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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11. Lebl DR, Hughes A, Cammisa FP Jr, O'Leary PF. Cervical spondylotic myelopathy: pathophysiology, clinical presentation, and treatment. HSS J. 2011;7(2):170–178. 
12. Hosono N, Sakaura H, Mukai Y, Kaito T, Makino T, et al. (2008) A simple performance test for quantifying the severity of cervical myelopathy. J Bone Joint Surg Br 90: 1210-1213.
13. Ebara S, Yonenobu K, Fujiwara K, Yamashita K (1988) Myelopathy hand characterized by muscle wasting. A different type of myelopathy hand in patients with cervical spondylosis. Spine 13: 785-791.
14. Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain. 1972;95:87–100.
15. Ranawat C, O’Leary P, Pellici P, Tsairis P, Marchisello P, et al. (1979) Cervical fusion in rheumatoid arthritis. JBJS Am 61A: 1003-1010.
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17. Bernhardt M, Hynes RA, Blume HW, White AA. Cervical spondylitic myelopathy. J Bone Joint Surg Am 1993; 75:119–128.
18. Muhle C, Metzner J, Weinert D, et al. Classification system based on kinematic MR imaging in cervical spondylitic myelopathy. AJNR 1998;19:1763–1771.
19. Kang Y, Lee JW, Koh YH, et al. New MRI grading system for the cervical canal stenosis. AJR Am J Roentgenol. 2011;197(1): W134–W140. 
20. Teresi LM, Lufkin RB, Reicher MA, et al. Asymptomatic degenerative disk disease and spondylosis of the cervical spine: MR imaging. Radiology. 1987;164(1):83–88. 
21. Campbell WW (1999) Focal neuropathies. In: Campbell WW(ed). Essentials of Electrodiagnostic Medicine: Williams & Wilkins publications. Baltimore, USA. pp. 255-278.
22. Nardone R, Höller Y, Brigo F, et al. The contribution of neurophysiology in the diagnosis and management of cervical spondylotic myelopathy: a review. Spinal Cord. 2016;54(10):756–766. doi:10.1038/sc.2016.82.
23. Kadanka Z, Mares M, Bednaník J, et al. Approaches to spondylotic cervical myelopathy: conservative versus surgical results in a 3-year follow-up study. Spine (Phila Pa 1976). 2002;27(20):2205–2211.
24. Kadaňka Z, Bednařík J, Novotný O, Urbánek I, Dušek L. Cervical spondylotic myelopathy: conservative versus surgical treatment after 10 years. Eur Spine J. 2011;20(9):1533–1538. 
25. Sumi M, Miyamoto H, Suzuki T, Kaneyama S, Kanatani T, Uno K. Prospective cohort study of mild cervical spondylotic myelopathy without surgical treatment. J Neurosurg Spine. 2012;16(1):8–14. 
26. Rhee JM, Shamji MF, Erwin WM, et al. Nonoperative management of cervical myelopathy: a systematic review. Spine (Phila Pa 1976). 2013;38(22 Suppl 1):S55–S67. 
27. Okada Y, Ikata T, Yamada H, et al. Magnetic resonance imaging study on the results of surgery for cervical compression myelopathy. Spine (Phila Pa 1976) 1993; 18:2024–2029. 
28. Yonenobu K. Cervical radiculopathy and myelopathy: when and what can surgery contribute to treatment? Eur Spine J 2000; 9:1–7.
29. Kim TH, Ha Y, Shin JJ, Cho YE, Lee JH, Cho WH. Signal intensity ratio on magnetic resonance imaging as a prognostic factor in patients with cervical compressive myelopathy. Medicine (Baltimore). 2016;95(39):e4649.
30. Epstein NE. High cord signals on magnetic resonance and other factors predict poor outcomes of cervical spine surgery: A review. Surg Neurol Int. 2018;9:13.
31. Fouyas IP, Statham PF, Sandercock PA. Cochrane review on the role of surgery in cervical spondylotic radiculomyelopathy. Spine (Phila Pa 1976). 2002;27(7):736–747.
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Lumbar Spinal Stenosis

                          Lumbar Spinal Stenosis

                                       DR KS DHILLON

What is 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 spinal stenosis classically present with neurogenic claudication in the lower limbs on standing and walking and the symptoms are relieved with bending forward, sitting and lying down. The neurogenic claudication symptoms include pain in the lower limbs radiating to the ankles during walking and standing, numbness, tingling, and weakness.
The prevalence of lumbar spinal stenosis in the USA is estimated to be 9% in the general population, and up to 47% in people over age 60 [1].

