Degenerative disk disease

Degenerative disk disease refers to a group of conditions in which disk material is displaced into the spinal canal. The condition can be asymptomatic or manifest as radiculopathy (due to compression of a spinal nerve root) or myelopathy (due to compression of the spinal cord). The site of nerve or cord compression can often be determined based on the patient's neurological deficits. Radiculopathy manifests with radicular pain, motor weakness, and loss of deep tendon reflexes in the dermatome and myotome territory of the compressed nerve root. Myelopathy is a medical emergency that typically manifests with motor weakness, sensory abnormalities (e.g., saddle anesthesia), and bowel and/or bladder disturbances. MRI findings consistent with physical exam findings confirm the diagnosis. Conservative management with analgesics and physiotherapy may be sufficient for isolated acute radiculopathy without severe paresis. Urgent surgical decompression is required for patients with spinal cord compression, conus medullaris syndrome, or cauda equina syndrome to prevent permanent neurological damage.

• Disk protrusion: protrusion of the vertebral disk nucleus pulposus through the annulus fibrosus
• Disk herniation: (disk extrusion or disk prolapse): complete extrusion of the nucleus pulposus through a tear in the annulus fibrosus
• Disk sequestration: extrusion of the nucleus pulposus and separation of a fragment of the disk
• Spondylosis: a broad term used to describe degenerative changes of the spine that may result in irritation and/or damage of the adjacent nerve roots or spinal cord

• Age: most common at 30–50 years
• Sex: ♂ > ♀ ^[1]
• Approx. 80% of all Americans suffer from significant back pain at some point in their lives. ^[2]
• Disk herniation is the cause of back pain in roughly 5% of cases.
  • Cervical and thoracic disk herniations: rare
  • Lumbosacral disk herniation
    • L5–S1 (most common site)
    • L4–L5 (second most common site)

Epidemiological data refers to the US, unless otherwise specified.

• The intervertebral disk consists of a dense outer ring (annulus fibrosus) and a gelatinous core (nucleus pulposus).
  • These structures work together as a shock absorber by distributing high axial pressure evenly onto the cover plates and base units of the vertebral bodies.
  • High pressure on the vertebral disks leads to fluid loss, and as a result, body height decreases physiologically by 1–2 cm during the day.
• Compression, tension, shear, and torque stresses on the spinal disk → degenerative changes (e.g., dehydration, annular tear) → disk protrusion or herniation through the annulus fibrosus into the central canal → adjacent nerve root impingement → sensorimotoric deficits in affected nerve root
• Posterolateral disk herniation/protrusion (common) → compression of the transversing nerve root → compressive radiculopathy ^[3]
• Central disk herniation/protrusion (less common) → compression of the spinal cord (above L1–L2) or cauda equina (below L2) → compressive myelopathy ^[3]

Intervertebral disks usually protrude/herniate posterolaterally, as the posterior longitudinal ligament is thinner than the anterior longitudinal ligament.

Degenerative disk disease may be asymptomatic and detected incidentally (e.g., on imaging performed for an unrelated condition). Examination findings vary depending on the location and severity of nerve root compression. ^[4][5]

• Acute onset of severe neck or back pain
  • Radicular pain: pain that radiates to the legs (sciatic pain) or arms ^[3]
  • The pain is either stabbing in nature or resembles an electric shock.
  • Pain increases with pressure (e.g., from coughing or sneezing).
  • Pain decreases with minor changes in position (e.g., taking a short walk).
• Features of radiculopathy: lower motor neuron signs of the affected nerve root (typically unilateral) ^[6][7]
  • Paresthesia of the affected dermatome
  • Muscle weakness and atrophy of the related myotome
  • Absent or diminished deep tendon reflexes
  • See “Compressive radiculopathy” for details.
• Features of compressive myelopathy (typically bilateral) or cauda equina syndrome ^[6]
  • Paresthesia below the level of compression
  • Motor deficits
    • At the level of compression: lower motor neuron signs
    • Below the level of compression
      • Upper motor neuron signs in spinal cord compression and conus medullaris syndrome
      • Lower motor neuron signs in cauda equina syndrome
  • May be associated with gait disturbances, bladder dysfunction, and/or bowel dysfunction
  • See “Compressive spinal emergencies” for details.

As dermatomal territories often overlap (except in autonomous sensory zones) and muscles are often supplied by several myotomes, sensory and motor deficits may be absent or minimal if a single spinal root is compressed.

The affected nerve root is typically the one below the level of disk herniation (i.e., C4–C5 disk herniation leads to C5 radiculopathy; L4–L5 disk herniation leads to L5 radiculopathy).

