Degenerative Disc Disease Spin11 Degenerative Disc Disease

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Degenerative Disc Disease

Last updated: April 4, 2016

Etiopathophysiology 1

Topography 2

Cervical 2

Lumbosacral 2

Pathology 3

Epidemiology 3

Clinical Features 4

Cervical herniation 4

Lumbosacral herniation 4

Pain 4

Examination 5

Thoracic herniation 5

Diagnosis 5

Plain X-ray 5

Electrophysiology 6


Myelography 10

Discography 11

Differential diagnosis 11

Treatment choice 11

Conservative therapy 12

Percutaneous nucleotomy 12

Chemonucleolysis 12

Surgical treatment 12

Indications 12

Contraindications 12

Preoperative 12

Approaches 13

Lumbar approach 13

Cervical approach 13

Thoracic approach 13

Posterior decompression 13

Microdiscectomy 14

Transmuscular tubular (s. Minimally invasive) diskectomy 14

Spinal Stabilization 14

Cervical 14

Lumbar 15

Intraoperative Complications 15

Postoperative Complications 15

Postoperative 16

Prevention of recurrence 17

Prognosis 17

  • anterior and posterior longitudinal ligaments blend with and strengthen annulus fibrosis.

  • in early childhood, nucleus pulposus is gelatinous, containing hydrophilic polysaccharides (water content > 80%).

  • annulus fibrosus is composed of concentric collagenous layers that are attached to adjacent vertebrae; fibers are directed obliquely (at ≈ 55° degrees to horizontal plane) between vertebrae in successive layers that are perpendicular to each other.

N.B. disk elasticity is provided in large measure by annulus fibrosus!


Disk degeneration (acceleration of aging effects):

    1. decreasing vascular supply, decreasing H2O & O2 contentdisc height↓ (desiccation & shrinkage).

    2. internal layers of annulus fibrosus progressively grow into nucleus pulposus → disk becomes amorphous, sometimes discolored, and increasingly fibrotic → more compressible, less elastic disk - more prone to tear and rupture.

    3. wear & tear (accumulation of axial loading, motion trauma effects) → cracks in inner layers of annulus fibrosus.

N.B. disc degeneration is universal accompaniment of aging! (degeneration is identifiable in virtually everyone over age 60 years)

  • propensity to develop degeneration is correlated with ↑mobility of spinal segments:

  • cervical region, L4-S1, upper lumbar and lower thoracic spine;

  • discs lying above / below fused spinal segments!!!

Reactive vertebral changes

- decreased capacity for shock absorption in degenerated discs → greater forces are transmitted directly onto adjacent vertebral bodies:

  1. Osteophytes

  2. End-plate changes:

Type I - edema: ↓signal on T1-MRI, ↑signal on T2-MRI; differentiate from edema seen in infectious discitis/osteomyelitis (with infection, disc is abnormally bright on T2-MRI, whereas degenerated discs are dark).

Type II - end-plate infiltration by fat; marrow is brighter on T1-MRI and dark on T2-MRI; represents burned-out type I.

Type III - degenerative discogenic sclerosis of end-plate: ↓signal on both T1- and T2-MRI.
Possible further changes:

  1. invasion of cancellous spaces by fibrovascular reactive tissue continuous with that of disc.

  2. end-plate fracture and displacement into vertebral body.

  3. very irregular end-plate → destructive diskovertebral lesion (may simulate infective spondylitis) → vertebral malalignment (scoliosis, retrolisthesis, anterolisthesis).

Disc displacements

  1. Bulge - circumferential extension of disc margin beyond vertebral body margins.

    • identified in 50% asymptomatic persons.

    • annulus normally may bulge diffusely little (< 2-3 mm) beyond vertebral margins, esp. in children.

  2. Herniation - focal displacement of disc material (nucleus pulposus and/or annulus) beyond margins of disc space; can occur in any direction (most clinically significant – posterolaterally).

  1. protrusion (hard disc protrusion, spondylosis) – hardened nucleus bulges beneath attenuated annulus; associated osteophytes add to mass effect;

    • identified in 25% asymptomatic persons.

  1. extrusion (herniation, soft disc protrusion, disc rupture) – soft nucleus extrudes through tear in annulus;

    • identified in < 1% asymptomatic persons.

  • sequestered fragment - extruded disc fragment separates entirely from its disc of origin, and may migrate within epidural space (occasionally, penetrates dura and can be seen intrathecally – can simulate neurinoma).

Schmorl node – nucleus pulposus herniation through cartilaginous end plate into vertebral body; usually incidental radiographic or postmortem finding (prevalence in general population ≈ 20%).

