Cervical Spondylosis

What it is. Cervical spondylosis is the age-related degenerative cascade of the cervical spine, involving the intervertebral discs, the vertebral bodies (osteophytes), the facet joints and the ligaments. It spans everything from an asymptomatic radiographic finding to debilitating myelopathy, and the same set of changes produces all three clinical syndromes: axial pain, radiculopathy and myelopathy.

Who has it. Prevalence increases linearly with age: 25% at age 40 and over 85% at age 60. The segments that give way are C5-6, the most mobile and the most commonly affected, and C6-7.

Risk factors. Age is the primary one, and a family history of early degeneration is the other that cannot be changed. The modifiable list is worth taking a history for:

• Smoking - accelerates disc desiccation
• Heavy labour - axial loading
• Vibration exposure - jackhammering
• Contact sports

Previous whiplash or cervical injury often initiates the cascade early.

Natural history. Generally benign, but be precise about what "benign" means. In the 10-year follow-up of 205 patients with neck pain (Gore, Spine 1987, PMID 3576350), 79% had a decrease in pain - yet only 43% became pain-free, and 32% still had moderate or severe residual pain. So the honest counselling line is that most people get better but a third do not get better enough, and that is a different sentence from "it resolves".

The same study found pain severity was not related to the degree of degenerative change, canal diameter or lordosis, which is why treating the radiograph rather than the patient goes wrong here. Myelopathy is the exception: it deteriorates in a stepwise fashion rather than improving spontaneously (Nurick, Brain 1972, PMID 5023079).

It begins in the disc. Disc desiccation - loss of water content - is the first event, and the rest of the cascade follows from it.

• Loss of disc height reduces the tension on the annular fibres and the ligaments
• Segmental instability follows, the vertebral bodies moving more than they should
• Osteophytes are the body's answer to that instability, increasing surface area to restabilise the joint
• Uncinate hypertrophy develops as the uncovertebral joints carry more load with the disc collapsed, and those osteophytes project into the foramen - radiculopathy
• Facet hypertrophy follows in the posterior joints, causing pain and encroaching on the canal
• Ligamentum flavum buckling completes it: with height lost the ligament is redundant and buckles inwards, compressing the cord from behind - myelopathy

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The Kirkaldy-Willis cascade divides the same degeneration into three stages by age.

• Dysfunction, age 15-45. Annular tears, endplate microfractures and facet synovitis, with the potential for disc herniation. Episodic neck pain.
• Instability, age 35-70. Disc height loss and a dark, desiccated disc, lax facet capsules, the beginning of osteophyte formation, and segmental instability.
• Stabilisation, age over 60. Advanced osteophytes bridging levels and facet hypertrophy leave a stiff, restabilised spine in which stenosis - foraminal or central - is the main problem.

OPLL. Ossification of the posterior longitudinal ligament is a distinct but related pathology, often co-existing, and particularly common in Asian populations (Japanese and Korean). It causes severe, hard compression of the anterior cord.

Applied Anatomy

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The ligaments. The anterior longitudinal ligament is a strong broad band that prevents hyperextension and is often the site of large anterior osteophytes (DISH). The posterior longitudinal ligament is a narrower band behind the bodies that prevents hyperflexion, and is the ligament that ossifies in OPLL. The ligamentum flavum connects the laminae and is elastic and yellow; it compresses the cord from behind when it hypertrophies or buckles in extension.

The neural foramen. Its boundaries and contents:

• Anterior: uncovertebral joint, disc and the posterior aspect of the vertebral body
• Posterior: facet joint (the superior articular process of the lower vertebra) and ligamentum flavum
• Superior and inferior: the pedicles of the levels above and below
• Contents: the exiting nerve root, with the dorsal root ganglion usually inside the foramen, the radicular artery and a venous plexus

So an uncinate osteophyte compresses the root from in front, and facet hypertrophy compresses it from behind.

Canal dimensions. The numbers worth carrying:

• Normal: 17-18mm
• Relative stenosis: under 13mm - watch for symptoms
• Absolute stenosis: under 10mm - high risk of cord injury
• Cord compression: under 8mm effective diameter

The Torg ratio, canal diameter divided by vertebral body diameter, suggests stenosis below 0.8, but it has a high false positive rate and an absolute measurement on MRI is preferred.

