2.  describe the multidimensional nature of pain,  explain the role of pain in preserving health and well-being,  discuss how the pain response can assist in evaluating an injured person,  describe how pain is sensed and how the “pain message” is transmitted to the central nervous system, and  discuss contemporary theories on modulating the pain message in the central nervous system.

3.  “An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage” – The International Association for the Study of Pain  Subjective sensation  Pain Perceptions – based on expectations, past experience, anxiety, suggestions ◦ Affective – one’s emotional factors that can affect pain experience ◦ Behavioral – how one expresses or controls pain ◦ Cognitive – one’s beliefs (attitudes) about pain  Physiological response produced by activation of specific types of nerve fibers  Experienced because of nociceptors being sensitive to extreme mechanical, thermal, & chemical energy.  Composed of a variety of discomforts  One of the body’s defense mechanism (warns the brain that tissues may be in jeopardy)  Acute vs. Chronic – ◦ The total person must be considered. It may be worse at night when the person is alone. They are more aware of the pain because of no external diversions.

4.  Cutaneous Pain – sharp, bright, burning; can have a fast or slow onset  Deep Somatic Pain – stems from tendons, muscles, joints, periosteum, & b. 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

5.  Fast vs. Slow Pain – ◦ Fast – localized; carried through A-delta axons in skin ◦ Slow – aching, throbbing, burning; carried by C fibers ◦ Nociceptive neuron transmits pain info to spinal cord via unmyelinated C fibers & myelinated A- delta fibers.  The smaller C fibers carry impulses @ rate of 0.5 to 2.0 m/sec.  The larger A-delta fibers carry impulses @ rate of 5 to 30 m/sec.  Acute vs. Chronic

6.  Types of Nerves  Neurotransmitters

7.  Afferent (Ascending) – transmit impulses from the periphery to the brain ◦ First Order neuron ◦ Second Order neuron ◦ Third Order neuron  Efferent (Descending) – transmit impulses from the brain to the periphery

8.  Stimulated by sensory receptors  End in the dorsal horn of the spinal cord  Types ◦ A-alpha – non-pain impulses ◦ A-beta – non-pain impulses  Large, myelinated  Low threshold mechanoreceptor; respond to light touch & low-intensity mechanical info ◦ A-delta – pain impulses due to mechanical pressure  Large diameter, thinly myelinated  Short duration, sharp, fast, bright, localized sensation (prickling, stinging, burning) ◦ C – pain impulses due to chemicals or mechanical  Small diameter, unmyelinated  Delayed onset, diffuse nagging sensation (aching, throbbing)

9.  Receive impulses from the FON in the dorsal horn ◦ Lamina II, Substantia Gelatinosa (SG) - determines the input sent to T cells from peripheral nerve  T Cells (transmission cells): transmission cell that connects sensory n. to CNS; neurons that organize stimulus input & transmit stimulus to the brain ◦ Travel along the spinothalmic tract ◦ Pass through Reticular Formation  Types ◦ Wide range specific  Receive impulses from A-beta, A-delta, & C ◦ Nociceptive specific  Receive impulses from A-delta & C  Ends in thalamus

10.  Begins in thalamus  Ends in specific brain centers (cerebral cortex) ◦ Perceive location, quality, intensity ◦ Allows to feel pain, integrate past experiences & emotions and determine reaction to stimulus

11.  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  Stimulation of the PGA in the midbrain & NRM in the pons & medulla causes analgesia.  Endogenous opioid peptides - endorphins & enkephalins

12.  Chemical substances that allow nerve impulses to move from one neuron to another  Found in synapses ◦ Substance P - thought to be responsible for the transmission of pain-producing impulses ◦ Acetylcholine – responsible for transmitting motor nerve impulses ◦ Enkephalins – reduces pain perception by bonding to pain receptor sites ◦ Norepinephrine – causes vasoconstriction ◦ 2 types of chemical neurotransmitters that mediate pain  Endorphins - morphine-like neurohormone; thought to  pain threshold by binding to receptor sites  Serotonin - substance that causes local vasodilation &  permeability of capillaries  Both are generated by noxious stimuli, which activate the inhibition of pain transmission  Can be either excitatory or inhibitory

