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  • Learning Objectives: Differentiate between the mechanisms of somatic pain, visceral pain, referred pain and phantom limb pain.
  • Learning Objectives: Explain the roles of the axon reflex and hyperalgesia in the Triple Response of Lewis.
  • Learning Objectives: Explain the responses of a thermal receptor to changes in temperature.
  • Learning Objectives: Explain the mechanisms of paradoxical cold and pain associated with stimulating thermal receptors.
  • Learning Objectives: Explain the adequate stimulus for nociceptors and compare the mechanisms of slow and fast pain.
  • Learning Objectives: Memorize the structures and functions of the spinothalamic somatosensory systems.
  • Learning Objectives: Explain how knowledge of the Brown-Sequard syndrome can be used to localize neural lesions.
  • Learning Objectives: Memorize the spinal organization of spinothalamic somatosensory system fibers.
  • Learning Objectives: Explain the gate control theory of pain.
  • Learning Objectives: Explain the relationship between serotonin and enkephalin in the perception of pain.
  • Learning Objectives: Compare and contrast the roles of the hypothalamus, the nonspecific thalamic nuclei and the ventrobasal thalamic nuclei on autonomic, emotional, motivational, discrimninatory and cognitive perceptual factors in somatosensory functions.
  • Learning Objectives: Memorize the structures and functions of the spinothalamic somatosensory systems.

    2. 2. PAIN <ul><li>Unpleasant sensory and emotional experience associated with actual or potential tissue damage </li></ul><ul><li>Functions: Stop Signal </li></ul><ul><ul><li>Warning of a threat </li></ul></ul><ul><ul><li>Basis of learning </li></ul></ul><ul><ul><li>Forces a person to rest </li></ul></ul>
    3. 3. Case Study #2 <ul><li>A 42 year-old female injured her neck in an automobile accident 2 months prior to seeking help. She noted a dull pain in her jaw during this period. Three weeks prior to admission a sharp, shooting pain (like an “electric shock”) was noted beginning in her neck and shooting to her jaw and face. The pain could be triggered by coughing, sneezing and straining to pick up heavy objects. </li></ul>
    4. 4. Case Study #2 (cont’d) <ul><li>The patient also reported parasthesia as a “tingling numbness” of the left cheek. Neurological examination revealed absent jaw jerk ( masseter deep tendon reflex ) on the left. Motor strength of the upper and lower limbs was normal and there were no Babinski signs . </li></ul>
    5. 5. Case Study #2 (Question) <ul><li>The pain this patient experienced is due to </li></ul><ul><li>Excitation of nociceptors </li></ul><ul><li>Excitation of medium- and large-diameter sensory nerve fibers </li></ul><ul><li>Excitation of small-diameter myelinated and unmyelinated sensory nerve fibers </li></ul><ul><li>Pressure on a dorsal root </li></ul><ul><li>More than one but not all of the above </li></ul>
    7. 10. Tissue Injury & Inflammation <ul><li>“ Inflame” – to set fire. </li></ul><ul><li>Inflammation is “dynamic response of vascularized tissue to injury.” </li></ul><ul><li>Is a protective response. </li></ul><ul><li>Serves to bring defense & healing mechanisms to the site of injury. </li></ul>
    8. 11. Triple Response of Lewis <ul><li>Flush : capillary dilatation. </li></ul><ul><li>Flare : arteriolar dilatation. </li></ul><ul><li>Weal : exudation, edema. </li></ul>
    9. 12. Red, Warm & Swollen (Flare, Flush & Weal – Lewis) Triple response HYPERALGESIA IN AREAS SURROUNDING INJURY
    10. 13. “ The Angry” Axon Reflex antidromic stimulation
    11. 16. Spinothalamic (Anterolateral) System
