Orthopedic Bone Healing, Fractures, and Biomechanics PDF

Bone-Mechanical Properties Compression best load for bone results in bone formation moderate consistent force is best bone is strongest when loaded through compression Tension bone has good strength against if loaded...

Bone-Mechanical Properties Compression best load for bone results in bone formation moderate consistent force is best bone is strongest when loaded through compression Tension bone has good strength against if loaded parallel to long axis of bone can result in bone resorption if too much Torsion bone is weak to this force causes fractures easily small loads can increase bone strength Shear Bone is weakest to this force Causes fractures easily small loads can increase bone strength -trabeculae formation Bone-Healing Inflammation Day of injury Soft Callus First 3-4 weeks fragile continue to immobilize stable once phase is over Hard Callus 4-6 weeks can resume normal activity once fully stabilized 3-4 months hard bony union Remodeling 1-2 years  Fixation Closed Reduction: cast, Can proper alignment be attained without surgery? splint, boot or brace to hold -May reduce with or without anesthesia position Open Reduction Surgically (open) realign bone for proper healing -if bone cannot be reduced and stay aligned w/o surgery -midshaft of long bones can be difficult to reduce -fractures close to ends of bones secondary to muscle attachment and resting tension in muscles -smaller bones with little blood flow Open Reduction Internal increase chance of infection (possibly years later) Fixation: rods, pins and large incisions (healing time and ability) wires, screws, plates may heal faster than OREF may not lead to long term strength usually permanent, but may be removed External Fixation Pins or wires used to secure an external scaffolding -can use compression or traction -post-traumatic, limb reduction, limb lengthening, arthrodesis, limb salvage -less soft tissue and periosteum disruption -may lead to increased long term bone strength Fracture Stress -Loading factors: biomech, training, strength, surface, shoe/orthotics -Factor that modify ability of bone to resist load=>genetics, nutrition, endocrine status, activity history, disease, meds Intraarticular Extraarticular Simple Complex Comminuted Open Closed Fibrous Connective Tissue-Tendon and Ligaments Fibroblasts in extracellular matrix structure Histology: Fibroblasts-20% Structure: Collagen, Elastin, Ground Substance-80% Mechanical Properties: Davis’s Law=>similar to Wolf’s Law Compare chart Tendons Ligaments Collagen is more organized Less volume of collagen and less organized More specific function Function may be less specific -carry tensile forces from muscle to bone -resist multiple directions of mvt -compress bone when acting as pulley -mechanoreceptors=>proprioception -20% length comes from crimp=>ability to stretch Mechanical Properties of Tendons and Ligaments Fibrous Connective Tissue Compression is destructive Respond well to tension Weak w/ torsion or shear Viscoelasticity Time dependent mechanical behavior Stress and strain relationship is not constant -creep -stress relaxation Muscle Charts Stress/Strain Curve:  Creep: Primary creep ​ The initial stage of creep deformation ​ A non-linear, high rate of creep strain ​ The strain rate decreases over time Secondary creep ​ A stable stage where the strain rate of deformation remains constant ​ The minimum strain rate of a creep deformation ​ The secondary stage contributes the majority of the total strain experienced by a material Tertiary creep ​ The final stage of creep deformation ​ A very high strain rate deformation that leads to failure Stress Relaxation: Once the specimen reaches the desired elongation, the strain is held constant for a predetermined amount of time. The stress decay, which occurs because of stress relaxation, is observed as a function of time. Tendinopathy Reactive Tendinopathy Cells activated, proteoglycans increased Dysrepair Extracellular matrix disruption with vascular ingrowth Degenerative Cell death, ECM degenerates, neovascularization Tendinopathy Tendon Healing and Rehab Healing Rehab needs load to heal do not completely rest-↓load to beneficial levels -tendons