Degenerative Cervical Myelopathy: Natural History, Clinical Presentation, Current Diagnosis and Treatment Review

Fernando Luís Maeda1, MD; Andrei Fernandes Joaquim2, MD, PhD

1 Neurosurgery Resident. Department of Neurosurgery, University of Campinas (UNICAMP), Campinas, Brazil;
2 Professor of Neurosurgery. Department of Neurosurgery, University of Campinas (UNICAMP), Campinas, Brazil.

Conflict-of-interest statement: The author(s) declare(s) that there is no conflict of interest regarding the publication of this paper.

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Correspondence to: Fernando Luís Maeda, MD, Department of Neurosurgery, University of Campinas (UNICAMP), 126, Tessália Vieira de Camargo, Campinas, São Paulo, 13083-887, Brazil.
Email: fernandomaeda89@gmail.com
Telephone: +55-19986020004
Fax: +55-1935217483

Received: May 25, 2020
Revised: July 5, 2020
Accepted: July 10 2020
Published online: August 28, 2020


Degenerative cervical myelopathy is a chronic, nontraumatic compression and progressive disease of the cervical spinal cord. Osteoarthritic degeneration (spondylosis, facet hypertrophy, degenerative disc disease), ligament changes (ossification of the posterior longitudinal ligament, hypertrophy of the ligamentum flavum) and ischemia (secondary ischemic injury) may lead to spinal cord compression and result in neurological deficits. Clinically, the appendicular function is mainly affected, as well as gait and urinary function. Duration and degrees of compression are negatively correlated with prognosis. Non-operative treatment can be performed in mild symptomatic cases; however, surgical treatment may possibly improve the natural course of cervical myelopathy disease by stopping progression or avoiding deterioration and, in some cases, restoring some neurological function.

Key words: Cervical Myelopathy; Degenerative Cervical Myelopathy; Degenerative Disc Disease; Cervical Spondylotic Myelopathy; Ossification of Posterior Longitudinal Ligament; Ossification of Ligamentum flavum; Anterior Cervical Discectomy and Fusion

© 2020 The Authors. Published by ACT Publishing Group Ltd. All rights reserved.

Maeda FL, Joaquim AF. Degenerative Cervical Myelopathy: Natural History, Clinical Presentation, Current Diagnosis and Treatment Review. International Journal of Orthopaedics 2020; 7(3): 1313-1321 Available from: URL: http://www.ghrnet.org/index.php/ijo/article/view/2909

ACDF: Anterior cervical discectomy and fusion
CSM: Cervical spondylotic myelopath
CT: Computed tomography
DCM: Degenerative cervical myelopathy 
DDD: Degenerative disc disease
DTI: Diffusio: n tensor imaging
JOA Score: Japanese Orthopaedic Association Score
LF: Ligamentum flavum
mJOA: score modified Japanese Orthopedic Association Score
MRI: Magnetic resonance imaging
OLF: Ossification of ligamentum flavum
OPLL: Ossification of the posterior longitudinal ligament
PEEK: Polyetheretherketone
PLL: Posterior Longitudinal Ligament
QALY Scale: Quality Adjusted Life Year Scale
SCI: Spinal Cord Injury
VAS: Visual analog scale


Degenerative Cervical Myelopathy (DCM) is a chronic, non-traumatic condition caused by disc, bone, and ligament changes in the cervical spine, which results in dynamic and static spinal cord narrowing and compression[1].

DCM includes a combination of disc disease [e.g. degenerative disc disease (DDD)], bone changes [e.g. cervical osteoarthritis (spondylosis), spondylolisthesis, subluxation] and ligament impairment [e.g. hypertrophy, calcification, ossification of the ligamentum flavum and calcification of the posterior longitudinal ligament (OPLL)][2,3] (Figure 1). All these anatomical changes contribute to the static and dynamic compression of the spinal cord. Flexion and extension movements can cause narrowing of the cervical canal through the “Pincer mechanism”[4,5] (Figure 2).

Figure 1 Cervical Spinal Cord normal anatomy and degenerative process. A: Uncinate process hypertrophy; B: Osteophyte, Hypertrophy of Posterior Longitudinal Ligament (LLL) or Ossification of PLL; C: Uncovertebral joint hypertrophy; D: Ossification or hypertrophy of ligamentum flavum.

