Pain – some facts

1. Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab. DCA, Dip. Software statistics Pain – some facts

2. An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. ISSP definition Definition

3. An unpleasant sensation, occurring in varying degrees of severity as a consequence of injury, disease, or emotional disorder. pain always has a subjective component Some say as

4. Whatever the patient says hurts. Margo McCaffrey

5. Nociception is the activation of a nociceptor by a potentially tissue-damaging (noxious) stimulus. It is the first step in the pain pathway What is nociception ??

6. nociceptor is a specialized, neurologic receptor that is capable of differentiating between innocuous and noxious stimuli Terminals of A delta and C fibres What is a nociceptor ??

7. Patient has no pain But the noxious stimulus is there Anaesthesia – all sensory modalities gone While analgesia – only pain Analgesia

8. Abnormal sensation Spontaneous or evoked Painful or painless Painful paraesthesia is dysaesthesia Formication is a form of paresthesia in which the patient feels as though bugs are crawling Paraesthesia

9. pain is felt in an area that is otherwise numb or desensitized Trigeminal neuralgia Trigeminal nerve is ablated no sensation but suddenly shooting pain comes Anaesthesia dolorosa

10. hyperpathia refers to an abnormally intense pain response to repetitive stimuli. Usually hyperpathic area of skin is not sensitive to a simple stimulus but over responds to multiple stimuli Pin prick Hyperpathia

11. Histamines, substance P, potassium, and prostaglandins, bradykinin, 5 HT are examples of algogenic substances Produced or injected – nociception Algogens

12. Hyperalgesia-shift of the stimulus pain response curve to the left • Primary • Pain to a non noxious stimulus in the area of injury • Pharyngitis – swallowing – painful • Secondary • Pain to a non noxious stimulus in the area by the side or encircling the injury P A I n stimulus

13. Primary secondary • Starts within minutes • Area of injury • Sensitive to heat and mechanical • Peripheral sensitization • Delayed onset • Wider area • Only thermal • Central role

14. Expansion of receptive field of nociceptor Sensitization of nociceptor Loss of central inhibition Increased CAMP levels Activation of protein kinase C Primary hyperalgesia – mechanisms

15. Antidromic release of algogens Dorsal horn neurons – sensitive WDR neurons – plastic changes Sometimes irreversible Post op pain - !!! Secondary hyperalgesia

16. Sensitization • shift of the stimulus - nerve fibre response curve to the left F I B res stimulus

17. Sensitization is a state in which a peripheral receptor or a central neuron either responds to stimuli in a more intense fashion than it would under baseline conditions or responds to a stimulus to which it is normally insensitive. Sensitization occurs both at the level of the nociceptor in the periphery and at the level of the second-order neuron in the spinal cord Sensitization

18. CLASSIFY PAIN

19. Nociceptive Somatic Visceral Nonnociceptive Peripheral Central Psychogenic Types of pain

20. Dull or sharp Localized Increased with movement Eg. Tooth ache Nociceptive – somatic

21. Skin, muscle, bone, joint etc….

22. Visceral nociception autonomic sensations including nausea, vomiting, and diaphoresis. There are often cutaneous referral sites

23. burning, electrical, and numbing Intervening normal Sudden Post herpetic, trigeminal, glossopharyngeal Neuropathic

24. Central pain syndrome is a neurological condition caused by damage or malfunction in the Central Nervous System (CNS) which causes a sensitization of the pain system. Trauma, tumors, stroke, Multiple Sclerosis, Parkinson's disease, or epilepsy . Pain can either be relegated to a specific part of the body or affect the body as a whole. Central pain

25. severe, persistent, paroxysmal, often intolerable, pains on the hemiplegic side, not yielding to any analgesic treatment Dejerineroussy syndrome

26. that state there are specific cellular and molecular changes that affect membrane excitability and induce new gene expression after nerve injury, thereby allowing for enhanced responses to future stimulation. the ectopic impulses of neuroma, changes of sodium and calcium channels in injured nerves, sympathetic activation, and deficient central inhibitory pathway contribute to the mechanisms of neuropathic pain theories have been proposed- neuropathic pain