    12. 17. The Spinothalamic System <ul><li>The spinothalamic system provides for temperature and pain sensibility. This small fiber, evolutionarily old system provides for perceptual capabilities that have a larger component of emotional tone, the affective component, than do perceptions provided for by the DCML system. Because its fibers ascend in the anterolateral portion of the spinal cord, the spinothalamic system is also called the anterolateral system. </li></ul>
    13. 18. Spinothalamic System <ul><li>Receptor = Nociceptor (responds to noxious stimuli such as pain and temperature) </li></ul><ul><li>Nociceptors are naked nerve endings of primary (first order) afferent neurons </li></ul><ul><li>Nociceptor signaling regulated by ion channels and membrane receptor proteins </li></ul><ul><li>Pain and temperature signals transmitted from nociceptors to first order primary afferents without synapse </li></ul><ul><li>First order neurons release SP and glutamate primarily and synapse in the Substantia Gelatinosa (SG) of spinal cord. </li></ul>
    14. 19. Decussation of Second Order Spinothalamic Neurons <ul><li>Pain signals transmitted to second order neurons contralaterally at spinal level of stimulated receptor or at a spinal segment above or below the stimulated receptor (tract of Lissauer) making pain and temperature difficult to localize to a single dermatome precisely. </li></ul><ul><li>Brown-Sequard syndrome (spinal cord hemisection) lesions produce ipsilateral and contralateral loss of pain and temperature sensation in the dermatomes at the spinal level of the lesion but only contralateral loss in the dermatomes below the spinal level of the lesion </li></ul>
    15. 20. Hemisection of Spinal Cord Brown-Sequard Syndrome
    16. 21. Brown-Sequard Syndrome
    17. 23. Role of Thalamus <ul><li>Second order neurons transmit pain and temperature signals to thalamus contralateral to stimulated receptor </li></ul><ul><li>VPM processes pain and temperature signals from trigeminal (CNV) analog of spinothalamic system for head and neck </li></ul><ul><li>VPL processes pain and temperature signals from peripheral regions of the body such as viscera, trunk and limbs </li></ul><ul><li>Medial (intralaminar) thalamic nuclei process pain and temperature signals from reticular formation (spinoreticular fibers) such as raphe nuclei and locus coruleus </li></ul><ul><li>Central (thalamic) pain signals cannot be localized (e.g., metastatic cancer) and central (thalamic) pain syndrome is relieved by producing electrical lesions in a thalamotomy procedure </li></ul>
    18. 24. Role of Cerebral Cortex <ul><li>Pain and temperature signals transmitted from VPL and VPM (specific thalamic nuclei) to somatosensory cortices SI and SII for localization </li></ul><ul><li>Pain and temperature signals transmitted from medial intralaminar (nonspecific) nuclei to all regions of cerebral cortex for “alerting” response, which induce wakefulness and inhibit sleep </li></ul><ul><li>Pain and temperature signals also transmitted from intralaminar nonspecific nuclei to limbic system, hypothalamus and associated structures for emotional, endocrine, stress and autonomic responses which produce fear, suffering, cardiovascular, respiratory, gastrointestinal, urogenital and stress-related hormonal responses </li></ul>
    19. 25. Functional Properties of the Spinothalamic System <ul><li>The spinothalamic system subserves pain and temperature sensibility and provides for a less precise, less well-localized, more emotion laden type of somatic sensibility than the DCML system. The affective component of the pain experience is due to the divergent projections of the spinothalamic system, especially those into the reticular formation, intralaminar thalamic nuclei, and limbic system. </li></ul>
    20. 27. GIII (A-delta) and GIV (C-fibers) Afferents for Pain
