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Therapeutic Exercise Notes by Aamir Memon TherTherapeutic
ExerThecise Notes
T
Therapeutic Exercise Notes by Aamir Memon[Type text] Page 1
NOTES FOR MEDICAL & ALLIED HEALTH PROFESSIONS
2012-14
TherTherapeutic ExerThecise
Notes Based on Kiner & Colby 5th Edition
Dpt. Aamir Raoof Memon
https://www.facebook.com/groups/653602987987375/
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* Disease Impairments Disability Handicap
ICF* --- Impairments Activity limitation 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. Post-
surgical 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)
Fractures, Osteotomy, Soft tissue trauma & repair
o 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”.
Appearance of involved muscles → Constant state of contraction
Inhibition procedures applied → decrease muscle tension
Causes of hypotonicity→ CVA, TBI, SCI
3. 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. Alignment
2. Stabilization
3. Intensity of Stretch/Magnitude of force
4. Duration of Stretch
5. Speed of Stretch
6. Frequency of Stretch
7. 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 tissue-
maintained. 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) Limited P-ROM in capsular pattern (ii) Firm end feel – when range limiting tissue is over pressured (iii) ↓ed joint-play movement with “Mobility tests” (iv) 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. Static Stretching. 2. Cyclic Stretching. 3. Ballistic Stretching. 4. PNF Stretching. 5. Manual Stretching. 6. Mechanical Stretching. 7. Active Stretching. 8. 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 Ensure → optimal muscle relaxation & Prevent tissue injury. o 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 (Range-limiting 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 weight-
pulley 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 No voluntary relaxation between the patterns. o 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 2) Stabilization 3) Intensity 4) Volume 5) Exercise order 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:
Fear of pain injury, re-injury Depression related to physical illness Impaired attention or memory – Aging Head injury Side effects of medication
Attention:
“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 & fibrosismuscle 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)
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.
1. Interscalene bordered by scalenus anterior, medius & 1st rib
2. 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 Emerge from lateral cord.
o Cross axilla with median nerve.
o Pierce & innervate Coracobrachialis.
o Travel distally to innervate biceps brachii & Brachialis.
o Continue between Biceps & Brachialis to flexor surface of elbow.
o Emerge from deep fascia at elbow.
o Continue as Lateral Cutaneous Nerve to Forearm.
o Affected by injury to lateralcord or upper trunk.
o Isolated impingement is uncommon.
o 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 ulnarisimpingement site
o Extrinsic musclesflexor carpi ulnaris & flexor digitorum profundus
(ulnar 1/2).
o Enter hand via the trough formed byPisiform & 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 distallywith
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 intosuperficial & deep branches.
o Deep BranchEntrapped under the edge of ECR brevis & fibrous slit in
the supinator.
Progressive weakness in wrist & finger extensor & supinator
muscles.
(Except ECR longusinnervated proximal to the bifurcation)
Impingement erroneously k/n Tennis elbow or lateral epicondylitis.
Pass around the neck of radiusinjury with radial head fractures.
o Superficial Branchundergoes direct traumasensory changes.
Enter the hand on dorsal surfacesensory only.
o Injury proximal to elbowResults in wrist drop & inability to actively
extend the wrist & fingers.
o Length – tension relationship of extrinsic finger flexors affected.
o Result in ineffective gripwrist splinted in partial extension.
o Injury to mid – forearmsupinator, extrinsic abductor & extensor
pollicis muscle affected.
Lumbosacral Plexus:
o Lumbarformed by anterior primary divisions of nerve rootsL1,3 & 4.
o SacralFormed fromL4-5, 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 Iliopsoassupplied superior to inguinal ligament.
o Injuries occur:
With traumafracture 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 nervedifferentiated 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 musclecompression & irritation of
nerve.
o Course between Ischial tuberosity & greater trochanter
Protected under gluteus maximus.
