DEGENERATIVE DISC DISEASE

REM KUMAR RAIMS ORTHO RESIDENTNAMS

DEFINITION

Degenerative disc disease (DDD) has been used to describe a wide variety of morphologic and radiographic changes in the adult spine

DEFINITION: DISC DEGENERATION The North American Spine Society

Consensus Committee on Nomenclature :

Changes in a disc characterized by desiccation, fibrosis, or cleft formation in the nucleus; fissuring or mucinous degeneration of the annulus; defects and sclerosis of the endplates; and/or osteophytes at the vertebral apophysis.

DEFINITION: DDD

Degenerative disc disease: as a clinical syndrome

characterized by manifestations of disc degeneration and symptoms thought to be related to those changes

Intervertebral disc Total 23 Hydrostatic, load

bearing , shock absorbing structure between the vertebral bodies

Each disc unit has strong outer ring of

fibers called the annulus fibrosus

a soft , jelly like center called the nucleus pulposus

2 endplates (Campbell)

Intervertebral Disc Annulus Fibrosus

Outer portion of the disc

Lamellae Great tensile, torsional

& radial strength

Great tensile, torsional & radial strength

– Made up of lamellae fibrocartilage

Annulus Fibrosus

– Layers of collagen fibers Type I Arranged obliquely 30° Some radial fibers Thicker anteriorly >posteriolry Attached to end plates

– Layers of collagen fibers Type I Arranged obliquely 30° Some radial fibers Thicker anteriorly >posteriolry Attached to end plates

Intervertebral Disc

Nucleus Pulposus Nucleus Pulposus– Inner structure

– Notochord remnant– Type II collagen

+Gelatinous GAG,H2O– High water content (70-

90%)– Resists axial forces

– Inner structure– Notochord remnant– Type II collagen

+Gelatinous GAG,H2O– High water content (70-

90%)– Resists axial forces

Vertebral End-Plate

Cartilaginous & osseous component Nutritional support for the nucleus Passive diffusion

The intervertebral disc in the adult is avascular.

blood vessels in the annulus until the age of 20 years and within the cartilage endplates until the age of 7 years.

The cells within the disc are sustained by diffusion of nutrients into the disc through the porous central concavity of the vertebral endplate

The discs vary in size and shape with their position in the spine. Discs also decrease in volume, resulting in a 16% to 21% loss in disc height after 6 hours of standing or sitting.

Anatomical Segment

Components:Vertebral body Attached posterior elementsDisc belowExiting and traversing Nerve root

Anatomical House with windows

Window of opportunity to the disc space, interlaminar and intertransverse window

The FUNCTIONAL UNIT of the spine

Comprises of: 1.Two adjacent

vertebrae 2.Intervertebral disc 3.Connecting ligaments:

including the ligamentum flavum, interspinous, supraspinous, intertransverse ligament

4.Two facet joints and capsules

The FUNCTIONAL UNIT of the spine

Comprises of: 1.Two adjacent

vertebrae 2.Intervertebral disc 3.Connecting ligaments:

including the ligamentum flavum, interspinous, supraspinous, intertransverse ligament

4.Two facet joints and capsules

Spine Motion Segment

Natural History of Disc Disease

Kirkaldy-Willis divided DDD into three separate stages with relatively distinct findings. There is recurrent episodes of pain followed by periods of significant or complete relief

Dysfunction seen in those 15 to 45 years of age, characterized by circumferential and radial (micro )tears in the disc annulus and localized synovitis of the facet joints.

Instability found in 35- to 70-year-old patients, characterized by internal disruption of the disc, progressive disc resorption, degeneration of the facet joints with capsular laxity, subluxation, and joint erosion

Stabilization present in patients older than 60 years, the progressive development of hypertrophic bone about the disc and facet joints leads to segmental stiffening or frank ankylosis

Each spinal segment degenerates at a different rate

As one level is in the dysfunction stage, another may be entering the stabilization stage

Disc herniationcomplication of disc degeneration in the dysfunction and instability stages

Spinal stenosis from

degenerative arthritis complication of bony overgrowth compromising neural tissue in the late instability and early stabilization stages

Pathoanatomy & pathogenesis

Kirkaldy-Willis Three phases of Degenerative process

DYSFUNCTION

INSTABILITY

STABILIZATION

Mechanism of DYSFUNCTION

Episode of rotational or compressive trauma( uncoordinated muscle contraction)

