Degenerative Spine Disease

What is degenerative spine disease?

A natural process of spinal aging—but not always “harmless.” In some patients, it progresses into a clinically significant condition.

The term degenerative spine disease (or spondylosis) describes long-term changes affecting:

• intervertebral discs (dehydration, loss of height, annular tears, herniation),
• joints (facet joints; uncovertebral joints in the cervical spine),
• ligaments and soft tissues (thickening, laxity, hypertrophy),
• bony margins (osteophytes, narrowing of the spinal canal and foramina).

These changes may remain silent or present with:

• axial pain in the neck or low back,
• radiculopathy — pain, numbness, tingling, or weakness in an arm or leg,
• myelopathy — progressive gait/balance difficulty, loss of fine motor control, and sometimes sphincter dysfunction.

How common is it, and who is at higher risk?

Extremely common on imaging—clinically important only in a portion of the population.

Spondylosis is an age-related process that occurs in most people. Imaging signs of disc and joint degeneration are seen:

• in roughly 10% of people around age 25,
• in rates approaching 95% around age 65.

Still, not everyone develops symptoms. Risk factors for symptomatic degeneration include:

• Smoking.
• Repetitive mechanical strain (heavy manual work, frequent heavy lifting, vibration exposure).
• Obesity and sedentary lifestyle.
• Genetic predisposition (disc/collagen quality).
• Prior trauma or surgery involving the spine.

Degenerative disease can occur at any age, but it becomes more common after 40–45. In younger adults, disc herniation and radiculopathy tend to dominate; later in life, stenosis and myelopathy become more frequent.

How does degeneration begin—what happens to discs and joints?

The intervertebral disc is often the starting point: disc dehydration triggers a chain of changes across the entire motion segment.

An early stage is disc dehydration (degenerative disc disease): biochemical composition changes, height decreases, and the disc becomes less elastic.

This can lead to:

• load transfer to the joints (facet and uncovertebral joints),
• ligament hypertrophy (ligamentum flavum, posterior longitudinal ligament),
• formation of osteophytes,
• foraminal narrowing where nerves exit,
• spinal canal stenosis.

When compression becomes focal and clinically relevant, it may produce a herniated disc and/or chronic stenotic disease affecting neural structures.

What is “simple” neck or low back pain (axial pain)?

Pain centered in the neck or low back without clear radiation into the arms or legs—often originating from discs, joints, or soft tissues.

Axial pain refers to pain localized to the spine (cervical or lumbar) without distinct radicular symptoms.

Main contributors include:

• Discogenic pain — annular tears, inflammation, or pressure within a degenerating disc.
• Facet-related pain — arthritic changes in facet joints with inflammation and paraspinal muscle spasm.
• Myofascial pain — overuse, posture-related strain, muscle spasm.

It often worsens with prolonged standing or sitting, poor ergonomics, heavy lifting, or specific movements, and improves with rest, gentle activity, and physiotherapy.

What is radiculopathy, and what symptoms should I watch for?

When a nerve root is compressed or irritated at its exit from the spine, pain and symptoms “track” along that nerve into the arm or leg.

Radiculopathy refers to symptoms caused by compression of a nerve root—commonly from a herniated disc or osteophytes narrowing the foramen. Classic patterns include:

• Cervical radiculopathy — arm pain, numbness/tingling, “electric” sensations, and weakness in a root-specific pattern (C5–C8).
• Lumbosacral radiculopathy (sciatica) — pain starting in the low back/buttock and radiating down the leg (L4–S1), with or without weakness.

Symptoms that require urgent evaluation include:

• Sudden or progressive weakness in an arm or leg.
• Loss of bladder/bowel control or “saddle” numbness — possible cauda equina syndrome (an emergency).
• Severe, persistent pain that does not respond to appropriate medication.

What is cervical myelopathy, and why is it considered serious?

Cervical myelopathy is progressive spinal cord dysfunction from chronic neck compression—without treatment, it may lead to permanent disability.

In some patients, spondylosis and cervical canal stenosis cause chronic compression of the spinal cord, leading to:

• Gait disturbance and imbalance (“tripping for no clear reason”).
• Loss of fine motor control (buttons, handwriting, handling small objects).
• Weakness in the arms and/or legs.
• Stiffness, spasticity or “electric shock” sensations in the limbs.
• In advanced stages: bladder/bowel symptoms.

