Degenerative Cervical Myelopathy (Cervical Spondylotic Myelopathy)

Disease/Disorder

Definition

• Degenerative Cervical Myelopathy (DCM), also referred to as Cervical Spondylotic Myelopathy (CSM), is a progressive degenerative process of the cervical spine that results in narrowing of the central spinal canal and compression of the cervical spinal cord. DCM has been suggested as a preferred term which broadly encompasses all age-related changes in the spinal axis that can cause progressive spinal cord compression independently or in combination, including spondylosis, ossification of the posterior longitudinal ligament (OPLL), and degenerative disc disease.^1-5
•  DCM is a clinical diagnosis based on symptoms and signs of myelopathy in the presence of imaging evidence of cord compression due to degenerative conditions of the cervical spine, typically on magnetic resonance imaging (MRI). It is an umbrella term that encompasses cervical spondylotic myelopathy and cervical degenerative disc disease.^1-4

Etiology

• DCM results from degenerative changes in the cervical spine, including the vertebrae, uncovertebral and facet joints, intervertebral discs, ligaments (ligamentum flavum hypertrophy, posterior longitudinal ligament ossification) and/or connective tissue. It usually develops insidiously but may be precipitated by trauma.^1-9
• It can occur directly by mechanical compression and abnormal movement, and/or indirectly by ischemia due to arterial compression or venous stasis.
• A congenitally narrow canal lowers the threshold by which trivial trauma or degenerative changes may cause myelopathy.^7,8,10
• Congenital and connective tissue disorders, including Klippel-Feil syndrome, Down Syndrome, or Ehlers-Danlos Syndrome can contribute to musculoskeletal instability and premature degenerative changes of the spine.³ Furthermore, genetic factors such as APOE4 and BMP polymorphisms have been associated with increased susceptibility to DCM.³

Epidemiology including risk factors and primary prevention

• DCM is the most common cause of spinal cord dysfunction in adults over age 55.^1-3,6,11
• Men are affected more than women (2.7:1).⁶
• Recent estimates suggest a prevalence of approximately 2.3 % worldwide, but this is likely an underestimate.³
• Despite its burden, diagnosis is often delayed, in part due to heterogenous and non-specific clinical presentations.^1-4 A recent systematic review and meta-analysis reported an average lag of 15 months from onset of symptoms to diagnosis and 11 months from onset of specifically myelopathic symptoms to diagnosis and assessment for surgery.⁴ Another study reported a mean time to diagnosis of about 2.3 years after the first physician visit.¹ This under-recognition contributes to poorer outcomes and underscores the need for greater awareness and standardized diagnostic criteria.
• The more mobile mid-cervical segments, C5 to C7, are most frequently involved.
• Patients over 60 often have multi-segmental disease, with C5 and C6 being the most frequent levels at which compression occurs.⁶
• The average anterior-posterior (AP) diameter of the canal measures about 17 mm from C3-C7. The space required by the spinal cord averages 10 mm. Absolute spinal canal stenosis exists with a sagittal diameter below 10 mm. Stenosis is relative if the diameter is 10-13 mm.¹⁰

