Therapeutic Exercise Notes

NOTESTherapeutic FOR MEDICAL & ALLIED HEALTH PROFESSIONS Exercise Notes by Aamir Memon TherTherapeutic ExerThecise Notes T

TherTherapeutic ExerThecise Notes Based on Kiner & Colby 5th Edition Dpt. Aamir Raoof Memon

2012-14

Therapeutic Exercise Notes by Aamir Memon[Type text] https://www.facebook.com/groups/653602987987375/

Page 1

Therapeutic Exercise Systemic, planned performance of bodily movements, postures or physical activities intended to provide a patient/client with a means to prevent impairments; improve, restore, or increase physical function, prevent or decrease the health-related risk factors; optimize overall health status, fitness, or sense of well-being. Patient → Individual with impairments & functional limitations (diagnosed by a PT), who is receiving Physical therapy care to improve function & prevent disability. Client → Individual without diagnosed dysfunction, who engages in Physical therapy services to promote health & wellness, & to prevent dysfunction.

Aspects of Physical Function 1. Balance → Ability to align body segments against gravity, to maintain or move the body segments within the available BOS without falling. OR Ability to move the body in equilibrium with gravity, via the interaction of sensory & motor systems. 2. Cardiopulmonary Fitness (Endurance) → Ability to perform the low-intensity,repetitivetotal body movements over an extended time period. 3. Flexibility → Ability to move freely,without restriction. 4. Postural control,stability & equilibrium → Synonym with static & dynamic balance. 5. Co-ordination → Correct timing & sequencing of muscle firing combined with appropriate intensity of muscular contraction leading to effective initiation, guiding & grading of movement. 6. Mobility → Ability of body structures or segments to move or be moved in order to allow the occurrence of ROM for functional activities.  Active → depends on Neuromuscular activation  Passive → depends on Soft tissue extensibility 7. Muscle performance → Capacity of muscle to produce tension & do physical work.  Encompasses → Strength, Power & Endurance. 8. Neuromuscular control → Interaction of sensory & motor systems that enables the muscle to anticipate or respond to the proprioceptive & kinesthetic information & subsequently to work in correct sequence to create co-ordinated movements. 9. Stability → Ability of neuromuscular system through synergistic muscle action to hold a proximal part/distal body segment in a stationary position or to control a stable BOS during superimposed movement. 10. Joint stability → Maintenance of proper alignment of bony partners of a joint by means of passive or the dynamic components.

Therapeutic Exercise Interventions  Aerobic conditioning & reconditioning.

       

Muscle performance exercises → Endurance, Power, & Strength Training Stretching techniques → Muscle lengthening procedures, Joint mobilization Neuromuscular control, Inhibition, Facilitation, & Postural awareness training Postural control, Body mechanics, & Stabilization exercises Balance exercises & agility training Relaxation exercises Breathing exercises, Ventilatory muscle training Task-specific functional training

Evidence Based Practice Conscious, explicit, & judicious use of current best evidence in making decisions about the care of an individual patient. Steps:1. Identify a patient problem & convert it into a specific question 2. Search the literature & collect clinically relevant, scientific studies than certain evidence related to the question 3. Critically analyze the patient evidence found during the literature search & the applicability of the information to the identified patient problem 4. Integrate the appraisal of the evidence with clinical expertise 5. Incorporate the findings & decisions into patient management 6. Assess the outcomes of interventions & ask another question if necessary

Disablement process & models Disablement → Impact & functional consequences of acute or chronic conditions on specific systems that comprise basic human performance & an individual’s ability to meet necessary, customary, expected & desired social functions & roles. Comparison of terminology in disablement models MODEL

TISSUE/CELLULAR

ORGAN/SYSTEM

PERSONAL

SOCIETAL LEVEL

Nagi

Active pathology

Impairments

Functional limitation

Disability

ICIDH* ICF*

Disease ---

Impairments Impairments

Disability Activity limitation

Handicap Participation restriction ICIDH →International Classification of Impairments, Disabilities & Handicapped (by WHO) NCMRR → National Center for Medical Rehab: & Research (added Physical & Social Factors) ICF → International Classification of Functioning, Disability,& Health (Biopsychosocial model of disablement) (added Contextual Factors → Environmental & Personal)

Pathology/Pathophysiology

Disruption of the body’s homeostasis as a result of acute or chronic diseses,disorders, or conditions characterized by set of abnormal findings-signs & symptoms- that indicate alterations/interruptions of body structures/function primarily identified at the cellular level.  Alteration of Anatomical,Physiological, & Psychological structures. Impairments Consequences of pathological conditions that reflect abnormalities of the body systems, organs, or tissue level.  Direct/Primary Impairment → arise directly from pathology  Indirect/Secondary Impairment → result of pre-existing impairments  Composite Impairment → combination of Primary & Secondary Impairment Categories of Impairments 1. Musculoskeletal  Pain,muscle weakness, ↓endurance, joint hypomobility  Muscle length & strength imbalances  Limited ROM → Restriction of joint capsule & periarticular connective tissue, ↓ muscle length 2. Neuromuscular  Pain, abnormal tone (hyper- or hypo- or dystonia)  Delayed motor development, Inco-ordination & faulty timing  Impaired balance, postural stability or control  Ineffective/inefficient functional movement strategies 3. Cardiopulmonary  ↓aerobic capacity→ cardiopulmonary endurance  Impaired circulation → Lymphatic,Venous, Arterial  Pain with sustained physical activity → intermittent claudication 4. Integumentary  Skin hypomobility → Immobile/Adherent scaring Functional Limitations Result of impairments characterized by decreased ability of a person to perform actions or components of motor skills in an efficient or typically expected manner  Physical, Social, Psychological nature  Synonym used by WHO → Ability Limitation Categories of Functional Limitations 1. Functional Limitations to perform ADLs  Bathing, Dressing, Feeding 2. Functional Limitations to perform IADLs  Occupational tasks, School-related tasks, community mobility, Housekeeping, Recreational activities.

3. Physical task related Functional Limitations  Reaching & grasping, Lifting & carrying, Pushing & pulling, Bending & stooping, Turning & twisting, Throwing & catching, Rolling & standing, Squating & kneeling, Standing up & sitting down, Getting in & out of the bed, Ascending & descending stairs, Kicking, Hopping, & Jumping. Disability Inability to perform/participate in activities/tasks related to one’s self, home, recreation, or community in a manner/to the extent that individuals/the community as a whole perceive as “normal”. Activities relevant to disability  Self-care, community mobility, occupational & school-related tasks, home management (indoor/outdoor), recreational & leisure activities, caring for dependents, community responsibilities & service.  “Participation Restriction” term used by ICF Disablement Risk Factors 1. Biological factors  Age, Sex, Race  Height/Weight relationship  Congenital abnormalities & disorders  Family history of a disease → Genetic predisposition 2. Behavioral/Psychological/Lifestyle factors  Sendentary lifestyle  Use of tobacco,alcohol, other drugs  Poor nutrition  Low level of motivation  Difficulty dealing with change  Negative effect 3. Physical Environment Characteristics  Architecture barriers in home, community, workplace  Engonomic characteristics of home, work, school environment 4. Socioeconomic factors  Low economic status  Low level of education  Inadequate access to health care  Limited family/social support

Clinical Decision Making Dynamic complex process of reasoning & analytical i.e. critical thinking that involves making judgements & determinants in context to the patient care.  Hypothesis Oriented Algorithm for Clinicians-II → HOAC-II

 “Clinical Prediction Rules” Tool → assist in & improve the decision making process Requirements for skilled clinical decision making             

Knowledge of pertinent information about the problem(s) Prior clinical experience with the same or similar problems Ability to recall relevant information Cognitive and psychomotor skills to obtain necessary knowledge of an unfamiliar problem Ability to integrate new and prior knowledge An efficient information-gathering and information processing style Ability to obtain, analyze, and apply evidence from the literature Ability to critically organize, categorize, prioritize, and synthesize information Ability to recognize clinical patterns Ability to form working hypotheses about presenting problems and how they might be solved An understanding of the patient’s values and goals Ability to determine options and make strategic plans Use of reflective thinking and self-monitoring strategies to make necessary adjustments

Prognosis Prediction of patient’s optimal level of function expected as a result of a course of treatment & anticipated length of time needed to reach a specified functional outcome.

Chapter 2

Health General physical, mental & spiritual condition of body

Wellness A state of good health often achieved through healthy lifestyle choices

Health promotion Contribution to growth & development of health

Prevention 1. Primary → preventing a target condition/problem in an individual/community at risk. Example → developing fitness program for children → prevent obesity 2. Secondary → decreasing the duration & severity of a disease Example → developing resistance program for individuals with Osteoporosis 3. Tertiary → decreasing degree of disability & promoting rehabilitation for individuals with chronic/irreversible disease Examples → developing fitness program for individuals with SCI

Determining readiness to change ― Behavioral Change Theories 1. Social cognitive theory → looks at brief systems of individuals 2. Health belief model → based on sufficient concern about developing an illness―perceived threat.  Belief that by following the health recommendations it is possible to achieve the desired outcomes at an acceptable cost 3. Transtheoretical model → looks at the stages required to make changes 1) Precontemptation 2) Preparation 3) Action 4) Contemptation 5) Maintenance

Chapter 3

Types of ROM Exercises 1. Passive ROM “Movement of a body segment within the unrestricted ROM that is produced entirely by an external force”.  There is no/little voluntary muscle contraction  External force → gravity, machine, another person/body part 2. Active ROM “Movement of a body segment within the unrestricted ROM that is produced by active contraction of muscles crossing that joint”. 3. Active-Assisted ROM “Type of A-ROM involving manual/mechanical assistance provided by an outside force because the prime mover muscles need assistance to complete the motion”.

Indication of ROM Exercises 1. Passive ROM  Acute inflamed tissue → 2-6 days  Comatose/Paralyzed/Completely bed-ridden patient 2. Active & Active-Assisted ROM  Active muscle contraction → Active ROM  Aerobic conditioning program → Active ROM  Region above & below the immobilized segment → Active ROM  Weak musculature → Active- Assisted ROM  Control gained → Manual/Mechanical Resistance Exercise → Improve muscle performance

Goals of ROM Exercises Passive ROM Primary Goal  Decrease complications of immobilization i.e. Cartilage degeneration, Adhesion & Contracture formation, Sluggish circulation Specific Goals  Maintain joint and connective tissue mobility     

Minimize the effects of the formation of contractures Maintain mechanical elasticity of muscle Assist circulation and vascular dynamics Enhance synovial movement for cartilage nutrition and diffusion of materials in the joint Decrease or inhibit pain



Assist with the healing process after injury or surgery

 Help maintain the patient’s awareness of movement Other uses 

Determine limitations of motion, to determine joint stability, and to determine muscle and other soft tissue elasticity.  Demonstrate the desired motion for an active exercise program.  Used preceding the passive stretching techniques.

Active & Active-assisted ROM Primary Goal  Similar to PROM in absence of inflammation & contraindication Specific Goals     

Maintain physiological elasticity and contractility of the participating muscles Provide sensory feedback from the contracting muscles Provide a stimulus for bone and joint tissue integrity Increase circulation and prevent thrombus formation Develop coordination and motor skills for functional activities

Limitations of ROM Exercises Passive ROM   

Prevent muscle atrophy Increase strength or endurance Assist circulation to the extent that active, voluntary muscle contraction does

Active ROM  

Maintain or increase strength in a strong muscle Develop skill or coordination except in the movement patterns used.

Contraindications  After acute tears, fractures, surgery  Disruption to the healing process  Increased pain & inflammation

Precautions  MI, CABAGE, Percutaneous transluminal coronary angioplasty  Venous stasis & thrombus formation

Principles & Procedures of Application 1. Examination, Evaluation, & Treatment planning 2. Patient Preparation 3. Application of Techniques

Self-assisted ROM → S-AROM Used to protect healing tissue when more intensive muscle contraction is contraindicated i.e. Postsurgical or Post-trauma

Forms of S-AROM  Manual  Equipment  Wand or T-bar  Finger ladder,Wall climbing, Ball rolling  Pulleys  Skate or Powder board (Hip abd: & adduction, Shoulder Horizontal flexion & extension)  Reciprocal Exercise devices → Bicycle, Upper/Lower body ergometer etc

Continuous Passive Motion (CPM) “Passive motion performed by a mechanical device that moves the joint slowly & continuously through a controlled ROM”.  Beneficial healing effects on diseased/injured structures Benefits ↓ Negative effects of immobilization→ Arthritis, Contractures, Intra-articular fractures ↑Recovery rate & ROM―post-surgical Demonstration by Salter    

Prevents development of adhesions and contractures and thus joint stiffness Provides a stimulating effect on the healing of tendons and ligaments Enhances healing of incisions over the moving joint Increases synovial fluid lubrication of the joint and thus increases the rate of intra-articular cartilage healing and regeneration  Prevents the degrading effects of immobilization  Provides a quicker return of ROM  Decreases postoperative pain  Decreases postoperative blood drainage & increases analgesia

Chapter 4

Mobility “Ability of structures/body segments to move/be moved to allow the presence of functional ROM”. OR “Ability of an individual to initiate, control, or sustain active movements of body to perform simple to complex motor skills is called Functional Mobility”.  Associated with Joint integrity & flexibility

Hypomobility “Restricted/decreased motion caused by adaptive shortening of soft tissues due to disorders/situations”.  Leads to functional limitations & disabilities  Stretching interventions → integral component  Causes → decreased ROM, Soft tissue stiffness, Contracture development Factors predisposing to Hypomobility  Prolonged immobilization o Extrinsic  (Casts & Splints, Skeletal traction) 

o

Fractures, Osteotomy, Soft tissue trauma & repair

Intrinsic  Pain  Microtrauma or macrotrauma; degenerative diseases  Joint inflammation & effusion  Joint diseases or trauma  Muscle, tendon, facial disorders  Myositis, tendonitis, fasciitis  Skin disorders  Burns, skin grafts, scleroderma  Bony block  Osteophytes, ankylosis, surgical fusion  Vascular disorders  Peripheral lymphedema

 Sedentary lifestyle and habitual faulty or asymmetrical postures o

Confined to bed or a wheelchair; prolonged positioning associated with occupation or work evironemt

 Postural malalignment : congenital or acquired o Scoliosis, kyphosis  Paralysis, tonal abnormalities, and muscle imbalances

o

Neuromuscular disorders or diseases ; CNS or PNS dysfunction

 spasticity, rigidity, flaccidity, weakness, muscle guarding, spasm  Tissue trauma resulting in inflammation & pain  Congenital or acquired deformities

Flaxiblity “Extensibility of soft tissues that surround/cross the joints (muscles,fascia,tensdons,capsules,ligaments, blood vessels,skin)”. OR “Ability to move a single joint/series of joints smoothly & easily through unrestricted, pain-free ROM”. OR “Degree to which an active muscle contraction moves a body segment through the available ROM”. Determinants → muscle length, joint integrity, periarticular soft tissue extensibility Depends on → muscle & connective tissue extensibility Factors preventing MSK injuries  Soft tissue mobility  Neuromuscular control  Muscle strength & endurance Passive flexibility (Passive mobility/ROM) “Ability due to which a joint can passively be moved through the available ROM”. Depends on → muscle & connective tissue extensibility Dynamic flexibility (Active mobility/ROM) “Degree to which an active muscle contraction move a body segment through the available ROM”. Depends on → degree of movement occurring & tissue resistance during movement

Muscle tightness “Adaptive shortening of contractile & non-contractile elements of a muscle.

Tightness “Restricted motion due to adaptive shortening of soft tissues”.

Contraction “Process of developing muscle tension during shortening/lengthening”.

Contracture “Adaptive shortening of muscle-tendon unit & other soft tissues crossing/surrounding a joint resulting in significant resistance to active/passive stretch & ROM limitation”. Contracture→ complete loss of motion Shortness → partial loss of motion Designation of Contractures:Shortened Elbow Flexors → No full elbow extension → Elbow Flexion Contracture Types of Contractures 1. Myostatic/Myogenic Contracture “Adaptive shortening of musculotendinous unit & loss of ROM without specific muscle pathology”.  Morphology → ↓ in sarcomere number →normal sorcomere size  Resolve with Stretching exercises in short time 2. Pseudostatic/Apparent Contracture “Impaired mobility & limited ROM due to hypotonicity (spasticity/rigidity),muscle spasm/guarding, & pain”.    3.

