Lecture I Intro Pain 2013

Physical Therapy

Interventions I

Introduction to Modalities

The Healing Process

Introduction to Pain

Today’s Objectives

Identify the stages of healing and associated

signs and symptoms

Introduce modalities used throughout the stages

of healing

Identify the different types of pain

Review how pain is relayed from the periphery

to higher brain centers

Review tools for assessing pain

Identify different mechanisms for controlling pain

Therapeutic Modalities

Electrical energy

Electrical stimulation, iontophoresis

Electromagnetic energy

SWD, MD, IR, UV, LLL

Thermal energy “Infrared Modalities”

Cold packs, hot packs, whirlpools, paraffin

Sound energy

Ultrasound

Mechanical energy

Massage, compression, traction

Healing Process

Inflammatory response

Fibroblastic repair phase

Maturation-Remodeling phase

All 3 Phases overlap each other

Healing Process

Inflammatory Response

Acute

24-48 hours

Subacute

Signs and Symptoms

Redness, swelling, heat, pain

Healing Process


Vascular

Immediate vasoconstriction slows

hemorrhage to allow for platelet aggregation

Brief vasoconstriction larger vessels

Prolonged vasoconstriction smaller vessels

Coagulation and platelet activation

Local vasodilation

Localized edema

***Therapy can have the greatest impact on the

vascular response

Healing Process


Cellular Reaction

Leukocytes and exudate are recruited for

phagocytosis of pathogens and damaged

tissue

Neutrophils, monocytes, macrophages

Allows for tissue repair and remodeling

Chemical mediators control the amount of

inflammation

Healing Process

Chronic inflammation

Interruption of the normal healing process Inflammatory phase fails to progress to fibroplastic

repair

Can be the result of repetitive microtrauma or autoimmune response

Not associated with cardinal signs of inflammation and neutrophil infiltration Macrophages, lymphocytes and plasma cells

Example: CTS

Healing Process Fibroblastic Repair Phase

Begins within few hours of injury & lasts 4-6 weeks

Granulation tissue matrix of collagen, fibroblasts and capillaries Fibroblasts and collagen lay down to create scar

Capillaries allows for re-oxygenation and new lymphatics

Fibroplasia (period of scar formation) Inflammation and acute pain subsides

Point tenderness

Pain with movements or stress applied

Collagen proliferates, tensile strength increases and fibroblasts decrease

Fibrosis if fibroplasia is extended Capsulitis

Healing Process Maturation-Remodeling Phase

Can last several years

Realignment and remodeling of collagen

fibers in scar tissue

Breakdown and synthesis of collagen

increases the tensile strength

Rarely as strong as normal tissue

Factors Impeding Healing

Extent of injury

Edema

Hemorrhage

Poor vascular supply

Separation of tissue

Muscle spasm

Atrophy

Corticosteroids

Keloids and

hypertrophic scars

Infection

Humidity, climate and

oxygen tension

Health, age and

nutrition

Treatment: Acute Injury

Goal is to prevent and limit edema,

provide analgesia and facilitate healing

Cryotherapy

Compression

Should be combined with elevation

Electrical stimulation

Ultrasound

Low level laser

Treatment: Inflammatory Phase

Goal is to control pain and swelling

Cryotherapy

Compression


Laser

AROM and PROM

Introduction of heat is dependent on the presence of edema

Contrast with cold with longer cold:hot ratio

Treatment: Fibroblastic Repair

Phase Goal is to increase circulation and lymphatic

flow to promote healing, remove injury by-products and decrease pain for progression of ROM and strengthening.

Thermotherapy

Intermittent compression


Laser

Exercise

Treatment: Maturation

Remodeling Phase Goal to promote healing and return to

activity

All modalities are safe

Ultrasound

Shortwave and microwave diathermy


Low- level laser

Wolf’s Law

Bone will respond to the physical demands

placed on them, causing them to remodel or

align along lines of the tensile force

Same is true for soft tissue

Healing tissue needs progressive and controlled

mobilization to promote:

Scar formation

Revascularization

Muscle regeneration, tensile strength

Injuries can initially benefit from immobilization

Also consider…

Does the daily routine need to be altered?

How is the patient going to maintain

current levels of strength, flexibility,

neuromuscular control and cardiovascular

endurance?

What are your contraindication and

indications?

Pain

Pain is defined as an unpleasant

sensation and emotional response

associated with actual potential tissue

damage, serving as a useful warning

signal so that an appropriate behavioral

response can result

-International Association for the Study of Pain

Pain

Positive aspects of pain

Indicates something is wrong

Provokes withdrawal

Generates muscle spasm or guarding to protect an

injury

Negative aspects of pain

Circulation deficiency

Atrophy

Disuse habits

Decreased function and disability

Types of Pain

Acute pain Caused by an event

Chronic pain Lasting > 6 mo., cause maybe unknown

Persistent pain (treatable condition vs. chronic)

Referred pain Felt in location different from injury

Radiating pain Pathology to nerve or nerve root

Deep somatic pain Deep achy feeling, can be caused by cancer

Not uncommon that site of pain differs from site of pathology

Pain Assessment

Identify type of pain

Quantify the intensity

Evaluate effect on patient’s level of

function

Assess the psychosocial impact of pain

Pain Assessment

Visual Analog Scale

Pain Assessment

Pain Charts

Pain Assessment

McGill Pain

Questionnaire

Pain Assessment

Numeric Pain Rating Scale (NPRS)

Eleven point scale: 0 (no pain) to 10 (worst

imaginable pain)

“I need you to rate your pain on a scale of

0 to 10, 0 being no pain at all and 10 being

the worst pain imaginable.”

