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 sensationPerception of actual or threatened damage Physiological response produced by activation of specific types of nerve fibersExperienced 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)Perception based on expectations, past experience, anxiety, suggestions, cognitive factors

AcuteChronic - 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.

What is pain? Many definitions………..“ pain is whatever the experiencing person says it is, existing when he says it does” (McCaffery, 1980)“ Pain is an unpleasant sensory or emotional experience associated with actual or potential tissue damage” (International Association for the study of pain 1986)Complex warning sign. Difficult to measure as peoples perception of pain varies

Pain SourcesCutaneous Pain – sharp, bright, burning; can have a fast or slow onsetDeep Somatic Pain – stems from tendons, muscles, joints, periosteum, & b. vesselsVisceral 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 SourcesFast vs. Slow Pain –

Fast – localized; carried through A-delta axons in skinSlow – aching, throbbing, burning; carried by C fibersNociceptive 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 monthsChronic – greater than 6 months

Acute pain

Sudden onset

Temporary (disappears once stimulus is removed)

can be somatic, visceral, referred

Associated anxiety

Physiological responses to acute pain include increased RR, HR, BP and reduction in gastric motility – sympathetic response)

Chronic pain

Persistent – usually lasting more than six months

Cause unknown – may be due to neural stimulation or a decrease in endorphins

Physiological responses are less obvious especially with adaptation.

Psychological responses may include depression

Referred PainOccurs away from pain site3 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

SOMATIC VS VISCERALSomatic pain

Superficial: stimulation of receptors in skinDeep: stimulation of receptors in muscles, joints and tendons

Visceral painStimulation of receptors in internal organs, abdomen and skeletonOften poorly localised as fewer receptors located in visceraVisceral pain can be referred.

Withdrawal Reflex (Starkey, Therapeutic Modalities3rd ed. P. 30)

Pain PathwayThere are four processes in the pain pathway 1. transduction

Noxious stimuli translated into electrical activity at sensory nerve endings

2. TransmissionPropagation of impulses along spinothalamic pathway.

3. ModulationTransmission is modified

4. PerceptionAffective / motivational aspect

Each of these processes present a potential target for analgesic therapy

Transduction -Receptor activation

When cellular damage occurs, tissues release chemicals that stimulate nociceptors

Bradykinin HistamineSerotonin AcetylcholinePotassium ions Prostaglandins (PGE2, PGI2)Substance P

The activity and sensitivity of nociceptors is profoundly altered by such mediators (enhances receptor response to noxious stimuli).

Types of stimuli

Receptors respond to injury• Thermal –excessive heat or cold• Mechanical –tearing, crushing, stretching etc• Chemical

Inflammatory mediators Lactic acid ischemia

Transduction - A delta fibres and C fibres

stimuli and covert energy at the site of the stimulus into neural impulsesNociceptors are terminal endings of primary afferent fibres. These can be classed into two main types

myelinated A-delta fibres• or

non-myelinated C fibres When the threshold level of the stimulus is reached, then depolarisation occurs along these fibres in the form of action potentials

Transduction - A delta fibres and C fibres

A-Delta fibres

myelinated

fast ( first) pain -conduct at 5-35m/sec

Associated with Sharp, brief, prinking pain

Well localised

Elicited by mechanical or thermal stimuli

C- fibres

unmyelinated

Slow (second) pain – conduct at 0.5-2.0m/sec

Associated with dull,burning, aching, prolonged pain

More diffuse

Elicited mainly by chemical stimuli or persisting mechanical or thermal stimuli

TransmissionA-delta and C ( primary) fibres enter the spinal cord via the dorsal rootThey synapse with secondary neurones in the grey matter of the dorsal horn

Marginal zone ( lamina I)Substantia gelatinosa ( lamina II)Lamina V

Evidence to suggest that:A-delta fibres synapse in lamina I, II and VC-fibres in lamina I and II

Pain Transmission PathwaySome neurones ascend directly to the thalamus allowing rapid analysisThe spinothalamic tract also sends collaterals to reticular formation, hypothalamus and other limbic structures (associated more with C-fibres and slow pain)This more indirect pathway mediates arousal and emotional reactions to pain. It is also responsible for somatic and autonomic motor reflexes.

