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by: Jerrell Klein


Jerrell Klein
GPA 3.93


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This 28 page Class Notes was uploaded by Jerrell Klein on Saturday September 12, 2015. The Class Notes belongs to KINS 4100 at University of Georgia taught by Cooper in Fall. Since its upload, it has received 67 views. For similar materials see /class/202066/kins-4100-university-of-georgia in Kinesiology at University of Georgia.

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Date Created: 09/12/15
Ch2 Concepts of Healing 342012 72600 PM Fun Key Terms and Phrases Acetylcholine 0 Causes vasodilation Angiogenesis 0 Provides for subsequent scar tissue formation and normal healing events that follow Arachidonic acid 0 Precursor in the production of leukotrienes prostaglandins and thrombaxanes Bradykinin 0 Local vasodilator o Increases vascular permeability and local pain receptors Chemotactin 0 Important factor in promoting healing process CoHagenase o Involved in degredation of collagen during tissue repair 0 Controls collagen content in a wound Elastin o Allows tissues to change shape with stress and resume normal conditions after stress removal 0 Important in remodeling Endothelial Leukocytes 0 Act as phagocytes to remove debris from an injured area Epinephrine o Stimulant of sympathetic nervous system and a powerful vasopressor o Increases metabolic activities Extracellular Matrix 0 Foundation on which new tissue is cast Fibrin 0 Important in clotting Fibrinogen o Converts fibrin to form a plug at injury site Fibrinolysin o Converts fibrin into a soluble substance to unplug lymphatics system at injury site Fibroblast 0 Forms the fibrous tissues that support and bind tissues Fibronectin o Crosslink to collagen in connective tissue thereby playing a role in the adhesion of fibroblasts to fibrin o Involved in collection of platelets in an injured area Granuloma o Occurs in chronic inflammatory conditions when the body produces collagen around a foreign substance to protect itself from that substance Granular Leukocytes 0 Release histamine and serotonin to produce vasoactive reactions following injury Granulation Tissue 0 Forms the scar of the wound Ground Substance o Reduces friction between connective tissue fibers 0 Adds to the area s density Hageman Factor 0 Initiates blood coagulation process following trauma by converting prothrombin to thrombin Histamine o Increases vascular permeability and fibronectin 0 Released by mast cells and granulocytes Hyaluronic Acid 0 Major component of early granulation tissue Promotes cell movement and migration during repair Stimulates fibroblast proliferation Produces edema by absorbing large amounts of water to increase fibroblast migration Kallikrein 0 Forms kinins and activates plasminogen o Increases vascular permeability and vasodilation Kinin o Mediates the classic signs of inflammation 0 Causes microvascular permeability O O O Leukocytes o Phagocytic properties to remove debris from an injury site Leukotriene o Regulates inflammatory reactions 0 Stimulate movement of leukocytes into the area Macrophages o Regulators of the repair process 0 Phagocytize the injured area of debris kill macroorganisms and secrete substances into injury site 0 Keeps inflammatory process localized Mast Cells 0 Connective tissue cells 0 Store and produce various mediators of inflammation Monocytes 0 Remove debris from an injury site Myoblast 0 Forms myotubes which eventually evolve into muscle fiber Myofibroblasts o Responsible for wound contraction Neutrophil 0 Contain toxic chemicals that bind to microorganisms to kill them 0 White blood cell Plateletderived growth factor 0 Essential fro the growth of connective tissue cells Plasmin o Converts fibrin to soluble substances Platelets 0 First cells seen at injury site 0 One of the regulatory cells of healing 0 Form plug at the injury site to stop bleeding Polymorphonuclear leukocyte o Chemotactic and phagocytic in the healing process Prostaglandin o Mediates cell migration during inflammation 0 Increase pain sensitivity induce fever and suppress lymphocyte transformation 9inhibiting the inflammatory response o Protease o Acts as a catalyst to split interior peptide bonds in protein 0 Causes increased vascular permeability and increases concentration of proteins and cells in wound space o Protoglycan 0 Provides a resilient matrix to inhibit cell migration 0 Regulates cell function and proliferation and regulates collagen fibrillogenesis o Reticulin 0 Forms the early framework for collagen deposition 0 