Patho-anatomy/physiology

• Static, dynamic, and molecular factors contribute to the pathophysiology of myelopathy.³
• Static factors
  • Disc degeneration is typically an initiating factor for DCM. Decreased height of desiccated intervertebral discs leads to increased sagittal diameter and disc bulging.¹
  • Reactive hypertrophy occurs and osteophytes form at the vertebral end plates.
  • Osteophytes can project from the uncovertebral and facet joints.
  • Hypertrophy of facet capsules and laxity of facet joints¹
  • Ossification or hypertrophy of the posterior longitudinal ligament and the ligamentum flavum^2,3
• Dynamic factors
  • During neck flexion, the spinal cord stretches and can be compressed against osteophytic spurs and intervertebral discs protruding into the canal. With a kyphotic sagittal alignment, the cord can become tethered over spondylotic anterior elements during flexion even though canal diameter is increased.³
  • Hyperextension can also compress the spinal cord between the posterior margin of a vertebrae or a degenerative protruding disc anteriorly, and the laminae or ligamentum flavum posteriorly. The ligamentum flavum buckles into the canal, and the degenerative disc bulges posteriorly.³
  • As spinal segments are stiffened by spondylotic change, adjacent segments may develop relative hypermobility and listhesis, causing cord impingement.
• Histopathological and cellular changes
  • Pressure from constant spinal cord compression can result in neuroischemia and rearrangement of blood supply, infarction, oligodendrocyte apoptosis and subsequent demyelination of adjacent neurons.^3,6,8,9
  • Mechanical compression on the spinal cord’s microvascular structures may result in cystic cavitation, gliosis, central gray and medial white matter degeneration, and Wallerian degeneration of posterior columns and posterolateral tracts and anterior horn cell loss^3,6
  • Chronic demyelination of the neurons in the spinal cord can lead to permanent nerve damage even after surgical decompression.
  • Secondary neural injury likely involves glutamate toxicity, free radical mediated cell injury, and apoptosis.^3,6

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

• Natural history of DCM is variable and inadequately defined, in part due to difficulty in diagnosing early and mild cases.⁴
• Onset is typically insidious but may be acute (e.g., after a fall with hyperextension injury).⁸
• Four unique phenotypes of patients with DCM were identified in a machine learning-based cluster analysis: severe multimodal impairment, minimal impairment, motor dominant, and pain dominant.⁵
• Some patients experience a benign clinical course with neurological improvement, but complete resolution is infrequent.⁸ Improvement rates tend to be higher with a short duration of symptoms.
• Many individuals experience neurological deterioration over time. Stepwise neurological worsening with interspersed periods of quiescent stability is common; less commonly, slow, steady progression may occur.^6,8,12
• Risk factors for neurologic progression are reported to include narrow canal size, circumferential cord compression, female sex, and cervical hypermobility.^6,13
• Balance loss is usually the first symptom patients notice, and it can become quite profound before it is addressed. The recovery of balance after surgical intervention is a slow process.⁷

Specific secondary or associated conditions and complications

• Cervical radiculopathy often occurs concomitantly with DCM.⁸
• Co-existing lumbar stenosis has been reported in a subset of patients.³
• Although DCM is typically a gradually progressive disorder, acute cord compression with central cord syndrome may occur with relatively minor hyperextension trauma.
• Differential diagnosis includes amyotrophic lateral sclerosis (ALS), multiple sclerosis and other demyelinating conditions, other causes of spinal cord dysfunction (tumors; syringomyelia; infectious myelopathy; toxic, inflammatory and nutritional myelopathies), movement disorders, peripheral and entrapment neuropathies, intracranial pathology, and systemic causes of hyperreflexia.^1,2

Essentials of Assessment

History

• Symptoms depend on the magnitude and chronicity of the spinal cord dysfunction.
• It is important to assess the presence, extent, and functional impact of myelopathy-specific symptoms affecting the upper extremities, lower extremities, and autonomic function in individuals with a suspected diagnosis of DCM.^1,2
• Early symptoms include neck pain and stiffness, diminished hand dexterity and subtle changes in balance and gait with leg stiffness, incoordination, and/or weakness.^1,2,6,12
• Pain is common in the neck, shoulders, and arms.
• Symptoms may be limited to the lower extremities in some cases
• Patients may present with frequent falls.⁷
• Initial sensory complaints often predominate in the upper extremities.^1,2
• Compromised bladder or bowel function is less common, and occurs with greater disease severity.^1,2,6,8
• Occipital headache, neck and/or upper extremity pain from associated radiculopathy is common.^1,2,9

