Pathophysiology

Back Pain

Daryo Soemitro
Department of Neurosurgery
Medical Faculty – University of Indonesia
 Definition

 Pain is "an unpleasant sensory and emotional

experience associated with actual or potential
tissue damage, or described in terms of such
damage" (Merskey, 1986)

 Low back pain problems are usually linked to two

areas :
1. Lifestyle, which includes stress, lack of exercise
and poor posture, and
2. Physical injury or disease.
 Definition

 Low back pain is pain, muscle tension, or stiffness

localized below the costal margin and above the
inferior gluteal folds, with or without leg pain
(sciatica).

 The term refers to pain in the lumbosacral area of

the spine encompassing the distance from the 1st
lumbar vertebra to the 1st sacral vertebra.

This is the area of the spine where the lordotic curve

forms. The most frequent site of low back pain is in the
4th and 5th lumbar segment .
 Terminology

 Localized.
In localized pain the patient will feel soreness or
discomfort when the doctor palpates, or presses on, a
specific surface area of the lower back.
 Diffuse.
Diffuse pain is spread over a larger area and comes
from deep tissue layers.
 Radicular.
The pain is caused by irritation of a nerve root. Sciatica
is an example of radicular pain.
 Referred.
The pain is perceived in the lower back but is caused
by inflammation elsewhere-- often in the kidneys or
lower abdomen.
 Terminology

 Acute pain (nociceptive) and chronic pain (neuropathic)

differ in their etiology, neuro–physiological processes,
diagnosis and therefore tend to respond to different
treatment modalities.
 Neuropathic should not be confused with neurogenic, a
term used to describe pain resulting from injury to a
peripheral nerve but without necessarily implying any
"neuropathy".
 Compression may directly stretch nociceptors in dura
or nerve root sleeve tissues, but ischemia from
compression of vascular structures, inflammation, and
secondary edema are also likely to play a role in some
cases
 Acute Pain & Pathophysiology

 Self–limiting and serves a protective biological

function by acting as a warning of on–going tissue
damage.
 NOCICEPTIVE in nature,
 occurs secondary to chemical, mechanical and
thermal stimulation of A–delta and C–polymodal
pain receptors, which are located in skin, bone,
connective tissue, muscle and viscera.
 useful role at localizing noxious chemical,
thermal and mechanical stimuli.
 can be somatic or visceral in nature
 usually responds to opioids and non–steroidal
anti–inflammatories (NSAIDS).
 Afferent nociceptor terminal

 The C-polymodal nociceptor terminals are sensitive

to direct heat, mechanical distortion, or chemicals
released from damaged cells.
 Chemicals released by tissue damage : potassium,
histamin, acetylcholine, serotonin, adenosine
triphosphate, bradykinin
Afferent nociceptor terminal

 Direct activation by intense

pressure and consequent cell
damage
 Cell damage leads to release of
potassium and to synthesis of
prostaglandin (PG) and
bradykinin (BK).
 Prostaglandin increase the
sensitivity of the terminal to BK
and other pain-producing
substance
Afferent nociceptor terminal

 Secondary activation. Impulses

propagated not only to the
spinal cord but into other
terminal branches, where they
induce the release of
substance P (SP).
 SP causes vasodilatation and
neurogenic edema with further
accumulation of bradykinin
 SP also causes the release of
histamin (H) from mast cells
and serotonin (5HT) from
platelets
 Afferent nociceptor terminal

 Histamin and serotonin levels rise in the

extracellular space, secondary sensitizing nearby
nociceptors
 This leads to a gradual spread oh hyperalgesia and /
or tenderness
Pain-sensing Structures
Pain-sensing Structures
 Chronic Pain & Pathophysiology

 The mechanisms involved in neuropathic pain are

complex and involve both peripheral and central
pathophysiologic phenomenon.
 Chronic, non–malignant pain is predominately
NEUROPATHIC in nature and involves damage
either to the peripheral or central nervous systems.
 The underlying dysfunction may involve
 deafferentation within the peripheral nervous
system (eg. neuropathy)
 deafferentation within the central nervous system
(eg. post–thalamic stroke) or
 an imbalance between the two (eg. phantom limb
pain).
 Chronic Pain & Pathophysiology

 serves no protective biological function, rather than

being the symptom of a disease process, chronic
pain is itself a disease process.
 unrelenting and not self–limiting, can persist for
years and even decades after the initial injury.
 can be refractory to multiple treatment modalities. If
chronic pain is inadequately treated, associated
symptoms can include chronic anxiety, fear,
depression, sleeplessness and impairment of social
interaction.
Nerve Vascularisation