Myelopathy is not simply “neck pain.” It is a neurological disorder of the spinal cord. Early recognition and neurosurgical decompression can stabilize—and often improve—function.

How is it diagnosed—tests and imaging

The clinical assessment comes first; MRI confirms. We treat the patient—not the scan.

Evaluation typically includes:

• Detailed history — timing, pain pattern, neurological symptoms, triggers, functional impact.
• Neurological examination — strength, reflexes, sensation, gait tests, fine motor assessment.
• Imaging:
  • MRI of the cervical and/or lumbar spine — the preferred test to assess discs, nerves, and spinal cord.
  • Standing X-rays — alignment, lordosis/kyphosis, and potential instability.
  • CT or CT myelography — selected cases (bony detail, preoperative planning, MRI contraindications).
• Electrodiagnostic testing (EMG/NCS) — helpful in selected cases to distinguish radiculopathy from peripheral neuropathy.

Treatment decisions are not based on MRI alone, but on correlation between symptoms, examination, and imaging.

When is conservative care and physiotherapy enough?

In most cases, first-line treatment is non-surgical—as long as there are no red-flag neurological signs.

Typical conservative measures include:

• Medication — analgesics, NSAIDs, muscle relaxants, and in selected cases neuropathic pain agents.
• Individualized physiotherapy — core strengthening, stretching, posture and ergonomics training.
• Lifestyle adjustments — weight management, smoking cessation, avoiding overload.
• Interventional pain options (with a specialist team) — facet injections, selective nerve root blocks, etc.

Conservative treatment is often appropriate when:

• there is pain but no progressive weakness or myelopathy,
• symptoms are of short duration (weeks to a few months),
• there is gradual improvement with treatment.

When is surgery needed for a disc herniation and radiculopathy?

Targeted nerve root decompression—when pain and neurological deficit persist despite appropriate conservative care.

Surgical treatment for a cervical or lumbar disc herniation and radiculopathy is considered when:

• there is persistent, severe radicular pain (sciatica, arm pain) for > 6–8 weeks despite structured conservative care,
• there is objective neurological deficit (weakness, significant sensory loss) correlating with MRI findings,
• there are recurrent episodes that substantially limit daily life and work.

Main surgical techniques include:

• Lumbar microdiscectomy — a small posterior incision using the operating microscope to remove disc material compressing the nerve.
• Anterior cervical discectomy and fusion (ACDF) — removal of disc/osteophytes, cage/graft placement, often with a plate.
• In selected patients: cervical disc arthroplasty (motion-preserving disc replacement).

The goal is nerve decompression and rapid relief of radicular pain, with minimal invasiveness while maintaining stability.

When is surgery needed for cervical myelopathy?

In cervical myelopathy, surgical decompression is typically the treatment of choice, since the condition tends to progress over time.

Indications for decompression in cervical myelopathy include:

• Clinically established myelopathy (gait dysfunction, spasticity, loss of fine motor control) with corresponding MRI findings.
• Progressive worsening despite observation/conservative measures.
• Significant cervical canal stenosis and spinal cord compression, especially with signal change on MRI.

Core surgical strategies:

• Anterior approach (ACDF, anterior corpectomy and fusion) — when compression is mainly anterior and limited to fewer levels.
• Posterior approach (laminectomy/laminoplasty with or without fusion) — for multilevel stenosis, particularly when lordosis is preserved or can be restored.

The goal is spinal cord decompression and stabilization where needed, to improve or stabilize neurological function and reduce the risk of future disability.

Postoperative course and long-term outlook

The goal is not only pain relief, but a safe return to daily life and long-term protection of function.

After surgery for disc herniation/radiculopathy:

• Often rapid relief of radicular pain within days.
• Gradual improvement of numbness and strength (when nerve injury is reversible).
• Return to light work and daily activities within weeks, depending on the case.

After surgery for cervical myelopathy:

• The primary objective is disease stabilization—and in many patients, improvement is also seen.
• Outcome depends heavily on duration and severity before surgery.
• Advanced deficits are not always fully reversible—this is why timely intervention matters.

Long-term outcomes are influenced by:

• adherence to guidance (exercise, weight control, ergonomics),
• risk-factor control (smoking, obesity),
• the presence of multilevel degeneration in other spinal segments.