    21. 28. Transient Receptor Potential Vanilloid-1 (TRPV1) Channels <ul><li>All animals need to sense temperature to avoid hostile environments and to regulate their internal homeostasis. A particularly obvious example is that animals need to avoid damagingly hot stimuli. The mechanisms by which temperature is sensed have until recently been mysterious, but in the last couple of years, we have begun to understand how noxious thermal stimuli are detected by sensory neurons. Heat has been found to open a nonselective cation channel in primary sensory neurons , probably by a direct action. In a separate study, an ion channel gated by capsaicin , the active ingredient of chili peppers, was cloned from sensory neurons. This channel (vanilloid receptor subtype 1, VR1) is gated by heat in a manner similar to the native heat-activated channel, and our current best guess is that this channel is the molecular substrate for the detection of painful heat. Both the heat channel and VR1 are modulated in interesting ways. The response of the heat channel is potentiated by phosphorylation by protein kinase C, whereas VR1 is potentiated by externally applied protons . Protein kinase C is known to be activated by a variety of inflammatory mediators, including bradykinin, whereas extracellular acidification is characteristically produced by anoxia and inflammation. Both modulatory pathways are likely, therefore, to have important physiological correlates in terms of the enhanced pain ( hyperalgesia ) produced by tissue damage and inflammation. </li></ul>
    22. 29. Vanilloid Receptor
    23. 30. Purinergic (ATP) Receptors <ul><li>It has been well known that pain is caused by nociceptive stimulation such as protons (i.e. acidic solutions), heat and capsaicin, a pungent ingredient of chili peppers. For a long period, the signal transduction mechanism of pain activated by these nociceptive stimuli has not been clarified. Recent advance, especially the identification of TRPV1 receptor (for which capsaicin, protons and heat are ligands), P2X and P2Y receptor (for which ATP is a ligand) and acid sensing ion channel made a remarkable progress in understanding the mechanism of nociceptive neurons. </li></ul>
    24. 32. Thermal and Pain Receptors <ul><li>The spinothalamic system receives its input from free (naked, bare) nerve endings that are the peripheral terminals of small- diameter myelinated (A) and unmyelinated (C) primary afferent fibers. </li></ul>
    25. 34. Capsaicin Menthol
    26. 35. Thermoreceptor: frequency proportional to delta-T Set point
    27. 37. Pin-prick test
    28. 38. Hmine, BK, PG, 5-HT, H+, K+ Ach, SP Sources of chemical stimuli: neurons, blood, damaged tissues, mast cells, platelets
    29. 41. Small Diameter Afferent Fibers <ul><li>Cutaneous mechanoreceptors </li></ul><ul><ul><li>Respond to nondiscriminative tactile stimuli </li></ul></ul><ul><ul><li>Pinch, rub, stretch, squeeze </li></ul></ul><ul><ul><li>A-delta and C fiber, high-threshold </li></ul></ul><ul><li>Cutaneous thermoreceptors </li></ul><ul><ul><li>Respond to transient change in temperature </li></ul></ul><ul><ul><li>Innocuous ward and cool stimuli </li></ul></ul>
    30. 42. Small Diameter Afferent Fibers <ul><li>Cutaneous nociceptors – cutaneous pain </li></ul><ul><ul><li>A-delta mechanoreceptors </li></ul></ul><ul><ul><ul><li>Mechanical tissue damage </li></ul></ul></ul><ul><ul><li>C-polymodal nociceptors </li></ul></ul><ul><ul><ul><li>Mechanical tissue damage, noxious thermal stimuli, endogenous algesic chemicals </li></ul></ul></ul><ul><li>C-fiber mechanonociceptors </li></ul><ul><li>A-delta heat thermonociceptors </li></ul><ul><li>A-delta, C-fiber cold thermonociceptors </li></ul><ul><li>C-fiber chemonociceptors – algesic chemicals </li></ul>
    31. 43. Deep Nociceptors <ul><li>Muscle nociceptors – GIII, GIV afferents </li></ul><ul><ul><li>Bradykinin </li></ul></ul><ul><ul><li>5-HT (Inflammation releases 5-HT in TMJD) </li></ul></ul><ul><ul><li>K+ </li></ul></ul><ul><ul><li>GLUT </li></ul></ul><ul><li>Joint nociceptors – GIII, GIV afferents </li></ul><ul><ul><li>Inflammation (K+, Bradykinin, 5-HT, GLUT) </li></ul></ul><ul><ul><li>Kaolin (experimental models) </li></ul></ul><ul><ul><li>Carregeenan (experimental models) </li></ul></ul>