Figure 2 Pincer mechanism. Narrowing of the cervical spinal canal due to flexion and or extension movement.

DCM is the main cause of nontraumatic spinal cord compression worldwide. Usually, it affects patients during the fifth or the sixth decade of life[6,7]. Patients can be asymptomatic or even present severe deficits, according to the compression degree and ischemic spinal cord injuries[8]. Fortunately, the majority of the cases are asymptomatic or mildly symptomatic. Symptoms include tingling, numbness, weakness, gait impairment, neck pain, radiculopathy, loss of coordination, fine motor skills deteriorations, and difficult bladder control[9,10]. Because of the mild cases, the incidence (4.1 / 100.000) and prevalence (60.5 / 100.000) seem to be underestimated[6,11-13].

Clinically, it causes a slow and progressive neurological impairment, with a stepwise pattern of quiescent disease periods before deterioration. Naturally, 20 to 62% of patients with DCM will deteriorate neurologically within 3 to 6 months[14]. Otherwise, acute presentation is not common, except when precipitated by trauma or acute disc herniation[15].

Asymptomatic and mildly symptomatic patients with evidence of spinal cord compression must be closely monitored, clinically and radiologically, and surgery should not be done unless they become more symptomatic[16,17]. Moderate and severe cases should be surgically treated[16,18]. However, long-term compression, age, spinal cord atrophy, low signal on T1-weighted images, and high signal on T2-weighted on MRI are signs of poor outcome[19-21].


Classically, the CSM pathophysiology is explained by a mixture of mechanical dysfunction and genetic disorders. Static factors (e.g. spondylosis, disc degeneration, OPLL, ossification of the ligamentum flavum, congenital stenosis, etc.) contribute to narrow the spinal canal and may cause direct spinal cord compression[10]. Dynamic dysfunctions (e.g. neck flexion and extension) contribute to additional narrowing of the spinal canal by the Pincer mechanism[14,22]. Neck flexion could result in anterior spinal cord compression against cervical osteophytes, hypertrophy, or OPLL, while neck extension could result in posterior spinal cord compression against hypertrophy of the uncinate process or facet and ossification or hypertrophy of ligamentum flavum[3,4,23]. Furthermore, additional stretching forces during flexion-extension movements could make the spinal cord more susceptible to physiological changes and secondary damage[5,24].

However, these mechanisms are not enough to explain differences in clinical presentations in patients with similar degrees of compression. Secondary injuries (e.g. decreased spinal cord perfusion, venous congestion, and spinal cord ischemia) and endogenous responses (e.g. neuroinflammation and apoptosis) are a complementary mechanism to the pathophysiology of CSM. The additional molecular mechanism remains unclear[25].

Natural History

Cervical Myelopathy (CM) most occurs in men (2.4:1) between the 5th and 6th decade of life[12]. The most frequently involved level is C5-6[26]. Historically, CM was described as a constellation of symptoms. At the onset, the patient may present clumsiness, gait impairment, weakness, daily activity compromises, neck pain, shoulder pain, and neurogenic bladder[1,8]. Once clinical manifestations start, remission to normality usually does not occur. Motor changes persist and tend to progress over time.

Patients present mild symptoms at the initial phase, usually described as Nurick grade II 27 (Table 1)[28]. Diagnosis and referral to a specialist are usually delayed and may result in later surgical treatment[29]. Good access to health care providers, greater technical knowledge about CSM, and improvements in diagnostic methods facilitated the diagnosis[30]. However, this reduction in time does not seem enough. In the 1950s, the delay in diagnosis from the first symptoms was 6.3 years, while recent studies show a delay of 2.2 years[29,31]. Since symptoms start, remission to normality does not occur and motor changes usually persist and tend to progress. Deterioration may occur in three different patterns. Stepwise progression is the most common form and occurs in 75% (Figure 3A). It means a sequence of stable and sudden worsening periods. In 20% of cases, occur slow and steady deterioration (Figure 3B) and only 5% of patients experience stability after an initial symptom 10 (Figure 3C).

Clinical treatment may be useful in the early stages and mild symptoms. Nevertheless, since symptoms get worse, especially in Nurick III, IV, and V, surgery should be considered[16].