Cervical radiculopathy ^[8]

Etiology

• Disk herniation
• Spondylosis

Symptoms

• Neck pain commonly associated with radiculopathy
• Can manifest with difficulty with fine motor skills
• Can be accompanied by headache and/or shoulder pain

Examination findings

May be normal or demonstrate specific motor or sensory deficits depending on the nerve root affected

Provocative maneuvers

• Hoffmann reflex: A positive result suggests cervical myelopathy. ^[10]
• Neck compression test (Spurling maneuver): screens for cervical radiculopathy ^[11]
  • Tilt and rotate the neck toward the affected side while applying downward pressure (axial loading) to the head.
  • The test is positive if it produces pain and/or paresthesia that radiates to the motor or sensory area of the affected nerve root.

Lumbosacral radiculopathy ^[3]

Symptoms

• Low back pain (lumbago) commonly associated with radiculopathy
• Pain characteristically worsens with lumbar flexion (e.g., on sitting).

Worsening of low back pain with lumbar flexion (e.g., on sitting) is suggestive of lumbar disk herniation, while improvement of pain with lumbar flexion is suggestive of lumbar spinal stenosis. ^[3]

Examination findings

May be normal or show specific motor or sensory deficits, depending on the affected nerve root

Back pain associated with bowel or bladder dysfunction is concerning for spinal cord compression, cauda equina syndrome, and conus medullaris syndrome.

Herniated lumbosacral disks commonly cause radiculopathy below the level of the herniated disk (e.g., L4–L5 disk herniation results in L5 radiculopathy). However, a far lateral disk herniation can cause radiculopathy above the level of the disk (e.g., L4–L5 far lateral disk herniation resulting in L4 radiculopathy). ^[12]

Provocative maneuvers

Leg raising maneuvers are used to screen for lumbosacral radiculopathy

• Straight leg raise test (Lasegue sign): A straight leg raise leads to increased pain in the ipsilateral leg with radiation to the motor or sensory area of the affected nerve root.
• Bragard sign: A straight leg raise leads to increased pain in the ipsilateral leg; lowering the leg to just below the level where pain is produced and pulling the foot to dorsiflexion reproduces the pain.
• Crossed straight leg raise test: A crossed straight leg raise leads to pain in the ipsilateral leg radiating to the motor and sensory area of the affected nerve root.
• Reverse straight leg raise test: A reverse straight leg raise leads to pain in the ipsilateral leg radiating to the motor and sensory area of the affected nerve root.

Degenerative disk disease is diagnosed on the basis of characteristic clinical features in conjunction with abnormal imaging.

Approach ^[13][14][15]

See also “Management of acute back pain” and “Compressive spinal emergencies.”

• Perform clinical evaluation focusing on red flags for acute back pain.
• Determine the need for imaging (see also “Approach to imaging in acute back pain”).
  • Red flags for acute back pain: MRI spine without IV contrast is preferred. ^[14]
  • No red flags for acute back pain: Urgent imaging is typically not required. ^[14][15]
• Consider additional studies (e.g., bladder scan) based on clinical suspicion.

MRI spine without IV contrast ^[8][13][16]

• Indications: preferred initial imaging modality for suspected radiculopathy, myelopathy, or cauda equina syndrome ^[13][14][15]
• Supportive findings
  • Disk degeneration: sclerosed, dehydrated disk that appears hypointense on T2-weighted images
  • Disk prolapse/herniation: herniation of disk tissue with surrounding edema
  • Evidence of impingement/compression of a spinal nerve or the spinal cord may be visible, e.g.:
    • Focal narrowing of the spinal canal
    • Compression of the thecal sac
    • Edema of the spinal cord (appears hyperintense on T2-weighted images)

A diagnosis of degenerative disk disease should not be made based on imaging alone; up to 30% of asymptomatic individuals have abnormal disk appearances on MRI. ^[16]

Other imaging modalities

CT myelogram ^[13][14][15]

• Indications
  • MRI unavailable
  • MRI contraindications
  • Surgical planning (better analysis of bone structure)
• Supportive findings
  • Similar to MRI
  • May rule out occult spondylolysis or tumors

X-ray spine ^[14][15]

• Indications
  • Consider for individuals with new or increasing nontraumatic cervical pain who do not have red flag features.
  • Flexion-extension views are useful for identifying spondylolisthesis and spinal instability. ^[14]
• Supportive findings (on AP and lateral views): disk space narrowing, vertebral body osteophytes, endplate and facet sclerosis

Additional investigations

• Bladder scan: Evaluate for urinary retention in patients with myelopathy or cauda equina syndrome.
• Laboratory studies
  • Not required to diagnose degenerative disk disease
  • Consider evaluation for alternative etiologies of radicular pain, radiculopathy, or myelopathy.
• Advanced studies: In patients with persistent radiculopathy and inconclusive imaging findings, consider electrodiagnostic testing to distinguish radiculopathy from a peripheral neuropathy. ^[17][18]

See “Acute back pain” for details on the distinguishing characteristics and management of the underlying etiology.

