transfer of heat from warmer to cooler source through conduction medium

EX: infrared lamp, laser, UV light

Rays rebound off the material

nerve fibers that are activated by noxious stimuli and received by the brain; noxious stimuli include pressure, heat/cold extremes, chemicals, and pain

nociceptors transmit stimuli through sensory nerves (afferent) to the motor nerves (efferent) through interneurons within the spinal cord

located in skin or muscle/tendons - detect temperature

• Krause's end bulbs - cold
• Ruffini corpuscles - heat

located in skin or muscle/tendons - detects change in tension/length

• muscle spindles -> length changes
• golgi tendon organs -> tension changes

reduction of frequency that occurs with a prolonged stimulus or with frequently repeated stimuli

Ex: modality used too often; receptors adapt to stimuli and decrease their impulses

info from dorsal horn of the spinal cord to the brain (thalamus)

• wide dynamic range (receive impulses from A-beta, A-delta, & C fibers)
• nociceptive specific (receive impulses from A-delta & C fibers)

carries info to relevant brain centers where acted upon

• perceives location, quality, intensity
• allows feeling of pain, emotions, determines reaction to stimulus

• NON PAIN
• high conduction velocity
• diameter: 6-12 microM
• velocity = 30-70 M/sec
• stimulus = touch, kinesthesia (nonpain)

• myelinated
• PAIN from mechanical pressure
• short duration, sharp/rapid, localized sensation
• diameter 1-6 microM
• velocity = 6-30 M/sec
• stimulus = sharp pain, pressure, temperature
• ACUTE PAIN!!
• larger/faster A-delta neuron, originates from receptors in the skin
• lasts only as long as there is stimuli (a-delta)
• localized & fast

• unmyelinated
• PAIN from chemical/mechanical
• delayed onset, diffuse nagging sensation (ache/throb)
• CHRONIC PAIN
• aching, throbbing, burning
• transmitted by C fiber neurons, originates from skin tissue and deeper ligament/muscle tissue
• delayed perception following injury, pain continues until long after stimuli is removed

Substantia gelantinosa

a mass of gelatinous gray matter that lies on the dorsal surface of the dorsal column and extends the entire length of the spinal cord into the medulla oblongata and that functions in the transmission of painful sensory information

(responsible for closing gate to painful stimuli)

• blocks passage of noxious stimuli from first to second order neurons
• released from interneurons
• inhibits the release of substance P (NT released from both ends of the neuron)

air/water particles move across the body, creating a temperature variation

Ex: WWP, CWP, contrast in WP

changing from 1 energy form into another

EX: US, diathermy

• line the skin, heart, blood, vessels, hollow organs, glands
• ability to generate
• ability to conduct heat/cold, US energy - but this tissue resists electrical currents (why you have to turn e-stim up)

• limited ability to regenerate
• ability to conduct heat/cold, US energy, electrical current

• cells located in the CNS have no ability to regenerate
• cells located in the PNS have limited ability to regenerate
• Ability to alter the conduction velocity of nerve through heat/cold and US
• slowing conduction rate can decrease pain perception

generated by high energy source, transmitted by movement of photons

• Energy can be:
• reflected - rays that rebound off the material
• refracted - ray passes from 1 material to another, changing its path
• transmitted - rays passing through a material
• absorbed

no reactions/changes can occur in the body tissues if the amount of energy absorbed is insufficient to stimulate the absorbing tissues

(AT goal is to deliver sufficient energy to stimulate the tissues to perform their normal function)

operate by conduction, used to produce a  local heating/cooling of superficial tissues with maximum depth of 1cm or less

• rate of heat transfer from 1 object to another is proportional to the difference in temperature between them
• if there is a greater temperature difference between the 2 objects = rapid heat transfer
• EX: cold pack (8F) to body (98.6F), so heat flow from skin to cold pack is rapid

• delivered by movement of charged particles
• associated with flow of elelctrons through an electric field
• an electrical current that passes through tissues will warm the tissues based on the resistance of the tissue to the flow off electricity

• produces sound waves (inaudible)
• US: depth of penetration is greater than electromagnetic energy
• great depth of penetration is because US travels well through tissue
• Extracorporal Shock Wave Therapy: high pressure, short duration sound wave - used to treat plantar fasciitis, epicondylitis, nonunion fractures

