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Cervical myelopathy

79 citationsUpdated Sep 2026

Overview

Cervical spondylotic myelopathy is a degenerative disorder of the cervical spine and represents the most common type of spinal cord dysfunction in patients over fifty-five years old [2]. Left untreated, the condition typically worsens clinically, with more than 50 percent of patients progressing to severe disability [4]. Surgical treatment is indicated for patients with objective myelopathic symptoms confirmed by imaging demonstrating spinal cord compression to halt progression of symptoms and improve function in some patients [22]. Patients with myelopathy or severe stenosis are best treated with surgical decompression [51], and decompression surgery remains a reasonable treatment option even in elderly patients [49]. While consensus on the optimal timing of surgical intervention remains lacking, particularly for patients with mild symptoms or asymptomatic cord compression [5], early operative management is beneficial for most patients with moderate or severe myelopathy [13]. It is essential to operate on patients as soon as they develop symptoms of myelopathy to improve surgical results [24], and satisfactory recovery is more likely in patients treated earlier in the course of the disease and those with less comorbidity [13].

The duration of myelopathic symptoms is an independent prognostic indicator of surgical outcome [19], and patients with Nurick grade 2 cervical spondylotic myelopathy are most likely to improve from surgery [19]. Patients being considered for anterior cervical diskectomy and fusion who have substantial preoperative motor deficits may benefit from earlier surgical intervention [66]. Absolute surgical indications for disc herniation include deteriorating neurological deficits with myelopathy or cauda equina syndrome [71]. Although appropriate patient selection can lead to successful surgical outcomes by restoring spinal stability and improving quality of life in the management of metastatic cervical spine tumors [14], the primary focus for degenerative disease remains decompression. Anterior and posterior decompression for degenerative cervical myelopathy resulted in similar postoperative outcomes and rates of complications [18]. Three anterior cervical surgical approaches have good curative effects on single level cervical spondylotic myelopathy [7], and posterior minimally invasive surgery is an effective and safe method for the treatment of cervical spondylosis [65].

Perioperative complications associated with cervical myelopathy surgery can be devastating [22]. Adverse events associated with anterior cervical spine surgery are infrequent but can be serious and potentially life-threatening [16], necessitating appropriate strategies to avoid them and an understanding of how to detect and manage them when they arise [16]. While most patients improve after decompressive surgery for degenerative cervical myelopathy, not all early results are durable [20]. Up to 17.9% of patients experience recurrent decline by 10 years after decompressive surgery for degenerative cervical myelopathy [20]. Diabetes with advanced age and long-term cervical spondylotic myelopathy symptoms adversely affected cervical laminoplasty outcomes [12]. There is a need to understand the prevalence and natural history of degenerative cervical cord compression without myelopathy [1], and biomarkers are needed to predict progression from degenerative cervical cord compression without myelopathy to symptomatic myelopathy [1]. A multicenter study is underway to establish a comprehensive prediction measure for neurologic recovery in patients with cervical myelopathy [9].

Anatomy & Pathophysiology

Bony Anatomy

The cervical vertebral body is an oblong structure with a coronal diameter larger than its sagittal diameter [84]. Cervical endplates exhibit a cup-in-saucer configuration, distinct from the flat endplates of the thoracic and lumbar vertebrae [84]. The posterior aspect of the cervical transverse process guides the spinal nerves as they exit the spinal canal, forming a half-pipe configuration that cradles the nerve [84]. The cervical pedicles project from the vertebral body in an orientation running posterolateral to anteromedial, forming the posteromedial border of the transverse foramina and the anterolateral aspect of the spinal canal [87]. The subaxial cervical spine includes the C3–C7 vertebral segments, which maintain a relatively uniform anatomical configuration analogous to the thoracic and lumbar spine [91].

The occipital bone forms the posterior part of the foramen magnum, which emits the spinal cord into the spinal canal [91]. The external occipital protuberance (inion) marks the thickest portion of the occipital bone, and the occiput curves sharply anterior from the superior nuchal line to the foramen magnum [91]. The occiput interfaces with the cervical spine through bilateral articular condyles on either side of the foramen magnum [91]. The tectorial membrane extends from the posterior border of the foramen magnum to the superior surface of the C1 ring and is analogous to the posterior longitudinal ligament in the lower cervical spine [91]. The posterior atlantooccipital membrane spans between the lower occiput and the posterior C1 ring and is analogous to the ligamentum flavum at other levels [91]. The vertebral artery enters the posterior atlantooccipital membrane approximately 1.5 cm from the posterior midline [91].

Ligamentous and Muscular Anatomy

The ligamentum flavum spans each interlaminar space and is noncontiguous in nature [87]. The ligamentum flavum, interspinous ligaments, and supraspinous ligaments (ligamentum nuchae) form the posterior ligamentous complex [87]. The ligamentum nuchae is a thick condensation of supraspinous fibrous bands that overlays the spinous processes of the cervical vertebrae and extends from the inion to C7 [91]. The apical ligament runs from the tip of the dens to the basion [93]. The alar ligaments attach on the lateral side of the tip of the dens and run horizontally to the anteromedial aspect of the occipital condyles [93]. The transverse ligament spans from the lateral masses of C1, running just dorsal to the dens [93]. The craniocaudal component of the cruciate ligament runs in the midline from the transverse ligament cranially to the basion and caudally to the C2 vertebral body [93]. The posterior occipito-atlantal membrane runs from the posterior arch of C1 to the posterior aspect of the foramen magnum (opisthion), with a gap laterally for the vertebral arteries [93].

The superior obliquus capitis muscle runs from the lateral aspect of the superior nuchal line to the transverse process of C1 [91]. The rectus capitis posterior minor attaches to the superior nuchal line and the C1 spinous process [91]. The rectus capitis posterior major muscle extends from the superior nuchal line to the spinous process of C2 [91]. The longissimus capitis blends with the deep muscles of the upper thoracic paraspinal region, spanning from the mastoid process of the skull [91].

Spinal Cord Anatomy

The anterior corticospinal tract is responsible for skilled movement and crosses to the opposite side of the body [85]. The lateral corticospinal (pyramidal) tract is responsible for skilled movement and remains on the same side of the body [85]. The vestibulospinal tract facilitates extensor muscle tone and remains on the same side of the body [85]. The dorsolateral fasciculus transmits pain and temperature signals bidirectionally [85]. The fasciculus proprius provides short spinal connections bidirectionally [85]. The fasciculus gracilis and the fasciculus cuneatus transmit position and fine touch signals on the same side of the body [85]. The lateral spinothalamic tract transmits pain and temperature signals to the opposite side of the body [85]. The anterior spinothalamic tract transmits light touch signals to the opposite side of the body [85].

Pathophysiology

Cervical spondylotic myelopathy is a degenerative disorder of the cervical spine that is the most common type of spinal cord dysfunction in patients over fifty-five years old [2]. Cervical spondylosis is defined as a generalized disease process affecting the entire cervical spine and related to chronic disk degeneration [40]. In approximately 90% of men older than 50 years and 90% of women older than 60 years, degeneration of the cervical spine can be demonstrated by radiographs [40]. The incidence of cervical myelopathy is twice as great in men as in women [40]. People older than 60 years are more likely to have multi-segmental cervical spondylotic disease [40]. The most frequently involved levels in cervical spondylosis are the more mobile segments: C5-C6, C6-C7, and C4-C5 [40].

Cervical degenerative disc disease peaks between age 40 and 50 years [63]. The C5 to C6 level is the most frequently involved in cervical degenerative disc disease, followed by C6 to C7 [63]. Risk factors for cervical degenerative disc disease include frequent lifting, cigarette smoking, and a history of excessive driving [63]. The degenerative spinal cascade in the cervical spine is the result of the interplay of the intervertebral disc and four other articulations: two uncovertebral joints (of Luschka) and two facet joints [63]. Facet joint capsules contain sensory receptors that may play a role in pain and proprioceptive sensation in the cervical spine [63].