Appearance of involved muscles → Constant state of contraction Inhibition procedures applied → decrease muscle tension Causes of hypotonicity→ CVA, TBI, SCI Arthrogenic & Periarticular Contracture

Arthrogenic→ result of intra-articular pathology Periarticular→ result of decreased /loss of connective tissue mobility that cross/attach to joint/joint capsule.  Changes include → adhesions, synovial proliferation, joint effusion, irregularities in articular cartilage,osteophyte formation. 4. Fibrotic & Irreversible Contracture Fibrotic→ result of fibrous changes in connective tissue of muscles & periarticular cartilage causing adhesions & contracture development  Stretching ↑ROM; Difficult to re-establish optimal tissue length Irreversible→permanent loss of soft tissue extensibility due to replacement of relatively nonextensible, fibrotic adhesions & soft tissue/heterotropic bone  Can’t be reversed by nonsurgical intervention  Occurs with chronic fibrotic contracture

Indications for Stretching    

Limited ROM → lead to structural deformities Muscle weakness & shortness of opposite tissue Part of total fitness program → minimize postexercise muscle soreness Causes of limited ROM→ Loss of Soft tissue extensibility→adhesions,contractures,scar formation

Contraindications to Stretching       

A bony block limits joint motion. Recent fracture and incomplete bony union. Acute inflammatory or infectious process (heat and swelling) or soft tissue healing could be disrupted in the tight tissues and surrounding region. Sharp, acute pain with joint movement or muscle elongation. Hematoma or other indication of tissue trauma. Hypermobility already exists. Shortened soft tissues o Provide necessary joint stability in lieu of normal structural stability or neuromuscular control. o Enable a patient with paralysis or severe muscle weakness to perform specific functional skills otherwise not possible.

Interventions to increase Soft tissue mobility Stretching & Mobilization → therapeutic maneuver to increase extensibility of restricted soft tissues. 1. Manual & Mechanical/Assisted & Passive Stretching “Sustained/intermittent external,end-range stretch force applied with overpressure via manual contact/mechanical device to elongate a shortened musculotendinous unit & periarticular connective tissue by moving a restricted joint just past the available ROM”.  Passive stretch → in relaxed patient  Active stretch → with patient assistance in moving the joint through a greater ROM 2. Self Stretching (Flexibility exercises or Active stretching) “Stretching exercise carried out independently by a patient after the instructions & supervision by a therapist”. 3. Neuromuscular Facilitation & Inhibition Techniques “Purported to relax tension in shortened muscle reflexively prior to/during muscle elongation”.  PNF→ Inhibition techniques to assist muscle elongation  Combined inhibition/muscle lengthening procedures → PNF, Active inhibition, Active/facilitated stretching 4. Muscle Energy Techniques/Post-isometric relaxation (based on neuromuscular inhibition principle) “Manipulative procedures to lengthen muscles & fascia to mobilize joints”.  Uses voluntary muscle contraction in a precisely controlled direction & intensity against a counterforce by the therapist.  Evolved from Osteopathic medicine.

5. Joint mobilization & manipulation “Manual therapy techniques applied to joint structures & used to stretch capsular restrictions or reposition a subluxed/dislocated joint”. 6. Soft tissue mobilization & manipulation “Techniques to improve muscle extensibility & involve the application of specific & progressive forces to effect the changes in the myofascial structures that can bind soft tissues & improve mobility”.  Techniques include → Friction massage, Myofascial release, Acupressure, Trigger point therapy. 7. Neuromeningeal mobilization/Neural tissue mobilization “Techniques to prevent post-traumatic & post-surgical adhesions or scar tissue formation around the meninges & nerve roots or at the site of injury at plexus on peripheral nerves”.

Selective Stretching “Process whereby the overall function of a patient may be improved by applying stretching techniques selectively to some muscles & joints but allowing limitation of motion to develop in other muscles & joints”.  Decision for selective stretching of musculotendinous units & joints is made in patients with permanent paralysis.

Overstretching & Hypermobility Overstretching→ stretch beyond the normal muscle length & the joint ROM & the surrounding soft tissues.  Results in hypermobility/increased mobility  Needed in sports requiring extensive flexibility  Create joint stability when:o There are insufficient supporting structures of joint o There is insufficient strength around a joint  Instability causes → pain & MSK injuries

Determinants of Stretching Interventions 1. 2. 3. 4. 5. 6. 7.

Alignment Stabilization Intensity of Stretch/Magnitude of force Duration of Stretch Speed of Stretch Frequency of Stretch Mode of Stretch

Properties of Soft tissue response to Immobilization Immobility due to injury,disease, or surgery results in: Decreased connective tissue extensibility→ Noncontractile element of muscle  Primary cause of Restricted ROM Factors affecting response of soft tissues: Direction, Velocity, Intensity, Duration & Frequency of Stretch force  Tissue temperature Tissue lengthening is affected by: Mechanical characteristics of Contractile & Noncontractile soft tissue  Neurophysiological properties of contractile tissue Soft tissues that become restricted & impair mobility are: Contractile & Noncontractile elements of muscle  Conective tissues → Tendons, Ligaments, Fascia, Capsule, Skin Soft tissue stretching causes →Elastic, Viscoelastic, & Plastic changes. 1. Elasticity →Ability of soft tissue to gain its prestretch resting length directly after the removal of short duration stretch force. 2. Viscoelasticity→ Time-dependent property of soft tissue that initially resists the deformation of tissue when a stretch force is first applied.  Possesed by connective tissue only(not the contractile element). 3. Plasticity→ Tendency of soft tissue to adopt a new & greater length after the removal of stretch force.

Mechanical Properties of Contractile Tissue  Contractile elements of muscle have →contractility & irritability  Noncontractile elements of connective tissue have →ability to resist deforming forces  Endomysium(muscle harness)→ separate muscle fibers & myofibrils  Perimysium→ encases fiber bundles  Epimysium→envelops fascial sheath around entire muscle  Connective tissue framework → primary source of muscle resistance to passive elongation.  Contracture→ adhesions b/w collagen fibers that resist movement. Contractile elements of Muscle Muscle→Muscle fibers(parallel)→Myofibrils→Sarcomere/Contractile unit(series)→Composed of overlapping Myofilaments i.e. Actin & Myosin

Mechanical Response of Sarcomere to Stretch & Immobilization  Changes occur in contractile unit (sarcomere) with stretch & immobilization.  Noncontractile structures also affect the response to stretch & immobilization. Response to Stretch  Stretch force is transmitted to muscle fibers via connective tissue  Passive stretch→ involves longitudinal & lateral transduction  Initial lengthening in series elastic component of connective tissue→ Tension rises sharply after a point→ mechanical disruption leading to abrupt sarcomere lengthening k/n Sarcomere Give.  Short-term stretch→ Elasticity observed in muscle  Stretch force maintained over an extended time period→ Plastic length increases occur

Response to Immobilization & Remobilization Morphological Changes Muscle immobilized for a prolonged time period, results in:   

Decay of contractile proteins Decrease in muscle fiber diameter Decrease in Myofibril number Decrease in Intramuscular capillary density o Results in Atrophy & weakness→ decreased muscle force o Increase in fibrous & fatty tissue

Atrophy occurs more quickly & extensively in: Tonic (Slow-twitch) postural muscles than Phasic muscles.  Singnificant deterioration in motor unit recruitment → EMG results. Immobilization in shortened position After surgery/fracture →↓ in muscle length,muscle fibers, sarcomere number due to Sarcomere Absorption Faster absorption than muscle’s ability to regenerate sarcomere: Results in muscle atrophy & weakness  Rapid in shortened than lengthened position Increased proportion of fibrous tissue & subcutaneous fat: Decreased extensibility of shortened muscle  Protect weakened muscles on stretch Immobilization in lengthened position Application of a series of positional casts→ serial casts

OR Use of dynamic splint to stretch a long-standing contracture & increase ROM: Muscle adopt by increasing sarcomere number―Myofibillogenesis o Maintain greatest functional overlap of Actin & Myosin  Relatively plastic (permanent) form of muscle lengthening Note: - Adoptation of sarcomeres to prolonged positioning is transient, lasting only 3-5 weeks if muscle resumes its preimmobilization use & degree of lengthening for functional activities.

Neurophysiological Properties of Contractile Tissue Two sensory organs of muscle-tendon unit → Muscle spindle & GTOs Mechanoreceptors that convey information to CNS about the changes in muscle tendon unit (length & tension) & affect muscle response to stretch. Muscle Spindle (Major Sensory Organ of Muscle) Sensitive to quick & sustained (tonic) stretch Receive & convey information about the changes in length & velocity of length changes Small, encapsulated receptors Composed of:1. Afferent Sensory fiber endings 2. Efferent Motor fiber endings 3. Specialized muscle fibers k/n Intrafusal fibers Intrafusal fibers lie b/w & parallel to Extrafusal fibers ―muscle body  Intrafusal fibers are connected at the ends to Extrafusal fibers  Only ends/Polar Regions are contractile Small diameter motor neurons k/n “ɣ-motor neurons” innervate Polar Regions of intrafusal fibers. Large diameter motor neurons k/n “ɑ-motor neurons” innervate extrafusal fibers. Intrafusal fiber types are:1. Nuclear Bag Fibers  Give rise to primary−type Ia afferent endings  Sense & cause muscle to respond to quick & sustained (tonic) stretch. 2. Nuclear Chain Fibers  Give rise to secondary−type II afferent endings  Sensitive to tonic stretch only. Primary & Secondary afferent fibers synapse ɑ- or ɣ-motor neurons

o

Stimulation→ Excitation of Extrafusal & Intrafusal fibers

Stimulation of Sensory fibers via stretch is caused by: Overall lengthening of the muscle  Stimulating intrafusal fiber contraction via ɣ-efferent neural pathway. Golgi Tendon Organs (GTOs) Sensory organ located near the musculotendinous junction of the extrafusal muscle fibers. Monitor changes in Tension of a musculotendinous unit Encapsulated nerve endings woven in collagen strands of a tendon Transmit sensory information via Ib fibers Tension develops in Muscle→GTOs inhibit ɑ-motor neuron activity→decrease tension in musculotendinous unit being stretched. Low threshold i.e. sensitive to slight changes of tension  Passive stretch & active muscle contraction.

Neurophysiological Response of Muscle to Stretch Quick/Slow stretch force to muscle-tendon unit→Primary & Secondary Intrafusal afferents sense length changes→Extrafusal fiberactivation via ɑ-motor neurons in spinal cord results in: Activation of stretch reflex→ decreased activity/inhibition of antagonist(inhibition of muscle on opposite side) k/n Reciprocal Inhibition  Increase/facilitate tension in stretched muscle→ cause resistance to lengthening→ effectiveness of stretching is compromised. GTOs impact in prolonged stretch force→ inhibitory on the level of muscle tension in muscle-tendon unit is k/n Autogenic Inhibition→ contributes to Reflexive muscle relaxation in stretching & enables muscle to elongate against less muscular tension. Low-intensity, prolonged stretch preferred → inhibit muscle tension & allow sarcomeres to remain relaxed & lengthen.

Mechanical Properties of Noncontractile Soft/Connective Tissue Adhesions & contractures develop in: Ligaments,Tendons, Joint Capsule, Skin &  Noncontractile elements of muscle (Endomysium,Perimysium,Epimysium)

Composition of Connective Tissue

Connective tissue is composed of: Collagen, Elastin & Reticulin fibers  Nonfiberous Ground Substance 1. Collagen Fibers Responsible for Tissue Strength→ Resist Tensile Deformation Collagen ɑ Tissue Stability Parallel fiber arrangement withstands greater tensile loads → Tendons 19 types & 6 Classes Type-I fibers in tendons & ligaments→ stable covalent bonds Topocollagen→myofibril→subfibril→fibril→fascicle(tendon,ligament,skin) 2. Elastin Fibers Provide extensibility Elastin ɑ Flexibility Increased elongation with smaller loads 3. Reticulin Fibers Provide tissue with bulk 4. Ground Substance Composed of→ Proteoglycans & Glycoproteins Proteoglycans  Hydrate the matrix, Stabilize collagen network, resist compressive forces  Most important in Cartilage & IV discs Organic Gel containing Water: Decrease friction b/w fibers  Transport nutrients & metabolites  Maintain space b/w fibers→ prevent excessive cross linkage

Stress-Strain Curve Interpret mechanical behaviour of connective tissue under stress loads Stress → force per unit area Mechanical stress→ resistance (internal reaction) to external load

Tension→ force applied perpendicular to cross-sectional area of tissue in a direction away from the tissue  Stretching force is an example of tension stress Compression→ force applied perpendicular to cross-sectional area of tissue in a direction towards the tissue  Examples include muscle contraction & loading in weight-bearing Shear → force applied parallel to cross-sectional area of tissue Strain →amount of deformation/lengthening when load (stress) or stretch force is applied.

Cyclic Loading & Connective Tissue Fatigue “Principle used for stretching by applying repetitive (cyclic) loading at a submaximal level on successive days”. Repetitive tissue loading→ increase heat production→ resulting in failure below yield point Applied load is inversely proportional to number of cycles needed for failure Load intensity is determined by patient tolerance Minimal load is needed for this failure Endurance limit→ below minimum load, apparently infinite number of cycles doesn’t cause failure Connective tissue fatigue from cyclic loading results in Stress Fractures & Overuse Syndrome Time is allowed b/w bouts of cyclic loading to allow for Remodeling & Healing in new range.

Regions of Stress-Strain Curve Toe-Region → Area where there is considerable deformation without the use of much force  Range where the most functional activity occurs Elastic Range/Linear Phase→ Stress is directly proportional to tissue’s ability to resist force    

Occurs when gentle stretch is applied at the End-ROM Some microfailure n/w collagen fibers begins Some water is displaced from the Ground substance Complete recovery from this deformation occurs

Elastic Limit→ Point beyond which the tissue doesn’t return to its original shape & size Plastic range→ Range beyond the elastic limit extending to the point of rupture  Permanent deformation occurs after the release of stress  Heat is released & absorbed in the tissue

 Rupturing of fibers results in increased length Ultimate Strength→ the greatest load the tissue can sustain  Increased strain/depolarization occurs without increase in stress Region of Necking→ region where there is considerable tissue weakening & if the stress is maintained results in complete tissue tearing  Ligaments may withstand strain of 20-40% Failure→ Rupture of tissue integrity

Structural Stiffness Tissues with increased stiffness: Increased slope in Elastic region  Less elastic deformation with greater stress Contracture & Scar formation: Increased stiffness  Increased degree of bonding b/w collagen fibers & surrounding matrix

Connective Tissue Response to Loads Creep→ occurs when load is applied for an extended time period, the tissue elongates & results in permanent deformation Related to viscosity & time-dependent Deformation depends on Amount & Rate of force applied Low magnitude loads applied in Elastic range for long periods→result in increase in connective tissue deformation & ultimately allow gradual remodelling of collagen fibers & Redistribution of water to surrounding tissue Increase in temperature → increase in creep→ increase tissue distensibility

Stress Relaxation “Principle used in prolonged stretching procedures where the stretch position is maintained for several hours or days”. Occurs when load is applied o stretch a tissue while the length is kept constant After initial creep there is: Decrease in force needed to maintain that length  Decrease in tissue tension

Related to: Viscoelastic qualities of coneective tissue  Redistribution of water content

Changes in Collagen affecting Stress-Stain Response Effects of Immobilization    

Tissue weakening due to collagen turnover & weak bonding b/w new fibers Adhesion formation due to increased cross-linkage b/w disorganized collagen fibers Decreased effectiveness of ground substance maintaining space & lubrication b/w fibers Rate of return to normal tensile strength is slow

Effects of Inactivity ― decreased normal activity  Decrease in size & amount of collagen fibers→ tissue weakening  Proportional increase in Elastin predominance→ increased compliance  5 months of regular cyclic loading→ recovery Effects of Age  Decrease in maximum tensile strength & elastin modulus  Decreased rate of adaptation to stress  Increased tendency for overuse syndromes, fatigue fractures, tears with stretching Effects of Corticosteroids  Long-lasting deleterious effect on mechanical properties of collagen  Decrease in tensile strength  Fibrocyte death Effects of Injury  Excessive tensile loading→ ligament & tendon rupture at the musculotendinous junction  Healing→ newly synthesized type-III collagen  Remodeling→ collagen type-I o Begins 3 weeks after injury till months-years

Precautions for Stretching General Precautions    

Do not passively force a joint beyond its normal ROM; be aware of age & sex related changes in flexibility. Use extra caution in patients with known or suspected osteoporosis due to disease, prolonged bed rest, age, or prolonged use of steroids Protect newly united fractures Avoid vigorous stretching of muscles and connective tissues that have been immobilized for an extended period of time→ loss of tensile strength in tendons, ligaments o High-intensity short-duration stretch→ more trauma→ soft tissues weakness.



Progress the dosage (intensity, duration, and frequency) gradually to minimize soft tissue trauma and post-exercise muscle soreness  Avoid stretching edematous tissue→ increased pain and edema  Avoid overstretching weak postural muscles

Special Precautions―Common Errors & Potential Problems Nonselective/Poorly balanced stretching activities  General flexibility programs include: - stretching the body regions that are mobile/hypermobile but may neglect the regions that are tight due to faulty posture/inactivity.  Faulty postures may worsen rather than the improvement Insufficient warm-up  Individuals in flexibility programs often fail to warm-up before stretching Ineffective stabilization  Exercise may fail to stretch the intended tight structure & transfer the force to the structures that are already mobile/hypermobile. Use of Ballistic Stretching  Uncontrolled stretching→ increase post-exercise muscle soreness & soft tissue injury Excessive Intensity  Effective flexibility routine should be progressed gradually & not cause pain or excessive tissue stress. Abnormal Biomechanics  Some exercises don’t respect regional biomechanics→ “Hurdler’s” Stretch Insufficient Information about Age-Related Differences  Result of normal aging process→ decreased connective tissue mobility→ decreased activity level

Adjuncts to Stretching Relaxation Training “Methods of general relaxation/total body relaxation that help the patient learn to relieve/decrease pain, muscle tension, anxiety/stress & associated physical impairments (tension headache, increased BP & RR)”.