Posterior joint strain( also annular strain)

SplintingPosterior joint Subluxationmaintained

Minor facet subluxation

Synovitis( pain)

Sustained segmental Hypertonicity of muscle

Ischemia ( pain)Altered muscle metabolism

Symptom sign & radiological changes in dysfunction

Symptom:- Low back pain Often localised axial Sometimes referred /radicular Movement painful

Sign:- Local tenderness Muscle contracted: PSM spasm Hypomobility Extension painful Neurologically usually normal

Radiograph:- Loss of physiological curvatures Spinous process malalignment Irregular facet Early disc changes

Mechanism of unstable phase

Severe dysfunction

Trauma Continuing stress

Increased dysfunction

facets disc

Degeneration of cartilage Coalescence of tears

Attenuation of capsuleLoss of nucleus, internal disruption

Laxity of capsuleBulging of annulus

Increased abnormal movement

Unstable phase

INSTABILITY Symptom:-

Those of dysfunction Giving away of back, “catch” in back( on

movement) Pain on coming to standing position after flexion

Sign:- Detection of abnormal movement( LOOK/FEEL) Observation of “catch” sway or shift when coming

erect after flexion Radiograph:-

AP:- Lateral shift Rotation Abnormal tilt Malaligned spinous process

OBLIQUE:- Opening facets

LATERAL:- Spondylolisthesis( in flexion) Retrolisthesis ( in extension) Narrowing foramen( in extension).Abnormal opening

of disc Abrupt change in pedicle height.Traction spurs

Mechanism of stabilization

Facets Disc

Destruction of cartilage Loss of nucleus

Fibrosis in joints Approximation of bodies

Enlargement of facets Destruction of plates

Locking facets Fibrosis in disc

Fibrosis arund joints osteophytes

Increased stiffness

stabilization

STABILIZATION Symptom:-

Low back pain of decreasing severity Sign:-

Muscle tenderness Stiffness Reduced movement Scoliosis

Radiograph:- Enlarged facet Loss of disc height Osteophytes Small foramen Reduced movement Scoliosis

Diagnostic Studies ROENTGENOGRAPHY 1. AP and Lateral 2. Oblique views:

useful in defining spondylolisthesis and spondylolysis

3. Lateral flexion and extension: X-ray may reveal segmental

instability 4. Ferguson view (20-

degree caudocephalic anteroposterior ): value in the diagnosis of the

"far out syndrome," that is, L5 compression produced by a large transverse process of the fifth lumbar vertebra against the ala of the sacrum

MYELOGRAPHY

Indicated if MRI is not available or for patient in whom MRI is contraindicated( cardiac pacemaker or brain aneurysm clip)

valuable in a previously operated spine and in patients with marked bony degenerative change that may be underestimated on MRI

improved by the use of postmyelography CT scanning

COMPUTED TOMOGRAPHY

extremely useful diagnostic tool noninvasive, painless, outpatient procedure

can supply more information about spinal disease

Unfortunately, CT does not demonstrate intraspinal tumors or arachnoiditis and is unable to differentiate scar from recurrent disc herniation.

MAGNETIC RESONANCE IMAGING

newest technological advance in spinal imaging

The advantages :- ability to demonstrate

intraspinal tumors, examine the entire spine, and identify degenerative discs based on decreased H2O content

costly and requires specially constructed facilities.

Modic Change Type I Signal intensity on

low T1-weighted High T2-weighted

replacement of the end-plate marrow with vascular fibrous tissue in response to chronic “injury.”

Clinical: annular tear, fissure

MODIC CHANGE Type II signal intensity

high T1-weighted and on FSE T2-weighted

Low T2

represents replacement of the end-plate marrow with fatty tissue.

Chronic marrow disuse

Type II changes tend to remain stable with time.

Modic Change Type III signal intensity

lowT1-weighted lowT2-weighted

severely degenerated end plates

only end plate change visible on CT scans or radiographs-sclerosis

Part of the normal aging process and must not be confused with other pathologic processes, such as tumor and infection

Other diagnostic tests

PET / SPECT- experimental & few centers have this facilities

Electromyography/ NCVadvantage of electromyography is in the identification of peripheral neuropathy and diffuse neurological involvement indicative of higher or lower lesions.