Etiology of spinal stenosis

Lumbar spinal stenosis results from degenerative, developmental, or congenital disorders. The most common cause is degenerative disease of the spine.
The following classification is useful in understanding the etiology and pathogenesis of spinal stenosis [2].

A.Congenital-developmental stenosis

• Idiopathic
• Achondroplasia or hypochondroplasia
• Hypophosphatemic vitamin D-resistant rickets
• Morquio's mucopolysaccharidosis
• Spinal dysraphism

B.Acquired stenosis

• Degenerative

         1.Spondylosis
         2.Spondylolisthesis
         3.Scoliosis
         4.Ossification of the posterior longitudinal ligament
         5.Ossification of the ligamentum flavum
         6.Intraspinal synovial cysts

• Postoperative

         1.Laminectomy
         2.Fusion

• Posttraumatic
• Metabolic or endocrine

         1.Epidural lipomatosis-Cushing's disease
         2.Osteoporosis
         3.Acromegaly
         4.Pseudogout-calcium pyrophosphate dihydrate deposition disease
         5.Renal osteodystrophy
         6.Hypoparathyroidism

• Other

        1.Paget's disease of bone
        2.Rheumatoid arthritis
        3.Ankylosing spondylitis
       4.Diffuse idiopathic skeletal hyperostosis

Congenital or developmental stenosis was first described by Sarpyener [3] in children and later in adults by Verbiest [4]. It is most frequently caused by an idiopathic reduction in the normal spinal canal dimensions or by achondroplastic dwarfism. In symptomatic adults with congenital or developmental stenosis, the anterior-posterior diameter of the lumbar spinal canal has been found to be 12 mm or less, which is much smaller than the 15- to 23-mm diameter in normal cadaver skeletons [5]. There have been suggestions that in familial developmental lumbar stenosis the dimensions of the spinal canal, may be regulated by genetic factors [6,7].

Developmental stenosis of the whole spinal canal is a known feature of achondroplastic dwarfism [8]. The vertebrae, in these patients, have short pedicles and decreased interpediculate distances, which leads to anteroposterior and lateral stenosis of the canal. In adulthood, these patients develop progressive compression of the spinal cord or cauda equina [9]. Minor trauma and disc extrusion in the thoracic or lumbar spine in these patients can lead to a sudden onset of flaccid or spastic paraplegia.

The main cause of acquired lumbar stenosis is degenerative disease of the spine. Degenerative disease is also known as lumbar 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. Increases in stresses on the posterior part of the spine lead to the formation of osteophytes and thickening of laminae, pedicles, and 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. The thickness of the ligamentum flavum can increase from its normal of 2 to 5 mm to as much as 5 to 10 mm in patients with spondylosis [2]. This hypertrophied ligamentum flavum is the major cause of lumbar stenosis in some patients [2].

Degeneration of the spine can lead to spondylolisthesis where relative anterior or posterior displacement of one vertebral body on an adjacent vertebra occurs. This can lead to narrowing of the spinal canal resulting in spinal stenosis. Degenerative spondylolisthesis is a frequent complication of advanced lumbar spondylosis [10].

Although acquired spinal stenosis is usually caused by spondylosis and spondylolisthesis, there are many other rarer causes of acquired spinal stenosis. These include vertebral deformities, ossification of posterior longitudinal ligament and the ligamentum flavum, spinal infections, intraspinal synovial cysts, surgical procedures (laminectomy or spinal fusion), trauma, and bony overgrowth due to Paget's disease, ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis, or rheumatoid arthritis. There are various metabolic and endocrine abnormalities, such as acromegaly, pseudogout, hypoparathyroidism, or renal osteodystrophy, which can be associated with lumbar stenosis.  Epidural lipomatosis, which can be seen in patients with endogenous obesity who are taking steroids or who have Cushing's syndrome, can cause spinal stenosis leading to radiculopathy [2].