Physical examination

• Limited range of motion reflects underlying spondylosis.
• Motor exam^1,2,6,7
  • Patients with DCM and hyperextension injury may present with central cord syndrome (weaker upper limbs compared to lower limbs, and sacral sparing)
  • Finger escape sign: when patient holds fingers extended and adducted, the small finger spontaneously abducts due to weakness of intrinsic muscle.⁷
  • Grip and release test: have the patient make a fist and release 20 times in 10 seconds. Myelopathic patients may struggle to perform this task.⁷
• Upper motor neuron signs
  • Spastic paraparesis is typical, reflecting early involvement of the corticospinal tracts.
  • Pathological reflexes such as Hoffman sign, inverted supinator sign, Babinski sign, lower extremity hyperreflexia, and clonus may indicate cord compression. A normal jaw reflex distinguishes from intracranial pathology.
  • Concomitant lumbar stenosis or peripheral neuropathy may mask lower extremity hyperreflexia.¹
  • Upper motor neuron signs may be accompanied by lower motor neuron signs at the level of cord or root compression (e.g., intrinsic atrophy of hand muscle or muscle wasting and fasciculations of shoulder girdle).
• Sensory exam
  • Altered vibratory and proprioceptive changes are common. Posterior column dysfunction may cause sensory ataxia.
• Gait and balance
  • Broad-based, unstable gait
  • Impaired toe-to-heel walk
  • Positive Romberg test
• Lhermitte sign may be positive ^1,2,6,7

Functional assessment

• Gait, balance, and fall risk should be assessed.^1-3
• Activities of daily living should be evaluated with upper extremity involvement.
• High quality evidence for content validity of outcome measures for assessing DCM is limited.¹⁴ 
• Some outcome instruments that provide clinically meaningful and interpretable information include the modified Japanese Orthopedic Association (mJOA) scale for neurological dysfunction, and the Neck Disability Index (NDI) and Visual Analog Scale (VAS) as pain-related measures.¹⁴
• The mJOA questionnaire is an18-point scale that is used to categorize neurological dysfunction as mild, moderate, or severe, although it doesn’t address other important aspects such as neck pain or frailty.^3,14  It has 4 categories:
  • Motor dysfunction of upper extremities
  • Motor dysfunction of lower extremities
  • Sensory dysfunction of upper extremities
  • Sphincter dysfunction
• The Japanese Orthopedic Association Cervical Myelopathy Evaluation Questionnaire (JOACMEQ) is a patient-reported tool developed to assess the severity of cervical myelopathy across five domains: cervical spine function, upper extremity function, lower extremity function, bladder function, and quality of life.¹⁴
• The NDI is a questionnaire that can been used to assess how DCM-associated neck pain affects daily living. It assesses pain intensity, frequency of headaches, and pain interference with personal care, lifting, reading, and concentration.¹⁴

Laboratory studies

Laboratory studies are done to rule out other conditions.

Imaging

• Radiographs of the Cervical Spine^1-3,6,7
  • Typically, the initial imaging modality
  • Degenerative changes are very common in the general population (more than 60% of patients aged 55 or older, and increasing with age), and positive radiograph findings should not be interpreted in isolation but clinically correlated.²
  • Anterior-posterior (AP), lateral, and oblique views with flexion and extension films provide valuable information. Lateral radiographs best evaluate spinal alignment, ideally under load bearing conditions (e.g., while sitting or standing). AP radiographs can assess vertebral bodies, intervertebral spaces, and pedicles and visualize uncovertebral joint spurs. Oblique views visualize neural foramina, uncovertebral and facet joints, and can reveal foraminal stenosis.^1,2
  • The absolute sagittal diameter of the spinal canal is measured from the posterior aspect of the mid-vertebral body to the spinolaminar line. A reduction to 13 mm or less at C3-C7, or a ratio of canal diameter to mid-vertebral body diameter of 0.8 or less is stenotic.⁷
  • Flexion and extension views assess sagittal range of motion, spondylolisthesis, and instability.^1,2
• At present, MRI is the imaging modality of choice to confirm the diagnosis and evaluate degree of spinal cord and nerve root compression, as it assesses soft tissues and neural elements.^1-3,8
  • Classification systems and tools can be used to characterize the severity of degenerative changes, canal stenosis, and cord compression on MRI.¹
  • However, it is important to keep in mind that the degree of cervical cord compression doesn’t always correlate with clinical severity. Cervical cord compression on MRI may be visualized in many asymptomatic individuals and, conversely, some symptomatic patients have only minimal imaging evidence of compression.³
  • Signal changes in the cervical cord have higher specificity and sensitivity for confirming DCM than imaging evidence of cord compression alone. Clinical severity of DCM has good correlation with hyperintensity signals in T2-weighted MR images (myelomalacia). ³
  • Signal changes of hypointensity on T1-weighted images are reported to correlate with poorer prognosis following surgical decompression.^3,4
  • MRI is also useful to exclude other disorders that may present like DCM (e.g., neoplasms, demyelination, or syringomyelia)^1-3
• Computerized tomography (CT)
  • CT without contrast can provide complementary information to MRI in some cases, and can be more useful in evaluating bony structures, including assessment of an ossified posterior longitudinal ligament.^1-3
  • CT myelography may be considered in patients who cannot have an MRI or have artifact from local hardware.^1-3

