Cervical disc herniation C5-C6 and C6-C7: symptoms and treatment

Cervical disc herniation is the most common cause of cervicobrachial neuralgia — arm pain of cervical origin — in adults under 50. Among the seven cervical disc levels, C5-C6 and C6-C7 together account for approximately 90% of all cervical disc herniations, making the C6 and C7 nerve roots the most frequently compressed in the cervical spine. Dr Christian Dimitriu, spine neurosurgeon in Paris, explains the anatomy, clinical presentation by level, diagnostic approach, and the full range of medical and surgical treatment options.

Anatomy: why do C5-C6 and C6-C7 herniate most often?

The cervical spine comprises seven vertebrae (C1 to C7) and six intervertebral discs. The lower cervical spine — specifically the C5-C6 and C6-C7 segments — is subjected to the greatest mechanical load and range of motion during everyday activities. This biomechanical predominance explains the higher incidence of disc degeneration and herniation at these two levels.

Each intervertebral disc consists of a central nucleus pulposus (gelatinous, hydrated core) surrounded by a fibrous annulus fibrosus (concentric lamellae of collagen). With age, physical stress, genetic predisposition, or acute trauma, the nucleus may herniate through a weakness in the posterior annulus and compress the adjacent nerve root as it exits through the intervertebral foramen. The direction of herniation determines the clinical picture: postero-lateral herniations compress the exiting nerve root, whilst central herniations may compress the spinal cord itself (producing myelopathy) in addition to, or instead of, nerve root compression.

In younger patients (under 45), herniations are predominantly soft — consisting of extruded nuclear material, with good potential for spontaneous resorption. In older patients, herniations are frequently hard — osteophytic bone spurs (cervical spondylosis) that narrow the foramen chronically and do not resolve without surgical intervention.

C5-C6 disc herniation: C6 root compression

A herniation at the C5-C6 level compresses the C6 nerve root. This is the second most frequently affected cervical root, accounting for approximately 20 to 25% of cervical radiculopathies. The C6 root supplies:

• Sensory territory (dermatome): lateral aspect of the arm and forearm, thumb and index finger. Patients describe burning, shooting or electric pain radiating from the neck to the thumb, sometimes with numbness and tingling in these fingers.
• Motor territory (myotome): biceps brachii (elbow flexion) and wrist extensors (extensor carpi radialis longus and brevis). Weakness manifests as difficulty lifting objects, curling weights, and maintaining wrist extension against resistance.
• Deep tendon reflex: the biceps reflex (assessed by tapping the biceps tendon at the elbow) is innervated by C5 and C6. Its reduction or absence on the affected side is a reliable clinical sign of C6 root compromise.

The Spurling test (axial cervical compression with ipsilateral lateral flexion towards the affected side) typically reproduces or exacerbates the radicular symptoms and is positive in approximately 90% of cases.

C6-C7 disc herniation: C7 root compression

A herniation at the C6-C7 level compresses the C7 nerve root, the most commonly affected cervical root overall, accounting for 45 to 60% of cervical radiculopathies. The C7 root supplies:

• Sensory territory (dermatome): posterior aspect of the arm, forearm, and the middle finger (index and ring fingers in some patients). Pain radiates down the back of the arm to the middle finger, often with a burning, electric quality. Numbness predominates on the dorsal aspect of the middle finger.
• Motor territory (myotome): triceps brachii (elbow extension) and wrist flexors (flexor carpi radialis). Weakness manifests as difficulty pushing, performing press-ups, or opening a heavy door.
• Deep tendon reflex: the triceps reflex (tapping the triceps tendon at the posterior elbow) is innervated predominantly by C7. Its reduction or absence is highly specific for C7 root compromise and is a key clinical sign.

MRI diagnosis: the reference investigation

MRI of the cervical spine is the reference imaging investigation for suspected cervical disc herniation. It is indicated when clinical examination suggests nerve root or spinal cord compression, and should be performed before any surgical planning. The following sequences are routinely acquired:

T2-weighted sequences

T2 sequences are the most informative for disc herniation. The herniated disc fragment appears as a darker (hypointense) structure against the bright (hyperintense) cerebrospinal fluid within the spinal canal. The degree of nerve root or cord compression is directly assessed on axial and sagittal T2 images. A T2 hyperintensity within the spinal cord at the level of compression indicates myelopathy — a finding that significantly changes surgical planning and urgency. The degree of foraminal stenosis (narrowing of the canal through which the nerve root exits) is also quantified on parasagittal T2 images.