    32. 44. Visceral Nociceptors <ul><li>Heart – A-delta and C afferents </li></ul><ul><ul><li>H+ </li></ul></ul><ul><ul><li>K+ </li></ul></ul><ul><ul><li>Ischemia </li></ul></ul><ul><ul><li>Bradykinin </li></ul></ul><ul><ul><li>PGE-2 </li></ul></ul>
    33. 45. Lung Nociceptors <ul><li>Lung Irritant Receptors – A-delta afferents </li></ul><ul><ul><li>Irritant aerosols and gases </li></ul></ul><ul><ul><li>Mechanical stimuli </li></ul></ul><ul><li>Lung “J” Receptors – C-fibers </li></ul><ul><ul><li>Capsaicin </li></ul></ul><ul><ul><li>Pulmonary congestion, edema </li></ul></ul><ul><ul><li>Inhaled irritants </li></ul></ul>
    34. 46. G.I. Tract Nociceptors <ul><li>Rapidly-adapting mechanoreceptors, slowly adapting mechanoreceptors, chemoreceptors (A-delta and C-fibers) </li></ul><ul><ul><li>Irritation of the mucosa </li></ul></ul><ul><ul><li>Distension </li></ul></ul><ul><ul><li>Powerful contraction </li></ul></ul><ul><ul><li>Torsion </li></ul></ul><ul><ul><li>Traction </li></ul></ul><ul><ul><li>Bloating </li></ul></ul><ul><ul><li>Cramping </li></ul></ul><ul><ul><li>Appendicitis </li></ul></ul><ul><ul><li>Impaction </li></ul></ul>
    35. 47. Distribution of Nociceptors <ul><li>UG Tract - C-polymodal (e.g., testis) </li></ul><ul><ul><li>Intense mechanical stimuli </li></ul></ul><ul><ul><li>Noxious heat </li></ul></ul><ul><ul><li>Algesic chemicals </li></ul></ul><ul><li>Bone - periosteum </li></ul><ul><li>Blood Vessels - walls </li></ul><ul><li>Brain – none </li></ul><ul><ul><li>C-fibers in dura mater </li></ul></ul>
    36. 48. CNS Neurotransmitters of A-delta and C-fibers <ul><li>Substance P (Neuropeptide) </li></ul><ul><li>Calcitonin Gene Realted Peptide (CGRP) </li></ul><ul><li>Excitatory amino acids – e.g., glutamate </li></ul><ul><ul><li>Release in ischemia/hypoxia - neurotoxicity </li></ul></ul>
    37. 49. Membrane Receptors of A-delta and C-fibers in CNS <ul><li>Purinergic (ATP) </li></ul><ul><li>GABA-ergic </li></ul><ul><li>Mu opioid receptor (MOR) </li></ul>
    38. 50. Large Multimodal RFs <ul><li>Receptive fields of central neurons within the spinothalamic system are often large. Individual neurons may respond to several different stimuli (multimodal responses). RFs may be bilateral. Some neurons are specifically sensitive to noxious stimulation; others are sensitive to temperature changes. </li></ul>
    39. 51. Spinal tract of CNV (Trigeminal Analog of STT) Spinal tract of CNV descends and crosses in medulla and cervical spinal cord
    40. 52. Spinal Tract of CNV <ul><li>Trigeminal analog of spinothalamic system transmits pain and temperature signals from head and neck to VPM of thalamus </li></ul><ul><li>Second order neurons in in spinal tract of CNV transmits pain and temperature contralaterally via decussations in pons, medulla or cervical spinal cord </li></ul><ul><li>Cervical spinal lesions can produce abnormal pain and temperature sensations in head and neck (e.g., cervical arthritis, whiplash injury producing temporomandibular disease) </li></ul>
    41. 53. Coarse Somatotopic Organization <ul><li>Somatotopic organization in the spinothalamic system is not as distinct as in the DCML system, except in the spinal cord. </li></ul>
    42. 54. STT fibers distribute widely to specific and nonspecific nuclei
    43. 55. Spinal cord distribution of STT fibers Pain and temperature deficits referred to receptor dermatome: Law of projection Hand/arm medial, foot/leg lateral distribution Inverse to DCML
    44. 56. Features of the Pain Experience