Progressive collapse of cervical discs results in loss of normal lordosis of the cervical spine and chronic anterior cord compression across the kyphotic spine or anterior chondroosseous/discoosteophytic spurs [63]. Subsequent loading of facet and uncovertebral joints results in spondylotic changes in foramina that may restrict motion and lead to spinal cord and/or nerve root compression [63]. "Soft" disc herniation refers to a herniated nucleus pulposus without bony osteophytes, usually located posterolaterally between the posterior edge of the uncinate process and the lateral edge of the posterior longitudinal ligament [63]. "Hard" disc herniation refers to a herniated nucleus pulposus with an associated discoosteophytic spur [63]. Myelopathy may be seen with large central herniation or spondylotic bars in the setting of a congenitally narrow canal [63]. Anterior herniation of the cervical disc may cause dysphagia, a rare occurrence [63].

Degenerative changes at the cervical disc and facet joints can be a source of symptoms due to the presence of nerve fibers and nociceptive nerve endings in the peripheral portions of the disc and in the capsule and synovium of the facet joints [10]. Biochemical and biomechanical changes with age result in a degenerative cascade where the intervertebral disc gradually loses height, posterior portions of the disc bulge into the spinal canal and neuroforamina, the ligamentum flavum and facet joint capsule infold, and osteophytes form [10]. These degenerative changes lead to decreases in canal and foraminal size [10]. Subluxation and hypermobility between vertebral bodies may occur as a result of degenerative changes [10]. It is generally believed that only an inflamed or irritated nerve root can result in radicular pain on compression [10]. Neurogenic chemical mediators of pain released from sensory neuron cell bodies and non-neurogenic mediators released from disc tissue may initiate and perpetuate an inflammatory response [10]. Chronic edema and fibrosis within the nerve root caused by compression can alter the response threshold and increase the sensitivity of the nerve root to pain [10]. The dorsal root ganglion is exquisitely sensitive to deformation and may be a source of pain [10]. The prolapsed nucleus pulposus elutes inflammatory mediators, initiating a local inflammatory response that leads to increased permeability at the dorsal root ganglion and pain [10].

Cord compression can cause myelopathy by an ischemic effect secondary to compression of the anterior spinal artery or by a direct mechanical effect on cord function [35]. The natural history of cervical myelopathy typically includes stable periods punctuated by unpredictable stepwise progression [35]. The natural history of cervical myelopathy for most patients is slow deterioration over time, typically in a stepwise fashion with variable periods of stable neurologic function [43]. Spondylosis producing cervical spondylotic myelopathy is the most common cause of cervical myelopathy in patients older than 50 years [35]. Anterior structures such as bulging, ossified, or herniated disks and osteophytic anterior spurs are the usual cause of cord compression in cervical spondylotic myelopathy [35]. Less commonly, conditions involving posterior structures such as ligamentum flavum hypertrophy or ossification of the ligamentum flavum may contribute to cervical spondylotic myelopathy [35]. Degenerative spondylolisthesis can exacerbate or cause compression in cervical spondylotic myelopathy [35]. Cervical spondylotic myelopathy commonly arises in the setting of a congenitally narrowed cervical canal [35]. Cervical spondylotic myelopathy often does not become symptomatic until the later decades of life because the cord may have sufficient space to avoid compression until a threshold amount of space-occupying degenerative changes accumulate [35]. Kyphosis, whether primary or postlaminectomy, is a less common cause of cervical myelopathy [35].

The sagittal cervical canal diameter is appreciably smaller, on average by 3 mm, in the myelopathic spondylotic spine than in the normal spine [40]. The anterior-posterior dimensions of the cervical spinal canal measure between 17 and 18 mm in normal individuals [40]. Spinal canal stenosis is present when the canal diameter becomes less than 13 mm [40]. Extension of the neck decreases both the spinal canal diameter and the neuroforaminal diameter [40]. Extension of the cervical spine often exacerbates the symptoms of spinal cord and nerve root compression [40]. In neck extension, the cord is compressed between the degenerative disc and spondylotic bar anteriorly and the hypertrophic facets and infolded ligamentum flavum posteriorly [63]. Neck flexion results in a slight increase in canal diameter and relief of cord compression [63]. Normal cervical spinal canal diameter is 14 mm or greater [63]. Relative cervical spinal stenosis is defined as a canal diameter of less than 14 mm (10–13 mm) [63]. Absolute cervical spinal stenosis is defined as a canal diameter of less than 10 mm [63]. The Pavlov (Torg) ratio is the ratio of the canal diameter to the vertebral body width, with a normal ratio of 1.0 [63]. A Pavlov (Torg) ratio less than 0.8 is considered abnormal and may be a risk factor for later neurologic involvement, though clinical significance is debated [63].

Disk degeneration starts with tears in the posterolateral region of the annulus [40]. Loss of water content and proteoglycans in the nucleus leads to a decrease of disk height [40]. Longitudinal ligaments degenerate and form bony spurs at their insertion into the vertebral body [40]. The converging of the cervical disk space may result in buckling of the ligamentum flavum, with further narrowing of the spinal canal [40]. Segmental instability results in hypertrophic formation of osteophytes by the uncovertebral joint of Luschka and by the facet joints [40]. Prominent osteophytes from the uncovertebral and facet joints result in compression of both the exiting nerve roots and the spinal cord [40]. Anterior spinal artery impingement by the disk or osteophyte is part of the pathogenesis of cervical spondylosis [40].

The nucleus pulposus is avascular in adults, receiving nutrients through perforations in the cartilaginous end plates of the intervertebral discs [88]. In adults older than 30 years, there is no direct vascular supply to the disc [88]. The microvasculature of the vertebral bony end plates contains vessels oriented obliquely that originate from circumferential vessels and nearby metaphyseal marrow vessels [88]. Perforations in the cartilaginous end plates of the disc may allow the ingress of bacterial or fungal pathogens into the disc [88]. Hematogenous spread of infection to the spine is more commonly arterial than venous [88].

Degenerative cervical myelopathy results from static compression, spinal malalignment leading to altered cord tension and vascular supply, and dynamic injury mechanisms [21]. Occupational hazards, including transportation of goods by weight bearing on top of the head, may accelerate cervical disk degeneration [21]. Potential genetic factors for degenerative disk disease include those related to MMP-2 and collagen IX [21]. Potential genetic factors for ossification of the posterior longitudinal ligament include those related to collagen VI and XI [21]. Congenital anomalies including spinal stenosis, Down syndrome, and Klippel-Feil syndrome may predispose to the development of cervical disk degeneration [21]. Cervical motion segment disorders are considered multifactorial, involving developmental size of the canal and foramina, pathological encroachment, biomechanical effects, and circulatory deficiencies [21]. Static and dynamic factors should be considered for the development of myelopathy in patients with cervical spondylotic spinal cord compression [21]. The pathophysiology of degenerative cervical myelopathy includes a cascade of events after compression of the spinal cord, including ischemia, destruction of the blood–spinal cord barrier, demyelination, and neuronal apoptosis [21].