synthesis and increased stiffness w/ no compressive loads load no rapid loads start with isometrics, then isometrics (eccentric do not stretch early and concentric) then plyometrics do not ignore pain-avoid more than 2 point increase -isometric and isotonic exercise decrease pain do not rely on passive treatments avoid wrapping of tendon, avoid end range takes 12 weeks for tendon changes and 6 mos for exercises with insertional tendinopathy significant change Ligament Injury Grade 1 Microscopic tears in substance with no effect on stability Grade 2 Macroscopic tear involving a partial tear-decreased joint stability, but ligament still partially intact Grade 3 Complete disruption-significant laxity in direction of motion that ligament restrains Intra-articular Ligaments Injury Limited ability to heal Surgical repair needed for non-copers Healing depends in type of repair -graft normally strongest initially~2 weeks -graft then degrades and “ligamentizes”~4 weeks Normal Healing 0-4 weeks structurally weak protected ROM minimal strength training 4-6 weeks structural union occurs begin to achieve normal ROM -BE CAREFUL!!! 6 weeks-3/4 months Protected strength training 3/4 months-8 months Fibers are becoming stronger Full ROM strengthening Possible start athletics 8-12 months remodeling of fibers -must load fibers return to full activity -full ROM, neuromuscular integration, strength Cartilage Articular Cartilage-Hyaline Cartilage -Chondrocytes -Extracellular matrix=>collagen (type II), proteoglycan, small amount of elastin, water Avascular and not innervated 4 zones=>superficial, transitional, deep (radial), tidemark (transition), calcified  Cartilage Injury Single insult vs. Degeneration High Impact force vs. Repetitive sub-threshold loads -compression: responds well to slow, low loads-high speed and high force is destructive -torsion and shear-can cause tears Chondral damage w/o visible disruption (cartilage at risk) Disruption of cartilage alone Disruption of cartilage and subchondral bone (osteochondral injury) Cartilage Classification Grade 0 normal Grade 1 Cartilage w/ softening and swelling=> @ risk Grade 2 A partial-thickness defect w/ fissures on the surface that do not reach subchondral bone or exceed 1.5 cm in diameter Grade 3 Fissuring to the level of subchondral bone in an area with a diameter more than 1.5 cm Grade 4 Exposed subchondral bone Surgical Procedures Microfracture -Most common tears 65, poor knee alignment, RA, non-full thickness tears -Complications: Mild transient pain, “Gritty” sensation,catching, effusion Osteochondral -Transfer of cartilage and bone “plugs” from NWB’ing portion of joint repair site Autograft -Better long term outcomes than microfracture Transplantation (OATs) -Indicated for young active pt w/o severe OA or RA and good donor site Matrix-Induced -Two step procedure Autologous -Chondrocytes harvested from pt in first surgery Chondrocyte -Chondrocytes are expanded in a culture then seeded into a collagen scaffold Implantation (MACI) -During a second procedure the matrix is cut to fit and secured with a fibrin glue -Indicated for 18-55 y/o, full thickness tears less than 3x5 cm w/o severe OA  Nerve Interface Common peroneal at fibular head Dura mater @ L4 Radial N attachment to radial head Suprascapular N to suprascapular notch Spinal nerve roots @ facet joints Spine tension points: C6,T6,L4 Neurodynamic Slump C6,T6,L4 and popliteal are tension points Neural tissue does not move in relation to movement of spinal canal Length of spine increases ~9cm from ext to flex Physical Stresses on Peripheral Nerve Tensile stress applied longitudinally to peripheral nerve creates an elongation of the nerve (an increase in strain) The transverse contraction that occurs during this elongation is greatest at the middle of the section undergoing tensile strength Indications and Contraindications Indications Contraindications -Subacute and chronic radiculopathy -Malignancy (cervical+lumbar) -Acute Inflammation -Adherent nerve root -Spinal Cord Injury -Peripheral neuropathy (peripheral nerve -Suspected HNP entrapment) -Cauda Equina -Status post severe trauma -CNS conditions -Deterioration of neurological sx Proposed Mechanisms of NM Physiological Central Effects