Intervertebral Disc Herniation

What is the intervertebral disc & how does herniation occur?

The intervertebral disc functions as a “cushion” between two vertebrae, absorbing load and allowing movement. When it fissures or ruptures, this is referred to as a herniated disc.

Anatomically, the disc consists of:

• Nucleus pulposus – rich in proteoglycans, highly hydrophilic, with high water content, providing elastic load-bearing capacity.
• Annulus fibrosus – concentric layers of collagen and elastic fibers surrounding the nucleus and anchoring to the vertebral endplates.
• Endplates – cartilaginous layers between the disc and the vertebral bodies.

A disc herniation represents the displacement of disc material beyond the confines of the annulus and vertebral margin, usually through annular rupture. Depending on its location (paracentral, central, foraminal) and size, it may compress a nerve root or the spinal cord itself.

Why does the disc degenerate – pathophysiology & mechanisms?

Disc degeneration is part of normal aging, but in some patients it progresses more rapidly and predisposes to herniation.

Key pathological changes:

• Loss of proteoglycans & water within the nucleus – the disc dehydrates, loses height, and becomes less elastic.
• Fissures & tears of the annulus fibrosus – due to chronic degeneration or acute microtrauma.
• Migration of disc material posteriorly or laterally, resulting in compression of the spinal cord or nerve roots.

Predisposing factors:

• age, genetic predisposition,
• smoking, obesity, sedentary lifestyle,
• chronic or repetitive loading (high-impact sports, heavy labor),
• pre-existing degenerative spinal disease.

The result is a disc that is shorter, less elastic, and more vulnerable to rupture, particularly during flexion–rotation or sudden loading.

How does a cervical disc herniation present clinically?

Cervical disc herniation may cause cervical radiculopathy (arm pain from root compression) or cervical myelopathy (spinal cord compression), or a combination of both.

Typical symptoms of cervical radiculopathy:

• Neck pain radiating to the shoulder, arm, forearm, or fingers.
• Numbness, tingling in a dermatomal distribution.
• Weakness in specific movements (e.g., shoulder elevation, wrist extension, grip).
• Worsening with neck movements (extension, rotation, axial loading).

If the herniation is paracentral or central and coexists with spondylosis (osteophytes, ligamentous hypertrophy), it may compress the spinal cord and cause:

• hand clumsiness, difficulty with fine motor tasks,
• gait instability, sensation of “heavy” legs,
• hypertonia, spasticity, pathological reflexes (Hoffmann, Babinski),
• in advanced cases, urinary dysfunction.

A thorough clinical and neurological examination is essential to distinguish between isolated radiculopathy and myelopathy.

How does a thoracic disc herniation present?

Thoracic disc herniation is relatively uncommon, but when it compresses the spinal cord it can result in significant neurological impairment.

Possible symptoms include:

• Thoracic or back pain – often band-like, radiating around the chest or abdomen.
• Hypoesthesia or dysesthesia in a circumferential “band” pattern.
• Weakness in the lower extremities, heaviness, or spasticity.
• Gait disturbances, imbalance.
• Sphincter dysfunction in advanced cases.

Because symptoms may be subtle or atypical, thoracic disc herniation is often diagnosed late, most reliably with thoracic spine MRI.

How does lumbar disc herniation & sciatica present?

Lumbar disc herniation is a classic cause of sciatica. Low back pain radiating into the leg is the hallmark presentation.

Typical symptoms:

• Low back pain worsened by bending, lifting, coughing, or sneezing.
• Sciatica – pain following a nerve root distribution (e.g., buttock–posterior thigh–below the knee to the foot).
• Numbness or paresthesias in dermatomal patterns.
• Weakness (foot drop, difficulty walking on toes or heels).

Cauda equina syndrome – a medical emergency

When a large central herniation compresses the cauda equina nerve roots in the lower lumbar spine, patients may develop:

• Acute or rapidly progressive urinary retention or incontinence.
• Saddle anesthesia in the perineal region.
• Bilateral lower extremity weakness.

This condition requires immediate neurosurgical evaluation and urgent decompression to reduce the risk of permanent sphincter dysfunction and gait impairment.

How is the diagnosis made (MRI, CT, CT myelography)?

Diagnosis is based on careful correlation of clinical history, physical examination, and imaging findings.

Key diagnostic studies:

• Spine MRI – the study of choice for identifying disc herniation, nerve root or spinal cord compression, and associated stenosis.
• Spine CT & CT myelography (CTM) – useful when detailed bony anatomy is required, in suspected osteophytes, calcified herniations, or ossification of the posterior longitudinal ligament.