Injury with hip dislocation or reduction.
o Tibial portion Innervateshamstrings & Adductor magnus (portion)
o Common peroneal protion innervatesshort head of biceps femoris.
o Terminate into tibial & common peroneal nervesproximal 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 ligamenttransverse tarsal tunnel.
Entrapment from space occupying lesionsTarsal tunnel
syndrome.
o Divides intomedial & 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 straintenderness of posteromedial plantar aspect.
Painful heelInflammed calcaneal nerve.
Pain in pes cavus foot.
Medial & lateral planter nerves:
o InnervateIntrinsic muscles of foot (expect extensor digitorum brevis)
o Innervation:
Lateral plantar nerveulnar nerve
Medial plantar nerve median nerve
o Nerve compressionweakness &postural changes in the foot.
Pes cavus & clowing of toes.
Common Peroneal Nerve L4 – S2
o Pass b/wbiceps 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 asleepsustained pressure with cross – legs.
o Bifurcate below fibular neck intosuperficial & 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 functionsensitive 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
ElectricityLightening 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 blockednerve damage.
Endoneurium:
o Maintain fluid pressure & provide nerve cushioning.
Insult to PNS:
o AcuteTrauma.
o ChronicRepetitive trauma or entrapment.
Sites Vulnerable to compression, friction, tension are:
o Tunnelssoft tissue, bony, fibro-osseous
o Branches of nervous systemnerve 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 tissuehypoxia & 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 nerveforaminal stenosis.
Adhesion of epineureum to another tissueligament.
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 pointnormal above
& below.
Temporary sensory symptomsno muscle atrophy.
Causemild ischemia from nerve compression or traction
RecoveryComplete.
Axontmesis:
Loss of axonal continuity but connective tissue covering remains
intact.
Wallerian degeneration distal to the lesion.
Sensory loss & muscle atrophy.
Causeprolonged compression or stretchcause infarction or
necrosis.
Recoveryincompletesurgical intervention.
Neurotmesis:
Complete severance of nerve fiber with disruption of connective
tissue coverings.
Wallerian degenerationdistal to lesion.
Sensory loss & muscle atrophy.
CauseGunshot, stab wound, avulsion, and rupture.
Recoverynot 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.
2nd
Degree injury – Axontmesis:
Complete axonal disruption.
Complete recovery.
3rd
Degree Injury – Axontmesis & Neurotmesis:
Disruption of axon & Endoneurium.
Poor prognosis without surgery.
4th
Degree injury – Neurotmesis:
Disruption of axon, Endoneurium & Perineurium.
Poor prognosis without surgery.
5th
Degree Injury – Neurotmesis:
Complete structural disruption.
Poor prognosis without Microsurgery.
RECOVERY OF NERVE INJURIES
Nerve tissue irritated from tension, compression, hypoxiashow 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 damagemore tissue reaction & scaring.
Disruption in proximal aspectfiber mismatchingregeneration
affected.
Regeneration rate1 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 injuriesdisrupt nerve integritysurgical
intervention
Regeneration potential based on grouping of specific nerves are:
Excellent regeneration potentialradial, Musculocutaneous,
femoral nerve.
Moderate regeneration potentialMedian, Ulnar, Tibial nerve.
Poor regeneration potentialPeroneal 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 territoryimproper input.
Recovery reinnervation in wrong territoryfalse 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 contractionmuscle positioned shortened
Electrical stimulationused to re – enforce active effort
Control gainedBegin gravity eliminated AA – ROM
Weak musclesprotected with splint or a brace.
Desensitization
Regenerationhypersensitivity in the area
Graded series of modalities & proceduresdecreased irritability &
increased awareness
Multiple texture & contactssensory 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 localizedprogress 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 testsNerve palpation, sensory testing, muscle testing
Test positions & maneuvers same as those of Rx
Tension signsStretch pain or paresthesia
Neurological system stretched across multiple joints
Caused bystress 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
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.