Mechanical -Decrease intraneural edema -Decrease dorsal horn and -Increase nerve excursion -Increased neural vascularity supraspinal sensitization (cortical and -Restore mvmt in neural tissues subcortical reorganization seen w/ and surrounding nerve interface neuropathic pain)  Neurodynamic Assessment SLR ULTT -Classic SLR w/ sensitizing mvmts of hip -Shldr abd 110°, shldr ER, forearm supination, wrist & finger adduction + Ankle DF=>Sciatic & Tibial ext, elbow ext=>Median -Ankle DF+Eversion=>Tibial -Shldr abd 10°, shldr ER, forearm supination, wrist & finger -Ankle DF+Inversion=>Sural ext, elbow ext=>musculocutaneous -Ankle PF+Inversion=>Common Peroneal -Shldr abd 50°, forearm pronation, shldr MR, wrist & finger flex+wrist UD+elbow ext=>Radial -Shldr abd 90°, elbow flex, wrist & finger ext, shldr LR=>Ulnar Treatment Sliders/Flossing Tensioners -combinations of joint mvmt that tense nerves at one -Combination of joint mvmts that elongate the nerve at end of nerve bed while releasing nerves at other end of both ends nerve bed -Goal: improve viscoelastic properties of nerve -Goal: glide nerve in relation to surrounding tissues Treatment Principles Irritable Tissue Non-irritable Tissue -Start with indirect techniques-removed from symbol area -Larger longer oscillating mvmts when -Technique should be pain-free initially extra-neural restrictions exist (interfacing -Use large amplitude (grade II) performed rhythmically through tissues); smaller quicker oscillations w/ range intra-neural disorders -Repeat for approx 20 sec then release-progress by oscillating -Optimal component mvmts should be for longer periods and with greater amplitudes, adding tension explored (direct vs indirect, addition of at different points along NS sensitizing mvmts, sequencing of mvmts) -constantly monitor sx Muscle Energy Techniques Voluntary contraction of a muscle in a controlled direction, at varying levels of intensity, against specific counterforce by examiner Used to lengthen short/contracted/spastic muscle, strengthen a weak muscle, reduce local edema Can be effective at mobilizing an articulation that is restricted b/c of contractile tissue dysfunction  Indications Restoring normal tone is hypertonic muscles Increasing joint mobility Strengthening weak muscles Increasing local circulation Preparing muscles for subsequent stretching Improving function Physiological Principles-Extrafusal Skeletal muscle tissue is comprised of both extrafusal and intrafusal muscle fibers Extrafusal fibers are typical skeletal muscle fibers innervated by alpha motor neurons Golgi tendon organ lies within extrafusal fibers -as muscle contracts or is put on stretch, tension in golgi tendon organ inhibits alpha motor neuron activity causing muscle to relax -Golgi tendon organ will respond to increased tension by inhibiting further muscle contraction (protective mechanism)=>BASIS BEHIND “POST ISOMETRIC RELAXATION” Post-Isometric Relaxation (PIR) Tension is caused by isometric contraction When sustained causes inhibition from GTO=>PHC=>AHC Reduction in tone lasts 20-25 sec Tissues can then be lengthened Physiological Principles-Intrafusal Intrafusal fibers comprise the muscle spindle and are innervated by gamma and beta motor neurons Respond to amount and rate of change in length of a muscle Intrafusal fibers serve a proprioceptive function Muscle spindle gives contant “real time” feedback to the muscle regarding length In response to stretch, muscle spindle discharges nerve impulses that increase contraction, thus preventing over stretching Excitatory activity of agonist muscle results in inhibitory activity in antagonist=>BASIS BEHIND “RECIPROCAL INHIBITION”  Reciprocal Inhibition (RI) Excitatory impulse of contracting agonist 20 second refractory period Inhibitory impulse of antagonist May be less effective than PIR Reduction in tone of antagonist Can use if contraction of muscle is painful Method of Application Take joint to point of resistance (point of bind) Ask pt. To isometrically contract muscle to be treated 20% of max force Slow contraction for 6-8 sec Move joint further into ROM during exhale of deep breath No discomfort and pt. Should be instructed to breathe Rest 15-30 sec in new ROM Repeat until no progress