A traumatic spinal cord injury without instability in the spondylotic or congenitally stenotic spine is most usually central cord syndrome [74]. Underlying cervical stenosis, arising from degenerative changes or a congenitally narrow canal, increases the risk of neural injury with abrupt movements of the neck that are not severe enough to result in a significant fracture or ligament injury [74]. Individuals with diffusely ankylosed spines, such as those with ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis, or severe osteoarthritic ankylosis, have a rigid, immobile spine that functions more like a long bone if injured [34]. Fractures in patients with diffuse idiopathic skeletal hyperostosis or ankylosing spondylitis are almost universally unstable and should be treated as such [34]. Bridging osteophytes in hyperostotic spines effectively fuse the spine into a solid, continuous piece of bone that generally sustains extensile injuries traversing the anterior and posterior elements [34]. A sudden increase in kyphosis and decrease in horizontal forward gaze is a common feature with acute fractures in patients with ankylosing spondylitis [34]. Patients with ankylosing spondylitis are predisposed to developing neurologic decline from epidural hematoma following injury [34]. Acute mortality rates for traumatic injuries to the hyperostotic spine have ranged from 17% to 30% [34]. A study documented a 38% mortality for patients with ankylosing spondylitis at 3 months and 63% by 1 year following injury [34]. Patients with ankylosing spondylitis demonstrated a statistically increased mortality compared to age-, sex-, and injury-matched controls, a finding not seen in patients with diffuse idiopathic skeletal hyperostosis [34].

The genetic influence on disc degeneration may be attributed to a small effect from multiple genes or a relatively large effect of a smaller number of genes [121]. Specific gene loci associated with disc degeneration include variations in the aggrecan gene, metalloproteinase-3 gene, collagen type IX, and alpha 2 and 3 gene forms [121]. Approximately 76% of asymptomatic matched controls show significant abnormalities on

Classification

Allen and Ferguson: This system categorizes subaxial cervical spine injuries into six common patterns based on mechanistic description and radiographic appearance [39]. It further subdivides each injury pattern into stages of severity regarding osseous and ligamentous injury [39]. Derived from a review of 165 subaxial injuries, it is described as the most widely used system for subaxial cervical spine injuries, and its terminology has become familiar to spine surgeons [39]. However, precise definitions of each stage are lacking, and the number of stages makes the system difficult to use precisely in clinical practice [39].

Subaxial Injury Classification (SLIC): Proposed by Moore et al. and subsequently modified by Vaccaro et al., this scoring system evaluates three categories: morphology, discoligamentous complex integrity, and neurologic status [39]. The SLIC system reincorporates the neurologic status of the patient as a component integral to the determination of spinal stability [39]. Scores from the three categories are summed to determine whether nonoperative or operative treatment should be performed [39].

White, Southwick, and Panjabi Checklist: This checklist assigns point values to specific radiographic and clinical criteria for the diagnosis of clinical instability in the subaxial cervical spine [39]. A total score of 5 points or more indicates that clinical instability is likely [39]. Specific criteria include sagittal translation of 3.5 mm on a lateral view and a difference of more than 11 degrees in sagittal rotation between two adjacent motion segments [39].

Nurick: This classification system grades neurological status from grade 0 (neurologically intact) to grade 5 (wheelchair-dependent or bedridden) [38].

Eismont et al.: This system quantifies motor recovery by grading individual muscles of the lower extremity, with the final grade based on the maximum strength found in any muscle [164]. Class A is assigned for grade 0 or 1 muscle strength, Class B for grade 2 or 3, Class C for grade 4, and Class D for grade 5 or normal motor strength [164].

MRI Compression Level: Patients with degenerative cervical myelopathy can be classified into groups based on the level of maximum compression identified on cervical MRI [172]. A high-level compression group includes patients with maximum compression at C3–4 or C4–5, while a low-level compression group includes patients with maximum compression at C5–6 or C6–7 [172]. For patients with multilevel compression, grouping is based on the level of maximum compression [172].

Other Considerations: The Allen and Ferguson system and the SLIC scoring system demonstrated similar reliability for treatment recommendations when compared among experienced spine surgeons [39]. Spinal stability is classically defined as the ability of the spine under physiologic loads to prevent damage or irritation of the spinal cord or nerve roots, and to prevent incapacitating deformity or pain from structural changes [39]. Acute spinal instability is caused by bone or soft-tissue injury that places neural elements at risk of injury with subsequent loading or deformity, whereas chronic spinal instability results from progressive deformity that may cause neurologic deterioration, prevent recovery of injured neural tissue, or cause increasing pain or decreasing function [39]. The subaxial region of the cervical spine (C3-T1) accounts for about 65% of all cervical spine injuries and most cervical spinal cord injuries [39]. The subaxial cervical spine supporting structures are divided into anterior and posterior groups; a motion segment remains stable under physiologic loads if it has all posterior elements and one anterior element, or all anterior elements and one posterior element [39].

Clinical Presentation

Cervical myelopathy is the most common type of spinal cord dysfunction in patients over fifty-five years old [2]. The clinical presentation and natural history of cervical degenerative conditions are variable due to the many ways these conditions can manifest [11]. Clinical manifestations, especially in early stages, can be quite subtle [35]. People older than 60 years are more likely to have multi-segmental disease [40].

Upper Extremity Symptoms

Patients often report a generalized feeling of clumsiness in the arms and hands, including dropping things [35]. Specific difficulties include an inability to manipulate fine objects such as coins or buttons [35], trouble with handwriting [35], and difficulty with buttons or a change in handwriting [41]. Loss of manual dexterity in the hands is a characteristic sign that can present insidiously [41]. Patients may also report diffuse, typically nondermatomal, numbness [35]. Subjective weakness may occur late or not at all [35].

Lower Extremity Symptoms

Gait disturbance is a characteristic sign of myelopathy [41]. Patients may report gait instability, including a sense of imbalance and bumping into walls when walking [35]. A stiff or spastic gait is characteristic [41], and patients demonstrate a wide-based gait with a history of loss of balance and falls [41]. Spasticity in the extremities is a characteristic sign that can present insidiously [41]. Patients with severe cord compression may report the Lhermitte phenomenon, described as electric shock–like sensations that radiate down the spine or into the extremities with certain offending positions of the neck [35].

Other Symptoms

Bowel and bladder symptoms may occur late or not at all [35]. Urinary symptoms are a characteristic sign that can present insidiously [41]. Loss of motor strength may occur, though many patients deny having this symptom [35]. Neck pain may be absent despite advanced degrees of spondylosis [35]. Radicular symptoms or signs are not present in many patients with cervical myelopathy [35]. Headache may be the presenting symptom of cervical spondylosis, usually worse in the morning and improving throughout the day, commonly located in the occipital region and radiating toward the frontal area [40]. Patients complaining of itching of the dorsolateral forearms of seemingly unknown etiology should undergo a workup of the cervical spine [106]. The presence of transient neurological abnormalities, especially those precipitated by the opening of a parachute, should warn the clinician of the possibility of serious cervical myelopathy [30].

Physical Examination Findings

Severe weakness of the major muscle groups in the upper or lower extremities is uncommon [35]. The motor examination may be completely normal even in cases of nerve root or spinal cord compression [41]. When upper extremity weakness is present, it often presents as diminished grip and/or intrinsic strength [41]. Sensory findings often include proprioceptive loss [41]. Dorsal column (proprioceptive) dysfunction occurs with advanced disease and carries a poor prognosis [35].

Hyperreflexia, which may be present in the upper and/or lower extremities, suggests spinal cord compression [35]. Patients with concomitant myelopathy and peripheral nerve disease from conditions such as diabetes, hypothyroidism, peripheral neuropathy, or severe multilevel cervical foraminal stenosis can have diminished or absent reflexes [35]. Patients with cervical myelopathy who have coexisting lumbar stenosis may exhibit brisk upper extremity reflexes consistent with upper motor neuron findings yet diminished lower extremity reflexes because of the root level compression in the lumbar spine [35].

