Cervical spinal stenosis

                            Cervical spinal stenosis

                                                     DR KS DHILLON

What is cervical spinal stenosis?

Spinal stenosis is a condition in which the spinal canal space available for the neural and vascular elements is reduced leading to compression of the spinal contents. Spinal stenosis is most often due to degeneration of the spine. Patients with cervical spinal stenosis can present with neck pain, weakness, or numbness in the shoulders, arms, and legs. Hand clumsiness and gait and balance disturbances may be present. Paraesthesias such as burning sensations, tingling, and pins and needles in the involved extremity, such as the arm or leg may sometimes be present. In severe cases, bladder and bowel disturbances can be present.

Cervical stenosis is estimated to be present in 4.9% of the adult population, 6.8% of the population fifty years of age or older, and 9% of the population seventy years of age or older [1].

Etiology of spinal stenosis

Cervical spinal stenosis (CCS) can be congenital, acquired or a combination of the two.
Congenital cervical stenosis is seen in individuals when the bony anatomy of the cervical canal is smaller than expected in the general population. This can predispose the individual to symptomatic neural compression.

Acquired cervical stenosis is most commonly caused by degenerative disease of the spine which develops with age. Diseases such as rheumatoid arthritis, ankylosing spondylitis, and ossification of the posterior longitudinal ligament (OPLL) can cause narrowing of the spinal canal leading to spinal stenosis. Tumour infiltration, such as metastatic disease of the spine and spinal infections with abscess formation can also lead to narrowing of the spinal canal. Paget disease can cause enlargement of the vertebral body resulting in spinal stenosis. Trauma to the spine can cause spinal stenosis and iatrogenic narrowing of the canal can result from surgery on the cervical spine.

Pathophysiology

The most common cause of cervical spinal stenosis is degenerative disease of the spine which is known as cervical spondylosis. After the age of 20 years, the water content of the nucleus pulposus begins to decline resulting in a decrease in disc height. This leads to migration of the facets, a reduction of interlaminar space, narrowing of the neural foramina and the spinal canal. Degeneration of the disc leads to disc bulges which cause narrowing of the canal. Increase in stresses on the posterior part of the spine leads to the formation of osteophytes and thickening of laminae and pedicles, as well as hypertrophy of the facets and ligaments. All these changes contribute to the narrowing of the spinal canal. In degenerative spondylosis, there is hyperplasia, fibrosis, and cartilaginous metaplasia of the annulus, posterior longitudinal ligament, as well as the ligamentum flavum which all contribute to stenosis of the spinal canal.

There is a close association between the presence of spinal stenosis and the occurrence of cervical myelopathy, although spinal stenosis is not the only cause of myelopathy. In patients with cervical spondylosis, there are restrictions of the spinal canal which result in release and shear forces on the spinal cord which lead to diffuse and focal axonal damage [2]. In patients with cervical spondylosis, there is instability of the spine with hypermobility of the spinal segments leading to more stress on the spinal cord [2].

In patients with spinal stenosis, the diameter of the spinal canal in flexion and extension is reduced due to posterior disc protrusion in the anterior part of the canal and folding of the ligamentum in the posterior part of the canal. Movements of the cervical spine affect the length of the spinal cord.
Extension of the cervical spine is associated with shortening of the spinal cord and an increase in the diameter of the cord [2].

In patients with spinal stenosis, the spinal cord can be further damaged by cervical spine movements by becoming pinched between the pincers of the posteroinferior end of one vertebral body and the lamina or ligamentum flavum of the caudal segment. This will not only cause local damage to the spinal cord but also compress the vessels which perfuse the cord. perfusing it [2].

The cervical movements in patients with spinal stenosis can cause direct compression of the anterior spinal artery. Flattening of the spinal cord due to compression can cause torsion in the sulcus vessels, which run transversely. These vessels perfuse the grey matter as well as the medial white substance, which are commonly affected early in the course of the disease [3].

Patients who have a congenitally narrow canal (< 13 mm) are at a higher risk for developing clinical features from static-mechanical compression of the spinal cord [3]. A narrowing of the spinal canal causes compression of the spinal cord, leading to tissue ischemia, neural cell injury, and neurological deficit. Thirty percent or more compression of the cord usually causes patients to become symptomatic, though this can vary between patients [4].

