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 PiaArachnoid 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
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Compressed spinal nerves are symptomatic when their nutrient supply is cut off and their venous return is impaired.
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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
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