Considered at type III collagen fiber o Satellite Cells 0 Regenerate new muscle tissue o Serotonin o Produces vasoconstriction in small vessels after norepinephrine activity is complete o Tenocyte o Converts to fibroblasts during healing of tendons o Thrombin 0 Enzyme that converts fibrinogen to fibrin to form a fibrin plug early in inflammation phase 0 Stimulates fibronectin production o Thromboaxane o Vasoconstrictor and important in platelet aggregation Primary and Secondary Healing o Primary Intention 0 Bridge of cells that binds the ends of the separated tissue together 0 Commonly occurs in minor wounds o Secondary Intention o Wound heals by producing tissue from the bottom and sides of the wound to fill in the space created by the wound o Occurs when the tissue is a farther distance away o Takes longer and results in a larger scar Healing Phases o The Inflammation Phase 0 When the body recognizes a problem and begins a series of defensive maneuvers to stabilize the injured site and protect it by rushing chemicals and cells to the area Takes up to 10 days to complete Usually lasts around 45 days An important and necessary step in the healing process Clinicians goal to minimize inflammation Best ways to control compression and elevation Massage helps encourage venous return Vasoconstriction and Vasodilation Immediate local vasoconstriction that happens locally right after injury Quickly followed by vasodilation Cellular Reactions Vasodilation causes release of blood and blood products into the injured site a Blood platelets and serum proteins Platelets a Release phospholipids which stimulate the clotting mechanism to stop bleeding n Bind to collagen fiber stumps that were exposed by the injury a Release fibronectin growth factors and fibrinogen Fibronectin binds together fibrin and collagen n Kallikrein enzyme o Initiates blood clotting process 0 Converts prothrombin thrombin afibrogene fibrin 9 temporary plug a Fibronectin and fibrin join together to form a lattice structure that acts as a plug to stop bleeding o Plug is temporary and very fragile O O O O O 0 Provides initial tensile strength o Replaced by type 3 collagen as healing process goes on Leakage from damaged lymph vessels halted by formation of fibrin plug a Unable to move fluids out of the joint when edema is present Once the area becomes stable fibrinolysin is released a Enzyme that converts fibrin from insoluble to soluble protein to promote absorption of the fibrin plug and allow lymph vessels to do theirjob Body attempts to remove debris during the first few hours a Begun by neutrophils o Contains toxic chemicals that allow them to bind to microorganisms and destroy them o Most plentiful WBC in the body o Presence is short lived o Replaced by mononuclear phagocytes o Monocytes and macrophages Monocytes and Macrophages n Become predominant in a cell within 2448 hours a Act as phagocytes to remove debris and dead tissue from area As inflammatory response proceeds inflammatory exudateis formed in fluid escaping from local vessels dead tissue and dying neutrophils n Commonly whitish and seen as pus though not an infection Debridement is necessary for healing to continue a Injury site must be cleared of excess fluid and other waste materials in order to continue healing a Macrophages release growth factors and may trigger termination of tissue growth when healing process is complete 0 Chemical Reactions Chemotaxis a Process of attraction or stimulation of cells Vascular permeability chemical reaction a Allows cells and chemicals to enter the injury site a Initiated by histamine in the area Released by cells such as platelets mast cells and neutrophils Chemotactic factor for leukocytes causing them to enter the area Function controlled by serotonin ad kinins Serotonin released by mast cells Kinins and platelets released by plasma a Presence of kinins followed by prostaglandin formation Complement system 0 Various proteins found in serum Turn into a complement cascade when surge of events following activation of complement system 0 n Prostag landin types PGEl continuing vascular permeability in localarea PGEZ responsible for attracting leukocytes to the site Both stimulate repair of the damaged area and permit advancement to the proliferative phase These are the ones influenced by NSAIDS Hageman factor a Factor XII production a Stimulate production of kallikrein Increases vascular permeability and vasodilaltion 0 Signs of Inflammation Localized redness edema pain increased temperature loss of normal function The increases in cellular and chemical activity