PAIN PERCEPTION, TRANSMISSION AND SUPPRESSION, THERMOREGULATION by prof charles.pptx

Health physiology

1. DEPARTMENT OF PHYSIOLOGY TOPIC; Pain perception, transmission, suppression and thermoregulation By Dr prof Charles 2024

2. “ Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage ” International Association for the Study of Pain

3. Why feel pain? Gives conscious awareness of tissue damage Protection: Remove body from danger Promote healing by preventing further damage Avoid noxious stimuli Elicits behavioural and emotional responses

4. free nerve endings in skin respond to noxious stimuli 1. Nociceptors

5. Nociceptors Nociceptors are special receptors that respond only to noxious stimuli and generate nerve impulses which the brain interprets as "pain".

6. Adequate Stimulation Temperature Mechanical damage Chemicals (released from damaged tissue) Bradykinin, serotonin, histamine, K + , acids, acetylcholine, and proteolytic enzymes can excite the chemical type of pain. Prostaglandins and substance P enhance the sensitivity of pain endings but do not directly excite them. Nociopectors

7. Hyperalgesia:  The skin, joints, or muscles that have already been damaged are unusually sensitive. A light touch to a damaged area may elicit excruciating pain;  Primary hyperalgesia occurs within the area of damaged tissue; Secondary hyperalgesia occurs within the tissues surrounding a damaged area.

8. 2. Localization of Pain Superficial Somatic Pain arises from skin areas Deep Somatic Pain arises from muscle, joints, tendons & fascia Visceral Pain arises from receptors in visceral organs localized damage (cutting) intestines causes no pain diffuse visceral stimulation can be severe distension of a bile duct from a gallstone distension of the ureter from a kidney stone

9. Most pain sensation is a combination of the two types of message. If you prick your finger you first feel a sharp pain which is conducted by the A fibres, and this is followed by a dull pain conveyed along C fibres. 3. Fast and Slow Pain

10. Fast pain (acute) occurs rapidly after stimuli (.1 second) sharp pain like needle puncture or cut not felt in deeper tissues larger A nerve fibers Slow pain (chronic) begins more slowly & increases in intensity in both superficial and deeper tissues smaller C nerve fibers

11. PAIN RECEPTORS Pain Receptors Are Free Nerve Endings. The pain receptors in the skin and other tissues are all free nerve endings. They are widespread in the superficial layers of the skin, as well as in certain internal tissues, such as the periosteum, the arterial walls, the joint surfaces, and the falx and tentorium in the cranial vault.

12. Impulses transmitted to spinal cord by Myelinated A δ nerves: fast pain (80 m/s) Unmyelinated C nerves: slow pain (0.4 m/s) nociceptor nociceptor A δ nerve C nerve spinothalamic pathway to reticular formation

13. Impulses ascend to somatosensory cortex via: Spinothalamic pathway (fast pain) Reticular formation (slow pain) reticular formation spinothalamic pathway thalamus somato- sensory cortex

14. 4. Visceral pain Notable features of visceral pain: Often accompanied by strong autonomic and/or somatic reflexes Poorly localized; may be “ referred ” Mostly caused by distension of hollow organs or ischemia (localized mechanical trauma may be painless)

15. Pain can be elicited by multiple types of stimuli, classified as mechanical, thermal, and chemical pain stimuli. In general, fast pain is elicited by the mechanical and thermal types of stimuli, whereas slow pain can be elicited by all three types. Some of the chemicals that excite the chemical type of pain are bradykinin, serotonin, histamine, potassium ions, acids, acetylcholine, and proteolytic enzymes. In addition, prostaglandins and substance P enhance the sensitivity of pain endings but do not directly excite them. The chemical substances are especially important in stimulating the slow suffering type of pain that occurs after tissue injury.

16. PATHWAY FOR THE TRANSMISSION OF PAIN SIGNAL TO CENTRAL NERVOUS SYSTEM PERIPHERAL PAIN FIBERS The fast-sharp pain signals are elicited by either mechanical or thermal pain stimuli. They are transmitted in the peripheral nerves to the spinal cord by small type Aδ fibers at velocities between 6 and 30 m/sec. Conversely, the slow-chronic type of pain is elicited mostly by chemical types of pain stimuli but sometimes by persisting mechanical or thermal stimuli. This slow-chronic pain is transmitted to the spinal cord by type C fibers at velocities between 0.5 and 2 m/sec.

17. Because of this double system of pain innervation, a sudden painful stimulus often gives a “double” pain sensation: a fast-sharp pain that is transmitted to the brain by the Aδ fiber pathway, followed a second or so later by a slow pain that is transmitted by the C fiber pathway. The sharp pain plays an important role in making the person react immediately to remove himself or herself from the stimulus. The slow pain tends to become greater over time, eventually producing intolerable pain and making the person keep trying to relieve the cause of the pain.

