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 Table of Contents  
Year : 2019  |  Volume : 2  |  Issue : 1  |  Page : 5-12

Natural history, prevalence, and pathophysiology of cervical spondylotic myelopathy

Department of Neurosurgery, AMRI Hospitals Salt Lake, Kolkata, West Bengal, India

Date of Web Publication11-Jan-2019

Correspondence Address:
Dr. Gomatam Raghavan Vijay Kumar
1702 Tritiya, Upohar Luxury Complex, 2052 Chakgaria, Kolkata - 700 094, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/isj.isj_48_18

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This study is a narrative review performed to summarize the current knowledge about the epidemiology, natural history and pathogenesis of cervical spondylotic myelopathy (CSM). A comprehensive search was undertaken to look at all available articles between January 1, 1956 to May 1, 2018, on PubMed and the Cochrane Collaboration Library. The natural history of CSM is variable. The main determinants of the clinical course of CSM are the extent of neurological impairment, age, cervical instability, abnormalities of cord conduction, canal diameter, congenitally stenotic spinal canal and the extent of involvement and tract disruption on diffusion tensor imaging (DTI) imaging. There is little data on the true incidence and prevalence of CSM across the globe and none from India. The pathoanatomic basis of CSM is cord compression, either dynamic or static. The biological events that are thought to play a significant role in the development of CSM are ischemia, derangement of the blood-spinal cord barrier, chronic neuronal inflammation, and apoptosis. Emerging knowledge about the molecular biology holds promise for potential intervention, both for prevention and for cure, of this common and debilitating condition.

Keywords: Cervical, epidemiology, incidence, myelopathy, natural history, pathophysiology, prevalence, spondylosis

How to cite this article:
Vijay Kumar GR, Ray DK, Das RK. Natural history, prevalence, and pathophysiology of cervical spondylotic myelopathy. Indian Spine J 2019;2:5-12

How to cite this URL:
Vijay Kumar GR, Ray DK, Das RK. Natural history, prevalence, and pathophysiology of cervical spondylotic myelopathy. Indian Spine J [serial online] 2019 [cited 2023 Apr 1];2:5-12. Available from: https://www.isjonline.com/text.asp?2019/2/1/5/249899

  Incidence and Prevalence of Cervical Spondylotic Myelopathy Top

Cervical spondylotic myelopathy (CSM) is the most common progressive, nontraumatic disorder of the spinal cord in adults.[1],[2] Delay in diagnosis is common, and patients usually present with bilateral neurological deficits like “clumsy hands,” “unsteady gait,” and Lhermitte's sign. A thorough search of the indexed medical literature was conducted to ascertain the incidence and prevalence of CSM.

In the international literature, magnetic resonance imaging (MRI)-based population studies have revealed that more than 85% of the adults aged above 60 years have severe degeneration of at least one cervical level.[3] Since the incidence of radiculopathy and myelopathy is much lower, it can be inferred that most patients are usually asymptomatic, with the average age at diagnosis being about 64 years. CSM is more common in men compared to women, with a ratio of 2.7:1.

Nouri et al. did a narrative review and concluded that the incidence and prevalence of CSM was about 41 and 605 respectively per 1,000,000 population in North America.[4] Wu et al. did a 12 year retrospective cohort study using the National Health Insurance Research Database and concluded that the overall incidence of CSM related hospitalization was 4.04 per 100,000 person-years in Taiwan, with a higher incidence in elderly males.[5] Boogaarts and Bartels estimated the prevalence of CSM to be 1.60 per 10,000 population based on the number of cases that were treated surgically at a hospital in The Netherlands.[6] Salemi et al. conducted a door-to-door survey in a Sicilian municipality and found the prevalence of cervical spondylotic radiculopathy to be 3.5 per 1000 population with a peak in the 50–59 year age group.[7] Patel et al. conducted a retrospective population-based genealogic database study of over 2 million residents of Utah, USA and found an inherited predisposition to cervical spondylosis with myelopathy.[8] They concluded that this would help in identification of high-risk CSM pedigrees. Using electrophysiology studies, Tani et al. documented a high incidence of conduction block at C3–C4 (55%) or C4–C5 (45%) level in the elderly Japanese population aged over 65 years, whereas C5–C6 was the most common site of involvement in middle-aged patients.[9] [Table 1] summarizes some of the studies in the literature with a brief description of the salient points of the publication. Unfortunately, we were unable to find studies documenting the incidence and prevalence of CSM in different regions of India.
Table 1: Summary of some studies of the natural history and prevalence of cervical spondylotic myelopathy