• energy acquired by the objects upon which work is done
• kinetic energy (energy of motion)= massage graston
• or potential energy (stored energy of position)= stretching, traction (holding position)

Primary: tissue destruction related to the actual trauma

Secondary: cell death caused by lack of oxygen to the injured cells/area

(cells die without oxygen which release their contents into the injured site, causing even more debris to clean up)

• once the damaged cells have released debris into the area, it triggers an inflammatory reaction (hemorrhage/edema)
• with the increase in fluids, pressure is placed on the nerve receptors in the area causing a clogging of blood flow (ischemia)
• this causes further cell death because of lack of oxygen (muscle spasm/atrophy, and loss of function of body parts)

• IMMEDIATELY FOLLOWING INJURY - lasts 24-48 hours
• inflammation very important to the healing process, without the physiological changes the later stages of healing will not occur
• CRITICAL to the entire healing process, if this phase is not completed in its entirety, the rest of the rehab could be altered
• S&S: redness, swelling, tenderness, increased temperature, loss of function

1. Chemical Mediators attracted to the area to limit swelling

• histamine: causes vasodilation (short period of time) and increased cell permeability
• leukotrienes: causes margination = (WBC line up along cell walls)
• also increase cell permeability locally, affecting the passage of fluid/WBC through cell walls to form exudate/swelling
• Cytokines: major regulators of leukocyte traffic, help attract leukocytes to the site which brings phagocytes to the inflammation

AMOUNT OF SWELLING DIRECTLY RELATED TO EXTENT OF TISSUE DAMAGE!

2. Vascular Response: involves vascular spasm, formation of platelet plug, blood coagulation, growth of fibrous tissue

• immediate response to tissue damage is vasoconstriction away from injured site for 5-10 minutes, then vasodilation of the area
• increase in blood flow is transitory, then the flow of fluid slows, leukocytes adhere to vascular wall (stagnation of fluid lasting for 24-36 hours)
• Platelet accumulation: platelets adhere to collagen fibers, create sticky matrix on vascular wall, causing additional platelet and leukocytes to adhere forming a plug
• plug abstructs local lymphatic fluid draining to localize the injury response

3. Clotting Process: caused by conversion of fibrinogen to fibrin

•  occurs because of a cascading effect
• clot formation begins within 12 hours, finishing within 48 hours
• injured area becomes walled off during most of the inflamatory phase
• leukocytes phagocytize foreign debris towards end of inflammatory phase, getting the area ready for fibroblastic phase

• about 72 hours until about 4-6 weeks
• scar formation period (fibroplasia - starts within the first few hours until 4/6 weeks)
• inflammatory symptoms decrease (decreased swelling/pain/point tenderness/heat)
• increased oxygen delivery along with increased blood flow bringing nutrients to the region
• the fibrin clots breaks down, replaced with granulation tissue (delicate connective tissue)
• fills in gaps of tissues
• fibroblasts arranged themselves parallel to the capillaries and begin to create an extracellular matrix made of collagen/elastic/ground substance
• day 6-7: fibroblasts produce collagen fibers in random patterns within the scar
• tensile strength of area increases in relation to collagen synthesis
• with increased tensile strength, fibroblasts formation decreases --> maturation phase

• can last several years
• realignment/remodeling of collagen fibers within scar tissue according to tensile forces
• increased tensile stress on the area ---> collagen fibers realign parallel to line of tension (maximum efficiency)
• scar is never as strong as original tissue

• occurs when acute inflammatory response does not eliminate the injuring agent and restore tissue to normal physiological state (often because low concentration of chemical mediators are present)
• can develop chronic inflammation without having acute inflammation
• low grade inflammation persists, causing damage to connective tissue causing tissue necrosis prolonged the healing/repair process

• extent of injury
• edema: caused increased pressure, creating separation of tissue, inhibits neuromuscular control, impedes nutrition to area
• hemorrhage: bleeding from damage to capillaries (same effects as edema)
• poor vascular supply: these areas heal poorly and at slow rate (scaphoid)
• muscle spasm: causes traction on torn tissues preventing approximation
• Atrophy
• corticosteroids: inhibits healing phase
• keloid/hypertrophic scars (raised): rate of collagen production exceeds rate of collagen breakdown (more common in brown people: more melanin)
• humidity/climate/oxygen tension: lack of scabbing
• health/age/nutrition: skin elasticity decreases with age