    45. 57. Features of the Pain Experience <ul><li>Pain is a complex perceptual experience. It is difficult, except at the conceptual level, to separate the objective sensory aspects from the cognitive and emotional reactions to the presence of pain. The complexity of the pain experience is matched by the complexity of the central pathways for nociceptive inputs. For pain from superficial tissues, it is customary to distinguish fast (pricking) pain, due to activation of A (GIII) fibers, from slow (burning) pain which is due to activation of C (GIV) fibers. Fast pain does not last much longer than the stimulus, is easy to endure, and is not accompanied by much of an affective, or emotional, component. It is like the pain from a hypodermic needle during an injection. Slow pain persists, is hard to endure, and has a large affective component; autonomic responses may occur. Slow pain is associated with suffering and is most often the kind of pain that brings the patient to the doctor's office. </li></ul>
    46. 58. Control of Nociceptive Inputs and Modulation of Pain <ul><li>The brain is able to modulate all the varieties of sensation via efferent connections to receptors or neurons in sensory pathways. This is also true for nociception and there are three (non-mutually exclusive) mechanisms by which nociceptive inputs are modulated. </li></ul>
    47. 59. Gate Control Theory of Pain <ul><li>Large-diameter primary afferent fibers (Aα and Aβ fibers) can inhibit, via inhibitory interneurons, dorsal horn neurons (projection neurons) that give rise to spinothalamic tract fibers. This form of control of nociceptive input is known as the gate control theory of Melzack and Wall, after the scientists who proposed it. Electrical stimulation of the dorsal columns or of large, myelinated peripheral nerve fibers by transcutaneous electrical nerve stimulation (TENS) may relieve pain by this mechanism. Acupuncture anesthesia may also be an example of dorsal column-anterolateral system interaction since it is reported to be effective only when needles are inserted near bundles of Group II fibers. Dorsal column-anterolateral system interactions may occur at several levels, including spinal cord dorsal horn, spinal V nucleus, and thalamus. </li></ul>
    48. 60. Gate Control Theory of Pain
    49. 61. Gate Control Theory of Pain <ul><li>Pain and temperature signals cause C and A-delta fibers to release an excitatory neurotransmitter (e.g., glutamate, SP) and stimulate second order neurons directly </li></ul><ul><li>Pain and temperature signals also cause C and A-delta fibers to release an inhibitory neurotransmitter (e.g., GABA, enkephalin) and inhibit an inhibitory interneuron, thereby, opening the gate for transmitting pain and temperature signals to second order neurons </li></ul><ul><li>Tactile signals cause A-fibers to release an excitatory neurotransmitter and stimulate the inhibitory interneuron which closes the gate for transmitting pain and temperature signals to second order neurons </li></ul><ul><li>Tactile stimulation such as stroking, massaging or kissing an affected area closes the gate and raises the pain threshold </li></ul>
    50. 62. Role of Enkephalins and Endorphins in Modulating Pain <ul><li>Enkephalins and endorphins are naturally occurring brain peptides with an opiate-like effect on pain transmission. Certain inhibitory interneurons in the dorsal horn use enkephalin as a neurotransmitter. The interneurons are activated by serotonergic fibers that descend from the reticular formation. Enkephalin causes a decrease in the EPSP produced by the first-order nociceptor via a presynaptic inhibitory action. In part, the effect is due to a decrease in the duration of the action potential in the C fiber terminal. When that occurs, less glutamate (GLU) and substance P are released from the terminal. Enkephalin also may cause a postsynaptic hyperpolarization due to a conductance-increase IPSP. </li></ul>
