Pain sensations

Undegraduate medical students ,pain physiology lecture ppt

1. Pain Physiology Dr Raghuveer Choudhary Associate Professor Department of Physiology Dr Sampurnanand Medical college Jodhpur

2. OBJECTIVES Definition of pain Types of pain Varieties of pain Pain pathway Pain inhibiting pathway Central analgesia Applied physiology

3. PAIN 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 1979)

4. Damaged tissues release proteolytic enzymes, K+ &histamine . Proteolytic enzymes act on globulins in the interstitial Fluid to release kinins . e.g bradykinin , K+ and histamine stimulate pain receptors Pain is a protective sensation.

5. Pain receptors . Free nerve endings Three types 1. Mechanical pain Receptors .: stimulated by mechanical injurious stimuli. 2. Thermal pain Receptors. : discussed before. 3. Chemical pain Receptors .: stimulated by chemical stimuli. Chemical stimuli include: bradykinin ( most important) serotonin, histamine & K+.

6. Distribution of pain receptors - More : Skin, periosteum , arteries, joint surfaces, & tentorium cerebelli and cranial sinuses. - Less : deep tissues. - Absent : liver parenchyma, lung alveoli and brain. ► Nerve fibres : A delta and C fibres . ► Adaptation: Slowly (static-tonic) or nonadaptive receptors .

7. Types of pain Pain is classified according to the : (a ) Site of pain 1. Cutaneous pain. 2. Deep pain. 3. Visceral pain. (b) Quality of pain 1. Epicritic i.e sharp pricking pain. 2. Protopathic i.e dull aching pain. 3. Burning pain.

8. Types of pain Fast pain is due to activity of myelinated A  fibres and it is appreciated as sharp bright and localized sensation. Slow pain is due to activity of unmyelinated C fibres and it is appreciated as dull aching and more diffuse. Slow pain follows fast pain. Peripheral Nerve C-Fiber A-delta Fiber

9. Fast pain & Slow pain Fast pain: is also described as sharp pain, pricking pain, Acute pain, electric pain . it is elicited by mechanical and thermal type of stimuli. Slow pain is also called as , slow burning pain, aching pain, throbbing pain, nauseous pain, chronic pain . slow pain can be elicited by mechanical, thermal and chemical stimuli.

10. Pain nerve fibers – fast pain and slow pain From the pain receptors, the pain stimulus is transmitted through peripheral nerves to the spinal cord and from there to the brain. This happens through two different types of nerves fibers: A-delta "fast pain” and C-fibers “slow pain” nerve fibers.

11. TYPES OF PAIN FIBRES TYPE OF NERVE CONDUCTION VELOCITY ( MTS/SEC ) MELINATED TYPE OF PAIN A- DELTA 20 (fast)   YES   SHARP, PRICKING,WELL LOCALIZED   C   1 (slow)   No DULL ACHE, DIFFUSE

12. Types of Pain Fast pain Slow pain Pin prick, cutting or burning of skin Associated with tissue destruction. Caused by mechanical or thermal stimuli. Caused mainly by chemical stimuli Transmitted by Aδ fibers (velocity 6-30 m/sec) NT- Glutamate Transmitted by C fibers (velocity 0.5-2 m/sec) NT- Substance P Neo- spinothalamic tract Paleo-spinothalamic tract

13. TYPES OF PAIN source of origin -- three types of pain. Superficial pain : pain arising from skin and mucous membrane. Deep (somatic) pain : pain originating from somatic structures deep to the skin are known as deep pain. Visceral pain : pain arising from different internal organs or viscera

14. Where Does Pain Come From? Cutaneous Pain – sharp, bright, burning; can have a fast or slow onset Deep Somatic Pain – stems from tendons, muscles, joints, periosteum , & bl. Vessels Visceral Pain – originates from internal organs; diffused @ 1 st & later may be localized (i.e. appendicitis) Psychogenic Pain – individual feels pain but cause is emotional rather than physical