Clinical diagnosis of lumbar spinal stenosis

Lumbar spinal stenosis (LSS) is a poorly defined clinical syndrome. Tomkins-Lane [11] carried out an International Delphi Study to arrive at a consensus on the clinical diagnosis of lumbar spinal stenosis. Their study showed that within 6 historical questions clinicians become 80% certain about the diagnosis of LSS. They, however, proposed a consensus-based on a set of “7 history items” that act as a practical criterion for defining LSS in the clinical setting.
The most commonly selected factors in the survey were:

• Leg pain while walking
• Flex forward while walking to relieve symptoms 
• Sit down or bend forward to relieve pain
• Normal foot pulses
• Relief with rest 
• Lower extremity weakness 

They found that significant change in certainty ceased after 6 questions at 81% certainty. The task force found that the 7th most popular question was “Does the patient have low back pain?”. The consensus of the Taskforce was that the presence of low back pain was an important component of history taking in patients with LSS diagnosis and they decided that this question should be included in the list of factors for diagnosis of LSS.

The question on top of the list, ‘Does the patient have leg or buttock pain while walking?’, refers to neurogenic claudication which is recognized to be the hallmark of LSS [12,13,14].
A systematic review by de Schepper et al [15] found that the most useful information for making a diagnosis of LSS included age, radiating leg pain which is made worse while standing/walking, absence of pain when seated, improvement of symptoms on bending forward, and a wide-based gait.
Important items identified in the study by Tomkins-Lane [11], that were shown to be less specific or sensitive in the systematic reviews included the presence of motor or sensory disturbances while walking, low back pain and lower extremity weakness. Patients with neurogenic claudication usually report a progressive reduction in the distance they can walk before symptoms are noticed. All patients with suspected neurogenic claudication must have their foot pulses examined to rule out vascular claudication in the lower limbs.

The pathogenesis of nerve root dysfunction in patients with neurogenic claudication, which produces poorly localized leg pain exacerbated with walking and relieved by rest or bending forward remains unclear. It is believed that the pain and weakness may result from intermittent ischemia caused by compression of the radicular microcirculation during periods of increased axonal activity [2].
Positional radiculopathy, which is characterized by radiating leg pain, paresthesias, numbness, or weakness occurring when the patient stands erect or bends backward, is a more common initial symptom of lumbar stenosis than is neurogenic claudication. Extension of the lumbar spine causes relaxing and buckling of the ligamentum flavum as well as increasing disc protrusion which further narrows the canal leading to radiculopathy [16]. Extension of the spine also brings the laminae
closer together and projects the superior facets farther upward, which causes further narrowing the spinal canal and foramina by as much as 60% as compared to their diameter during lumbar flexion [2].

Cauda equina syndrome is uncommon in patients with spinal stenosis. The symptoms in LSS develop gradually unlike in patients with acute disc prolapse where the symptoms appear abruptly. In patients with LSS demonstrable sensory or motor, deficits are usually absent. Since LSS has
a predilection for the mid lumbar spine, patients may present with quadriceps weakness or atrophy and a depressed or absent knee jerk.  Major motor weakness such as a footdrop may be seen in some patients after prolonged walking. Examination of the patient with LSS after making them walk till the symptoms appear may show motor and/or sensory deficit.

Diagnostic test for spinal stenosis

In patients with suspected LSS, plain x rays of the lumbar spine is the first diagnostic test that is carried out. The x rays cannot confirm the diagnosis of LSS but it can show the presence of lumbar spondylosis and/or spondylolisthesis.

The North American Spine Society (NASS) Evidence-Based Clinical Guidelines for diagnosis and treatment of degenerative spinal stenosis [17] recommend that ‘in patients with history and physical examination findings consistent with degenerative lumbar spinal stenosis, MRI is suggested as the most appropriate, noninvasive test to confirm the presence of anatomic narrowing of the spinal canal or the presence of nerve root impingement’. The grade of recommendation is grade B.

