1. Neuroanatomy/Pain Review

2. Anatomy Cell body (in ganglion) nucleus Dendrites Dendrite Body axon
Synapse

3. Anatomy Cont. Axons (actual nerve fibers)
peripheral nervous system: may be covered by myelin sheath (schwann cell) which allows for regrowth
CNS: oligodendrocytes are the “myelin” but it doesn't allow for regrowth

4. Anatomy 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.

5. Nerve Types Afferent; sensory nerves (ascending tracts)
AA 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 pain
See Prentice Table 1-2 for Classes of Afferent Neurons
Note: First pain is from Adelts (faster), second pain is C

6. Nerve Types Cont. Efferent Nerves: motor nerves (descending tracts)
Gamma: motor neuron
Ascending and descending tracts:
myelination increases conduction velocity
Diameter increases conduction velocity (less resistance)

7. Nerve Types:
Afferent Nerves
CNS
A Beta
Adelta C

8. Physiology
Excitable Tissue: only nerves and muscles are excitable tissue due to the fact only they have a resting membrane potential

9. Physiology 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 mV
semipermeable membrane which is impermeable to Sodium at rest

10. Physiology Cont.
Sodium Potassium pump keeps the potential by pump in K+ in and Na+ out
Na+ want in the cell but if it gets in an action potential is formed
to +30 mV (a 100 mV difference)
hormone , chemical, electrical, thermal or mechanical factors may create action potentials
As athletic trainers we try and change this status and create an action potential

11. Threshold
The minimum amount of stimulus necessary to create an action potential
Polar: refers to negative
depolarize: less negative
repolarize: becoming negative
hyperpolarize: more negative

12. Physiology Cont.
All or none theory: If stimulus meets the threshold, action potential will always go to +30mV, even if supra-threshold stimulus is given

13. Physiology 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 produced
Absolute refractory period: NO stimulus will create a response no matter how strong
Relative refractory period: resting potential is much lower, therefore a higher stimulus is needed

14. How is this class affecting your pain receptors?

15. Pain
The 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 are
Acute
Chronic
Referred

16. Acute Pain
First 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)

17. Acute Pain Treatment Goal block the pain through: inhibition
blocking A fibers (Gate Control)

18. Chronic 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

19. Chronic Pain Goals in treating unlearn the Pain
Acute pain control techniques are usually ineffective
Exercise my affect pain by distraction
Important to have guidance under a physician

20. Referred Pain (projected pain)
Felt at other site than injured area
Dermatome (skin represented by nerve root)
Myotome (muscle innovated by nerve root)
Sclerotome (bones innovated by nerve root)

21. Pain 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
& Cortex
Thalamus and Cortex
location and discrimination
Pain Transmitted to
Higher Brain Centers
Descending Control Mech.
Activated here once noxious
stimuli reaches higher centers
of brain. Incoming stimuli can
be inhibited at various levels
and endoginous opiates released
Retinacular Formation &
Periaquductal Gray (PAG)
Motor, sensory and autonomic Response
Discrimination and Location of
pain occurs during this sequence

22. Pain theories
Specificity Theory
Pattern Theory
Gate Control Theory

23. Specificity 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.

24. Pattern 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.

25. Gate 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.

26. Blocking entry of c-delta Fibers
Gate Control Theory
First 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 stimulus
Brain/Pain centers
A-beta
non-painful
stimulus
Blocking entry of c-delta Fibers
C delta
noxious stimulus

27. Gate 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 afferent
Works 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

28. Gate Control In Dorsal Horn of Spinal Cord Brain . A-Beta
Sensory, Proprioception, Etc T SG
Inhibitory Synapse
A-Delta, C Fibers
Pain Transmission
Facilitator Synapse

29. The 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-cell
If the S.G. is relatively inactive the “gate” is open
the balance of activity in the large and small diameter sensory neurons determines the position of the “gate”

30. Gate Control Theory
Large 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

31. Gate 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

32. Gate Control Theory
When 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.

33. Gate Control Theory
The 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

34. Pain modulation: Levels Theory of Pain Control
Spinal Levels of Pain Control
Gate Control Theory
Central Biasing (hyperstimulation analgesia)
Endogenous Opiate (Pituitary level)

35. Level 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 closed
If accommodation occurs (electrical stimulus) the gate is then open and pain returns

36. Level 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 pain
Impulses from higher centers act to close the gate and block transmission of the pain message at the dorsal horn synapse
Transmission of sensory
input ot higher
brain centers
Transmission
Cell
Central
Control + - + -
Substantia
gelitinosa + -
A-beta fiber
Afferents
A-Delta & C
fiber afferents

37. Level 3: -Endorphin modulation Endogenous Opiate
Opiate like substance made by the body
Norepinephrine
Seratonin
These opiates inhibit the depolarization of second order nociceptive nerve fibers (thus no pain)
Found in substantia gelatinosa - activated in tract
Causes degeneration of prostaglandin and dorsal horn inhibition

38. The purpose of knowing all the pain control theories is to use modalities to assess these pain theories and decrease the athlete/patient’s pain