Supplemental assessment tools

• Electrodiagnostic testing (nerve conduction studies and electromyography) evaluates concomitant root involvement and excludes other mimicking conditions such as ALS or neuropathies.^1-3,7,8 Findings of radiculopathy often accompany development of DCM. ¹²
• Lumbar spinal imaging assesses concomitant lumbar spinal stenosis.
• While conventional MRI remains the gold standard, advance in imaging techniques such as diffusion tensor imaging (DTI) and magnetic resonance spectroscopy (MRS) show promise for a potential future role in early detection and tracking progression.³

Early predictions of outcomes

• Favorable prognostic indicators: symptoms for less than one year duration, mild myelopathic symptoms, and younger age at initial presentation.^1,3,14
• Motor symptoms tend to be more progressive and less likely to improve than sensory abnormalities.
• MRI findings of T1 hypointense signal changes, and multi-level (but not single-level) T2 hyperintensity signals, have been associated with decreased recovery potential after surgery.⁵

Environmental

Given a high risk of falls, environmental interventions such as eliminating loose rugs to prevent tripping, optimizing ambient lighting, and installing grab bars in the bathroom are important.

Social role and social support system

Old age and associated co-morbidities contribute to a high risk of loss of independence, especially without an adequate social support system.

Professional issues

Symptoms of DCM are often subtle and varied, thus the diagnosis may be missed or misattributed to other conditions.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Lack of high quality, randomized studies and varied natural history of the disease contribute to paucity of definitive treatment guidelines.

At different disease stages

• Although the defining criteria to characterize DCM as mild, moderate, or severe are not standardized, the use of mJOA scale with a score of 15-17 as mild, 12-14 as moderate, and 0-11 as severe myelopathy has been proposed.^3,14 Recent clinical guidelines recommend that patients with mild DCM be conservatively managed with structured rehabilitation and medications, while patients with moderate to severe DCM be evaluated for possible surgical intervention, although a few reports suggest that surgery may be an option even in some mild cases with potential for improving function and quality of life.^5,11,15
• Patients without major neurological deficits but with radiological evidence of cord compression may be treated conservatively and monitored. Function is a more important determinant for surgery than imaging or physical exam findings. The role of surgical decompression in this population remains controversial.
  • Symptomatic treatment with non-steroidal anti-inflammatory drugs (NSAIDs) and gabapentin or other similar medications for neuropathic pain
  • Lifestyle changes include avoiding high-impact activities associated with hyperextension and avoiding aggressive manipulation such as chiropractic treatment or high velocity osteopathic manipulation. Traction has not been proven to improve symptoms or outcomes
  • A soft cervical collar may prevent additional injury by providing sensory feedback to restrain extremes of movement; proof of effectiveness is limited.¹³
• Surgical decompression should be considered in the setting of progressive neurological deterioration, or possibly in other patients with moderate to severe DCM.^3,11,15 The long-term effectiveness of surgery remains inconclusive.
  • Both anterior and posterior surgical approaches have been used and are reported to show similar levels of neurologic and functional recovery, pain and quality of life.^{5, 11,16}Choice of technique depends upon location of the primary compressive lesion, presence of spinal instability, spinal alignment, number of levels involved, and surgeon preference. Ventral surgery may be associated with a higher risk of dysphagia and overall complication rates, while dorsal surgery may be associated with higher incidence of new radiculopathy and impaired wound healing and infections. The differing adverse event profile should be considered as part of shared decision-making with patients.⁵
  • Anterior approaches include anterior cervical discectomy and fusion or cervical corpectomy. The presence of cervical kyphosis usually requires an anterior approach.^11,16
  • Patients with widespread stenosis and multi-segment cord compression, ligamentum flavum buckling, or with technical/mechanical factors that interfere with an anterior approach, may be candidates for posterior decompression. ¹¹
  • Laminectomy alone carries the risk of developing postoperative kyphotic deformity, which is decreased with laminoplasty or laminectomy with fusion. ¹¹
• Rehabilitation interventions depend on the extent and type of deficits and should be considered before surgery, post-operatively, and when surgery is not indicated.^17,18 Mobility assessment, gait training, and fall risk management are essential. Patients with upper extremity weakness and impaired hand dexterity need ADL assessment and training and prescription of appropriate adaptive equipment.
  • Complications of myelopathy such as urinary infections, incontinence, and pressure ulcers should be prevented and promptly managed.