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 PainP-Q-R-S-T formatPROVOCATION – Ask how the injury occurred & what activities or the painQUALITY (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 scaleTIMING – When does it occur? At night, a.m., after activity, all the time

TerminologyNoxious – harmful, injurious

Noxious stimuli – stimuli that activate nociceptors (pressure, cold/heat extremes, chemicals)

Nociceptor - specialized receptor on n. that transmit pain impulsesNociception – impulse giving rise to sensation of painAccommodation 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, tinglingInhibition – 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 painfulPain 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, Merkel’s corpuscles

Encapsulated – end bulbs of Krause Meissner’s 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. (Meissner’s c. & Pacinian c.)

Tonic receptors produce impulses as long as the stimulus is present. (muscle spindles, free n. endings, Krause’s end bulbs)

Sensory ReceptorsMechanoreceptors – touch, light or deep pressure

Meissner’s corpuscles (light touch), Pacinian corpuscles (deep pressure), Merkel’s corpuscles (deep pressure, but more slowly than pacinian c.; hair follicle deflection)

Thermoreceptors - heat, coldKrause’s end bulbs ( temp & touch), Ruffini corpuscles (in the skin) – touch, tension, heat; (in joint capsules & ligaments – change of position)

Proprioceptors – change in length or tensionMuscle Spindles, Golgi Tendon Organs

Nociceptors – painful stimuli mechanosensitivechemosensitive

NociceptorsSensitive to repeated or prolonged stimulationMechanosensitive – excited by stress & tissue damageChemosensitive – excited by the release of chemical mediators

Bradykinin, Histamine, Prostaglandins, Arachadonic Acid

Primary Hyperalgesia – due to injurySecondary 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 NeuronsStimulated by sensory receptorsEnd in the dorsal horn of the spinal cordTypes

A-alpha – non-pain impulsesA-beta – non-pain impulses

• Large, myelinated• Low threshold mechanoreceptor; respond to light touch & low-

intensity mechanical infoA-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)

NeurotransmittersChemical substances that allow nerve impulses to move from one neuron to anotherFound in synapses

NorepinephrineSubstance P - neurotransmitter thought to be responsible for the transmission of pain-producing impulsesAcetylcholineEnkephalins2 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 NeuronsReceive 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

TypesWide 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 NeuronsTransmit impulses from the brain (corticospinal tract in the cortex) to the spinal cord (lamina)

Periaquaductal Gray Area (PGA) – release enkephalinsNucleus 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 ScalesVisual Analog ScaleNone Severe 0 10Locate area of pain on a pictureMcGill 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 TheoriesWhere have we been?

Where are we now?

Where have we been?Specificity Theory

4 types of sensory receptors – heat, cold, touch, painA nerve responded to only one typeNerve was continuous from the periphery to the brain

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

Gate Control TheoryMelzack & Wall, 1965 – the basis for theories todayNon-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 TheorySubstantia Gelatinosa (SG) in dorsal horn of spinal cord acts as a ‘gate’ – only allows one type of impulses to connect with the SONTransmission 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 neuronsIf 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 PainMelzack & 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

Pain

Heat, Cold, Mechanical

Gate (T cells/ SG)

Level II – Central Biasing Theory

Descending neurons are activated by: stimulation of A-delta & C neurons, cognitive processes, anxiety, depression, previous experiences, expectationsCause release of enkephalins (PAG) and serotonin (NRM)Enkephalin interneuron in area of the SG blocks A-delta & C neuronsExamples: brief, intense TENS, acupressure

Level III – Endogenous Opiates Theory

Least understood of all the theoriesStimulation 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)

The Pathway of PainIrritation 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.