Cervical myelopathy is very likely to be present when the dynamic canal space during extremes of flexion or extension is less than 11 mm [3].

One study even went to the extent of measuring changes in disc bulge, ligamentum flavum bulge, and anteroposterior canal diameter, in response to tension-compression forces and combined loading forces in the lower cervical spine (C4-7) in human cadavers [5]. They found that from tension to compression, the average disc bulge changed 1.13 mm (10.1%) of the original canal diameter, the ligamentum flavum bulge changed 0.73 mm (6.5%) of the canal diameter. From flexion to extension of the cervical spine the average disc bulge changed 1.16 mm (10.8%) of the canal diameter, and the ligamentum flavum bulge changed 2.68 mm (24.3%) of the canal diameter. These measurements show that neck flexion reduces cord compression by increasing the sagittal diameter of the canal and neck extension in the presence of a ligamentum flavum bulge increases the canal stenosis [5].

Clinical manifestations

The clinical presentation in patients with cervical myelopathy resulting from spinal stenosis (especially spondylotic stenosis), can be varied. A good history, proper clinical examination and supporting radiological findings are essential in making a clinical diagnosis of cervical myelopathy [6].

Chiles et al [7] carried out a retrospective review of 76 patients with cervical spondylotic myelopathy who had cervical decompression and fusion. They found that the most common preoperative symptoms in the patients were deterioration of hand use (75%), upper extremity sensory complaints (82.9%), and gait difficulties (80.3%). In the upper extremities, weakness was most common in the intrinsic muscles of the hand (56.6%) and tricep muscles (28.9%), whereas in the lower extremities, weakness was most common in the iliopsoas (38.8%) and the quadriceps muscles (26.3%).

Crandall and Batzdorf [8] classified the pathology of cervical spondylotic myelopathy (CSM) into 5 types. They came up with 5 syndromes based on clinical presentation which include:

Syndrome                                                 Clinical features
1.Brachial cord                       Motor (paralysis) and sensory deficits (and                                                         
                                                pain) in upper extremities.

2.Central cord                         Motor and sensory deficits in upper     
                                                extremities more than in lower extremities.

3.Anterior cord                       Spasticity

4.Brown-Squared syndrome   Ipsilateral motor deficits with contralateral   
                                                sensory deficit.


5.Transverse lesion              Corticospinal, spinothalamic, and posterior cord
                                             tracts are all involved.

Ferguson and Caplan [9] described 4 syndromes based on clinical presentation which include:

Syndrome                     Clinical features
1.Medial                      Long-tract symptoms

2.Lateral                     Radicular symptoms

3.Combined                Combined medial and lateral syndromes

4.Vascular                  Vascular insufficiency causing a rapidly progressive 
                                    myelopathy

Mihara et al [10] found that many patients with CSM did not fit into any of the several types of myelopathy syndromes described in these classification systems. They introduced a new classification system. Their study included 315 consecutive patients who were diagnosed to have cervical myelopathy and underwent surgical treatment. They were able to classify all but two patients into 5 types.

The five types include [10]:

Type I: Anterior lesion syndrome, which involves dysfunction of one upper extremity (13.1%).
Type II: Central lesion syndrome, which involves dysfunction of both upper extremities (8.6%).
Type III: Posterior lesion syndrome, which involves bilateral lower extremity dysfunction with deep sensory disturbance (5.4%).
Type IV: Hemilateral lesion syndrome, which involves unilateral upper and lower limb palsy (12.1%).
Type V: Transverse lesion syndrome, which involves the presence of neurological symptoms in all four extremities (60.7%).


Anterior lesion syndrome is caused by damage to the anterior horn and/or anterior rootlet resulting in neurological deficit in one upper limb. This type of clinical presentation may also be seen in patients with radiculopathy caused by eccentric disk bulging, with/without osteophyte formation in the nerve root foramen. Hence, it is important to differentiate between the two causes of the clinical presentation since the treatment will be different in the two groups of patients. It is necessary to carefully exclude patients with pure radiculopathy or peripheral nerve entrapment syndrome from those with myelopathy [10].

