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Cauda equina syndrome

40 citationsUpdated Sep 2026

Overview

Cauda equina syndrome lacks a universally agreed definition, and its diagnostic subcategories demonstrate poor interobserver reliability [1, 2]. Consequently, these subcategories should no longer be used for decision-making, prognosis, research, or medicolegal purposes [2]. Clinical signs do not reliably correlate with MRI findings [1], so triage must rely on a synthesis of symptoms, signs, and bladder ultrasound results [2]. A post-void residual volume of ≥ 200 ml is considerably more accurate in predicting the condition than clinical assessment alone [6]. For patients under 55 years of age, a limited sequence lumbosacral MRI can safely diagnose the syndrome, though further research is needed to assess its safety and efficacy before existing protocols change [17].

MRI should be performed within one hour of suspicion of cauda equina syndrome [1]. When compression is confirmed, urgent surgical decompression of the spinal canal is the indicated treatment [1, 3]. Specific etiologies may require tailored approaches; for instance, acute syndrome following in situ arthrodesis is best treated by immediate decompression including resection of the posterosuperior rim of the sacrum and the adjacent disc, with consideration for posterior instrumentation and reduction [10]. Combined epiconus and cauda equina syndrome due to multilevel stenosis has been successfully treated with combined two-stage anterior and posterior decompression [11]. Surgeons must monitor for early symptoms to prevent compression from fat grafts, maintaining graft thickness between one-half and one centimeter to avoid this complication [9, 12].

Long-term follow-up reveals that autonomic and non-autonomic dysfunction is common, even in patients with the most optimistic prognosis [8]. Sexual issues persist at rates of 14% to 100% [5]. Early decompression did not show a statistically significant correlation with improved outcomes in long-term follow-up [8]. Internet information regarding the condition is of variable quality and largely set at an inappropriate readability level [7].

Anatomy & Pathophysiology

Spinal Cord and Cauda Equina

In most adults, the spinal cord terminates around L1-L2 [16]. The conus medullaris marks the caudal end of the spinal cord and is tethered to the coccyx by the filum terminale [16]. Peripheral nerves distal to the conus medullaris, generally from L2 to S5, form the cauda equina [16]. Compression at the conus level is called conus medullaris syndrome (CMS) [16]. The conus medullaris most typically lies between the levels of T11-L1 [16]. Female spinal cords are generally longer, terminating at L1-L2 in female patients versus T12-L1 in male patients [16]. CMS includes upper motor neuron symptoms, contrasting with CES’s lower motor symptoms [16]. The detrusor urinae muscle and internal bladder sphincter are governed by sacral nerve roots (S2-S4) and the hypogastric plexus (T11-L3) [16]. Dysfunction of a single nerve disrupts both sensory perception and muscle control, leading to urinary retention [16].

Osseous Anatomy

The bony anatomy of the spine consists of 7 cervical vertebrae, 12 thoracic vertebrae, 5 lumbar vertebrae, 5 fused sacral vertebrae, and 4 or 5 fused coccygeal vertebrae [64]. The spinal column is composed of 33 vertebrae comprising five distinct regions: the cervical, thoracic, lumbar, sacral vertebrae, and the coccyx [69]. The vertebral column comprises 33 vertebrae divided into five sections (7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4 coccygeal) [72]. The sacral and coccygeal vertebrae are fused, which typically allows for 24 mobile segments [72]. The vertebral body is connected by the pedicles to the posterior arch of the vertebra, which consists of the lamina and spinous process [64]. A typical vertebra comprises an anterior body and a posterior arch that enclose the vertebral canal [72]. Each vertebra is composed of an anterior portion (vertebral body) and a posterior arch formed by the pedicle, facet, lamina, and spinous process [69]. The vertebral body is composed of an inner region of cancellous bone surrounded by a thin shell of cortical bone [69]. The neural arch is composed of two pedicles laterally and two laminae posteriorly that are united to form the spinous process [72]. To either side of the arch of the vertebral body is a transverse process and superior and inferior articular processes [72]. The articular processes articulate with adjacent vertebrae to form synovial joints [72]. The relative orientation of the articular processes accounts for the degree of flexion, extension, or rotation possible in each segment of the vertebral column [72]. The spinous and transverse processes serve as levers for the numerous muscles attached to them [72]. The length of the vertebral column averages 72 cm in men and 7 to 10 cm less in women [72].

The spinal canal is created by the body anteriorly, lamina posteriorly, and pedicles laterally [64]. The vertebral canal extends throughout the length of the column and provides protection for the spinal cord, conus medullaris, and cauda equina [72]. The vertebral bodies function primarily to bear weight and transfer forces to the pelvis and hips [64]. The posterior elements provide protection to the neural structures and function as a tension band [64].