1. Fascicular Pia-
Arachnoid
2. Intra- and Interfasicular
Arterial Coils
3. Major Radicular
Longitudinal artery
4. Radicular Vein
5. Arterio-Venous
Anastemoses
6. Collateral Radicular
Arteries
7. Radicular Pia-Arachnoid
Nerve Compression

• Compressed spinal nerves

are symptomatic when their
nutrient supply is cut off
and their venous return is
impaired.
• Anatomist Wesley Parke
has shown that impairment
of venous return is the
primary reason that
compressed nerves
become pain generators.
 Pain Pathophysiology

 Peripheral Nerve Sensitivity

 Dorsal Horn Transmission
 Supraspinal Modulating Loops
 the dorsolateral pontine tegmentum
 the rostral ventral medulla
 the dorsal medulla
 the caudal medulla
 the lateral hypothalamus
 Other Descending Pain Modulating Pathways
 Spinocerebral Ascending Pathways
 "Cortical Pain Centre"?
Pain Pathophysiology
Pain Pathophysiology
 Causes Of Low Back Pain

 Mechanical causes
 98% of low back pain. Sitting produces the
highest load on the spine, typically worsens the
pain.
 sprained / strained ligaments, tendons, and
muscles
 Rheumatologic
 Neoplastic Disease
 Infections : acute or chronic
 Vascular or Hematologic
 Endocrine / Metabolic
 Referred pain
 Other non-mechanical causes
 Psychological factors
 Facet Joint Syndrome

A B
A is computerized picture of the lumbar spine showing 
where the facet joints are located. B is radiographic 
anatomy of a facet joint

Pain from facet joints is not constant and 
only occurs several times a year
 Lumbar Stenosis

 Etiology : congenital or acquired.

 In most cases, may be attributed to acquired
degenerative or arthritic changes of the
intervertebral discs, ligaments and facet joints
surrounding the lumbar canal.
 Cartilaginous hypertrophy of the articulations
 Intervertebral disc herniations or bulges
 Hypertrophy of the ligamentum flavum
 Osteophyte formation.
 Compression of the microvasculature of the lumbar
nerve roots, resulting in ischemia, is believed to be a
major contributing factor in the development of
neurogenic claudication
 Lumbar Stenosis

Osteophyte formation result from subperiostel bone

formation, which result from elevation of periosteum by
disc bulging (A). A spondylotic ridge then develops (B
and C)
Lumbar Stenosis
Lumbar Stenosis
Lumbar Stenosis
 Adhesive Arachnoiditis

 This entity, represents an advanced form of

inflammation where prominent fibrosis (scarring)
involving nerve structures has occurred.
 It is important to clarify this neuropathologic entity
because it can lead to a lifetime of suffering due to
intractable pain, neurologic deficit, and even death.
 In the 20th century the most common cause of
clinically significant adhesive arachnoiditis has
been ill-advised myelography with oil based agents
such as Pantopaque and Myodil.
 In the 21st century ill-advised epidural steroid
injections have now become the primary etiology of
new cases.
Anatomy of Arachnoid
 Progression of
Adhesive Arachnoiditis
 Progression of
Adhesive Arachnoiditis

First Stage :
Nerve Roots markedly
swollen

Second Stage :
Nerve Roots Atrophy
with Scar Proliferation

Final Stage :
Empty Cavity
Nerve Totally Enveloped
in Dense Scar
 Cause of Adhesive Arachnoiditis

Chemically induced AA
This arises when chemicals are introduced into or around the
subarachnoid space.

 Myelogram
 Epidural / intrathecal steroid injection
 Epidural anaesthetics
 Chymopapain
 Intraspinal chemotherapy agents
 Chemical meningitis
 Cause of Adhesive Arachnoiditis

Mechanically-induced AA
 Spinal surgery : especially multiple surgeries.
 Trauma
 Multiple lumbar punctures
 Spinal stenosis (when chronic)
 Anatomical abnormalities : especially degenerative
conditions : e.g osteophytes (bony protuberances)
 Chronic disc prolapse : including leaked disc
material, which is known to be highly irritant to
nerves.
 Blood

Infection :
 Meningitis
 Tuberculosis
 THANK YOU
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