15. VARIETIES OF PAIN ACUTE PAIN CHRONIC PAIN CUTANEOUS PAIN DEEP SOMATIC PAIN VISCERAL PAIN REFERRED PAIN NEUROPATHIC PAIN PHANTOM PAIN

16. What is “fast pain” and “slow pain”? A pain stimulus, e.g. if you cut yourself, consists of two sensations. first “fast pain” sensation-is experienced as sharp. “slow pain”, more a dull and burning. Occurs after a short time lasts a few days or weeks, Chronic pain-if inappropriately processed by the body, it can last several months

17. Fast pain nerves are called A-delta fibers. relatively thick size nerve fibers allow the pain stimulus to be transferred very fast (at a speed of five to 30 meter/second), hence the name This is all to make the body withdraw immediately from the painful and harmful stimulus, in order to avoid further damage.

18. Slow Pain starts immediately after the fast pain is transmitted by very thin nerve fibers, called C-nerve fibers (their diameter is between 0.2 to 1 thousandth of a millimeter). pain impulse can only be transmitted slowly to the brain, at a speed of less than 2 meters per second. Body response -immobilization (guarding, spasm or rigidity), so that healing can take place.

19. (1) Cutaneous Pain Fast (Immediate, acute sharp or pricking) Felts within 0.1 sec ond . Short-duration. Mechanical &Thermal R. A delta fibres . Ends in cerebral cortex. Well localized. Not felt in deep tissues Blocked by hypoxia & pressure Neospinothalamic tract Neurotransmitter: Glutamate . Slow (Chronic, burning, aching throbbing nauseous) After one second . Prolonged;annoying,intolerable . Elicited by All types of R. C fibres Ends in non specific thalamic nuclei & Reticular formation. Poorly localized . Occurs in skin & deep tissues Blocked by local anesthesia. Paleospinthalamic tract Neurotransmitter Substance P.

20. Nociceptive Pathways Fast A Delta Fibers Glutamate Neospinothalamic Mechanical, Thermal Good Localization Sharp, Pricking Terminate in VB Complex of Thalamus Slow C Fibers Substance P Paleospinothalamic Polymodal/Chemical Poor Localization Dull, Burning, Aching Terminate; RF Tectal Area of Mesen. Periaqueductal Gray

21. Nociceptive Pathways Spinothalamic - Major Neo- Fast (A Delta) Paleo- Slow (C Fibers) Spinoreticular Spinomesencephalic Spinocervical (Mostly Tactile) Dorsal Columns (Mostly Tactile)

22. PAIN A-DELTA→ Noxious Stimulation → change in Membrane Potential → Receptor Potential → A. P. C-FIBERS: Damaged Cell → Proteolytic Enzymes Circulating Gamma Globulins Bradykinin, Substance P Stimulation of Nerve Ending

23. Fast pain is transmitted by A delta fibers (5-15 m/sec.) from skin (mainly), parietal pleura, peritoneum a & Synovial membrane.

24. (1) Somatic (motor) reflexes:- Spinal reflexes . Flexor withdrawal reflex. (2) Autonomic reactions:- Cutaneous pain: Pressor effects (increased heart rate & ABP). DEEP & visceral pain: Depressor effects (decreased heart rate & ABP). (3) Emotional reactions:- -Acute pain: Crying and anxiety. (4) Hyperalgesia :- mainly due to skin lesion. (increased pain sensibility).

25. Deep pain C. Fibres Diffuse, Dull aching and Depressor effects. Causes: - inflammation, ischaemia or muscle spasm. - Bone fractures; due to stimulation of periosteal pain receptors. Characters of deep pain 1. Dull aching or rhythmic cramps. 2. Diffuse (poorly localized). Depressor autonomic changes: decreased heart rate, decreased arterial blood pressure ,nausea & vomiting.

