Degenerative disc disease is a condition characterized by changes in the discs between vertebrae. As discs degenerate they lose water content and height. Fissures can form in the annulus fibrosus and the nucleus pulposus loses structure. This can lead to bulging of the disc and potentially protrusion or extrusion of disc material. Kirkaldy-Willis divided the process into three stages: dysfunction, instability, and stabilization. Symptoms include back pain and pain that may radiate into the legs. Diagnostic imaging includes x-rays, CT, MRI, and discography which can help identify problematic discs.

1. DEGENERATIVE DISC DISEASE
REM KUMAR RAI
MS ORTHO RESIDENT
NAMS

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

3. 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.

4. DEFINITION: DDD
 Degenerative disc disease:
 as a clinical syndrome characterized by
manifestations of disc degeneration and
symptoms thought to be related to those
changes

5. 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)

6. Intervertebral Disc
 Annulus Fibrosus
 Outer portion of the disc
Annulus
Fibrosus
– Made up of lamellae fibrocartilage
– Layers of collagen fibers Type I





Arranged obliquely 30°
Some radial fibers
Thicker anteriorly >posteriolry
Attached to end plates
Great tensile, torsional
& radial strength
Lamellae

7. Intervertebral Disc
 Nucleus Pulposus
– Inner structure
– Notochord remnant
– Type II collagen
+Gelatinous GAG,H2O
– High water content (7090%)
– Resists axial forces
Nucleus
Pulposus

8. Vertebral End-Plate
 Cartilaginous & osseous component
 Nutritional support for the nucleus
 Passive diffusion

9.  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.

10. Anatomical Segment
Components:
Vertebral body
Attached posterior elements
Disc below
Exiting and traversing Nerve root

11. Anatomical House with windows
Window of opportunity to the disc space, interlaminar and intertransverse window

12. Spine Motion Segment
 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

13. 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.

14.  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

15.  Each spinal segment degenerates at a different
rate
 As one level is in the dysfunction stage, another
may be entering the stabilization stage
 Disc herniationcomplication 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

16. Pathoanatomy & pathogenesis
 Kirkaldy-Willis Three
DYSFUNCTION
phases of
Degenerative process
INSTABILITY
STABILIZATION

17. Mechanism of DYSFUNCTION
Episode of rotational or compressive trauma
( uncoordinated muscle contraction)
Posterior joint strain
( also annular strain)
Splinting
Posterior joint
Subluxation
maintained
Minor facet subluxation
Synovitis( pain)
Sustained segmental
Hypertonicity of muscle
Ischemia ( pain)
Altered muscle metabolism

18. 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

19. Mechanism of unstable phase
Severe dysfunction
Continuing stress
Trauma
Increased dysfunction
disc
facets
Degeneration of cartilage
Coalescence of tears
Loss of nucleus, internal disruption
Attenuation of capsule
Bulging of annulus
Laxity of capsule
Increased abnormal movement
Unstable phase

20.  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

21. Mechanism of stabilization
Disc
Facets
Destruction of cartilage
Loss of nucleus
Fibrosis in joints
Approximation of bodies
Enlargement of facets
Destruction of plates
Locking facets
Fibrosis in disc
osteophytes
Fibrosis arund joints
Increased stiffness
stabilization

22.  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

23. 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

24. 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

25. 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.

26. 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.

27. 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

28. 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.

29. Modic Change
 Type III
 signal intensity
 lowT1-weighted
 lowT2-weighted
 severely degenerated end
plates
 only end plate change visible
on CT scans or radiographssclerosis
 Part of the normal aging
process and must not be
confused with other
pathologic processes, such as
tumor and infection

30. Other diagnostic tests
 PET / SPECT- experimental & few centers
have this facilities
 Electromyography/ NCVadvantage 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.

31.  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.

32. 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.

33. 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.

34. 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

35. 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

36. 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.
4.
5.
6.
7.
8.
9.
AF develops fissures parrallel to the vertebral
end plates.
Compressive loads transfer away from nucleus
to margins
Sclerosis of endplate reduces disc nutrition.
Facet joints wear away cartilage, begin to
override
Motion segment becomes hypermobile
Osteophytes develop to attempt to stabilize
motion segment
Osteophytes may encroach on neural
structures.

37. Prolapse intervertebral disc
Pathophysiology:
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.

38. 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

39. 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.

40. 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

41. CLASSIFICATION DD
 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

42. CLASSIFICATION
 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

43. 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

44. 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

45. 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

49. 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

50. 
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.

51. 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

52. 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

53. 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.

54. Thank you