Central lesion syndrome is caused by damage to the grey matter of the central part of the spinal cord. It is characterized by motor dysfunction with/without sensory disturbance, in both upper extremities. Patients in this group have no obvious neurological deficit in the lower extremities. If the damage reaches the corticospinal tract, the patient will usually display hyperreflexia in the lower extremities. This type of cervical myelopathy can progress to transverse lesion syndrome if the neural damage extends to the entire corticospinal tract [10].

Patients with posterior lesion syndrome exhibit motor dysfunction involving both lower extremities, without upper extremities involvement. Patients with this type of cervical myelopathy have ataxic gaits (not spastic gaits), and they have deep sensory disturbances in both lower limbs. Posterior lesion syndrome, in patients with neurological deterioration in both lower limbs who have cord compression at the C6-C7 or C7-T1 level, can be difficult to differentiate from transverse lesion syndrome. In such patients for diagnosis of posterior lesion syndrome, tests for deep sensory disturbances and equilibration function need to be carried out [10].

In patients with hemilateral lesion syndrome, there is damage to one half of the spinal cord which produces symptomatology similar to that seen in Brown-Séquard syndrome [10]. In such patients, there is an ipsilateral corticospinal deficit characterized by ipsilateral spastic paresis with loss of vibration and joint position sense (destruction of ipsilateral dorsal column fibres), and ipsilateral loss of position, light touch and vibration sensation at the level of the lesion. The reflexes are brisk with upgoing plantar reflex. In these patients, there is contralateral loss of pain and temperature beginning a few segments below the lesion (because the spinothalamic tracts enter the cord and travel ipsilaterally for a few segments before decussating). There is no plantar response on this side because of the loss of pain sensation. Ipsilateral Horner's syndrome may be present. Sphincter disturbances may also be present. This syndrome might progress to transverse lesion syndrome.

Transverse lesion syndrome is the most common and the most advanced type of cervical myelopathy. In these lesions, there is involvement of the corticospinal, spinothalamic, and other tracts as well as the grey matter in the spinal cord which produces neurological signs and symptoms in all four limbs [10].

Clinical presentation

Symptomology in patients with CSM can vary widely. Patients with mild symptoms may report neck pain and limitation of neck motion. In the later stages, history taking can elicit difficulty with motor tasks such as slowness and clumsiness with activities such as buttoning and using keys. There may be changes in handwriting. There can be difficulty with common tasks such as using a computer keyboard, pushing buttons on a mobile phone, or text messaging. As myelopathy progresses the patient may need assistive devices, such as a cane, walker, or wheelchair, to mobilise due to balance or weakness issues. The need for the use of handrail while negotiating stairs can be a manifestation of balance problems. Paresthesias and weakness are often present in the extremities and patients can have concomitant radicular signs and symptoms [11].

CSM most commonly affects the lower cervical spinal cord at C5 to C7. The C5 to C7  dermatomes and muscle groups include [6]:

Cord level       Sensory Dermatome                     Motor function
C5              Radial side of cubital fossa        Shoulder abduction and elbow
                                                                        flexion.                                                               
C6             Thumb                                          Elbow flexion and wrist 
                                                                        extension.   
C7             Middle finger                               Elbow flexion and wrist
                                                                       extension.
C8            Little finger                                   Finger flexion

Patients with CSM can have difficulty with the 15-second hand dexterity test. The test is performed by asking the patient to grip and release their fingers as rapidly as possible for 15 seconds [12]. A normal person is usually able to grip and release their hand 25 to 30 times in 15 seconds but a person with CSM will have difficulty doing so.

Examination will often show localised wasting and weakness of the extrinsic and intrinsic muscles of the hand [13]. The ‘finger-escape sign’ may also be present where there is spontaneous abduction of the little finger due to intrinsic muscle weakness.

In the upper limbs both upper and lower motor neuron signs may be present. Muscular wasting may also be present. Sensory loss may be present depending on the level of cord lesion. Vibration, proprioception,  and touch sensation can be impaired on the ipsilateral side to the lesion, and pain and temperature sensation can be impaired on the contralateral side. Hyporeflexia or hyperreflexia may be present in the upper limbs.

