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Cervical Disc Disease

Cervical disc disease refers to degeneration or herniation of the intervertebral disc resulting in compression of the spinal cord or the exiting nerve root. Symptoms arise from mechanical compression, local inflammatory irritation by cytokines such as TNF- and IL-6, and ischemic compromise of the root. Herniation occurs posterolaterally where the annulus is thinnest and the posterior longitudinal ligament offers least support.

 

Q. Which levels are most commonly affected?

 

C5–C6 and C6–C7 are the commonest levels, followed by C4–C5. Accordingly, C6 and C7 roots are the most frequently involved.

 

Q. What are the predisposing factors?

 

Advancing age, repetitive neck movements, trauma, smoking, poor posture, and genetic predisposition contribute to disc degeneration and herniation.

 

Q. How does cervical disc disease present?

 

Typical presentation is neck pain radiating to one upper limb along a dermatomal pattern, often associated with paresthesia or numbness in the same distribution. The pain increases on neck extension or rotation. There may be segmental weakness and reflex loss corresponding to the affected root. Central or large herniations cause cervical myelopathy presenting as hand clumsiness, spasticity, gait disturbance, and sphincter urgency.

 

Q. What are the characteristic root-wise findings?

 

C4 root (C3–C4 disc, uncommon): Lower neck or trapezial pain with or without shoulder-tip paresthesia; no reliable reflex; mild hemidiaphragm weakness possible due to phrenic involvement; movement affected: neck elevation and inspiration (diaphragmatic component).

 

C5 root (C4–C5 disc): Pain from neck to lateral upper arm; weakness of deltoid and biceps; diminished biceps reflex; sensory loss over lateral upper arm; movement affected: shoulder abduction and elbow flexion.

 

C6 root (C5–C6 disc): Pain radiating to lateral forearm and thumb; weakness of wrist extensors and biceps; decreased brachioradialis reflex; sensory loss over lateral forearm, thumb, and index finger; movement affected: elbow flexion and wrist extension.

 

C7 root (C6–C7 disc): Pain from neck and interscapular region to dorsal forearm and middle finger; weakness of triceps, wrist flexors, and finger extensors; decreased triceps reflex; sensory loss over middle finger; movement affected: elbow extension, wrist flexion, and finger extension.

 

C8 root (C7–T1 disc): Pain in lower neck radiating to medial forearm and ring–little fingers; weakness of finger flexors and intrinsic hand muscles; no reliable deep tendon reflex; sensory loss over ulnar digits; movement affected: finger flexion and grip strength.

 

T1 root (rare disc above T1): Medial arm pain and paresthesia; weakness of interossei causing impaired finger abduction; movement affected: finger abduction and adduction.

Q. What are the typical signs on examination?

 

Spurling’s test reproduces radicular pain when the head is extended and rotated toward the symptomatic side. Weakness, sensory loss, and reflex depression correspond to the affected root. The inverted radial reflex may appear in C5–C6 lesions.

Myelopathy produces long-tract signs: hyperreflexia below the lesion, Hoffman or Babinski positivity, spasticity, gait imbalance, and loss of fine motor dexterity. Lhermitte’s phenomenon (Barber’s Sign) may be elicited by neck flexion. Hoffman’s becomes positive only when the corticospinal tract is compressed; it is absent in pure radiculopathy (long tract sign present in myelopathy).

 

Q. How will you differentiate between root involvement and cord involvement?

 

Root involvement causes lower motor neuron features at a single level: segmental weakness, flaccidity, atrophy, and reflex depression with preserved tone and reflexes below.

Cord involvement produces upper motor neuron signs below the lesion: hyperreflexia, spasticity, Hoffman/Babinski positivity, and gait disturbance. The coexistence of both indicates combined spondylotic myeloradiculopathy.

 

Q. What are the upper cervical presentations?

 

C1 involvement causes deep suboccipital pain without sensory loss. C2 lesions produce occipital neuralgia radiating to the vertex. C3 lesions cause pain along the lateral neck and angle of the jaw. These levels have no limb weakness or reflex changes. If pyramidal signs are present, the compression lies at the cervicomedullary junction.

 

Q. What imaging work-up will you perform and what do you expect to find?

 

Plain radiographs (AP, lateral, and flexion–extension) are done to assess alignment and instability; obliques show foraminal osteophytes. MRI is the investigation of choice, it defines the level of disc herniation, canal diameter, and any cord compression or myelomalacia. Axial MRI best demonstrates posterior or paramedian disc displacement and root sleeve indentation. CT delineates osteophytes or ossified posterior longitudinal ligament. CT-myelography is reserved for patients in whom MRI is contraindicated.

 

Q. What are the EMG and nerve-conduction findings?

 

Needle EMG shows fibrillation potentials, positive sharp waves, and reduced recruitment in muscles supplied by the affected root. Sensory conduction studies are usually normal because the lesion is proximal to the dorsal root ganglion, while motor conduction may show mild delay if axonal loss exists. These studies help differentiate radiculopathy from peripheral entrapment neuropathies or plexopathies.

 

Q. How will you manage cervical disc disease initially?

 

Most acute radiculopathies recover with conservative therapy. This includes rest, short-term soft collar immobilization, NSAIDs, muscle relaxants, neuropathic pain agents, cervical traction, and physiotherapy. Epidural or selective nerve-root steroid injections may be used for persistent radicular pain.

 

Q. When is surgery indicated?

 

Surgery is considered for progressive neurological deficit, intractable radicular pain persisting beyond 6–12 weeks of adequate conservative treatment, or evidence of myelopathy or acute cord compression.

 

Q. What are the surgical options?

 

Anterior cervical discectomy and fusion remains the standard approach for ventral or central compressive pathology. Cervical disc arthroplasty is a motion-preserving alternative in young patients with one or two-level soft-disc disease and no instability or advanced spondylosis. Posterior keyhole foraminotomy or laminoforaminotomy is useful for lateral or foraminal soft-disc herniations. For multilevel canal stenosis or ossified posterior longitudinal ligament, posterior laminectomy or laminoplasty is performed depending on sagittal alignment.

 

Q. What are the common complications of surgery, especially after ACDF?

 

Complications include dysphagia, hoarseness from recurrent or superior laryngeal nerve injury, esophageal or tracheal injury, vertebral artery or spinal-cord injury, dural tear with CSF leak, graft or cage displacement, pseudoarthrosis, infection, airway obstruction due to hematoma, and late adjacent-segment degeneration.

 

Q. How will you manage recurrence?

 

Recurrence is evaluated with MRI to confirm the level and exclude pseudarthrosis or adjacent-segment disease. If pain is predominant without deficit, conservative measures and selective root blocks may be tried. For recurrent foraminal stenosis after anterior fusion, a posterior foraminotomy can decompress the root; if pseudarthrosis, graft collapse, or central compression is present, revision anterior fusion is indicated. Persistent or recurrent compression after posterior decompression is treated by anterior discectomy and fusion. Pseudarthrosis requires revision fusion, anterior or posterior, based on alignment and stability.

 

Q. What is the prognosis after treatment?

 

Radicular pain improves in most patients. Motor recovery depends on the severity and duration of preoperative weakness. In cases with established myelopathy or cord signal changes, residual spasticity or gait disturbance may persist despite adequate decompression.

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