    51. 65. Role of Serotonin and Norepinephrine <ul><li>Reticulospinal fibers from raphe nuclei project to dorsal horn of spinal cord and release serotonin which stimulates interneurons to release enkephalin </li></ul><ul><li>Enkephalin inhibits transmission of pain and temperature signals in second order neurons </li></ul><ul><li>Reticulospinal fibers from locus coruleus also project to dorsal horn of spinal cord and release norepinephrine which inhbits pain and temperature signals by an unknown mechanism </li></ul><ul><li>Mental illnesses such as depression decrease serotonin and norepinephrine and lower pain thresholds while antidepressant drugs and therapies (e.g., exercise) which increase serotonin and norepinephrine levels raise pain thresholds </li></ul>
    52. 66. Role of Efferent Pathways in Modulating Pain <ul><li>Some individuals may, in the midst of great exertion or focused activity, fail to notice a major injury. One factor that may account for this type of modulation of nociceptive inputs is that nerve fibers arising from cortex, reticular formation, etc., can inhibit spinothalamic system neurons. For instance, corticospinal tract fibers that originate in SI cortex and which are active during voluntary movements terminate in the dorsal horn of the spinal cord. Activity in these fibers could cause inhibition of second order neurons in the spinothalamic system. </li></ul>
    53. 67. Cortex and Pain <ul><li>The cortical contribution to pain perception is not well understood. Surgical excision of SI cortex is not an effective therapy for chronic pain. However, electrolytic lesions of the thalamus can produce analgesia or hypalgesia (lost or decreased pain perception). Lesions of the ventrobasal complex may cause loss of touch and cutaneous pain; lesions of the intralaminar nuclei may cause loss of deep pain. Vascular lesions along the somatosensory pathway may cause a late-developing &quot;central pain&quot; that appears in the anesthetic limb. This type of pain is called thalamic pain. It is similar to phantom limb pain and may arise due to the loss of inhibitory control by large-diameter fibers over nociceptive neurons representing the affected limb. These data have led to the notion that pain is appreciated at a subcortical, probably thalamic, level. </li></ul>
    54. 69. Plasticity of Pain Perception <ul><li>The pain experience is complex and remarkably plastic. Drugs, fear, stress, joy, hypnosis, ritualistic participation, psychosurgery, etc., may profoundly influence it. Both the perception of pain (knowledge that tissue has been damaged) and the emotional reaction to it (the degree of suffering) can be altered. Pain is not necessarily commensurate with the extent of tissue damage. </li></ul>
    55. 70. Clinical Features of Spinothalamic Lesions <ul><li>Decrease in pain sensibility (hypalgesia or analgesia). Decrease in temperature sensibility. Increase in pain sensibility (hyperpathia or hyperalgesia). </li></ul>
    56. 71. Stress Analgesia <ul><li>Release of NE by sympathetic neurons </li></ul><ul><li>Stimulates release of Enk in spinal cord </li></ul>
    57. 72. Movement Analgesia <ul><li>Rhythmic movement releases 5-HT </li></ul><ul><li>Gum chewing </li></ul><ul><li>Locomotion </li></ul>
    58. 73. Projected Pain <ul><li>Activation of nociceptive fibers anywhere along their course is felt (projected) as a pain in the peripheral distribution of the fibers. Examples: &quot;to hit one's funny bone&quot; or pain in the leg due to pressure on a spinal nerve at its entrance to the spinal cord. </li></ul>
    59. 74. Referred Pain <ul><li>Pain arising from disease of the viscera, but felt at a relatively distant superficial site. Referred pain appears in parts of the periphery supplied by the same segment of the spinal cord as the affected organ; referred pain occurs in the associated dermatome. It probably arises due to convergence of visceral nociceptive afferents (sympathetic afferents) and skin afferents onto the same dorsal horn neurons. Hyperpathia and reflex muscle spasms may also be present. </li></ul>