Coordination of care

DCM typically occurs in older individuals with co-morbidities that cumulatively impact function, thus a coordinated, interdisciplinary approach to care is important.

Patient & family education

Patients should be informed of the risks, benefits, and limitations of various surgical and nonsurgical treatment options.

Impairment-based measurement

• Gait analysis, particularly walking speed, e.g., 30-meter-walk test (30MWT)^4,9
• Grip strength evaluation with a dynamometer
• 10-second open-and-close-hand test
• Nine-hole-peg test (9-HPT)^4,9
• mJOA scale⁴

Translation into practice: practice “pearls”

• DCM should be considered if unexplained subtle gait abnormalities or hyperreflexia are present in elderly patients.
• Do not assume that DCM is the primary cause of neurological impairment, just because there is radiological evidence of cervical spondylosis. One still needs to evaluate for other conditions that may explain the patient’s impairment.
• Involvement of the face or cranial nerves, visual or swallowing changes, cognitive impairment, or seizures point to an alternate or co-existing diagnosis.¹

Cutting Edge/Emerging and Unique Concepts and Practice

• Determining the role of genetics in DCM is a promising area of research to individualize treatment.³
• Advances in neuroimaging technology such as spinal diffusion tensor imaging (DTI) and magnetic resonance spectroscopy (MRS), and molecular-based diagnosis, may play a key future role in assessment and management.^3,9
• Minimally invasive techniques can make surgery less invasive in the future.
• Application of artificial intelligence and machine learning analyses has promise to improve categorization of clinical phenotypes with individualization of treatment plans.⁵

Gaps in the Evidence-Based Knowledge

• Controversies persist about the natural history of DCM, the role of conservative versus surgical treatment in patients with mild symptoms, and the comparative merits of various surgical approaches.
• Research is needed to evaluate specific interventions to optimize rehabilitation outcomes.¹⁸
• Research in applying advances in neuroprotective, neuroregenerative, and neuromodulation interventions, which are being studied for traumatic spinal cord injury and other neurological disorders, is very limited in DCM and has been recognized as a future priority.¹⁹
• Riluzole, an FDA-approved agent for ALS, although not found to be effective for primary neurological recovery outcomes, may have promise in reducing neck pain perhaps by attenuating glutaminergic excitotoxicity.  Further investigation is warranted to determine if there is a role of riluzole or other neuroprotective agents such as ibudilast, in a sub-set of patients with DCM. ^2,3,19
• Evaluation of surgical outcomes has been largely based on retrospective cohort studies and further high-quality studies are needed to guide selection of surgical methods and optimal timing of surgical intervention.²⁰