    • seen most frequently in lower thoracic and upper lumbar spine.

    • occur through defects of end-plate (e.g. gaps in chondrification formed by vessels arising from vertebral body).

    • may be consequence of trauma.

    • reactive sclerosis forms around herniated cartilage nodule and it becomes easily visible radiographically.

    • thinning of disc space may or may not accompany herniation (caused not so much by actual herniation of disc material but by disc desiccation).

N.B. term “herniation” should be reserved for situations in which more precise classification cannot be made!

Disc degeneration + Traumatization is prime cause of disc herniation.

  • genetic predisposition in many cases!

  • commonly trauma is trivial.

  • major trauma is usually cause in children and young adults.

Time course of herniation:

  1. development of radial fissure through inner* concentric rings of anulus fibrosus; nucleus pulposus may begin to extend into this fissure; patient may experience low back pain and perhaps some referred pain into buttock or hip.

*outer layers of anulus fibrosus are tightly bound to adjacent vertebral end-plates

  1. nucleus protrusion causing bulging of outer layers of anulus and of posterior longitudinal ligament (sufficient to pinch adjacent nerve root between protruding disc and lamina or intervertebral facet).

  2. free disc fragment is completely extruded and becomes wedged anterior to nerve root.

d:\viktoro\neuroscience\spin. spinal disorders\00. pictures\41-26.jpg
Disc displacement causes symptoms by several mechanisms:

  1. Local pain (provided by sinuvertebral nerve):

    1. mechanical stress on pain-sensitive structures (outer fibrous annulus, ligaments, periosteum, dura).

N.B. intervertebral disks (at least, nucleus pulposus) are not pain-sensitive!

    1. exposed disc material has direct toxic effect → local inflammatory response.

    2. regional muscle spasm.

  1. Radiculopathy / myelopathy – due to compression by mass of disc material:

    1. herniation into lateral recess or neural foramen (posterolateral herniation) → spinal root compression.

    2. herniation into spinal canal (central herniation) → spinal cord compression (in cervical ÷ thoracic region) or cauda equina compression (in lumbosacral region).

N.B. spinal stenosis & spondylosis are major contributors to compression syndromes of cord and cauda equina! (even bulges and small protruding discs may compress neural structures).

  • disc extrusion is more likely to be source of symptoms than is disc protrusion (protrusions and annular bulges do cause symptoms, but this depends on additional anatomic factors - proximity of disc material to roots, caliber of bony spinal canal).

  • mechanisms by which compression causes neurological dysfunction: mechanical alteration of axonal membranes, impaired axonal flow, ischemia, eventual demyelination.

In many cases, symptoms are self-limited:

  1. reparative processes

  2. desiccation (shrinkage) of herniated disc fragment.


Absence of C8 vertebral body but presence of C8 spinal segment means that:

roots above C8 exit above corresponding vertebral body;

remaining roots exit below their respective vertebral bodies.

  • as spinal nerve exits through intervertebral foramen, it lies between intervertebral disc anteromedially and facet joint posterolaterally.

  • roots occupy ≈ 25-30% of space in intervertebral foramina.

  • > 2/3 herniations are lumbosacral.


Most common sites: C6-7 (55%) > C5-6 (30%) > C7-T1 > C4-5.

Roots above C8 exit above corresponding vertebral body + spinal segment and vertebral levels are roughly aligned:

  • posterolateral herniation compresses caudal root (e.g. C6-7 herniation affects C7 root; C7-T1 herniation affects C8 root) - the same rule as in lumbar region!

  • central (midline posterior) herniation compresses ≈ same level spinal segment (rare event, unless spinal stenosis, or massive herniation).

d:\viktoro\neuroscience\spin. spinal disorders\00. pictures\cervical disc herniation (scheme).jpg


Most common sites: L5-S1 (80%) > L4-5 > L3-4 (4-5%) > L2-3 & L1-2 (< 1%)

Roots exit below corresponding vertebral bodies + emerging root usually escapes entrapment above protruding disc:

  • large central (midline posterior) herniation may compress cauda equina (multiple bilateral roots).

see p. Spin1 >>

  • posterolateral herniation compresses caudal root (traveling downward to emerge one level below); e.g. L4-5 herniation affects L5 root – i.e. the same rule as in cervical region!

Disc annulus is weakest posterolaterally – most frequent lumbar herniations are posterolateral.

d:\viktoro\neuroscience\spin. spinal disorders\00. pictures\disk herniations (scheme).gifd:\viktoro\neuroscience\spin. spinal disorders\00. pictures\disk herniations (scheme)2.gif

  • far lateral (foraminal, lateral extraforaminal) herniation (≈ 10% lumbar herniations; tend to affect higher levels - L2-4) - lateral to spinal canal and root sleeve - compresses rostral root (e.g. L3-4 herniation may compress L3 root).

