SPINE DISIORDERS

DEPARTEMEN NEUROLOGI
FAKULTAS KEDOKTERAN UNIVERSITAS
SUMATERA UTARA
Normal Radiographic Anatomy
The Basics

 Five basic densities

• Metal – bright white
• Bone – White
• Water/Soft Tissue – Shades of Lighter Gray
• Fat – Darker Gray
• Air – Black
 Radiolucent = black
 Radiopaque = white
C1 Posterior Arch and ANATOMY C1 Anterior Tubercle
Tubercle
Odontoid Process

C2

Vertebral Bodies
C3
Spinous Processes

C4

C5
Intervertebral Discs
C6

C7

Neutral
Articular Processes
Lateral
Cervical
 C1 Posterior Arch
and Tubercle
C1 Anterior Tubercle

Intervertebral
Foramina

C3

C4
Articular Processes
C5

T1 Transverse
Process C6

C7

T1
Pedicles

1st Ribs
Oblique
Cervical
 T1

Posterior Ribs Pedicles

T6

Transverse
Intervertebral Discs Processes

T12
AP Thoracic
 Superior Articular
Processes

Pedicles

T6
Vertebral Bodies
Intervertebral
Foramina
Intervertebral Discs

Spinous Processes

T12

Lateral
Thoracic
 Superior Articular
Processes

Inferior Articular
Processes

Pedicles

Spinous Processes
Transverse
Processes

Sacroiliac Joints
Median Sacral Crest AP Lumbar
 Pedicles Superior Articular
Processes

Vertebral Bodies

Spinous Processes

Intervertebral
Discs

Inferior Articular
L5 Processes

Intervertebral
Foramina Sacral Canal
Lateral
Sacrum Lumbar
 Transverse
Processes
Inferior Articular
Processes

Superior Articular
Processes

Pedicles Partes
Interarticulares

“Scotty Dog”
Appearance

Sacroiliac Joint

Oblique
Lumbar
 Inferior Articular Spinous Processes
Superior Articular Processes
Processes

L5 Transverse
L5 Processes

Ventral Sacral Sacroiliac Joints

Foramina

Median Sacral Crest

Coccyx

Pubic Symphysis
AP Pelvis
SPINE DISORDERS
Tuberculosis Spondylitis
(TB spine/Pott’s diseasis)

 Tuberculous spondylitis has been documented in ancient

mummies from Egypt and Peru
 It is one of the oldest demonstrated diseases of humankind.
 Percival Pott presented the classic description of TB spine in
1779.
 TB spine causes serious morbidity, including
permanent neurologic deficits and severe
deformity.
 Medical treatment or combined medical and
surgical strategies can control the disease in
most patients
 Epidemiology

 TB spine is common in developing countries>

developed countries
 Internationally approx. 1-2% of total TB cases
are attributable to Pott disease.
 As with other forms of TB, the frequency is
related to socioeconomic factors and historical
exposure to the infection.
 Sex: Males are more often affected
(1.5-2:1).
 Age: In developed countries Pott dx
primarily occurs in adults.
 In countries with higher rates of
infection, it mainly occurs in
children
 Mortality/Morbidity : Pott disease is the
most dangerous form of musculoskeletal TB.
 It can cause bone destruction, deformity, and
paraplegia
 It commonly involves the thoracic and
lumbosacral spine.
 Pathophysiology

 Pott disease is usually secondary to an

extraspinal source of infection.
 The basic lesion is a combination of
osteomyelitis and arthritis.
 Typically, more than one vertebra is involved.
 The area usually affected is the anterior aspect of
the vertebral body adjacent to the subchondral
plate
 Tuberculosis may spread from that area to
adjacent intervertebral disks.
 In adults, disk disease is secondary to the spread
of infection from the vertebral body.
 Inchildren, because the disk is vascularized, it
can be a primary site.
 Progressive bone destruction leads to vertebral
collapse and kyphosis.
 The spinal canal can be narrowed by abscesses,
granulation tissue, or direct dural invasion
 This leads to spinal cord compression and
neurologic deficits.
 Kyphotic deformity occurs as a consequence of
collapse in the anterior spine.
 Lesions in the thoracic spine have a greater
tendency for kyphosis than those in the lumbar
spine.
A cold abscess can occur if the infection extends
to adjacent ligaments and soft tissues.
 Abscesses in the lumbar region may descend
down the sheath of the psoas to the femoral
trigone region and eventually erode into the skin.
Clinical presentation
 Presentation depends on the following:
• Stage of disease
• Site
• Presence of complications such as neurologic deficits,
abscesses, or sinus tracts.

