Low Back Pain &

HNP (hernia nucleus pulposus)

Dr. dr. Farhad Bal’afif, SpBS(K)

Prof. Dr. dr. M. Istiadjid ES, SpS, SpBS(K)

SMF Bedah Saraf RSSA – FKUB

LOW BACK PAIN
& HNP (hernia nucleous pulposus)
Introduction
• Lower back pain is
commonly seen in primary
care.
• The initial treatment of the
most common causes of low
back pain is symptomatic.
• Physical exam can help
confirm the diagnosis and
assess functional status.
Epidemiology
• 85% of people experience LBP
in their lifetime.
– 2nd leading symptom (behind
URI’s) prompting all physician
visits in the US.
– Up to 50% of working age people
admit to low back pain during the
year.
– General prevalence in US
population 15-20%.
• LBP often recurs; becomes
chronic in 5-10% of patients.
Epidemiology
• Back symptoms are the most
common cause of disability for
persons younger than age 45.
• 1% of US population is disabled
due to LBP.
• Total societal costs for low
back pain exceed 50 billion
dollars
Anatomy
• 5 lumbar vertebra
• Components
– Body
– Pedicles
– Facets
– Lamina
– Spinous and transverse
processes
Anatomy of Lumbar Vertebrae
• AnteriorElements:
•Vertebral body: provide bulk
and height; Sustain
compression loads.
• Middle Elements:
• Pedicles: transfer forces
from posterior to anterior
elements.
• Posterior Elements:
•Articular processes and
facet jts, laminae, spinous
processes.
•Lock spine to prevent
forward sliding and twisting;
Insertion sites for muscle
Lumbar Joints
• 3 Joint Complex:
– Intervertebral disc: principal
joint between vertebrae.
– 2 Facet Joints: formed by
superior and inferior articular
processes.
• Disc consists of:
– Nucleus polposus
– Annulus fibrosis
– Vertebral endplates
 Lumbar Spine Ligaments

• Serve to aid spinal stability.

They include:
– Interspinous Ligament: connects
spinous process.
– Ligamenum Flavum: connects
laminae; roof for spinal canal.
– Ant / Post longitudinal ligaments:
cover vertebral body for stability.
 Lumbar Spine

• Include
–Vertebra
–Diskus
–Spinal Cord dan Nervus
Intervertebral Disc
• Hydrostatic, load bearing structure between the
vertebral bodies
• Nucleus pulposus + annulus fibrosus
• No blood supply
• L4-5, largest avascular structure in the body
Nucleus Pulposus
• Type II collagen strand + hydrophilic proteoglycan
• Water content 70 ~ 90%
• Confine fluid within the annulus
• Convert load into tensile strain on the annular fibers
and vertebral end-plate
• Chondrocyte manufacture
the matrix component
Annulus Fibrosus
• Outer boundary of the disc
• Concentric layer of overlapping lamellae of type I
collagen
• Fibers are oriented 30-degree angle to the disc
space
• Helicoid pattern
• Resist tensile, torsional, and radial stress
• Attached to the cartilaginous and bony end-plate
at the periphery of the vertebra
Vertebral End-Plate
• Cartilaginous and osseous component
• Nutritional support for the nucleus
• Passive diffusion
Facet Joint
• Synovial joint
• Rich innervation with sensory nerve fiber
• Same pathologic process as other large synovial joint
• Load share 18% of the lumbar spine
Vital Functions
•Restricted intervertebral joint motion
•Contribution to stability
•Resistence to axial, rotational, and bending load
•Preservation of anatomic relationship

Biochemical Composition
•Water : 65 ~ 90% wet wt.
•Collagen : 15 ~ 65% dry wt.
•Proteoglycan : 10 ~ 60% dry wt.
•Other matrix protein : 15 ~ 45% dry wt.
Disc Degeneration
•Environmental factor
•Genetic predisposition
•Normal aging process

* Biomechanical stress
 Degeneration of soft tissue and bone
 progressive morphologic change
 Intervertebral Disc
Cellular and Biochemical Change

•Decrease proteoglycan content

•Loss of negative charged proteoglycan
side chain
•Water loss within the nucleus pulposus
•Decrease hydrostatic property
•Loss of disc height
•Uneven stress distribution on the
annulus
Morphologic Changes
•bulging of the annulus fibrosus
•radial tear
•in-growth of granulation tissue in the annulus
•annular defect, cleft and fissure
•cellular necrosis  loss of distinction between the nucleus
and annulus
•focal extrusion of disc material