Intervertebral Disk

The intervertebral disk is composed of an inner nucleus pulposus (NP) and an outer ring termed the anulus fibrosus (AF) [69]. The NP serves as an osmotic pump to attract water and generate hydraulic pressure when subjected to significant loads [69]. The AF encapsulates the gelatinous NP and provides mechanical support to contain NP pressure and constrain intervertebral rotations [69]. The outer AF is integrated with the vertebral rim via a fibrocartilage enthesis that consists of a thin layer of calcified cartilage, or “tidemark” [69]. The end plate is a bilayer of cartilage and bone that separates the disk from adjacent vertebrae [69]. The cartilage end plate integrates with the inner AF to fully encapsulate the NP [69]. The IVD separates each successive vertebral body and provides a unique combination of compressive stiffness and flexibility to support normal spine biomechanics [69]. The end plate facilitates important but potentially conflicting biophysical functions: it must be strong and thick to resist significant loads but must also be permeable to favor chemical transport and disk cellular vitality [69].

Thoracic Spine Specifics

The thoracic spine has the most variable anatomy and represents two transitional zones [66]. The upper thoracic vertebrae share some similar features as cervical vertebrae, and the lower thoracic levels share some features with the lumbar vertebrae [66]. The outstanding characteristic of the thoracic spine is its rigidity [66]. In conjunction with the ribs and the sternum, the thoracic region essentially forms a bony “cube,” which is an inherently stable structure [66]. The vertebral bodies of the thoracic spine are larger than those of the cervical spine, but smaller than the lumbar vertebrae [66]. The pedicles of the thoracic spine arise more superiorly from the posterior vertebral body than in the cervical or lumbar spine and project more obliquely from superodorsal to inferoventral [66]. The pedicles of T1 and to a lesser degree T2 have a more medial trajectory [66]. Moving caudally, the remaining thoracic pedicles have significantly less medial angulation, projecting almost straight forward [66]. The upper thoracic pedicles (T1 and T2) have fairly generous cross-sectional area [66]. Moving caudally, the pedicles narrow in diameter until the midthoracic spine and then increase again toward the most caudal levels [66]. The posterior arch of thoracic vertebrae encloses the spinal canal, which is narrowest in this region of the spine [66].

The spinous processes of the upper four thoracic vertebrae project more horizontally, with only slight inferior angulation [66]. In the midthoracic spine, the spinous processes project sharply obliquely, overlapping the lamina and spinous processes inferiorly [66]. From T10 to T12, the spinous processes again transition to a more horizontal projection, consistent with lumbar vertebrae [66]. The laminae of the midthoracic spine overlap considerably [66]. The superior articular facets project cranially from the junction of the laminae and pedicles and are oriented coronally [66]. The inferior articular facets are essentially contiguous with the ventral aspect of the lamina [66]. The orientation of the thoracic facets permits only a small arc of motion [66]. The rib heads articulate with the lateral aspect of the vertebral bodies [66]. There is a shared articulation at the level of the disk space with the rib head articulating with the superolateral aspect of the vertebral body for which it is named and the inferior aspect of the level above [66]. The first, eleventh, and twelfth vertebral bodies have only a single articulation for the same-numbered rib head [66]. The transverse processes project obliquely superolaterally [66]. Along the ventral aspect of the transverse process is the costotransverse joint, the point at which the rib articulates with the same-numbered transverse process [66]. There is no costotransverse articulation at T11 or T12 [66]. The transverse processes of T11 and T12 are shorter and project more laterally than the levels above [66].

Alignment and Biomechanics

The alignment of the spine varies by region [68]. Normal cervical alignment is approximately 15° of lordosis [68]. The thoracic spine generally ranges from 20° to 40° of kyphosis [68]. The lumbar spine has approximately 40° to 50° of lordosis [68]. The sacrum is again kyphotic [68]. Kyphotic segments (thoracic, sacral) are considered “primary” curvatures as they are already present in utero and at birth [68]. The lordotic curvatures of the cervical and lumbar spine develop secondarily later in life to allow the growing child to develop an upright posture [68]. The center of gravity of the spinal column runs from the odontoid process proximally through the sacral promontory caudally [68]. Changes in sagittal balance that shift the center of gravity too far ventrally can result in significant pain and disability [68].

The basic motion segment of the spine consists of the “functional spinal unit” [68]. The functional spinal unit is comprised of two vertebrae, the disk between them, and the facet joints (and their capsules) [68]. The functional spinal unit serves to limit motion of the spine within the confines of protecting the neural structures contained therein [68]. Vertebral bodies are loaded in series; the more caudal levels must support more weight than more cranial segments [68]. The vertebral bodies bear 70% to 90% of the static axial load of the spine [68]. The facet joints support 10% to 20% of axial load in a standing, neutral alignment [68]. In extension, the facet joints may bear up to 30% of the axial load [68]. In flexion, the facet joints may be burdened with up to 50% of the anterior shear load [68]. The intervertebral disk helps absorb axial loads [68]. As compressive forces are applied to the disk, the nucleus pulposus deforms, redistributing axial forces radially [68]. This radial pressure is then resisted by the tensile properties of the alternating bands of fibers within the anulus fibrosus [68]. The spinous processes and transverse processes act as lever arms, providing mechanical advantage for the muscles that insert along their surfaces [68].

