2Anatomy Cell body (in ganglion) nucleus Dendrites Dendrite Body axon Synapse
3Anatomy Cont. Axons (actual nerve fibers) peripheral nervous system: may be covered by myelin sheath (schwann cell) which allows for regrowthCNS: oligodendrocytes are the “myelin” but it doesn't allow for regrowth
4Anatomy Cont.Nodes of Ranier: breaks in myelin. Action potentials jump from node to node (salutatory condition) myelin acts as resistance and insulation and thus needs nodes for function.
5Nerve Types Afferent; sensory nerves (ascending tracts) AA Beta): sensory, large diameter with myelin (Fastest)A delta: pain fibers, smaller with less myelin (4-30m/s)C: pain, smallest, non myelinated (.5-2m/s) dull slow painSee Prentice Table 1-2 for Classes of Afferent NeuronsNote: First pain is from Adelts (faster), second pain is C
6Nerve Types Cont. Efferent Nerves: motor nerves (descending tracts) Gamma: motor neuronAscending and descending tracts:myelination increases conduction velocityDiameter increases conduction velocity (less resistance)
8PhysiologyExcitable Tissue: only nerves and muscles are excitable tissue due to the fact only they have a resting membrane potential
9Physiology Cont.Resting membrane Potential: a chemical and electrical balance with a pump to aid in return to homeostasis.at rest membrane in -70 mV to -90 mVsemipermeable membrane which is impermeable to Sodium at rest
10Physiology Cont.Sodium Potassium pump keeps the potential by pump in K+ in and Na+ outNa+ want in the cell but if it gets in an action potential is formedto +30 mV (a 100 mV difference)hormone , chemical, electrical, thermal or mechanical factors may create action potentialsAs athletic trainers we try and change this status and create an action potential
11ThresholdThe minimum amount of stimulus necessary to create an action potentialPolar: refers to negativedepolarize: less negativerepolarize: becoming negativehyperpolarize: more negative
12Physiology Cont.All or none theory: If stimulus meets the threshold, action potential will always go to +30mV, even if supra-threshold stimulus is given
13Physiology Cont.Refractory period: membrane potential goes below the resting potential of -70mV and may not be stimulated for a given period of time. This limits how many action potentials may be producedAbsolute refractory period: NO stimulus will create a response no matter how strongRelative refractory period: resting potential is much lower, therefore a higher stimulus is needed
14How is this class affecting your pain receptors?
15PainThe purpose of pain is as a protective mechanism. Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage:The types of pain areAcuteChronicReferred
16Acute PainFirst pain: carried in A-delta fires: larger diameter fibers contain myelin, reflex to get off source, goes to cognitive level (more discrete - very localized)Second Pain: carried in C fibers. Smaller diameter, non myelinated, slower. (less discrete - more diffuse)
17Acute Pain Treatment Goal block the pain through: inhibition blocking A fibers (Gate Control)
18Chronic Pain:Any pain which lasts for six months or more (in athletes we may consider chronic pain to be pain which is continue from months but is not in proportion to tissue injury or activity... i.e... chronic tendinitis may be long lasting but have organic root)No real purpose (?)numerous by-passes. Also goes to limbic system (emotional control)- learned response
19Chronic Pain Goals in treating unlearn the Pain Acute pain control techniques are usually ineffectiveExercise my affect pain by distractionImportant to have guidance under a physician
20Referred Pain (projected pain) Felt at other site than injured areaDermatome (skin represented by nerve root)Myotome (muscle innovated by nerve root)Sclerotome (bones innovated by nerve root)
21Pain Transmission A-Beta C-Delta Doral Horn Acute Pain Acute Pain Noxious Stimulus travel Via A-Delta and C-delta Fibers to Dorsal Horn (spinal Cord)STT (Spinal thalamic Tract)Limbic System& CortexThalamus and Cortexlocation and discriminationPain Transmitted toHigher Brain CentersDescending Control Mech.Activated here once noxiousstimuli reaches higher centersof brain. Incoming stimuli canbe inhibited at various levelsand endoginous opiates releasedRetinacular Formation &Periaquductal Gray (PAG)Motor, sensory and autonomic ResponseDiscrimination and Location ofpain occurs during this sequence
22Pain theoriesSpecificity TheoryPattern TheoryGate Control Theory
23Specificity theory: specific stimulus has a specific receptor which goes to a location in the brain The specific location identifies the pain’s quality. Thus any noxious stimulus applied to the surface of the skin results in a pain sensation. The evaluation of the type of pain occurs in the brain.