Hyperreflexia is usually seen in both the upper and lower extremities.

Abnormal long tract signs, such as the Babinski, Hoffman's, and inverted radial reflexes (tapping the brachioradialis tendon that elicits firing of the long finger flexors is considered a positive response) are often present in patients with CSM. Sustained clonus may also be present. It has poor sensitivity (~13%) but high specificity (~100%) for cervical myelopathy.

Gait and balance abnormality which is often present can be tested by doing toe-to-heel walk and Romberg test. Posterior column dysfunction leads to a positive Romberg test where the patient loses balance when he/she is asked to stand with arms held forward and eyes closed.

Lhermitte's sign (also known as Lhermitte's phenomenon or the barber chair phenomenon) may be positive in patients with CMS. It is characterised by the presence of an electric shock-like sensation which radiates down the spine, often into the legs, arms, and sometimes to the trunk, on extreme cervical flexion.

There are several disease severity classifications which have been used such as the European Myelopathy Score, Nurick’s Functional Scale, Ranawat Classification of Neurological Deficit, and the modified Japanese Orthopaedic Association scoring system. Although they are helpful in determining the severity of the disease, they do have some limitations.

The Nurick’s classification [14] is based on gait, ambulatory function, and employability.

Nurick's classification system for myelopathy.

Grade  Root signs  Cord involvement      Gait                    Employment
0            Yes             No                         Normal                      Possible
I            Yes              Yes                        Normal                      Possible
II           Yes             Yes                   Mild abnormality           Possible
III          Yes             Yes                  Severe abnormality         Impossible
IV         Yes             Yes                  Only with assistance        Impossible

The Ranawat classification [15] is based on neurological and ambulatory status.

Ranawat Classification for myelopathy

Class I          Pain, no neurologic deficit.
Class II         Subjective weakness, hyperreflexia, dysesthesias.
Class IIIA    Objective weakness, long tract signs, ambulatory.
Class IIIB    Objective weakness, long tract signs, non-ambulatory.

Diagnostic test for spinal stenosis

In patients with suspected cervical spinal stenosis, plain x rays of the cervical spine is the first diagnostic test that is carried out. Plain X-ray radiographic evaluation should include AP and lateral views. Disc space narrowing, facet joint arthrosis, osteophytes, ossification of the posterior longitudinal ligament (OPLL), spondylolisthesis and kyphotic alignment of the spine can be visualized on a lateral plane X-ray. Flexion-extension lateral view of the cervical spine is useful to assess hypermobility of the segments adjacent to the stiff spondylotic segment. This hypermobility can cause dynamic compression of the spinal column and may not be seen on routine MRI imaging. Oblique views of the cervical spine are useful for visualizing foraminal narrowing. Important information about the stability and motion of the cervical spine under a physiologic load can be obtained by comparing standing radiographs to supine radiographs [11].

The canal diameter can be measured on the x rays. Sagittal canal diameter of less then 10mm is defined as ‘absolute stenosis’ and diameters of less than 13 mm is defined as ‘relative stenosis’ [6].
In assessment of spinal stenosis, the Torg-Pavlov ratio can be calculated.  In this method, the ratio of the diameter of the cervical canal to the width of the cervical body on the lateral view of the cervical spine is calculated. A ratio of less than 0.8 is taken as an indication of cervical stenosis [16].

Currently, MRI is by far the most commonly used imaging method for the accurate evaluation of spinal canal stenosis. It can show the width and length of the spinal canal besides depicting in detail the spinal cord, intervertebral disks, osteophytes, and ligaments, all of which can cause spinal canal stenosis [17].

Muhle et al [18] classified cervical canal stenosis according to the following grading system based on MRI findings:

Grade 0.  Normal.
Grade 1.  Partial obliteration of the anterior or posterior subarachnoid
                space. 

Grade 2. Complete obliteration of the anterior or posterior
                subarachnoid space. 
Grade 3. Cervical cord compression or displacement.