increases local temperature Histamine causes redness Edema is also the result of increased substances in the area of blockage of lymph vessels whose normal responsibility of drainage is restricted by the newly formed fibrin plug Pain chemicals n Histamine prostaglandins bradykinin o Proliferation Phase 0 O O 0 Growth of new blood vessels and granulation tissue Beginning marked by transition from debridement to angiogenesis and formation of granulation tissue Angiogenesis occurs rapidly Important because forming scar tissue requires vascular production and supply for healing to continue Fibroblasts Development of new caps and extracellular matrix Cells responsible for the production of new growth Seen in increased numbers three to five days following injury Hallmark of proliferation beginning Responsible for development of new capillaries and the extracellular matrix a Matrix holds wound together and helps protect from stress and infection a Soon replaced by collagen matrix o Stronger and protects new blood vessels that are forming Produce substances that will eventually make up the collagen matrix a Required for scar tissue formation Significant increase in extracellular collagen production Increased proteoglycans Increased epithelial mitosis Granulation Tissue O Combination of matrix and newly formed capillary buds Typically a bright red beefy color Endothelial cells a Most important cells in capillary formation a Contain plasminogen activator o Breaks down and removes the fibrin network that was formed during inflammation phase so the lymphatic flow can be restored Components of the Extracellular Matrix Fibrous Elements both combined add tensile strength a Type III collagen scar tissue o Lays down very unorganized collagen o Makes new tissue not as elastic if it is not laid down in a functional pattern a Reticulin inelastic n Elastin elastic NonFibrous Elements n Ground substance o Gellike substance composed of glycosaminoglycan proteoglycans and glycoproteins o Fills in the spaces between fibrous elements of matrix and reduces friction between fibers when stress is applied to the tissue As the epithelium progresses across the wound epithelial cells and fibroblasts release collagenase Enzyme that prevents overproduction of collagen in the wound Prevents keloid formation Early collagen produced is type III Seen forming 4872 hrs after the injury occurs Weak and thin structure Misaligned and randomly dispersed Provides primary tensile strength Later replaced by type I collagen Tensile strength is directly related to the amount type and arrangement of collagen in the area Replaced by day 12 o Hyaluronic Acid Draws water to the area during all of these processes Provides additional room for the proliferating fibroblasts in the wound site 0 Signs Redness and swelling in the area Pressure sensitive nerve endings cause the area to be sensitive to pressure and tension o Remodeling Phase 0 Wound tissue converts to scar tissue 0 Some proliferating activities continue on into remodeling phase 0 Wound Contraction Makes the scar smaller Myofibroblasts migrate to wounds periphery and pull the wound edges toward the center to contract the wound s size Detrimental in situations in which joints are involved a Scar tissue contraction and adhesions can cause a loss of motion in the joint 0 Collagen Transition As type I collagen is synthesized type III is destroyed When the construction rate equals the destruction rate the healing process evolves to the final and longest phase of remodeling n Lasts about 618 months depending on the tissue Clinician obstacles a Pain edema patient compliance n Physicians typically want immobilization n We must know the tissue o How much stress we can put on the new tissues O O O O O c We need to know how aggressive we can be with mobilization techniques 0 The further we get into the motion the more stress we put on the structure 0 We have to apply some force in order to align the fibers correctly 0 Need to know direction of fibers in a resting state Large number of capillaries are no longer needed and begin to recede Fibroblasts and myofibroblasts begin to diminish Loss of the scar s red color Lessening of swelling and wound sensitivity Scar develops tensile strength Maturation of the wound s collagen structure and arrangement is the primary activity Growth Factors Proteins that serve many functions Interact with each other and other substances to promote the healing process Complex and not yet fully understood Perform specific tasks that affect specific cells to speed and enhance the healing process Named for the