PathophysiologyBack Pain

Daryo SoemitroDepartment 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.

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

Terminology

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 SyndromeFacet Joint Syndrome

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

anatomy of a facet jointanatomy of a facet joint

A B

Pain from facet joints is not constant and Pain from facet joints is not constant and only occurs several times a yearonly 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 ofAdhesive Arachnoiditis

Progression ofAdhesive Arachnoiditis

First Stage :Nerve Roots markedlyswollen

Second Stage :Nerve Roots Atrophywith Scar Proliferation

Final Stage :Empty CavityNerve Totally Envelopedin 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

This image honors a Burmese (Padaung Tribe) beauty.

THANK YOU