Mamisch et al [18] carried out a Delphi survey to develop a list of radiologic criteria for describing lumbar spinal stenosis. The survey found that there are no widely accepted quantitative criteria for the diagnosis of lumbar spinal stenosis though there are partially accepted qualitative criteria for the diagnosis of lumbar spinal stenosis. The partially accepted criteria include disc protrusion, loss of perineural intraforaminal fat, hypertrophic facet joints, absent cerebrospinal fluid around the cauda equina, and hypertrophy of the ligamentum flavum.

The survey found that cutoff values for the highest-rated quantitative parameters were 12 mm for the midsagittal diameter of the dural sac, 3 mm for the diameter of the foramen, and 3 mm for the lateral recess height.

Generally, these quantitative criteria for the diagnosis of LSS were not accepted by the authorities who were surveyed.

Steurer et al [19] carried out a systematic review of the literature to investigate which quantitative radiological signs are described in the literature and which radiological criteria are used to establish inclusion criteria for a diagnosis of LSS.

They found that there were 10 different parameters which were used to quantify lumbar spinal stenosis. The most often reported measures for central stenosis were the anteroposterior diameter (< 10 mm) and the cross-sectional area (< 70 mm2) of spinal canal. A lateral recess height equal to or less than 2 mm and/or lateral recess depth equal to or less than 3 mm or a lateral recess angle of less than 30° has been described as diagnostic for lateral recess stenosis.

For foraminal stenosis, the only quantitative criterion was the diameter of the foramen and a diameter of 2 to 3 mm is considered to indicate stenosis.

The NASS guidelines [17] recommend that in patients with suspected LSS in whom MRI is either contraindicated or inconclusive, CT myelography is the most appropriate test to confirm the presence of anatomic narrowing of the spinal canal and the presence of nerve root impingement. In patients in whom MRI and CT myelography are contraindicated, inconclusive or inappropriate, CT scan is the preferred test to confirm the narrowing of the spinal canal and presence of nerve root impingement.
The presence of spinal canal narrowing on radiological imaging does not indicate a diagnosis of spinal stenosis because degenerative changes in the spine are common in asymptomatic individuals. Brinjiki et al [20] did a systematic review of literature of imaging features of spinal degeneration in asymptomatic populations. They found that the prevalence of disk degeneration in asymptomatic individuals increased from 37% among 20-year-old individuals to 96% among 80-year-old individuals. The prevalence of disk bulge increased from 30% among 20 years old individuals to 84% among 80 years old individuals. The prevalence of disc protrusion increased from 29% of those 20 years of age to 43% of those 80 years of age.

Boden et al [21] did MRI scans in 67 individuals who never had back pain, sciatica and neurogenic claudication in the past. They found 21% of the individuals had radiological evidence of spinal stenosis.

Wiesel et al [22] did CT scans of the spine in asymptomatic individuals and found the presence of disc herniation, facet degeneration or spinal stenosis in about 50% of the subjects. They also found that there was no significant correlation between the area of the dural sac in axially loaded CT and the clinical symptoms of spinal stenosis.

False-positive and false-negative CT scan and MRI findings of nerve compression have been well documented, which makes radiological imaging as a sole means of diagnosing spinal stenosis untenable [21,22,23]. There is also an element of significant variation of image interpretation of  MRI and CT scan in the diagnosis of spinal stenosis [24].

Therefore the diagnosis of spinal stenosis has to be clinical and it can be confirmed and correlated with imaging studies.

There are several radiological criteria for defining the severity of spinal stenosis but their role remains unclear. Several classifications for defining radiological spinal stenosis have been published in the literature [25].

Lee et al [26] have offered a simple MRI based classification system for central stenosis. They described a 4-grade (0, 1, 2, and 3) system based on the degree of separation of the cauda equina on T2-weighted axial images. They did not measure the parameters. They defined grade 0 as no lumbar stenosis when there was no obliteration of the CSF space in front of the cauda equina; mild or grade 1 stenosis was present when there was no CSF in front of the cauda equina and the cauda equina remained separated; grade 2 or moderate stenosis was present when there was some cauda equina aggregation or bunching and grade 3 or severe stenosis was present when there was no space between the cauda equina elements and the roots cannot be visually separated. They found that with this classification the interobserver reliability was substantial to excellent for all levels and the intraobserver reliability was excellent. This classification system has been independently validated by Park et al [27] who showed that there was substantial interobserver reliability in the diagnosis of spinal stenosis with this classification. The authors also showed that none of the patients with grade 0 stenosis had neurological symptoms and almost all patients with grade 3 stenosis had neurological symptoms. The relevance of grade 1 and 2 stenosis remained unclear.