Aging Progress
•disc become more fibrous and disorganized
•replaced by amorphous fibrocartilage
•no clear distinction between nucleus and annulus
•gas formation and vacuum disc sign
Vertebral End-Plate
• Become thinner and hyalinized
• Decrease permeability
• Inhibit nucleus metabolism
• Disc space narrowing
• Osteophyte formation at the end-plate and
annular junction
• Marrow change with increased axial loading
• Subluxation and instability
Facet Joint

Disc height reduction 

• Facet joint capsule become lax
• Increased load transfer to the
facet joint
• Accelerate degeneration
• Joint subluxation, hypertrophy,
osteophyte formation

** Primary disc degeneration

 Secondary change in the
posterior facet joint and
soft tissue
• Degeneration
– dehydration of the disc
• Protrusion
– The disc bulges Ply w/o
rupture of the Ann Fibrosus
• Prolapse
– Only the outer most fibers
of the annulus fibrosus
contain the nucleus
• Extrusion
– The ann fibrosus is
perforated and discal
material moves into the
epidural space
• Sequestration
– A formation of discal
fragments from the AF & NP
outside the disc proper
Lumbar Disc Disease

Discogenic Back Pain

A. Internal Disc Disruption (IDD)

B. Degenerative Disc Disease (DDD)
C. Segmental Instability

Lumbar Disc Herniation and Radiculopathy

 Lumbar Disc Herniation
How pain is generated?

• Inflammatory
• Biochemical
• Vascular
• Mechanical
compression
Inflamation
• Central role in radiculopathy
• Olmarker(1995, spine)
Epidural application of autologous nucleus
without any pressure
 Nerve function impairment
 Axonal injury with significant primary
cell damage
• Nucleus is totally avascular
 Perceived as an antigen
 Intense inflammation response
• Application of annulus fibrosus
 No reduction of nerve conduction velocity
Biochemical Effect
• Nuclear herniation
 Incsease phospolipase A2, prostaglandin E2
cytokine, nitric oxide
• Disc herniation and sciatica
 Neurofilament protein and S-100 increase
in CSF
 Axonal and Schwann's cell damage

Mechanical Compression
• Local damage and intraneural ischemia
Vascular Pathophysiology

* Application of nucleus pulposus to nerve root

 increase endoneurial pressure
 decrease blood flow in the dorsal root
ganglia
 compartment syndrome
HNP LUMBALIS
HNP LUMBALIS
Clinical Anatomy
• Disc injury
- annular disruption, fissuring, annular defect

• Contained herniation
Noncontained herniation
Extruded
Sequestrated

• L4-5 and L5-S1 herniation most common

- 90% of disc herniation
- Great axial load, lordotic shear
History
• symptom of disc herniation : acute or gradual
• after trauma or without and inciting event
• most common 3rd and 4th decade

Chief Complain
• Pain, radiating from the back or buttock into the leg
• Numbness and weakness
• Sharp, lancinating, shooting/radiating down the leg
posteriorly below the knee
• Coughing, Valsalva maneuver  increase intracecal
pressure  increase pain
• Sitting position, driving  out of lordosis 
increase intradiscal pressure  increase pain
How Severe Is Your Pain?
• Are you able to
work?
• What activities
does the pain
prevent you from
doing?
• What have you
used to relieve
the pain, and did
it work?
Sciatica
- radiating pain down the leg

Radiculopathy
- radiating pain down the leg as a
result of nerve root irritation
Back Pain
• irritation of the posterior primary
ramus
- facet capsule, local musculature
• sinuvertebral branch - posterior
annulus
• change in disc loading and shape,
biomechanics
• loss of viscoelasticity.
• 90% of radiating pain have long-
standing prior episodic low back
pain
Physical Exam for LBP
• Important that you:
– Confirm what you suspect
from history.
– Assess severity.
– Reassure patient when there
is nothing serious.
• Start with patient standing
for inspection, palpation and
ROM.
• Have patient sitting for
strength and neurologic
exam.
Neurologic Examination
 Root Tension Signs

• Straight-leg raising : L5, S1 root

• Contralateral SLR : sequestrated or
extruded disc
• Femoral stretching, reverse SLR : L3,
L4 root
Physical Examination
Physical Examination

Laseque or Straight Leg Raising (SLR)