Spinal cord compression with myelopathy can manifest with abnormal upper motor neuron signs such as Hoffman’s sign, inverted radial reflex, pathological clonus, and Babinski’s sign [41]. The Hoffman’s sign is described as quick flexion of both the thumb and index finger when the middle finger nail is snapped [41]. Clonus is a series of abnormal reflex movements of the foot in plantar flexion, induced by sudden dorsiflexion [41]. The Babinski reflex occurs after the sole of the foot has been firmly stroked, resulting in the big toe moving upward or toward the top surface of the foot while the other toes fan out [41]. The inverted radial reflex is noted by flexion of the fingers without flexion of the forearm when the distal end of the radius is tapped [41]. Lhermitte’s sign is an electric shock–like sensation that runs down the center of the patient’s back and enters the limbs during flexion of the neck [41].

Myeloradiculopathy is associated with spinal stenosis with concurrent compression of the neuroforaminal contents, which produces lower motor neuron signs at the level of the cervical cord lesion and upper motor neuron signs caudal to the level of compression [41]. Posterior cord syndrome is a rare syndrome best diagnosed clinically and should be considered in cases of cervical spondylotic myelopathy in which motor strength testing is preserved [27].

Diagnostic Criteria and Screening

A simple self-administered questionnaire has been developed to screen for cervical myelopathy [32]. Typical clinical manifestations of cervical spondylotic myelopathy include chronic neck pain, walking instability, chest band sensation, muscle weakness, and atrophy, as well as positive pathological findings [52]. Patients with DCM may present with common signs and symptoms of neurological dysfunction, such as paresthesia, abnormal gait, decreased hand dexterity, hyperreflexia, increased tone, and sensory dysfunction [21].

Investigations

Plain radiography: Plain radiographs serve as the initial imaging modality due to their low cost and ease of acquisition [53]. They provide information on the location and severity of spinal degeneration, instability, and deformity [53]. Routine series include AP, lateral, and flexion-extension views [53]. The lateral cervical spine view is the most important radiographic view; inadequate imaging can miss over 20% of cervical injuries [42]. Imaging must encompass the entire cervical spine, including the occipitocervical and cervicothoracic junctions [42]. All seven vertebrae should be visible on the lateral view, often requiring gentle upper extremity traction or a swimmer’s view to visualize C7 [42]. Careful scrutiny of the prevertebral soft tissue, vertebral body borders, spinal canal, and posterior elements is mandatory [42]. Prevertebral swelling may indicate a hematoma and serve as the only clue to a traumatic lesion [42]. Normal prevertebral space limits are 10 mm at C1, 5 mm at C2, 7 mm at C3 and C4, and 20 mm at C5, C6, and C7 [42]. Subtle incongruities in bony contours may indicate significant instability [42]. The atlantodental interval (ADI) normally measures less than 3 mm in adults and less than 4 mm in children [42]. On the AP radiograph, vertical widening of the interspinous distance greater than 1.5 times the level above and below indicates a hyperflexion injury with posterior instability or interlocking facets [42]. Traumatic tilting may be noted in the AP plane but not on the lateral view [42]. Oblique views at 45 degrees visualize facet joint articulations [42]. The open-mouth view evaluates the odontoid process, lateral masses, and their articulations [42]. In atlantoaxial rotatory subluxation, the rotated forward lateral mass of the atlas is closer to the midline (medial offset), while the opposite mass is farther away (lateral offset) [42]. Burst fractures of the C1 ring cause overhang of the C1 lateral masses on C2; a combined overhang exceeding 6.9 mm correlates highly with transverse ligament insufficiency and C1-C2 sagittal instability [42]. This series is also important for evaluating congenital defects in infants and children, as well as insidious neck pain in adults [42]. Arthritic changes, including osteophytes, disk space narrowing, and facet sclerosis, may be subtle or apparent [42]. Bone quality can also be assessed [42].

MRI: MRI is noninvasive and provides visualization of intervertebral disks, the spinal cord, and nerve roots [53]. It offers good visualization of spinal cord and nerve root compression [53]. Signal changes within the spinal cord suggest severe compression and injury [53]. T1- and T2-weighted signal changes have a moderate ability to predict surgical outcomes [53]. Diffuse T2 hyperintensity without clear bordering is associated with potentially reversible changes such as edema, Wallerian degeneration, demyelination, and ischemia [53]. Substantial T2 hyperintensity with sharp bordering and T1 hypointensity represent irreversible changes such as cavitation, neural tissue loss, myelomalacia, necrosis, and spongiform changes in gray matter [53]. Myelopathic signs are significantly more common in patients with cord signal changes suggestive of myelomalacia [53]. MRI is complementary to CT in trauma, primarily evaluating spinal cord integrity and soft tissues [103]. It allows detailed assessment of the posterior ligamentous complex (PLC), anterior and posterior longitudinal ligaments (ALL/PLL), intervertebral discs, and surrounding soft tissues [103]. MRI characterizes the degree of spinal cord injury by assessing edema, compression, and continuity of the cord and nerve roots [103]. It demonstrates fluid in the spinal canal, including compressive epidural hematomas, and cerebrospinal fluid in traumatic durotomy [103]. The presence and extent of spinal cord signal and hematoma help determine the prognosis for neurologic recovery [103]. However, MRI has relatively low specificity in distinguishing clinically relevant tension band injuries from less worrisome soft tissue injuries; indiscriminate reliance may overestimate instability and lead to unnecessary surgery [103]. Because MRI is inferior to CT for osseous injuries, it is used primarily as a complementary study [103]. It is particularly useful when evaluating spinal cord integrity or compression, or when the neurologic examination is inconsistent with CT findings [103]. MRI should be used with caution when posterior tension band integrity is unclear [103]. Limitations include increased cost, longer acquisition time, and lower availability relative to CT [103]. MRI and CT myelography exhibit 83% to 95% agreement in predefined surgical threshold measurements of cervical spinal stenosis and cord compression, with axial MRI achieving the highest agreement rate of 95% [130]. Dynamic MRI has high reliability and accuracy in diagnosing cervical spondylotic myelopathy [81]. T2-weighted MRI high signal is associated with dynamic change [52]. MR T2-hyperintensity is an independent risk factor for rapidly progressive cervical spondylotic myelopathy [123]. In patients with cervical radiculopathy, the type and extent of disc herniation on MRI prior to surgery correlated neither with symptom severity at presentation nor with clinical outcomes at two years postoperatively [79]. Structural and functional changes in the cervical spinal cord and brain occur in CSM patients, with brain reorganization playing an important role in maintaining symptoms [83].

CT: CT myelography is a good alternative if a patient cannot undergo MRI due to medical reasons or if metal or scar tissue obscures visualization on MRI [53]. CT is helpful if ossification of the posterior longitudinal ligament (OPLL) is suspected [53]. It also better visualizes the vertebral artery if corpectomy or C2 pedicle screws are planned [53]. CT allows excellent visualization of bony architecture and paravertebral soft tissues [42]. Pedicles, laminae, spinous processes, and the bony spinal canal are examined with significantly better resolution than with conventional radiographs [42]. CT with myelography or intrathecal contrast permits visualization of spinal canal contents [42]. It is appropriate for evaluating congenital variations and malformations, including spinal canal stenosis and spina bifida [42]. Pars defects, atlantoaxial joint diseases, inflammatory changes, primary tumors, and metastatic carcinoma are well appreciated with CT [42]. Although cervical disk disease is detectable with thin cuts and contrast enhancement, it is better visualized with MRI [42]. In trauma patients with questionable plain radiograph findings, CT is integral in evaluating possible fractures or instability [42]. Atrophy, deformity, and displacement of the spinal cord from acute or chronic injury are appreciable with intrathecal contrast [42]. With the advent of MRI, CT is reserved for the assessment of bony architecture, which it does better than MRI [42]. In patients with hyperostotic disease (AS, DISH, severe osteoarthritic ankylosis), CT and MRI are invaluable in delineating injuries [34].