Muscular Stabilization

The spinal column is also stabilized by a set of paraspinal muscles that include the erector spinae, psoas, and multifidus [69]. The erector spinae runs longitudinally on the dorsal surface of the spinal column and functions to extend the spine [69]. The psoas runs longitudinally on the ventrolateral surface of the spinal column and serves to flex the hip (bilateral contraction) or laterally bend the trunk (unilateral contraction) [69]. The multifidus connects intersegmentally to stabilize the spine by acting like a bowstring to maintain lordosis [69].

Vascular Supply

The thoracic and lumbar levels are supplied by paired segmental arteries which originate directly from the aorta along its posterior surface [73]. Branches of the segmental arteries supply the vertebral body, the paraspinal musculature, and the spinal cord [73]. The cervical spine derives its circulation primarily from the vertebral arteries [73]. The vertebral arteries arise from the subclavian arteries on either side, coursing superiorly [73]. The vertebral arteries typically enter the transverse foramen at the C6 level and run proximally through the transverse foramina to C1 [73]. The vertebral arteries course posteriorly over the superior aspect of the C1 ring before turning proximally again and entering the foramen magnum [73]. In the foramen magnum, the vertebral arteries merge to form the basilar artery [73]. Segmental branches to each cervical vertebra arise from the vertebral artery and the deep cervical branch of the costocervical trunk [73]. Typically one side of the vertebral artery is more dominant, having a larger diameter than the other [73]. Occasionally, the vertebral artery enters through the transverse foramen of C7 rather than C6 [73]. It is not uncommon to see anomalous courses of the vertebral artery where the vessel loops through a cervical vertebral body before returning to its longitudinal course through the transverse foramen [73].

The vascular supply of the spinal cord is primarily from the medullary branches of the segmental spinal arteries [73]. These branches merge to feed the anterior spinal artery, which is responsible for supplying approximately 80% of the vascular supply to the spinal cord [73]. Typically, three anterior medullary arteries supply the cervical region, one or two supply the thoracic region, and one supplies the lumbosacral spinal cord [73]. This vascular arrangement creates several watershed areas within the spinal cord at the distal ends of these vascular trees [73]. The artery supplying the lumbosacral spinal cord is known as the arteria medullaris magna (AMM), arteria radicularis magna, or the artery of Adamkiewicz [73]. The AMM is the largest anterior segmental artery and typically arises on the left side anywhere between the T8 and L1 level [73]. Right-sided origins of the AMM are not uncommon [73].

Neural Anatomy

A typical mixed spinal nerve has three distinct components: motor, sensory, and sympathetic [74]. Several rootlets leave the anterolateral sulcus of the spinal cord and unite to form each motor root [74]. The fibers traversing these roots arise from the anterior horn cells and innervate the skeletal muscles [74]. The sensory fibers arise from pain, thermal, tactile, and stretch receptors [74]. Cell bodies for sensory fibers are located within the dorsal root ganglia with axons entering the posterolateral sulcus of the cord via several rootlets [74]. The fibers conveying joint or position sensibility and some tactile fibers turn cephalad in the dorsal columns and do not synapse before reaching the gracile and cuneate nuclei at the cervicomedullary junction [74]. Pain and temperature fibers synapse in the substantia gelatinosa and cross to ascend in the dorsal spinothalamic tract [74]. Tactile fibers enter, synapse, and cross to ascend in the ventral spinothalamic tract [74].

The sympathetic component of all 31 mixed spinal nerves leaves the spinal cord along only 14 motor roots [74]. The cells of origin for sympathetic fibers are in the intermediolateral cell column that extends throughout the thoracic and upper lumbar cord segments [74]. The sympathetic fibers exit from the cord with the 12 thoracic and first two lumbar motor roots, enter the respective mixed spinal nerve, and promptly emerge from it as white rami [74]. The white rami pass anteriorly to the corresponding sympathetic ganglion [74]. Synapse may occur within the ganglion with which the ramus is associated, and postganglionic fibers pass back to the mixed spinal nerve as a gray ramus [74]. More often, the fibers entering the ganglion via the white rami pass for variable distances up or down the paravertebral chain to synapse at higher or lower levels [74]. The postganglionic fibers pass along gray rami to cervical, lower lumbar, or sacrococcygeal mixed spinal nerves having no white rami [74]. Sweat glands, blood vessels, and erector pili are innervated also in a segmental pattern [74].

Mixed spinal nerves, having left the intervertebral foramina, receive their sympathetic component and promptly branch into anterior and posterior primary rami [74]. The posterior primary rami are directed posteriorly and supply the paraspinal musculature and the skin along the posterior aspect of the trunk, the neck, and the head [74]. The upper three cervical posterior rami are larger than their corresponding anterior rami, supplying relatively large areas of the scalp posteriorly and the musculature around the craniocervical junction [74]. With these exceptions, posterior primary rami are small, and the major part of each spinal nerve continues laterally in an anterior primary ramus to enter a plexus or to become an intercostal nerve [74]. Anterior primary rami of all the cervical, the first thoracic, and all the lumbosacral nerves join in the formation of plexuses [74]. The upper four cervical anterior rami form the cervical plexus [74]. The lower four cervical and first thoracic anterior rami form the brachial plexus [74]. The first three and a part of the fourth lumbar anterior rami form the lumbar plexus [74]. The sacral anterior rami along with the fifth lumbar and a part of the fourth join to form the lumbosacral plexus [74]. The area of skin supplied by the fibers of a single spinal root is called a dermatome [74]. Segmental dermatomal patterns are well preserved in the thoracic region but not in the limbs [74]. Migration of the limb buds accounts for the displacement of midcervical dermatomes along the lateral aspect of the arm and radial aspect of the forearm [74]. Migration of the limb buds accounts for the displacement of lower cervical and upper

Classification

Diagnostic Subcategories: The diagnostic subcategories of cauda equina syndrome should no longer be used for decision-making, prognosis, research, or medicolegal purposes [2].

