fibrous tissue derived from the pia mater, lacking functional nervous elements, and is enveloped by the spinal meninges along its course.^[1]^[3] Anatomically, the filum terminale is divided into two segments: the filum terminale internum, which measures about 15 cm and lies within the lumbar cistern surrounded by cerebrospinal fluid and the cauda equina nerve roots up to the level of the S2 vertebra, and the filum terminale externum, the shorter distal portion that pierces the dura mater and arachnoid mater, fuses with the periosteum of the coccyx via the coccygeal ligament, and contains all three meningeal layers.^[1]^[2] This structure emerges from the conus medullaris, typically positioned at the L1-L2 intervertebral disc space in adults, and maintains a central position within the thecal sac, occasionally appearing fatty on imaging in up to 19% of individuals without symptoms.^[2]^[3] The primary function of the filum terminale is to provide caudal anchorage for the spinal cord and meninges, thereby stabilizing the structure against excessive cephalad or lateral displacement during body movements and transmitting tensile forces to prevent upward migration of the conus medullaris.^[1]^[3] In clinical contexts, abnormalities such as a thickened (>2 mm), low-lying, or lipomatous filum terminale can contribute to tethered cord syndrome, a condition where abnormal tension on the spinal cord leads to neurological deficits including lower extremity weakness, sensory disturbances, bladder and bowel dysfunction, and orthopedic deformities like scoliosis, often requiring surgical sectioning for relief.^[2]^[3] Radiographically, it is visible on MRI as a thin, T2-hypointense line within the thecal sac, with variants like fatty infiltration being incidental in most cases but diagnostic markers in tethered cord pathology.^[2]

Anatomy

Gross anatomy

The filum terminale is a slender fibrous filament that extends caudally from the apex of the conus medullaris, typically located at the L1-L2 vertebral level, to the dorsal surface of the coccyx.^[4] It measures approximately 15-20 cm in length and serves as a non-neural connective tissue extension beyond the termination of the spinal cord.^[5] The conus medullaris ends at the L1 or L2 vertebral level in adults, with the filum terminale continuing inferiorly through the vertebral canal.^[6] The structure is divided into two main portions: the filum terminale internum and the filum terminale externum. The internum is the intradural segment, approximately 15 cm long, extending from the conus medullaris to the S2 vertebral level, and is covered by extensions of the pia mater.^[4] The externum is the shorter extradural segment, about 5 cm in length, which pierces the dura mater at the S2 level and blends with the periosteum of the coccyx.^[4] Positioned centrally within the lumbar cistern, the filum terminale is surrounded by cerebrospinal fluid (CSF) and the nerve roots of the cauda equina.^[4] It has a typical diameter of 1-2 mm, tapering distally from proximal measurements of about 1.7 mm to 1.1 mm or less.^[4] Within its structure, small nerve filaments may be present as remnants or connections to coccygeal nerves (typically 2-3), observed in some specimens as gross attachments containing S100-positive nerve fibers.^[6]

Histology

The filum terminale consists primarily of dense connective tissue. The bulk of its structure is formed by longitudinally oriented bundles of type I collagen fibers measuring 5 to 20 μm in thickness and separated by 3 to 10 μm intervals.^[7] These collagen bundles are connected by a delicate meshwork of finer transversal type III collagen fibers (0.05 to 1.5 μm thick).^[7] Abundant elastic and elaunin fibers, also longitudinally oriented and interspersed among the collagen, contribute to its elastic properties.^[7] An internal core of looser connective tissue contains glial scars and occasional neuroglial cells, which stain positive for glial fibrillary acidic protein (GFAP), surrounded by a denser outer collagenous sheath. Residual neural elements include ependymal cells, sometimes lining patent central canal remnants or forming cysts, along with scattered unmyelinated axons in some specimens. In studies of surgical specimens from patients with tethered cord syndrome, ependymal cells were observed in 70.8% of cases, ependymal cysts in 3.1%, and elastic fibers in 3.1%.^[8] The filum terminale internum may exhibit more prominent glial remnants compared to the externum. In histological preparations, the collagen fibers stain blue under Masson's trichrome, highlighting the dense fibrous composition, while elastic fibers appear black with Verhoeff-van Gieson staining, revealing their even dispersion in normal tissue.^[7]