Lee et al 28] have also developed a grading system for foraminal stenosis. They divided the stenosis into 4 grades, from 0 to 3 based on sagittal MRI images of the lumbar spine. In this classification grade 0 refers to the absence of foraminal stenosis. In grade 1 stenosis there is mild foraminal stenosis with perineural fat obliteration in the two opposing directions, vertical or transverse. In grade 2  stenosis there is moderate foraminal stenosis with perineural fat obliteration in all four directions without morphologic change and grade 3 refers to severe foraminal stenosis with nerve root collapse or morphologic change. The authors concluded that this ‘new grading system for foraminal stenosis of the lumbar spine showed nearly perfect interobserver and intraobserver agreement and would be helpful for clinical study and routine practice’.

Wildermuth et al [29] have similarly divided foraminal stenosis into four Grades (1-4) based on the presence of perineural fat as seen on MRI imaging. Grade 1 is the absence of stenosis with normal perineural fat. In grade 2 or slight stenosis, there is compression of perineural fat but the fat is still present all around the nerve root. In grade 3 or marked stenosis, there is a loss of perineural fat on at least one side of the nerve and in grade 4 or advanced stenosis, there is a complete loss of perineural fat.

There are no universally accepted criteria for radiological diagnosis of lateral canal stenosis. Steuer et al [30] did a systematic review of the literature and found that the height and the depth of the lateral recess and the lateral recess angle are the criteria used for describing lateral canal stenosis. The measurements are done on a CT scan or an MRI (axial T2 weighted) images of the lumbar spine. The depth refers to the measurement between the top of the pedicle and the superior articular facet. The height refers to the distance between the most anterior point of the superior articular facet and the posterior border of the vertebral body and the lateral recess angle as the angle between the lines parallel to the floor and the roof of the lateral recess. A lateral recess height ≤ 2 mm and/or lateral recess depth ≤ 3 mm or a lateral recess angle < 30° has been described as diagnostic for lateral recess stenosis.

Treatment of lumbar spinal stenosis

There is no evidence in the literature to show that the outcome of treatment of spinal stenosis is better as compared to the natural history of the disease (no treatment) [31].

Conservative treatment

Anti-inflammatory medications, physical therapy and conditioning is the usual mode of conservative treatment to relieve pain and improve function in patients with spinal stenosis [32]. Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used in the treatment of LSS. In the elderly population NSAIDs have to be used with caution because of their potential gastrointestinal and cardiovascular adverse effects.

There is no credible evidence that other pharmaceutical agents such as methylcobalamin, gabapentin, prostaglandin E, intranasal calcitonin, and intramuscular calcitonin are of value in the treatment of spinal stenosis [31].

Unfortunately there is insufficient evidence in literature ‘to make a recommendation for or against the use of pharmacological treatment in the management of spinal stenosis’ [31].
There, however, is level II therapeutic evidence that an exercise program which includes stretching, strengthening and low-intensity cycling exercises, in the short term, improves pain and disability in patients with lumbar spinal stenosis [33].

Physical therapy has shown some improvement in physical function in patients with spinal stenosis although the evidence is not so robust [34,35].

Epidural steroid injections

Epidural steroid injections are widely used for the treatment of patients with spinal stenosis despite the absence of credible evidence regarding its efficacy and safety. Friedly et al [36] carried out a multisite, double-blind, randomized trial in 400 patients with spinal stenosis who had moderate to severe leg pain and disability. One group was given epidural injections of glucocorticoids plus lidocaine and the other group lidocaine alone. The epidural injections were fluoroscopically guided. At six weeks they found no difference between the two groups in the primary outcomes as measured by the Roland-Morris Disability Questionnaire (RMDQ) scores and the rating of the intensity of leg pain. Likewise, there was no difference between the subgroups who received interlaminar or foraminal injections. The authors concluded that ‘in the treatment of lumbar spinal stenosis, epidural injection of glucocorticoids plus lidocaine offered minimal or no short-term benefit as compared with epidural injection of lidocaine alone’.