Presentation Modes: In a retrospective chart review of thirty-one patients with cauda equina syndrome secondary to a central disc lesion, two modes of presentation were identified: an acute mode and a slower onset mode [14]. The acute mode is characterized by abrupt, more severe symptoms and signs, and carries a slightly poorer prognosis after decompression, especially for the return of bladder function [14]. The slower onset mode is characterized by prior symptoms for varying time-intervals before the more gradual onset of the syndrome [14].

Shi Classification: A retrospective multi-center cohort study assessed the distribution of patients according to the Cauda Equina Syndrome Classification (Shi Classification), finding Early (3.1%), intermediate (84.4%), and late (12.5%) [42].

Other Considerations: A study assessed the inter-rater reliability of dividing patients with cauda equina syndrome into categories including ‘suspected CES’, ‘early CES’, ‘incomplete CES’, and ‘CES with urinary retention’ [29]. The pathophysiology of cauda equina syndrome is thought to be related to damage to the nerve roots from direct mechanical compression and resulting ischemic damage [16]. Specific causes of direct mechanical compression include external trauma, excessive retraction of the dural sac intraoperatively, postoperative hematoma, epidural anesthetic misplacement, abscess, and tumors [16]. Ischemic damage to the nerve roots is an often-overlooked pathology when considering treatment [16]. The blood supply to the nerve roots is provided by distal radicular arteries and ventral proximal radicular arteries, which receive their ultimate blood supply from the anterior spinal artery [16]. Spinal canal stenosis elevates spinal fluid pressure caudally [16].

Compression at the conus level is called conus medullaris syndrome [16]. Female spinal cords are generally longer, with termination at L1-L2 in female patients versus T12-L1 in male patients [16]. Anatomic variance in spinal cord termination does not alter the diagnosis of conus medullaris syndrome versus cauda equina syndrome for an individual patient [16]. Conus medullaris syndrome includes upper motor neuron symptoms, contrasting with cauda equina syndrome’s lower motor symptoms, aiding in clinical localization before imaging [16]. Dysfunction of a single nerve disrupts both sensory perception and muscle control, leading to urinary retention, a notable indicator of cauda equina syndrome [16].

In the retrospective review of thirty-one cases, all patients had urinary retention preoperatively [14]. Bladder function was the most seriously affected function preoperatively and remained so postoperatively [14]. The prognosis for return of motor function was good, with twenty-seven of the thirty patients who were operated on regaining normal motor function [14]. Preoperatively, all patients had sciatica, which was bilateral in fourteen and unilateral in seventeen [14]. The average time to surgical decompression after the patient was seen ranged from 1.1 days for more acute lesions to 3.3 days for the second group [14]. There was no correlation between the time to surgical decompression and return of function [14]. Decompression for cauda equina syndrome does not have to be performed in less than six hours if recovery is to occur, as has been suggested in the past [14].

Clinical Presentation

Diagnostic Reliability and Classification

Clinical signs do not reliably correlate with MRI findings in cauda equina syndrome [1]. Assessment of inter-rater reliability for categorizing patients with cauda equina syndrome demonstrates poor agreement among consultant spinal surgeons, neurosurgical registrars, and medical students [29].

Clinical Signs and Symptoms

Cauda equina syndrome presents with lower motor neuron symptoms, contrasting with the upper motor neuron symptoms of conus medullaris syndrome [16]. Dysfunction of the detrusor urinae muscle and internal bladder sphincter, governed by sacral nerve roots (S2-S4) and the hypogastric plexus (T11-L3), leads to urinary retention, a notable indicator of cauda equina syndrome [16]. In a retrospective review of 31 patients with cauda equina syndrome secondary to a central disc lesion, all patients had urinary retention preoperatively [14]. Bladder function was the most seriously affected function preoperatively and remained so postoperatively [14]. All patients in this cohort had sciatica preoperatively [14], which was bilateral in 14 patients and unilateral in 17 patients [14]. Long-term follow-up of cauda equina syndrome patients revealed that many continued to experience sexual issues, with a reported range of 14% to 100% [5].

Diagnostic Accuracy and Imaging

Use of a post-void residual (PVR) volume ≥ 200 ml was considerably more accurate in predicting cauda equina syndrome compared to clinical assessment [6]. A limited sequence lumbosacral MRI could be used to diagnose cauda equina syndrome safely in patients under the age of 55 years, though further research is needed to assess safety and efficacy before changes to existing protocols can be recommended [17].