is made (3-4 reps) Hold final position 25-30 sec Keys to Success No pain should be caused by MET Keep contractions light (20-30% of strength) Communicate effectively and ensure client is not experiencing discomfort at any time Client can help to locate tissue tension or restriction barrier Never over-stretch the muscle Spine Key Considerations Imagining findings must be interpreted in the context of the pt’s clinical condition Must be considered a multi-dimensional model to understand spine pain Morphological changes occur as a result of loading/stress on spinal structures Clinical picture may reflect pathological changes in spine tissue structure and function  Models Kinesiopathology Mvmt impairment precedes pathological change Pathokinesiology Injury leads to mvmt impairment Mixed Model Interactive-mvmt impairment contributes to abnormal loading on tissues and structural changes alter mvmt Physical Stress Theory (PTS) Expansion of “SAID” principle =>Specific Adaptation to Imposed Demand 5 characteristics responses of tissues to stress: 1.​ atrophy=>not enough 2.​ Maintenance=> constant 3.​ Hypertrophy=>overload 4.​ Injury=>too much 5.​ Death=>way too much Consider the problem of overall deconditioning when applying PTS to spine pathology Functional Spinal Unit AKA Motion Segment Smallest physiological motion unit of spine exhibiting biomechanical characteristics similar to entire spine =>2 vertebrae, the zygapophyseal joints, IVD, soft tissue structures FSU concept illustrates interdependence of all of these bony and soft tissue structures Clinical relevance: no pathological process can exist w/o affecting the function of other parts of the FSU  Degenerative Disc Disease Cartilaginous end plates (hyaline) cranially and Proteoglycans in NP allow for absorption of water (ability caudally at junction of vertebral bodies (weak to attenuate compressive force) junction) Type II collagen in NP, type I in AF Innervation by sinuvertebral nerves, ventral rami, gray rami communicantes Water content in IVD decreases with age Fissures in AF can occur “Age related changes in molecular composition of Changes can have biomechanical=>clinical disc” consequences Genetic component exists (twin models and animal Environmental factor believed to be a secondary studies) consideration (ie. weightlifters have lower than expected prevalence) “An aberrant, cell-mediated response to progressive Signs of disc degeneration often present by 3rd decade structural failure” of life Most common condition affecting adult spine Occurs in 3 phases 1.​ Dysfunction 2.​ Instability 3.​ Stabilization 3 Phases of DDD Facet Joints Intervertebral Disc Synovitis Circumferential Tears Hypomobility Dysfunction Radial Tears Early Degeneration ⇓ Continued Degeneration Internal Disruption Capsular Laxity Instability Loss of Disc Height Subluxation ⇓ Disc Resorption Enlargement of Articular Stabilization Osteophytes Processes  3 Phases Characteristics Dysfunction Phase Unstable/Instability Phase Stabilization Phase -Physiologic changes -Subluxation of facets -Subchondral bone growth leads to predominate, structural changes -Internal disc disruption osteophyte formation are minimal -Annular bulging -Continued erosion of articular -Facet joint -Disc space narrowing cartilage inflammation=>synovitis -Retrolisthesis -Bony ankylosis -Formation of intraarticular -Lateral canal stenosis -Central/Lateral canal stenosis adhesions and synovial folds -Clinical instability -Disruption of articular cartilage; thinning, fissuring, and fibrillation -Joint hypomobility -Annular fiber tearing: circumferential/radial Modic Changes (Modic Sign) Type I Vascular development in vertebral body, no bone damage or red marrow changes (inflammation and pain) Type II Fatty replacement of red marrow Type III Fractures of trabecular bone Disc Herniation w/ NR Involvement SLR test + for referred leg pain ¾ hx or physical examination findings: -dermatomal pain location in concordance w/ a nerve root -corresponding sensory deficits -diminished reflex -motor weakness Supplementary physical examination finding -crossed SLR test may be + Sacroiliac Joint No centralization of sx Dominant pain in SIJ ⅗ physical examination findings: -distraction -compression -thigh thrust -Gaenslen’s test -Sacral thrust  Spinal Stenosis (Lateral Canal) w/ Radiculopathy Pain and/or limitation w/ ext, ipsilateral LB and rotation; flexion may decrease sx Neurological: -dermatomal sensory loss -diminished reflexes -motor loss (depends on severity) -variable nerve tension signs Special Test: -SLR/Slump test + -Quadrant test + Spinal Stenosis (Central) 3/5 hx findings Supplementary physical exam findings -age more than 48 hrs -improved walking tolerance w/ spine in flexion -bilateral sx -relief by forward bending -leg pain more than back pain -pain during walking/standing -pain relief upon sitting Spondylolisthesis Intervertebral slip inspection or palpation Segmental hypermobility by use of manual passive physiological intervertebral motion Supplementary physical exam finding in older adults Facet Joint No valid tests for facet joint pain General clinical criteria include: -local pain -pain w/ active or passive ext -joint mobility impairment TBC 2 levels of initial patient triage -level of 1st contact healthcare provider -level of rehab provider Includes a biopsychosocial model of LBP mgmt -risk assessment -addresses psychological factors 3 levels of classification  Level I Classification Medical Management Pts referred to appropriate medical provide due to suspicion of serious pathology Rehabilitation Management Pts who can be managed by PT Self-care Management Pts who do not require tx by a healthcare provider Level II Classification Symptom Modulation Severe pain and high levels of disability status consistent w/ high level of irritability Movement Control Pain severity low to moderate, moderate disability, sx stable-goal resolution of sxs and improvement in function Functional Optimization Pain low or absent, disability low-goal to return to high level function w/o recurrence Level III Classification Stage 1: Treatment-Based Stage 2: Treatment Impairment Stage 3 Subgroups Based -Manipulation -Flexibility Impairment -Activity Intolerance -Stabilization -Strength Impairment -Work Intolerance -Traction -Endurance Impairment -Work Conditioning -Specific Exercise -Motor Control Impairment -CardioVascular Impairments -Poor body mechanics Pt Examination-Level I Triage Detailed Hx Comprehensive pt exam Medical Screening FABQ score and/or STarT Back Tool Review of pt data generated by other healthcare ODI score providers  STarT Back Screening Tool (SBST) 9 item validated tool Screens primary care pts w/ LBP for prognostic indicators relevant to initial decision making Identifies modifiable risk factors (biomedical, psychological, social) 3 categories of risk for poor outcome -low risk=>3 or less -medium risk=>4 or more then 3 or less psych -high risk=>4 or more for both Reduces back pain related disability=>Subgroup and Targeting Treatment Psych Score=>Questions 5-9 Lumbar Manipulation Classification Criteria Tx Approach -No sx distal to the knee or local sx -Spinal Manipulation techniques directed to -Recent onset of sx (If # of criteria met was 4+, there was 95% chance of successful outcome Stabilization Classification Criteria Tx Approach -Younger age (91°, postpartum (ES,EAO) -Aberrant mvmts during active mvmt testing for -Exercises to enhance co-contraction local spinal flexion/extension stabilizers (multifidi, TA) -+Prone lumbar instability test -CPR=>if 3+ criteria met, 80% chance of successful -Segmental hypermobility outcome -Tendency toward episodic pain Traction Classification Criteria Tx Approach -S&S:of nerve root compression (Positive Well-leg -Mechanical Traction Raise/SLR) -Manual Traction -No centralization of sx during exam -General Lack of evidence to support use of traction for LBP -PT should not use mechanical traction for pts w/ chronic LBP w/ leg pain, based on the lack of benefit when added to other interventions  Specific Exercise: Extension Classification Criteria Tx Approach -Sx improve or centralize w/ lumbar extension -End range extension exercise -Sx peripheralize w/ lumbar flexion -Mobilizationmanipulation to promote extension -Directional preference for extension -Temporary avoidance of flexion postures and activities Specific Exercise: Flexion Classification Criteria Tx Approach -Older age (>50 yo) -flexion based exercises -Directional preference for flexion -mobilization to promote flexion -Imaging evidence of lumbar stenosis -exercise directed at impairments of strength/ROM/muscle length impairments -body weight-supported ambulation -avoidance of sustained extension postures/activities Specific Exercise: Lateral Shift Classification Criteria Tx Approach -Observation of Lateral Shift -pelvic translatory exercises -directional preference of lateral translation -lateral shift correction in non-WB Cervical Mobility Classification Criteria -no sx of root compression -no sx below elbow -duration of sx 7 -Referred sx extending to upper quarter -Poor tolerance for examination/irritabile -Tx to include cervical spine mobilization and cervical ROM ex Headache Classification Criteria -CC HA w/ onset preceded by neck pain -Sx affected by neck mvmts or pressure on neck -No dx or sxs of migraine -Tx to include cervical spine mobilization or manipulation + strengthening ex for DNF and upper quarter MDT Basic Principles A system of assessment and treatment of spinal disorders Focuses on pt directed intervention Not just extension!!! Uses repeated mvmts and loading strategies (mechanical) Responses to mvmt directs tx Manual therapy only to add specific force  MDT Attributes Encourages Self Tx Proven to be Reliable Noninvasive Screens for red flags Nonspecific tissue Dx (not pathoanatomic) Easily transitions to HEP Mechanical Dx Less reliance on practitioner Predictability 4 steps: =>Assess,Classify,Treat,Prevent Prevention MDT Syndromes Derangement Dysfunction Postural Others Disruption within the Abnormally shortened Abnormal force being Spinal stenosis, hip motion segment (eg. this tissue resulting in pain (eg. places on normal tissues pathology, Si disorder, is where we normally see scarring, fibrosis, adherent (eg. seated PT student Spondylolysis, centralization) nerve root) posture) Spondylolisthesis, Postsurgical Derangement (80%) Reducible (78%) Irreducible (22%) -Typically responds to repeated mvmt (Directional Preference) -Does not respond to loading: sx do -Sx decrease or centralize w/ preference not decrease or centralize w/ -Sx may increase or peripheralize w/ opposite mvmt repeated mvmt -Severity based on area of sx: central, unilateral above knee/elbow, unilateral below knee/elbow -Tx is based on directional preference: extension (70%), Flexion (6%), Lateral (24%), Combo -Progress from unloaded midrange to loaded end range Dysfunction (15%) May be adaptively shortened tissue, adhered or scarred Pain noted at end range of restriction Named for direction of Restriction Flexion,Extension,Lateral Tx based on loading into direction of dysfunction Aim to remodel tissue  Postural (5%) Pain arising from deformation of tissue from prolonged end range loading Pain when postures are assumed Pain w/ static loading-rest of exam normal Low load w/ longer duration of load Tx approach is postural correction and education MDT Examination Terms FIS=>flexion in standing Rep FIL Rep FIS EIL=>extension in lying EIS=>extension in standing Rep EIL Rep EIS SGIS=>side glide in standing FIL=>flexion in lying Rep SGIS McKenzie Method Chart Classification Conceptual Model Clinical Findings Derangement Internal articular displacement causing a Rapid and lasting changes in pain intensity and Syndrome disturbance in the joint, which produces location occurring for a few mins to a few days; pain and impairment often accompanied by mechanical improvements; sx centralization/peripheralization may be present Dysfunction Pain resulting from deformation of Pain is felt consistently when the abnormal tissue Syndrome structurally impaired soft tissue is loaded at the end ROM and abates when the surrounding or within the spine resulting loading is released; ROM is restricted; no rapid from previous trauma, degeneration, or change in pain is seen development of an imperfect repair; examples include contraction, scarring, adherence, and adaptive shortening Posture Mechanical deformation of normal soft Local mechanical pain occurs only after Syndrome tissues arising from prolonged postural prolonged positioning at joint end range (eg. stresses that lead to pain; local sitting slouched); and abates when position mechanical pain occurs after