Complications with epidural injections were not uncommon. The complication rate in the glucocorticoid–lidocaine group was 21.5% and in the lidocaine-alone group was 15.5%. Complication rates were higher in the transforaminal injection group. Cortisol suppression was significantly higher in the glucocorticoid–lidocaine group.

In this study patients in both treatment groups had improvement in function and decreased pain probably due to a placebo effect, the natural history of spinal stenosis, and other factors present in both study groups. Unfortunately this excellent study did not have a sham group.

Chou et al [37] in 2015 did a systematic review and meta-analysis of the published data on the use of epidural corticosteroids in the treatment of lumbar radiculopathy and spinal stenosis. They evaluated 30 placebo-controlled trials of epidural corticosteroid injections for radiculopathy, and 8 trials were for spinal stenosis. They found that with epidural corticosteroid injections for radiculopathy there was an immediate reduction in pain and function but the benefits were small and not sustained. There was also no effect on long term surgical risk. There was some evidence to suggest that there are no benefits of epidural steroids in the treatment of spinal stenosis. They found that ‘serious harms were rare, but harms reporting was suboptimal’.

Nancy E. Epstein [38] in 2013 did a comprehensive review of the literature to assess the risks of epidural and transforaminal steroid injections in the spine. Epidural injections for the management of spinal conditions, though not approved by the FDA, are being performed with an increased frequency (160%). They are typically short-acting with no long term benefit and their use can be associated with major risks/complications. According to Nancy Epstein, there have been reports of contaminated epidural steroid injections which had resulted in meningitis, stroke, paralysis, and even death. Though many of the complications go unreported, other reported complications include ‘life-threatening infections, spinal fluid leaks (0.4-6%), positional headaches (28%), adhesive arachnoiditis (6-16%), hydrocephalus, air embolism, urinary retention, allergic reactions, intravascular injections (7.9-11.6%), stroke, blindness, neurological deficits/paralysis, hematomas, seizures, and death’ [38].
In 2009 FDA started investigations into adverse events related to epidural injections and they found that between 1997 and 2014 there were 90 serious and sometimes fatal neurological complications associated with the use of epidural glucocorticoid injections. The complications included paraplegia, quadriplegia, spinal cord infarction, and stroke. Following this investigations, in 2014, the FDA issued a mandatory requirement that ‘all injectable glucocorticoid product labels carry a warning stating that “serious neurologic events, some resulting in death, have been reported with epidural injection of corticosteroids” and that the “safety and effectiveness of epidural administration of corticosteroids have not been established and corticosteroids are not approved for this use” [39].
Ammendolia et al [40] in 2013 did a Cochrane database systematic review to evaluate the effectiveness of non-operative treatment of patients with spinal stenosis and neurogenic claudication. The review included pharmaceutical and physical therapy interventions as well as epidural injections and they found that ‘moderate and high-quality evidence for nonoperative treatment is lacking’. What about surgical treatment for spinal stenosis?

Surgical treatment of spinal stenosis

Spinal decompression

Since the symptoms of spinal stenosis are due to narrowing of the spinal canal, surgical decompression was considered to be the logical treatment for symptomatic spinal stenosis from time immemorial. However, over the years clinical experience showed that many patients did well without surgery.

There have been many reports in the literature with variable outcomes after surgical treatment for spinal stenosis. The outcome varied from 26% to 100% good results at 4 years [41], 77% good results at 8 years [42], and  68% good results at 12 years [43].

Johnsson et al [44] compared the outcome of surgical and conservative treatment of patients with spinal stenosis. They found that 60% of the patients treated surgically improved and 25% deteriorated at 53 months follow up and of those treated conservatively 30% improved and 60% remained unchanged at 31 months follow up.