Other Considerations: The sagittal cervical canal diameter was appreciably smaller (3 mm on average) in the myelopathic spondylotic spine than in the normal spine [40]. With neck extension, both spinal canal and neuroforaminal diameters decrease [40]. The most frequently involved levels are the more mobile segments: C5-C6, C6-C7, and C4-C5 [40]. Cervical myelopathy is the most common form of spinal cord dysfunction in people older than 55 years [40]. Degenerative changes at the cervical disc and facet joints can be a source of symptoms [10]. Nerve fibers and nociceptive nerve endings are present in the peripheral portions of the disc and in the capsule and synovium of the facet joints [10]. Findings of discography and provocative injections of the facet joint have supported the role of these structures in the causation of neck pain [10]. Biochemical and biomechanical changes that occur with age result in a degenerative cascade [10]. The intervertebral disc gradually loses height, posterior portions of the disc bulge into the spinal canal and neuroforamina, the ligamentum flavum and facet joint capsule infold, and osteophytes form [10]. All of these degenerative changes lead to decreases in canal and foraminal size [10]. Subluxation and hypermobility between vertebral bodies may occur [10]. Neurogenic chemical mediators of pain released from the cell bodies of the sensory neurons and non-neurogenic mediators released from disc tissue may play a role in initiating and perpetuating an inflammatory response [10]. Chronic edema and fibrosis within the nerve root caused by compression can also potentially alter the response threshold and increase the sensitivity of the nerve root to pain [10]. It may be that the dorsal root ganglion is the source of pain, as it is exquisitely sensitive to deformation [10]. In addition to mechanical compression of the dorsal root ganglion, the prolapsed nucleus pulposus elutes inflammatory mediators, initiating a local inflammatory response that leads to increased permeability at the dorsal root ganglion and pain [10].

Individuals with diffusely ankylosed spines have often been considered as a single group when discussing cervical trauma, although this may not be entirely appropriate [34]. AS, DISH, and severe osteoarthritic ankylosis all result in a rigid, immobile spine that may be exceedingly prone to fracture and functions more like a long bone if injured [34]. Patients who present with neck pain and/or neurologic deficit after major, or minor, trauma should be considered to have a cervical spine injury until proven otherwise when there is known hyperostotic disease [34]. Degenerative spondylotic changes, such as vertebral body osteophytes, fixed subluxations, and facet hypertrophy, can make the radiographic diagnosis of fracture difficult [34]. Unless a frank dislocation, or a translational or intervertebral extension deformity, is present, plain radiographs may not be helpful in identifying an injury in patients with hyperostotic disease [34]. MRI also has the additional advantage of demonstrating spinal cord contusion, cord edema, and epidural hematoma [34]. Bridging osteophytes, whether marginal, as in AS, or nonmarginal as in DISH, are the radiographic characteristics of the hyperostotic spine [34]. The condition effectively fuses the spine into a solid, continuous piece of bone that generally sustains extensile injuries that traverse the anterior and posterior elements [34]. Fractures in patients with DISH or AS are almost universally unstable and should be treated as such [34]. A sudden increase in kyphosis and decrease in horizontal forward gaze is a common feature with acute fractures in patients with AS [34]. Patients with AS, particularly following injury, are also predisposed to developing neurologic decline from epidural hematoma [34].

A simple self-administered questionnaire was successfully developed to screen for cervical myelopathy [32]. The presence of transient neurological abnormalities, especially those precipitated by the opening of the parachute, should warn the clinician of the possibility of serious cervical myelopathy [30]. Congenital hypoplasia of the atlas is a rare cause of myelopathy that often presents in the seventh decade of life when accompanied by degenerative changes or torticollis [23]. Nontraumatic upper cervical spine instability is a rare condition in children that can lead to permanent neurologic compromise if not diagnosed and managed correctly [33]. The article emphasizes the need to understand the prevalence and natural history of degenerative cervical cord compression without myelopathy [1]. The article calls for identifying biomarkers to predict progression to symptomatic myelopathy [1]. A new assessment method based on preoperative MRI cumulative score is simple and useful to assess preoperative severity and predict the results of cervical laminoplasty for cervical spondylotic myelopathy [80]. Congenital spinal stenosis was identified as an independent risk factor for rapidly progressive cervical spondylotic myelopathy [123]. Resting-state Amplitude of Low-frequency Fluctuation is a potentially useful prognostic functional biomarker in cervical myelopathy [9]. To establish a comprehensive prediction measure for neurologic recovery in patients with cervical myelopathy, a multicenter study is underway [9].

Treatment

Non-Operative

For patients with mild degenerative conditions, nonsurgical options may be tried with careful observation [11]. If nonsurgical care is elected, careful and frequent follow-up is mandatory [35]. Firm orthoses, anti-inflammatory medications, isometric exercises, and epidural steroids can be considered for nonsurgical care [35]. Observation, not surgery, is recommended for patients with only radiographic cord compression from spondylosis without clinical myelopathy or radiculopathy [35].

Operative

Indications: Surgical treatment is indicated for patients with objective myelopathic symptoms confirmed by imaging demonstrating spinal cord compression to halt progression of symptoms and improve function [22]. Surgical intervention has shown to be superior for conditions where there is symptomatic moderate to severe spinal cord and nerve root compression [11]. Early operative management is beneficial for most patients with moderate or severe myelopathy, with satisfactory recovery more likely in patients treated earlier in the course of the disease and those with less comorbidity [13]. Patients with cervical canal stenosis and cord compression secondary to spondylosis, without clinical evidence of myelopathy, and who present with clinical or electrophysiological evidence of cervical radicular dysfunction or central conduction deficits seem to be at higher risk for developing myelopathy and should be counseled to consider surgical treatment [21].

Surgical Approach / Technique: The goal of surgery is to decompress any spinal cord or nerve root compression, correct any deformity, and stabilization to maintain correction or prevent deformity [11]. Alignment and the characteristics and location of spinal cord compression help determine the ideal surgical approach [48]. Most spine surgeons prefer an anterior approach when one to two levels are involved [76]. An anterior approach offers direct decompression of pathologies in the anterior cervical spine, a muscle-sparing dissection to minimize postoperative pain, lower infection rates, and the ability to decompress and correct cervical kyphosis [76]. Kyphotic patients exhibited greater improvement when approached by an anterior or combined approach [76]. When three or more levels are involved, the complication rates with an anterior approach rise and a posterior approach may be more efficacious [76]. The posterior approach allows for a wider decompression and is dependent on the ability of the cord to drift away from anterior lesions [76]. Lordotic patients exhibited similar improvement when approached anteriorly or posteriorly [76]. Laminoplasty technique is often ideal for the patient with spinal stability, good cervical lordosis, and minimal neck pain [76]. Laminoplasty offers the opportunity to preserve some of the natural cervical biomechanical motion without necessitating fusion [76]. In deciding between laminoplasty and laminectomy, the risks of surgical and neurological complications, and radiologic and clinical outcome, must be taken into consideration if both options are available in multi-level cervical spondylotic myelopathy [8]. In 2 years of clinical observation, laminoplasty with selective fusion (LPSF) was effective in maintaining the stability of the cervical spine with less sacrifice of mobility and surgical trauma for multilevel myelopathy with segmental instability compared to laminectomy with fusion (LCF) [47]. Posterior minimally invasive surgery is an effective and safe method for the treatment of cervical spondylosis and is a recommended optional surgical procedure for single-segment myelopathy and radiculopathy [65]. Endoscopic decompression of posterior cervical vertebral disorders is a safe, effective, and minimally invasive surgical procedure with rapid recovery times [107]. In a comparison of microendoscopic laminotomy with conventional laminoplasty for cervical spondylotic myelopathy, neurologic outcomes were similar at 5-year follow-up, but patients with microendoscopic laminotomy had significantly less postoperative axial pain and improved subaxial cervical lordosis [73]. In a comparison of microendoscopic selective laminectomy to conventional laminoplasty in patients with degenerative cervical myelopathy, microendoscopic laminectomy resulted in better outcomes in terms of postoperative range of motion, axial pain, and quality of life, although both procedures showed good neurologic improvement [73].