26. DEEP PAIN Arises from Periosteum & Ligaments Continuous Contraction of Muscles Poorly Localized Associated with Sweating & Changes in Blood Pressure Often Nauseating Transmitted via Antero Lateral System

27. Ischaemic pain Type of deep pain felt in muscles when their blood supply is decreased. The Patients complains of severe pain in the muscles upon walking or running due to accumulation of pain producing substances as lactic acid. Examples 1 . Cardiac muscle: angina pectoris. 2. Skeletal muscle: intermittent claudication.

28. Visceral pain C Fibres Most of viscera contain only pain receptors. Pain from viscera is carried a long; C fibres . Pain from peritoneum, pleura or pericardium: Adelta . It differs from cutaneous pain . Sharp cut in the viscera does not cause pain (why). . Diffuse stimulation of pain nerve ending ® severe pain.

29. Causes Of Visceral Pain 1. Ischaemia : increased acidic metabolites, bradykinin & proteolytic enzymes. 2. Inflammation of peritoneal covering of viscera. 3. Irritation (chemical irritation by HCI in peptic ulcer). 4. Overdistension of a hollow viscus e.g urinary bladder. 5. Spasm of a hollow viscus e.g gut, gall bladder or ureter . Both 4 & 5: Obliteration of blood vesssels ® Ischaemic pain.

30. Characters of visceral pain 1. Dull aching or rhythmic cramps. 2. Diffuse (poorly localized ). 3. Depressor autonomic changes: decreased heart rate, decreased arterial blood pressure ,nausea & vomiting. 4. Rigidity of the overlying muscles. Limitation of the spread of infection. Decrease the mobility of the diseased viscus for relief of pain. 5. Referred to the surface area i.e referred pain.

31. VISCERAL PAIN Arises from Visceral Organs Receptors Free Nerve Endings of A Delta & C Fibers Sparsely Distributed Stimulus: Spasm, Distension, Ischemia, Chemical Ischemia Release Acid Metabolites Tissue Degeneration Products Produce Bradykinin & Proteolytic Enzymes Chemicals Release of Proteolytic Acid Gastric Juice

32. VISCERAL PAIN Input to CNS via Autonomic Nerves Cell Bodies of I st Order Neuron DRG & Homologous Cranial Nerve Ganglia of VII, IX , X & Trigeminal Nerve Afferent also Enters via Sympathetic Ganglia for Reflex Control of Visceral Functions

33. VISCERAL PAIN In CNS Fibers Follow Same Route as that of Other Pain Fibers Poorly Localized, Unpleasant Associated with Autonomic Changes & Nausea Usually Referred to Superficial Parts of Body REFERRED PAIN Visceral Pain Usually Referred Deep Pain May Also be Referred

34. Referred pain Definition Pain originating from viscera but felt in somatic structures which supplied by the same spinal dorsal root ( the same dermatome) of the diseased viscus .

35. Referred pain Examples 1. Cardiac pain: is felt in left shoulder. 2. Gall bladder pain: is felt in tip of right shoulder. 3. Appendicular pain: is felt around the umbilicus. 4. Gastric pain: is felt between the umbilicus & xiphoid process. 5. Renal pain: is felt in the back, inguinal region & testicles. 6. Teeth pain: referred to other teeth.

36. REFERRED PAIN Superficial Pain Never Referred Visceral Pain - Local & Referred May also Radiate to Distant Site Cardiac Pain Inner Aspect of Left Arm, Right Arm, even to Neck & Abdomen Distension of Ureter Pain in Testicles Irritation of Parietal Plura & Peritoneum Pain Referred to Overlying Surface of Body Of Diaphragm Tip of Shoulder

37. Referred Pain

38. REFERRED PAIN Mechanism Dermatome Rule Parts Develop from Same Embryonic Segment or Dermatome Diaphragm Migrate from Neck Heart & Arm have Same Segmental Origin Convergence Somatic and Visceral Pain Afferents Converge on Same Second Order Neuron Brain Unable to Differentiate Site of Origin Hence Pain Felt at Somatic Sites

39. Mechanism of referred pain Convergence – projection theory Afferent pain fibers from the skin and viscous converge on the same cells of SGR or thalamus and will finally activate the same cortical neurons . Whatever the source of pain, the cortex will project it to the skin being the commonest source of pain.