    60. 75. Neuralgia <ul><li>&quot;Spontaneous&quot; pains arising in a root or nerve distribution due to relatively long-term damage (tension, pressure, crushing). An innocuous stimulus in the nerve distribution can elicit the pain, which is often severe. Examples: herpes zoster (shingles) infection, trigeminal neuralgia. </li></ul>
    61. 76. Causalgia <ul><li>&quot;Spontaneous&quot; pains arising in a nerve or root distribution following rapid, violent injury to a nerve, such as due to a bullet wound. Probably due to a disorder of sensory processing. Example: anesthesia dolorosa (tactile anesthesia with intense pain in the affected area). </li></ul>
    62. 77. Phantom Limb Pain <ul><li>Burning, shooting, or crushing pains may be experienced in the missing part following amputation. When triggered from the stump, they may be a type of neuroma pain. In other cases, a disorder of central processing is implicated. </li></ul>
    63. 78. Stress-Related “Tight” Muscle Pain <ul><li>Sympathetic neurons release NE </li></ul><ul><li>Skeletal muscle spindles stimulated </li></ul><ul><li>Increased neuronal activity in m. spindles </li></ul><ul><li>Increased tension (tone) of muscles </li></ul><ul><li>Decreased blood flow to skeletal muscles </li></ul><ul><li>Ischemia-induced pain (release of LA, BK, </li></ul><ul><li>K+, H+, etc. in skeletal muscle) </li></ul>
    64. 79. Hyperalgesia vs Allodynia <ul><li>Allodynia </li></ul><ul><li>Pain to stroking </li></ul><ul><li>stimuli </li></ul><ul><li>A-beta fiber mediated </li></ul><ul><li>Decreases with </li></ul><ul><li>ischemic block </li></ul><ul><li>Hyperalgesia </li></ul><ul><li>Pain to punctate </li></ul><ul><li>stimuli (von Frey) </li></ul><ul><li>A-delta and C-fiber mediated </li></ul><ul><li>Persists with ischemic block </li></ul>
    65. 83. Case Study #2 (Question) <ul><li>The pain this patient experienced is due to </li></ul><ul><li>Excitation of nociceptors </li></ul><ul><li>Excitation of medium- and large-diameter sensory nerve fibers </li></ul><ul><li>Excitation of small-diameter myelinated and unmyelinated sensory nerve fibers </li></ul><ul><li>Pressure on a dorsal root </li></ul><ul><li>More than one but not all of the above </li></ul>
    66. 84. Case Study #2 (Answer) <ul><li>Two of the statements are true. The pain is caused by pressure on a dorsal root. The pressure causes excitation of small-diameter GIII and GIV primary afferent fibers within the dorsal root. Their activity leads to the perception of pain and their peripheral terminals, the nociceptors themselves, are not being excited by a noxious stimulus. (Law of Projection). </li></ul>
    67. 85. Case Study #2 (Question) <ul><li>Does the patient’s localization of pain indicate the site of the injury? </li></ul><ul><li>A. No, the injury was distant from the pain </li></ul><ul><li>B. No, the injury was on the opposite side </li></ul><ul><li>B. Yes, the injury was in the vicinity </li></ul><ul><li>C. Yes, the injury was to the jaw muscle </li></ul>
    68. 86. Shortcut to ovation Spinal tract of CNV (Trigeminal Analog of STT) Spinal tract of CNV descends and crosses in medulla and cervical spinal cord
    69. 87. – Lewis Carroll , Alice’s Adventures in Wonderland <ul><li>Alice, speaking to the Cheshire Cat: </li></ul><ul><li>“ Would you tell me, please, which way I ought to go from here?” </li></ul><ul><li>“ That depends a good deal on where you want to get to,” said the Cat. </li></ul><ul><li>“ I don’t much care where,” said Alice. </li></ul><ul><li>“ Then it doesn’t matter which way you go,” said the Cat. </li></ul><ul><li>“ – so long as I get somewhere,” Alice added as an explanation. </li></ul><ul><li>“ Oh, you’re sure to do that,” said the Cat, “if you only walk long enough.” </li></ul>