Pain Sensation Physiology PDF

Pain sensation - The chemicals that excite the chemical type of pain are bradykinin, serotonin, histamine, potassium ions, acids, Pain is a protective mechanism...

Pain sensation - The chemicals that excite the chemical type of pain are bradykinin, serotonin, histamine, potassium ions, acids, Pain is a protective mechanism acetylcholine, and proteolytic enzymes - Pain occurs whenever tissues are being damaged - It causes the individual to react to remove the pain stimulus - Bradykinin: Fast pain Slow pain ➔ Seems to be more painful than others Felt Within about 0.1 second 1 second or more and then ↑ ➔ Agent most responsible for causing pain by tissue damage after pain stimulus slowly over seconds or minutes ➔ The greater the rate of metabolism of the tissue, the more Speed 6-30 m/sec 0.5-2 m/sec Stimuli Mechanical, & thermal Mechanical, thermal, & chemical rapidly the pain appears Terms Sharp, pricking, acute, Burning, aching, throbbing, and electric pain nauseous, and chronic pain - Ischemia (blood flow to a tissue is blocked) Site Felt on the skin but not Felt on the skin and in almost ➔ The tissue often becomes very painful within minutes on deep tissue or organs any deep tissue or organ ➔ Due to accumulation of large amounts of lactic acid Tract Neospinothalamic tract Paleospinothalamic ➔ Other agents: bradykinin and proteolytic enzymes Fibers Fast type Aδ pain fibers Slow type C pain fibers NT Glutamate Substance P - Prostaglandins and substance P: ➔ Enhance the sensitivity of pain endings Classification of pain ➔ Do not directly excite them - Superficial pain (cutaneous pain): ➔ Arises from superficial structures: skin & SC tissues Non-adapting nature of pain receptors ➔ It is a sharp, bright pain with a burning quality - Pain receptors adapt very little and sometimes not at all ➔ May be abrupt or slow in onset - To allow the pain to keep the person apprised of a tissue- - Deep somatic pain: damaging stimulus as long as it persists ➔ Originates in deep body structures such as periosteum, muscles, tendons, joints & blood vessels Rate of tissue damage as a stimulus for pain ➔ Dull aching and poor localization - Person begins to perceive pain when skin is heated > 45 °C ➔ Usually accompanied by prolonged contraction of skeletal - This is the temp. at which the tissues begin to be damaged muscles → induces ischemia and aggravates pain - The pain (resulting from heat, bacterial infection, tissue Pain receptors (nociceptors) ischemia and tissue contusion) is closely correlated with the - In the skin and other tissues are all free nerve endings rate at which damage to the tissues is occurring and not with - Pain is elicited by: mechanical, thermal, & chemical stimuli the total damage that has already occurred - Fast pain is elicited by mechanical and thermal types of stimuli - Slow pain can be elicited by all three types of stimuli  - In spinal cord, the pain signals take two pathways to the brain: ➔ The neospinothalamic tract: ▪ For fast pain by fast type Aδ pain fibers ▪ Transmits mechanical and acute thermal pain ▪ On entering cord, fibers may travel up or down 1-3 segments and terminate on neurons in dorsal horn ▪ Glutamate: excitatory NT of Aδ fiber nerve ending ▪ 2nd neuron crosses to the opposite side and passes to the brain in the anterolateral columns: ✓ Some neurons terminate in reticular substance ✓ Most fibers → thalamus ventrobasal complex ▪ Composed of nociceptive fibers from laminae I & II ▪ 3rd order neurons go to the cortex ➔ The paleospinothalamic tract: ▪ For slow-chronic pain by type C pain fibers ▪ 2nd neuron crosses immediately to opposite side Dual pathways for transmission of pain signals to the CNS and passes to the brain in anterolateral columns ▪ Composed of axons of wide dynamic range (WDR) - Free nerve endings use two separate pathways: neurons from laminae IIa and V with only small number of nociceptive specific (NS) neurons ➔ Fast-sharp pain pathway: ▪ Substance P: excitatory NT of C fiber nerve ending ▪ Elicited by mechanical or thermal pain stimuli ▪ Only 10 to 25 % of fibers terminate in thalamus ▪ Transmitted to the spinal cord by small Aδ fibers ▪ Most terminate diffusely in reticular nuclei of ▪ Velocities between 6 and 30 m/sec medulla, pons and mesencephalon; tectal area of mesencephalon; periaqueductal gray region ➔ Slow-chronic pain pathway: ▪ Elicited mostly by chemical types of pain stimuli Possible NTs or neuropeptides that can be released at SC: ▪ May be by persisting mechanical/thermal stimuli - Glutamate: ▪ Transmitted to the spinal cord by type C fibers ➔ Excitatory neurotransmitter that activates NMDA receptors ▪ Velocities between 0.5 and 2 m/sec ➔ Decreases activation threshold and extends depolarization ➔ Activation of the dorsal horn neurons  - Glycine and gamma-amino-butyric-acid (GABA): Allodynia vs Hyperalgesia ➔ Inhibitory neurotransmitters ➔ Glycine can bind onto NMDA - Allodynia: ➔ GABA has its own specific receptor ➔ Pain due to a stimulus that does not normally provoke pain ➔ An example would be a light feather touch - Substance P: ➔ It is an excitatory neuropeptide in C-fibers in the periphery - Hyperalgesia: ➔ Response to tissue injury: vasodilation, inflammation, pain ➔ Exaggerated response from a usually painful stimulus ➔ Thought to mediate lower back pain, arthritis, fibromyalgia ➔ Ex: intense pain when touching a recently burned area ➔ Over-the-counter creams containing capsaicin: ➔ Primary hyperalgesia: ▪ Made from chili peppers & used to relieve pain ▪ Occurs at the site of injury ▪ Deplete substance P from local nerve endings ▪ Hyperalgesia to mechanical and heat stimuli ▪ Ex: a person has surgery on elbow, and the pain - Endorphins and serotonin: starts to worsen over time instead of improving ➔ Released in the descending pathway ➔ Secondary hyperalgesia: ➔ Also help with gate control and the modulation of pain ▪ Occurs outside the injury ▪ Characterized by mechanical hyperalgesia only There are two types of second order neurons: ▪ When the pain spreads to non-injured tissue - Wide dynamic range (WDR) neurons: Neuropathic pain ➔ Synapse to Aβ, Aδ, and C fibers - By damage or disease affecting the somatosensory system ➔ Activated by noxious and non-noxious stimuli - May be associated with: - Nociceptive specific (NS) range neurons: ➔ Abnormal sensations called dysesthesia ➔ Only synapse to Aδ and C fibers ➔ Allodynia ➔ Activated by noxious stimuli - Peripheral nerves: The appreciation of pain ➔ Traumatic brachial plexus injury - Removal of somatic sensory areas of cortex: ➔ Diabetes mellitus ➔ Does not destroy the ability to perceive pain ➔ Carpel tunnel syndrome ➔ Pain impulses to lower areas: conscious perception of pain ➔ Herpes zoster infection ➔ Cortex is important for determining the quality of pain - Central nervous system: - Stimulation of reticular areas of brain stem and intralaminar ➔ Central post stroke pain nuclei of thalamus causes widespread arousal of the NS ➔ Spinal cord injury Visceral pain ➔ Non-noxious large diameter Aβ fibers → inhibitory - Pain from the different viscera of the abdomen and chest is response → gate is closed → no pain signals sent to brain one of the few criteria that can be used for diagnosing visceral ➔ The activation of the large diameter Aβ fibers can reduce inflammation, infectious disease, and other visceral ailments and inhibit the transmission of the Aδ and C fibers - The viscera have sensory receptors for no other modalities of sensation besides pain - Visceral pain differs from surface pain in several aspects: ➔ Highly localized types of damage to the viscera seldom cause severe pain: a surgeon can cut the gut entirely in two in a patient who is awake without causing pain ➔ Any stimulus that causes diffuse stimulation of pain nerve endings throughout a viscus causes pain (can be severe): ▪ Ischemia - As the stimulus passes through brain stem: ▪ Chemical stimuli ➔ It may cause an interaction between periaqueductal grey ▪ Spasm of hollow viscus matter (PAG) and the raphe nucleus in the mid brain ▪ Overdistension of hollow viscus ➔ They form part of the descending pain suppression system ➔ Their neurons lead to the excitation of substantia Referred pain gelatinosa cells → inhibition of the pain transmission - Feeling pain in a part of the body that is fairly remote from the tissue causing the pain - The endogenous opioids: - Mechanism: branches of visceral pain fibers synapse in the ➔ Endogenous opioids and their corresponding receptors: spinal cord on the same second-order neurons that receive ▪ Enkephalins: δ receptors pain signals from the skin → the person has the feeling that ▪ Endorphins: μ-receptors the sensations originate in the skin ▪ Dianorphins: κ -receptors ➔ Involved in pain modulation: Pain modulation (Gate-control theory) ▪ At periaqueductal grey (PAG) and the raphe nucleus - First described by P.D. Wall & Melzack (1965) ▪ Produce analgesia related only to prolonged pain - There is an interaction between pain and touch fiber input - The interneurons in substantia gelatinosa forms the pain gate ➔ The inhibitory effects of higher centers influence the pain ➔ If the gate is open: pain signals can pass to the brain transmission mediated through C fibers ➔ If the gate is closed: pain signals will be restricted ➔ Note: systemically administered opioids at analgesic doses - If the interneurons in substantia gelatinosa are stimulated by: activate spinal and supraspinal mechanisms via μ, δ, ➔ Smaller diameter A-δ or C fibers, excitatory response is and κ type opioid receptors and modulate pain signals produced → gate is open → pain signals are sent to brain