40. b. Facilitation theory Afferents of diseased viscera, give facilitation to cutaneous pain cells in Substantia Gelatinosa of Rolandi (SGR), Which leads to facilitation of their stimulation.

41. REFERRED PAIN Facilitation Effect: ↑ Activity in Visceral Pain Afferents Collaterals Fibers → EPSP in Spinal Neurons Receiving Somatic Inputs → ↑ Activity in Somatic Neurons → Continuous Pain

42. PAIN Intensity of Pain is Proportional to Degree of Tissue Damage Ischemic Pain → Lactic Acid → Nerve Ending Stimulation Muscle Spasm Mechanoreceptor Stimulation Ischemia Transmission of Pain A – Delta Fibers: 6 to 30 M/Sec C – Fibers: 0.5 to 2 M/Sec

43. How pain is transmitted to brain

44. Process of pain physiology TRANSDUCTION TRANSMISSION PERCEPTION MODULATION

45. Transduction: Pain stimuli is converted to electrical energy. This is known as Transduction. This stimulus sends an impulse across a peripheral nerve fiber ( nociceptor ).

46. Perception Person is aware of pain – somatosensory cortex identifies the location and intensity of pain Person unfolds a complex reaction-physiological and behavioral responses is perceived.

47. Modulation Inhibitory neurotransmitters like endogenous opioids work to hinder the pain transmission. This inhibition of the pain impulse is known as modulation

48. sensory cortex C fibre Final pain perception depends on activity of the Ascending pain impulse transmitting tracts Descending pain modulatory (inhibitory) tracts

49. Dual pathways for pain transmission From peripheral receptors to spinal cord: A δ fibers (fast fibers ) – for fast pain C fibers (slow fibers) – for slow pain From spinal cord to brain: via Anterolateral ( Spinothalamic ) tract Neo- spinothalamic tract – for fast pain Paleo-spinothalamic tract – for slow pain

50. PAIN Mixed Spinal Nerve Dorsal Root Ganglia Dorsal Root Dorsal Horn A – Delta Fibers Terminate in Lamina I of Dorsal Horn Gray Matter (Fast Pain)Give Local Collateral Branch for Spinal Reflexes Second Order Neuron Cross to Opposite Side Form Anterior Spino -Thalamic Tract ( Neospinothalamic Tract) Joins Medial Laminiscus → Few Collaterals to R.F.

51. First synapse in spinal cord is substantia gelatinosa substantia gelatinosa Neurotransmitter at the first synapse of the pain pathway is substance P Acute pain : glutamate Chronic pain: substance P Pain inhibitory neurotransmitters: enkephalin , GABA

52. Ascending pathway Crosses the midline Ascends up as the lateral spinothalamic tract Pain lateral spinothalamic tract C fibre substantia gelatinosa

53. PAIN Second Order Neuron Thalamus Post Central Gyrus Localization is Good Neurotransmitter is Glutamate Few Fibers Ascends in Dorsal Column

54. Slow pain: C –Fibers I st Order Neuron Lamina II and III Substantia Gelatinosa of Rolando Interneuron Lamina V Second Order Neuron Cross → Lateral Spinothalamic Tract ( Paliospinothalamic Tract → Brain Stem Joins → Medial Leminiscus → Thalamus → Cortex

55. Pain Brain Stem: Collaterals Given to: Reticular Formation at All Levels of Brain Stem Hypothalamus Peri Ventricular Gray Matter Peri Aqueduct Gray Matter Most Fibers End in Intralaminar and Reticular Nuclei of Thalamus Non Specific Thalamo Cortical Projections to All Part of Cerebral Cortex To Somato Sensory Cortex SI and SII