Amundsen et al [45] did a long term prospective study in 100 patients to compare the outcome of conservative and surgical treatment of spinal stenosis. In this study there were 19 patients with severe symptoms who had surgical treatment and 50 patients with moderate symptoms had conservative treatment, and another 31 patients were randomized between the conservative treatment group (18 pts) and surgical treatment group (13 pts). All patients were followed up for 10 years.

In the conservative treatment group, good results were reported in 70% of the patients at 6 months, 64% at 1 year and 57% at 4 years. In the surgical group, good results were reported in 79% at 6 months, 89% at 1 year and 84% at 4 years. In patients who were randomly assigned to the conservative and surgical group, the results were much better in the surgical group as compared to the conservative group.

This study provides Level IV evidence that patients with severe symptoms at presentation, who undergo surgical decompression, the outcome will be good 80-90% of the time and in patients with moderate symptoms who undergo conservative treatment, the results will be good in about 70% of the time (31).

Mariconda et al [46] reported a prospective study of 44 patients which compared laminectomy with conservative treatment in patients with mild to moderate leg pain. At 4 years follow up they found that 68% of the surgical group had good results while 33% in the conservative group had good results. There was a 9 percent reoperation rate in the surgical group and 9% crossover rate. This study provides level IV evidence that surgical decompression gives good results in 68% of the patients [31].

The outcome of spinal decompression for the treatment of LSS is very variable. There is only level IV evidence to show that the outcome is good in 68% to 90% of the patients. There is also level IV evidence that conservative treatment can give good results in about 70% of the patients.

Spinal fusion

Spinal fusion is often done after spinal decompression due to a belief that posterior spinal decompression can destabilize the spine. Spinal fusion prolongs the operating time and increases blood loss and can be associated with more complications. Is spinal fusion necessary after posterior decompression?

Grob et al [47] did a study to address this issue. They did a randomized, controlled trial of 45 patients with symptomatic lumbar stenosis with no spinal instability. The patients were randomly assigned to one of the three groups. Group 1 patients had laminotomy with medial facetectomy. In group 2 the patients had decompression with fusion of the most stenotic segment and in group 3 the patients had decompression with fusion of all decompressed segments. At an average follow up  28 months all groups showed an increase in walking ability and a decrease in pain and there was no difference in the outcome between the groups. This study provides Level II therapeutic evidence that there is no difference in the clinical outcome in patients, with spinal stenosis and no spinal instability, who had posterior decompression alone and in those who had decompression with fusion [31].

Patients with spinal instability as defined by Posner’s method [48] generally do not do well if a laminectomy is done without fusion. Yone and Sakou [49] studied 60 patients who had surgery for spinal stenosis. Thirty-three of the 60 patients had spinal instability as defined by the Posner’s criteria. Of the 33 patients with instability 19 had laminectomy with fusion and the other 14 refused fusion and had laminectomy alone. Twenty-seven other patients without instability had laminectomy alone. Eighty percent of the patients without instability and 80% of those with instability and fusion had good outcomes whereas only 43% of patients with instability and no fusion had a good outcome.This study provides Level II  evidence that in patients with spinal stenosis and spinal instability, decompression with fusion is more effective than decompression alone [31]. There are other authors who believe that all patients with spinal stenosis can be treated by decompression alone without fusion.

Iguchi et al [50] studied the long term outcome of posterior spinal decompression without fusion in patients with spinal stenosis. They did laminectomy with partial facetectomy without fusion in 122 patients with spinal stenosis. At a minimum of 10 years (average 13 years) follow up, 37 patients were available for evaluation. In 62.2% of the patients, there was no impairment in activities of daily living. The outcome was excellent in 13 (35.1%), good in 8 (21.6%), fair in 8 (21.6%) , and poor in 8 patients (21.6%). Three of the 8 patients (8.1%) required additional surgery. The outcome was the same in patients with preoperative spondylolisthesis and those without spondylolisthesis. Similarly, the outcome was the same in patients with preoperative scoliosis and those without scoliosis. At least 2 levels of laminectomy was performed in each patient. Preoperative sagittal rotation of more than 10° with multilevel laminectomy was thought to be a risk factor for poor outcome. The authors concluded that acceptable results can be obtained with a laminectomy without spinal fusion in patients with spinal stenosis on long term follow up.