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  Natural History Top

CSM was described as far back as the late 19th century by C. Aston Key, who based on autopsies, opined that many of the cases of paraplegia were attributable to affection of the ligaments of the spine.[17] The prevalence of cervical spondylosis along with associated myelopathy is increasing with increase in life expectancy. Given the near universal occurrence of degeneration and spondylosis with age, the natural history of the disease needs to be elucidated and understood so as to guide appropriate therapeutic choices. Unfortunately, while the management of severe CSM is well defined, there is no such consensus on the natural history or appropriate form of intervention for more subtle forms of the disease. There remains a lack of clarity regarding its course, and as a result, management suffers from wide variation resulting from individual experiences and institutional dogmas. This is, at least in part, because the disease behaves differently in different individuals with some experiencing a progressive decline and others having long periods of dormancy during which they improve or are neurologically stable. It may also not be ethically sound to prospectively randomize patients with progressive or severe forms of the illness.

Early investigators reported a relatively benign course in their patients. Clarke and Robinson reported a clinically stable course interrupted by episodes of deterioration in 75% of their conservatively treated patients while 5% remained stable throughout after an initial symptomatic phase.[10] Only 20% showed progressive deterioration over time. Lees and Turner reported that about 67% of their conservatively treated patients with CSM improved over time.[18] Subsequently, Symon and Lavender took a different view in their published series which pointed at a more relentless and disabling course.[19] Phillips in 1973 reported a series of 102 cases accumulated over a 10-year period and his results favored surgery with most of his operated patients showing sustained improvement.[20] Sadasivan et al. in a retrospective analysis of 22 patients reported a mean time lapse of 6.3 years between the first appearance of symptoms and diagnosis, all of whom showed progression in the intervening period. This study, however, included only those patients who were subjected to surgical intervention and may suffer from selection bias.[12]

In a large, prospective study involving over five hundred patients, Sampath et al. reported greater improvement in neurological symptoms, activities of daily living, and functional status in patients treated by surgery. The study was, however, nonrandomized and may suffer from a selection bias resulting from the influence of severity of disease on the decision-making process, with more severely affected patients being offered surgery.[14]

One sees a shift in opinion in more recent literature, owing perhaps to advancements in diagnostic tools, both in the realm of radiodiagnosis and neurophysiological testing and better and more objective quantification of myelopathy and consequent disability.

Kadanka et al. in a prospective randomized study comparing mild-to-moderate CSM treated with surgery and nonsurgical methods, concluded that the canal diameter (Pavlov's index), the severity of symptoms (modified Japanese Orthopedic Association and subjective assessment), neurophysiological parameters (somatosensory evoked potential (SSEP) and motor evoked potential indicating the central conduction time), age of the patient were all significant predictors of progression of disease. The authors found no correlation between intensity changes on MRI and the subsequent clinical course.[15] In another study by the same group it was reported that abnormal electrophysiology in asymptomatic patients with spondylotic cord compression on MRI correlated with progression to clinical myelopathy over time.[13] Other authors have stressed on abnormal electrophysiological findings in predicting progression to clinical myelopathy.[21] Along with the factors detailed above, the mobility of the cervical spine also needs to be factored in while deciding the treatment modality applied. It has been shown that increased cervical mobility portends to a progressive clinical course.[11]

A description on the natural history of spondylotic myelopathy and its outcomes would be incomplete without discussing the recent advances in application of MR tractography in its diagnosis as well as in predicting treatment outcomes. DTI sequences have been shown to be more sensitive in diagnosing spinal cord injury even when conventional MR sequences do not show intensity changes. Their main application is in visualising the long tracts and their structural continuity. Authors report better surgical outcomes in patients with intact long tracts. However, there is no consensus on the correlation of tractography and severity of neurological symptoms.[16] In a study involving more than 40 patients with up to 2 years of follow-up by Wen et al., DTI was reported to be superior to measures of central conduction (SSEP) and conventional MRI. In addition, they found a correlation between fractional anisotropy on DTI and the surgical outcomes in their patients.[22] Correlation between outcomes of surgical decompression and DTI has also been reported by other authors.[23]

Fehlings et al. have proposed management guidelines based on current knowledge of the natural history of CSM and systematic review of literature for non-surgical and surgical treatment of cervical myelopathy. This was proposed by a guideline development group under the aegis of AOSpine and the Cervical Spine Research Society. Their recommendations favor surgical intervention in all patients with moderate and severe cervical myelopathy. In mild myelopathy and in nonmyelopathic patients with significant cord compression, they recommend supervised trial of structured rehabilitation or close serial clinical follow-up.[24]

To summarize, the main determinants of the clinical course of CSM are the extent of neurological impairment, age, cervical instability, abnormalities of cord conduction, canal diameter, congenitally stenotic spinal canal, and the extent of involvement and tract disruption on DTI imaging.