Root compression may occur at level of disc space (1) or from rostrally migrated fragment into foramen of upper nerve root (2):

Extraforaminal hernia may even compress root from level above as it descends in paravertebral muscles immediately adjacent to spine!

d:\viktoro\neuroscience\spin. spinal disorders\00. pictures\far lateral lumbar herniation (scheme).jpg


  • markedly degenerated, gritty calcified deposits; thoracic disc protrusion is more granular and yellowish.

  • some surgeons continue to submit disc material for histologic diagnosis - yield is exceedingly low and of questionable benefit.


Women ≥ men (according to other sources: males – 80%).

  • 5% males and 2.5% females experience sciatica at some time in their lifetime.

Peak incidence - ages 30-50 yrs (rare before 25 and uncommon after 60):

  1. accumulated some degenerative changes in annulus.

  2. preserved expansile gelatinous nucleus.

  3. job and sports-related activities.

  • incidence falls in older population (osteoarthritis becomes more frequent cause of symptoms):

    1. ↓mobility of desiccated disc

    2. physical activity↓.

Risk factors

      1. Congenital spinal anomalies (e.g. fused and malformed vertebrae, lumbar spinal stenosis due to short pedicles) – may cause tendency toward disc herniation in some families.

      2. Acquired spinal disorders (e.g. degenerative arthritis, ankylosing spondylitis).

      3. Increased weight, heavy lifting

      4. Tall stature

      5. Physical inactivity (e.g. sedentary occupations)

      6. Spinal trauma (repeated occupational)

      7. Motor vehicle use, vibration

      8. Smoking, diabetes

      9. Genetic predisposition

      10. In younger women:

        1. pregnancy and delivery → lumbosacral herniation.

        2. bending and lifting involved in child rearing → cervical herniation.

Clinical Features

Signs & symptoms relate to geometry:

  1. size and strategic location of disc fragments

  2. size and configuration of spinal canal (incl. foramina).

  1. Local pain (s. axial pain) – may be absent, or may precede herniation for weeks or months.

  2. Compressive lesion:

  1. radiculopathy see p. PN1 >>

N.B. radicular pain may radiate into extremity episodically, extending further down extremity with each episode.

  1. myelopathy (may be preceded by spinal shock) - paresis, with loss of pain and temperature sensations below level of lesion; vibration and position sensations are frequently retained (posterior location of dorsal columns). see p. Spin1 >>

Cervical herniation

  • onset of symptoms:

  1. follows trauma (e.g. sudden rotation of head)

  2. spontaneous.

  • begins with stiff neck (reactive splinting of erector capital muscles), discomfort at medial border of scapula.

  • local neck pain (axial pain) radiates to interscapular region, shoulders, arms (radicular pain).

  • palpation of brachial plexus and supraclavicular fossa is often painful.

  • symptoms are worsened by:

  1. Valsalva maneuvers

  2. stretching dependent arm

  3. neck movements (esp. extension, lateral flexion to side of herniation – i.e. lateral flexion toward painful side*).

*vs. in trivial muscle spasm – pain on lateral flexion to opposite side (i.e. during stretch of painful muscle)!

vs. cervical spondylosis - exacerbated by any neck movements!

d:\viktoro\neuroscience\spin. spinal disorders\00. pictures\cervical pain (bates-355, 356).jpg

Source of picture: Barbara Bates “A Guide to Physical Examination”, 3rd ed. (1983); J.B. Lippincott Company; ISBN-13: 978-0397543991 >>

  • for relief patient adopts recumbent position with arm elevated and flexed behind head (vs. shoulder disease - patient maintains arm in dependent position, avoiding elevation or abduction at shoulder joint).

  • axial loading test, Spurling test (support diagnosis of cervical root disease) → see p. D1 >>

N.B. do not omit motor and sensory examination in lower extremities - to detect cord compression!

Lumbosacral herniation

  • bouts of nonspecific low back pain (usually remittent) already begin in twenties.

  • in majority, there is no history of antecedent trauma - herniation follows lifting* / twisting injuries (or may result from accumulated low-level trauma); sneeze, cough, or trivial movement may also be trigger.

N.B. in many cases, inciting event cannot be identified!

*increasing intra-abdominal pressure during heavy lifting even adds to compressive load on vertebrae but otherwise stabilizes spinal column and may prevent twisting injury

  • patient appears uncomfortable.