Common element is to involve→ decrease in muscle tension in entire body/region that is painful/restricted by conscious effort & thought. Mechanism→ Patient performs deep breathing exercises/visualizes a peaceful scene Examples include:1. Autogenic Training―Schultz & colleagues “Invade conscious relaxation via autosuggestion & progression of exercises & medications”. 2. Progressive Relaxation―Jacobson “Use systematic, distal to proximal, progression of voluntary muscle contraction & relaxation”.  Incorporated into childbirth education 3. Awareness through Movement―Feldenkrais “Combines sensory awareness, movements of limbs & trunk, deep breathing, conscious relaxation,& self-massage to alter muscle imbalances & abnormal postural alignment to remediate muscle tension & pain”. Indicators      

Decreased muscle tension, HR, BP, RR, & distractibility Increased skin temperature in limbs―Vasodilation Constricted pupils Little/no body movement Eyes closed & flat facial expression Jaw & hands relaxed with palms open

HEAT:



Pre-stretch warm-up → Common practice in Rehab. Programs.

 ↑ in Intramuscular temperature→ ↑ in soft tissue extensibility (contractile & non contractile)  ↑ in amount & time of stretch force.





↓ in Firing of type-2 efferent from muscle spindle



↑ in Sensitivity of GTO’s

↓ Post exercise muscle sorness and risk of soft tissue injury.

Methods of warm-up:



Thermal agents → used to heat small areas prior to or during stretching (individual joints, muscle groups, tendons) →Superficial heating agents → Hot packs, paraffin. →Deep heating agents →Ultrasound, SWD.



Low-intensity Active exercises → ↑se the circulation and body temperature. →Pre-stretching warm-up of large group of muscles. EXAMPLES → Brief walking, non fatiguing stationary bicycling, active heel raises, use of stair-stepping machine, Active arm exercises for few minutes.

Effectiveness of warm-up:



Heat combined with stretching procedures → Produce great Long-term gain in tissue length.



Pre-stretching cryotherapy → ↓ muscle tone & sensitivity during stretch ( healthy & spasticity secondary to UMNL) → Immediately after soft tissue injury → ↓ pain & muscle spasm. → Ineffective when healing & scar formation begins. → 24-48 hrs Post-soft tissue injury → ↓ swelling, pain & muscle spasm. → Soft tissues in lengthened position- Post stretching → Promote more lasting Soft tissue length & minimize Post-stretch Muscle soreness.



STRETCHING CONTRAINDICATION: inflammation & acute phase of healing.

BIOFEEDBACK – AUDIOVISUAL TOOL

   

Tool to help patient learn & practice the process of relaxation. Monitor & learn to → ↓ the amount of muscle tension, HR, & B.P. ↓sed muscle tension → ↓ pain & ↑flexibility. Help the patient learn how to Activate a muscle. o Quadriceps setting – post surgery KNEE.

Massage - For Relaxation    

Light or Deep stroking techniques → ↑ local muscle relaxation. ↑ muscle relaxation & ↓ muscle spasm. Effleurage (light stroking) → relaxation in stress & anxiety, pain management. Sports & conditioning programs → ↑recovery after sternous physical activity.

Soft Tissue Mobilization techniques – DEEP MASSAGE    

↑ mobility of adherent or shortened connective tissue – fascia, tendons, ligaments. Long enough stress applied for CREEP & stress relaxation of tissues. Myofascial massage → Stretch force applied across facial planes or between the muscles & septae. Friction massage → Deep circular or Cross-fiber massage applied → break the adhesions or minimize rough surfaces B/w Tendons & synovial sheaths. o Use: → mobility of scar tissue in healing muscle.

Joint Traction or Oscillation – Pendular Joint Motion

   

Slight manual distraction of joint surfaces. Pre or conjunct to Joint mobilization or Muscle-tendon stretching techniques o Use: inhibit joint pain & muscle spasm around a joint Uses weight of limb → distract joint surface & simultaneously oscillate & relax the limb. Further distraction → add 1-2 lbs weight to the extremity → stretch force on joint surfaces.

Chapter # 5 Mobilization and manipulations :

Joint mobilizations: Manual therapy techniques used to modulate pain and RX joint dysfunction that limits ROM via addressing altered joint mechanics.  Specifically address restricted capsular tissues & minimize abnormal compression (stress) on articulating cartilage.  Anatomy, arthrokinematics, pathology, neuromuscular system. Terms: Manipulations: ↑ Velocity, ↓amplitude, forced passive movement that cannot be prevented by the patient - THRUST

Mobilizations: Passive, skilled manual therapy techniques applied to the joints & related soft tissues at varying speeds and amplitudes using physiological and accessory movements.

Self-mobilizations (auto-mobilizations): Self stretching techniques using joint traction or glide that direct the stretch force t the joint capsule.

Mobilization with movement (MWM): Concurrent application of the sustained accessory mobilizations applied by the therapist and an active physiological movement to the End range by the patient.  Always applied in Pain-free direction.  Brain mulligan- New Zealand

Accessory movements (Arthro kinematics): movements in joint & the surrounding tissue that cannot be actively performed by patient. Component motions → accessory movement → motion that accompanies active motion but is not under volunteer control. →Upward scapular rotation & rotation of clavicle → shoulder flexion → →Rotation of fibula → Ankle motion. EXAMPLES: Distraction, sliding, compression, rolling, spinning.$

Physiological movements (Osteokinematics): Classic or traditional movements the patient can do voluntarily. Examples: Flexion, abduction, rotation

Joint Play: Motion b/w joint surfaces & Dispensibility or “give” in the joint capsule which allows the bone to move. Thrust: High velocity, short-amplitude motion at the end-range of physiological limit of joint which cannot be prevented by the patient.  Alter positional relationships, Snap adhesions, stimulate joint receptors Manipulation under Anesthesia: Medical procedure to restore full Rom by breaking adhesions around a joint while the patient is anesthetized.  Rapid thrust or passive stretch using physiological or accessory movements Muscle energy: Techniques using active contraction of deep muscles that attach near the joint & whose line of pull can cause desired accessory motion.  Command for Isometric muscle contraction → cause Accessory movement

Joint motion provides sensory input relative to:  Static position & sense of speed of movement → Superficial joint capsule → Type I  Change of speed of movement → Deep layer (capsular), articular fat pad → Type II  Sense of direction of movement → Ligaments → Type-I&III receptors  Regulation of muscle tone → Type I, II, III receptors  Nociceptive stimuli → Capsule, ligament, Articular fat, peritoneum, vessel walls → Type-IV receptors BASIC CONCEPTS OF ARTHROKINEMATICS: Joint shape → Influence b/w bony partners in a joint Ovoid joints → Convex & concave Seller joints → Concave & Convex

Types of motion Swing → movement of bone lever  Flexion, extension, abduction, adduction, rotation  Amount of movement measured in degrees with a goniometer k/n ROM  Motion of bone surfaces → Rolling, sliding, spinning Roll → one bone rolling n another     

Surfaces are incongruent – new points on surface meets opposing one. Results in angular motion of bone – SWING Cause compression of surfaces on the side to which bone is swinging Combined with sliding and spinning Passive stretching using bone angulation → cause stressful compressive forces → joint damage Slide or Translation → One bone sliding (translating) across another.  Congruent surfaces → flat or curved  Some points on one surface come In contact to other one  Doesn’t occur in joints → surface not absolutely congruent

Convex – concave rule → Basis to determine the direction of mobilization  Sliding in Same direction → moving surface in Concave  Sliding in Opposite direction → moving surface in Convex Spin → Rotation of a segment about a stationary mechanical axis  Same point on moving surfaces creates an Arc of a circle  Combined with → Rolling Sliding Examples: Shoulder → flexion/extension Hip → flexion/extension Radiohumeral joint → pronation/supination

Combined Roll-Slide  Congruent joint surface ∞ Sliding  Incongruent Joint surface ∞ Rolling  Active muscle contraction → Sliding caused or Controlled → Caudal sliding of humeral head in shoulder abduction by rotator cuff muscle → Posterior sliding of tibia in knee flexions by hamstrings. → Abnormal biomechanics → Microtrauma & Joint dysfunction  Sliding → Restore joint play & Remove joint hypomobility → Traumatic glide, translation, glide.  Rolling(Passive angular stretching) → Cause joint compression PASSIVE ANGULAR STRETCHING → Bony lever — Used to stretch tight joint capsule Cause ↑ed pain or joint trauma — Because:  Use of a lever magnifies force at joint surface  Force causes excessive joint compression in direction of rolling  Roll without a slide doesn’t replicae normal joint mechanics

Joint Glide (Mobilization) Stretching → Translatoric glide — used to stretch a tight capsule Safer and more relative because:  Fore applied close o joint surface — Controlled intensity w.r.t Pathology  Direction of force replicates sliding — No cartilage compression  Small amplitude motion yet specific to Restricted (Adherent) capsule/ligament  Force is selectively applied OTHER ACCESSORY MOTIONS Compression → ↓ joint space b/w the bony patterns    

Normally occur in — Extremity and spinal joints in weight bearing Occur with muscle contraction — Provide joint stability Occur during — Rolling Normal intermittent compression loads — Articular cartilage changes & deterioration Traction(Long-axis traction) & Distraction(Joint traction, joint separation):

Traction → Longitudinal pull  Traction of humeral shaft → Glide of joint surface Distraction → separation or pulling the surface apart  Distraction of glenohumeral joint → Need pull at right angle to Glenoid force  Used to → control or relief pain when applied gently  Used to → stretch capsule when applied with stretch force

EFFECTS OF JOINT MOBILIZATION

 MORE SYNOVIAL FLUID — Bring nutrients to:  Avascular articular cartilage of joint surface  Intra-articular fibrocartilage of menisci.  Joint immobilization → Atrophy of articular cartilage  Extensibility & tensile strength of articular & periarticular tissuemaintained.  IMMOBILIZATION → Fibrofatty proliferation → Intra-articular Adhesions → Biomechanical changes (Tendon, ligament, Capsule) ↓ Joint contracture & ligament weakening

4) Progressive Limitation  Rx with joint play techniques → Maintain available ROM → Retard progressive mechanical restriction  Distraction/Glide dosage depends on → Patient response & Disease state 5) Functional Immobility — Inability to move joint for a time period Non-stretch gliding/Distraction techniques:  Maintain available Joint play  Prevent degeneration & Restricting effects of immobility Limitations  Can’t change disease process — Rheumatoid arthritis.  Can’t change inflammatory process  Rx goals:  Minimize pain  Maintain available joint play  ↓ effect f any mechanical limitation  Too vigorous application → joint trauma & hyper mobility  Outcomes depend on — Skill of therapist Contraindications 1. Hypermobility  Potential necrosis of ligament and capsule  Painful hypermobile joints→ Gentle joint-play techniques within limits of motion. 2. Inflammation  Stretching → ↑ pain & muscle guarding→ ↑ed tissue damage.  Gentle oscillatory or distraction motions → Temporarily inhibits pain.

3. Joint effusion — Traumatic or Pathological  Rapid swelling — Indicate bleeding in joint → Hemephilia or trauma. → Medical intervention (aspiration) required: o Minimize necroting effects of articular cartilage  Slow swelling — Arthritis, Mild trauma or irritation. o Indicate serious effusion — build u of excessive synovial fluid.

 Capsule is stretched → distend to accumulate extra-fluid  Extra-fluid & Muscle response to pain → Limit motion  Gentle oscillating motions — Don’t stress/stretch capsule o Block nociceptive transmission o Help improve fluid flow — maintain available joint play. Precautions       

Malignancy Bone disease detectable on radiograph Unhealed fracture — Depends upon: Site & Stabilization. Excessive pain — determine the cause & Modify Rx Hypermobility in associated joints — proper stabilization of them. Total joint replacement Systemic connective tissue disease — rheumatoid arthritis – weaken C.T.  Newly formed or weakened connective tissue → Post-trauma, surgery, disease & corticosteroid use.  Joint mobilization — safer than Passive Angular stretching

Procedure of application 1)

Examination & evaluation  Determine → Tissue limiting the function, state of pathology.  Rx directed to → relieve pain or stretch joint(soft tissue) limitation. (a) Quality of pain → Determine →stage of recovery & Dosage of technique used. (i) Pain before tissue limitation – Gentle pin-inhibiting jint techniques used → Muscle guarding after acute injury or during active stafe o disease (ii)

Pain concurrent with tissue limitation – gentle stretching techniques used → damaged tissue begins to heal — CAVITATIN

(iii) Pain after tissue limitation – Aggressive stretching with joint play techniques → Tight capsular or periarticular tissue

(b)

Capsular Restriction → Capsular limitation — Responds to Mobilization in these signs: (i) (ii) (iii) (iv)

Limited P-ROM in capsular pattern Firm end feel – when range limiting tissue is over pressured ↓ed joint-play movement with “Mobility tests” Adherent or contracted ligament limits motion:  ↓ed Joint-play when ligament fibers are stressed.

Grades & Dosage of movement: 1. Graded oscillation techniques a. Grade-I: Small amplitude, Rhythmic oscillations at the beginning of the range. b. Grade-II: Large amplitude, Rhythmic oscillations with in the range — doesn’t reach the limits. c. Grade-III: Long amplitude, rhythmic oscillations at the limit of motion & stressed into tissue resistance d. Grade-IV: Small amplitudes, rhythmic oscillations at the limit of available motion & stressed into tissue resistance e. Grade-V: Small amplitude, high velocity thurst, perfrmed to snap adhesions at the limit of motion. USES:  Grade – I & II: used primarily to Rx pain  Oscillations → inhibit nociception via Mechanoreceptor stimulation  Non-stretch motions → More synovial fluid → cartilage nutrition.  Grade – III & IV: primarily stretching maneuvers TECHNIQUES:  Oscillations performing using:  Physiological motions → Osteokinematics  Joint-play techniques → Arthrokinematics 2. Sustained Translatory Jint Play Techniques a. Grade-I: Small mplitude distraction with no stress on capsule. → Eqiuilize → Cohesive forces, muscle tension & Atmosphere pressure (joint). b. Grade-II: TIGHTEN → Enough distraction to tighten tissue around the joint → “Taking up the slack” — called Kaltenborn c. Grade-III: STRETCH → Long enough distraction/glide to stretch capsule & surround periarticular structures.

USES: GRADE-I: LOOSEN → used with all gliding motions, to relieve pain GRADE-II: TIGHTEN→ Used for initial Rx determine joint Sensitivity.  Intermittent → Inhibit pain  Glides → Maintain joint play – Without ROM GRADE-II: STRETCH → used to stretch structures → ↑ joint play. Indication ----Mobilization 1. Joint pain, reflux muscle guarding & muscle spasm  Rx with gentle joint – play techniques → Stimulate neurophysiological effects → Stimulate Mechanical effects a) Neurophysiological effects: Small- amplitude oscillatory and oscillatory and distraction movements.  Stimulate Mechano-receptors  Inhibit Nociceptive stimuli at spinal cord/Brain-stem level b) Mechanical effects Small-amplitude distraction or gliding movements  Cause --Synovial fluid motion  Bring nutrients to Avascular portion of Articular cartilage (Intra-articular and Fibrocartilage) Gentle joint-play techniques  Help maintain nutrient exchange  Prevent painful and degenerative effects of stasis in pain and Inflammation 2. Reversible joint Hypomobility  Rx with – progressively vigorous Joint-play stretching  Elongate hypomobile capsular & ligamentous connective tissue  Sustained or Oscillatory stretch forces  Distend shortened tissue mechanically 3. Positional faults/Subluxations  Muscle imbalances, traumatic injury, long-term Immobilization  Malposition of bony partners  Limited ROM and pain with Neuromuscular imbalances 

MWM techniques---- Realign the bony partners.

 Manipulation→ Reposition on obvious subluxation 

→ Pulled elbow or Capitate - lunate subluxation

TYPES OF STRETCHING: 1. 2. 3. 4. 5. 6. 7. 8.

Static Stretching. Cyclic Stretching. Ballistic Stretching. PNF Stretching. Manual Stretching. Mechanical Stretching. Active Stretching. Passive Stretching

Static stretching: commonly used method Elongation of soft tissues just past the point of tissue resistance & then held in elongated position with a sustained stretch force over a period of time.     

Duration of single stretch cycle → 5-sec to 5 min/repetition. Muscle tension → ½ the ballistic stretching. ↑ flexibility. Low intensity → less tissue trauma & post exercise muscle soreness. Facilitate impulses from primary afferents of muscle spindle – 1a fibers → contribute to muscle relaxation via Inhibiting tension in contractile

units.

Static progressive stretching:

Shortened soft tissues held in comfortably lengthened position until a degree of relaxation is felt & are the incrementally lengthened even further & held in a new End range position for additional duration of time.  Examine effectiveness of → DYANMIC ORTHROSIS.