Investigations

Diagnostic Criteria and Triage

A post-void residual (PVR) volume of ≥ 200 ml is considerably more accurate in predicting cauda equina syndrome compared to clinical assessment [6].

Imaging Modalities

MRI: MRI is the standard for advanced imaging of the spine and is superior to CT in most circumstances, particularly for identification of infections, tumors, and degenerative changes within the discs [85]. It provides excellent assessment of the spinal cord [84] and allows evaluation of the intervertebral discs, nerve roots, posterior longitudinal ligament, and intervertebral foramen due to high soft-tissue contrast and resolution [84]. MRI is superior to CT for imaging the disc and directly imaging neural structures [85]. However, MRI consistently underestimates the lumbar spinal canal cross-sectional area compared to CT [48], a discrepancy that could impact surgical planning and outcomes [48]. Further research is needed to assess the safety and efficacy of limited sequence MRI for cauda equina syndrome before changes to existing protocols can be recommended [17]. Patients undergoing lumbar decompressive surgery should have sagittal whole spine MRI studies pre-operatively to exclude proximal neurological compression [142]. MRI combined with paraspinal mapping or diffusion tensor imaging showed clear benefits in determining decompression levels of lumbar spinal stenosis compared to MRI combined with neurological examination [143].

CT: CT myelography is reserved for patients who have contraindications to MRI or who have equivocal MRI examinations [84].

Other Imaging: Myelography and lumbar venography are complementary diagnostic studies which should be used together in doubtful cases [50].

Imaging Interpretation and Correlation

The presence of a high-intensity zone (HIZ) on a lumbar MRI T2-weighted image indicates abnormal disc morphology [47]. Findings on magnetic resonance scans were not predictive of the development or duration of low-back pain [25]. The presence of a morphological variation from 'normal' in an imaging study does not confirm the diagnosis [82]. Imaging studies must be concordant with clinical symptoms and signs to be of diagnostic value [82], and an imaging study alone is insufficient to qualify for a diagnosis excepting spinal fractures [82]. MRI evidence of disc degeneration has been reported in the cervical spine in 25% of patients younger than 40 years and in 60% of patients 60 years and older [85]. Lumbar disc degeneration was found in 35% of patients 20 to 39 years old and in 100% of patients older than 50 [85]. Consequently, MRI findings must be carefully correlated with the clinical impression [85]. The best way to obtain meaningful clinical information from MRI is to have a specific question derived from the patient’s history and careful physical examination [85]. Specific questions for MRI should be posed using the parameters of neural compression, instability, and deformity [85]. Failure to interpret an imaging study in a clinically targeted way would inevitably lead to poor clinical choices and outcomes [85]. No relationships between MRI findings and symptoms or walking capacity were found in patients with surgically confirmed lateral lumbar spinal canal stenosis [147]. The surgeon should consider the correlation of symptoms and physical findings with the results of imaging [52].

Other Investigations

Negative discography in patients with probable symptoms of discogenic low back pain cannot absolutely exclude the diagnosis of discogenic pain [60]. Anterior rupture of the disc is a rare lesion that can be identified by discography when other investigations are inconclusive [151].

Treatment

Diagnostic Triage and Imaging

There is no universally agreed definition of cauda equina syndrome, and clinical signs do not reliably correlate with MRI findings [1]. Consequently, the diagnostic subcategories of cauda equina syndrome have poor interobserver reliability and should no longer be used for decision-making, prognosis, research, or medicolegally [2]. A limited sequence lumbosacral MRI could be used to diagnose cauda equina syndrome safely in patients under the age of 55 years, but further research is needed to assess safety and efficacy before changes to existing protocols can be recommended [17].

Surgical Indications and Timing

Decompressive surgery is clearly indicated in cases of progressive neurologic deficit, cauda equina syndrome, and disabling lower-extremity weakness [20]. In a retrospective review of thirty-one patients with cauda equina syndrome secondary to a central disc lesion, the average time to surgical decompression after the patient was seen ranged from 1.1 days for more acute lesions to 3.3 days for the second group [14]. There was no correlation between the time to surgical decompression and return of function in patients with cauda equina syndrome secondary to a central disc lesion [14]. Decompression does not have to be performed in less than six hours if recovery is to occur, as has been suggested in the past [14]. In a retrospective multi-center cohort study of 32 patients with cauda equina syndrome caused by lumbar herniated intervertebral disc, the duration of symptoms to surgery ranged from 12 to 164 hours, with an average of 44.81 ± 32.69 hours [42].

Operative Techniques and Complications

An acute cauda equina syndrome following in situ arthrodesis is best treated by immediate decompression including resection of the posterosuperior rim of the sacrum and the adjacent disc, with consideration for posterior instrumentation and reduction [10]. Surgeons should monitor for early symptoms of cauda equina syndrome and ensure fat graft thickness is between one-half and one centimeter to prevent compression [12]. In the absence of myelopathy, simultaneous decompression may be considered in patients who can tolerate longer operative times [27].

Outcomes and Prognosis

Twenty-seven of the thirty patients who were operated on for cauda equina syndrome secondary to a central disc lesion regained normal motor function [14]. Bladder function was the most seriously affected function preoperatively and remained so postoperatively in patients with cauda equina syndrome secondary to a central disc lesion [14]. Long-term follow-up of cauda equina syndrome patients revealed that many continued to experience sexual issues, with a range of 14% to 100% [5].

