Cervical Disc Disease

Cervical disc disease covers both the acute soft disc herniation and the chronic spondylotic hard disc, and the same pathology can present as a nerve root syndrome, a cord syndrome, the two together, or axial neck pain with no signs of neural compression at all. C5-C6 and C6-C7 are the levels that fail most often, C6-C7 most commonly of all.

Risk factors. What to ask about in the history:

• Degenerative change with age
• Smoking
• Heavy manual labour
• Prior disc disease
• Genetic predisposition

Companion pages. This page is the disc disease - the pathology, the ACDF and arthroplasty decision, and the myelopathy. If the picture is cord rather than root - gait, hands, hyperreflexia - the syndrome, its grading and its urgency belong to cervical myelopathy, where delay costs recovery rather than comfort. The nerve-root syndrome, with its dermatomal patterns, examination cluster and conservative management, is set out in cervical radiculopathy, and when the trial fails the operation is ACDF. Before accepting a root at all, note that two of the commonest mimics are peripheral rather than spinal - cubital tunnel syndrome for the C8 picture and thoracic outlet syndrome for the positional lower-trunk one.

The disc. The nucleus pulposus is the central gelatinous material, with a high water content, and it does the cushioning; the annulus fibrosus is the outer fibrous ring that contains it and attaches to the vertebrae. The posterior longitudinal ligament is thin in the cervical spine, so there is less protection against a posterolateral herniation.

The uncovertebral joints of Luschka sit posterolaterally and are a common site of osteophyte formation - the same corner of the foramen a posterolateral herniation occupies. So hard disc and soft disc arrive at the root by the same route.

How compression happens. Disc degeneration costs height and provokes osteophyte formation, the neural foramen narrows, and the neural element is compressed; inflammatory mediators act alongside the mechanical compression.

The foramen and the cord. The foramen is bounded by the disc in front and the facet behind, and osteophyte from either narrows it, which compresses the exiting root. The cord sits centrally in the canal, where a central disc-osteophyte complex compresses it: myelopathy rather than radiculopathy.

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Why these levels. Flexion and extension are greatest at C5-C6, rotation at C1-C2 (atlantoaxial), and lateral bending is coupled with rotation. C5-C6 and C6-C7 carry the most motion and the most stress, which is why disc disease concentrates there - and why preserving motion is the argument for arthroplasty over fusion.

The standard radiological lexicon separates a disc bulge from a true herniation and then grades herniations by shape and by continuity with the parent disc. This matters clinically because the morphology predicts the likelihood of spontaneous resorption and therefore supports the conservative-first approach.

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A herniation is additionally described as contained when the annulus or posterior longitudinal ligament still covers the displaced material, and uncontained when that barrier is breached.

By pathology. The first question about a compressive lesion is whether it is soft or hard, because that decides both whether it can resolve and what the operation has to remove.

A soft disc herniation may resolve naturally; a hard disc rarely does.

By clinical syndrome. The second question is which syndrome is in front of you, because that sets the urgency rather than the technique.

Myelopathy requires urgent attention, and outcomes are worse with delay.

Once myelopathy is diagnosed it should be quantified, because severity guides the urgency of surgery and predicts recovery. Two scales are used.

The modified Japanese Orthopaedic Association (mJOA) score is an 18-point scale, where higher is better, summing four domains: upper-limb motor function (0 to 5), lower-limb motor function (0 to 7), upper-limb sensation (0 to 3) and bladder (sphincter) function (0 to 3). It defines the standard severity bands used in AO Spine pathways.

The older Nurick grade (0 to 5) is a purely gait and ambulation-based scale: grade 0 root signs only without cord involvement; grade 1 cord signs without walking difficulty; grade 2 mild gait difficulty not preventing employment; grade 3 gait difficulty preventing employment; grade 4 walking only with assistance or a frame; grade 5 chairbound or bedridden.

Record the score before the operation is discussed: the debate about timing in mild disease turns on which band the patient is in.

History. Take the pain first: where it sits in the neck and how far down the arm it travels, in a radicular pattern or not. Then the sensory symptoms, numbness and tingling, and the motor ones, weakness and clumsiness. Extension and rotation of the neck are the movements that aggravate it, and the answers that change the pathway are the red flags - gait disturbance, bladder symptoms, and bilateral arm symptoms.

Examination. The Spurling test reproduces the radicular pain and confirms that the origin is a root. Bakody's sign, the shoulder abduction relief sign, works in the opposite direction: pain eases with the arm lifted over the head, and that relief is a cervical radiculopathy finding. Then work through the motor groups (deltoid, biceps, triceps, grip), the dermatomal sensory pattern and the reflexes, and finish with the upper motor neurone signs that say the problem is the cord and not the root.

Differential Diagnosis

Arm pain and hand symptoms have many causes outside the cervical disc. The examiner will reward a structured differential that distinguishes neural compression from peripheral entrapment, referred pain and non-musculoskeletal mimics.

MRI is the gold standard. Its soft tissue detail is what the diagnosis and the surgical decision rest on. Request it for suspected radiculopathy or myelopathy, for failed conservative treatment, for a progressive neurological deficit, and for preoperative planning.