Table 1 NURICK Clinical Scale 31.
0Signs or symptoms of root involvement but without evidence of spinal cord disease
1Signs of spinal cord disease but no difficulty in walking
2Slight difficulty in walking which does not prevent full-time employment
3Difficulty in walking which prevented full time employment or the ability to do all housework, but which was not so severe as to require someone else's help to walk
4Able to walk only with someone else's help or with the aid of a frame.
5Chairbound or bedridden.

Figure 3 Three different patterns of clinical deterioration of CSM patients. A: Stepwise pattern; B: Slow and steady deterioration and C: stability after initial symptom.

Evaluation and Diagnosis

Symptomatic cervical spondylosis (CS) may present axial neck pain, radiculopathy, myelopathy, or a combination of these entities. The medical history and clinical evaluation should be considered in order to differentiate and exclude the differential diagnosis[32], which should receive some special attention. Amyotrophic lateral sclerosis, multiple sclerosis, low hydrocephalus pressure, carpal tunnel, and radiculopathies can cause misdiagnosis[33].

Myelopathy may present itself with weakness, clumsiness, gait impairment, neurogenic bladder. Axial cervical pain may result in muscular strain, regional myofascial pain, referred shoulder pain, while radiculopathy generates symptoms along with nerve roots[34].

The unspecific symptoms delay the diagnosis in early myelopathic stages. Limb weakness and gait impairment tend to be undervalued. Evaluation by an expert and monitoring with assessment tools facilitate the follow-up of these patients and the decision for the best treatment. Nurick score and modified Japanese Orthopedic Association score (mJOA) are the most common, useful and standardized assessment tools for CSM evaluation. However, Cooper myelopathy scale (CMS), Prolo Scale (PS) and European Myelopathy Score (EMS) also have their relevance[28,35-37].

The physical examination should include cervical range motion, evaluation of pyramidal signs (Hoffmann, Tromner, Babinski, ankle clonus), sensorial, tendon reflexes, gait and balance evaluation[38-40]. Classical findings include limitations of cervical motion, spasticity, hyperreflexia, pyramidal signs, and abnormal gait[41-43]. As a degenerative disease of the spinal cord, concomitant lumbar spinal stenosis may be present in 15 to 33 % of CSM patients[44,45]. In these cases, lower limb hyporeflexia may be present as well.

Spurling maneuver composed by cervical extension, side bending, and axial compression may reproduce ipsilateral radicular pain, generally in the setting of an ipsilateral foraminal stenosis[46]. In myelopathic patients, cervical flexion may trigger a sudden transient electric-like shock extending down the spine (Lhermitte’s sign)[47].

Evaluation of strength, sensitivity, and tendon reflexes contributes to the differentiation between cervical radiculopathy, peripheral nerve compression syndromes, and global deficits 48. Special signs contribute to cervical myelopathy diagnosis, including shoulder girdle muscular atrophy, fasciculations and myelopathic hand defined by failing in 10 seconds of grip and release test (10SGRT), 30-meter walking test (30MWT), 10 seconds step test (10SST), uncoordinated finger motion and Wartenberg’s sign (finger escape sign)[49-52].

The finger escape sign is involuntary abduction of the fifth finger caused by weakness in finger adduction in CSM evidenced by keeping the fingers extended and abducted for 30-60 seconds[53]. The 10SGRT is used to assess impairment in the upper limbs and manual dexterity. This test is positive when the patient is unable to rapidly open and close the hand into a fist at least 20 times in 10 seconds[54]. The 30 MWT and the 10SST are used in clinical practice and research to objectively measure gait impairment[55,56].

In myelopathic patients, not only gait balance is impaired, but also the gait pattern. Instead of heel-to-toe walk, severe myelopathic gait is characterized by limited propulsion due to weakness in the lower limb and compensation by the proximal hip musculature[57,58]. It results in decreased knee flexion, limb hyperextension, decreased step speed and length and increased stance width in stance phase, and slower plantar flexion in the swing phase[59].