13.  Nociceptive - normal nerves transmit info to CNS about trauma to tissues  Neuropathic - disease/ degeneration of NS

14. Nociceptors = specialized terminal peripheral branches of sensory nerve fibers that are sensitive to noxious stimuli

15.  Sensitive to repeated or prolonged stimulation  Mechanosensitive – excited by stress & tissue damage  Chemosensitive – excited by the release of chemical mediators ◦ Bradykinin, Histamine, Prostaglandins, Arachadonic Acid  Primary Hyperalgesia – due to injury  Secondary Hyperalgesia – due to spreading of chemical mediators

16.  A delta fibers - sharp, immediate pain  C fibers - small, unmyelinated, transmit prolonged, burning pain

17.  A  (small myelinated) fibres ◦ 2-5  m diameter ◦ conduct at 12-30 m/sec ◦ cause sharp, localised sensation  C (unmyelinated) fibres ◦ 0.4-1.2  m diameter ◦ conduct at 0.5-2 m/sec ◦ cause dull, diffuse feeling Activated byActivated by –low pH, heat (via TRPV 1 etc) –local chemical mediators (eg bradykinin, histamine, prostaglandins)

18.  Occurs in about 0.1 seconds  Subjective description; sharp, acute, electric or prinking  A  fibers synapse on cells in lamina I (lamina marginalis) in the dorsal horns  Secondary neurons cross and travel through the anterolateral pathway to ventral complex of the thalamus  Tertiary neurons go to the primary sensory cortex

19. I II III IV V VI IX VII VIII SUBSTANTIA GELITANOSA LAMINA MARGINALIS VENTROBASAL NUCLEUS ANTEROLATERAL PATHWAY

20.  Occurs after a second or more  Often associated with tissue destruction  Subjectively described as burning, aching, throbbing, nauseous or chronic  C fibers synapse in the synapse substatnia gelitanosa  Final projection is the frontal cortex

21. I II III IV V VI IX VII VIII SUBSTANTIA GELITANOSA LAMINA MARGINALIS VENTROBASAL NUCLEUS ANTEROLATERAL PATHWAY

23.  Fast pain is generally mechanical or thermal  Slow pain can be all three  Chemical pain receptors; bradykinin, serotonin, histamine, potassium ions, acids, acetylcholine and proteolytic enzymes.  Prostaglandins enhance pain perception

24.  Respond best to one but some to all ◦ Thermal ◦ Mechanical ◦ Chemical  NTs: glutamate and Substance P  Capsaicin causes release of Sub P from nociceptor axons  Large amounts of capsaicin cause analgesia due to depletion of sub P from synapses

25.  Aspirin suppresses synthesis of prostaglandins

26.  Nociceptive fibres synapse in the dorsal horn  Projection neurones cross the midline and travel in the antero-lateral spinothalamic tract ◦ some to the thalamus & cortex  fine localization of sharp pain ◦ some to the reticular formation  diffuse, chronic pain

27.  DRGN enters dorsal horn at each spinal cord level  Ascend/descend in Lissaur’s tract  Synapse in Substantia Gelatinosa  Decussate in ventral spinal cord  Ascend ventrally in spinal cord as the Spinothalamic Tract  Synapse in thalamus (Ventral Posterior and intralaminar Nuclei)  Thalamic axons travel to S1 somatosensory cortex and synapse in layer 4.

28. Thalamus Cortex Gracile/cuneate nucleus A/A/ Reticular formation A  /C

29.  Gate control theory ( by Melzack & Wall, 1965 ) ◦ activity in Aa/b fibres inhibits transmission from nociceptive fibres to spinothalamic neurones ◦ Substantia Gelatinosa (SG) in dorsal horn of spinal cord acts as a ‘gate ’ Brain Pain Heat, Cold, Mechanical Gate ( T cells/ SG)

30. Thalamus Cortex Gracile/cuneate nucleus A/A/ Reticular formation A  /C

31.  Descending controls ◦ stimulation of periaqueductal grey and nucleus raphe magnus inhibit nociceptive transmission ◦ Stimulation of A-delta & C fibers causes release of B-endorphins from the PAG ◦ Mechanism of action – similar to enkephalins to block ascending nerve impulses