24Pattern Theory: a pattern or coding of sensory information is created by different sensations. This theory is faulty due to the number of different types of receptors proven to exist.
25Gate Control Theory (1965)Melzack and Wall originally described a neurophsiologic mechanism which involved the concept of peripheral and central “gating”. The gate theory utilizes the specificity theory and the pattern theory and added the interaction of peripheral afferents with a modulation system in the spinal cord gray matter. Additionally Melzack and Wall believed there also exists a descending modulation system.
26Blocking entry of c-delta Fibers Gate Control TheoryFirst Order neurons: the theory focuses on the first order neurons (primary afferents): the A-beta (large diameter sensory neurons) and A-delta and C neurons (both small diameter sensory neurons).A non-painful stimulus can block the transmission of a noxious stimulusBrain/Pain centersA-betanon-painfulstimulusBlocking entry of c-delta FibersC deltanoxious stimulus
27Gate Control Theory Cont. The second order neuron, the T-cell and the substantia gelatinosa (Rexed’s laminae II and II of the dorsal horn of the spinal gray matter) can exert affects on the primary afferentWorks on the premise that the SG (located in dorsal horn) modulates afferent nerve impulses and influence transmission of T cells. This activates a central controlling mechanism
28Gate Control In Dorsal Horn of Spinal Cord Brain . A-Beta Sensory, Proprioception, EtcTSGInhibitory SynapseA-Delta, C FibersPain TransmissionFacilitator Synapse
29The second order neuron When the substantia gelatinosa is active the “gate” is closed and there is a decrease in the amount of sensory input to the T-cellIf the S.G. is relatively inactive the “gate” is openthe balance of activity in the large and small diameter sensory neurons determines the position of the “gate”
30Gate Control TheoryLarge diameter afferents cause an initial increase in the T-cells followed by a reduction of activity. The initial increase is due to direct activation of the second-order neuron by primary afferents. The reduction is an indirect result due to large-diameter afferents also activating the s.g. cells which causes the gate to close
31Gate Control Theory Cont. Small diameter afferents increase T-cell activity by these primary afferents also activate inhibitory interneurons that reduce activity in the s.g which open the gate
32Gate Control TheoryWhen the balance of small to large diameter sensory neuronal input is no longer maintained and reaches a critical value the second-order neurons are activated. This activation is of the ascending system and leads to the perception of pain and the subsequent behavioral responses.
33Gate Control TheoryThe Descending control system in which emotion and past experience evoke descending input, impinging upon the gating mechanism to block pain sensation at the spinal level.PAIN is an excellent “bible” for those working clinically with pain control
34Pain modulation: Levels Theory of Pain Control Spinal Levels of Pain ControlGate Control TheoryCentral Biasing (hyperstimulation analgesia)Endogenous Opiate (Pituitary level)
35Level I: Presynaptic inhibition Gate Control Theory The concept that when several sensory stimuli reach the spinal cord at the same location and time. one of them becomes dominant.As long as the stimulation is causing firing of the sensory nerve, the gate to pain should be closedIf accommodation occurs (electrical stimulus) the gate is then open and pain returns
36Level 2: Descending inhibition Central Biasing A theory of pain modulation where higher centers such as the cerebral cortex influence the perception of and response to painImpulses from higher centers act to close the gate and block transmission of the pain message at the dorsal horn synapseTransmission of sensoryinput ot higherbrain centersTransmissionCellCentralControl+-+-Substantiagelitinosa+-A-beta fiberAfferentsA-Delta & Cfiber afferents
37Level 3: -Endorphin modulation Endogenous Opiate Opiate like substance made by the bodyNorepinephrineSeratoninThese opiates inhibit the depolarization of second order nociceptive nerve fibers (thus no pain)Found in substantia gelatinosa - activated in tractCauses degeneration of prostaglandin and dorsal horn inhibition
38The purpose of knowing all the pain control theories is to use modalities to assess these pain theories and decrease the athlete/patient’s pain