Pain: Definition, Gate theory and its pathways
- 1. PAIN Dr. Samidha M. Patil (PT) Assistant professor MPT (MSK) (MUHS)
- 2. OBJECTIVES • Pain Pathway • Pain gate theory • Descending pain suppressing system • Physiological block
- 4. INTRODUCTION • Definition: - Sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage. - BIOPSYCHOSOCIAL - Pain: response to stimulation of peripheral nociceptive structures
- 5. • FAST PAIN: - Shrap, pricking, acute, electric • SLOW PAIN: - Burning, aching, throbbing, nauseous, chronic
- 6. Pain receptors: free, non-corpuscular peripheral nerve endings consisting of a series of spindle-shaped, thick segments linked by thin segments to produce "string-of-beads" appearance. Pain receptors are sensitive to: Mechanical, thermal and chemical stimulus Nociceptors are present in almost all types of tissue (Except in nucleus pulposus and the inner part of the annulus fibrosus) Nociceptors —---> convert the initial stimulus into electrical activity —--> in the form of action potentials (TRANSDUCTION)
- 7. Nociceptors —-----> release neuropeptides from peripheral terminals —---> which are substance P and a no. of breakdown products of arachidonic acid such as prostaglandins and leukotriene
- 8. Peripheral Nerve Pathway • Nociceptors give rise to two types of first-order afferent nerve fibers: - C fibers and A-delta fibers.
- 9. C fibers (group IV afferents): - - small, unmyelinated nerve fibers that transmit action potential slowly. (1.0 to 4.0 meters/second). - Respond to noxious levels of mechanical, thermal, and chemical stimulation - The pain sensations are slow onset, long lasting, emotionally difficult, and diffusely localized. - accompanied by autonomic responses such as sweating, increased heart rate and blood pressure, or nausea.
- 10. A-delta fibers (group III afferents) - Small-diameter fibers - Transmit rapidly than C fibers, at a rate of about 30 meters/second, because they are myelinated. - Most sensitive to high-intensity mechanical stimulation, also respond to heat or cold and are capable of transmitting non-noxious information. - The pain is quick onset after the painful stimulus, lasts only for a short time, is generally localized to the area.
- 12. CENTRAL PATHWAY C and A-delta afferents project —----> gray matter of the spinal cord —------> these fibers synapse, with second-order neurons (transmission or T cell) in the superficial dorsal horn of the gray matter (the substantia gelatinosa). - T cells make local connections within the spinal cord. - Continued or repetitive C-fiber activation can sensitize the T cells, causing them to fire more rapidly —----> increasing their receptor field size, and input from other interneurons originating in the substantia gelatinosa of the spinal cord or from descending fibers originating in higher brain centers can inhibit T-cell activity.
- 13. Continued or repetitive C-fiber activation can sensitize the T cells, causing them to fire more rapidly —----> increasing their receptor field size, and input from other interneurons originating in the substantia gelatinosa of the spinal cord or from descending fibers originating in higher brain centers can inhibit T-cell activity.
- 15. - These inhibitory interneurons release various neurotransmitters, including norepinephrine, serotonin, and enkephalins, to modulate the flow of the afferent pain pathways. - The inhibition of pain by inputs from non-nociceptive afferents is known as pain gating. T Cells Excitation Inhibition C fibers and A-delta nociceptor afferents From large-diameter non- nociceptive sensory afferents and From descending fibers from higher brain centers.
- 16. Transmission cell activation —--> increase muscle spasm —--> via a spinal cord reflex in which the transmission cell synapses with anterior horn cells to cause muscle contractions. - The ongoing muscle contractions —---> accumulation of fluid and tissue irritants. The contracting muscles cause nociceptive impulses by mechanically compressing the nociceptors.
- 17. - Neospinothalamic Tract for Fast Pain (LATERAL SPINOTHALAMIC TRACT). - The fast type Aδ pain fibers transmit mainly mechanical and acute thermal pain. - They terminate mainly in lamina I (lamina marginalis) of the dorsal horns excite second- order neurons of the neospinothalamic tract. - These give rise to long fibers that cross immediately to the opposite side of the cord through the anterior commissure and then turn upward, passing to the brain in the anterolateral columns.
- 18. Termination of the Neospinothalamic Tract in the Brain Stem and Thalamus - Terminate in the reticular areas of the brain stem, (some in the ventrobasal complex along with the dorsal column– medial lemniscal tract for tactile sensations). - Few fibers also terminate in the posterior nuclear group of the thalamus.
- 19. Glutamate: Neurotransmitter of the Type Aδ Fast Pain Fibers.
- 20. Paleospinothalamic Pathway for Transmitting Slow-Chronic Pain. -Transmits pain from the peripheral slow-chronic type C pain fibers. - In this pathway, the peripheral fibers terminate in the spinal cord in laminae II and III of the dorsal horns, which together are called the substantia gelatinosa, - Most of the signals then pass through one or more additional short fiber neurons within the dorsal horns lamina V (dorsal horn) give rise to long axons that mostly join the fibers from the fast pain pathway passing first through the anterior commissure to the opposite side of the cord, then upward to the brain in the anterolateral pathway.
- 22. Sympathetic Nervous System Influences- - component of the autonomic nervous system. - The ANS: sympathetic and parasympathetic systems. (activities of smooth and cardiac muscles and with glandular secretion.) - The sympathetic nervous system: "fight or flight," response such as increasing heart rate etc - sympathetic nervous system: activated by acute pain or injury but does not cause pain. - However abnormal sympathetic activation, can increase pain severity and cause exaggerated signs and symptoms such as excessive vasomotor or sweating reactions.
- 23. Gate Control Theory: - According to this theory, severity of the pain sensation is determined by the balance of excitatory and inhibitory inputs to the T cells in the spinal cord. C and A delta fibers Excitatory inputs T cells Inhibitory input Substantia gelatinosa and Large diameter a delta (non-nociceptive sensory afferents) Closes gate for pain sensation to cerebral cortex
- 25. Many physical agents and intervention help in managing pain by activating non nociceptive sensory nerves, thereby inhibiting activation of pain transmission cells and closing the gate to the transmission of pain
- 26. PAIN MODULATION •THE ENDOGENOUS OPIOID SYSTEM •PAIN GATE THEORY
- 27. Pharmacological Approach s control pain by modifying inflammatory mediators at the perihery, altering pain transmission from the periphery to the cortex, or altering the central perception of pain
- 28. REFERENCE • Essentials of medical physiology by sembulingam • Guyton and hall textbook of medical physiology • A. K. Jain, medical Physiology • Physical agents in rehabilitation, Cameron • Wall and Melzacks textbook of pain
- 29. THANK YOU