The SSEP is an extremely sensitive monitoring technique.

Bone scans positive findings usually are not indicative of intervertebral disc disease, but they can confirm neoplastic, traumatic, and arthritic problems in the spine.

complete blood count, differential white cell count, biochemical profile, urinalysis, and sedimentation rate good screening procedures

Rheumatoid screening studies such as rheumatoid arthritis latex, antinuclear antibody, lupus erythematosus cell preparation, and HLA-B27 also are useful when indicated by the clinical picture.

ZYGAPOPHYSEAL (FACET) JOINT INJECTIONS Cause of facet joint pain:-

Meniscoid entrapment and extrapment, synovial impingement, chondromalacia facetae, capsular and synovial inflammation, and mechanical injury to the joint capsule.

Osteoarthritis No noninvasive pathognomonic findings

distinguish facet joint–mediated pain from other sources of spine pain.

Fluoroscopically guided facet joint injections therefore are commonly considered the gold standard for isolating or excluding the facet joint as a source of spine or extremity pain.

DISCOGRAPHY provocative testing for concordant pain to provide information regarding the clinical significance of the disc abnormality. Indications :- surgical planning of spinal fusion, testing of the

structural integrity of an adjacent disc to a known abnormality such as spondylolisthesis or fusion, identifying a painful disc among multiple degenerative discs, ruling out secondary internal disc disruption or suspected lateral or recurrent disc herniation, and determining the primary symptom-producing level when chemonucleolysis is being considered.

Lumbar spine in an oblique position with superior articular process (arrow) dividing disc space (d) in half

Disc entry point is just anterior (arrow) to base of superior articular process (s) and just above superior endplate of vertebral body

Curved procedure needle (c) passing through straight introducer needle (n

Lumbar Disc Disease

Symptomatic LDH occurs during the lifetime of approx. 2% of the general population

Factors associated with LDH:- Male gender Age 30 -50 yrs Job requiring heavy lifting Lifting in a twisted or asymmetric posture Stressful occupation Lower income Cigarette smoking Exposure to prolonged vibration in the

range of 4 to 5 Hz

Degenerative Disc Disease Pathophysiology:

1. Disc gradually dries out, loses height and volume.

2. NP changes from a turgid gelatinous bulb to brownish dessicated structure.

3. AF develops fissures parrallel to the vertebral end plates.

4. Compressive loads transfer away from nucleus to margins

5. Sclerosis of endplate reduces disc nutrition.

6. Facet joints wear away cartilage, begin to override

7. Motion segment becomes hypermobile

8. Osteophytes develop to attempt to stabilize motion segment

9. Osteophytes may encroach on neural structures.

Prolapse intervertebral discPathophysiology:

1. Acute disc prolapse is due to flexion +compression.

2. More at L4/5,L5/S1 (stress is more severe).3. Disc rupture = stress + disturbances in the

hydrophilic properties of the NP.4. Disc rupture = fibrocartilaginous material

extruded posteriorly and annulus bulges to one side.

5. Part of the nucleus may sequestrated freely.6. Large central rupture may cause pressure of

the cauda equina.

Boos et al. decrease in 

nutritional transport  water content absolute number of viable cells proteoglycans pH

increase in an increase keratin sulfate to chondroitin sulfate

ratio  lactate degradative enzyme activity

Pathophysiology: Pain= arises due to disruption of outermost layer

of the annulus fibrosus, stretching or tearing of the posterior longitudanal ligament and pressure on the dura. symptoms worsened by coughing, valsalva, sneezing

Sciatica= if disc protudes to oneside it may irritate the dural covering of the adjacent nerve root causing pain in the buttock, posterior thigh and calf.

Pressure on the nerve root itself causes paraesthesia and/or numbness in the corresponding dermatome, as well as weakness and decreased reflexes in the muscles suppllied by that nerve root.

STAGES OF DDD

Dessication Loss of fluid in nucleus pulposus.