T1-weighted and STIR sequences

T1 sequences define bone marrow signal and help distinguish soft disc herniations from osteophytic hard compressions. STIR sequences suppress fat signal and are useful for detecting inflammatory changes in the soft tissues surrounding a recently herniated disc.

Conservative treatment: effective in 80–90% of cases

In the absence of significant motor deficit, myelopathy or rapidly progressive neurological signs, conservative management is the appropriate first-line treatment for C5-C6 and C6-C7 disc herniation. Published data consistently demonstrate that 80 to 90% of patients improve clinically within 6 to 12 weeks without surgery.

The biological basis for this favourable natural history is well established: soft disc herniations — the most common type in younger patients — undergo spontaneous resorption through a process mediated by macrophage infiltration, phagocytosis of disc material, and neovascularisation. This process is most vigorous for extruded and sequestered fragments (those that have escaped through a complete annular tear) and less active for contained sub-ligamentous bulges.

Conservative protocol

• NSAIDs: naproxen, ibuprofen, or celecoxib for 10 to 14 days at standard anti-inflammatory doses. Target the prostaglandin-mediated inflammatory component of acute radicular pain. Gastroprotection with a proton pump inhibitor is recommended for courses beyond 5 days.
• Short corticosteroid course: methylprednisolone (Medrol dose pack) or prednisolone 0.5 mg/kg/day for 5 to 7 days. Highly effective for severe acute radicular pain with a significant inflammatory component. Not appropriate as ongoing treatment.
• Neuropathic agents: gabapentin (300 to 900 mg/day) or pregabalin (75 to 150 mg/day) for the burning, electric, or shooting quality of nerve root pain.
• Physiotherapy: supervised programme including deep cervical flexor strengthening, postural correction, and neural mobilisation. Cervical traction is contraindicated.
• Foraminal epidural steroid injection: CT- or fluoroscopy-guided injection of corticosteroid adjacent to the affected nerve root. Indicated when pain is severe or when rapid improvement is needed to facilitate physiotherapy. Achieves significant short-term pain relief in 60 to 80% of patients.

Surgical indications: when to operate?

Surgery is indicated in the following circumstances:

• Failure of conservative treatment after 6 to 12 weeks: persistent disabling radicular pain, functional limitation, and inability to return to normal activities despite appropriate medical management
• Motor deficit ≤ 3/5 on the MRC scale: biceps or triceps weakness below the threshold of movement against gravity should not be left untreated beyond 4 to 6 weeks due to the risk of irreversible muscle denervation atrophy
• Rapidly progressive neurological deficit: any worsening of neurological signs over days to weeks, regardless of pain duration
• Concomitant myelopathy: a cervical disc herniation that also compresses the spinal cord has a lower surgical threshold than pure radiculopathy. Even mild myelopathic signs (subtle gait disturbance, hand dexterity impairment, brisk reflexes) should prompt early surgical assessment
• Intractable neuropathic pain: pharmacologically refractory pain severely impairing quality of life, sleep, and daily function

Surgical options: ACDF versus cervical disc arthroplasty

Two principal surgical techniques address C5-C6 and C6-C7 disc herniation via an anterior approach: ACDF and cervical disc arthroplasty (CDA). Both achieve equivalent nerve root decompression; they differ in what is done with the disc space after decompression.

ACDF: anterior cervical discectomy and fusion

ACDF remains the reference standard for surgical treatment of cervical disc herniation worldwide. Via a 3 to 4 cm transverse skin incision on the front of the neck, the anterior surface of the cervical spine is exposed by retracting the carotid sheath laterally and the trachea-oesophagus medially. Under microscopic magnification, the disc at C5-C6 or C6-C7 is completely removed, the posterior longitudinal ligament is opened, and the nerve root is decompressed in its foramen under direct visualisation. An interbody cage (titanium or PEEK) packed with synthetic bone substitute is inserted and stabilised with a low-profile titanium plate and screws. Solid osseous fusion develops over 3 to 6 months. ACDF achieves radicular pain relief in 90 to 95% of patients, and its long-term outcomes are supported by more than 40 years of clinical literature.

The main long-term concern of ACDF is adjacent segment disease: the fusion transfers mechanical stress to the adjacent disc levels, accelerating their degeneration. The radiographic incidence is approximately 3% per year; the clinical (symptomatic) incidence is lower, estimated at 1 to 2% per year. Over a 10-year follow-up, approximately 10 to 15% of ACDF patients develop symptomatic adjacent segment disease requiring treatment.