Complications

Iatrogenic and Postoperative Complications

Direct Mechanical Compression: Specific causes of direct mechanical compression leading to cauda equina syndrome include excessive retraction of the dural sac intraoperatively, postoperative hematoma, and epidural anesthetic misplacement [16]. Acute cauda equina syndrome can also occur following in situ arthrodesis for severe spondylolisthesis at the lumbosacral junction [10].

Fat Graft Complications: Cauda equina syndrome has been reported as a complication following surgical treatment of lumbar spinal stenosis with application of free autogenous fat grafts [12]. To prevent compression from fat grafts, surgeons should ensure fat graft thickness is between one-half and one centimeter [12]. Surgeons should monitor for early symptoms of cauda equina syndrome following the use of free autogenous fat grafts [12].

Infection: Discitis occurred in 15 of 502 lumbar disc operations, representing a rate of 2.8 per cent [34].

Long-Term Functional Outcomes and Residual Deficits

Bladder Function: Bladder function was the most seriously affected function preoperatively and remained so postoperatively in patients with cauda equina syndrome secondary to central disc lesions [14]. All patients in a retrospective review of cauda equina syndrome secondary to central disc lesions had urinary retention preoperatively [14]. The prognosis for return of bladder function was slightly poorer in patients with an acute mode of presentation compared to those with a slower onset [14].

Motor Function: In a retrospective review of 31 patients with cauda equina syndrome secondary to a central disc lesion, 27 of the 30 patients who were operated on regained normal motor function [14].

Recovery

Functional milestones: The first study to use validated patient-reported outcome measures to assess the CES Core Outcome Set reported the long-term outcome of patients with cauda equina syndrome [43].

Key Evidence

  • [L4] There is no universally agreed definition of cauda equina syndrome, and clinical signs do not reliably correlate with MRI findings; MRI should be performed within one hour of suspicion, and patients with confirmed compression should undergo emergency surgery. [1] (10.1302/0301-620x.97b10.35922)
  • [L5] The diagnostic subcategories of cauda equina syndrome have poor interobserver reliability and should no longer be used for decision-making, prognosis, research, or medicolegally; triage should instead be based upon a synthesis of symptoms, signs, and bladder ultrasound results. [2] (10.1302/0301-620x.106b3.bjj-2023-1016.r1)
  • [L5] Regardless of the setting, when cauda equina syndrome is diagnosed, the treatment is urgent surgical decompression of the spinal canal. [3] (10.5435/00124635-200808000-00006)
  • [L2] However, long-term follow-up of cauda equina syndrome patients revealed that many continued to experience sexual issues (14% to 100%). [5] (10.1186/s12891-025-08736-3)
  • [L2] Use of a PVR volume ≥ 200 ml was considerably more accurate in predicting cauda equina syndrome compared to clinical assessment. [6] (10.1302/0301-620x.102b6.bjj-2020-0195.r1)
  • [L4] Internet information relating to cauda equina syndrome is of variable quality and largely set at an inappropriate readability level. [7] (10.1097/brs.0000000000000282)
  • [L3] Autonomic and non-autonomic dysfunction is common in long-term follow-up of cauda equina syndrome patients, even in those with the most optimistic prognosis, and early decompression did not show a statistically significant correlation with improved outcomes. [8] (10.1302/0301-620x.103b9.bjj-2021-1152)
  • [L4] Herniation of a free epidural fat graft into the spinal canal can cause cauda equina syndrome, a complication not previously reported. [9] (10.2106/00004623-198870080-00023)
  • [L4] An acute cauda equina syndrome following in situ arthrodesis is best treated by immediate decompression including resection of the posterosuperior rim of the sacrum and the adjacent disc, with consideration for posterior instrumentation and reduction. [10] (10.2106/00004623-199173040-00026)
  • [Case_report] Combined epiconus and cauda equina syndrome due to multilevel spinal canal stenosis was treated successfully with combined two-stage anterior and posterior decompression. [11] (10.1007/s00402-007-0555-9)
  • [L4] Surgeons should monitor for early symptoms of cauda equina syndrome and ensure fat graft thickness is between one-half and one centimeter to prevent compression. [12] (10.2106/00004623-198971070-00018)
  • [L4] [14] (10.2106/00004623-198668030-00011)
  • [L5] [16] (10.2106/jbjs.rvw.24.00156)
  • [L4] A LS lumbosacral MRI could be used to diagnose CES safely in patients under the age of 55 years, but further research is needed to assess safety and efficacy before changes to existing protocols can be recommended. [17] (10.1302/0301-620x.102b4.bjj-2019-0645.r2)
  • [L5] [20] (10.5435/00124635-199907000-00004)
  • [L2] The findings on magnetic resonance scans were not predictive of the development or duration of low-back pain. [25] (10.2106/00004623-200109000-00002)
  • [L2] In the absence of myelopathy, simultaneous decompression may be considered in patients who can tolerate longer operative times. [27] (10.5435/jaaos-d-25-00824)
  • [L4] [29] (10.1302/0301-620x.105b9.bjj-2022-1343.r1)
  • [L4] Discitis occurred in 15 of 502 lumbar disc operations (2.8 per cent). [34] (10.2106/00004623-196951040-00009)
  • [L4] [42] (10.1186/s13018-025-05594-6)
  • [L3] This study reports the long-term outcome of patients with CES and is the first to use validated patient-reported outcome measures to assess the CES Core Outcome Set. [43] (10.1302/0301-620x.103b9.bjj-2021-0094.r1)
  • [L1] The presence of an HIZ on a lumbar MRI T2-weighted image indicates abnormal disc morphology. [47] (10.1186/s13018-017-0523-1)
  • [L4] MRI consistently underestimated the lumbar spinal canal cross-sectional area compared to CT, which could impact surgical planning and outcomes. [48] (10.1186/s13018-025-05653-y)
  • [L3] Myelography and lumbar venography are complementary diagnostic studies which should be used together in doubtful cases. [50] (10.2106/00004623-197759020-00003)
  • [L4] The surgeon should consider the entire spectrum of pathological changes of the discs, the patient's symptoms, physical findings, and any adverse psychosocial factors, and correlation of symptoms and physical findings with the results of imaging. [52] (10.2106/00004623-198971080-00024)
  • [L2] Negative discography in patients with probable symptoms of discogenic low back pain cannot absolutely exclude the diagnosis of discogenic pain. [60] (10.1007/s00402-011-1448-5)
  • [L4] The authors advise that patients undergoing lumbar decompressive surgery should have sagittal whole spine MRI studies pre-operatively to exclude proximal neurological compression. [142] (10.1302/0301-620x.95b10.31222)
  • [L2] MRI + (PM or DTI) showed clear benefits in determining decompression levels of lumbar spinal stenosis than MRI + NE. [143] (10.1186/s13018-016-0382-1)
  • [L3] However, no relationships between the MRI findings and symptoms or walking capacity were found, suggesting their multifactorial etiology. [147] (10.1186/1471-2474-15-247)
  • [L4] Anterior rupture of the disc is a rare lesion that can be identified by discography when other investigations are inconclusive; the information obtained allowed for a more effective operative approach. [151] (10.2106/00004623-198365080-00025)