Cyclic or intermittent stretching:

Relative Short-duration stretching force thet is repeatidly but gradually applied, released & then applied. OR. End range stretch force with ↓ed Velocity & intensity & in a controlled manner. o o

Ensure → optimal muscle relaxation & Prevent tissue injury. 5-10 sec. in each cycle of stretch.

Ballistic stretching:

Rapid, forceful, intermittent stretching → High speed & intensity.    

Quick, bouncing movements. Greater tissue trauma & residual muscle soreness. ↑ROM safely in young & healthy subjects. Contraindication: Elderly & sedentary subjects, patients with MSK pathology or chronic contractures. o Recommended rationale: 1. weakened tissues – immobile or Disuse → Easily injured. 2. Dense connective tissue in chronic contractures → become more brittle & tears more rapidly.

MODES OF STRETCHING: Manual Stretching: Therapists

or other person applies external force to move the involved body segment slightly

beyond the point of tissue resistance & the available ROM.     

Takes soft tissues beyond their available length to ↑ ROM. Employs → Controlled, End-range, static, Progressive stretch with comfortable consistant intensity for 15-60 sec. & is repeated for several times. High-Intensity, short duration stretch. ↑ muscle length & ROM in non-impaired subjects. CONSIDERATION:

Self-stretching---- Flexibility exercises OR Active stretching: Stretching procedures carried out independently by the patient after careful instructions & supervised practice.   

Enable the patient to → Maintain or ↑ ROM Integral component of HOME EXERCISE PROGRAM. Necessary for long-term self-management of many repetition. → Safest type of self stretching.

CONSIDERATIONS:

Mechanical Stretching: 

Stretching via using → Cuff weight or weight-pulley system, orthosis or automated stretching machines.



Provide → constant load with variable displacement. → constant displacement with variable load.



Apply very low-intensity stretch force → Low loads over a prolong time provide to create permanent (maintained) soft tissue lengthening. Due to → Plastic deformation. o Effective to → ↓ Long-standing contractures o Long duration of stretch needed for patients with chronic contractures due to Neurological or Musculoskeletal disorders o Duration → substantially longer overall duration of stretch. →15-30 mins → as long as 8-10 hrs. at a time → continuous throughout the day.

Proprioceptive Neuromuscular Facilitation --- PNF: Active or facilitative stretching – Knott & Vos, Kabat. 

Muscle fibers reflexively inhibited via Autogenic or Reciprocal inhibition. → Less resistance to elongation by contractile elements of the muscle.



Combines functionally based diagonal patterns of the movements with Neuromuscular facilitation techniques. →Evoke Motor responses & improve neuromuscular control & function.



Requires normal innervations & voluntary control of either shortened muscles or muscles on opposite side of the joint. Effective in Neurorehabilitation & rehabilitation of MSK conditions. USE: → Develop muscle strength & endurance & facilitate mobility & stability. → Develop neuromuscular control & coordinated movements.

 

→ Restoration of function.     

Can’t be used effectively in patients with Paralysis or spasticity resulting neuromuscular disease and injury. Procedures designed to affect contractile elements of muscle & non contractile connective tissue → more appreciated when muscle spasm limits motion & less appropriate for Fibrotic contractures. Performed with combined muscle groups acting in a diagonal patterns → ↑ flexibility & ROM. Strong muscle groups of a diagonal pattern facilitate responsiveness of weaker muscle groups. Important for → strength, Endurance, Dynamic stability development.



Useful throughout the rehabilitation : →early phase of tissue healing →isometric techniques used. →final phase of rehabilitation→ High-speed diagonal movements against Maximum Resistance



HALLMARK → use of diagonal patterns & appropriate sensory uses. Sensory uses → Proprioceptive, audiovisual, cutaneous.→ elecit or augment motor responses.

FOUNDATION → analysis on → Theories of motor development, control & learning, and Principles of Neurophysiology.

Types Of Proprioceptive Neuromuscular Facilitation:

HOLD RELAX(HR) & CONTRACT RELAX(CR) 1. range limiting muscle is 1st lengthened to point of limitation or the comfortable extent. 2. patient performs pre-stretch, end-range, isometric contractions for the 5-10 sec. followed by Voluntary relaxation of tight muscles. 3. Limb passively moved into new range → Range-limiting muscle elongated.

HR technique → limb rotators are allowed to contact concentrically whereas all other muscle groups contract Isometrically during the prestretch contraction of resisting muscle. → Prestretch contraction is Isometric in all muscles of diagonal pattern.

CR & HR technique → Make passive elongation of muscle more comfortable for the patient than manual passive stretching.

Assumption: → sustained prestretch contraction followed by Reflexive relaation. → ↓ in EMG activity in range limiting muscles

Due to

AUTOGENIC INHIBITON.

Multiple repetitions of Maximal Presretch Isometric Contraction. → Acute ↑ in Arterial BP.

Valsalva maneuver (↑sed BP) avoided by : → Breathing regularly when performing Submaximal (Low-intensity) isometric contractions for 5-10 sec each repetitions.

AGONIST CONTRACTION OR DYANAMIC RANGE OF MOTION – DROM Agonist→ muscle opposite to range-limiting muscle. Antagonist→ Range-limiting muscle.

1. Short Antagonists limits → Full movement of prime mover- Agonist. 2. Patient concentrically contracts (shortens) the muscle opposite to the Range limiting muscle & holds the End- Range position for atleast several seconds. 3. After brief rest period, the procedure is repeated.

When antagonist is activated & concentrically contracted.

Antagonist(Range-limiting muscle) is Reciprocally inhibited.

Maximum agonist relaxation & lengthening.

OBSERVATION:     

Effective when significant muscle guarding restricts muscle lengthening & joint movement. Less effective to ↓ choronic contractures. Useful when patient cannot generate → Strong, pain-free contraction of the Range-limiting muscle→ HR-PROCEDURE. Useful to initiate Neuromuscular control in new range → DYNAMIC FLEXIBILITY. Less effective in Close to Normal flexibility

PRECAUTION: Avoid full range, ballistic movements when performing concentric contraction of Agonist muscle group. 

Rest after each repetition → avoid muscle cramping..

Hold-Relax With agonist contraction: HR-AC or Slow-reversal Hold- Relax Techniques.

1. Move the limb to the point where tissue resistance is felt in the Tight muscle (Rangelimiting muscle). 2. Patient performs → resisted, prestretch isometric contraction of the range-limiting muscle. 3. Relaxation of the muscle & Immediate concentric contraction of the muscle opposite to the tight muscle.

Diagonal patterns   

Multijoint, Multiplaner, Diagonal, Rantional patterns of movement. Multiple muscle groups contract simultaneously. Diagonal patterns → D1 and D2 – flexion and extension, patterns identified by: → Motion occurring at proximal Pivot points → Shoulder or Hip joints. → Position of shoulders or hip when diagonal patterns are completed.



Diagonal patterns carried out → Unilaterally or Bilaterally. →Symmetrically →Asymmetrically →Reciprocally

Basic procedures of PNF patterns: Diagonal patterns used with → various forms of Mechanical resistance.(free weights, simple weightpulley system, Elastic resistance , Isokinetic units)

Manual Contacts “How & where the therapist’s hands are placed on the patient”.  

Placed over → Agonist muscle groups or Tendinous insertions. One manual contact placed Distally ( where movement begins), Other placed proximally.

Maximal Resistance 

Greatest resistance applied during → Dynamic concentric muscle contraction. → Smooth movement without pain through the ROM.



Adjusted resistance → Accommodate strong & weak components of pattern.

Position & Movement of therapist:  

Therapist position → Shoulders & Trunk facing in the direction of moving limb. Therapist movement → move pivot over wide BOS to allow rotation.

Traction  

“Slightly separation of joint surfaces to inhibit pai & facilitate movement”. Most often applied in 3 Antigravity (flexion) pattern.

Approximation 

“Gentle compression of joint surfaces by means of Manual compression or Weight-bearing” → Stimulate agonist & antagonist contraction. → ↑ dynamic flexibility 7 postural control → via joint & muscle mechanoreceptors.

Normal timing   

Sequence of Distal to proximal, Coordinated muscle contractions occur. Distal component motions should be completed ½ way through the pattern. Correct sequencing 3 Promote Neuromuscular control & coordinated movements.

STRETCH: → Stimulus → Reflex

Stretch stimulus: winding up the part or taking up the slack. “Placing the body segments in the position that lengthen agonist muscle” Example: for D1-flexion → Limb is placed in D1 Extension  Rotation(utmost consideration) → ↑ Extensibility & responsivness of muscle. Stretch Reflex:    

Facilitated by a rapid stretch (overstretch) just past the point of tension to already elongated agonist muscle. Quick stretch followed by sustained resistance to agonists. → Keep contracting the muscle under tension. Directed to a distal musce group → Elicit a Phasic muscle contraction → Initiate PNF patterns. Prior to Resisted Isometric contraction during early stages of soft tissue healing. → Post-trauma or post surgical.

PRECAUTION→ Acute or active arthritic conditions. Verbal commands:  

Auditory cues → ↑ motor output. Sharp verbal commands simultaneous with Stretch Reflex. → Synchronize Phasic, reflexive motor response with sustained volitional effort.

Visual Cues: 

↑ control of movement throughout the ROM.

Specific techniques With PNF: 

stimulate weak mmucles further & ↑ movement or stability,.

Rhythmic Initiation  use → promote the ability to initiate a movement pattern.  Helps → Understand the rate at which movement is to ossur.  Assisted or Active movements → Helps the patient Learn a movement pattern. Process: Voluntary relaxation→ Passive motion throughout the available Rom – several times → Patient familiar with Sequence of movements in pattern.

Repeated Contractions 

Repeated, dynamic contractions at any point in Rom. → Strengthen weak agonist component of the pattern. Pattern Initiated with repeated quick stretches followed by Resistance.

Reversal of Antagonists    

Involve → Stimulation of weak agonists by Resisting Antagonist contraction. Based on → Sherrington’s Law of SUCCESSIVE INDUCTION. Instituted just before the previous pattern has been fully completed. Activities involving Quick reversal are: → Sawing or chopping wood, Dancing, Playing tennis, Grasping or Releasing objects.



Types – Slow reversal - Slow reversal hold. Slow Reversal: o

INVOLVES → Dynamic concentric contraction of stronger agonist.

↓ Immediately followed by Dynamic concentric contraction of weaker Antagonist. o o

No voluntary relaxation between the patterns. Promotes → Rapid, reciprocal action of Agonists & Antagonists.

Slow Reversal Hold: o

Add ISOMETRIC contraction at the End-Range to ↑ End-Range holding of a weakened muscle. o No relaxation period o USE → ↑ dynamic stability in proximal muscle groups. Procedure: Direction of movement rapidly reversed by Dynamic contraction of Agonist group.

↓Quickly followed by Isometric contraction of Agonist muscle group. ALTERNATING ISOMETRICS: 

Improve → Isometric strength of Agonist and Antagonists. → Stability of postural muscles of Trunk. → Proximal stabilizing muscle of shoulder gridle and Hip.

 

No joint motion should occur. Applied with extremities in → Close-Chain or Open-chain positions. Procedure Manual resistance gradually applied & released. → IN single plane or One side of body segment & then on other.

RHYTHEMIC STABILIZATION --- Progression of Alternating isometrics  

Promote stability via Coordination of proximal stabilizing musculature of the Trunk, Shoulder and Pelvic gridle. Multiple muscle groups around the joint must contract → Rotators mostly. Procedure -

Performed in weight-bearing position → Joint approximation → facilitate contraction. Multidirectional resistance applied via placing manual contacts on the opposite side of the body. → Resistance applied simultaneously in opposite directions.

PNF Pattern Motion Components:

UPPER LIMB: SHOULDER: D1 –Flexion → Flexion, Adduction, External rotation. D1 – Extension → Extension, Abduction, Internal Rotation. D2 – Flexion → Flexion, Adduction, External rotation SCAPULA: D1 – Flexion → Elevation, abduction, Upward Rotation. D1 – Extension → Depression, Adduction, Downward Rotation. D2 – Flexion → D2 – Extension → ELBOW: D1 – Flexion → Flexion or Extension D1 – Extension → Flexion or Extension D2 – Flexion → Flexion or Extension D2 – Extension → Flexion or Extension FOREARM D1 – Flexion → Supination D1 – Extension → Pronation D2 – Flexion → D2 – Extension → WRIST D1 – Flexion → Flexion, Radial Deviation D1 – Extension → Extension, Ulnar Deviation D2 – Flexion → Extension, Radial Deviation D2 – Extension → Flexion, Ulnar Deviation

FINGERS AND THUMB D1 – Flexion → Flexion, Adduction D1 – Extension → Extension, Abduction D2 – Flexion → Extension, Abduction D2 – Extension → Flexion, Adduction

LOWER LIMB:

HIP D1 – Flexion → Flexion, Adduction, External Rotation D1 – Extension → Extension, Abduction, Internal rotation D2 – Flexion → Flexion, Abduction, Internal Rotation D2 – Extension → Extension, Adduction, External Rotation

KNEE D1 – Flexion → Flexion or Flexion or Extension D1 – Extension → Flexion or Extension D2 – Flexion → Flexion or Extension D2 – Extension → Flexion or Extension ANKLE D1 – Flexion → Dorsiflexion, Inversion D1 – Extension →Plantar flexion, Eversion D2 – Flexion →Dorsiflexion, Eversion D2 – Extension → Plantar flexion, Inversion

TOES D1 – Flexion →Extension D1 – Extension → Flexion D2 – Flexion → Extension D2 – Extension → Flexion

MUSCLE PERFORMANCE “Capacity of a muscle to do work” Affected by → Morphological qualities of a muscle, Neurological, biochemical & biomechanical influences, metabolic, CVS, Respiratory, cognitive and emotion function. Key Element → Strength, power, endurance Impaired by → Injury, Disease, immobilizations, disuse, Inactivity

Resisted exercise – resistive training Active exercise in which dynamic or stable muscle contraction is resisted by an outside force applied manually or mechanically.

Strength: Ability of a contractile tissue to produce tension & a resultant force based on the demands placed on the muscle. OR Greatest measurable force exerted by muscle or group of muscle to overcome the resistance during a single maximum effort.

Functional strength: Ability of a neuromuscular system to produce, reduce or control forces, Comtempted or imposed, during functional activities in a smooth coordinated manner.

Strength training ---- Strengthening exercises Systematic procedure of a muscle or muscle group Lifting, Lowering or controlling heavy loads (resistance) for a relatively low number of repetitions or a short period of time. *most common adaptation: ↑ maximum force producing capacity of muscle. → Neural adaptation & ↑ in muscle fiber size.

Power: Work produced by muscle per unit time → F×d/t OR Rate of performing work.  

Aerobic & Anaerobic power Expressed by → single burst of high intensity activity → Repeated burst of Low intensity activity

Power training:  

↑se intensity (muscle work) & ↓se time → ↑se power. Polymetric training or Stretch- Shortening drills. → speed of movement manipulated

Endurance Ability of a muscle to perform low- intensity, repetitive, sustained activities aver a prolonged period of time

Cardiopulmonary Endurance--- total body endurance: Repetitive, dynamic motor activities which involve the use of large body muscle.  Walking, cycling, swimming, upper body ergometry. Muscle Endurance --- Local endurance or aerobic power Ability of muscle to contract repeatedly against a load, generate & sustain tension & resist fatigue over an extended time period.    

Key Elements→ Low intensity muscle contraction, Prolonged time period, Large number of repetitions. Adaptability: ↑ Oxidative & metabolic capacities →Better O2 delivery & use. Minimize adverse forces on joints. Produce less irritation to soft tissue & Comfortable.

Overload principle: To improve muscle performance, a load exeding the metabolic capacity of the muscle must be applied.

Application → focus on progressive muscle loading by manipulation(joint).  

Strength training→ Resistance incrementally & progressively ↑sed. Endurance training→ ↑se time of a muscle contraction is sustained or ↑ number of repetitions.

Reversibility Principle: Adaptive changes in a body systems in response to resistance exercise program → are transient unless training-induced improvements are regularly used for functional activities. Detraining ↓ in muscle performance begins within 1-2 weeks after the cessation of resistance exercises & continues until the training effects are lost

SAID Principle--- Specific adaptations to imposed demands:    

Framework of specificity is necessary for the foundation to build exercise program. Applies to all body systems Extension of wolf’s law Helps therapists → Determine exercise prescriptions and parameters

Specificity of training --- specificity of Exercise: Adaptive effects of training ( ↑ in strength, power, endurance) are highly specific to the training method employed.  Relative to: o Mode and velocity of exercise. o Limb position ----- Joint angle o Movement pattern during exercise  Basis related to: o Morphological and metabolic changes o Neural adaptations to the stimulus associated with motor learning.  Desired functional outcome → Ascend or Descend stairs: o Eccentric and concentric exercise in a weight-bearing pattern.

Transfer of training --- Over-flow or Cross training  Occurs to a very limited basis w.r.t velocity training & mode of exercise  Effects can occur from exercised limb to nonexercised contralateral limb in a resistance training program.