Implant Selection: Anterior decompression and arthrodesis with autogenous bone-grafting can be performed safely, and is associated with a high rate of neurological recovery, functional improvement, and pain relief, in patients who have cervical spondylotic myelopathy [109]. Clinical series have demonstrated successful arthrodesis in most patients (92% to 96%) after single-level ACDF with satisfactory clinical outcomes [76]. The incidence of nonunion increases with the number of levels being fused in multilevel ACDFs [76]. Anterior cervical plating increases the fusion rates in patients undergoing multilevel surgery [76].

Other Considerations: Complications of anterior procedures include postoperative dysphagia (2% to 48%), hoarseness (temporary in 3% to 11%, permanent in 0.33%), and injury to the vertebral artery (0.03%) [76]. Anterior cervical surgery carries an incidence of adjacent segment disease of 3% per year [76]. 'Skip' corpectomy displays safety comparable to that of posterior decompression and better efficacy for treating four-level cervical spondylotic myelopathy [101]. Anterior cervical surgery effectively improves both physical symptoms and mental health outcomes in patients with cervical spondylotic myelopathy, regardless of preoperative psychological distress [108]. In long-course symptomatic cervical OPLL, anterior en bloc resection (ACOE) provided a modest but clinically meaningful improvement in neurological recovery at 48 months compared with posterior laminectomy with instrumented fusion (PLF) [46]. Patients with Nurick grade 2 CSM are most likely to improve from surgery, while the duration of myelopathic symptoms is an independent prognostic indicator of surgical outcome [19]. While most patients improve after decompressive surgery for degenerative cervical myelopathy, not all early results are durable, with up to 17.9% experiencing recurrent decline by 10 years [20]. These findings help predict which patients are likely to experience meaningful improvements following surgery for degenerative cervical myelopathy [36]. A compression ratio of less than 0.4 is associated with a poor prognosis [35]. An increase in the compression ratio to more than 0.4 postoperatively correlates with clinical recovery [35]. The article argues for a general agreement on the definition and terminology of degenerative cervical cord compression without myelopathy, emphasizes the need to understand its prevalence and natural history, and calls for identifying biomarkers to predict progression to symptomatic myelopathy [1].

Complications

Natural History and Progression

Neurological survivorship following primary decompressive surgery for degenerative cervical myelopathy is 89.3% at 5 years and 77.3% at 10 years [68].

Surgical Complications: Anterior Approach

Dysphagia: Postoperative dysphagia occurs in 2% to 48% of patients undergoing anterior cervical procedures [76]. Hoarseness: Hoarseness is temporary in 3% to 11% of cases and permanent in 0.33% [76]. Vascular Injury: Injury to the vertebral artery has an incidence of 0.03% [76]. Adjacent Segment Disease: Anterior cervical arthrodesis carries an incidence of adjacent segment disease of 3% per year [76]. Nonunion: The incidence of nonunion increases with the number of levels being fused in multilevel anterior cervical discectomy and fusion [76]. Risk Factors for Laminoplasty: Diabetes, advanced age, and long-term cervical spondylotic myelopathy symptoms adversely affect cervical laminoplasty outcomes [12].

Surgical Complications: Posterior Approach and General

Decision Making: In deciding between laminoplasty and laminectomy for multi-level cervical spondylotic myelopathy, the risks of surgical and neurological complications must be taken into consideration [8]. Comparative Rates: Anterior and posterior decompression for degenerative cervical myelopathy resulted in similar rates of complications [18]. White Cord Syndrome: White cord syndrome is a potential complication following anterior cervical discectomy and fusion, characterized by acute hemiparesis after posterior cervical decompression and fusion for chronic cervical stenosis [17, 50]. Surgeons should explain the possibility of white cord syndrome before cervical decompression surgery and perform a neurological examination immediately after surgery [50]. OPLL Management: In long-course symptomatic cervical ossification of the posterior longitudinal ligament, anterior en bloc resection and posterior laminectomy with instrumented fusion have low and broadly similar complication rates [46].

Adjacent Segment Disease

Risk Factors: A single-level arthrodesis involving the fifth or sixth cervical vertebra and preexisting radiographic evidence of degeneration at adjacent levels appear to be the greatest risk factors for new disease at adjacent segments [54]. Etiology: The incidence of symptomatic non-fusion segment disease after anterior cervical arthrodesis has multifactorial causes [77].

Traumatic and Ankylosed Spine Complications

Morbidity and Mortality: Perioperative morbidity for traumatic injuries to the hyperostotic spine has been reported at percentages similar to acute mortality rates [34]. A 50% mortality rate has been reported for patients with ankylosing spondylitis at 2 years postinjury [34]. A 38% mortality rate has been documented for patients with ankylosing spondylitis at 3 months postinjury, increasing to 63% by 1 year [34]. Patients with ankylosing spondylitis demonstrated a statistically increased mortality when compared to age-, sex-, and injury-matched controls, a finding not seen in patients with diffuse idiopathic skeletal hyperostosis [34]. Traction Risks: Inline traction can lead to catastrophic neurologic compromise in patients with ankylosing spondylitis due to pre-existing kyphotic deformity [34].

Recovery

Prognosis and Natural History: Patients with spinal cord edema due to cervical spondylosis demonstrate an earlier onset and more rapid progression of disease compared to those without spinal cord edema [180].

Surgical Outcomes and Timing: Single-level arthrodesis involving the fifth or sixth cervical vertebra, combined with preexisting radiographic evidence of degeneration at adjacent levels, represents the greatest risk factors for new disease [54].

Long-Term Durability and Survivorship: Neurological survivorship following primary decompressive surgery for degenerative cervical myelopathy is reported at 89.3% at 5 years and 77.3% at 10 years [68]. Through long-term follow-up, the effect of decompression becomes observable [72]. In long-course symptomatic cervical ossification of the posterior longitudinal ligament, anterior en bloc resection provides a modest but clinically meaningful improvement in neurological recovery at 48 months compared with posterior laminectomy with instrumented fusion [46].

Comparative Surgical Recovery: In two years of clinical observation, laminoplasty with selective fusion maintains cervical spine stability with less sacrifice of mobility and surgical trauma for multilevel myelopathy with segmental instability compared to laminectomy with fusion [47]. Significant improvement in cervical myelopathy and absence of recurring symptoms at long-term follow-up have been documented in cases of posttraumatic osteophytes resulting from long-standing neglected posterior atlanto-occipital dislocation [3]. Additionally, neurological improvement at midterm follow-up is observed with spinal cord decompression and fusion for cervical myelopathy due to ossification of the transverse atlantal ligament [67].

Predictors and Biomarkers: The complete disappearance of deficits in spinal cord function after surgery is the most robust predictor of survival in metastatic spinal cord compression from non-small-cell lung cancer [125].