18. On entering the spinal cord from the dorsal spinal roots, the pain fibers terminate on relay neurons in the dorsal horns. Here again, there are two systems for processing the pain signals on their way to the brain,

19. Dual pain pathway in the cord and brainstem On entering the spinal cord, the pain signals take two pathways to the brain, through : The neospinothalamic tract The paleospinothalamic tract.

20. Neospinithalamic tract for fast pain 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, and there they excite second-order neurons of the neospinothalamic tract. These second-order neurons 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.

21. Termination of the neospinothalamic tract in brain stem and thalamus A few fibers of the neospinothalamic tract terminate in the reticular areas of the brain stem, but most pass all the way to the thalamus without interruption, terminating 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. From these thalamic areas, the signals are transmitted to other basal areas of the brain, as well as to the somatosensory cortex.

22. The Nervous System Can Localize Fast Pain in the Body. The fast-sharp type of pain can be localized much more exactly in the different parts of the body than can slow-chronic pain. However, when only pain receptors are stimulated, without the simultaneous stimulation of tactile receptors, even fast pain may be poorly localized, often only within 10 centimeters or so of the stimulated area. Yet, when tactile receptors that excite the dorsal column–medial lemniscal system are simultaneously stimulated, the localization can be nearly exact.

23. Glutamate, the Probable Neurotransmitter of the Type Aδ Fast Pain Fibers. It is believed that glutamate is the neurotransmitter substance secreted in the spinal cord at the type Aδ pain nerve fiber endings. Glutamate is one of the most widely used excitatory transmitters in the central nervous system, usually having a duration of action lasting for only a few milliseconds.

24. Paleospinothalamic Pathway for Transmitting Slow-Chronic Pain The paleospinothalamic pathway is a much older system and transmits pain mainly from the peripheral slow-chronic type C pain fibers, although it also transmits some signals from type Aδ fibers. In this pathway, the peripheral fibers terminate in the spinal cord almost entirely in laminae II and III of the dorsal horns, which together are called the substantia gelatinosa , as shown by the lateral most dorsal root type C fiber . Most of the signals then pass through one or more additional short fiber neurons within the dorsal horns before entering mainly lamina V, also in the dorsal horn. Here, the last neurons in the series 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 and then upward to the brain in the anterolateral pathway.

25. Substance P, the Probable Slow-Chronic Neurotransmitter of Type C Nerve Endings. Type C pain fiber terminals entering the spinal cord release both glutamate transmitter and substance P transmitter. The glutamate transmitter acts instantaneously and lasts for only a few milliseconds. Substance P is released much more slowly, building up in concentration over a period of seconds or even minutes. In fact, it has been suggested that the “double” pain sensation one feels after a pinprick might result partly from the fact that the glutamate transmitter gives a faster pain sensation, whereas the substance P transmitter gives a more lagging sensation. Regardless of the yet unknown details, it seems clear that glutamate is the neurotransmitter most involved in transmitting fast pain into the central nervous system, and substance P is concerned with slow-chronic pain.

26. Projection of Paleospinothalamic Pathway (Slow Chronic Pain Signals) Into the Brain Stem and Thalamus. The slow-chronic paleospinothalamic pathway terminates widely in the brain stem, in the large shaded area. Only 10% to 25% of the fibers pass all the way to the thalamus. Instead, most terminate in one of three areas: 1) the reticular nuclei of the medulla, pons, and mesencephalon; 2) the tectal area of the mesencephalon deep to the superior and inferior colliculi; 3) the periaqueductal gray region surrounding the aqueduct of Sylvius

27. Pain suppression system in the brain and spinal cord The analgesia system consists of three major components: The periaqueductal gray and periventricular areas of the mesencephalon and upper pons surround the aqueduct of Sylvius and portions of the third and fourth ventricles. Neurons from these areas send signals to The raphe magnus nucleus, a thin midline nucleus located in the lower pons and upper medulla, and the nucleus reticularis paragigantocellularis , located laterally in the medulla. From these nuclei, second order signals are transmitted down the dorsolateral columns in the spinal cord to A pain inhibitory complex located in the dorsal horns of the spinal cord. At this point, the analgesia signals can block the pain before it is relayed to the brain.

28. Analgesia system to the brain and spinal cord

29. Several transmitter substances, especially enkephalin and serotonin, are involved in the analgesia system. Many nerve fibers derived from the periventricular nuclei and from the periaqueductal gray area secrete enkephalin at their endings. The endings of many fibers in the raphe magnus nucleus release enkephalin when stimulated. Fibers originating in this area send signals to the dorsal horns of the spinal cord to secrete serotonin at their endings.