 The reported average duration of symptoms at the

time of diagnosis is 3-4 months.
 The average duration of symptoms at the time of
diagnosis is 3-4 months
 Back pain is the earliest and most common
symptom.
• Patients have usually had back pain for weeks prior to
presentation.
• Pain can be spinal or radicular.
 Constitutional symptoms include fever and
weight loss.
 Neurologic abnormalities occur in 50% of cases
and can include spinal cord compression with
paraplegia, paresis, impaired sensation, nerve
root pain, or cauda equina syndrome.
 Cervicalspine tuberculosis is a less common
presentation but is potentially more serious
because severe neurologic complications are
more likely.
• This condition is characterized by pain and stiffness.
• Patients with lower cervical spine disease can present with
dysphagia or stridor.
• Symptoms can also include torticollis, hoarseness, and
neurologic deficits.
 The clinical presentation of TB in HIV
patients is similar to that of HIV negative
patients; however, the relative proportion of
individuals who are HIV positive seems to be
higher.
 Physicalexamination should include the
following:
• Careful assessment of spinal alignment
• Inspection of skin, with attention to detection of sinuses
• Abdominal evaluation for subcutaneous flank mass
• Meticulous neurologic examination
 The thoracic spine is frequently reported as the
most common site of involvement followed by
lumber spine
 The remaining cases correspond to the cervical
spine.
 Spine deformity (KYPHOSIS) of some degree
occurs in almost every patient.
 There may be large cold abscesses of paraspinal
tissues or psoas muscle that protrude under the
inguinal ligament.
 They may erode into the perineum or gluteal
area.
 Neurologic deficits may occur early in the
course of disease.
 Signs depend on the level of spinal cord or
nerve root compression
 Workup

1 Lab studies
 Tuberculin skin test demonstrates a positive
finding in 84-95% of patients who are non–HIV-
positive.
 ESR may be markedly elevated (>100 mm/h).
 Microbiology studies to confirm diagnosis:
Obtain bone tissue or abscess samples to stain for
acid-fast bacilli (AFB), and isolate organisms for
culture and susceptibility.
 These study findings may be positive in only
about 50% of the cases.
Imaging studies
 PLAIN RADIOGRAPHY demonstrates the
following characteristic changes of spinal
tuberculosis:
• LYTIC DESTRUCTION of anterior portion of vertebral
body
• Increased anterior wedging
 • COLLAPSE OF VERTEBRAL BODY
• Reactive sclerosis on a progressive lytic process
• Enlarged psoas shadow with or without calcification
 Additional findings
• Vertebral end plates are osteoporotic.
• Intervertebral disks may be shrunk or destroyed.
 CT scanning
• CT scanning provides much better bony detail of irregular
lytic lesions, sclerosis, disk collapse, and disruption of
bone circumference.
• Low-contrast resolution provides a better soft tissue
assessment, particularly in epidural and paraspinal areas.
 MRI
• MRI is the criterion standard for evaluating disk space
infection and osteomyelitis of the spine and is most
effective for demonstrating the extension of disease into
soft tissues and the spread of tuberculous debris under the
anterior and posterior longitudinal ligaments
Histologic Findings:
 Since microbiologic studies may be nondiagnostic,
anatomic pathology can be very significant.
 Gross pathologic findings include exudative granulation
tissue with interspersed abscesses.
 Coalescence of abscesses results in areas of caseating
necrosis.
Treatment