Sensory Receptors

Receptor nerve endings

Meissner’s corpuscles Light touch

Pacinian corpuscles Deep pressure

Merkel’s corpuscles Deep pressure

Hair follicle deflection

Ruffini corpuscles Skin: Touch, tension and heat

Joint capsule and ligament: change in position

Sensory Receptors

Krause’s end bulbs

Thermoreceptor

Decrease in temperature and touch

Nociceptors/ free nerve endings

Pain receptors

Mechanical, thermal or chemical energy

Sensory Receptors

Proprioceptors

muscle spindles and golgi tendon organs respond to

changes in length and tension in muscle

Phasic receptors

Respond when stimulus is increasing or decreasing

Tonic receptors

Respond to stimulus as long as the stimulus is

present

Adaptation – decrease in generator potential and

decrease of frequency with a prolonged stimulation or

with frequently used or repeated stimulation

Pain – Neural Transmission

1st order or primary afferent (Sensory receptor to dorsal horn)

A-alpha and A-beta (large diameter)

A-delta and C fibers (small diameter)

2nd order afferent fibers (Dorsal horn to brain)

Wide dynamic range input from A-beta, A-delta and C fibers

Nociceptor specific respond only to noxious stimuli from A-delta and C fibers

3rd order neurons Brain to sensory cortex where information is

processed

Pain – Neural Transmission

Neurotransmitter such as acetylcholine

passes information between neurons

Also facilitating or inhibiting synaptic

activity

serotonin, norepinephrine, substance P,

enkephalin, B-endorphin

Serotonin blocks pain messages in efferent

pathways

Enkephalin inhibits depolarization of 2nd order

nociceptive nerve fibers

Pain – Nociception

Injury to cell

Release prostaglandin & bradykinin

Stimulate nociceptors

Pain response


Primary Hyperalgesia

Nociceptor depolarization threshold lowered

Enhanced pain response

Secondary Hyperalgesia

(next several hours)

Chemicals increase in concentration to

increase size of pain area and hypersensitivity


Fast Pain

Larger, faster conducting a-delta afferents in skin

Brief and well-matched to stimulus

Well localized

Slow Pain

C fibers originate in skin and deeper tissue

Aching, throbbing, burning

Poorly localized

Pain Control Theories

Gate Control Melzack, Wall and Castel

Blocking ascending pathways by providing sensory stimulation to A-beta afferents

Sensory stimulation by A-Beta afferents found in the skin and muscle stimulate the substantia gelatinosa in the dorsal horn

Substantia gelatinosa inhibits synaptic transmission (pain message) in small diameter A-delta and C fibers

Pain impulses carried by small fibers is never transmitted to 2nd order neurons


Gate Control: Blocking Ascending

Pathways


Gate Control

Blocking ascending pathways with

enkephalin release (Castel)

Increased activity A-alpha and A-beta triggers

the release of enkephalin

Enkephalin in the dorsal horn inhibits synapse

in the A-delta and C fibers, blocking pain

before reaching sensory levels

Block Ascending Pathway

Enkephalin Release


Gate Control

Descending pain control mechanism

Impulses from higher centers can block pain

transmission in the dorsal horn

Pain carried by A-delta and C fibers provide input to

Periaqueductal gray region in midbrain and the

Raphe Nucleus in pons and medulla

PAG and RN activate descending mechanism

Impulses descend via efferent fibers to release

enkephalin

Synaptic transmission to 2nd order neuron is inhibited


Gate Control: Descending Control

Note:

Pons to dorsal horn

is a another

descending

mechanism


Endogenous Opioids

Beta-endorphin and dynorphin can be

released when A-delta and C fibers are

stimulated

Stimulation to small fiber afferents for 20-40

minutes can trigger release of endogenous

opioids from anterior pituitary gland


Beta-Endorphin and Dynorphin

Pain Management

Cognitive influences

Modulate pain perception via descending

systems

Behavior modification, focusing, hypnosis,

suggestion

Facilitating or inhibiting pain perception

Past experience, culture, anger, fear, aggression

Pain Management

Identify sources of pain

Select modality most appropriate for each individual patient

Have clear rationale supporting clinical decision TENS, massage stimulate large diameter afferents

Decrease pain fiber transmission with cold

Stimulate small diameter afferents and descending pain control with acupressure, deep massage, TENS or trigger points

Stimulate release of endogenous opioids via small fiber stimulation with TENS

Conclusion

What are the signs of the phases of healing you

will see in your patient?

Can you tell the difference between stages?

What are some factors that will impede healing?

How are you going to chose a tool for assessing

pain?

What are the mechanisms by which we try to

control pain?

Lecture I Intro Pain 2013

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Transcript of Lecture I Intro Pain 2013