56. PAIN While Entering Spinal Cord Fibers Ascends or Descends Few Segments → Enters Spinal Cord Through Many Inter-Neurons Information Relayed to Anterior Horn Cells of Same & Opposite Side for Local & Segmental Reflexes of Spinal Cord

57. Thalamus – ventrobasal complex Reticular formation Spinothalamic tract Spinal cord (lamina I – lamina marginalis) Peripheral fibers A δ fibers Pain receptor (Free nerve endings) Somatosensory cortex Other basal areas of brain

58. Pain pathway

59. Reticular nuclei,Tectal area & periaqueduvtal grey region Thalamus Spinothalamic tract Spinal cord (lamina II & III – substantia gelatinosa) Peripheral fibers C fibers Pain receptor (Free nerve endings) Thalamus (IL & VL nuclei) Hypothalamus Other basal areas of brain

60. CENTER FOR PAIN SENSATION The center for pain sensation is in the post central gyrus of parietal cortex. Fibres reaching Hypothalamus are concerned with arousal mechanism due to pain stimulus. Substance P is the neurotransmitter involved in pain sensation. It is secreted by the ending of pain nerve fibres in dorsal grey horn.

61. Appreciation of pain - Fast pain; is appreciated in thalamus and cortex. - Slow pain; is appreciated mainly in thalamus. Functions of the cortex in pain appreciation 1. Localization of pain 2. Discrimination of type of pain. 3. Modulation of pain by emotional and behavioral factors.

62. Arousal reaction to pain signals The non specific thalamic nuclei (intra-laminar nuclei) and reticular formation have a strong arousal effect on the brain which prevents sleep during pain.

63. PHYSIOLOGY OF PAIN PERCEPTION Injury Descending Pathway Peripheral Nerve Dorsal Root Ganglion C-Fiber A-beta Fiber A-delta Fiber Ascending Pathways Dorsal Horn Brain Spinal Cord 76

64. lateral spinothalamic tract thalamus sensory cortex C fibre thalamocortical tracts

65. Physiological Basis of Medical measures to relieve pain The CNS has its own control system which inhibits the impulse of pain sensation. This is also called Analagesia system . This control system is present in both brain and spinal cord. Pain control system in spinal cord: This is in dorsal grey horn. The dorsal grey horn is considered as the gateway for pain impulses to reach the brain (via) spinothalamic tract.

66. Pain Control Mechanisms Peripheral Gating Theory Involves Inhibitory Inter-Neuron in Cord impacting Nociceptive Projection Neurons Inhibited by C Fibers Stimulated by A Alpha & Beta Fibers TENS Central Direct Electrical + to brain → Analgesia Nociceptive control Pathways Descend to Cord Endogenous Opioids

67. GATE CONTROL THEORY Melzack & Wall, 1965 Substantia Gelatinosa (SG) in dorsal horn of spinal cord acts as a ‘gate’ – only allows one type of impulses to connect with the SON If A-beta neurons are stimulated – SG is activated which closes the gate to A-delta & C neurons If A-delta & C neurons are stimulated – SG is blocked which closes the gate to A-beta neurons

68. Gate control theory When pain fibre is stimulated, gate will be opened & pain is felt pain pain is felt + gate is opened

69. Gate control theory When pain and touch fibres are stimulated together, gate will be closed & pain is not felt pain is not felt touch pain + - gate is closed

70. GATE CONTROL MECHANISM S.G.Cells T- Cells Type II Fibers A-DELTA & C Fibers (-) (-) (+) (-) (+) Spino Thalamic Pathway (-)

71. GATE CONTROL THEORY Gate - located in the dorsal horn of the spinal cord Smaller, slower n. carry pain impulses Larger, faster n. fibers carry other sensations Impulses from faster fibers arriving @ gate 1 st inhibit pain impulses (acupuncture/pressure, cold, heat, chem. skin irritation). Brain Pain Heat, Cold, Mechanical Gate ( T cells/ SG)