MEDICAL TREATMENT
 Medical therapy requires combination regimens
with at least 3 antituberculous drugs.
 A 3-drug regimen usually includes INH,
rifampin, and pyrazinamide.
 The duration of treatment ranges from 9-12
months
Surgical treatment
 Indications
• Neurologic deficit (acute neurologic deterioration,
paraparesis, paraplegia)
• Spinal deformity with instability
• No response to medical therapy
 In disease involving the cervical spine, the
following factors justify early surgical
intervention:
• High incidence and severity of neurologic deficits
• Severe abscess compression that may induce dysphagia or
asphyxia
• Instability of the cervical spine
 Contraindications
• Vertebral collapse of a lesser magnitude is not considered
an indication for surgery because with appropriate
treatment and therapy compliance, it is less likely to
progress to severe deformity.
• Vertebral damage is considered significant if more than
50% of the vertebral body is collapsed or destroyed or if
there is spinal deformity of more than 5°.
Lumbar Disc Herniation and
Radiculopathy
 BACK PAIN: THE STATISTICS
 Eight out of ten adults will experience low back pain sometime during their lifetime

 After the common cold problems related to the low back are the most frequent
cause of lost workdays in individuals over 45 years of age

 Back pain ranks second to headaches as the most frequent location for pain

 Greater than 65 million Americans experience back pain every year

 Back injuries are one of the most common causes for disability

 The annual costs associated with back pain runs into the tens of billions of dollars
considering lost productivity, medical expenses and worker’s compensation benefits
 CAUSES OF BACK PAIN
Includes but is not limited to

 Facet Syndrome  Fracture

 Segmental Dysfunction
 Disc Herniation
 Tumor
 Cyst
 Radiculopathy
 Scar Tissue (Fibrosis)
 Infection
 Primary Cancer
 Metastatic Cancer
 Spinal Stenosis
 Surgical Instrumentation
 Transitional Segment
 COMMON SPINE CONDITIONS
 Facet Syndrome
 Segmental Dysfunction
 DISC HERNIATION
 SPONDYLOSIS
 DEGENERATIVE DISC DISEASE
 RADICULOPATHY
 Scoliosis
 Myelopathy
 Spondylolithesis
 Spinal Stenosis
 Muscular Deconditioning
 Disc Bulge
 Transitional Segment
Lumbar Spine Motion Segment
 Three joint complex
 Intervertebral disc + 2 facet joint
 Ligamentous structure, vertebral body
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
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.
Spondylosis
 Generalized process of the axial skeleton
 Sequence of degenerative change
 Start biochemical and cellular level
 Manifest biomechanical and morphologic level
Initiating Factor in Degenerative Cascade

 Injury to annulus fibrosus

 Matrix composition alteration of the nucleus pulposus
 Vascularity and permeability change of end-plate

 Primary causitive agent??

 The process of disc degeneration is multifactoral
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
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
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
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
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
Quality of pain and associated symptom

 dullache or sharp, stabbing pain?

 eletricity, tingling, numbness, shooting down the leg?
 any associated weakness?
 dose anything make the pain better or worse?
 forward flexion or hyperextension exacerbate or relieve pain?
 standing more comfortable than sitting?

** Back pain abated when leg pain developed

 relief of annular tensile stress, nerve root irritation
** Isolated leg pain  acute disc extrusion
Differential Diagnosis
 Vascular claudication
 Vascular assessment and flow study
 Dorsalis pedis palpation
 Spinal stenosis
 leg pain, dysesthesia, paresthesia, often not dermatomal
 pain d/t mechanical compression of spinal canal and foramen
 lordosis and axial loading
 symptomatic on walking, relief by sitting
 Thrombophlebitis
 Metabolic and peripheral neuropathy
Physical Examination
Inspection
 Old scar, muscle spasm, cutaneous stigma, spinal alignment,
loss of lordosis
Palpation
 Midline, sciatic notch, iliac crest, SI joint, coccyx
 Paraspinal tenderness, rigidity
 Costovertebral angle, abdomen
 Kidney, stone, retroperitoneal abnormality

Hip pathology
 Patrick test

Skin
 Temperature and atrophic change
Neurologic Examination
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
Nonoperative Treatment

 90% of patient improve with conservative treatment

 Short-term rest, NSAID, analgesics,

antispamodic medication, exercise

 Physical therapy
 Oral corticosteroid

** Conservative treatment should continue for

6 weeks, 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
surgery
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