Key Evidence

  • [L5] The article argues for a general agreement on the definition and terminology of degenerative cervical cord compression without myelopathy, emphasizes the need to understand its prevalence and natural history, and calls for identifying biomarkers to predict progression to symptomatic myelopathy. [1] (10.3389/fneur.2024.1341371)
  • [L5] This article reviews the evaluation and management of patients with cervical spondylotic myelopathy, a degenerative disorder of the cervical spine that is the most common type of spinal cord dysfunction in patients over fifty-five years old. [2] (10.2106/jbjs.m.01030)
  • [L5] The cervical myelopathy significantly improved, and the patient was doing well without recurring symptoms at a long-term follow-up. [3] (10.5435/jaaosglobal-d-21-00129)
  • [L5] Most patients with cervical spondylotic myelopathy become worse clinically if the disorder is left untreated, with more than 50 percent progressing to severe disability. [4] (10.2106/00004623-199409000-00020)
  • [L5] The review highlights that consensus on the optimal timing of surgical intervention for degenerative cervical myelopathy remains lacking, particularly for patients with mild symptoms or asymptomatic cord compression. [5] (10.1530/eor-2025-0070)
  • [L3] Three anterior cervical surgical approaches have good curative effects on single level cervical spondylotic myelopathy. [7] (10.1186/1471-2474-15-233)
  • [L2] In deciding between the two procedures, the risks of surgical and neurological complications, and radiologic and clinical outcome, must be taken into consideration if both options are available in multi-level cervical spondylotic myelopathy. [8] (10.1186/1749-799x-8-45)
  • [L2] To establish a comprehensive prediction measure for neurologic recovery in patients with cervical myelopathy, a multicenter study is underway. [9] (10.1097/corr.0000000000001157)
  • [L5] [10] (10.2106/00004623-200706000-00026)
  • [L2] Diabetes with advanced age and long-term cervical spondylotic myelopathy symptoms adversely affected cervical laminoplasty outcomes. [12] (10.2106/jbjs.n.00064)
  • [L5] Early operative management is beneficial for most patients with moderate or severe myelopathy, with satisfactory recovery more likely in patients treated earlier in the course of the disease and those with less comorbidity. [13] (10.2106/jbjs.f.00014)
  • [L5] Appropriate patient selection can lead to successful surgical outcomes by restoring spinal stability and improving quality of life. [14] (10.5435/jaaos-23-01-38)
  • [L4] Patients in both the laminectomy with fusion and laminoplasty cohorts reported similar functional improvements after treatment for cervical spondylotic myelopathy. [15] (10.1007/s11999-010-1653-5)
  • [L4] Adverse events associated with anterior cervical spine surgery are infrequent but can be serious and potentially life-threatening; appropriate strategies must be utilized to avoid these events, and surgeons must understand how to detect and manage them when they arise. [16] (10.5435/00124635-200812000-00005)
  • [L3] Anterior and posterior decompression for degenerative cervical myelopathy resulted in similar postoperative outcomes and rates of complications. [18] (10.2106/jbjs.16.00882)
  • [L3] Patients with Nurick grade 2 CSM are most likely to improve from surgery, while the duration of myelopathic symptoms is an independent prognostic indicator of surgical outcome. [19] (10.1302/0301-620x.95b7.31363)
  • [L5] This commentary notes that while most patients improve after decompressive surgery for degenerative cervical myelopathy, not all early results are durable, with up to 17.9% experiencing recurrent decline by 10 years. [20] (10.2106/jbjs.22.01250)
  • [L5] Surgical treatment is indicated for patients with objective myelopathic symptoms confirmed by imaging demonstrating spinal cord compression to halt progression of symptoms and improve function in some patients, though perioperative complications can be devastating. [22] (10.5435/jaaos-d-25-00026)
  • [L4] Congenital hypoplasia of the atlas is a rare cause of myelopathy that often presents in the seventh decade of life when accompanied by degenerative changes or torticollis. [23] (10.1097/01.blo.0000223991.26529.45)
  • [L3] It is essential to operate on patients as soon as they develop symptoms of myelopathy to improve surgical results. [24] (10.1007/s004020050296)
  • [L4] Posterior cord syndrome is a rare syndrome best diagnosed clinically and should be considered in cases of cervical spondylotic myelopathy in which motor strength testing is preserved. [27] (10.5435/jaaosglobal-d-23-00027)
  • [L5] The presence of transient neurological abnormalities, especially those precipitated by the opening of the parachute, should warn the clinician of the possibility of serious cervical myelopathy. [30] (10.1016/0020-1383(84)90102-5)
  • [L3] We successfully developed a simple self-administered questionnaire to screen for cervical myelopathy. [32] (10.1186/1471-2474-11-268)
  • [L5] Nontraumatic upper cervical spine instability is a rare condition in children that can lead to permanent neurologic compromise if not diagnosed and managed correctly. [33] (10.5435/00124635-200604000-00005)
  • [L2] These findings help predict which patients are likely to experience meaningful improvements following surgery for degenerative cervical myelopathy. [36] (10.3171/2016.3.focus1665)
  • [L4] [38] (10.2106/00004623-199907000-00007)
  • [L5] [43] (10.5435/00124635-200111000-00003)
  • [L3] In long-course symptomatic cervical OPLL, ACOE provided a modest but clinically meaningful improvement in neurological recovery at 48 months compared with PLF, with low and broadly similar complication rates. [46] (10.1186/s12891-026-09661-9)
  • [L3] In 2 years of clinical observation, LPSF was effective in maintaining the stability of the cervical spine with less sacrifice of mobility and surgical trauma for multilevel myelopathy with segmental instability compared to LCF. [47] (10.1186/s12891-021-04297-3)
  • [L5] Alignment and the characteristics and location of spinal cord compression help determine the ideal surgical approach. [48] (10.5435/jaaos-d-14-00250)
  • [L4] Decompression surgery can be a reasonable treatment option for cervical myelopathy, even in elderly patients. [49] (10.1097/01.blo.0000201156.21701.86)
  • [Case_report] Surgeons should explain the possibility of white cord syndrome before cervical decompression surgery and perform a neurological examination immediately after surgery. [50] (10.1186/s12891-020-3162-3)
  • [L4] Patients with myelopathy or severe stenosis are best treated with surgical decompression. [51] (10.5435/jaaos-22-07-420)
  • [L3] [52] (10.1186/s13018-025-05715-1)
  • [L3] A single-level arthrodesis involving the fifth or sixth cervical vertebra and preexisting radiographic evidence of degeneration at adjacent levels appear to be the greatest risk factors for new disease. [54] (10.2106/00004623-199904000-00009)
  • [L4] Posterior minimally invasive surgery is an effective and safe method for the treatment of cervical spondylosis and is a recommended optional surgical procedure for single-segment myelopathy and radiculopathy. [65] (10.1186/s13018-022-03274-3)
  • [L3] Patients being considered for anterior cervical diskectomy and fusion who have substantial preoperative motor deficits may benefit from earlier surgical intervention. [66] (10.5435/jaaos-d-16-00606)
  • [Case_report] The patient obtained neurological improvement at midterm follow-up with spinal cord decompression and fusion. [67] (10.1016/j.otsr.2011.10.014)
  • [L3] The study reports neurological survivorship of 89.3% at 5 years and 77.3% at 10 years following primary decompressive surgery for DCM. [68] (10.2106/jbjs.22.00218)
  • [L5] Absolute surgical indications for disc herniation include deteriorating neurological deficits with myelopathy or cauda equina syndrome. [71] (10.1302/2058-5241.6.210020)
  • [Paper] Through long-term follow-up, the effect of decompression became observable. [72] (10.1007/s00402-013-1719-4)
  • [L3] The incidence of symptomatic non-fusion segment disease after anterior cervical arthrodesis has multifactorial causes. [77] (10.1186/s13018-018-0717-1)
  • [L2] In patients with cervical radiculopathy, the type and extent of disc herniation measured on MRI prior to surgery correlated neither to the severity of the symptoms at presentation, nor to clinical outcomes at two years postoperatively. [79] (10.1302/0301-620x.104b11.bjj-2022-0657.r2)
  • [L3] The new assessment method based on preoperative MRI cumulative score is simple and useful to assess preoperative severity and predict the results of cervical laminoplasty for cervical spondylotic myelopathy. [80] (10.1007/s004020100288)
  • [L3] [81] (10.1186/s12891-022-06097-9)
  • [L3] Structural and functional changes have taken place in the cervical spinal cord and brain of CSM patients, with brain reorganization playing an important role in maintaining symptoms. [83] (10.1186/s12891-024-07539-2)
  • [L3] 'Skip' corpectomy displays safety comparable to that of posterior decompression and better efficacy for treating four-level cervical spondylotic myelopathy. [101] (10.1186/s13018-014-0063-x)
  • [L5] The case highlights that patients complaining of itching of the dorsolateral forearms of seemingly unknown etiology should undergo a workup of the cervical spine. [106] (10.5435/jaaosglobal-d-19-00178)
  • [L4] Endoscopic decompression of posterior cervical vertebral disorders is a safe, effective, and minimally invasive surgical procedure with rapid recovery times. [107] (10.1186/s12891-019-2920-6)
  • [L3] Anterior cervical surgery effectively improves both physical symptoms and mental health outcomes in patients with cervical spondylotic myelopathy, regardless of preoperative psychological distress. [108] (10.1186/s12891-025-09168-9)
  • [L3] MR T2-hyperintensity and congenital spinal stenosis were identified as independent risk factors for rapidly progressive cervical spondylotic myelopathy. [123] (10.1186/s13018-021-02227-6)
  • [L4] The complete disappearance of deficits in spinal cord function after surgery was the most robust predictor of survival. [125] (10.2106/jbjs.n.01124)
  • [L3] MRI and CTM exhibit a favorable level of agreement (83% to 95%) in predefined surgical threshold measurements of cervical spinal stenosis and cord compression, with axial MRI achieving the highest agreement rate (95%). [130] (10.5435/jaaos-d-25-00122)
  • [L4] [164] (10.2106/00004623-198971020-00002)
  • [L3] [172] (10.1186/s12891-026-09889-5)
  • [L3] The disease showed an earlier onset and more rapid progression in the patients with spinal cord edema due to cervical spondylosis (SCECS) than in those without SCECS. [180] (10.1186/s12891-019-2673-2)