• Musculoskeletal: muscle strain; , spinal stenosis; , spinal disk herniation; , degenerative spondylolisthesis, vertebral fractures
• Neurological: spinal cord compression, cauda equina syndrome, conus medullaris syndrome, spinal epidural hematoma
• Malignancy: bone metastases (extradural metastatic lesions)
• Infections: diskitis, spinal epidural abscess, vertebral osteomyelitis
• Inflammatory: ankylosing spondylitis, reactive arthritis, psoriatic arthritis, autoimmune myelopathy (e.g., multiple sclerosis, neuromyelitis optica), transverse myelitis
• Referred pain: acute pancreatitis, ureteric stone, abdominal aortic aneurysm, aortic dissection

The differential diagnoses listed here are not exhaustive.

Approach

• Identify and treat compressive spinal emergencies immediately, if present.
• For isolated radiculopathy or pain due to DDD without any red flags for acute back pain:
  • Initiate conservative management.
  • Urgent imaging is typically not required; consider imaging if symptoms do not improve within 6 weeks. ^[14][15]
  • Consider referral to neurosurgery to assess whether surgery is required for persistent symptoms.
• Educate the patient on symptoms of compressive spinal emergencies and the need to seek immediate medical help if symptoms develop.

Urgently obtain an MRI and consult neurosurgery to evaluate any of the following red flags for acute back pain associated with DDD: new or progressive neurological deficits, especially motor weakness, saddle anesthesia, and/or bowel, bladder, or sexual dysfunction; intractable or progressive pain; recent spinal surgery.

Conservative management ^[8][17][18]

• Treatment is similar to that for nonspecific back pain and neck pain.
  • Physiotherapy with exercises to strengthen the back and neck
  • Continuation of daily activities (minimize bed rest) ^[19][20]
  • Analgesics (e.g., NSAIDs) ^[21]
  • Consider a short course of oral glucocorticoids for pain related to radiculopathy. ^[17][18]
• Advise patients that symptom improvement is typically gradual (several weeks).
• For patients with severe pain, consider periradicular therapy: image-guided injection of local anesthetic (e.g., ropivacaine) and glucocorticoids at the intervertebral foramen to reduce inflammation and edema at the affected nerve root ^[8][22]

About 90% of lumbar disk herniations with acute radiculopathy start to improve within 6 weeks and resolve by 12 weeks with conservative management. ^[23]

Surgery ^[8][18]

• Indications
  • Urgent: significant or progressive neurological deficits, bowel or bladder incontinence, compressive spinal emergencies
  • Elective: persistent or progressive radiculopathy despite conservative management
• Procedure: diskectomy ^[8][18]
  • Surgical removal of the herniated portion of the intervertebral disk
  • Can be performed via an open approach, via minimally invasive surgery (microdiskectomy), or under fluoroscopic guidance (percutaneous diskectomy)
• Complications
  • Damage of large prevertebral blood vessels (rare)
  • Failed back surgery syndrome: Persistent back pain, radicular pain, or paresthesias occurs in ∼ 20–40% of patients after disk surgery due to scarring, vertebral instability, or arachnoid adhesions to nerve roots. ^[24]

See also “Urgent spinal causes of back pain.”

Overview

The following table outlines common symptoms following compression of the spinal cord or cauda equina. Patients may also present with symptoms of incomplete spinal cord syndromes depending on the location of the herniated disk.

Spinal cord compression, conus medullaris syndrome, and cauda equina syndrome are medical emergencies that have the potential to cause permanent neurological damage. ^[28]

Cauda equina syndrome typically manifests with lower motor neuron signs. Spinal cord compression and conus medullaris manifest with a combination of lower motor neuron signs (at the level of compression) and upper motor neuron signs (below the level of compression).

Management

Consider empiric management of other urgent spinal causes of acute back pain, e.g., vertebral osteomyelitis, vertebral fracture, or spinal epidural abscess as directed by clinical suspicion.

• Obtain an urgent MRI spine without contrast.
• Consult neurosurgery for urgent surgical decompression.
• Document the patient's current neurological deficits and reassess frequently. ^[29]
• Obtain bladder scan to evaluate postvoid residual and insert Foley catheter for patients with urinary retention.
• Administer analgesics (preferably NSAIDs, see “Pain management”). ^[28][30]
• Treat the underlying cause.
• Admit the patient for frequent neurological examinations and definitive management.

Treatment of acute spinal cord compression varies based on the underlying etiology and may include decompressive surgery (e.g., for disk herniation) or IV steroids and radiation therapy (for malignant compression).

Initiate immediate management of back pain with new neurological symptoms in patients with back pain and new motor weakness, saddle anesthesia, and/or bowel/bladder dysfunction.

• Perform clinical evaluation focusing on red flags for acute back pain.
• Order urgent MRI spine and consult neurosurgery to evaluate for surgical decompression if red flags for acute back pain are present.
• Order bladder scan with postvoid residual and catheterize patients with bladder dysfunction.
• Manage acute pain (preferably with NSAIDs) after baseline neurological function and pain severity are documented.
• Treat the underlying cause (e.g., IV steroids for malignant cord compression, empiric antibiotic therapy for spinal infections).
• Admit for serial neurological examination and definitive management.