target cells they affect their source or their behavior Their Vital Roles in Healing O O O O O O 0 Control migration and prolieration of cells vital to wound heaHng Act as stimulators of vasoconstriction and vasodilation Affect formation of fibrin plug Controlling macrophages and preventing phagocytization of healthy cells Coordinate capillary endothelial production Angiogenesis granulation tissue and collagen production Stimulate degredation of type III and synthesis of type I o Primary Players in Healing o EGF39S Stimulate production of cells including epithelial endothelial and fibroblasts Draw epithelial cells into damaged areas to stimulate fibroblasts to produce GAG o Fibroblast Growth Factor FGF Formation of new vascular and granulation tissue Promote angiogensis Stimulate chondrocytes keratinocytes and myoblasts o Platelets Platelet Derived Growth Factor Stimulate events during proliferation and encourages healing of chronic ulcers Facilitate production of collagenase by stimulating fibroblast activity a Active during remodeling phase Transforming Growth Factors n TGFb o Stimulates healing during inflammation and angiogenesis stages by increasing macrophage activity and stimulating epithelialization o Stimulates extracellular matrix production o Leads to granulation tissue formation n n Ligamentous Healing Frayed stump ends where the ligament was separated are present Undergoes inflammation process including local edema The quantity of collagen being synthesized is greater than the amount being degraded 0 Increase in net collagen at this time Ligament stumps become surrounded with fluid 0 Causing ends become fragile Within first 2448 hours macrophages and monocytes enter to begin debridement 0 Vascular proliferation fibroblastic activity and clot formation occur during first 6 weeks Collagen and ground substance work to bridge torn ends of ligaments via scarring Scar maturation will occur and collagen tensile strength will increase 4872 hours fibroblasts produce the extracelluar matrix Proliferation takes up to 6 weeks Final stage may take 18 months to complete 4050 weeks before nearnormal tensile strangth is restored Important to know who the key players in stabilization within the joint are 0 Capsule muscle ligaments etc 0 Do we need to involve these other structures in our rehab plan Extra Articular Sprains o Bleeding in subcutaneous space Intra Articular Sprains o Bleeding within capsule Factors Affecting Ligament Healing o Surgically repaired extraarticular Heal with less scarring Stronger than unrepaired 0 Non Surgically Repaired Heal via fibrous scarring resulting in ligament lengthening and joint stability 0 Intraarticular ligament damaqe Results in synovial fluid presence diluting hematoma disrupting clot and healing o Ligament healing and immobilization Strength training can enhance joint stability Musculotendinous o 4 traits of skeletal muscle 0 elasticity extensibility irritability contractility o muscle size and architecture often contribute to magnitude and magnitude of motion O 0 all depends on thickness of the muscle and the function gross vs fine powerful vs coordinated o Muscle Healing O O O 0 Unique due to the presence of satellite cells Fuse with adjacent myofibers to repair and regenerate muscle tissue Restore and replace muscle cells routinely damaged during activity Hemorrhaging and edema lead to phagocytosis Fibrogen and ground substance form gel like matrix leading to fibrosis and scarring Myoblastic cells infiltrate the area Promoting myofibril regeneration Collagen undergoes maturation With active contractions being critical to apply tensile stress Final regeneration is completed with development of the neural aspect of the neuromuscular structure Larger muscles are unable to repair with regeneration and must resort to scar tissue as the means of healing Lengthy recovery Must be very patient o Tendon Healing O O O O Inflammatory phase lasts about three days Collagen formation begins rapidly and lasts for about four weeks During the second week Collagen starts becoming more organized End of second week fibers align themselves in the direction of stress Large amounts of collagen required for adequate healing Collagen synthesis can become excessive Resulting in fibrosis and interfering with tendon sliding action Scar tissue will gradually elongate allowing for appropriate tendon motion o If synovial sheath surrounds the injured tendon the injury could be devastating o By three weeks the synovial sheath is reconstructed Important so the tendon has smooth gliding surface within which to move 