See Also

References

[1] Cauda equina syndrome. The Bone & Joint Journal. 2015. DOI: 10.1302/0301-620x.97b10.35922

[2] The failure of subcategorization of cauda equina syndrome. The Bone & Joint Journal. 2024. DOI: 10.1302/0301-620x.106b3.bjj-2023-1016.r1

[3] Cauda Equina Syndrome. Journal of the American Academy of Orthopaedic Surgeons. 2008. DOI: 10.5435/00124635-200808000-00006

[5] The implications of surgery on sexual dysfunction in patients with lumbar disc herniation with cauda equina syndrome: a systematic review. BMC Musculoskeletal Disorders. 2025. DOI: 10.1186/s12891-025-08736-3

[6] A prospective study of the role of bladder scanning and post-void residual volume measurement in improving diagnostic accuracy of cauda equina syndrome. The Bone & Joint Journal. 2020. DOI: 10.1302/0301-620x.102b6.bjj-2020-0195.r1

[7] Cauda Equina Syndrome. Spine. 2014. DOI: 10.1097/brs.0000000000000282

[8] Infographic: Long-term core outcomes in cauda equina syndrome. The Bone & Joint Journal. 2021. DOI: 10.1302/0301-620x.103b9.bjj-2021-1152

[9] Cauda equina syndrome as a complication of free epidural fat-grafting. A report of two cases and a review of the literature.. The Journal of Bone & Joint Surgery. 1988. DOI: 10.2106/00004623-198870080-00023

[10] Cauda equina syndrome after in situ arthrodesis for severe spondylolisthesis at the lumbosacral junction.. The Journal of Bone & Joint Surgery. 1991. DOI: 10.2106/00004623-199173040-00026

[11] Two-stage decompression for combined epiconus and cauda equina syndrome due to multilevel spinal canal stenosis of the thoracolumbar spine: a case report. Archives of Orthopaedic and Trauma Surgery. 2008. DOI: 10.1007/s00402-007-0555-9

[12] Cauda equina syndrome after surgical treatment of lumbar spinal stenosis with application of free autogenous fat graft. A report of two cases.. The Journal of Bone & Joint Surgery. 1989. DOI: 10.2106/00004623-198971070-00018

[14] Cauda equina syndrome and lumbar disc herniation.. The Journal of Bone & Joint Surgery. 1986. DOI: 10.2106/00004623-198668030-00011

[16] Cauda Equina Syndrome: A Review of Classification, Diagnosis, Treatment, and Best Practices. JBJS Reviews. 2025. DOI: 10.2106/jbjs.rvw.24.00156

[17] Limited sequence MRI to improve standards of care for suspected cauda equina syndrome. The Bone & Joint Journal. 2020. DOI: 10.1302/0301-620x.102b4.bjj-2019-0645.r2

