Chapter 4

Pain and Pain Relief

What is Pain?

An unpleasant sensory & emotional experience associated with actual or potential tissue damage.

Why is dealing with pain so tough?

1. Modalities are directed to relieve pain2. Knowledge of pain improves the ability to

evaluate the injured athlete, empathize with & understand the response to injury & pain.

3. Understand that all pain experiences are not related to acute inflammatory responses & that chronic and persistent pain are significant challenges.

4. We are called to provide scientific basis & outcomes data for treatments.

Pain is Multidimensional

Intensity dimensionMotivational: Affective dimension – feelings and

emotions

Mediators of the response to injury and pain

1. Past experience2. Family experience3. Culture4. Expectations5. Context in which injury occurs or

pain is experienced

Pain as a warning or symptom vs. pain as a disease entity

1. Acute Pain: protection from injury or a signal that something is wrong

2. Acute Pain is of sudden onset and results in muscle spasm & guarding. This corresponds to the events of the acute inflammatory response (usually resolves in <6 wks)

Persistent Pain

Lingering or recurrent painSymptom of a treatable conditionSeveral causative factors

1. Rest-reinjury cycle2. Inaccurate or incomplete diagnosis &

eval3. Myofascial pain

Stress, posture, length-tension imbalance, trauma, somatization

Chronic Pain

Pain lasting beyond usefulnessNo identifiable or treatable causeDisease entity unto itself

1. RSD2. Rheumatic diseases3. Intractable back pain4. Intractable phantom limb pain

Chronic vs. Persistent Pain

Chronic Defy intervention What affect does

it have on the quality of life?

Persistent Pain Generally

tolerable once all contributing factors are identified and addressed.

Individual’s response to persistent/chronic pain

Anger and frustration with their situation and the inability of the health care system to help themErosion of family and social life and supportLoss of identity and self esteemDecreased quality of life

Pain & Patient Evaluation

What can injured physically active people tell us about their pain experience that can aid in the evaluation?

Here is a formula to try!

P = Provocation: sudden onset or insidiousQ = Quality: aching/burning/sharp/dullR = Region: where? Radiating-dermatome referred pain S = Severity: pain scale 0 = no pain; 10 = cut my arm offT = Timing: when did it begin, is there a

particular time of day it is worse, present when you wake up, increase with activity?

Physiology of Sensation – Sensory Receptors

SuperficialMeissner’s

corpuscles Pacinian corpuscles

Found in the hair follicles – easily stimulated

Ruffini corpusclesskin pressure

DeepGolgi Tendon

OrgansMuscle spindles

changes in muscle length and tension

1. Mechanoreceptors-touch & pressure

Sensory Receptors cont.

2. Thermoreceptors

Response to temperature change:

Issues with COLDWARMHOT

3. NociceptorsFree nerve endings

Stimulated by:*mechanical stress*thermal stress*chemical stress*acute inflam. response

Neural Transmission1st order afferent neurons (Primary) transmit impulses from sensory receptors to higher order centers.

-Amount of myelination determines rate of conductivity

-Type AI,II,III deal with proprioception, kinesthesia, & pain due to deep-tissue damage

-Type A-beta are found in the skin -Type A-delta: temperature, pressure,

noxious mech. -Type C – unmyelinated:slow conduction

Neural Transmission-Ascending Spinal Pathways

2nd Order AfferentsSensory transmission to the brainPathways of the Ventral Spinal Cord

Spinothalamic tract Spinoreticular tract Spinoencephalic tract

Nociceptive-specific second-order afferents

3rd & 4th Order Afferents

3rd – connect input from reticular formation to the thalamus4th – transmission between centers within the cerebral cortexInterneurons – connection between afferent and efferent neurons and play a role in pain modulation

Transmitter Substances

1. Neurotransmitters – acetylcholine2. Biogenic amine transmitters –

1. Serotonin2. Norepinepherine

3. Neuroactive peptides1. Substance P- facilitate synaptic trans. in

nociceptive pathways2. Enkephalins & Beta-endorphins (opioid

peptides) – inhibit transmission of pain impulses

Key Concept!

Synaptic transmission will occur only if the net effect of the transmitter substances acting on the synapse is facilitory. MOST transmitter substances act to inhibit, rather than facilitate, synaptic transmission. CONTEMPORARY PAIN CONTROL THEORY hinges on the notion that many therapeutic interventions inhibit the transmission of the pain message through activation of inhibitory transmitter substances.

Higher Centers in the Nociceptive System

1. Reticular formation of the medulla & ponsSensory discrimination & motivation

(affective)2. Mesencephalon (PAG)

Sensory discrimination & motivation (afective)3. Thalamus

Somatosensory cortexLimbic System – emotions, autonomic

responses, and endocrine responses to injury and pain. Allows memory and senses to regulate responses

Gate Control Theory of Pain

A theory that proposes that pain sensation could be altered by blocking or gating impulses in the pain pathways.States that the large, myelinated afferent fibers such as Type IA, IIA, and A-beta can block transmission of noxious stimuli at dorsal horn, thereby prevent input reaching the brain.Birth of TENS

TENS

How does it work? – depolarize afferent fibers, thereby allowing for the blockage of the transmission.A-beta fibers high input rate via low-intensity stimulation, an analgesic effect is produced.

Castel’s Model of Pain Control

Level I: Endogenous opioids1. Release of enkephalin interneurons;

inhibition of substance P; prohibits synaptic transmission; blocks pain at 1st synapse of nociceptive pathway; therefore, similar to GATE Theory, pain is modulated at the dorsal horn.

Level II Level III

Analgesia through brief intense stim.PAG raphe nucleus release serotonin depolar. enkephalin interneurons: block substance P = PAIN

Analgesia through prolonged intense stimulusBeta-endorphin (lg. peptide similar to morphine) stimulates raphe nucleus enkephalin interneuron analgesia at segmental level system

Descending Influence Beta-Endorphin Mediated

What about Cold & US?

COLD: slows nerve conduction in 1st order

afferents of nociceptive pathways This theory based on a DECREASED

neural input the dorsal horn (not an inc. seen previous models)

US: Slows nerve conduction also

What else do we know?

Other methods to block out pain: Relaxation techniques Imagery Placebo effect Belief in the modality “ just give me

some ultra sound, it always makes me feel better!”

Thank you