45 weeks until strong contraction can be imparted on tendon healing takes up to a year but you re still not 100 Surgical Repair Tendon and surrounding soft tissue become one wond Area fills with sticky gel n Has potential to become a thick dense scar u If formed will limit the gliding of the tendon and thereby impede function of the muscle o Often limits rehab success 0 O O Nerve Tissue o Generally involve contusion or inflammation o More severe crushing or severing 0 Causes life long disability o Peripheral nerves can be regenerated if cell body is not impacted o Slower regeneration with proximity to cell body o Regeneration requires optimal environment Cartilage Healing o Limited healing capacity 0 Depends on three variables The depth of the defect Maturity of the cartilage Location of the defect Small fullthickness defects or articular cartilage 0 Repair with fibrocartilage via the blood supply in the bone adjacent to the lesion Partial thickness defects 0 Do not repair the degenerate because there is no vascular supply available 0 Become necrotic and lead to osteoarthritis Variable healing depending on damage to cartilage and or subchondral bone Bone Articular cartilage fails to undergo clot formation or cellular response 0 Defective region remains defective When subchondral bone is involved the inflammatory process proceeds as normal For regeneration to occur the following conditions must be present Cells that will proliferate and differentiate into chondrocytes must be located in or migrate to the wound site A mechanical stimulus that enhances articular cartilage formation must be present Protection from excessive loads must be significant to allow cartilage repair with causing damage A normal joint conformation must be maintained or restored O O O O Inflammatory phase lasts 35 days Necrotic ends of the fractured bone and metabolic wastes are debrided by osteoclasts to clear the way and set the stage for the next phases Can We Impact the Healing Process RICE EStim enhancing protein sythesis and tensile strength EStim for spasm Ultrasoundheat Medication o NSAIDs to inhibit prostaglandin production of nocioceptors Manual techniques Clinician s Role In Healing PreSurgical Phase Involves athletes requiring surgery If surgery can be delayed exercise may help to improve outcome 0 Mainting or increasing ROM strength CV fitness neuromuscular control May enhance athlete s ability to perform rehab after surgery 0 O o Phase I Acute Injury Phase 0 Initial swelling and pain control are crucial Can t be aggressive in first 48 hours Immobilization necessary for first 2448 hours 0 By days 34 athlete should be engaged in some mobility exercises and gradually encouraged to weight bear 0 Use of NSAIDs o Phase II Repair 0 As the inflammatory process has subdided and pain decreases with passive ROM exercises Increase CV fitness Restore full ROM Restore or increase strength Establish neuromuscular control 0 Continued modality use for pain modulation and swelling control Cryotherapy and Estim Edema control still important o Phase III Remodeling 0 Longest phase with ultimate goal being RTP Promote functional alignment of fibers Continued collagen realignment Regain sport specific skills Return to play testing Heating modalities Ultrasound diathermy Increase circulation in deeper tissue If decreased ROM causing inflammation heat is a good way to go Know what you re trying to accomplish 0 Manual Therapy Massage reduce guarding spasms pain 0 Enhanced lymphatic flow will deliver essential nutrients and increase breakdownremoval of waste respectively Using Medication to Effect Healing o Primarily used for pain modification 0 O O NSAIDs o Aspirin acetaminophen ibuprofein naproxen sodium ketoprofen o Aspirin o Interferes with pain signal transmission from thalamus 0 Tissue damage results in release of arachindoic acid 0 Effects Blocks prostaglandin synthesis Modulates lysosomal membrane destruction Inhibits cyclooxygenase Alters sympathetic control of pain Ibuprofein o Anitpyretic effects 0 400 mg serves as analgeis and antiinflammatory agent Acetaminophen Use NSAIDs carefully if athlete is dehydrated o Ischemia within kidneys can occur Other factors such as 0 Surgical repair age disease severity infection nutrition spacticity edema CH 5 Restoring ROM and Improving Flexibility 342012 72600 PM Importance of Flexibility o Need to improve to preinjury status 0 Decrease injury risk 0 Increases function 0 Increases power Combo of speed of contraction and the lengthdistance it can contract o With injury there is a loss of ROM 0 Due to pain swelling muscle