[20] Degenerative Lumbar Stenosis: Diagnosis and Management. Journal of the American Academy of Orthopaedic Surgeons. 1999. DOI: 10.5435/00124635-199907000-00004

[25] The Value of Magnetic Resonance Imaging of the Lumbar Spine to Predict Low-Back Pain in Asymptomatic Subjects. The Journal of Bone and Joint Surgery-American Volume. 2001. DOI: 10.2106/00004623-200109000-00002

[27] Tandem Spinal Stenosis: A Proposed Therapeutic Algorithm Based on a Systematic Review and Meta-Analysis. Journal of the American Academy of Orthopaedic Surgeons. 2026. DOI: 10.5435/jaaos-d-25-00824

[29] Cauda equina syndrome. The Bone & Joint Journal. 2023. DOI: 10.1302/0301-620x.105b9.bjj-2022-1343.r1

[34] Discitis (Closed Space Infection) Following Removal of Lumbar Intervertebral Disc. The Journal of Bone & Joint Surgery. 1969. DOI: 10.2106/00004623-196951040-00009

[42] Biportal endoscopic lumbar discectomy surgery in patients with cauda equina syndrome caused by lumbar herniated intervertebral disc: a retrospective multi-center cohort study. Journal of Orthopaedic Surgery and Research. 2025. DOI: 10.1186/s13018-025-05594-6

[43] Long-term core outcomes in cauda equina syndrome. The Bone & Joint Journal. 2021. DOI: 10.1302/0301-620x.103b9.bjj-2021-0094.r1

[47] The correlation between the high-intensity zone on a T2-weighted MRI and positive outcomes of discography: a meta-analysis. Journal of Orthopaedic Surgery and Research. 2017. DOI: 10.1186/s13018-017-0523-1

[48] MRI underestimates lumbar spinal canal cross-sectional area compared to CT in patients with lumbar spinal stenosis. Journal of Orthopaedic Surgery and Research. 2025. DOI: 10.1186/s13018-025-05653-y

[50] Ascending lumbar venography in lumbar-disc disease. The Journal of Bone & Joint Surgery. 1977. DOI: 10.2106/00004623-197759020-00003

[52] Surgical management of lumbar intervertebral-disc disease.. The Journal of Bone & Joint Surgery. 1989. DOI: 10.2106/00004623-198971080-00024

[60] Diagnosis of discogenic low back pain in patients with probable symptoms but negative discography. Archives of Orthopaedic and Trauma Surgery. 2012. DOI: 10.1007/s00402-011-1448-5

[64] Orthopaedic Knowledge Update 13 Ebook Without Multimedia. Spinal Anatomy > Osseous Anatomy.

[66] Orthopaedic Knowledge Update 13 Ebook Without Multimedia. Spinal Anatomy > Osseous Anatomy > Thoracic Vertebrae.

[68] Orthopaedic Knowledge Update 13 Ebook Without Multimedia. Spinal Anatomy > Biomechanics.

[69] Orthopaedic Basic Science Fifth Edition Print Ebook. Biology and Mechanics of the Skeletal Extracellular Matrix > Anatomy.

[72] Campbell S Operative Orthopaedics 4 Volume Set. RECONSTRUCTION OF THE PATELLOFEMORAL AND PATELLOTIBIAL LIGAMENTS WITH A SEMITENDINOSUS TENDON GRAFT > ANATOMY OF VERTEBRAL COLUMN.

[73] Orthopaedic Knowledge Update 13 Ebook Without Multimedia. Spinal Anatomy > Vascular Anatomy.

[74] Campbell S Operative Orthopaedics 4 Volume Set. PERIPHERAL NERVE INJURIES OF THE UPPER AND LOWER EXTREMITIES > ANATOMY OF THE SPINAL NERVES > COMPONENTS OF MIXED SPINAL NERVES.

[82] Queensland Guidelines for Evaluation of Permanent Impairment, 2nd edition. Queensland Guidelines for Evaluation of Permanent Impairment, 2nd edition > Spine, p. 29.

[84] Campbell S Operative Orthopaedics 4 Volume Set. INTERVERTEBRAL DISC DISEASE.

[85] Campbell S Operative Orthopaedics 4 Volume Set. OVERVIEW OF LUMBAR AND THORACIC DISC DEGENERATION AND HERNIATION > MAGNETIC RESONANCE IMAGING.

[142] Neurological deterioration due to missed thoracic spinal stenosis after decompressive lumbar surgery. The Bone & Joint Journal. 2013. DOI: 10.1302/0301-620x.95b10.31222

[143] Reducing surgical levels by paraspinal mapping and diffusion tensor imaging techniques in lumbar spinal stenosis. Journal of Orthopaedic Surgery and Research. 2016. DOI: 10.1186/s13018-016-0382-1

[147] Correlation of lateral stenosis in MRI with symptoms, walking capacity and EMG findings in patients with surgically confirmed lateral lumbar spinal canal stenosis. BMC Musculoskeletal Disorders. 2014. DOI: 10.1186/1471-2474-15-247

[151] Anterior rupture of the lumbosacral disc. Report of a case.. The Journal of Bone & Joint Surgery. 1983. DOI: 10.2106/00004623-198365080-00025

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