Determinants and correlates that affect tension generation in a skeletal muscle:

Factors → Cross-section & size of muscle → Muscle fiber number and size. Influence →larger muscle diameter → Greater T

Factors → Fiber arrangement & fiber length → cross-sectional diameter of muscle Influence → Short fiber with Pinnate and multipinnate design → High force producing  Quadriceps, gastronemius, Deltoid , biceps brachii. → Large parallel design → High rate of shortening and less force production 

Sartorius, lumbricals.

Factors → fiber-type distribution of muscle → Type-1→ Tonic, slow twitch → Type-II A & IIB → phasic, fas twitch

Influence → High percentage type-1 phase → low force production→ resistance to Fatigue, slow rate of maximum force Development. → High percentage type-IIA&B fibers→ Rapid force production, rapid fatigue, Rapid high force production

Factors → Length tension relationship of muscles at the time of contraction

Influence → Muscles produce greatest tension near or at physiological resting Position at the time of contraction.

Factors → Recruitments of motor unit Frequency of firing of motor units.

Influence → Number and synchronization of motor unit firing ∞ force production

Frequency of firing ∞ Tension generation

Factors → Type of muscle contraction Speed f muscle contraction

Influence → Force output (Greatest to least) → Eccentric, concentric, isometric. → concentric contraction → ↑sed speed, ↓ tension → Eccentric contraction → ↑ speed, ↑ tension

Factors influencing tension generation in normal skeletal muscle:

 Determinants & Correlates include: → Morphological, biomechanical, neurological, metabolic and ciochemica factors  Contribute to: → Magnitude, Duration, Speed of force production. → Resistance OR suscecibility of muscle to fatigue.\

1. Energy stores and Blood supply  Energy needed for → contraction, tension generation, Resist fatigue.  Tension producing capacity & resistance to fatigue – depends on: → Predominant muscle fiber type & Adequacy of blood supply → brings O2 & nutrients, removes wastes.  Main Energy systems: → ATP-PC system, Aerobic ( Glycolytic or lactic acid) system, aerobic system

2. Fatigue:  Complex phenomenon affecting muscle performance.

a) Muscle (Load) fatigue: → Most relevant phenomenon of 3 skeletal muscle fatigue. “Dimeinshed response of muscle to a repeated stimulus”

→ Progressive decrement in amplitude of motor unit potentials.  Occur when muscle contracts (static or dynamic) against load.  Acute physiological response to exercise → normal and reversible → Charachterised by 3 ↓ed force producing capacity of Nm system. → temporary state of exhaustion 3 Failure → Lead to → ↓se in muscle strength.  Diminished muscle response → Due to: → Inhibitory (protective) influence from CNS → ↓ed conduction ( impulse) at myoneural junction 3 fast-twitch fibers. → Disturbances in muscle contractile system → due to → ↓ed Energy stores, insufficient O2, H+ build up.

b) Cardiopulmonary (General) fatigue: Diminshed response to entire body as a result of prolonged physical activity. → Walking, Jogging, cycling, Repetitive- Loading, Digging. Caused by: → ↓ed Blood sugar(Glucose) levels. → ↓ed Glycogen stores → muscle & liver. → depletion of K+ Ion → Elderly.

Sign and Symptoms of Muscle fatigue:      

Uncomfortable sensation in muscle → Pain & cramping. Tremulousness in contracting muscle. Jerky active movements → Not smooth. Use of substitute motion to complete pattern. ↓ed peak torque during Isokinetic training. Inability to complete movement pattern through full ROM during dynamic exercise with same resistance. Threshold of Fatigue:  Level of exercise which cannot be sustained indefinitely.  Length of time a contraction is maintained OR Number of repetitions of an exercise that initially can performed.

Factors influencing fatigue:  Patients health status, lifestyle- sedentary v/s active.  Abrupt onset – Abrupt, more rapid, at predictable intervals as: → Neuromuscular, Cardiopulmonary, Oncogenic, Inflammatory, Psychological disorder.  Multiple sclerosis → Awaken rested & function well – Early morning → Peak of fatigue reached, noteable weakness – Mid-afternoon → Fatigue diminished, strength return – Early Evening.  Deficits compromising the O2- transport system. → Cardiac, peripheral vascular, pulmonary disease → Chemotherapy or radiotherapy – Cancer. → Fatigue readily – Longer periods of recovery required.  Environmental factors→ Onside v/s Room temperature, Air quality Altitude → effect onset of fatigue & recovery (time duration) Recovery from Exercise → Intrasession & Intersession recovery:  After vigorous exercise → body must be given time to restore itself.  Recovery from acute exercise: → force producing capacity of muscle return to 90% to 95% of pre-exercise capacity. → takes 3-4 minute → greatest proportion of recovery during !st minute.  Changes occurring are: → O2 restores replenished in muscle → Energy stores replenished. → Glycogen replaced from skeletal muscle & Blood within → 1 hour (Post-exercise)  Recovery occurs more rapidly with: → Light exercise performed during recovery period → Active recovery. →than → Total resistance → Passive recovery.

Muscle fiber types & resistance to fatigue:

Type- I → Tonic, slow-twitch → Postural muscle  High resistance to fatigue.  High capacity density

 Aerobic energy system  Small diameter  Slow twitch  Slow maximum muscle shortening velocity Type II A  Intermediate  High  Aerobic.  Intermediate  Fast  Fast Type II B → Phasic, Fast-twitch – Gastrocnemius, bicep brachii → lift entire body weight, Lower, push heavy loads.      

Low Low Anaerobic Large Fast Fast

Physiological adaptation to resistance exercise:

1. Skeletal muscle structure:

Strength training → Hypertrophy (muscle fibers) → Greater in Type-II fibers Hyperplasia Remodeling of type II B to IIA fibers Capillary bed density → Decrease or no change Mitochondrial density & Volume → ↓ Endurance training → Hypertrophy → minimal or no change Capillary bed density → ↑ Mitochondrial density & Volume → ↑

2. Neural system:

Strength and Endurance training → Motor unit recruitment → ↑ motor unit firing Rate of firing → ↑ → ↓ twitch contractions Synchronization of firing → ↑ 3. Metabolic system: Strength and Endurance training → ATP & C storage → ↑ Myoglobin storage → ↑ Stored trigyceides → ↑ with endurance not Known → Strength 4. Enzymes: Strength and Endurance training → Creatine Phosphokinase → ↑ Myokinase → ↑ 5. Body composition: Strength and Endurance training → % Body fat → ↓se Lean body mass → ↑ with strength no change with endurance. 6. Connective tissue: Strength training → tensile strength (tendon, ligament, muscle connective tissue) → ↑ Bone → ↑ mineral density–No change in bone mass. Endurance training →Tensile strength → ↑ Bone → ↑ Mineralization with weight bearing activities

Determinants of resistance exercise program: 1) Alignment 4) Volume

2) Stabilization 5) Exercise order

3) Intensity 6) Frequency

7) Rest Interval

8) Duration

9) Mode of exercise

10) Velocity of exercise

11) Periodization

12) Integration of exercise into functional activities

Characteristics of Periodized training:

Period of training → Preparation Intensity → lower loads Volume & frequency → High number of repetitions & sets More exercise per session More frequent exercise sessions per day & week

Period of training → Competition Intensity → High loads – peaking just prior to competition Volume & frequency → ↓ed number of repetitions & sets Fewer exercises per session Less frequent exercise sessions per day & week

Period of training → Recuperation Intensity → gradual ↓se in exercise loads Volume & frequency → Additional ↓ in repetitions, sets, number of exercise & frequency Muscle performance

Strength

Power

Endurance

Types of Muscle Contraction

Dynamic Concentric

Isometric(static)

Dynamic Eccentric

Age Related Changes In Muscle & Muscle Performance:

Infancy, Early Childhood, Preadolescence:       

Muscle mass → 25% of body weight – At birth Total muscle fiber number established – Pre & during Infancy Postnatal muscle fiber distribution complete – End of 1st year Muscle mass & fiber size → ↑ Linearly – From infancy to puberty Muscle strength & Endurance → ↑ Linearly – From infancy to puberty Muscle mass and strength – Greater in Boys than Girls – Early childhood to Puberty Training induced strength gain without hypertrophy – Both sexes

Puberty  Rapid acceleration in muscle mass & fiber size → Boys more. → Muscle mass - ↑ by 30% per year     

Rapid ↑ in muscle strength – Both sexes Strength differences → Marked between Girls and Boys Boys → Muscle mass, Body weight & Height – Peak before muscle strength Girls → strength – peaks before body weight Resistance training – induced Relative strength gain – Both sexes → Greater muscle hypertrophy – Boys

Young & middle Adulthood  Muscle mass peaks → Women → b/w 16-20 years → Men → b/w 18-25 yeas  ↓ in muscle mass – by 25 yeas  Muscle mass → 40% of Total Body weight – Early adulthood → Muscle mass – Greater in men than women     

Strength development - 2nd decade – men Muscle strength, Endurance – peaks in 2nd decade – Earlier in women Strength decline – in 3rd decade – b/w 8-10% per decade via 5-6th decade Muscle strength & endurance deterioration – Rapid in sedentary adults Muscle strength & endurance improvement – possible with modest ↑ in physical activity

Late Adulthood  Rate of muscle strength decline – accelerate to 15-20% per decade – 6-7th decade → ↑ t 30% per decade after 6-7th decade  Loss f muscle mass - ↓ed by 50% of peak muscle mass(young adulthood) – 8th decade  ↓ in muscle fiber size & number & in ∞ - motor neuron number → Atrophy of type-II muscle fibers     

↓ed speed of muscle contraction & peak power Progressively gradual ↓ in Endurance & Maximum O2 uptake Loss of flexibility → ↓ed force-producing capacity of muscle Minimal ↓ in performance of functional skills – 6th decade Significant functional ability deterioration associated with ↓ed muscle endurance – 8th Decade  Significant improvement in – Muscle strength, endurance, power, - with resistance – training program.

Psychological & cognitive factors Ability to develop or sustain sufficient muscle tension for execution or acquisition of functional motor tasks – Adversely affected by:      Attention:

Fear of pain injury, re-injury Depression related to physical illness Impaired attention or memory – Aging Head injury Side effects of medication

“Ability to process relevant data while screening out irrelevant information from environment & to respond to internal cues from the body” Necessary For → patient safety & optimal Long-term effects

Motivation and feedback

Sequence of Rx to Gain & Reinforce Functional Mobility: 1. Warm the tissues 2. Relax the muscles  Hold-relax inhibition techniques  Grade-I or II joint oscillation techniques 3. Joint mobilization stretches  Position & dosage – for level of tissue tolerance 4. Passive stretch — Periarticular tissues 5. Patient actively uses new range  Reciprocal inhibition  Active ROM  Functional activities 6. Maintain new range, patient instructions  Self stretching  Auto-mobilization  Active, Resistive ROM  Functional activities using new ranges

BALANCE AND CONTROL: Balance and Postural Stability “Dynamic process by which a person’s position is maintained in equilibrium  Equilibrium → Static → at rest → Dynamic → at rest  Greatest when — COM or COG → maintained over BOS Center of mass — COM “Point corresponding to center of total body mass & point where body is in perfect equilibrium”.  Determined by finding — weight COM of each body segment Center of Gravity — COG “Vertical projection of COM to the ground”  Located → Slightly anterior to S2- Vertebrae or ≈ 55% of person’s height Momentum “Product of mass times velocity (m×v)”  Linear → Velocity of the body along straight line → Example → saggital or transverse planes  Angular → Rotational velocity of the body. Base of support — BOS “Perimeter of contact area b/w & its support surface”  Foot placement alters BOS → change postural stability (balance) of person.  Wide stance — elderly → ↑stability  Tendem stance or Walking → ↓ stability

Limits of stability “Sway boundaries in which person can maintain equilibrium without changing BOS”  Sway boundaries — Constantly changing — depending on: → Tasks, Biomechanics(person’s), Environmental aspects.  Quick stance — Area encompassed by outer edges of feet in contact with ground.  Normal adult — Anterioposterior sway limit — 12° from most posterior to most anterior  Adult with 4 inches B/W feet — standing — 16° lateral sway limit  Sitting without trunk support — ↑ed limits of stability then ……. → Height of COM above BOS is less & BOs is larger( buttocks in contact with surface) Ground reaction force & center of pressure — COP Ground reaction force → “Reaction from ground due to contact b/w our bodies & ground due to gravity (action forces)” Center of pressure

→ “Location of vertical projection of ground reaction force”

 Equal and opposite to — weighted average of downward forces acting on the area in Contact with ground.    

One foot on ground — COP lies within that foot Both feet on ground — Net COP lies somewhere b/w the two feet Both feet are in contact — Cop under each, can be measured separately COP is —“Reflection of body’s neuromuscular responses to COG imbalances” → Muscle force to stabilize (body) & control COG position — change COP location  Force plate — traditionally used to measure → Ground reaction force (N) → COG movements (meters) Balance Control “Complex motor control task involving detection & integration of sensory information to assess the position & motion of the body in space & the execution of appropriate Musculoskeletal responses to control body postion within the context of Environment and Task.  Require interaction of → nervous & musculoskeletal system, contextual effects.

1. Nervous system i. Sensory processing for the perception of body orientation in space → Provided by — visual, vestibular, somatosensory system ii. Sensory motor integration → Essential for linking sensation to motor responses & for adaptive & anticipatory aspects of postural control iii. Motor strategies for planning, programming & executing balance responses.

2. Musculoskeletal contributions Includes:  Postural alignment, Musculoskeletal flexibility (ROM), Joint integrity, Muscle performance(strength, endurance, power), Sensation (touch, pressure, vibration, proprioception, Kinesthesia) 3. Contextual effects — Environmental Interaction  Open environment → Unpredictable & with distractions  Closed environment → Predictable with no distractions  Support surface → Firm v/s slippery  Amount of lightening, effects of gravity, internal forces on body.  Tasks characteristics: o Well learned v/s new o Predictable v/s unpredictable o Single v/s Multiple Sensory Control & Balance Control Perception of body position & movement in space requires:  Information from → peripheral receptors in → Visual → somatosensory → Vestibular system 1. Visual system Provide information about:  Position of head relative to environment  Orientation of head to maintain level gaze  Direction & speed of head movements → surrounding objects move in opposite Direction  Used to improve → stability when → Proprioceptive or vestibular inputs are unreliable by fixating the gaze.

 Some provide inaccurate information balance → illusion of movement. 2. Somatosensory system  Provide information about:  Position and motion of body, body parts w.r.t each other, support surface. o Proprioceptors → sensitive to → muscle length and tension o Joint receptors → sensitive to → joint position, movement, stress o Mechanoreceptors → sensitive to → vibration, light touch, deep pressure, stretch  Inappropriate inputs about body position due to o Surface is moving → on a boat o Non horizontal surface  Local anesthetization of joint tissue & total joint replacement o Donnot impair joint position awareness

 Muscle spindle receptors → Provide joint position sense  Joint receptors → assist ∂-motor system  Regulate muscle tone and stiffness → provide anticipatory postural adjustments & counteract postural disturbances

3. Vestibular system  Provide information about → position and movement of head w.r.t Gravity and Inertia.  Semicircular canal(SSC) receptors → detect angular acceleration of head →sensitive to → Fast head movements → walking or during episodes of imbalances (slips, trips, stumbles)  Otoliths (uterlie, saccule) receptors → detect linear acceleration, head position. → Respond to → Heaad movements → postural sway  Additional information from mechanoreceptors in Neck – provide CNS with: → True picture of orientation of head relative to the body  It uses motor pathways → originating from vestibular nuclei of postural control and coordination of eye & head movements o Vestibular reflex → bring postural changes to compensate for tilts. → via vestibulospinal tracts projections to Antigravity muscles o Vestibulo-occular reflex → Stabilize vision during head and body movements. → via vestibular nuclei projections to extra-occular muscles.

Sensory orientation for balance control:  Vestibular, visual, somatosensory, inputs combined →sense o orientation and movements.  Incoming sensory information — integrated & processed in : → cerebellum, basal ganglia, supplementary motor area.  Somatosensory information → Fastest processing time for rapid response → visual → vestibular  CNS suppress input from one system(Environment/injury) & combine appropriate sensory inputs from other two systems. → Adaptive process k/n SENSORY ORGANISATON Types of balance control: Functional tasks require: 1. Static balance control → maintain stable antigravity position while at rest. EXAMPLES: Standing & Sitting 2. Dynamic balance control → stabilize the body when support surface is moving or body moves on a stable surface. EXAMPLES: Sit to stand transfer or Walking 3. Feed forward or open loop motor control → utilized for → Anticipatory aspects of postural control → Movements occurring too fast to rely on sensory feedback(Reactive Responses. 4. Anticipatory control → involve postural muscle activation In advance of performing skilled movements → Activation of posterior leg & back extensors (muscles) before pulling on a Handle when standing or planning how to navigate to avoid obstacles 5. Closed loop control → utilized for → precision of movements which need sensory feedback EXAMPLE: maintain balance while sitting on ball or standing on balance beam.