Imaging methods are essential for diagnosis, outcome, surgical planning, and postoperative follow-up. Radiography, computed tomography (CT) and magnetic resonance image (MRI), have specific peculiarities and goals. All patients with a compatible clinical history and neurological abnormalities detected during the physical examination should be evaluated with a cervical spine MRI[60]. Anteroposterior cervical X-ray may reveal a cervical rib or scoliosis, while the lateral view may reveal a reduced disc space, osteophytes, and sagittal alignment. Besides, dynamic examination with flexion and extension x-rays can provide important information about segmental instability, usually adjacent to hypomobile segments[61]. CT allows visualization of details of bone anatomy, evaluation of spondylosis, OPLL, ossification of the ligament flavum, bone compression and it is also useful for surgical instrumentation planning, and 3D reconstruction[62]. However, it is limited to soft tissue analysis[63]. MRI gives details of soft tissue anatomy, spinal cord compression, intervertebral disks, ligaments, microhemorrhage, syrinx, myelomalacia, intramedullary signal change, but it lacks information regarding bone anatomy[64]. Of note, MRI is considered the gold standard exam for CSM diagnosis and to rule out differential diagnosis.

The normal diameter of the cervical spinal canal on the sagittal plane varies from 17 mm on C3 to 13 mm on the C7 level[65]. Cervical canal stenosis can be measured in the midsagittal plane through the ratio between the spinal canal and the vertebral body diameter of the same level (Figure 4). Ratio < 0.8 represents severe cervical stenosis, while ratio < 0.4 is related to poor outcome (table 1)[66-68]. In the axial plane, spondylosis causing narrowing greater than 30% or below 60 mm2 is related to compression of long tracts and appearance of symptoms[69].

Figure 4 Cervical canal measure for stenosis evaluation. Torg-Pavlov ratio: canal / vertebral body width (A/B).

Meantime, isolated radiological findings without clinical symptoms do not confirm a diagnosis of cervical myelopathy. Degenerative changes are commonly found in asymptomatic patients and tend to become more prevalent with aging. In patients up to 50 years old, only 25-50% of the MRI show degenerative changes, while at a 65-year-old population almost 75-85% present degeneration and that is due to aging[13,70]. Therefore, the diagnosis of CSM should always consider the medical history and physical examinations compatible with the clinical condition.

Electrophysiological tests usually provide additional information to clinical and neuroimaging findings[34,71]. They are useful to localize spinal cord lesions or radiculopathy syndromes in pre-operative evaluation. They are also useful for post-operative evaluation and follow-up. Somatosensory Evoked Potential (SSEP) and Motor Evoked Potential (MEP) are helpful to evaluate the integrity of the spinal cord tracts, while Electromyography (EMG) and Nerve Conduction Study (NCS) are sensitive tests used to differentiate peripheral nerve disorders that can mimic CSM[72].

Prognostic factors

Many prognostic factors in CSM has been studied and evaluated. Patient’s age, duration of symptoms, preoperative neurological status, radiological findings including the number of levels of compression, effective canal diameter, and intrinsic signal changes in the cord, are the most important of them[36,73-75]. Understanding the clinical factors that predict a proper surgical treatment outcome is of fundamental importance to make therapeutic decisions[76].

Studies differ concerning the cutoff point of the age group that would present the best prognosis for surgical treatment[77-79]. It is known that younger patients have a greater chance of clinical improvement, especially when they are under 65 years old[80].

On MRI studies, preoperative spinal cord area and intramedullary signal changes are related to poor outcome[81]. The intramedullary signal is related to tissue relaxation and increased water content in spinal cord injuries. Due to this fact, T2 sequences are affected earlier than T1 and T1 hypointense signals will always be accompanied by T2 hyperintense signals[82]. Therefore, T2 hyperintense signal is a marker of early myelopathy and the T1 hypointense signal is correlated to advanced spinal cord injury[83,84]. The hyperintense signs of the spinal cord were described as three types of Increased Signal Intensity (ISI) on T2-weighted MRI images: Type-1: none, Type-2: light and diffuse area, and Type-3: bright, strong hyperintense well-circumscribed[85]. Only the Type-2 was correlated to poor outcome[86].

Prolonged MEPs and SSEPs, MRI abnormalities, and symptomatic radiculopathy have been described as important predictors of early myelopathy development[87]. When compared to MRI, electrophysiological tests tend to detect earlier the risk of progression into myelopathy[88].


Asymptomatic patients with positive MRI or electrophysiological tests should be observed closely due to the risk of myelopathy development. Mild symptomatic patients may be treated non-operatively with bed rest, physical therapy, medication, injections, and orthoses. Recent studies showed similar outcomes for conservative and surgical treatment used in mild symptomatic patients (mJOA ≥ 13)[89-91].