  Pathogenesis of Cervical Spondylotic Myelopathy Top

CSM is thought to be the most common cause of cervical spinal cord dysfunction in people aged over 55 years.[25] However, our understanding of the etiogenesis of this common clinical problem remains incomplete. Current evidence and understanding of the pathogenesis of this condition can be broadly categorized into two groups: pathoanatomical and pathophysiological.


The basic premise of the pathoanatomic basis of CSM is hinged on compression of the cervical spinal cord. The compressive element can be static or dynamic.

Static Cord Compression

As far back as 1911, Bailey and Casamajor[26] on the basis of their surgical observation in two patients with paralysis secondary to cervical cord compression proposed that osteoarthritis of the spine could lead to compression of the spinal cord due to bony overgrowth. They postulated that thinning of the intervertebral disc and subsequent trauma to the body leads to bone overgrowth resulting in spinal cord compression. In the same year, Middleton and Teacher[27] described compression of the spinal cord by a ruptured disc leading to paraplegia. Goldthwait,[28] also in 1911, reported a case of lumbago, sciatica, and paraplegia due to a protruded and herniated intervertebral disc. Unfortunately, these reports stayed unnoticed and the credit for describing CSM goes to Stookey in 1928, who felt that the pathological cause was compression of the cervical spinal cord by cartilaginous nodules of degenerated disc material.[29]

Age-related degenerative changes occurring in the spinal column are labeled as spondylosis. Spondylotic changes are produced by noninflammatory disc degeneration, facet joint, and uncovertebral joint osteoarthritis, degenerative changes in the posterior longitudinal ligament (PLL) and ligamentum flavum. Asymptomatic degenerative changes are quite common and are present in 95% of men and in 70% of women in the age group 60–65 in a study by Gore et al.[30] Nearly 60% of people over 40 years of age have a degenerated and narrowed cervical disc.[31] Modic changes in the cervical vertebrae are seen in 40% of people over 50 years of age.[32] Age over 40 years, male gender and preexisting disc disease were felt to be risk factors for developing type 2 Modic changes in asymptomatic individuals.[34] Age-related disc degeneration, which is perhaps the primary event in the spondylosis cascade, ultimately leads to reduction in disc height and volume due to dehydration, alteration in the chemical composition and viscoelastic property, fissuring/tears in the annulus.[34] The resultant loss of cervical lordosis leads to alteration in the biomechanics of the cervical spine with increased strain on the facet joints producing degenerative changes and facet hypertrophy, buckling and hypertrophy of the ligamentum flavum and the PLL, flattening and hypertrophy of the uncovertebral joints.[35],[36] Formation of osteophytes around the disc margins, facet, and uncovertebral joints is attributed to natures' attempt to stabilize this abnormal segmental motion and increase the weight-bearing surface area.

The annular bulging, ligamental buckling and osteophytes all contribute to creating circumferential compression on the spinal cord. The level most commonly affected is C5/6, followed by C6/7, C4/5, and C3/4.[31],[33] The normal anteroposterior cervical canal diameter is 17–18 mm and a diameter less than 13 mm is considered to be congenital stenosis. It then seems intuitive that people with congenitally narrow cervical canals would be more likely to develop symptomatic CSM. This is borne out by the study by Nagata et al., who reported on a population-based survey of 959 individuals evaluated by X-ray and MRI and confirmed a higher incidence of myelopathy in people with a congenitally narrow canal.[37]