Characteristics of Three motor systems for balance control 1. REFLEX Mediating pathway → Spinal cord Mode of activation → External stimulus Latency of Response → fastest Response → localized to point of stimulus, Highly stereotyped Role in balance →Muscular force regulation Response modifying factors → Musculoskeletal or Neurological abnormalities 2. AUTONOMIC Mediating pathway → Brainstem/Subcortical Mode of activation → external stimuli Latency of Response → Intermediate Response → Co-ordinate among leg & trunk muscles, stereotypical but adaptable Role in balance → Resist disturbances Response modifying factors → Musculoskeletal or Neurological abnormalities, Configuration of support, prior experience

3. VOLUNTARY: Mediating pathway → Cortical Mode of activation → External or Internal stimulation Latency of Response → Slowest Response → co-ordinated, highly variable Role in balance → Generate purposeful movements Response modifying factors → Musculoskeletal or Neurological abnormalities, Conscious effort, prior experience, task complexity

Balance assessment & interventions: 1. Static balance CLINICAL TESTS/ MEASURES → observations of patients maintaining different postures Single-leg stance, Romberg & stroke stand test INTERVENTIONS-If deficits Present → Vary postures, vary support surface, incorporate external loads. 2. Dynamic balance CLINICAL TESTS → observations of patient standing/sitting on unstable surface Tinetti Performance Oriented Mobility Assessment (POMA) Timed-up & Go Test(TUG), Berg balance scale, Dynamic gait index, Gait Abnormality Rating Scale(GARBS). INTERVENTIONS → Moving support surfaces; Move head, trunk, arms, legs. Transitional & Locomotor activities 3. Anticipatory —Feed Forward CLINICAL TESTS → Observation of patient catching ball, Opening door, Lifting objects Functional reach & Multidirectional reach test INTERVENTIONS → Resting, Catching, kicking, Lifting, Obstacle course

4. Reactive —Feedback CLINICAL TESTS → Observations of patient responses to pushes → small v/s large, slow v/s rapid, Anticipated v/s Unanticipated Pull, Backward release, Postural stress test INTERVENTIONS → standing sway, Ankle +Hip +Stepping strategy, Perturbations. 5. Sensory organization CLINICAL TESTS → Clinical test of sensory Integration on balance test (CTSIB) → Also k/n → Foam & Doam test INTERVENTION → Reduce visual inputs & somatosensory cues.

a. Safety during Gait, Locomotion, Balance CLINICAL TESTS → Observations, Home assement INTERVENTIONS → Balance with stability limits, Enviromental modifications, External support, Assistive devices b. Balance during functional activities CLINICAL TESTS → Physical performance test, Barthel ADL index, Katz ADL Index, Functional Independence Measure(FIM), Progressive Mobility Skills, Assesment task, Lawton IADL scale. INTERVENTIONS → Functional activities, Dual or Multitask activities

SOFT TISSUE LESION – MUSCLOSKELETAL DISORDERS: SPRAIN: Severe Stress, Stretch or tear of soft tissues. (Joint Capsule, ligaments, tendons or muscle) Referred: Superficially to injury of a ligament. Grades: 1st Degree (Mild) 2nd Degree (Moderate) 3rd Degree (Severe) STRAIN: Overstretching, Over exertions & Over use of soft tissues caused by slight trauma or unaccustomed repeated trauma of a minor degree. Referred superficially to distribution of “Musclotendinous Unit”. DISLOCATION: Displacement of a part (Usually bony partners in a joint) resulting in loss of anatomical relationship, leading to soft tissue damage, inflammation, pain & muscle spasm. SUBLUXATION: Incomplete or partial dislocation of bony partners in a joint often involving secondary trauma to surrounding tissue. MUSCLE / TENDON RUPTURE OR TEAR: PARTIAL: Pain is experienced in the region of breach when muscle is stretched or when it contracts against resistance. COMPLETE: Muscle does pull against the injury, so stretching or muscle contraction does not cause pain. TENDINOUS LESIONS OR TENDINOPATHY: TENOSYNOVITIS: Inflammation of synovial membrane covering a tendon. TENDINITIS: Inflammation of a tendon. (Results in: Scarring OR Calcium deposits) TENOVAGINITIS: Inflammation with thickening of tendon sheath. TENDINOSIS: Degeneration of a tendon due to repetitive micro trauma. SYNOVITIS: Inflammation of synovial membrane.  Excess of normal synovial fluid in a joint or tendon sheath.  Caused by trauma or disease. HAEMARTHROSIS: Bleeding into joint.  Caused by severe trauma. GANGLION: Ballooning of a wall of a joint capsule or tendon sheath.

 Ganglia arise after trauma & sometimes with RA. CONTUSIONS: Bruising from direct blow.  Resulting in Capillary rupture. Bleeding, edema & Inflammatory response. OVERUSE SYNDROME OR CUMULATIVE TRAUMA DISORDER (REPETITIVE STRAIN INJURY): “Repeated overuse, sub maximal overload & frictional wear to a muscle or a tendon”  Results in Inflammation & pain. CLINICAL CONDITIONS RESULTING FROM TRAUMA OR PATHOLOGY – SECONDARY: DYSFUNCTION: Loss of normal function of tissue or a region caused by adaptive shortening of soft tissues, adhesions & Muscle weakness or conditions resulting in loss of normal mobility. JOINT DYSFUNCTION: Mechanical loss of normal joint play in synovial joints.  Causes: Loss of function & pain.  Precipitating Factors: Trauma, Immobilization, Disuse, Aging or serious pathological condition. CONTRACTURES: Adaptive shortening of skin, fascia, muscle or joint capsule.  Prevents normal mobility or flexibility of structures. ADHESIONS: Abnormal adherence of collagen fibers to surrounding structures during immobilization, after trauma or as a complication of a surgery.  Restricts normal elasticity & gliding of structures involved. REFLEX MUSCLE GUARDING: Prolonged contraction of muscle in response to a painful stimulus.  Primary pain causing lesion is in nearby or underline tissue or referred pain source.  Ceases when painful stimulus is removed. INTRINSIC MUSCLE SPASM: Prolonged contraction of a muscle in response to a local circulatory & metabolic changes occurring when a muscle is in continuous state of contraction.  Response of muscle to viral infection, cold. Emotional trauma, prolonged period of immobilization or direct trauma to muscle.

MUSCLE WEAKNESS: Decrease in strength of muscle contraction.  Result of systemic, chemical or local lesion of nerve of CNS or PNS or Myoneural Junction.  Result of a direct insult to muscle or simple inactivity. MYOFASCIAL COMPARTMENT SYNDROME: Increased interstitial pressure in closed, non – expanding, myofascial compartment compromising the function of blood vessels, muscles & nerves.  Results in Ischemia & irreversible muscle loss.  Caused by fractures, repetitive trauma, crush injuries, skeletal traction & restricted clothing, wraps or casts. SEVERITY OF TISSUE INJURY:  Grade – 1(1st Degree): o Mild pain. o At the time of injury or within 1st 24 hours. o Mild swelling, local tenderness, pain when tissue is stretched.  Grade – 2 (2nd Degree): o Moderate pain requiring stopping of activity. o Stress & tissue palpation increases pain. o Ligament injury or tearing of some fibers result in increase joint mobility.  Grade – 3 (3rd Degree): o Near complete or complete tear or avulsion of tissue (tendon or ligament) & severe pain. o Tissue stress is painless. o Palpation may reveal the defect. o Torn ligament results in joint instability. IRRITABILITY OF TISSUE – STAGES OF INFLAMMATION & REPAIR:  Acute stage (Inflammatory reaction): o Cardinal signs of inflammation are present. o Painful ROM. o Reflex muscle guarding. o Causes of pain & impaired movement are:  Altered chemical state irritating nerve endings.  Increased tissue tension due to edema or joint effusion & muscle guarding.

o Lasts for 4 – 6 days unless insult is perpetuated.  Sub acute Stage (Repair & healing): o Signs of inflammation progressively decrease & eventually are absent. o Pain synchronous with encountering tissue resistance at the end of ROM. o Stressing tight tissue or developing tissue tension beyond its tolerance causing pain. o Weak muscles & limited function. o Lasts for 10 – 17 days (14 – 21days after the onset of injury). o May lasts up to 6 weeks in tissues with limited circulation (tendon).  Chronic Stage (Maturation & Remodeling): o No signs of inflammation. o Contractures or adhesions may limit the ROM. o Muscle weakness limits normal function. o Connective tissue continues to strengthen & remodel. o Stretch pain may be felt at the end of ROM of tight structures. o Function limited by muscle weakness, poor endurance & poor N.M Control. o Lasts for 6 months – 1 year depending on “Tissue involved & Amount of tissue damage”.  Chronic Pain Syndrome: o State that persist for more than 6 months. o Includes pain, not linked to the source of irritation or inflammation. o Functional limitation & disability of physical, emotional & psychological parameters. CHARACTERISTICS & CLINICAL SIGNS OF STAGES OF INFLAMMATION, REPAIR & MATURATION OF TISSUE.  Acute Stage (Inflammatory Reaction): Characteristics: o Vascular Changes. o Exudation of cells & chemicals. o Clot Formation. o Phagocytosis, Neutralization of irritants. o Early fibroblastic activity. Cardinal Signs or Clinical Signs: o Inflammation. o Pain before tissue resistance.

Physical Therapy Interventions (Protection Phase): o Control effects of Immobilization. o Modalities. o Selective rest / Immobilization. o Promote early & prevent deleterious effects of rest. o Passive movement, Massage & muscle setting with caution.  Subactue Stage (Repair & Healing): Characteristics: o Removal of noxious stimuli. o Growth of capillary beds into the area. o Collagen formation. o Granulation tissue. o Very fragile, easily injured tissue. Cardinal & Clinical signs: o Decreasing inflammation. o Pain Synchronous with tissue resistance. Physical Therapy Interventions (Controlled Motion Phase): o Promote heating, develop mobile scar. o Non – destructive active, resistive, open & closed chain stabilization & muscular endurance exercise, carefully progressed in intensity & range.  Chronic Stage (Maturation & Remodeling): Characteristics: o Maturation of connective tissue. o Scar tissue contracture. o Scar Remodeling. o Collagen aligns to stress. Clinical Signs: o Absence of inflammation. o Pain after tissue resistance. Physical therapy Interventions (Return to Function Phase): o Increase strength & alignment of scar. o Develop functional independence. o Progressive stretching, strengthening, endurance training. o Functional exercise & specificity drills.

ACUTE STAGE OR PROTECTION PHASE MANAGEMENT GUIDELINES:  Plan of Care: o Educate the patient. o Control pain, edema, and spasm. o Maintain soft tissue &joint integrity & mobility. o Reduce joint swelling if symptoms are present. o Maintain integrity & function of associated areas.  Interventions: o Inform the patient of anticipated recovery time & how to protect the part while maintaining appropriate functional activities. o Cold, compression, elevation, massage (48 Hrs); o Immobilize the part (Rest, splint, tape, cast); o Avoid position of stress to the part; o Avoid position of stress to the part; o Gentle (Grade – 1) joint oscillations in pain free position. o Appropriate dosage of passive movements within the limits of pain, specific to the structures involved; o Appropriate dosage of intermittent muscle setting or electrical stimulation; o May require medical intervention if swelling is rapid (Blood); o Provide protection (Splint, Casts). o Active – Assisted, resistive, modified Aerobic Exercises; o Depends on  Proximity of associated areas.  Effects on primary lesion. o Adaptive or Assistive devices  Protect the part during functional activities.  Precautions: o Proper dosage of rest & movement during inflammatory stage. o Signs too much movement (increased pain & Inflammation)  Contraindications: o Stretching with resistance exercises. (Should not be performed at the site of inflamed tissue) SUBACUTE STAGE OR CONTROLLED MOTION PHASE.  Plan of Care: o Educate the patient. o Promote healing of injured tissue. o Restore soft tissue, muscle, joint mobility.

o Develop N.M. Control, Muscle endurance & strength in the involved & related muscle. o Maintain integrity & function of associated areas.  Interventions: o Inform the patient of anticipated healing time & importance of the following guidelines; (Teach home exercises & encourage functional activities) (Modify & Monitor as the patient progresses). o Monitor the tissue response to exercise program; (Decrease in the intensity if inflammation increases) o Protect healing tissue with assistive devices (Splints, tape, Wrap); o Progressively increase the amount of time, the joint is free to move each day; o Decrease use of assistive devices as strength in supporting muscle increases o Progress from PROM to AAROM to AROM within pain limits; o Gradually increase the mobility of scars (specific to involved structures); o Progressively increase the mobility of related tight structures (Specific to tight structures) o Initially, progress multiple angle isometric exercises within the patient. o Tolerance (begin with mild resistance with caution). o Initiate AROM + protected weight bearing + stabilization exercises. o ROM + joint play + Healing improves progress isotonic exercise with increased repetition; o Emphasize control & proper mechanics. o Progress resistance later in this stage. o Apply progressive strengthening & stabilizing exercises; (Monitor effect on primary lesion) o Resume low intensity functional activities involving the healing tissue that don’t exacerbate the symptoms.  Precautions: o Signs of inflammation or joint swelling decrease early in this stage. o Discomfort with progression in activity level (not more than few hours) o Signs of too much motion or activity are:  Resting Pain, Fatigue, Increase weakness, Spasm.

CHRONIC STAGE OR RETURN TO FUNCTION PHASE.  Plan of Care: o Educate the patient. o Increase soft tissue, muscle & joint mobility. o Improve N.M control, strength & muscle endurance. o Improve cardiovascular endurance. o Progress Functional activities.  Interventions: o Instruct the patient in safe progression of exercises & stretching.  Monitor understanding & complains.  Teach ways to avoid re – injury & safe body mechanics.  Provide ergonomics counseling. o Stretching techniques specific to tight structures are:  Joint & selected ligaments (Joint mobilization).  Ligaments, tendons, soft tissue adhesions (Cross fiber massage).  Muscle NM inhibition, passive stretch, Massage, Flexibility Exercise. o Progress Exercise:  Submaximal to maximal resistance.  Specificity of exercise using resisted concentric & eccentric, weight bearing & non – weight bearing.  Single plane to multi – plane motions.  Single to complex motions emphasizing movements that stimulate functional activities.  Controlled proximal stability, super – imposed distal motion & safe biomechanics.  Increase time of slow speed, progress complexity & time, progress speed & time. o Progress aerobic exercises using safe activities. o Continue using supportive & assistive devices until the ROM & functional joint play & muscle strength is adequate. o Progress functional training stimulated activities from protected & controlled to unprotected & variable. o Continue progressive strengthening exercises & advance training activities  Muscle capable to respond to the required functional demands.  Precautions: o No signs of inflammation. o Discomfort with progression in activity level. o Signs that activities are progressing too quickly are:

    

Joints swelling. Pain (for more than 4 Hours) Decreased strength. Fatiguing more easily. Need medications.

ARTHRITIS – ARTHROSIS  Arthritis o Inflammation of a joint.  Inflammatory & non – inflammatory.  Most Common Types: o Rheumatoid Arthritis & Osteoarthritis.  Arthrosis: o Joint limitation without inflammation.  Traumatic Arthritis: o Bloody effusion  Aspiration. CLINICAL SIGNS & SYMPTOMS.  Impaired Mobility: o Signs of inflammation & joint involvement.  Characteristic pattern of limitation (CAPSULAR PATTERN)  Firm End – Feel.  Guarded end –feel in acute cases. o Decreased & painful joint play. o Joint swelling (Effusion).  Arthrosis in o Recovery from a fracture. o Problems requiring immobilization.  Impaired Muscle performance: o Poor muscle support:  Joint susceptible to trauma. o Good muscle support:  Protects arthritic joint. o Asymmetry of muscle pull:  Deforming forces that can be prevented via Splinting & Bracing. o Swollen or Restricted joints:  Stabilizing the muscle  inhibited.  Impaired Balance

o Altered or decreased sensory input (Mechanoreceptors & muscle spindle).  Develop balance deficit.  Problem with weight – bearing joints.  Functional Limitations o Minimal or significant restriction of  home, community, work related social activities. o Adaptive or Assistive devices  Improve function or prevent deforming forces.