References

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2. Balmaceno-Criss M, Singh M, Daher M, Buchbinder R, Diebo BG, Daniels AH. Degenerative Cervical Myelopathy: History, Physical Examination, and Diagnosis. J Clin Med. 2024 Nov 25;13(23):7139. PMID: 39685599; PMCID: PMC11642449.
3. Hejrati N, Pedro K, Alvi MA, Quddusi A, Fehlings MG. Degenerative cervical myelopathy: Where have we been? Where are we now? Where are we going? Acta Neurochir (Wien). 2023 May;165(5):1105-1119. PMID: 37004568.
4. Malone A, Sofiany M, Dawood G, Wright J, Ryan R, Treanor C, Gallagher C, Lenehan W, Doyle F, Bolger C. Duration of symptoms before diagnosis in degenerative cervical myelopathy: A systematic review and meta-analysis. Brain Spine. 2025 Apr 16;5:104252. doi: 10.1016/j.bas.2025.104252. PMID: 40343073; PMCID: PMC12059671.
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6. Kalsi-Ryan S, Karadimas SK, Fehlings MG. Cervical spondylotic myelopathy: the clinical phenomenon and the current pathobiology of an increasingly prevalent and devastating disorder. Neuroscientist. 2013;19(4):409-21.
7. McCormick JR, Sama AJ, Schiller NC, Butler AJ, Donnally CJ III. Cervical spondylotic myelopathy: a guide to diagnosis and management. J Am Board Fam Med 2020;33:303–313.
8. Onofrei LV, Henrie AM. Cervical and Thoracic Spondylotic Myelopathies. Semin Neurol. 2021 Jun;41(3):239-246. doi: 10.1055/s-0041-1725144.
9. Tu J, Vargas Castillo J, Das A, Diwan AD. Degenerative Cervical Myelopathy: Insights into Its Pathobiology and Molecular Mechanisms. J Clin Med. 2021 Mar 15;10(6):1214.
10. Morishita Y, Naito M, Hymanson H, Miyazaki M, Wu G, Wang JC. The relationship between the cervical spinal canal diameter and the pathological changes in the cervical spine. Eur Spine J. 2009 Jun;18(6):877-83.
11. Wu JC, Ko CC, Yen YS, Huang WC, Chen YC, Liu L, Tu TH, Lo SS, Cheng H. Epidemiology of cervical spondylotic myelopathy and its risk of causing spinal cord injury: a national cohort study. Neurosurg Focus. 2013 Jul;35(1):E10
12. Klineberg E. Cervical spondylotic myelopathy: a review of the evidence. Orthop Clin North Am. 2010;41(2):193-202.
13. Shimomura T, Sumi M, Nishida K, Maeno K, Tadokoro K, Miyamoto H, Kurosaka M, Doita M. Prognostic factors for deterioration of patients with cervical spondylotic myelopathy after nonsurgical treatment. Spine (Phila Pa 1976). 2007 Oct 15;32(22):2474-9.
14. Yanez Touzet A, Bhatti A, Dohle E, Bhatti F, Lee KS, Furlan JC, Fehlings MG, Harrop JS, Zipser CM, Rodrigues-Pinto R, Milligan J, Sarewitz E, Curt A, Rahimi-Movaghar V, Aarabi B, Boerger TF, Tetreault L, Chen R, Guest JD, Kalsi-Ryan S, McNair AG, Kotter M, Davies B; AO Spine RECODE-DCM Steering Committee. Clinical outcome measures and their evidence base in degenerative cervical myelopathy: a systematic review to inform a core measurement set (AO Spine RECODE-DCM). BMJ Open. 2022 Jan 19;12(1):e057650. PMID: 35046007.