Blood supply of the cord. The anterior spinal artery supplies the anterior two-thirds - the motor tracts and the spinothalamic tracts - and is prone to compression from anterior osteophytes and disc herniation. The paired posterior spinal arteries supply the posterior columns and therefore proprioception. The grey matter is highly vascular, but the watershed zone leaves the anterior cord susceptible to ischaemia from compression by osteophytes, and that ischaemia contributes to the pathophysiology of cervical spondylotic myelopathy. Radicular arteries enter through the foramen; the largest is the artery of Adamkiewicz, usually T9-L1 but it can be higher.

The vertebral artery. It ascends in the transverse foramen from C6 to C1, usually skipping the C7 transverse foramen, and is described in four segments: V1 pre-foraminal, V2 foraminal from C6 to C2, V3 the extradural loop at the atlas, and V4 intradural. It is vulnerable during lateral dissection and during lateral mass or pedicle screw insertion. The left is often larger than the right, and occlusion of a dominant artery can be fatal (Wallenberg syndrome, stroke).

History. The first task is to work out which of the three syndromes is in front of you.

Red flags. These take the patient out of the degenerative pathway and into urgent MRI.

Differential Diagnosis

The double crush. Concurrent proximal compression at the cervical root and distal compression such as a carpal tunnel can produce symptoms greater than either lesion alone, so examine the whole limb before settling on one level.

Which page you need. Spondylosis is the substrate; what it does is what has its own page. If the picture is root - dermatomal arm pain, Spurling - go to cervical radiculopathy. If it is cord - gait, hands, hyperreflexia - go to cervical myelopathy, where the grading and the urgency live and where delay costs recovery. The disc itself and its operative thresholds are cervical disc disease, and when the operation is anterior it is ACDF. Note the asymmetry the Boden study (PMID 2398088) forces on this whole page: degenerative change is near-universal on MRI in asymptomatic people, so the imaging cannot make the diagnosis - the syndrome does.

Physical Examination

Provocative tests. These are the bedside tests that separate a compressed root from a compressed cord.

• Spurling test - extension, lateral rotation and axial load. Reproduction of radicular pain is positive, and specificity is 93%, so a positive test rules radiculopathy in.
• Shoulder abduction (Bakody) test - relief of arm pain with the hand on the head is C5/C6 radiculopathy, the position relieving tension on the root.
• Lhermitte's sign - a shock sensation down the spine on flexion, indicating myelopathy or cord compression.
• Finger escape sign - the patient cannot hold the fingers extended and adducted (C8/T1 weakness in myelopathy).
• Grip and release test - 20 times in 10 seconds is normal; the myelopathic hand is slower.
• Inverted radial reflex - tapping the supinator produces finger flexion instead of the wrist or supinator response, indicating C5/6 cord compression.
• Valsalva manoeuvre - raises intrathecal pressure and aggravates radicular pain.

The myelopathic patient. The story is hand clumsiness, weak grip and wasting of the intrinsics in the first web space, together with a broad-based, spastic, unsteady gait. The long-tract signs to elicit are Hoffman, Babinski, hyperreflexia and clonus.

Root levels. The motor, sensory and reflex findings that localise the root:

• C5: deltoid, lateral arm, biceps reflex
• C6: wrist extension, thumb and index finger, brachioradialis reflex
• C7: triceps, middle finger, triceps reflex
• C8: finger flexion, little finger
• T1: interossei, medial forearm

The airway. After an anterior approach the airway is the first concern: a postoperative haematoma is an emergency, and oedema adds to it.

Dysphagia. The commonest complaint after an anterior approach, transient in up to 70%. Set that beside the measured trajectory in the Bazaz series below - 50.2% at one month falling to 12.5% at a year - and the two figures say the same thing: the early rate is high, most of it settles, and chronic dysphagia is rare.

Preventing it. Minimise retractor pressure, relax the retractors intermittently, and deflate the endotracheal tube cuff during retraction.

Managing it. Reassurance, since most resolve, with speech pathology review, a nasogastric tube if the aspiration risk is high, and intraoperative dexamethasone, which may help the oedema.