72. Gate control theory When pain sensation is produced-- other afferents particularly the touch fibres reaching the posterior column of spinal cord are also activated. These dorsal column fibres send collaterals to the cells of substantia gelatinosa in the dorsal grey horn. Thus impulses ascending via dorsal column fibres pass through the collaterals and reach substantia gelatinosa. Here these impulses inhibit the release of substance P by the pain nerve endings. So that the pain sensation is suppressed. Thus the gating of pain in dorsal grey horn level is similar to presynaptic inhibition.

73. Inhibition of pain transmission by tactile sensory signals Rubbing the skin near painful areas and applying liniments often relieves pain. This is due to the stimulation of Aβ sensory fibres from peripheral tactile receptors depress transmission of pain signals. This results from a type of local lateral inhibition.

74. Presynaptic inhibition substance P enkephalin pain impulse blocking of pain impulse

75. DESCENDING NEURONS Descending Pain Modulation (Descending Pain Control Mechanism) Transmit impulses from the brain (corticospinal tract in the cortex) to the spinal cord (lamina) Periaquaductal Gray Area (PGA) – release enkephalins Nucleus Raphe Magnus (NRM) – release serotonin The release of these neurotransmitters inhibit ascending neurons Endogenous opioid peptides - endorphins & enkephalins causes analgesia.

76. PAIN DESCENDING PAIN INHIBITING SYSTEM : Fibers Arise from: Peri-Aqueductal Gray matter Peri -Ventricular Gray Matter Hypothalamus Medial Forebrain Bundle Neurons around IIIrd & IV ventricle Nucleus Reticularis in Medulla Spinal Cord Nucleus Raphe Magnus Encephalins

77. PAIN Nucleus Raphe Magnus Dorsal Horn of Spinal Cord in Substantia Gelatinosa Pre-Synaptic and Direct Inhibition by Blocking Ca ++ Channels Blocking of Pain Signals Serotonergic Neurons

78. Periaqueductal grey Periventricular nuclei Raphe magnus nucleus Nucleus reticularis paragigantocellularis Spinal cord (pain inhibiting complex in dorsal horn) Hypothalamus (periventricular nucleus & MFB) Pain suppression (Analgesia) system of brain & spinal cord Neurotransmitters Serotonin Opiates ( enkephalins )

79. Pain Control Systems (I) Analgesic system a) The neurons of the periaqueductal gray area are stimulated by B endorphin reaching them from hypothalamus (neurons of periventricular area) or pituitary (through blood). b) Fibres of periaqueductal and interneurones of sp.cd. Secrete ( Enkephalin ) c) Fibres of raphe magnus nucleus secrete (Serotonin) d) Inhibitory interneurones in spinal cord secrete ( Enkephalin ).

80. Natural Opioids -Endorphins released from their storage areas in the brain when a pain impulse reaches the brain, bind to receptors in the pain pathway to block transmission and perception of pain.

81. opioid pain inhibition at multiple levels spinal cord brain-stem thalamus

82. (II) Brain Opiate System Opiate receptors in the brain cause pre and postsynaptic inhibition of the nociceptive pathway . Sites of opiate receptors Periaqueductal gray area Periventricular aea . Raphe magnus nucleus in medulla . Substantia nigra .

83. Opioid peptides (1 ) Enkephalins . Act as neurotransmitters at the analgesic system. (2 ) Endorphins -In hypothalamus act as neurotransmitters. -In pituitary act as hormone. Release during stress leading to stress analgesia. (3) Dynorphin Very potent analgesic. Types of opiate receptors Delta , Mu, Kappa, Sigma & Epislon .

