PAIN CONTROL THEORIES

Managing Pain

What is Pain?
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 Perception of actual or threatened damage 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 bodys defense mechanism (warns the brain that tissues may be in jeopardy) Perception based on expectations, past experience, anxiety, suggestions, cognitive factors
Acute 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.

Pain Sources
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 @ 1st & later may be localized (i.e. appendicitis) Psychogenic Pain individual feels pain but cause is emotional rather than physical

Pain Sources
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

Acute less than 6 months Chronic greater than 6 months

Referred Pain
Occurs away from pain site 3 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

Dermatomic pain irritate A-delta fiber; sharp, well-localized pain

Withdrawal Reflex

(Starkey, Therapeutic Modalities3rd ed. P. 30)

Goals in Managing Pain

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

Other ways to control pain

Encourage central biasing motivation, relaxation, positive thinking Minimize tissue damage Maintain communication w/ the athlete If possible, allow exercise Medications

Questions to Ask about Pain

P-Q-R-S-T format PROVOCATION Ask how the injury occurred & what activities or the pain QUALITY (characteristics of pain) Is it aching pain (impingement), burning pain (n. irritation), sharp pain (acute injury), radiating within dermatome (pressure on n.)? REFERRAL/RADIATION
Referred site distant to damaged tissue that does not follow the course of a peripheral n. Radiating follows peripheral n.; diffuse

SEVERITY how bad is it? Pain scale TIMING When does it occur? At night, a.m., after activity, all the time

Terminology
Noxious harmful, injurious
Noxious stimuli stimuli that activate nociceptors (pressure, cold/heat extremes, chemicals)

Nociceptor - specialized receptor on n. that transmit pain impulses Nociception impulse giving rise to sensation of pain Accommodation phenomenon adaptation by the sensory receptors to various
stimuli over an extended period of time (e.g. superficial hot & cold agents). Less sensitive to stimuli. Hyperesthesia abnormal acuteness of sensitivity to touch, pain, or other sensory stimuli Paresthesia abnormal sensation, such as burning, pricking, tingling Inhibition depression or arrest of a function Inhibitor an agent that restrains/retards physiologic, chemical, or enzymatic action Analgesic a neurologic or pharmacologic state in which painful stimuli are so moderated that, though still perceived, they are no longer painful Pain Threshold level of noxious stimulus required to alert an individual for possible tissue damage

Sensory Receptors
A n. ending is the termination of a n. fiber in a peripheral structure. (Prentice, p. 37) N. endings may be sensory (receptor) or motor (effector). Sensory endings may be:
Capsulated free n. endings, Merkels corpuscles Encapsulated end bulbs of Krause Meissners corpuscles

Sensory Receptors
Some sensory receptors respond to phasic activity & produce an impulse when the stimulus is or , but not during sustained stimulus. They adapt to a constant stimulus. (Meissners c. & Pacinian c.) Tonic receptors produce impulses as long as the stimulus is present. (muscle spindles, free n. endings, Krauses end bulbs)

Sensory Receptors
Mechanoreceptors touch, light or deep pressure
Meissners corpuscles (light touch), Pacinian corpuscles (deep pressure), Merkels corpuscles (deep pressure, but more slowly than pacinian c.; hair follicle deflection)

Thermoreceptors - heat, cold

Krauses end bulbs ( temp & touch), Ruffini corpuscles (in the skin) touch, tension, heat; (in joint capsules & ligaments change of position)

Proprioceptors change in length or tension

Muscle Spindles, Golgi Tendon Organs

Nociceptors painful stimuli

mechanosensitive chemosensitive

Nociceptors
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

Types of Nerves
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

First Order Neurons

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 & lowintensity 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, NCV - .5-2m/sec Delayed onset, diffuse nagging sensation (aching, throbbing)

Neurotransmitters
Chemical substances that allow nerve impulses to move from one neuron to another Found in synapses
Norepinephrine Substance P - neurotransmitter thought to be responsible for the transmission of pain-producing impulses Acetylcholine Enkephalins 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

Second Order Neurons

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

Third Order Neurons

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

Descending Neurons
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 (substances released by the body that reduce
the perception of pain by binding to pain receptor sites)

Pain Scales
Visual Analog Scale None Severe 0 10 Locate area of pain on a picture McGill pain questionnaire
Evaluate sensory, evaluative, & affective components of pain
20 subcategories, 78 words

Pain Threshold level of noxious stim. required to alert an individual of a potential threat to tissue

Pain Tolerance amount of pain a person is willing or able to tolerate Referred Pain - Mix-up in spinal cord in the transmission of pain impulses

Pain Control Theories

Where have we been? Where are we now?

Where have we been?

Specificity Theory
4 types of sensory receptors heat, cold, touch, pain A nerve responded to only one type Nerve was continuous from the periphery to the brain

Pattern Theory
A single nerve responded to each type of sensation by creating a code (i.e. different telephone rings)

Gate Control Theory

Melzack & Wall, 1965 the basis for theories today Non-painful stimulus can block the transmission of a painful stimulus

Where are we now?

Level I Gate Control Theory Level II Central Biasing Theory Level III Endogenous Opiates Theory

Level I Gate Control Theory

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
This can be overridden by Level II

Gate Control Theory of Pain

Melzack & Wall, 1965 The gate is 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 1st inhibit pain impulses (acupuncture/pressure, cold, heat, chem. skin irritation). Brain

Gate (T
cells/ SG)

Pain Heat, Cold, Mechanical

Level II Central Biasing Theory

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 Examples: brief, intense TENS, acupressure

Level III Endogenous Opiates Theory

Least understood of all the theories Stimulation of A-delta & C fibers causes release of Bendorphins 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)

The Pathway of Pain

Irritation on n. endings result in the depolarization of pain fibers. All noxious impulses are transmitted via afferent pathways to the
thalamus.

Pain response is initiated by stimulation of nociceptors. Mechanical stress excites mechanosensitive nociceptors Chemicals bradykinin, serotonin, histamine, prostaglandins excite chemosensitive nociceptors

The initiation of the pain process always begins with chemical stimulus.