RHEUMATOID ARTHRITIS “Autoimmune, Chronic, Inflammatory, systemic disorder affecting synovial lining of joints & connective tissue”.  Characteristics: o Periods of exacerbation (active disease) & remission (fluctuating course). o Early inflammatory changes in:  Synovial membrane.  Peripheral portion of articular cartilage.  Subchondral narrow spaces. o Granulation tissue (PANNUS) forms, covers, erodes  Articular cartilage, bone, ligaments in the joint capsule. o Adhesion formation (Restricted joint mobility) o Cancellous bone exposed with disease progression. o Deformity & disability caused by:  Fibrosis, Ossific ankylosis, Subluxation. o Inflammatory changes in tendon sheath (TENOSYNOVITIS).  Recurring friction Tendon fray or rupture. o Extra – articular changes are:  Rheumatoid nodules.  Atrophy & fibrosismuscle weakness associated.  Fatigue.  Mild cardiac changes. o Progressive deterioration & decreased functional level  progressive muscle weakness. o Irreversible loss of function of joint.  Criteria For Diagnosis:

o Morning stiffness (in & around the joint) lasting for ≥ 1Hour before maximal improvement. o At least three joint areas with soft tissue swelling or fluid  simultaneously. o Swelling in the  wrist, MCP, PIP Joints. o Symmetrical arthritis  bilateral PIP, MCP, MTP involvement. o Rheumatoid nodules. o Serum rheumatoid factor. o Radiographic changes.  Erosions or periarticular osteopenia in hands & wrist joints. NOTE: At least 6 / 7 should be present at least for six (6) weeks.  Signs & Symptoms (Period of active disease) o Synovial inflammation  Joint effusion & swelling  aching & limited motion. o Prominent joint stiffness in the morning. o Pain on motion. o Slight increase in skin temperature over joints. o Pain & stiffness worsen after strenuous activity. o Onset in smaller foot & hand joints  most commonly in PIP joints. o Bilateral symptoms. o Joint deformity with progression  Ankylose & subluxate. o Pain in adjoining muscles  Muscle atrophy & weakness. o Asymmetry in muscle strength & alteration in line of muscles & tendon pull.  Non – specific Symptoms: o Low – grade fever. o Loss of weight & appetite. o Malaise. o Fatigue. OSTEOARTHRITIS (DEGENERATIVE JOINT DISEASE): “Chronic degenerative disorder affecting articular cartilage of synovial joints with bony remodeling & outgrowth at joint margins (Spurs & lipping)” Progression of synovial & capsular thickening & joint effusion.  Characteristics: o Degeneration  bone remodeling & capsular distention  capsular laxity

(Hypermobility / Instibility) 



 

o Pain & decreased willingness to move  Contractures in the portions of capsule & overlying muscle. Unknown Etiology: o Mechanical injury to the joint  Major stress.  Repeated minor stress. o Poor movement of synovial fluid  immobilized joint.  Rapid destruction of articular cartilage with immobilization.  (Deprivation of nutritional supply) o Genetics  Hands, Hips, knees. Other Risks factors are: o Obesity. o Weakness of Quadriceps. o Joint impact. o Sports with repetitive impact & twisting  soccer, baseball, football. o Occupational activities. o Jobs requiring  Kneeling.  Squatting with heavy lifting. o Cartilage splits & Thins out:  Crepitations & loose bodies (joints)  Subchondral bone exposed. o Increased bone density in joint line:  Cystic bone & osteopenia in adjacent metaphysis. Enlarged Joints: o Heberden’s nodes  Finger DIP enlargement. o Bouchard’s nodes  PIP enlargement. Most Commonly Involved joints: o Weight bearing joints. o Cervical & lumbar spine. o Finger DIPs & Thumb CMC joints.

FIBROMYALGIA (NON – INFLAMMATORY, NON – DEGENERATIVE, NON – PROGRESSIVE DISORDER) “Chronic condition recognized by widespread pain which covers ½ of the body (right or left ½ , upper or lower ½) & lasts for more than 3 months”.  Symptoms: o 11 out of 18 tender pints at specific bony sited. o Non – restorative sleep. o Morning stiffness. o Fatigue with diminished exercise tolerance.

 Characteristics: o Symptoms usually appear in  early – middle adulthood. o Symptoms after physical trauma:  Motor vehicle accident, viral infection  30% Dx.  Hallmark Complaints: o Pain (Muscular origin)  scapula, head, neck, chest & low back. o Fluctuating symptoms is common.  Pain – free to marked increase in pain.  Higher Incidence of: o Tendonitis. o Headaches. o Irritable bowel. o Temporomendibular joint dysfunction. o Restless leg syndrome. o Mitral valve prolapsed. o Anxiety, depression, memory problems.  Contributing Factors: o Environmental, physical, emotional stress aggravates F.M.  Environmental Stress: o Weather changes  baroreceptor pressure changes, cold, dampness, fog rain, fluorescent lights.  Physical stress: o Repetitive activities  Typing, playing piano, vacuuming. o Prolonged periods of standing or sitting. o Working rotating shifts.  Emotional stress: o Life stresses. MYOFASCIAL PAIN SYNDROME (MPS) “Chronic regional pain syndrome”  Hallmark Classification: o Myofascial trigger points in a muscle with referred pattern of pain.  Trigger Points: o Hyperirritable area in tight band of muscle. o Pain is dull, aching, deep.  Types: o Active  produce classic pain pattern. o Passive or latent  asymptomatic unless palpated.  Impairments: o Decreased ROM with stretching a muscle. o Decreased muscle strength.

o Decreased pain with stretching a muscle.  Possible Causes (of Trigger points): o Chronic Overload of Muscle with:  Repetitive activities.  Maintained shortened position. o Acute Overload of Muscle:  Slipping & catching one self.  Following a trauma  Motor vehicle accident.  Picking up object with unexpected weight. o Postural Stresses:  Prolonged time sitting.  Leg – length differences. o Poorly conditioned muscles. o Poor body mechanics.

OSTEOPROSIS “Bone disease leading to decreased mineral content & bone weakness” Lead to fractures  Spine, Hip and Wrist. Diagnosed by determining T – Score or a BMD Scan.  T – Score: o Number of standard deviations (SD) above or below a reference value.  Normal: -1 or Higher.  Osteopenia: -1.1 to -2.4  Osteoporosis: -2.5 or less  Risk factors: o Primary osteoporosis:  Post menopause.  Low body weight.  Family History.  Little or no physical activity.  Smoking  Caucasian or Asian descend.  Prolonged bed rest.  Advanced age. o Secondary Osteoporosis:  Medical Conditions:  G.I – Disease.  Hyperthyroidism.  Chronic renal failure.

 Excessive alcohol consumption.  Medical Use:  Glucocorticoids. o Radiograph Defects:  Cortical Thinning.  Osteopenia Increased bone radiolucency.  Trbecular changes.  Fractures.  Prevention: o Diet rich in Ca++ & Vitamin – D. o Weight bearing exercises. o Healthy life style  Moderate alcohol consumption. o No Smoking. o Testing Bone density & medications (if needed) FRACTURES  POST – TRAUMATIC IMMOBILIZATION “Structural break in continuity of a bone, epiphyseal plate, cartilaginous joint surface” Serious soft tissue injury  Major artery or Peripheral nerve involved. Central fracture  Brain, Spinal cord & Viscera involved.  Position of fracture (Distal w.r.t Proximal fragment): o Non – Displaced. o Medial displaced. o Lateral displaced. o Distracted. o Over – riding with posterior with superior displacement. o Distracted & laterally rotated.  Direction of fracture w.r.t Longitudinal axis: o Transverse. o Longitudinal. o Oblique. o Spiral.  Frequently occurring comminuted fracture patterns: o Wedge shaped or Butter pattern. o Two or three – segmental level fracture. o Fracture with multiple fractures.  Identification of fracture via: o Site: Diphyseal, epiphyseal, metaphyseal, intra – articular. o Extent: Complete, Incomplete. o Configuration: Transverse, oblique or spiral, comminuted. o Relationship of fragments: Undisplaced, dispersed.

o Relationship to environment: Close, open.  Risk Factor: o Sudden impact: Accidents, Abuse & Assault. o Osteoporosis: Women > Men. o History of falls: increased age, low BMI.  Symptoms & Signs of possible fracture: o History of falls, direct blow, twisting injury, accident. o Localized pain aggravated by movement. o Muscle guarding with passive movement. o Decreased function part. o Swelling, deformity & abnormal movement. o Sharp, localized tenderness at fracture site.  Phases of Fracture Healing: o Inflammatory phase  Hematoma formation.  Cellular proliferation. o Reparative phase  Callous formation (unite breach).  Ossification. o Remodeling phase  Consolidation.  Bone remodeling.  Types of Abnormal fracture healing: o Malunion  Fracture healing in unsatisfactory position resulting in bone deformity. o Delayed Union  Fracture takes longer than normal to heal. o Non – Union  Fracture fails to unite with a bony union.  Fibrosis union or pseudoarthrosis.  Complications of Fracture: o Swelling  Contained within a compartment (facial compartment / Tight cast).  Lead to nerve &circulation compromise. o Fat Embolism  Migrate to lungs & block pulmonary vessels  fatal.  Fracture in long bones & pelvis. o Problems with fixation devices  displacement of screws & breakage of wires. o Infection  local or systemic. o Re – fracture. o Delayed or Malunion.

CAUSES WITH TYPES OF FRACTURE  Force  bending (Angulatory).  Effects  Long bones bend  failure on convex side of bend.  Fracture type  Transverse or oblique fractures Greenstick Fx (Children).  Force  Twisting (torsional).  Effects  spiral tension failure in long bones.  Fracture type  Spiral Fracture.  Force  straight pulling (traction).  Effects  Tension failure from pull of ligament or muscle.  Fracture types  Avulsion fracture.  Force  Crushing (Compression).  Effects  usually in Cancellous bone.  Fracture types  Compression Fracture. Torus (buckle) Fracture (Children)  Force  repetitive micro trauma.  Effects  small cracks in bone unaccustomed to repetitive/rhythmic stress.  Fracture types fatigue fracture/stress fracture.  Force  Normal force or abnormal bone.  Effects  with osteoporosis, bony tumor, other bone disease.  Fracture type  pathological fracture.

NERVE STRUCTURE  Peripheral Components of Neuromuscular system are: o Alpha & Gamma motor neurons & axons. o Skeletal muscles. o Sensory neurons & receptors (Connective tissue, joints, blood vessels). o ANS Neurons.  Connective Tissue o Around Axon  Endoneurium. o Around Fascicle  Perineurium. o Around Nerve fiber  Epineurium. Axolemma  Schwann cells  Endoneurium  Perineurium  Epineurium.  Peripheral Nerve Contains a mixture of: o Sympathetic neurons. o Sensory neurons. o Motor neurons.  Alpha – Motor neurons (Somatic efferent fibers) o Cell bodies located in anterior column of spinal cord. o Innervate skeletal muscles.  Gamma – motor neurons (Efferent fibers) o Cell bodies located in lateral column of spinal cord. o Innervate intrafusal muscle fibers.  Sensory neurons (Somatic afferent fibers) o Cell bodies located in dorsal root ganglia. o Innervate sensory receptors.  Sympathetic Neurons (Visceral afferent fibers) o Cell bodies located in sympathetic ganglia. o Innervate sweat glands, blood vessels, viscera, Glands.  Common sites of injury to peripheral nerve o Injury can occur anywhere along the pathway from nerve roots to their termination in the tissues of the trunk & extremities due to tension, compression or injury.  Nerve roots o Emerge from spinal cord & transverse foramina of spine. o Impinged as a result of various pathologies of spine (decrease space in foramina):  Degenerative disc disease (DDD)  Degenerative joint disease (DJD).  Disc lesions.  Spondylolisthesis

 Decreased spinal canal or foraminal space (stenosis) perpetuate symptoms with: o Extension, side bending & rotation to the side.  Adhesions place tension on a nerve root o Nerve mobility tests reproduce symptoms with contra lateral flexion.  Nerve roots of upper quarter  C5 – T1  Nerve roots of the lower quarter  L1 – S3 KEY MUSCLES FOR TESTING UPPER & LOWER QUARTER MAYOTOMES  Upper Quarter: o C1 – 2  cervical flexion o C3  cervical side flexion o C4 scapular elevation o C5  shoulder abduction o C6 Elbow flexion & wrist extension o C7  Elbow extension & wrist flexion o C8  Thumb extension. o T1  Finger abduction.  Lower Quarter: o L1 – 2  Hip flexion o L3  knee extension o L4  Ankle dorsi flexion o L5  Big toe extension o S1  Ankle eversion, plantar flexion, hip extension o S2  Knee flexion. o S3  No specific test action – intrinsic foot muscles (except, Abd. Hallucis)    

1. 2.

BRACHIAL PLEXUS Vasomotor fibers from sympathetic trunk join anterior primary rami. o Course within brachial plexus & peripheral nerves to extremities. Formed by  Anterior primary division of C5 – T1 nerve roots. Function as  distribution center for organizing the contents of each peripheral nerve. Course through thoracic outlet (Vascular & neurological symptoms  TOS) o 3 primary sites for compression or entrapment of neuromuscular structures. Interscalene  bordered by  scalenus anterior, medius & 1st rib Costoclavicular space  between clavicle(superiorly) & 1st rib (inferiorly)

3. Axillary interval  between deltopectoral fascia, pectoralis minor, coracoids process.  Structural anomalies (cervical rib or Malunion of clavicular fracture) o Compress or entrap a portion of plexus.  Upper plexus injuries (C5 – 6): o Most common injury  compression or tearing of upper trunk o Mechanism  Shoulder depression & neck contra lateral flexion o Result  loss of  shoulder abduction & lateral rotation Weakness in  Elbow flexion Weakness in  forearm supination  Erb’s Palsy or Waiter’s Tip Deformity: o Occur with birth injuries  shoulder stretched downward. o Maternal & infant factors described by Benjamin  Stinger  land on upper torso & shoulders with head & neck contra lateral lateral flexion (playing football) Middle plexus injuries C7 (rarely alone). Lower plexus injuries C8, T1 Compression by cervical rib or overhead arm stretching  Klumpke’s Paralysis  paralysis of “hand intrinsic” o Occurs with birth injuries  baby with overhead arm.  Complete or Total injuries of plexus o As a complication of birth (Erb – Klumpke’s paralysis)  Associated with “Horner’s syndrome” PERIPHERAL NERVES IN UPPER QUARTER  Brachial plexus terminates in the 5 primary peripheral nerves: o Musculocutaneous, Axillary, Median, Radial, & Ulnar nerve.  Axillary Nerve C5 – 6 o Emerge from posterior cord. o Pass laterally via Axilla. o Send branches to teres minor. o Course behind surgical neck of humerus. o Innervate deltoid & overlying skin. o Vulnerable to injury with  Shoulder dislocation, fracture of surgical neck. o Affected by injury or stretch to upper trunk. o Shoulder abduction & lateral rotation is impaired.  Musculocutaneous Nerve C5 – 6

o o o o o o o o o o

Emerge from lateral cord. Cross axilla with median nerve. Pierce & innervate Coracobrachialis. Travel distally to innervate biceps brachii & Brachialis. Continue between Biceps & Brachialis to flexor surface of elbow. Emerge from deep fascia at elbow. Continue as Lateral Cutaneous Nerve to Forearm. Affected by injury to lateralcord or upper trunk. Isolated impingement is uncommon. Impaired elbow flexion, forearm supination & shoulder instability.

 Median Nerve C6, 7 & 8 o Formed by bundles from medial & lateral cord in upper part of arm. o Course medial aspect of humerus to elbow. o Deep in cubital fossa under bicepital Aponeurosis. o Medial to tendon of biceps & brachial artery. o Move into forearm between two heads of pronator teres. o Pronator teres hypertrophy lead to the compression of median nerve. o Symptoms mimic carpal tunnel syndrome. o Forearm &intrinsic muscles are involved. o Forearm muscles  pronator teres, wrist flexion & extrinsic finger flexors o Pass via Carpal tunnel at wrist with flexor tendons. o Tunnel is covered by thick inelastic transverse carpal ligament. o Entrapment causes carpal tunnel syndrome.  Carpal Tunnel Syndrome: o Sensory changes & progressive weakness in muscle distal to the wrist.  Ape – hand deformity: o Thenar atrophy & thumb positioned in plane of the hand. o Occurs as a complication of Carpal tunnel syndrome.  Branch to Opponens muscle  hook over the carpal ligament 2/3rd the way up the thenar eminence.  Ulnar Nerve C8, T1 o Emerge from medial cord at the lower border of the Pectoralis minor. o Descends along the medial side of humerus in the arm. o Pass posterior to elbow joint in groove between medial epicondyle & ulnar Olecrenon.  Groove is covered by a fibrous sheath forming cubital tunnel.  Easily irritated here because of its superficial location.

o Pass b/w humeral & ulnar head of flexor carpi ulnarisimpingement site o Extrinsic musclesflexor carpi ulnaris & flexor digitorum profundus (ulnar 1/2). o Enter hand via the trough formed byPisiform & Hook of Hemate.  Trough is covered by Volar carpal ligament & Palmaris brevis.  Forms the tunnel of Guyon. o Tunnel of Guyon:  Sensory changes & progressive muscle weakness distallywith tumor, entrapment.  Injury after the bifurcation  partial involvement.  Radial Nerve C6 – T1 o Emerge directly from posterior cord at the lower border of Pectoralis mior. o Descends in arm, wound around humerus posteriorly in musculospinal groove.  Continue to radial aspect of elbow. o Innervate Triceps, Anconeus, upper portion of forearm extensors & supinators. o Injury with shoulder dislocation & mild humeral fractures. o Crutch Palsy:  Condition of nerve compression due to leaning on Axillary crutches. o Saturday night Palsy:  Occurs when sleeping with person’s head on arm, slung over the back of a chair or open car window.  Triceps involve if compression or injury occurs close to the axilla. o Pierce lateral muscular septum, anterior to lateral epicondyle. o Pass under the origin of extensor carpi radialis brevis.  Divide intosuperficial & deep branches. o Deep BranchEntrapped under the edge of ECR brevis & fibrous slit in the supinator.  Progressive weakness in wrist & finger extensor & supinator muscles.  (Except ECR longusinnervated proximal to the bifurcation)  Impingement erroneously k/n Tennis elbow or lateral epicondylitis.  Pass around the neck of radiusinjury with radial head fractures. o Superficial Branchundergoes direct traumasensory changes.  Enter the hand on dorsal surfacesensory only. o Injury proximal to elbowResults in wrist drop & inability to actively extend the wrist & fingers. o Length – tension relationship of extrinsic finger flexors affected. o Result in ineffective gripwrist splinted in partial extension.

o Injury to mid – forearmsupinator, extrinsic abductor & extensor pollicis muscle affected.  Lumbosacral Plexus: o Lumbarformed by anterior primary divisions of nerve rootsL1,3 & 4. o SacralFormed fromL4-5, S1, S2, S3(part). o Anterior primary rami receive postganglionic sympathetic nerve fibers from sympathetic chain.  Innervate sweat glands, blood vessels, piloerrector muscle. o Isolated injuries are uncommon. o Symptoms commonly arise from:  Disc lesions.  Spomdylitic deformities affecting greater than or equal to 1 nerve roots.  Tension or compression of specific peripheral nerves.