Moderate and severe CSM cases should be surgically treated since the disease will progress with neurological deterioration in the majority of the cases[92]. Surgery should be done as soon as possible because when performed at earlier stages it presents better functional outcomes [93].

The objectives of surgical treatment are to decompress the cervical spine, restore cervical alignment, and ensure the stabilization of the involved segments. To obtain these results, several anterior, posterior, or combined approaches were described. The choice of the most appropriate technique is out of the scope of this review, but should consider the patient’s age, general medical condition, number of levels to be treated, site of compression, cervical alignment, and instability, previous treatment, bone quality, and surgeon’s preference[94-97].

Clinical Cases

Case 1

We report two illustrative cases. A 46-year-old man who had cervical pain radiating to his right upper arm with weakness sensation in both arms. He was diagnosed with CSM and radiculopathy and underwent surgical treatment 2 months after the diagnosis. During the physical examination, he had normal motricity, a positive Spurling maneuver, pyramidal sign (Hoffman and Tromner) in the right side. He had a Nurick Scale grade 1 and scored 15 on mJOA scale.

Pre-operative Cervical computed tomography showed three levels of cervical stenosis (C3/4, C4/5 and C5/6). Further evaluation with MRI showed three levels of anterior compression due to herniated disc and posterior ligament hypertrophy on the right portion of spine canal (Figure 5).

Initially, the patient was treated conservatively with pain killers, however, pain became unbearable with limitation of daily activities. We performed three levels of anterior cervical discectomy and fusion (ACDF), with good decompression, lordosis restauration and clinical improvement (Figure 6).

Patient evaluated with pain control and improved muscle strength in the right side. According to clinical evaluation scales, patient improved his results. He scored 18 at mJOA and was classified as Nurick grade 0.

Figure 5 Pre-operative images. A: Sagittal CT of cervical spine showing C3/4, C4/5, C5/6 cervical stenosis and degenerative process. B and C: Axial MRI of cervical spine showing spinal cord compression mainly on antero-lateral portion. D: Sagittal T1 MRI showing C3/4, C4/5 and C5/6 anterior compression. E: Sagittal T2 MRI showing C3/4, C4/5 and C5/6 anterior compression.

Figure 6 Post-operative images. A: Sagittal CT showing Anterior cervical discectomy and fusion C3/4, C4/5 and C5/6. B: Sagittal view of 3D-CT reconstruction of ACDF.

Case 2

We present a 64-year-old man with difficulty to walk and weakness in his right side. He was diagnosed with CSM and underwent surgical treatment after 3 months. The patient presented instable gait and needed support to walk. Babinski reflex, Hofmann and Tromner signs were bilaterally present. He scored 12 at mJOA scale and was classified as Nurick grade 3.

Imaging evaluation demonstrated cervical stenosis at C4/5 and C5/6 levels (Figure 7). Patient underwent surgical treatment with posterior cervical decompression and fusion (Figure 8).

Patient improved his gait and strength. He scored 17 at mJOA scale and was reclassified as Nurick 1.

Figure 7 Pre-operative CT images. A: Axial view of cervical spine at most critical cervical stenosis level (C5/6). B: Sagittal view of cervical spine showing C4/5 and C5/6 cervical stenosis.

Figure 8 Post-operative images. A: Left posterior cervical fusion C3-6. B: Posterior cervical spinal canal decompression C4-6. C: Right posterior cervical fusion C3-6. D: Axial view of posterior cervical decompression. E: Coronal 3D-CT reconstruction of posterior cervical fusion.


CSM is the main cause of spinal cord dysfunction in adults. Symptoms may be unspecified, which delays the diagnosis. From the point when patients present neurological impairment, it usually tends to progress over time, with a stepwise progression occurring in 75% of the cases.

Mild symptomatic cases could be treated non-operatively by an expert with bed rest, physical therapy, medications, injections, and orthoses. A regular follow-up should be done to assess the clinical conditions. If the symptoms progress and the patient gets a worse score at mJOA or Nurick scale, a surgery should be done.

Surgical treatment aims to decompress the spinal canal, keep the cervical alignment, and avoid or correct cervical instability. Anterior, posterior or combined approaches for the cervical spine were described. The choice for the best treatment should consider the patient’s age, comorbidities, clinical status, previous surgery, bone quality, number of levels to treat, site of compression, cervical alignment, and stability. When there is no evidence of the superiority of any techniques, the surgeon’s preference must be considered.


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