Kang et al [19] more recently developed an MRI grading system for cervical spinal stenosis with excellent overall intraobserver agreement. They classified cervical canal stenosis based on T2-weighted sagittal images. They graded the stenosis from grade 0 to grade 3:

Grade 0. Absence of central canal stenosis
Grade 1. Obliteration of more than 50% of subarachnoid space without any sign of cord deformity.
Grade 2. Central canal stenosis with cord deformity but without spinal cord signal change.
Grade 3. Presence of spinal cord signal change near the compressed level.

The presence of cord impingement does not imply that the patient has symptomatic spinal stenosis. A study by Teresi et al [20] showed cord impingement in 16% of asymptomatic patients under age 64 years and in 26% of asymptomatic patients aged greater than 64 years.

In patients with suspected cervical spine stenosis in whom MRI is either contraindicated due to pacemaker or hardware or is inconclusive, CT myelography is the most appropriate test to confirm the presence of anatomic narrowing of the spinal canal, degree of spinal cord compression and the presence of nerve root impingement. The contrast for CT myelography is usually given via a C1-C2 puncture.

In patients in whom MRI and CT myelography are contraindicated, inconclusive or inappropriate, CT scan is the preferred test to confirm narrowing of the spinal canal and presence of nerve root impingement.

Electromyography (EMG) and Somatosensory Evoked Potentials (SSEPs) are diagnostic investigations that are infrequently used in patients with suspected cervical spondylosis. These tests are usually used to exclude differential diagnoses such as multiple sclerosis, amyotrophic lateral sclerosis, and peripheral neuropathy [21]. Nerve conduction studies, however, can have high false negative rates.

There are others who believe that ‘electrophysiological studies are very useful complementary investigations for assessing cervical cord dysfunction and have an important role in diagnosis and management of CSM’ (cervical spondylogenic myelopathy) [22].

Treatment of cervical spinal stenosis

There is insufficient good-quality evidence in literature to help physicians decide whether surgery or conservative treatment is the preferred method for the treatment of patients with myelopathy secondary to spinal canal stenosis.

Kadanka et al [23] carried out a 3-year prospective randomized study to compare the outcome of conservative and operative treatment of mild and moderate, nonprogressive, and slowly progressive forms of spondylotic cervical myelopathy. Their study, on average, did not show that surgery was superior to conservative treatment in patients with mild and moderate forms of spondylotic cervical myelopathy.

Kadaňka et al [24] carried out a similar study, comparing the outcome of conservative and surgical treatment in patients with mild and moderate spondylotic myelopathy, with a 10 years follow up. As with their previous study, in this study as well, they found that on average, there was no significant difference in the outcome between the two groups. The authors did, however, admit that the drawback of their study was that the number of patients at the final follow up (47 patients) were too small to answer the question of which treatment is definitely better for the patients with mild and moderate non-progressive CSM.

Sumi et al [25] carried out a prospective cohort study of patients with mild cervical spondylotic myelopathy without surgical treatment. Their study included 60 patients with mild CSM who presented with scores of 13 or higher on the Japanese Orthopaedic Association (JOA) scale. The patients were initially treated with cervical traction without surgery. They defined deterioration of myelopathy as a decline in JOA score to less than 13 with a decrease of at least 2 points. They found deterioration in myelopathy in  25.5% of the patients and in 74.5% of the patients there was no deterioration in myelopathy through the follow-up period (mean 94.3 months). They concluded that the tolerance rate of mild CSM was 70% in their study, which proved that the prognosis of mild CSM without surgical treatment was relatively good.

Rhee et al [26] carried out a systematic review to investigate the efficacy, effectiveness, and safety of conservative treatment of patients with cervical myelopathy and to find out whether the severity of myelopathy affects outcomes of nonoperative treatment.

They found that there was low evidence that showed that conservative treatment may yield equivalent or better outcomes than surgery in patients with mild myelopathy. In patients with moderate to severe myelopathy, conservative treatment had inferior outcomes as compared to surgery in 2 cohort studies.
Patients with mild CSM and those who are not fit for surgery are usually treated conservatively. There are several conservative treatment options which include analgesics, physiotherapy, lifestyle changes, and neck braces.