Cauda Equina Syndrome
• Caused by massive midline disc
herniation or mass compressing cord or
cauda equina.
– Rare (<.04% of LBP patients).
– Needs emergent surgical referral.
• Symptoms: bilateral lower extremity
weakness, numbness, or progressive
neurological deficit.
• Ask about:
– Recent urinary retention (most common) or
incontinence?
– Saddle anesthesia?
– Fecal incontinence?
Psycho-social Assessment
• Social, economic and psych
factors often play role in LBP
symptoms and response to
treatment.
• Need to consider:
– Affect on work.
– Disability issues.
– Pending legal issues.
– Family and job stress.
– Depression (30-40% of LBP
patients).
Diagnostic Test
Simple x-ray
• Disc space narrowing

MRI(magnetic resonance imaging)

• Disc pathology, neural structure,
musculoligamentous structure
• Soft tissue edema, hematoma,
intrinsic cord abnormality
• Synovial cyst, neurofibroma, perineural cyst
• 30% of asymptomatic individual have abnormal
MRI

CT, Myelography
Indication of Surgery
Ideal candidate
• history, physical examination, radiographic
finding, are consistent with one another
• when discrepancy exist, the clinical picture
should serve as the principal guide.
Absolute surgical indication
• cauda equina syndrome
• acute urinary retension/incontinence,
saddle anesthesia, back/buttock/leg pain,
weakness, difficulty walking
Relative indication
• progressive weakness
• no response to conservative treatment
Best predictive factor
1. persistent leg pain, that fail to respond to a 6-
week trial of nonoperative care
2. well-defined neurologic deficit
3. positive SLR test
4. positive imaging that correlates anatomically to
clinical findings
** 3 of these factor, at least 90% success rate

Other factors
• duration of sciatica, sick leave stress, depression,
level of education, work/disability
Timing of Surgery
• Cauda Equina Syndrome
- emergency
• Relative Indications
– Lack of scientific evidence on optimal timing
– Rarely <6 weeks
• Period in which improvement in symptoms generally
known to occur
– Should not be delayed beyond 3-4 months
• Chances of improvement in radicular pain are slight
and decrease further after 6 months
Available Surgical Interventions
• Open Discectomy

• Microdiscectomy

• Chemonucleolysis with Chymopapain

• Automated Percutaneous Nucleotomy

• Manual Percutaneous Discectomy
• Percutaneous Endoscopic Discectomy
• Endoscopic or Percutaneous Laser Discectomy
Complications of Surgery
• Wrong Level 1.2 – 3.3 %
• Durotomy 0.8 – 7.2 %
• Nerve Root Lesions 0.2 %
• Infection 2 – 3 %
• Recurrent Herniations 5 – 15 %
• Epidural Fibrosis
– Difficult to distinguish from recurrent herniation
– Contrast MRI investigation of choice
– No correlation between extent and symptoms
– No intervention or material shown to alter incidence
• Epidural Haematoma
• Cauda Equina Syndrome
• Iatrogenic Instability
Results of Surgery
• 85 – 95 % good to excellent short term results

• Long Term good to excellent results diminish to

55 – 70 %
– 10 – 18 % having required additional surgery
– Lower back pain usually the cause of dissatisfaction
• No difference between surgery or conservative

• Microdiscectomy
– Shorter hospital stay
– Faster return to sedentary work
– No difference c/w open discectomy after 8 –12 weeks

• No statistically significant difference in recovery

of established motor deficits with or without
surgery
LAMINECTOMY
“Discectomy”

• Mikrodiskektomi
• Laminotomi
• Laminektomi
CANAL STENOSIS
`
Nonoperative Treatment

• Short-term rest, NSAID, analgesics,

antispamodic medication, exercise
• Physical therapy
• Oral corticosteroid

** Conservative treatment should continue

for
6weeks, before other measure are
attempted
Exercise
• stretching and strengthening exercise
• debate on mechanism of pain relief
• protective effect of strong abdominal
muscle
 load share, partially shield the disc
from
excessive load

Physical therapy
• heat, cold, massage, ultrasonography
• helpful but scientifically not proven
Epidural steroid injection
• If leg pain persist beyond 4 weeks
• Maximum 3 injection per year

• Response vary greatly

- Hagen,2002 : short-term effect 40%. no
significant
long-term effect
- Wiesel, 1995 : 82% relief for 1 day, 50% for 2
weeks,
16% for 2mo.
- White 1983 : 77% avoid surgery after injection
- Carette, 2002 : neither significant functional
benefit nor reduction in
need for