15. Fehlings MG, Tetreault LA, Riew KD, Middleton JW, Aarabi B, Arnold PM, Brodke DS, Burns AS, Carette S, Chen R, Chiba K, Dettori JR, Furlan JC, Harrop JS, Holly LT, Kalsi-Ryan S, Kotter M, Kwon BK, Martin AR, Milligan J, Nakashima H, Nagoshi N, Rhee J, Singh A, Skelly AC, Sodhi S, Wilson JR, Yee A, Wang JC. A Clinical Practice Guideline for the Management of Patients With Degenerative Cervical Myelopathy: Recommendations for Patients With Mild, Moderate, and Severe Disease and Nonmyelopathic Patients With Evidence of Cord Compression. Global Spine J. 2017 Sep;7(3 Suppl):70S-83S
16. Yoshii T, Egawa S, Chikuda H, Wakao N, Furuya T, Kanchiku T, Nagoshi N, Fujiwara Y, Yoshida M, Taguchi T, Watanabe M. A systematic review and meta-analysis comparing anterior decompression with fusion and posterior laminoplasty for cervical spondylotic myelopathy. J Orthop Sci. 2021 Jan;26(1):116-122.
17. Catz A, Watts Y, Amir H, Front L, Gelernter I, Michaeli D, Bluvshtein V, Aidinoff E. The role of comprehensive rehabilitation in the care of degenerative cervical myelopathy. Spinal Cord. 2024 May;62(5):200-206. doi: 10.1038/s41393-024-00965-y. Epub 2024 Mar 4. PMID: 38438531; PMCID: PMC11176072.
18. Boerger TF, Hyngstrom AS, Furlan JC, Kalsi-Ryan S, Curt A, Kwon BK, Kurpad SN, Fehlings MG, Harrop JS, Aarabi B, Rahimi-Movaghar V, Guest JD, Wilson JR, Davies BM, Kotter MRN, Koljonen PA. Developing Peri-Operative Rehabilitation in Degenerative Cervical Myelopathy [AO Spine RECODE-DCM Research Priority Number 6]: An Unexplored Opportunity? Global Spine J. 2022 Feb;12(1_suppl):97S-108S. PMID: 35174735; PMCID: PMC8859699.
19. Gharooni AA, Kwon BK, Fehlings MG, Boerger TF, Rodrigues-Pinto R, Koljonen PA, Kurpad SN, Harrop JS, Aarabi B, Rahimi-Movaghar V, Wilson JR, Davies BM, Kotter MRN, Guest JD. Developing Novel Therapies for Degenerative Cervical Myelopathy [AO Spine RECODE-DCM Research Priority Number 7]: Opportunities From Restorative Neurobiology. Global Spine J. 2022 Feb;12(1_suppl):109S-121S. doi: 10.1177/21925682211052920. PMID: 35174725; PMCID: PMC8859698.
20. Fehlings MG, Badhiwala JH, Ahn H, Farhadi HF, Shaffrey CI, Nassr A, Mummaneni P, Arnold PM, Jacobs WB, Riew KD, Kelly M, Brodke DS, Vaccaro AR, Hilibrand AS, Wilson J, Harrop JS, Yoon ST, Kim KD, Fourney DR, Santaguida C, Massicotte EM, Kopjar B. Safety and efficacy of riluzole in patients undergoing decompressive surgery for degenerative cervical myelopathy (CSM-Protect): a multicentre, double-blind, placebo-controlled, randomised, phase 3 trial. Lancet Neurol. 2021 Feb;20(2):98-106. PMID: 33357512.

Bibliography

Sabharwal S. Cervical Spondylotic Myelopathy. In: Sabharwal S, ed. Essentials of Spinal Cord Medicine. New York, NY: Demos Medical Publishing; 2014.

Original Version of the Topic

Sunil Sabharwal, MD. Cervical Spondylotic Myelopathy. 6/7/2013

Previous Revision(s) of the Topic

Jennifer Yang, MD, Nasser Ayyad, DO, Sunil Sabharwal, MD. Cervical Spondylotic Myelopathy. 11/18/2017

Jaimie John, MD, Rafer Willenberg, MD, PhD, Sunil Sabharwal, MD. Cervical Spondylotic Myelopathy (Degenerative Cervical Myelopathy). 7/14/2022

Author Disclosures

Sunil Sabharwal, MD
Demos Medical publishing, Receipt of Royalties, Book author/editor

Ankur Gupta, MBBS
Nothing to Disclose

Hank Shipman, MD
Nothing to Disclose

Kyutae “Alex” Kim, MD
Nothing to Disclose