Non-steroidal anti-inflammatories (NSAIDs) are widely used for conservative treatment.The use of systemic and epidural steroids for myelopathy remains controversial [6].

Physiotherapy usually involves strengthening the neck, upper quadrant, and scapular muscles as well as heat and ultrasound therapy. Cervical collars or braces are sometimes useful for neck immobilization. Intermittent cervical traction for several days is sometimes warranted.

Lifestyle changes include avoiding activities that exacerbate the patients symptoms. Activities such as lifting heavy objects and activities that involve excessive neck extension and flexion can exacerbate the patient's symptoms.

Patients should be informed that even minor trauma to the neck leading to hyperextension of the neck can result in spinal cord injury leading to a central cord syndrome. Hence trauma to the neck should be avoided.

Patients with mild myelopathy who have hyperreflexia or slight balance disturbance should be closely followed up with clinical and radiographic examination [11].

Surgical treatment 

The decision for surgical treatment of spinal stenosis must take into consideration several factors such as, patient's age, functional ability, rate and degree of neurological deterioration, severity of symptoms, and general health of the patient [11].

The generally agreed upon indications for surgical treatment of spinal stenosis include, symptoms refractory to conservative treatment, intolerable symptoms, progressive neurological deterioration, bowel and or bladder dysfunction and generalised weakness [11]. Surgery is usually carried out in patients with severe myelopathy (Japanese Orthopedic Association [JOA] score, 0–9), as well as in patients with moderate myelopathy (JOA score, 10–12) [27,28]. Surgery is also indicated in patients with mild myelopathy (JOA score, 13–17) who have progressive neurologic deficits [29].

Patients with spinal stenosis should be informed that surgery is effective in preventing further decline in function, but it may, however, not result in substantial improvement from their current level of function [11].

Generally, patients with cervical compressive myelopathy with intramedullary signal intensity (SI) changes on MRI have a poor prognosis after surgical decompression.

A literature review by Epstein [30] showed that Grade/Types 2-3 high cord signals (HCS) on T1 and T2-weighted MR images on preoperative and postoperative MR studies, failure of HCS regression, cord re-expansion at the site of a prior HCS (reflecting cord atrophy), and a triangular cord configuration all contributed to poorer outcomes following surgery. The review found that higher the grade of HCS, greater is the likelihood of poorer outcome. Multisegmental HCS was also associated with worst outcomes.

Generally, surgery is recommended earlier for patients with myelomalacia (seen as edema within the cord on MRI). Signal change within the cord itself, however, may not correlate with neurological function or postoperative recovery [11].

A Cochrane Review of randomized controlled trials for the role of surgery in mild CSM was carried out by Fouyas et al [31]. They found that the early results of surgery were superior to conservative treatment in terms of pain, weakness, and sensory loss but at 1 year follow-up there was no significant differences between the two groups. They reviewed another trial and found that there was no significant difference between surgical and conservative treatment at 2 years follow-up. Overall, the authors concluded that the data from the reviewed trials was not adequate to provide definitive conclusions on the role of surgery in the treatment of spondylotic radiculopathy or myelopathy.

Surgical Techniques

There are several surgical techniques described for the treatment of spinal stenosis.The ideal surgical strategy has to be tailored according to the characteristics and location of cord compression. The main aim of surgical treatment is to decompress the spinal cord and at the same time to preserve the spine alignment and stability.

In patients with cervical myelopathy special precautions have to be taken when positioning the patient for surgery. The preoperative range of cervical motion must be recorded. Excessive cervical extension should be avoided when intubating the patient and when positioning the patient on the table because excessive extension of the neck in a patient with a tight cervical canal can lead to severe neurological injury [11].

The surgical approach to the cervical spine may be anterior, posterior or a combination of both anterior and posterior. The choice of approach, however, remains debatable. There are several factors which are taken into consideration when making a decision. These include sagittal alignment of the spine, the number of segments involved, morphology of the stenosis, quality of bone and any history of prior surgery [11].