Relations

The filum terminale occupies a central position within the cauda equina, surrounded by the lumbosacral nerve roots in the lumbar cistern of the subarachnoid space.^[9] It lies in the midline, posterior to the anteriorly directed lumbosacral roots, facilitating its role as a stabilizing structure amid the mobile nerve bundle.^[10] This central placement allows the nerve roots to move freely around the filum during spinal motion, while it remains bathed in cerebrospinal fluid (CSF) within the subarachnoid space, which extends to approximately the S2 level.^[11] Superiorly, the filum terminale attaches to the apex of the conus medullaris through extensions of the pia mater, often referred to as the filum terminale internum or proximal segment.^[10] The central canal of the spinal cord, continuous with the fourth ventricle, extends into the proximal portion of the filum terminale for approximately 5-6 mm, forming the terminal ventricle (ventriculus terminalis), lined by ependymal cells.^[11] Inferiorly, the filum terminale externum anchors to the periosteum of the coccyx, thereby stabilizing the entire dural sac and preventing excessive upward displacement of the spinal cord during movement.^[11] In terms of proximity to adjacent nerves, the filum terminale is positioned superior to the coccygeal nerve (Co1), the smallest and most caudal root of the cauda equina, which emerges near the conus medullaris.^[11] Laterally, it relates to the sacral nerve roots (S1-S5), which course around it within the thecal sac, maintaining the filum's midline orientation throughout its descent.^[9]

Development

Embryonic origins

The filum terminale originates as a vestigial remnant of the caudal eminence, also known as the caudal cell mass, during the early stages of human embryonic development, specifically between weeks 4 and 8 of gestation.^[12] This structure forms from undifferentiated mesenchymal cells at the caudal end of the embryo, following primary neurulation and the closure of the neural tube by the end of week 4.^[13] The caudal cell mass contributes to the formation of the distal spinal cord, including the conus medullaris, cauda equina, and filum terminale precursors, through a process of secondary neurulation.^[14] The formation of the filum terminale involves regression and cavitation of the primitive neural tube's caudal end, where vacuoles and cysts develop within the caudal cell mass around day 30, fusing to create a tubular secondary neural tube that eventually regresses.^[15] This regression process results in the transformation of neural elements into glial and ependymal scar tissue, characterized by fibrous connective tissue interspersed with glial cells and ependymal cell nests.^[16] Sonic hedgehog (Shh) signaling plays a key role in patterning the caudal neural tube during this phase, promoting ventral identity and contributing to the dedifferentiation of caudal cells into non-neuronal fibrous tissue rather than functional neural structures.^[17] As development progresses, the ascension of the conus medullaris from its initial sacral position to the lumbar levels by birth, driven by differential growth between the spinal cord and vertebral column, stretches the caudal filament into the definitive filum terminale.^[18] This process establishes the precursors to the filum terminale internum and externum by around week 12, following the completion of caudal regression.^[19] The central canal of the neural tube persists in the proximal filum as a terminal ventricle, or ventriculus terminalis, lined by ependymal cells, which represents a remnant of the original lumen.^[20]