What to assess on the scan:

• The level and side of the herniation
• Neuroforaminal stenosis
• Cord compression, and any signal change within the cord
• Whether the disease is multilevel

T2 signal change within the cord is myelomalacia, and it carries a poorer prognosis.

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Radiographs. AP, lateral and flexion-extension views. They show what the bone is doing - disc space narrowing, osteophyte formation, foraminal narrowing, alignment including kyphosis, and instability on the dynamic views - and they are useful for that overall assessment, but they cannot see soft tissue.

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CT gives the better bone detail, so it is the study for assessing an osteophyte, and CT myelography is the fallback when MRI is contraindicated.

EMG and nerve conduction studies confirm a radiculopathy, distinguish it from a peripheral neuropathy and show denervation changes; they earn their place when the clinical and radiological pictures do not match. The changes take 2 to 3 weeks to develop after the injury.

The decision. A pure radiculopathy with no myelopathy and no motor deficit gets a conservative trial of 6 to 12 weeks, and most settle in that window. Weakness with grade 4 power or better still earns a conservative trial, with close follow-up. A progressive motor deficit is an urgent surgical problem, decompressed by ACDF, and myelopathy is a surgical indication in its own right.

Conservative care runs in three phases, the last of which is a decision point.

Injections. A cervical epidural steroid injection may give temporary relief and has diagnostic value; the risks are cord injury and infection. A selective nerve root block is both diagnostic and therapeutic, and it confirms which root is generating the pain. Evidence for long-term benefit is limited, but either can bridge a patient to recovery.

When to operate. Four situations turn a non-operative problem into an operative one, and myelopathy is the most urgent of them, because earlier surgery yields better outcomes.

ACDF is the standard operation for single or two-level disease. The anterior Smith-Robinson exposure passes between the carotid sheath and the midline, and the disc is excised under the microscope or loupes, which removes the offending disc directly, decompresses the neural elements and restores disc height.

The key steps:

• Complete discectomy, including the posterior annulus
• Bilateral decompression of the neural foramina
• Endplate preparation that preserves the subchondral bone
• Cage placement, PEEK or titanium
• Plate fixation, optional at a single level

Fusion rates are over 95% with modern cage-and-plate technique.

Cervical disc arthroplasty preserves motion at the treated level, and the argument for it is a reduction in adjacent segment disease - reduced, not eliminated. It suits single-level disease with preserved disc height, no significant facet arthropathy and a young patient, and it is unsuitable for instability or multilevel disease. For radiculopathy the outcomes are similar to ACDF, and adjacent segment disease rates may be lower.

Posterior approaches avoid the anterior risks, dysphagia and the recurrent laryngeal nerve, and carry limitations of their own. A posterior foraminotomy deals with a lateral disc herniation and preserves motion, but does nothing for central stenosis. Laminoplasty or laminectomy is the answer to multilevel disease and myelopathy, preserving the posterior elements or sacrificing them respectively.

Prognostic Factors

What predicts a better result. A short symptom duration, single-level disease, arm pain rather than neck pain as the dominant complaint, and no myelopathy.

What predicts a worse one. Long-standing symptoms, multilevel disease, myelopathy with cord signal change, and a workers' compensation claim, the last of these psychosocial rather than structural.

Controversies and Areas of Uncertainty

Arthroplasty versus ACDF. Arthroplasty reduces reoperation and superior-level degeneration in pooled RCTs, but most trials are industry-sponsored non-inferiority designs. Whether motion preservation truly prevents rather than delays adjacent-segment disease over 15-plus years remains unresolved. Note the awkward fact underneath the whole debate: in Hilibrand's original series, multilevel fusion carried a LOWER risk of adjacent-segment disease than single-level fusion, which is the opposite of what a stress-transfer mechanism predicts and points instead to progressive spondylosis in a susceptible spine.

Timing in mild myelopathy. Surgery clearly helps moderate-severe myelopathy. For mild myelopathy (mJOA 15 or above) the choice between early surgery and structured surveillance is debated, though prospective data show benefit even in mild disease. State both sides of that trade-off honestly: in the same AOSpine cohort the complication rate was 18.7 percent, and a patient at mJOA 16 has only two points of headroom, so the case for operating early rests on preventing decline and on the disability and quality-of-life scores rather than on a large mJOA gain.

Plate versus standalone cage. Anterior plating raises fusion rates and reduces subsidence but increases dysphagia and adjacent-level ossification. Standalone and zero-profile cages reduce dysphagia; the trade-off in multilevel constructs is unsettled.

Anterior versus posterior for myelopathy. For multilevel myelopathy with neutral or lordotic alignment, anterior and posterior approaches give comparable neurological recovery. Alignment, number of levels and ossified PLL drive selection more than outcome superiority.

Global Epidemiology

• Cervical radiculopathy has a reported annual incidence of approximately 80 per 100,000 population, peaking in the fifth and sixth decades.
• C7 (from C6-C7 disc) is the most commonly affected root, followed by C6 (from C5-C6).
• Cervical spondylotic myelopathy is the leading cause of acquired spinal cord dysfunction in adults worldwide and rises sharply with age.
• A minority of acute radiculopathy is true soft-disc herniation; most chronic presentations reflect spondylotic (hard-disc/osteophyte) compression.

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