30. The serotonin causes local cord neurons to secrete enkephalin as well. The enkephalin is believed to cause both presynaptic and postsynaptic inhibition of incoming type C and type Aδ pain fibers where they synapse in the dorsal horns. Thus, the analgesia system can block pain signals at the initial entry point to the spinal cord.

31. Gate control theory Psychologist Ronald Melzack and the anatomist Patrick Wall proposed the gate control theory for pain in 1965 to explain the pain suppression According to them, the pain stimuli transmitted by afferent pain fibers are blocked by gate mechanism located at the posterior gray horn of spinal cord. If the gate is opened, pain is felt. If the gate is closed, pain is suppressed.

32. Mechanism of gate control at spinal level 1. When pain stimulus is applied on any part of body, besides pain receptors, the receptors of other sensations such as touch are also stimulated. 2. When all these impulses reach the spinal cord through posterior nerve root, the fibers of touch sensation (posterior column fibers) send collaterals to the neurons of pain pathway, i.e. cells of marginal nucleus and substantia gelatinosa

33. 3. Impulses of touch sensation passing through these collaterals inhibit the release of glutamate and substance P from the pain fibers 4. This closes the gate and the pain transmission is blocked

34. Role of brain in gate control mechanism According to Melzack and Wall, brain also plays some important role in the gate control system of the spinal cord as follows: 1. If the gates in spinal cord are not closed, pain signals reach thalamus through lateral spinothalamic tract .These signals are processed in thalamus and sent to sensory cortex

35. 3. Perception of pain occurs in cortical level in context of the person’s emotional status and previous experiences 4. The person responds to the pain based on the integration of all these information in the brain. Thus, the brain determines the severity and extent of pain. 5. To minimize the severity and extent of pain, brain sends message back to spinal cord to close the gate by releasing pain relievers such as opiate peptides
6. Now the pain stimulus is blocked and the person feels less pain.

36. Significance of gate control gating of pain at spinal level is similar to presynaptic inhibition. It forms the basis for relief of pain through rubbing, massage techniques, application of ice packs, acupuncture and electrical analgesia. All these techniques relieve pain by stimulating the release of endogenous pain relievers (opioid peptides), which close the gate and block the pain signals.

37. TO BE CONTINUED ON THERMOREGULATION

38. Thermoregulation This is the biological mechanism responsible for maintaining steady internal body temperature

39. Thermal receptors and their excitation People can perceive different gradations of cold and heat, from freezing cold to cold to cool to indifferent to warm to hot to burning hot. Three types of sensory receptors are involved The cold receptor, the warmth receptors and the pain receptors

40. Stimulation of Thermal Receptors Sensations of Cold, Cool, Indifferent, Warm, and Hot Nerve fibres involved in different temperature effects 1. Pain fibre stimulated by cold 2. Cold fibre 3. Warmth fibre 4.pain fibre stimulated by heat

41. in the very cold region, only the cold pain fibers are stimulated (if the skin becomes even colder so that it nearly freezes or actually does freeze, these fibers cannot be stimulated). As the temperature rises to +10°C to 15°C, the cold-pain impulses cease, but the cold receptors begin to be stimulated, reaching peak stimulation at about 24°C and fading out slightly above 40°C. Above about 30°C, the warmth receptors begin to be stimulated, but these also fade out at about 49°C. Finally, at around 45°C, the heat pain fibers begin to be stimulated by heat and, paradoxically, some of the cold fibers begin to be stimulated again, possibly because of damage to the cold endings caused by excessive heat

42. Discharge frequencies at different skin temperatures of a cold pain fiber, a cold fiber, a warmth fiber, and a heat pain fiber.

43. The human body uses three mechanisms for thermoregulation: a) Efferent responses. Efferent responses are the behaviors that humans can engage in to regulate their own body temperature. Examples of efferent responses include putting on a coat before going outside on cold days and moving into the shade on hot days.

44. Afferent sensing. Afferent sensing involves a system of temperature receptors around the body to identify whether the core temperature is too hot or cold. The receptors relay the information to the hypothalamus, which is part of the brain. Central control. The hypothalamus acts as the central control, using the information it receives from afferent sensing to produce hormones that alter body temperature. These hormones send signals to various parts of the body so that it can respond to heat or cold in the following ways:

45. Heat and cold exposure Response to heat Response to cold Sweating Shivering or thermogenesis Dilated blood vessels Constricted blood vessels Decrease in metabolism Increase in metabolism