Variations and anomalies

The filum terminale exhibits common anatomical variations in its length, thickness, and attachment sites, which can influence its mechanical properties without necessarily causing pathology. In adults, the mean length is approximately 15.6 cm, with a reported range of 11.3 to 21.1 cm based on cadaveric measurements. Thickness typically measures between 0.4 and 2.5 mm at its initial segment, with a mean of 1.38 mm, and narrows to about 0.76 mm at the midpoint. Attachment sites also vary, with the filum most frequently originating from the mid-L1 vertebral level (19.5% of cases) and fusing to the coccyx at the upper S2 level (31.7% of cases), though origins below L2 or variable coccygeal fusions occur in up to 5% of individuals. These variations correlate with body height and weight, such that taller or heavier individuals tend to have longer and thicker fila.^[21]^[21]^[21]^[21]^[21] Anomalies of the filum terminale often arise from incomplete regression during caudal embryonic development and predispose to conditions like tethered cord syndrome. A short filum, typically less than 12 cm, or one thickened beyond 2 mm in diameter, restricts spinal cord mobility and increases traction risk. Bifid or duplicated fila, where the structure splits into two strands, represent rare developmental deviations, potentially complicating detethering if unrecognized. Absent or rudimentary fila occur in severe caudal dysgenesis, leading to unstable cord anchoring. Ectopic nerve roots or ganglion cells embedded within the filum, observed in surgical specimens, indicate persistent neural tissue from embryogenesis and may contribute to abnormal signaling.^[22]^[22]^[23]^[24]^[25] Lipomas of the filum terminale involve fatty infiltration that replaces normal fibrous tissue, a common cause accounting for 13-26% of lipoma-related cases of tethered cord syndrome associated with occult spinal dysraphism.^[26]^[22]^[27] These lipomas often extend along the filum, linking to broader dysraphic processes like spina bifida occulta. Minor variations, such as fatty infiltration without symptoms, affect 4-6% of individuals based on cadaveric and imaging studies, while clinically significant anomalies like thickened or lipomatous fila are relatively rare.^[28] Genetic factors contribute to filum anomalies through mutations disrupting caudal development; for instance, alterations in VANGL1 are implicated in neural tube defects that can affect filum formation.^[24] Magnetic resonance imaging (MRI) is the primary modality for detecting these variations and anomalies, revealing a thickened filum greater than 2 mm in diameter or a low-lying conus medullaris below the L1-L2 level as key indicators.^[29]^[30]

Function

Anchoring and stabilization

The filum terminale primarily functions to tether the conus medullaris to the coccyx, anchoring the distal spinal cord and preventing its upward displacement during body movements such as extension. This tethering is facilitated by the filum terminale externum, a fibrous extension that attaches the dural sac to the periosteum of the coccyx, maintaining the overall position of the spinal cord within the vertebral canal.^[31] By securing the conus medullaris, typically at the L1-L2 level in adults, the structure ensures stability against cephalad migration that could occur with postural shifts or gravitational forces.^[11] The intradural portion, known as the filum terminale internum, blends histologically with the dura mater at the caudal end of the dural sac, thereby stabilizing the thecal sac and distributing mechanical tension across the lumbosacral region. This fusion allows the filum to act as an extension of the meninges, sharing load and preventing localized stress concentrations at the conus-dura junction during spinal loading. The biomechanical properties of the filum terminale support this role, with the intradural segment exhibiting near-perfect elasticity and an exponential relationship between applied weight and strain, enabling it to deform under tension while protecting the more rigid conus medullaris from excessive traction.^[32] This anchoring contributes to posture maintenance by limiting excessive flexion and extension at the lumbosacral junction, as the elastic nature of the filum permits only slight controlled movement of the conus medullaris in response to these motions. The overall length of the filum terminale externum correlates positively with body height, ensuring proportional tension distribution that supports upright posture without undue strain on neural elements. In the lumbar cistern, the filum terminale is suspended within cerebrospinal fluid (CSF), allowing its controlled movement alongside the cauda equina nerves without causing compression of adjacent roots, thus preserving unobstructed CSF flow and neural gliding.^[33]

Stress buffering

The filum terminale possesses elastic properties derived from its content of elastin fibers, which contribute to elastic recoil and absorption of linear traction forces applied to the spinal cord. This elasticity allows the structure to deform and recover, thereby reducing the transmission of peak stress to the conus medullaris during movements that involve caudal displacement of the cord.^[8]^[32] In addition to static anchoring, the filum terminale functions as a viscoelastic band that buffers the distal spinal cord against axial loading, such as occurs during high-impact activities like jumping or traumatic events. Through viscoelastic damping, it dissipates energy and prevents excessive stretching of the cord, maintaining its integrity under dynamic forces.^[34]^[35] The biomechanical characteristics of the filum terminale enable significant deformation—up to 15% strain—without structural failure, as evidenced by stress measurements reaching 1.9-3.3 MPa under controlled loading. This compliance supports its role in load distribution without rupture.^[36]^[35] The filum terminale also contains stretch-sensitive and nociceptive nerve endings, which may contribute to sensory functions such as proprioception or pain signaling in response to mechanical stress.^[37] Age-related changes in the filum terminale include a progressive decrease in elasticity with aging, attributed to fibroadipose deposition and collagen alterations, which heighten susceptibility to mechanical injury and traction-related stress on the spinal cord.^[38]^[39]