Dynamic Cord Compression

Cervical canal stenosis is a common finding, increasing in prevalence with age.[38] This is, however, clinically asymptomatic in the majority of individuals. Dynamic factors are proposed to play a role in the development of CSM. The normal cervical spine has a reserved space to accommodate changes in the spinal cord with flexion and extension. In extension, the cervical laminae get shingled, and there is inward buckling of the ligamentum flavum, which contributes to reducing the available spinal canal transverse area by 11%–16%. Along with this, there is a potential increase in the transverse area of the spinal cord by 9%–17%.[39] In addition, if there is any segmental translation of the vertebral bodies, either an antero or a retrolisthesis, this would further reduce the sagittal diameter of the canal and produce spinal cord compression.[40] As we know, an acute hyperextension of the cervical spine can pinch and injure the spinal cord between an osteophyte anteriorly and the lamina/buckled ligamentum flavum posteriorly to the extent of creating a central cord syndrome.[41]

Increased segmental motion has also been shown to accelerate spondylotic changes with resultant compression. This is particularly noted in patients with congenital fusions such as Klippel-Feil or in postsurgical fusions, at the levels adjacent to the fusion.[42],[43],[44]

Early or accelerated degenerative changes are seen following repetitive neck movements and trauma. This is supported by findings in rugby players, cervical dystonia patients, and in farm workers exposed to repetitive neck extension strain.[45],[46],[47] In patients with movement disorders associated with cervical stenosis, myelopathy occurs earlier and with greater frequency.[48]

Stretch and strain

The spinal canal elongates during normal spinal flexion, causing stretching of the spinal cord. Stretching of the cervical spinal cord produces axial strain, which has been proposed to be harmful.[49],[50],[51] This was confirmed in the cadaver study by Bilston and Thibault.[52] In human cadaver studies, Reid demonstrated an average 6.8 mm upward movement of the cervical spinal cord at T1 level with neck flexion.[53] The initial compliance of the spinal cord is overcome by progressive elongation and tensile loading.[54] Progressive stretch has been shown to damage the anatomical and physiological integrity of the neuronal axons. This ranges from increased membrane permeability causing transient conduction block to irreversible conduction loss, cytoskeletal collapse and secondary axotomy.[51],[54],[55] Tethering of the spinal cord over a small or large disc protrusion, osteophytic bar or at the apex of a kyphotic deformity has also been shown to exacerbate stretch injury, often also at a locus different from the site of deformation.[54]

Role of Minor Trauma

There is scant evidence for minor traumatic events producing or worsening clinical myelopathy in asymptomatic patients with cervical cord compression. Bednařík et al.[56] examined the risk of developing myelopathy in a group of asymptomatic cervical cord stenosis patients who were followed-up for a median 3.7 years. In their group, only 7% (one of 14 patients) developed myelopathy following an episode of minor trauma. This is in comparison to 24% (44 of 185 patients) who progressed to myelopathy over the study period in the absence of any traumatic event. This study did not demonstrate that traumatic events precipitate or worsen myelopathy. However, the small patient numbers do not allow for a definite conclusion to be made.

The study by Katoh et al.[57] showed markedly different results in their group of 27 patients with and without myelopathy who sustained minor trauma. In the cohort of patients who did not have myelopathy before the trauma, 68% developed myelopathy. Of those who had myelopathy before the minor trauma, 87% (7 of 8 patients) were clinically worse. However, this study was on patients with OPLL, and therefore, the results may not be directly translatable to patients with CSM.


There continue to remain many puzzling facts in CSM. Patients with similar degrees of radiological cord compression can have different symptomatology and clinical findings. Although some risk factors for disease progression have been identified, they are by no means definitive or comprehensive. It is fair to state that the molecular mechanisms underlying CSM are still to be fully defined. One of the significant roadblocks in greater elucidation of the molecular mechanisms underlying CSM has been the lack of a reliable animal model. Reliance had been placed on extrapolating data from acute injury models in animals. The pathophysiology of CSM is distinct from that of acute spinal cord injury. CSM is a chronic condition with poorly defined progression, where there is usually no acute injury. Histopathologically, there is no acute hemorrhagic necrosis seen within the spinal cord.[58]

The biological events that are thought to play a significant role in the development of CSM are ischemia, derangement of the blood-spinal cord barrier (BSCB), chronic neuronal inflammation and apoptosis. The recent development of animal models which more robustly mimic the chronic compressive pathological changes in human CSM is already adding to the available knowledge of the molecular biology in CSM.[59],[60],[61] This additional knowledge holds the promise of potential future interventions, both for prevention and for treatment of this common but difficult condition. The available evidence for these contributing factors is presented in this review.