PERIPHERAL NERVES IN LOWER QUARTER Lumbosacral plexus terminate in the three primary peripheral nerves: 1. Femoral & Obturator nerve  From lumbar plexus. 2. Sciatic Nerve  From sacral plexus.  Femoral Nerve L2 – 4 o Arise from 3 posterior divisions of lumbar plexus. o Emerge from lateral border of Psoas major (superior to inguinal ligament) o Descent under Inguinal ligament to femoral triangle (lateral to femoral artery) o Innervate the Sartorius & Quadriceps. o Iliopsoassupplied superior to inguinal ligament. o Injuries occur:  With traumafracture of upper femur & pelvis.  During reduction of CDH (Congenital dislocation of hip)  From pressure during a forceps labor & delivery. o Weakness of hip flexion, loss of knee extension. o Symptoms from neuritis in D.M.  Obturator Nerve L2 – 4 o Arise from three anterior divisions of Lumbar plexus. o Descend to medial side of thigh via Obturator canal in the medial Obturator foramen. o Innervate Abductor muscle group & Obturator externus. o Injury via hernia pressure & damage during labor. o Adduction & external rotation (thigh) impaired difficulty in crossing legs.

 Sciatic Nerve L4 – S3 o Emerge from sacral plexus as largest body nerve. o Component parts Tibial & common peroneal nervedifferentiated in common sheath. o Small nerves from sacral plexus (proximal to sciatic nerve formation) innervate buttock muscles  external rotators & gluteal muscles. o Exit pelvis via greater sciatic foramen & course below via piriformis muscle.  Piriformis Syndrome:  Occurs from shortened musclecompression & irritation of nerve. o Course between Ischial tuberosity & greater trochanter  Protected under gluteus maximus.  Injury with hip dislocation or reduction. o Tibial portion Innervateshamstrings & Adductor magnus (portion) o Common peroneal protion innervatesshort head of biceps femoris. o Terminate into tibial & common peroneal nervesproximal to popliteal fossa.

 Tibial & posterior Tibial nerve L4 – S3 o Form from anterior primary rami of sacral plexus (proximal to popliteal fossa) o Course in popliteal fossa:  Sends branch that joins branch from common peroneal nerve.  Form Sural nerve & continue as Posterior Tibial nerve. o Innervate muscles of posterior compartment of the leg:  Plantar flexors, popliteus, Tibialis posterior, Extrinsic toe flexors. o Occupy the groove behind medial maleollus in the foot.  Along with the tendons of Tibialis posterior, Flexor Hallucis longus, Flexor digitorum longus.  Groove covered by a ligamenttransverse tarsal tunnel.  Entrapment from space occupying lesionsTarsal tunnel syndrome. o Divides intomedial & lateral plantar & calcaneal nerve.  Plantar & Calcaneal Nerve: o Turn under medial side of foot & pass via opening in abductor Hallucis. o Entrapment via:  Over pronation of foot.  Stressed nerves against the fibrous edged opening in the muscle. o Symptoms similar to:  Acute foot straintenderness of posteromedial plantar aspect.

 Painful heelInflammed calcaneal nerve.  Pain in pes cavus foot.  Medial & lateral planter nerves: o InnervateIntrinsic muscles of foot (expect extensor digitorum brevis) o Innervation:  Lateral plantar nerveulnar nerve  Medial plantar nerve median nerve o Nerve compressionweakness &postural changes in the foot.  Pes cavus & clowing of toes.  Common Peroneal Nerve L4 – S2 o Pass b/wbiceps femoris & Gastrocnrmius (lateral head) o Sends branch to join Tibial nerve & form sural nerve. o Come laterally around fibular neck. o Pass via an opening in Peroneus longus muscle.  Pressure or force causes neuropathy.  Sensory changes & muscle weakness in Anterior & lateral leg compartments. o Injury occurs with:  Fracture of fibular head.  Rupture of lateral co – lateral ligament of knee.  Tightly applied cast. o Foot falling asleepsustained pressure with cross – legs. o Bifurcate below fibular neck intosuperficial & deep peroneal nerve.  Superficial Peroneal Nerve: o Descends along the Anterior part of fibula. o Innervate  Peroneus longus & brevis & cutaneous supply. o Injury results in impaired (lost) eversion  Unopposed Inversion  Equinovarus developed.  Deep peroneal nerve: o Decends along Interosseous membrane & distal tibia. o Innervate  Ankle ankle dorsiflexors, toe extensors, Peroneus tertius  Foot  Extensor digitorum brevis. o Injury results in foot drop:  Unopposed eversion  Pes valgus developed.

NERVE INJURY & RECOVERY Peripheral nerve injury  sensory, motor, sympathetic impairment. Pain (Symptom of nerve compression or tension) Connective tissue & vascular associated with peripheral nerve  innervated. Peripheral nerve functionsensitive to hypoxic status.  Mechanism of Nerve injury: o Types of nerve injuries: o Compression  Soft tissue impingement  Sustained pressure applied  Externally  tourniquet.  Internally  Bone, tumor, Soft tissue impingement. “RESULTS IN MECHANICAL OR ISCHEMIC INJURY” Laceration  knife, gunshot, surgical complication, infection injury. Stretch Excessive tension, tearing from traction forces. Radiation ElectricityLightening strike, electrical malfunction.  Partial or Complete Injury: o Symptoms based on location.  Biomechanical injuries to PNS: o Most commonly from  friction, compression, stretch.  Secondary injury from: o Blood or edema.  Compressive forces: o Affect nerve microcirculation  venous congestion & decreased axoplasmic transport impulses blockednerve damage.  Endoneurium: o Maintain fluid pressure & provide nerve cushioning.  Insult to PNS: o AcuteTrauma. o ChronicRepetitive trauma or entrapment.  Sites Vulnerable to  compression, friction, tension are: o Tunnelssoft tissue, bony, fibro-osseous o Branches of nervous systemnerve with abrupt angle. o Specific tension points. o Points where nerve is fixed, passing close to rigid structures (bony prominence)  Pathophysiological or Pathochemical response to injury can be:

o Intraneural:  Pathology affecting.  Conduction tissuehypoxia & demylination.  Connective tissue of nerve o Scaring of Epineurium or irritation of dura mater.  Restricted elasticity of nervous system. o Extraneural:  Pathology affecting  Nerve bed blood.  Swelling of tissue adjacent to nerveforaminal stenosis.  Adhesion of epineureum to another tissueligament.  Restrict gross movement of nervous system. CLASSIFICATION OF NERVE INJURIES  Seddon’s Classification o Three levels of pathology.  Sunderland’s Classification o Five levels of injury & potential for recovery.  Seddon’s Classification & Characteristics of Nerve Injury  Neuropraxia:  Segmental demyelination.  A.P decreased or blocks at the demyelination pointnormal above & below.  Temporary sensory symptomsno muscle atrophy.  Causemild ischemia from nerve compression or traction  RecoveryComplete.  Axontmesis:  Loss of axonal continuity but connective tissue covering remains intact.  Wallerian degeneration  distal to the lesion.  Sensory loss & muscle atrophy.  Causeprolonged compression or stretchcause infarction or necrosis.  Recoveryincompletesurgical intervention.  Neurotmesis:  Complete severance of nerve fiber with disruption of connective tissue coverings.  Wallerian degenerationdistal to lesion.  Sensory loss & muscle atrophy.  CauseGunshot, stab wound, avulsion, and rupture.

 Recoverynot without surgery & depends on:  Surgical intervention.  Correct re – growth of nerve fibers in endoneural tubes.  Sunderland’s Classification of Nerve Injury  1st Degree injury – Neuropraxia:  Minimal structural disruption.  Complete recovery. nd  2 Degree injury – Axontmesis:  Complete axonal disruption.  Complete recovery. rd  3 Degree Injury – Axontmesis & Neurotmesis:  Disruption of axon & Endoneurium.  Poor prognosis without surgery. th  4 Degree injury – Neurotmesis:  Disruption of axon, Endoneurium & Perineurium.  Poor prognosis without surgery. th  5 Degree Injury – Neurotmesis:  Complete structural disruption.  Poor prognosis without Microsurgery. RECOVERY OF NERVE INJURIES Nerve tissue irritated from tension, compression, hypoxiashow signs of recovery.  Recovery of Injured nerve depends on  Nature & level of Injury.  Timing & techniques of repair.  Age & motivation of the patient.  Extent of injury to axon & surrounding connective tissue sheath.  Nature & level of injury  More nerve damagemore tissue reaction & scaring.  Disruption in proximal aspectfiber mismatchingregeneration affected.  Regeneration rate1 inch per day (0.5 – 0.9mm/day)  Depends on  Nature & severity of the injury.  Duration of dennervation.  Condition of tissues.  Timing of Techniques & repair:  Laceration or crush injuriesdisrupt nerve integritysurgical intervention  Regeneration potential based on grouping of specific nerves are:

 Excellent regeneration potentialradial, Musculocutaneous, femoral nerve.  Moderate regeneration potentialMedian, Ulnar, Tibial nerve.  Poor regeneration potentialPeroneal Nerve.  Age & motivation of the patient:  Smith’s 5 possible outcomes of nerve regeneration  Exact reinnervation of its nature target organ with return of function  Exact reinnervation of its nature target organ but no return of function (Degeneration of End organ)  Wrong receptor reinnervated in proper territoryimproper input.  Recovery reinnervation in wrong territoryfalse localization of input  No connection with the end organ. MANAGEMENT GUIDELINES – RECOVERY FROM NERVE INJURY Recovery from nerve injury occurs in 3 phases.  Acute phase  Early after injury or surgery  Emphasis on  healing & complication prevention.  Recovery phase  Reinnervation occurs  Emphasis on  retraining & re – innervations  Chronic phase  Potential for re – innervations has peaked & significant residual deficits are present  Emphasis on  training compensatory function  Acute Phase  After injury or surgery (decompression & release or lacerated nerve)  Immobilization (brief period)  Protect the nerve.  Minimize inflammation.  Minimize tension at injured or repeated site.  Movement (ROM)  Minimizing joint & connection.  Splinting or Bracing:  Prevent deformities due to strength imbalances  Radial nerve splint  Prevent Wrist drop

 Median nerve splint  position the thumb in opposition  Plantar flexion splint  Prevent foot drop  Prevent undue stress on healing nerve  Patient Education:  Prevent extremity to avoid injury  due to sensation loss.  Chronic Phase  Re – innervations peaked & minimal or no sign of re – innervations  Train for compensatory function  Continue wearing supportive splint or brace  Preventive care continues (to avoid injury)  Recovery Phase  Begins with the signs of reinnervation  (Volutional muscle contraction & hypersensitivity)  Motor retraining  Signs of volutional muscle contractionmuscle positioned shortened  Electrical stimulationused to re – enforce active effort  Control gainedBegin gravity eliminated AA – ROM  Weak musclesprotected with splint or a brace.  Desensitization  Regenerationhypersensitivity in the area  Graded series of modalities & proceduresdecreased irritability & increased awareness  Multiple texture & contactssensory stimulation  Pattern of recovery after nerve injury:  Pain (Hypersensitivity)  Perception of slow vibration (30cps), moving touch, constant touch  Perception of rapid vibration (256cps), awareness from proximal to distal  Discriminative sensory re – education “Process of retraining the brain to recognize a stimulus once the hypersensitivity diminishes”  Begins with moving touch stimulus & stroke over the area  Open eyed followed by closed eye  Constant touch localizedprogress to identify various sizes, shapes, textures  Hand  keys, eating utensils, blocks, tooth brush, safety pins  Feet  Grass, sand, wood, pebbles, uneven surfaces  Patient education  Resume the use of the extremity

 Monitor pain, swelling, discoloration  Modify or temporarily avoid aggravating factors  Preventive care to avoid injury.

SYMPTOMS & SIGNS OF NERVE MOBILITY IMPAIRMENT  History  Vascular & mechanical factors  nerve pathology  Pain  most common symptom  Sensory response stretch pain or paresthesia with neural stretch position  Tests of provocation  Neurodynamics tests  detect tension signs in neural tissue  Upper limb tension test  ULTT  Upper limb Neurodynamics test ULNT  Straight leg raise  SLR  Slump test  Additional testsNerve palpation, sensory testing, muscle testing  Test positions & maneuvers same as those of Rx  Tension signsStretch pain or paresthesia  Neurological system stretched across multiple joints  Caused bystress on nerve proximal or distal to the compression site  Principles of Management  Nerve irritability increased with intensity of the maneuver  Tension or primary restriction  “stretch force applied into the tissue resistance & held for 15 – 20 sec, released & then repeated”  Stretched released  neurological symptoms (tingling, increased numbness) vanish  Position the patient at the point of tension (Beginning of symptoms)  Actively or passively move the joint  stretch & release the tension  Teach self stretching.  Neural Tension Disorder  Nerves vulnerable to increased pressure or tension with  Excessive or repetitive stress or strains imposed  Nerve compressed  passing near a bony structure or a confined space  Adhesive scar tissue or swelling  restrict the mobility  Tests of provocation performed

NEURAL TESTING & MOBILIZATION TECHNIQUES  Median nerve  Position  supine  Application  Shoulder  depression   abduction (slight)  Elbow  extension  Arm  lateral rotation  Fore arm  supination  Wrist  extension  Fingers  extension  Thumb  extension  Neck  contra lateral side flexion  Examine & Rx problems with:  Shoulder girdle depression (Thoracic Outlet Syndrome)  Carpal tunnel syndrome  Radial Nerve  Position  supine  Application  Shoulder  depression   abduction  Elbow  extension  Arm  medial rotation  Fore arm  pronation  Wrist  ulnar deviation   flexion  Fingers  flexion  Thumb  flexion  Neck  contra lateral side flexion  Examine & Rx symptoms related to:  Shoulder girdle depression  Tennis elbow & de Quevaion’s syndrome

 Ulnar nerve  Position  supine  Application  Shoulder  depression   abduction   external rotation  Elbow  flexion  Fore arm  supination  Wrist  extension  Neck  contra lateral side flexion  Important in symptoms related to  C8 – T1 nerve roots, lower brachial plexus, ulnar nerve  Medial epicondylitis  Femoral Nerve  Position  neutral (not extended) & hip extended to 0 o  Apply  knee flexion.  LBP or sensation changes in anterior of thigh  Upper lumbar nerve root tension  Femoral nerve tension  Spine Hyper – extension  Decreased foraminal space  nerve root pressure  Spinal movement  facet pain  Thigh pain  Rectus femoris tightness  Alternate positions & procedures  Position  side lying with involved leg upper most  Application  Pelvis  Stabilization  Hip  Extension  Knees  flexion  Sciatic Nerve (SLR with ankle dorsiflexion)  Position  supine  Apply  SLR with ankle dorsiflexion  Variations :  Hip  adduction   medial rotation  Ankle  Dorsiflexion   plantar flexion   Inversion  Neck  flexion (passive)  Variations are used to differentiate

 Tight or strained hamstrings  Nerve mobility in Lumbosacral plexus & sciatic nerve    

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Ankle dorsiflexion + Eversion  tension on tibial tract Ankle planter flexion + inversion  tension on common peroneal tract Ankle dorsiflexion + inversion  tension on sural nerve Hip adduction with SLR  tension on sciatic nerve(lat:to Ischial tuberosity)  Medial rotation with SLR  tension on sciatic nerve  Neck flexion (passively) with SLR  pull spinal cord cranially & stretch the nervous system Slump Sitting  Slump:  Neck  flexion (Over pressure on cervical spine)  Thorax  flexion (Over pressure on cervical spine)  Low back  flexion (Over pressure on cervical spine)  Knees  extension (as much as possible)  Ankle dorsiflexion Prevention  Neural Rx (testing) in early Rx after injury or surgery  Prevent restrictive adhesion development  Rule out “RED FLAG” condition prior to neural tension testing & Rx Precautions:  Know what other tissues are affected by position & maneuvers  Recognize involved tissues irritability & don’t aggravate symptoms  Identify the condition & rate of worsening  Care taken if active disease or pathology of nervous system is present  Watch for the signs of vascular compromise Contraindication  Acute or unstable neurological signs  Spinal cord injury or symptoms  Neoplasm & infection  Cauda equine symptoms related to spine  Changes in bowel or bladder control & peripheral sensation.