Clinical significance

Associated disorders

The primary disorder associated with the filum terminale is tethered cord syndrome (TCS), a condition arising from excessive tension on the spinal cord due to an abnormally tight or inelastic filum terminale that anchors the conus medullaris below its normal level.^[22] This traction leads to progressive neurological symptoms, including bladder and bowel dysfunction, lower limb weakness, sensory deficits, gait abnormalities, scoliosis, and back pain.^[22]^[27] Filum lipoma, a fatty infiltration within the filum terminale, often coexists with TCS and is frequently linked to spina bifida occulta, contributing to cord tethering through mechanical restriction.^[40] When symptomatic, it causes progressive neurological deficits such as lumbosacral pain, leg weakness, sensory loss, and urinary or fecal incontinence, typically worsening with growth or physical activity.^[40] Post-traumatic filum scarring, resulting from adhesions formed after spinal injury or prior surgery (such as myelomeningocele repair), can mimic primary TCS by creating inelastic tethers that restrict cord mobility.^[41] This secondary tethering presents with neurological deterioration, including motor and sensory changes in the lower extremities, sphincter dysfunction, pain, and orthopedic deformities like foot anomalies or spasticity.^[41] The underlying pathophysiology of these filum terminale disorders involves chronic stretch-induced ischemia of the spinal cord due to impaired perfusion and oxidative stress from traction on the conus medullaris.^[22] This mechanical stress can also promote syringomyelia through cerebrospinal fluid flow obstruction and cavitation within the cord, as well as compression of lumbosacral nerve roots leading to radiculopathy.^[42]^[22] Epidemiologically, the incidence of spinal dysraphisms, often associated with TCS and related filum disorders, is approximately 0.5 to 1 per 1,000 live births, while TCS itself is estimated at 1 in 4,000 births, with a higher prevalence among those with neural tube defects such as myelomeningocele, where 10-30% of cases develop symptomatic tethering.^[43]^[44] These conditions show variable gender distribution across studies, with some reporting slight female predominance and others male.^[45]^[46]

Surgical and diagnostic considerations

Diagnosis of filum terminale-related issues, particularly in tethered cord syndrome (TCS), relies on multimodal approaches to assess anatomical and functional abnormalities. Magnetic resonance imaging (MRI) serves as the gold standard, revealing a low-lying conus medullaris below the L1-L2 level and a thickened filum terminale exceeding 2 mm in diameter, which are indicative of tethering.^[47] Urodynamic studies evaluate associated bladder dysfunction, detecting issues such as detrusor hyperreflexia or sphincter dyssynergia that may precede overt symptoms in TCS patients.^[48] Somatosensory evoked potentials (SSEPs) provide electrophysiological evidence of nerve tension, often showing prolonged central conduction times that improve post-intervention.^[48] Surgical management primarily involves microsurgical transection of the filum terminale to release tension in cases of tight filum terminale syndrome. This procedure yields symptom improvement in 40-75% of patients for various symptoms, with 73% improvement in urodynamic studies.^[49] Risks include cerebrospinal fluid (CSF) leak, occurring in about 5.9% of cases, alongside pseudomeningocele formation in 4.1%; these complications are not mitigated by extended postoperative bed rest durations of 24 to 72 hours.^[50] Intraoperative histopathology of the filum terminale in TCS surgeries frequently uncovers abnormal elements, such as ependymal cells in 70.8% of specimens and fatty infiltration in 41%, reflecting persistent embryonic tissue that contributes to tethering.^[8] These findings, including lipomatous changes, aid in confirming the pathological basis during dissection. Postoperative care emphasizes vigilant monitoring for retethering, which affects roughly 5.2% of patients within the first year, identifiable via serial MRI to detect unchanged conus position or persistent syringomyelia.^[51] Routine follow-up with imaging and clinical assessments at 3, 6, and 12 months helps manage recurrence risks. Recent advances include endoscopic untethering techniques, which minimize tissue trauma through biportal approaches and reduce recovery time compared to traditional open methods.^[52] As of 2025, novel approaches like one-stage tandem detethering for complex cases and untethering without dural opening in myelomeningocele patients have been reported.^[53]^[44] Multimodality intraoperative neuromonitoring, incorporating transcranial motor evoked potentials and triggered electromyography, enhances nerve root identification and preserves motor function, with no new deficits reported in monitored cases.^[54]

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