27. Psychogenic pain, also called psychalgia, is pain that is caused by increased, or prolonged by mental, emotional, or behavioural factors Headache, back pain, or stomach pain are some of the most common types of psychogenic pain. It accompanies or induced by social rejection, broken heart, grief, love sickness, or other such emotional events. Psychogenic pain

28. No nociception No neuropathic mechanism But some evidence of psychologic symptoms to meet criteria for somatoform pain disorder, depression, Usually chronic Psychogenic pain

29. Origin of pain Treatment modalities Prognosis Why do we need to classify pain ??

30. Acute Acute pain is temporally related to injury and resolves during the appropriate healing period Chronic pain that persists for more than 3 months or that outlasts theusual healing process. Recurrent Duodenal ulcer Temporal classification

31. Etiology Arthritic Cancer Site Appendix Mastitits Other classifications

32. Aristotle believed that pain was due to evil spirits entering the body through injury, Hippocrates believed that it was due to an imbalance in vital fluids. it was thought that pain originated outside the body, perhaps as a punishment from God In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain History and theory

33. body has a separate sensory system for perceiving pain just as it does for hearing and vision— Von Frey (1895) and this system contains its own special receptors for detecting pain stimuli, its own peripheral nerves and pathway to the brain, and its own area of the brain for processing pain signals Theories of Pain - Specificity theory

34. SPECIFICITY THEORY • when someone pulls the rope to ring the bell, the bell rings in the tower. • Proved not correct

35. there is no separate system for perceiving pain, receptors for pain are shared with other senses, such as of touch. people feel pain when certain patterns of neural activity occur. Pattern theory- Goldschneider (1920)

36. Wilhelm Erb's (1874) "intensive" theory, that a pain signal can be generated by intense enough stimulation of any sensory receptor, has been soundly disproved Central processing theory Inputs – same but the central processing differs to produce pain Other theories

37. pain stimulation is carried by small, slow fibers that enter the dorsal horn of the spinal cordWall highlighted that pain messages are carried by the specific nerve fibresthat can be blocked before reaching the brain by the actions of other nerves andpsychological factors Melzack Wall gate control theory

38. The gate opens and closes

39. The gate control theory states that non painful stimulus such as distraction competes with the painful impulse to reach the brain. This rivlary limits the number of impulses that can be transmitted in the brain by creating the hypothetical gate Distraction – mechanical , endorphins, psychological Only theory – multifaceted pain approach The gate control theory

40. if the large fibers remain un stimulated, the pain signal will be propagated, but if they are activated, they act as an electrical gate, blocking the transmission of pain up the C fiber. the idea is

41. How is pain perceived ??

43. Aα Proprio, somatic Motor yes 12–20 70–120 Aβ Touch, pressure yes 5–12 30–70 Aγ Motor muscle spindle Yes 3–6 15–30 Aδ Pain, cold, touch Yes 2–5 12–30 BPreganglionic autonomic Yes 3 3–15 C Pain, temperature,No 0.4–1.2 0.5–2 Types of fibres myelin – dia mm velocity mm/s

44. Pain receptors (nociceptors) The sensation of pain then travels from the periphery to the spinal cord along A-delta and C fibers Lissauer’s tract synapse on second order neurons in substantiagelatinosa in dorsal horn (second order neuron) Pain starts

45. Spino thalamic tract (Neo and paleo) crossing via the anterior white commissure before ascending contralaterally. Before reaching the brain, the spinothalamic tract splits into lateral neospinothalamic tract and medial paleospinothalamic tract

46. Neo - posterolateral nucleus of the thalamus Paleospinothalamic neurons carry information from C fibers and terminate throughout the brain stem, a tenth of them in the thalamus and the rest in the medulla, pons and periaqueductal grey matter

47. Spinomesencephalic Midbrain – behavioural responses to pain Spino reticular Alerting and arousal motivational aspects -pain Pontine and medullary reticular formation Other second order neurons

48. Third order neurons from thalamus to cortex anterior cingulate cortex (emotional aspect ) Somatosensory cortex

49. Simple neuroanatomy of pain

50. Descending influence