Adjacent segment disease. The rate is about 2.9% per year for symptomatic disease, reaching 25.6% by ten years (Hilibrand), of whom more than two-thirds needed a further operation. Radiographic change is far commoner: 92% of 180 patients followed beyond five years had additional degeneration at an adjacent level (Goffin 2004). Keep the two numbers apart, because one is a new radiculopathy or myelopathy and the other is an appearance on a film.

The cause is genuinely two competing mechanisms, and the evidence does not cleanly favour the biomechanical one. Increased stress at the levels above and below a fusion is the intuitive explanation, but Hilibrand found adjacent-segment disease was less common after multilevel than single-level fusion - the opposite of what stress transfer predicts - and Goffin found the same rate of progression in younger trauma patients as in older degenerative ones, concluding that fusion biomechanics and the natural progression of pre-existing spondylosis both contribute. Manage conservatively at first and extend the fusion if symptoms are concordant, and counsel before the index operation, because this is the commonest reason a fused patient returns years later.

C5 palsy. The incidence tracks the operation: 3.3% after ACDF, 5.1% after laminoplasty alone, 7.5% after anterior corpectomy and fusion and 11.0% after laminectomy with fusion, pooling to 5.3% across 13,621 patients.

Posterior drift of the cord tethering the shorter, more direct C5 root is the classic explanation, but it is contested. Pooled across 107 studies, anterior decompression for myelopathy carries a similar rate to posterior (4% versus 7%, p=0.999) despite causing no posterior drift, while anterior surgery for pure radiculopathy causes essentially none - so the presence of a compressed cord, not the direction of approach, is what predicts it. Reperfusion injury of the cord is the better-supported mechanism, with tethering at most contributory.

The prognosis splits by approach, and the usual line that most resolve in 6-12 months needs qualifying. Pooled recovery at one year is 100% after ACDF but only 52.9% after laminoplasty and 50% after posterior decompression and fusion, so after the posterior operations roughly half are still not fully recovered at a year.

Other major risks. The remaining items on the consent list:

• Cord injury and carotid injury
• Recurrent laryngeal nerve palsy - hoarseness in 1-2%, more common on the right where the nerve is variable. ENT scope if it persists
• Oesophageal injury - rare but catastrophic and can lead to mediastinitis. Early recognition is key; immediate repair or a flap
• Vertebral artery injury - rare, during drilling or screw insertion. Tamponade, or sacrifice if the contralateral vessel is patent
• Horner's syndrome - sympathetic chain injury, with ptosis, miosis and anhidrosis
• Dural tear - CSF leak, repaired primarily or with a patch or sealant, with bed rest or a drain
• Pseudarthrosis and malposition of the fusion - the late construct failures, alongside adjacent segment disease

Global Epidemiology

Degenerative cervical myelopathy (DCM) is the most common cause of non-traumatic spinal cord dysfunction in adults worldwide, a point emphasised by both the AOSpine/CSRS clinical practice guideline (Fehlings et al, 2017) and the AOSpine North America cohort. Radiographic spondylosis rises steeply with age and is near-universal in older adults, yet only a minority become symptomatic. Ossification of the posterior longitudinal ligament (OPLL) is a major contributor to cervical stenosis in East Asian populations (notably Japan and Korea) and shifts surgical decision-making toward posterior or corpectomy strategies.

Side-by-Side Guidance

Registry & Practice Variation

Spine procedures are tracked in national datasets such as the British Spine Registry and various European spine registries, which consistently show that ACDF and posterior decompression are the dominant constructs, with cervical disc arthroplasty used selectively for single-level disease in younger patients. Practice varies internationally: a higher prevalence of OPLL drives greater use of laminoplasty in Japan and Korea, whereas anterior approaches predominate for focal one- to two-level pathology elsewhere. Across systems, progressive myelopathy is prioritised for earlier surgery over isolated axial pain.

Medication & Rehabilitation Notes

Neuropathic agents (gabapentin, pregabalin) are used for radicular pain but show modest benefit and carry sedation and misuse risk; access may be restricted under national subsidy schemes. Opioids are discouraged for chronic non-cancer neck pain in favour of multidisciplinary, exercise-based rehabilitation. High-velocity cervical manipulation should be avoided where myelopathy or instability is suspected.

Return to Driving

Patients should not drive in a rigid collar and should resume driving only when able to comfortably rotate the head to check blind spots and perform an emergency stop — typically a few weeks postoperatively, guided by local licensing authority advice.