guarding Flexibility o Ability of neuromuscular system to allow for efficient movement of a joint or series ofjoints through full pain free ROM o Musculotendinous unit s ability to elongate with application of a stretching force o Prolonged loss can reduce ROM o Lack of can lead to uncoordinated motion 0 Impacts performance Agility power balance ROM o Amount of mobility about a joint o Determined by the soft tissue and bony structures in the area Limited if flexibility is limited Connective Tissue o Connective Tissue Composition 0 Looselax o Ligaments joint capsules Can lose elasticity during periods of disuse or immobilization o Collagen 5x stronger than elastin provides tissue with strength and stiffness o Elastin The more elastin you have the more flexible the tissue Provides the extensibility Able to withstand elongation stress and return to normal lenght o Reticulin Type III collagen Important in repair following injury 0 Ground Substance Decreases friction between collagen fibers and elastin Structureless organic gel Maintain distance between fibers to prevent excessive cross linking transports nutrients to fibers o Three Types of Connective Tissue o Areolar loose irregular Skin Long distance between collagen crosslinks n Lots of elastin Lots of freedom of motion a Movement in all directions Lies between structures in areas where motion occurs a Joint capsular fascia intermuscular layers subcutaneous tissue 0 Dense Regular Tendonsligaments More cross links Parallel fiber pattern Resist high tensile loads while still providing some flexibility Need to work a lot with these fibers to align them correctly 0 Dense Irregular Joint capsule Elasticity is less due to fibers Running all directions Multidimensional fiber pattern a Allows tissue to provide resistance to forces in multiple directions Provides for tensile strength but has little extensibility to deform Effects of Immobilization Ground substance is reduced so crosslinks increase Fiber meshwork becomes hard dense less supple New collagen formation encourages new crosslink formation Wound contraction reduces ROM Fibrosis increases Detrimental to ROM and flexibility Normal collagen replacement comes as dense network Collagen binds to other structures and limits mobility Structure becomes weaker Loss of ROM end result Immobilization of Muscle o Decreased fiber size number of myofibrils and oxidative capacity 0 Increase in fibrous and fatty tissue in the muscle and a reduction in the intramuscular capillary density 0 The longer the muscle is immobilized the greater the number of muscle fibers that degenerate and the greater number of fibrous and fatty tissue 0 Atrophy in 24 hours Rate of atrophy depends on the muscle 0 Reduced capillary density 0 Prolonged immobilization Loss of normal feedback 0 Clinical changes Atrophy weakness and lower endurance Delayed reflex response a For every week of immobilization takes three weeks to undo atrophy Immobilization of Cartilage 0 Changes depend on whether or not the joint is weight bearing during immobilization position of the immobilization and duration 0 Less matrix organization Creates scar tissue within the joint space Makes tissue softer Irreversible damage with continued immobilization Adhesive capsulitis o Necrosis o Periarticular Connective Tissue 0 Soft tissue surrounding the joint Ligaments capsule fasica tendons and synovial membrane 0 CT becomes thick and fibrotic 0 Reduced GAG and water Causes a diminution of extracellular matrix 0 Loss of motion in the affected joint Effects of Remobilization o Effectively realigns collagen to improve its strength o Muscle Fibers 0 Best results if immobilization is short followed by active motion 0 Initially recovery is rapid but slows as recovery continues 0 Movement causes more rapid absorption of hematoma an increase in tensile strength improved myofiber regeneration and arrangement o Articular Cartilage 0 Promote WB ASAP 0 Controlled WB or loading of articular cartilage may even encourage repair of damaged cartilage o Periarticular o Helps prevent abnormal crosslink formation 0 Fatty tissue buildup around the joint limits mobility and must be broken by techniques such as stretching and joint mobilizations Mechanical Properties of Connective Tissue o Elasticity 0 Ability to return to normal length after elongation 0 Due to stored potential energy o Viscoelasticity O O O 0 Ability to resist change of shape when force is applied 0 eccentrics o Plasticity 0 Ability of tissue to undergo permanent change Physical Properties of CT o Force Deformation 0 Amount of force applied to