See Also

References

[1] Evidence-based commentary on the diagnosis, management, and further research of degenerative cervical spinal cord compression in the absence of clinical symptoms of myelopathy. Frontiers in Neurology. 2024. DOI: 10.3389/fneur.2024.1341371

[2] Surgery for Cervical Spondylotic Myelopathy: Right Evidence or Evidence Right Now?. Journal of Bone and Joint Surgery. 2013. DOI: 10.2106/jbjs.m.01030

[3] Cervical Myelopathy Caused by Posttraumatic Osteophytes Resulting From Long-Standing Neglected Posterior Atlanto-Occipital Dislocation More Than 30 years: A Case Report. JAAOS: Global Research and Reviews. 2021. DOI: 10.5435/jaaosglobal-d-21-00129

[4] Evaluation and Management of Cervical Spondylotic Myelopathy. The Journal of Bone & Joint Surgery. 1994. DOI: 10.2106/00004623-199409000-00020

[5] Degenerative cervical myelopathy: timing of surgery. EFORT Open Reviews. 2025. DOI: 10.1530/eor-2025-0070

[7] Comparisons of three anterior cervical surgeries in treating cervical spondylotic myelopathy. BMC Musculoskeletal Disorders. 2014. DOI: 10.1186/1471-2474-15-233

[8] Laminoplasty versus laminectomy for multi-level cervical spondylotic myelopathy: a systematic review of the literature. Journal of Orthopaedic Surgery and Research. 2013. DOI: 10.1186/1749-799x-8-45

[9] Resting-state Amplitude of Low-frequency Fluctuation is a Potentially Useful Prognostic Functional Biomarker in Cervical Myelopathy. Clinical Orthopaedics & Related Research. 2020. DOI: 10.1097/corr.0000000000001157

[10] Degenerative Cervical Spondylosis. The Journal of Bone & Joint Surgery. 2007. DOI: 10.2106/00004623-200706000-00026

[11] Orthopaedic Knowledge Update 13 Ebook Without Multimedia. Cervical Degenerative Conditions > Summary.

[12] Risk Factors for Poor Outcome of Cervical Laminoplasty for Cervical Spondylotic Myelopathy in Patients with Diabetes. The Journal of Bone and Joint Surgery-American Volume. 2014. DOI: 10.2106/jbjs.n.00064

[13] Operative Treatment of Cervical Spondylotic Myelopathy. The Journal of Bone & Joint Surgery. 2006. DOI: 10.2106/jbjs.f.00014

[14] Management of Metastatic Cervical Spine Tumors. Journal of the American Academy of Orthopaedic Surgeons. 2015. DOI: 10.5435/jaaos-23-01-38

[15] Laminoplasty versus Laminectomy and Fusion for Multilevel Cervical Spondylotic Myelopathy. Clinical Orthopaedics & Related Research. 2011. DOI: 10.1007/s11999-010-1653-5

[16] Adverse Events Associated With Anterior Cervical Spine Surgery. Journal of the American Academy of Orthopaedic Surgeons. 2008. DOI: 10.5435/00124635-200812000-00005

[17] Campbell S Operative Orthopaedics 4 Volume Set. ANTERIOR CERVICAL DISCECTOMY AND FUSION WITH PLATING > REFERENCES > GENERAL.

[18] Comparison of Anterior and Posterior Surgery for Degenerative Cervical Myelopathy. Journal of Bone and Joint Surgery. 2017. DOI: 10.2106/jbjs.16.00882

[19] Clinical predictors of surgical outcome in cervical spondylotic myelopathy. The Bone & Joint Journal. 2013. DOI: 10.1302/0301-620x.95b7.31363

[20] Are Functional Gains Durable After Decompressive Surgery for Cervical Myelopathy?. Journal of Bone and Joint Surgery. 2023. DOI: 10.2106/jbjs.22.01250

[21] Orthopaedic Knowledge Update 13 Ebook Without Multimedia. Cervical Degenerative Conditions > Annotated References.

[22] Diagnosis and Management of Degenerative Cervical Myelopathy. Journal of the American Academy of Orthopaedic Surgeons. 2025. DOI: 10.5435/jaaos-d-25-00026

[23] Case Reports: Cervical Myelopathy from Atlantal Hypoplasia and Torticollis. Clinical Orthopaedics and Related Research. 2006. DOI: 10.1097/01.blo.0000223991.26529.45

[24] Multiple regression analysis of the factors influencing the results of expansive open-door laminoplasty for cervical myelopathy due to ossification of the posterior longitudinal ligament. Archives of Orthopaedic and Trauma Surgery. 2005. DOI: 10.1007/s004020050296

[27] Failure of Surgical Equipoise in Posterior Cord Syndrome Myelopathy. JAAOS: Global Research and Reviews. 2023. DOI: 10.5435/jaaosglobal-d-23-00027

[30] Cervical myelopathy and transient tetraplegia during free-fall parachuting: a case report. Injury. 1984. DOI: 10.1016/0020-1383(84)90102-5

[32] Development of a self-administered questionnaire to screen patients for cervical myelopathy. BMC Musculoskeletal Disorders. 2010. DOI: 10.1186/1471-2474-11-268

[33] Nontraumatic Upper Cervical Spine Instability in Children. Journal of the American Academy of Orthopaedic Surgeons. 2006. DOI: 10.5435/00124635-200604000-00005

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