84. BRAIN OPIOID SYSTEM Opium Alkaloid Morphine Derived from Opium → Analgesia Receptors are Opioid Receptors Found in Many Areas of Brain Limbic System Hypothalamus, Peri-Ventricular Areas, Pituitary & Spinal Cord Endogenous Substances which Mimic Action of Opium → Opioid Peptides Brain’s Own Morphine Act like Neurotransmitter on Opioid Receptors

85. BRAIN OPIOID SYSTEM Opioid Peptides Beta Endorphins Derived from Pro-opiomelanocortin Met-and Leu-Encephalins Derived from-Proencephalins Dynorphin Derived from Prodynorphin Opioid Peptides Cause Pre-synaptic Inhibition At Spinal Cord to Block Pain Inhibit Release of Substance P

86. BRAIN OPIOID SYSTEM Cause Post Synaptic Inhibition Produce IPSP In Limbic Areas & Hypothalamus Pain Modulation Act Peripherally at Site of Injury Opioid Mediated Endogenous Analgesia System → Activated by Administration of Exogenous Morphine Descending Analgesia System Under Tonic Inhibitory Control of Mid Brain & Medulla Opiates Inhibit these Inhibitory Inter-Neurons

87. Pain Modulation Examples Stress Analgesia War Situation When Person Emotionally Charged Pain Relieved by Acupressure & Acupuncture and Electrical Vibrator Gate Control Mechanism Proposed by Malzek & Wall

88. Pain control system in Brain Acupuncture is also used to relieve pain. This is based upon the pain inhibitory mechanism of encephalins and endorphins released by this procedure. Pain control NSAIDs (inhibit COX) Opiates (inhibit NT release)

89. Surgical procedure that relieve pain Different surgical procedures are done in the course of pain pathway to relieve pain. They are - Sympathectomy -Cordotomy -Thalamotomy -Prefrontal lobotomy

90. 2)Thalamic gate: The same "gating" mechanism for pain is found also at the thalamus where pain signals could be blocked by corticofugal fibers or facilitated by intralaminar thalamic nuclei. In this way, the thalamus considered as a secondary gate far pain transmission.

91. Stress analgesia; During stress , Pain is blocked at two levels : A) At the thalamus: (the second gate of pain transmission ). Corticofugal fibers to the thalamus block by presynaptic inhibition the transmission of pain signals in the thalamus before they reach the cerebral cortex. B) At the dorsal horn of the spinal cord: (the first gate of pain transmission ) . The hypothalamus, and other parts of the central analgesia system, activate the spinal PIC which blocks the transmission of pain signals at the dorsal horn.

92. PAIN Pain & Other Crude Sensations Perceived Even in Absence of Cerebral Cortex Cortex is Concerned With Discriminative, Exact & Meaningful Interpretation of Pain Emotional Components of Pain Post Injury Pain Irritation of Nerve Endings Allodynia Minor Touch Causes Pain Neuropathic Pain Occur at Sites Even after Healing of Injury Often Resistant to Analgesics

93. VARIOUS TERMINOLOGIES TERM DESCRIPTION ALLODYNIA PERCEPTION OF NON-NOXIOUS STIMULUS AS PAIN ANALGESIA ABSENCE OF PAIN PERCEPTION ANESTHESIA ABSENCE OF ALL SENSATIONS ANESTHESIA DOLOROSA PAIN IN AN AREA THAT LACKS SENSATION DYSESTHESIA UNPLEASANT SENSATION WITH OR WITHOUT STIMULUS HYPOALGESIA DIMINISHED RESPONSE TO NOXIOUS STIMULUS HYPERALGESIA INCREASED RESPONSE TO NOXIOUS STIMULUS HYPERASTHESIA INCREASED RESPONSE TO MILD STIMULUS HYPOASTHESIA REDUCED CUTANEOUS SENSATION NEURALGIA PAIN IN THE DISTRIBUTION OF A NERVE PARASTHESIA ABNORMAL SENSATION PERCEIVED WITHOUT AN APPARENT STIMULUS RADICULOPATHY FUNCTIONAL ABNORMALITY OF NERVE ROOTS