maintain change of length or other deformation of tissue o Creep o Elongation of tissue when a low load is applied over an extended period of time Results in permanent change in tissue s length 0 When appropriate Use in repair phase because it helps put fibers back into correct alignment 0 Low load over stretching o StressStrain 0 Load required to change the length of connective tissue is directly related to the tissue s strength and the tissue s strength is directly related to its ability to resist a load Factors Affecting Stress o Depends on the amount of collagen and elastin in the structure amount of force applied amount of time the force is applied and tissue s temperature o Hook s Law 0 Strain of an object is directly related to the object s ability to resist stress Stress a Force that changes the form or shape of a body a Tension o Pulls apart a Compression o Crushes the tissues n Shear o Force that moves across parallel organization of tissue Strain n Amount of deformation that occurs when a stress is applied o Plastic takes us to our end range 0 Have to create some microtearing to increase our mobility at end range Factors Influencing Fail Point o Tissue width o Tissue slack length 0 Which type of tissue muscle can withstand greater loads o Tissue microstructure and orientation of structure to the forces appHed Neuromuscular influences on ROM o Muscle spindles o Sensitive to changes in muscle length 0 The more precise the movement the more muscle spindles in the muscles Golgi Tendon Organs 0 Less sensitive to stretch than spindle but more to muscle contraction 0 Protective mechanism An autogenic mechanism Fire at end range to protect body from reaching failure point Inhibits contraction of agonist o Inhibits against contraction This is why we do dynamic stretching AROM o Dynamic flexibility o Joint movement via muscle contraction o Ability to move joint with little resistance PROM Checks movement about the joint Motion ofjoints to end points without contraction Static flexibility Critical in injury prevention o Muscles can be forced to stretch beyond normal limits 0 Without elasticity it is likely that the musculotendinous unit will be injured Stretching Techniques o Ballistic Bouncing movement in which repetitive contractions of agonist work to stretch antagonist muscle Can cause damage to already injured tissue Stimulates both muscle spindles and GTOs Control of the stretch only limited by the velocity of the force applied to the stretch o Helps increase dynamic flexibility o Static Stretch and hold at point of discomfort Hold 68 seconds at maximal stretch Hold 1530 seconds 34x Small chance of injury but not dynamic o Proprioceptive Neuromuscular Facilitation Combination of active and passive stretching Also can be used as a strengthening exercise Alternating contractions and stretches Slowreversalholdrelax Contractrelax Holdrelax o Myofascial and Neural o Enhances NM system s ability to control movement o Passive Velocity Flexibility Program 0 Stretches that include increased velocity and range lengthening o Progressively controlled 0 O O O O O O O O O O 0 Slow static stretches Slow short end range stretching Slow full range stretching Fast short end range stretching Fast full range stretching o Allows for control of range and velocity without therapist assistance The Pain Response 342012 72600 PM Pain o Primary reason for seeking medical attention o Involves sensory behavioral emotional and cultural components o Learned response 0 Pain threshold can be influenced by our parents Pain Scales o Provides an objective measure to a subjective response o Come up with a pain scale that you like best 0 Make up anchors to help your athletes know parameters o Ask questions 0 where when duration pn after activity pn at night what makes it better or worse o Types of Scales 0 Visual analog no numbers 0 Color scale works best with children Referred Pain o Pain not in the injured area o Brain cannot localize the pain 0 Nerve fibers become cross branched and pain signal becomes mixed up and confused 0 Brain misinterprets the messages and sends pain elsewhere Chronic Pain o Continuous pain for 6 months or more o Can be a learned response o Gate remains open o People just learn to deal with it Few objective medical findings Taking medications for a long period of time Sleep difficulty Depression Manipulative behavior Nocioceptor pain impulse Mechanoreceptor stress of damage to tissue Chemoreceptor Afferent carry impulses to the brain Efferent carry messages from brain to body


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