Ischemia of the spinal cord as a mechanism for the development of myelopathy was first proposed by Brain in 1948.[62],[63] Breig, on the basis of microangiopathic studies, also proposed ischemia as a cause, induced by a combination of vessel narrowing and mechanical cord compression due to spondylosis.[50],[52] The normal blood supply of the spinal cord consists of a centripetal and a centrifugal system of vessels, with a watershed in the region of the inner one fourth of the white matter and the outer edge of the gray matter.[64],[65] Taylor proposed the compression of radicular arteries in the narrowed spondylotic foramen, along with fibrosis of the perineural root sheaths as a cause of ischemia in CSM because of impairment of blood flow in the radicular arteries.[66] Hyalinization and thickening of the walls of the anterior spinal artery and parenchymal arterioles have been reported by Mair and Druckman.[63]

Shimomura concluded on the basis of canine experiments that ischemia resulting from obstruction of blood vessels on the surface of the spinal cord, including the anterior spinal artery, the dorsolateral spinal arteries and the medullary part of the radicular arteries, is responsible for CSM. This obstruction was also the reason for the development of intramedullary cavitation.[67] Animal experiments have lent support to the combination of compression and ischemia in the etiogenesis of CSM. al-Mefty et al. produced chronic compression on the cervical spinal cord of dogs by anteriorly and posteriorly placed spacers and reported evidence of disturbed microcirculation leading to neuronal loss, necrosis, and cavitation.[68] Canine experiments involving a combination of anterior cord compression and segmental vessel ligation by various groups showed histological and neurological changes similar to that found in human CSM.[69],[70]

However, the evidence for ischemia as a cause of CSM is conflicting. Some studies have shown only mild local ischemia in animal experiments with moderate CSM.[65],[68] Carlson, in their study on the effect of compression and decompression on spinal cord blood flow in beagles, found only a 30% reduction in blood flow despite fairly profound neurological changes.[71] Fehlings et al. have argued from a molecular level. Their logic is that although ischemia can elicit an apoptotic response, it usually leads to cell death through necrosis. Increasing evidence available in human and experimental studies that suggest oligodendrocyte and neuronal cell death as a result of apoptosis argues against ischemia as a principal protagonist.[72]

Blood Spinal Cord Barrier (BSCB)

Like the blood-brain barrier, there exists a BSCB which is designed to provide a protected micro-environment for the functioning of the spinal cord. The anatomical features of the BSCB are similar to the blood-brain barrier, with the main feature being the presence of non-fenestrated endothelial cells linked with tight junctions.[73] These endothelial cells lack pinocytic vacuoles confirming restricted transcellular movement of molecules. They have numerous cytosolic mitochondria suggestive of high metabolic activity needed for selective active transport of molecules. The other components of the BSCB are the pericytes, basal lamina, and the astrocytic foot processes. To date, some structural and functional differences of the BSCB with the BBB have been identified. Of note are the presence of glycogen deposits in BSCB microvessels, increased permeability of the BSCB to some tracers such as [3H]-D-mannitol, [14C]-carboxyl-inulin; cytokines such as interferon-α, interferon-γ, and tumor necrosis factor-α (TNF-α). It has also been observed that the permeability of the BSCB shows regional differences and is not uniform across the whole of the spinal cord, with higher permeability to cytokines in the cervical spinal cord compared to the lumbar.[74] The functional implications of these differences remain to be fully understood.

Injury to the spinal cord will result in damage to the BSCB. Maikos in a well-designed experiment demonstrated that the gray matter was more affected than the white matter and that the degree of damage was correlated more to the rate of spinal cord compression than to the depth of compression.[75] This suggests that microvascular pathological damage is contributed to by tissue level strain factors. This study has important implications in CSM, where there is often very slow progression of compression and hence potential compensation of tissue level strain.