Cervical disc arthroplasty: motion-preserving alternative

Cervical disc arthroplasty (CDA) — also called total cervical disc replacement — offers identical decompression to ACDF but replaces the removed disc with a mobile prosthesis (such as the Mobi-C, ProDisc-C, Prestige LP, or Bryan disc). The prosthesis preserves physiological motion at the treated level, reducing stress concentration at adjacent levels.

The clinical evidence for CDA is now substantial. Multiple large randomised controlled trials — including the Mobi-C IDE trial (Davis et al., J Neurosurg Spine 2013), the ProDisc-C trial (Murrey et al., Spine J 2009), and the CSCP randomised trial published in Neurochirurgie (2013) — demonstrate non-inferiority to ACDF at 7 to 10 years for pain relief and neurological outcomes, with a statistically significant reduction in adjacent-level reoperation rates (relative risk reduction of approximately 50%). The 2019 AOSpine clinical practice guidelines recommend CDA as an appropriate alternative to ACDF for single and two-level cervical radiculopathy in appropriately selected patients.

CDA is the preferred option when all of the following criteria are met:

• Patient age under 55 years (active patients with longer prosthesis life expectancy)
• Single or two-level disease at C5-C6, C6-C7, or both
• Preserved facet joint health (no facet arthritis on CT or MRI)
• Adequate bone density (no significant osteoporosis — DXA T-score above −2.5)
• No significant cervical instability, deformity, or previous cervical fusion at an adjacent level

The difference from lumbar disc herniation: a lower surgical threshold

Patients and referring physicians sometimes ask why Dr Dimitriu recommends surgical intervention more promptly for cervical disc herniation than for lumbar disc herniation. The answer lies in a fundamental anatomical difference between the two regions of the spine.

In the lumbar spine, below the level of the L1-L2 vertebrae, the spinal cord has already ended and the spinal canal contains only the cauda equina — a bundle of peripheral nerve roots surrounded by cerebrospinal fluid. Peripheral nerves have an excellent capacity for regeneration and are remarkably tolerant of compression. This is why lumbar disc herniation and sciatica can be managed conservatively for extended periods with low risk, and why even severe lumbar radiculopathy often resolves without surgery.

In the cervical spine, the spinal cord itself runs within the canal. The spinal cord has a very limited regenerative capacity compared to peripheral nerves. A cervical disc herniation that causes even partial spinal cord compression (myelopathy) carries a real risk of permanent neurological deficit if not treated appropriately and in a timely manner. This fundamentally changes the risk-benefit calculation: for a cervical herniation causing myelopathic signs — even mild ones such as subtle gait disturbance or increased reflexes — the risk of permanent cord injury justifies prompt surgical decompression.

Surgical outcomes and return to activity

Surgery for C5-C6 and C6-C7 disc herniation delivers excellent and highly predictable outcomes when performed for the correct indication at the accurately identified level:

• Radicular arm pain relief in 90 to 95% of patients: the shooting, electric arm pain is typically eliminated or profoundly reduced. Many patients describe immediate relief upon waking from anaesthesia.
• Motor recovery: motor deficits (biceps weakness for C6, triceps weakness for C7) recover progressively over 3 to 6 months. Complete recovery is expected when the deficit was mild (4/5 or better) and of short duration. More severe deficits (3/5 or below) may only partially recover if present for more than 6 to 8 weeks prior to surgery.
• Sensory recovery: tingling and numbness in the thumb and index (C6) or middle finger (C7) resolve over 3 to 12 months, as the compressed nerve gradually recovers its conductivity.
• Hospitalisation: 24 to 48 hours for both ACDF and CDA, in an approved surgical facility in the Ile-de-France region.
• Return to sedentary work: 2 to 4 weeks after surgery.
• Return to manual or physical work: 6 to 8 weeks.
• Return to sport: 6 weeks for low-impact activities after CDA; 3 months for contact sport or heavy lifting after ACDF (to allow radiographic fusion).

Frequently asked questions

Sources: Radhakrishnan K et al., Neurology 1994 — Murrey D et al., Spine J 2009 — Davis RJ et al., J Neurosurg Spine 2013 — Bydon M et al., Neurosurgery 2015 — AOSpine Guidelines 2019 — SFNC, EANS — Laigle-Donadey et al., Neurochirurgie 2021.