In all cases, the neurosurgeon does not “treat the MRI,” but rather the patient: imaging findings must correlate with symptoms and the neurological examination.

When is conservative treatment sufficient & what does it include?

Many disc herniations improve without surgery, with appropriately structured conservative management and close follow-up.

Common conservative measures:

• Short-term relative rest – avoiding heavy strain without complete immobilization.
• Analgesics & anti-inflammatory medications – NSAIDs, pain relievers, and occasionally short courses of oral corticosteroids.
• Neuropathic pain agents (e.g., gabapentin, pregabalin) when pain has prominent neuropathic features.
• Physical therapy – core strengthening, stretching, ergonomic training, decompression techniques.
• Epidural steroid injections in selected cases of severe radicular pain refractory to other measures.

In the absence of significant neurological deficit, a 6–8 week period of conservative treatment is often appropriate, with careful clinical monitoring.

When is surgery required in the cervical, thoracic & lumbar spine?

The decision for surgery is not based solely on MRI findings, but primarily on the severity, duration, and progression of neurological symptoms.

General indications for surgery

• Progressive neurological deficit (weakness, foot drop, gait disturbance).
• Cauda equina syndrome or severe myelopathy.
• Severe, intractable radicular pain persisting despite adequate conservative therapy.
• Recurrent episodes with substantial impact on function or work.

Cervical spine

• Cervical radiculopathy with persistent pain > 6 weeks, functional limitation, and concordant imaging findings.
• Cervical myelopathy – surgical decompression is generally recommended to halt or slow neurological deterioration.

Thoracic spine

• Myelopathy, spastic paraparesis, sphincter dysfunction – indication for early decompression.
• Severe, refractory pain unresponsive to conservative therapy.

Lumbar spine

• Cauda equina syndrome – emergent decompression.
• Significant motor deficit (e.g., foot drop) with clear discogenic etiology.
• Sciatica persisting > 6–8 weeks despite intensive conservative therapy, with clear radiographic correlation.

Which surgical techniques are used in the cervical spine?

The choice of approach depends on the location of the herniation, number of levels, presence of myelopathy, and overall spinal alignment.

Main options:

• Anterior cervical discectomy and fusion (ACDF) – the standard approach for central or paracentral herniations; the disc is removed, decompression is performed, and stability is restored using a cage and/or plate.
• Anterior disc replacement (arthroplasty) – in selected patients, to preserve motion at the treated level.
• Posterior foraminotomy and microdiscectomy – primarily for lateral/posterior herniations, preserving motion with targeted nerve root decompression.
• Multilevel decompressions (laminectomy with or without fusion) – for extensive multilevel myelopathy or stenosis.

In cases of kyphosis or significant instability, decompression is combined with instrumented fusion to restore alignment and long-term stability.

Which techniques are applied in the thoracic & lumbar spine?

The goal is adequate decompression of the spinal cord or nerve root with minimal neural manipulation and preservation of stability.

Thoracic spine

Representative approaches depending on location and disc characteristics:

• Posterior–transpedicular approaches (laminectomy, transpedicular decompression) – for lateral or paracentral soft herniations.
• Posterolateral approaches (e.g., costotransversectomy) – improved access to the anterior thoracic canal.
• Anterior/thoracoscopic approaches – optimal for central or calcified herniations with significant cord compression.

Lumbar spine

The standard procedure for symptomatic lumbar disc herniation is microdiscectomy:

• Unilateral posterior approach through a small incision, using microscopy or tubular retractors.
• Direct decompression of the affected nerve root by removing extruded disc material.
• Careful removal of loose disc fragments to reduce recurrence risk, without overly aggressive discectomy that may predispose to chronic back pain.

In cases of associated instability or severe stenosis, decompression may be combined with spinal fusion.

What is the prognosis & course of recovery?

The majority of patients with disc herniation experience significant improvement, whether treated conservatively or surgically, when management is timely and appropriately targeted.

In general:

• Symptoms from most lumbar herniations gradually resolve over weeks to months with appropriate conservative treatment.
• After successful microdiscectomy, radicular pain often improves immediately or within days; full neurological recovery may take several months.
• In myelopathy, the primary goal of surgery is to halt neurological deterioration. Improvement is possible but may be incomplete, depending on duration and severity of preoperative injury.
• In cauda equina syndrome, the earlier the decompression, the greater the likelihood of recovery of sphincter and gait function.

Long-term recovery is strongly influenced by ergonomics, physical therapy, weight management, and smoking cessation, all of which reduce the risk of recurrence and further degeneration.