Disc bulge:- diffuse symmetrical outpouching of the annulus fibrosus caused by early disc degeneration& collapse

Protrusion:- base wider than any diameter of the material displaced beyond disc space

Extrusion:- displaced portion has a greater diameter than its connection with the parent disc at its base

Sequestration:- when disc extrusion has lost all connection with the parent disc

Migration:- an extruded disc, whether sequestrated or not, that has been displaced above or below the edge of the disc space

Depending upon whether the displaced portion is completely enveloped by intact outer annulus or combination of annulus and PLL( s/t called capsule):-

Contained:- Un contained:-

Subligamentous:- disc material contained beneath the PLL

Transligamentous Submembranous:- disc

material contained only by peridural menbrane

CLASSIFICATION DD

Depending upon the relationship of the herniated material to the posterior annulus and PLL: Central( midline):- herniation along the

posterior annulus Posterolateral:- along the weaker lateral

expansion of PLL Foraminal( lateral ) Extraforaminal ( far lateral)

In relation to nerve root: Shoulder herniation Axillary herniation

According to the level of LDH:- High LDH:- L1-L2, L2-L3, L3-L4 Low LDH:- L4-L5, L5-S1

CLASSIFICATION

SIGNS AND SYMPTOMS LDD

Age:- 3rd or 4th decade in healthy adult

Mostly relate to traumatic incident but Intermittent back pain of months or year

Back or leg pain, radiating Aggravating :-heavy exertion,

repetitive bending, twisting, or heavy lifting, relieved with rest in semi-Fowler position

weakness and paresthesias, localized to the neurological level of involvement

Clinical examination

Standing pt who declines to sit, with loss of normal lumbar lordosis & PVM spasm suggestive of PIVD

List Limited spine ROM Point tenderness may be present

over the spinous process at the level of the disc involved

Atrophy of muscles – chronic cases

LSR testing During SLR maneuver , the L5 and S1

nerve root either moves or passively deforms approx. 2 to 6 mm at the level of foramen

Maximum tension is realized in the sciatic nerve at 30* to 70* of elevation from the supine

Crossed SLR is more specific of a disc herniation( pathognomonic of micromotion in affected side nerve roots while raising normal side leg)

Large cenrtal or lateral recess herniation Free disc fragment

Lasegue sign Bowstring sign

Management

Goal:- Prompt return to normal function and pain

relief through the efficient and effective use of diagnostic tests and efficacious treatments

Non operative:- Reassurance, medications, and activity

modification Bed rest in a semi Fowlers position for 1 to 2

days in acute cases Aerobic conditioning including abdominal and

back strengthening exercises Application of heat, ice, TENS, USG massage,

Traction Manipulative therapy Back school programme

EPIDURAL STEROIDS:-

offer relatively prolonged pain relief without excessive narcotic intake if conservative care is elected.

Methylprednisolone is the usual steroid injected.

The dosage may vary from 80 to 120 mg.

The anesthetics used may include lidocaine, bupivacaine, or procaine.

current protocol is to inject the patient three times. These injections are made at 7- to 10-day intervals.

Indication of surgery Emergent/ absolute:-

Presence of cauda equina syndrome Progressive neurologic deficit

Relative:- Persistent radiculopathy despite an adequate trial of non

surgical treatment( min of 6 wks) Recurrent episodes of incapacitating sciatica Significant motor deficit with persistent tension signs and

pain Pseudoclaudication( activity related leg pain) caused by

canal stenosis resulting from a disc herniation Goal of surgery:-

Alleviate the neural compression without further injury to the affected nerve root

Minimal disruption of surrounding normal tissues and maintenance of spinal stability

Waddell’s Non-organic sign (DOReST)

Finding Description

1. Tenderness a. superficial - pain with light touch to skin

b. deep - nonanatomic widespread deep pain

2. Simulation a. pain with light axial compression on skull 

b. pain with light twisting of pelvis

3. Distraction No pain with distracted SLR

4. Regional a.nonanatomic or inconsistent motor findings during entire exam 

b. nonanatomic or inconsistent sensory findings during entire exam

5. Overreaction Overreaction noted at any time during exam

Surgical procedure

Standard open lumbar disectomy Microlumbar disc excision Endoscopic disc excision Additional exposure Hemilaminectomy usually is required when

identifying the root is a problem. This may occur with a conjoined root.

Total laminectomy usually is reserved for patients with spinal stenoses that are central in nature, which occurs typically in cauda equina syndrome.

Facetectomy usually is reserved for foraminal stenosis or severe lateral recess stenosis.

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