Several authors have pointed out the role of inflammation in the initiation and propagation of myelopathy in cervical spondylosis. The inflammatory process may result from direct mechanical compression of the cord or from on-going ischemia.[72] The presence of interleukin-6 (IL-6) was documented in the CSF of great Danes with CSM.[76] Nagashima et al. did a CSF analysis in 21 patients with CSM and found that there was a higher level of the proinflammatory cytokine IL-6. High level of IL-6 was also noted in 19 patients with lumbar radiculopathy, prompting them to suggest that IL-6 was a marker of spinal cord and nerve root damage. However, the study did not find any evidence of increase in the other proinflammatory cytokines tested, namely IL-1β and TNF-α.[77] Wang et al. collected PLL specimens from 30 CSM patients undergoing surgery and found that another proinflammatory cytokine TGF-beta1 was related to PLL degeneration.[78] IHC studies demonstrated that the TGF–beta 1 was secreted by macrophages. They concluded that anti-inflammation may serve as alternative non-surgical management or prophylactic strategy for PLL degeneration. Takano et al. did an experimental study using tip-toe walking Yoshimura mice and found using microarray analysis that the genes expressed in higher levels in mice with severe cord compression were “enriched for the terms related to regulation of inflammation in the compressed spinal cord.”[79] They found that M1 macrophage-dominant inflammation was present in the group with severe spinal cord compression, and cysteine-rich protein 61, an inducer of M1 macrophages was markedly upregulated in these spinal cords. To examine the mechanism of neurodegeneration in chronically compressed spinal cords, they focused on the complement system and further observed that C1qa, C1qb, and C1qc, which initiates the complement cascade, had higher levels in mice with severe cord compression compared to those with milder cord compression. Electron microscopic studies revealed that classically activated microglia/macrophages had migrated to the compressed spinal cord and eliminated the synaptic terminals. Using an experimental mouse model, Vidal et al. have noticed that delayed decompression of the compressed spinal cord was associated with prolonged elevation of pro-inflammatory cytokines and an elevated peripheral monocytic response in the spinal cord, which led to poorer response after decompression of the cord.[80] Their findings may be stated as:

  1. Prolonged spinal cord ischemia increases spinal cord blood flow after decompression. This gives rise to reperfusion injury of the spinal cord
  2. Delayed surgical decompression induces a sustained systemic and local postischemic inflammatory response
  3. Early decompression reduces astrogliosis in contrast to delayed decompression
  4. Early decompression provides better functional outcome
  5. Hyperalgesia is reduced by early surgical decompression
  6. Shorter duration of symptoms (≤6 months) leads to better outcome.


Neuropathological features of CSM characteristically include loss of neurons, glial scar formation, axonal degeneration, and demyelination.[72] In the neuronal degeneration and demyelination that accompanies spondylotic myelopathy, the phenomenon of apoptotic cell death of neuronal cell and oligodendrocytes has been studied by some investigators. Uchida et al. did an experimental study using spinal hyperostotic mouse (Yoshimura) and showed that spinal cord mechanical compression is characterized by the loss and exfoliation of anterior horn cells with progressive spongy necrosis and demyelination of white matter, demonstrated by a decrease in TUNEL positive cell count.[81] Several others have also opined that neuronal apoptosis is the underlying mechanism of spinal cord damage after traumatic injury, and it has been reported that the extent of demyelination and  Wallerian degeneration More Details in the white matter increased proportionately to the compression of the spinal cord.[82],[83] It has also been reported that in spinal cord injury, apoptotic oligodendrocytes are found along the spinal cord longitudinal axis, not only significantly at the site of injury, but also both proximal and caudal to the lesion.[84] The axonal damage caused by the injury leads to the depletion of neurotrophic factors which contributes to apoptosis of oligodendrocytes. Yu et al. did an autopsy study on six patients of CSM and found evidence of increased number of Fas-positive cells in the gray and white matter at the epicenter of all CSM spinal cords.[85] Double labeling with Fas and cell-specific markers revealed Fas immunoreactivity in neurons, astrocytes, microglia/macrophages, and oligodendrocytes. In addition to the Fas-mediated pathway, TNF-α, mitogen-activated protein kinase pathways, and the nuclear factor-kappa B have all been implicated in the initiation and propagation of apoptosis in spondylotic myelopathy.

  Conclusions Top

CSM is the most common degenerative spinal cord lesion mostly affecting people in the fifth and sixth decades of life. The incidence and prevalence vary by region, and we were unable to find any epidemiological study based on the Indian subcontinent. The natural history of CSM is variable and ranges from relentless progression to clinically stable with intermittent deterioration. The main determinants of the clinical course of CSM are the extent of neurological impairment, age, cervical instability, abnormalities of cord conduction, canal diameter, congenitally stenotic spinal canal and the extent of involvement and tract disruption on DTI imaging. The anatomic basis of CSM is cord compression, either dynamic or static. The biological events that are thought to play a significant role in the development of CSM are ischemia, derangement of the BSCB, chronic neuronal inflammation, and apoptosis. This additional knowledge holds the promise of potential future interventions, both for prevention and for treatment, of this common but debilitating condition.

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Conflicts of interest

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