Satisfactory long term outcome (8 years to 13 years) of surgical treatment for spinal stenosis ranges from 55% [51], 56.7% [50] and 71% [45].

The risk factors for unsatisfactory outcomes following surgery for spinal stenosis are numerous. Katz et al [52] found that poor long-term outcome, defined as severe pain or the need for a repeat operation, or both, included comorbidities such as osteoarthrosis, cardiac disease, rheumatoid arthritis, or chronic pulmonary disease, longer duration of follow-up, and laminectomy at a single level. However, Iguchi et al [50] found that patients who had multilevel laminectomies and a 10° or more of sagittal rotation had a poorer outcome. Patients undergoing repeat spinal surgery have poorer prognosis [53]. Lower-income, presence of anxiety and depression, existence of compensation claims, absences of preoperative neurological deficit, less severe canal stenosis and absences of preoperative subjective difficulty in walking, are all associated with poorer outcomes after surgery [54].

Despite the existence of a large number of publications in the scientific literature regarding the treatment of spinal stenosis, there appears to be no consensus as to what is the best form of treatment for spinal stenosis. Zaina et al [55] in 2016, did a systematic review of the literature for the Cochrane group to compare conservative and surgical treatment for spinal stenosis. They were unable to conclude whether surgical treatment or a conservative approach is better for lumbar spinal stenosis. They, however, noted that there was a complication rate of between 10% to 24% in patients treated with surgery and there were no side effects of conservative treatment. There were no clear benefits of surgery when comparison was made with conservative treatment. Their conclusion was that ‘clinicians should be very careful in informing patients about possible treatment options, especially given that conservative treatment options have resulted in no reported side effects’.

There is also no good evidence in the literature on the efficacy of surgery for spinal stenosis. Machado et al [56] in 2016 did a systematic review of literature for the Cochrane group to evaluate the outcome of surgical treatment for spinal stenosis. They found that there was very little literature on the efficacy of surgical treatment of spinal stenosis. There were no trials comparing ‘surgery with no treatment, placebo or sham surgery’ though ‘placebo-controlled trials in surgery are feasible and needed in the field of lumbar spinal stenosis’. They also found that decompression with fusion and interspinous process spacers were not superior to decompression alone.

Conclusion

Clinical or symptomatic spinal stenosis has been well defined with little ambiguity and the etiology has been well elucidated. Radiological narrowing of the spinal canal of the spine has been well studied and classified. However, the natural history of symptomatic spinal stenosis is not known because there are no studies comparing treatment and no treatment. However, from the little evidence available, it appears that the outcome is favorable in one third to half of the patients with mild to moderate spinal stenosis even without treatment. The natural history of patients with severe stenosis remains unknown. Rapid neurological decline does not happen in patients with lumbar spinal stenosis.

The use of anti-inflammatory medications, physical therapy, and conditioning remains the mainstay of conservative treatment of symptomatic spinal stenosis. There is no robust evidence to support the use of other pharmaceutical agents in the treatment of spinal stenosis.

Epidural steroid injections are widely used for the treatment of patients with spinal stenosis despite the absence of credible evidence regarding its efficacy and safety. Complications are not uncommon with epidural injections. Complication rates as high as 21.5% have been reported in the literature. Life-threatening infections, paralysis, and even death has been reported.

Despite the presence of a large number of publications in the scientific literature regarding the treatment of spinal stenosis, there appears to be no consensus as to what is the best form of treatment for spinal stenosis. There is no evidence in the literature as to whether surgical or conservative treatment is better for the treatment of spinal stenosis. Surgical treatment can be associated with up to 24% complication rate. Conservative treatment is not known to be associated with side effects. There is no good evidence on the efficacy of surgical treatment for spinal stenosis. Studies show that the outcome of spinal decompression alone is the same as that with decompression with fusion. Interspinous process spacers do not provide any additional benefits to patients in the treatment of spinal stenosis.

Till good evidence is available the treatment of patients has to be individualized and the least invasive treatment which will provide maximum relief with minimal or no side effects should be offered to the patient.

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