32. Thalamus Cortex Gracile/cuneate nucleus A/A/ Reticular formation A  /c PAG

34.  Increased sensitivity to pain after tissue injury  Damaged tissue also releases molecules sa bradykinin that gate other channels/bind receptors  Secretion of substances, substance P, bradykinin, prostaglandin that cause inflammation  Can cause long lasting intracellular changes that increased sensitivity of nociceptive ion channels

36.  Occurs away from pain site  Types of referred pain: ◦ Myofascial Pain – trigger points, small hyperirritable areas within a m. in which n. impulses bombard CNS & are expressed at referred pain  Active – hyperirritable; causes obvious complaint  Latent – dormant; produces no pain except loss of ROM ◦ Sclerotomic & Dermatomic Pain – deep pain; may originate from sclerotomic, myotomic, or dermatomic n. irritation/injury  Sclerotome: area of bone/fascia that is supplied by a single n. root  Myotome: m. supplied by a single n. root  Dermatome: area of skin supplied by a single n. root

37.  Due to mixing of nociceptive axons from viscera with those from skin at the level of spinal cord.  Perception of visceral information as coming from skin areas

38. Angina: low oxygen in heart is perceived as chest and arm pain

39.  Gate Control Theory  Central Biasing Theory  Endogenous Opiates Theory

40.  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  Transmission Cell (T-cell) – distal end of 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

41.  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)

42.  Descending neurons are activated by: stimulation of A-delta & C neurons, cognitive processes, anxiety, depression, previous experiences, expectations  Cause release of enkephalins (PAG) and serotonin (NRM)  Enkephalin interneuron in area of the SG blocks A- delta & C neurons

43.  Least understood of all the theories  Stimulation of A-delta & C fibers causes release of B-endorphins from the PAG & NRM Or  ACTH/B-lipotropin is released from the anterior pituitary in response to pain – broken down into B-endorphins and corticosteroids  Mechanism of action – similar to enkephalins to block ascending nerve impulses  Examples: TENS (low freq. & long pulse duration)

44. ◦ Peripheral pain modulation  Targets desensitization of peripheral nociceptors  Cryotherapy lessens the effects of chemical mediators and slows conduction velocity of sensory input ◦ Spinal level pain modulation  Gate control theory is proposed mechanism  Can be evoked using “counterstimulation” techniques

45. ◦ Noxious pain modulation  Elicits pain in affected region to achieve desired analgesic affect  Possibly evokes descending pain modulation ◦ Nerve block pain modulation  Application of medium-frequency currents creates an action potential failure—Wedenski’s inhibition Wedenski’s inhibition ; damping of muscle response resulting from application of a series of rapidly repeated stimuli to the motor nerve where less frequent stimulation produces muscle response  Used briefly for superficial areas

46. ◦ Suprapinal and descending pain modulation  Involves reticular formation—PAG, Raphe nucleus, and enkephalin  Serotonin released by stimulation of Raphe nucleus activates inhibitory interneurons that block pain transmission  Hypothalamus and pituitary also stimulated by pain impulses and release precursors to analgesic and anti-inflammatory agents  ◦ Motor stimulation—electroacupuncture  Goal is to enhance endorphin production through pulsed, rhythmic, low-frequency stimulation  Low-frequency stimulation of trigger and acupuncture points also valuable

47.  Reduce pain!  Control acute pain!  Protect the patient from further injury while encouraging progressive exercise

48. Inhibition of pain transmission Higher brain center Large diameter afferents Cutaneous receptors jt. Receptors, muscle receptor TENS Massage Manipulation Thermal Traction Compression, etc Therapist

49. ◦ Pain can be characterized as acute, persistent, or chronic. These types of pain differ in purpose and treatment. ◦ The physical therapist should understand the contemporary pain theories that form the basis for the analgesic response to therapeutic modalities.

50.  Compare and contrast the fast pain and slow pain.  In your own words, describe the gate control theory of pain control.