  • symptoms are often episodic (remissions are characteristic).


  • pain may be restricted to parasacral area or may radiate to buttocks, thigh, leg, foot.

sciatica – L5 or S1 * radicular pain.

*any of L4-S3 roots (take part in ischiadic nerve) may produce sciatica to varying degree

  • paresthesias are common.

  • pain is aggravated by: see p. PN1 >>

  1. Valsalva maneuvers

  2. heavy lifting from bent position

  3. back movement (extension or twisting).

  4. provocative root stretch maneuver:

    1. passive straight-leg rising s. Lasègue sign (for roots L5 and S1);

    2. femoral stretch test (for root L4).

  • pain is characteristically relieved promptly when patient lies down* (no matter how severe pain is when patient is erect!; vs. spinal tumor - pain is not relieved or even worsens!) on one side with hips and knees flexed.

*some patients are more comfortable standing and some can find no comfortable position

  • patient may not be able to stand erect because paraspinal muscles contract so vigorously, yet pain may be relieved as soon as patient lies down, only to return again on any attempt to stand.

  • most uncomfortable position is sitting - causes increased intervertebral pressure!

  • later, short walks can bring relief, but long walks or extended sitting (especially driving) can aggravate pain.


  • protective splinting of paraspinal muscles:

  1. asymmetric prominence of long erector muscles.

  2. loss of lumbar lordosis (flattening of lumbar spine), lumbar scoliosis.

  3. elevated one iliac crest (list or tilt) – “longer leg on one side” (erroneous assignment of back pain to leg length asymmetry) – often causes patient to raise heel on shoe of “short” leg to level pelvis).

  4. reduced range of motion of lumbar spine (attempted movement in some planes [esp. flexion] → severe back pain).

    • tenderness of adjacent vertebrae.

    • muscle atrophy and weakness (fasciculation is rare). see p. PN1 >>

e.g. wasted gluteus - one gluteal fold hangs down and shows added skin creases when patient is erect.

    • sciatic tenderness on direct pressure at some point along nerve (e.g. popliteal).

    • with sacral roots involvement, disturbances of bladder & bowel function are common.

Thoracic herniation

- herniations are uncommon! (suspect other underlying lesions – tumor, abscess, etc).

  • motion trauma (wear and tear) plays no role (vs. cervical, lumbosacral disc degenerations) - thoracic vertebrae are designed for stability rather than excursion, and heavy rib cage contributes to rigidity of this structure.

  • small capacity of thoracic canal → spinal cord compression is more frequent and more critical than root compression - early recognition is important! (to avoid irreversible myelopathy)

  • thoracic disc disease may result from Scheuermann disease with later trauma.


N.B. asymptomatic patients have high incidence of anatomical lesions – try to establish closest possible clinical correlation with anatomical findings!
Question about:

  1. trauma

  2. cancer

  3. infections, recent fever

  4. bleeding disorders, anticoagulant medications

Immediately establish major deficits that demand rapid diagnosis & surgical treatment (see below – clear indications for surgery).
Findings consistent with ruptured disc + no ÷ moderate deficit → plain X-ray of affected area → no unexpected lesions → conservative therapy.

  • this approach is justified by good prognosis for spontaneous recovery of acute radiculopathy with up to moderate deficits.

  • if clinical examination leaves doubt about lesion localization (root vs. peripheral nerve or plexus) → EMG, nerve conduction studies (more sensitive if delayed until at least 10-14 days after onset of new deficit).

  • if surgery is considered necessary, it should be preceded by MRI or CT myelography.

Plain X-ray

  1. Indirect diagnostic information (radiographs cannot show neural tissues or disc itself!):

  1. isolated loss of disc space height

    • normal cervical ÷ thoracic discs are almost equal in height.

    • normal lumbar discs progressively increase in height from T12-L1 through L4-5; L5-S1 disc has variable height because of its transitional status.

  1. other degenerative changes: osteophytes, end-plate sclerosis, malalignment (scoliosis, retrolisthesis, anterolisthesis).

Degenerative changes do not mean patient has “arthritis” as many asymptomatic patients (esp. young females) have some changes!

  • gas may be visible within degenerated discs (nitrogen drawn from blood by negative pressure generated during spine extension within airtight disc fissures).

  • severe degenerative disc disease may progress to spontaneous fusion between adjacent vertebrae.

  1. Screen for unexpected infection, tumor, bony deformity.

  • many disc syndromes are genetic - abnormal skeletal features should be sought throughout spine (spinal stenosis, spondylolisthesis, widespread disc disease, Marfan disease, etc).

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