Physical Therapy Interventions I

Introduction to Modalities The Healing Process Introduction to Pain

Todays 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
Inflammatory Response
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
Inflammatory Response 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 Inflammation and acute pain subsides Point tenderness Pain with movements or stress applied Collagen proliferates, tensile strength increases and fibroblasts decrease

Fibroplasia (period of scar formation)

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 Electrical stimulation 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 byproducts and decrease pain for progression of ROM and strengthening.

Thermotherapy Intermittent compression Electrical stimulation Laser Exercise

Treatment: Maturation Remodeling Phase

Goal to promote healing and return to activity All modalities are safe Ultrasound Shortwave and microwave diathermy Electrical stimulation Low- level laser

Wolfs 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

Chronic pain

Caused by an event Lasting > 6 mo., cause maybe unknown Persistent pain (treatable condition vs. chronic) Felt in location different from injury Pathology to nerve or nerve root Deep achy feeling, can be caused by cancer Not uncommon that site of pain differs from site of pathology

Referred pain

Radiating pain

Deep somatic pain

Pain Assessment
Identify type of pain Quantify the intensity Evaluate effect on patients 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 Meissners corpuscles
Light touch

Pacinian corpuscles

Merkels corpuscles
Ruffini corpuscles
Deep pressure Hair follicle deflection

Deep pressure

Skin: Touch, tension and heat Joint capsule and ligament: change in position

Sensory Receptors
Krauses 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 Brain to sensory cortex where information is processed

3rd order neurons

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

Pain Nociception

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

Pain Nociception
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

Pain Control Theories Gate Control: Blocking Ascending Pathways

Pain Control Theories 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

Pain Control Theories 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

Pain Control Theories Gate Control: Descending Control

Note: Pons to dorsal horn is a another descending mechanism

Pain Control Theories 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

Pain Control Theories 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?