The sagittal alignment of the cervical spine is a very important consideration when deciding on the surgical approach to the spine. When a fixed cervical kyphosis is present, the anterior procedure will allow  decompression of the spinal canal as well as correction of the deformity. A posterior procedure will not be suitable in such circumstances because it will leave the spinal cord compressed anteriorly by spondylotic bars and disc bulges [11].

The commonly performed anterior procedure is a single or multilevel anterior cervical discectomy and fusion (ACDF). Sometimes corpectomy or hemi-corpectomy and fusion is required. Anterior surgery is usually recommended for patients in whom the disease is limited to one or a few segments and in patients who have a fixed cervical kyphosis.

Interbody bone graft is always needed for the fusion. The most commonly used graft is an iliac crest autograft. Sometimes a plate may be required for stabilization of the spinal segments. The use of plates, however, have inherent risks of late instrumentation-related complications.

Posterior procedures are usually carried out in patients with dorsal compression due to ligamentum flavum infolding and in patients with multisegmental stenotic disease who have a neutral to lordotic spinal alignment [11]. The type of posterior procedures for CSM can vary widely and can include central decompression by laminotomy or laminectomy with fusion, or decompression by laminoplasty.

In complex cases, where there is compression from both anterior and posterior structures, a combination of anterior and posterior procedure is required to treat the myelopathy associated with spinal stenosis.

Complications of Surgery

Cervical spine surgery as with other spinal surgery can be associated with complications such as infection, bleeding, nerve injury, dural leak and fistula formation.

Anterior surgery can be associated with risk of superior and recurrent laryngeal nerve injury, esophageal injury as well as vertebral artery injury.

Breakage of hardware, hardware migration, fusion failures, graft dislodgement, Horner's syndrome, and airway compromise has also been reported [32]. Many patients will experience dysphagia which is usually self-limiting.

Neurological deterioration can occur following cervical surgery for myelopathy. Yonenobu et al [33] reported a 5.5% incidence of neurologic deterioration following surgery for compression myelopathy. They performed 134 anterior interbody fusions, 70 subtotal corpectomies with strut bone graft, 85 laminectomies, and 95 laminoplasties. Twenty-one patients (5.5%) developed deterioration of spinal cord function or of nerve root function. Manifestations of deterioration of spinal cord function varied from weakness of the hand to tetraparesis. The causes of neurological deterioration included spinal cord injury during surgery, epidural hematoma and malalignment of the spine associated with graft complication.

Posterior laminectomy can lead to posterior shifting of the spinal cord which can cause neurological deterioration, such as C5 palsy [34]. The overall incidence of C5 nerve root palsy following cervical spine surgery is between 5–6%, and it ranges from 0–26.4% for anterior and 0–50% for posterior cervical procedures [35,36]. It usually presents with severe weakness of the deltoid muscle and a mild to moderate weakness of the biceps muscle. There is associated sensory loss and pain in the C5 dermatome [37,38].

Conclusion

Cervical spinal stenosis is usually the result of age-related degenerative changes in the spine which is also known as cervical spondylosis. The degenerative cascade starts with disc desiccation followed by facet hypertrophy, ligamentum flavum thickening with infolding, and kyphotic collapse of the cervical spine. In some patients there can be congenital narrowing of the spinal canal. Spinal stenosis can lead to cervical myelopathy from direct cord compression and ischemic dysfunction.
Static as well as dynamic factors play a role in the pathogenesis of myelopathy and these should be kept in mind when planning treatment options.

A good history and clinical examination can establish the diagnosis and MRI studies are invaluable in confirming the diagnosis and localizing the level/levels of the lesion.

The treatment of mild myelopathy is usually conservative. Operative treatment is often reserved for patients with moderate to severe myelopathy.

Anterior surgery is usually carried out in patients with stenotic disease limited to few segments and in those with kyphotic deformity. Posterior surgery is usually done in patients with multiple segment disease.

A Cochrane review, however, found that the data from the literature was not adequate to provide definitive conclusions on the role of surgery in the treatment of spondylotic radiculopathy or myelopathy.

Patients with spinal stenosis should be informed that surgery is effective in preventing further decline in function, but it may, however, not result in substantial improvement from their current level of function. The patient should also be made aware that surgery can be associated with serious complications including neurological deterioration.

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