prolonged changes; ROM is full and repeated motions have positioning at joint end range (eg. sitting no effect slouched) Other Does not fit criteria for derangement; No lasting change in pain location or intensity in dysfunction, or posture syndrome response to therapeutic loading strategies  Derangement Tx=>REDUCTION Anterior Disc=>Flexion Based Find Directional Preference Directional Preference is Mvmt that: Anterior Lateral Disc=>Mixed May be unidirectional or Multiplanar Centralizes Flexion and Lateral Based Lateral Disc=>Lateral Based First correct lateral shift if noted Reduces or abolishes sx Posterior Lateral Disc=>Mixed Start unloaded and work toward Restores function (increase ROM, Extension and Lateral Based increased loading as tolerated decrease stretch, improve gait, improve SLR) Posterior Disc=>Extension Based Steps for Tx Derangement *Use the least amount of force necessary 1.​ Reduce Derangement 2.​ Maintain Reduction 3.​ Recover Function 4.​ Prevent Reoccurrence Green Light: Pt w/ mechanical response that lasts after mvmt=>KEEP GOING!!! Yellow Light: Pt may respond during mvmt (increase or decrease in sx), but no change after mvmt=>change force: may need more reps, more or less loading, or more or less force, but keep direction Red Light: sx worsen or peripheralize and remain after mvmt or new sxs that remain after mvmt=>STOP!!! Try a different direction or fully re-evaluate  Dysfunction Tx=>REMODELING Restricted or adhered tissues causing pain Focus on stretching into restriction Easier when less chronic Will produce some discomfort Temporary and mild May take weeks to respond and months to recover Green Light: pain is produced at end range, but abolishes when stretch is removed=>Keep GOING!!! Red Light: pain is produced or worsens and remains after stretch is removed=>STOP!!! Decreases force or time spent at end-range-may have to give rest or re-evaluate Postural Tx=>RE-EDUCATION Focus on education Show pt link b/w posture and pain Show alternatives to faulty posture Teach strategies to change posture throughout the day MDT Cervical Tx IV Disc Derangement Dysfunction Postural -Anterior=>flex, protraction -Reduction -Remodeling -Reeducation (lower), retraction (upper), -Repeated movements in -Stretch shortened tissue -Educate on posture retraction w/ OP directional preference w/ and progress as ROM and pain and how to -Lateral=>Side bend, increased loading as increases and sx decrease change and avoid rotation tolerated postures -Posterior=>retraction (lower), retraction-extension, extension in prone, protraction (upper)  MLI vs CLI Mechanical Lumbar Instability Functional(Clinical) Lumbar Instability -Based upon imaging findings or PA mobility assessment -Related to poor neuromuscular control of (increased angular mvmt or translator mvmt vertebral segments -Addressed via surgery (fusion) or PT -Better addressed through PT -Disruption of passive stabilizers and decreased structural -’A significant decrease in the capacity of the integrity stabilizing system of the spine to maintain the -”Loss of spinal motion segment stiffness such that applied IV neutral zones within physiological limits forces produce displacements exceeding those found in a which result in pain and disability” normal spine” Copers vs Non-Copers Copers Non-copers -Can develop strategies to cope w/ altered -develop signs and sx of clinical instability segmental mvmt Clinical Lumbar Instability Signs and Sx Hx of painful locking/catching during Pain worsens w/ sustained positions Positive response to motion immobilization Pain on return from forward bend Clusters of sx are of more value in Responds to manipulation-short terms of diagnostic accuracy term, dramatic results Pain during transitional activities Frequent prior episodes of pain Hx of trauma or surgery Pain w/ sudden or trivial activities Extreme fluctuations of sx w/ minimal No clear postural preference perturbation Problems w/ unsupported sitting Transient deformity w/ prior episodes Difficulty w/ activities requiring extensor muscle activity Physical Examination Criteria Aberrant mvmt during AROM (sagittal plane) -”instability catch” -painful arc -thigh climbing (Gower’s sign) -reversal of lumbopelvic rhythm Segmental hypermobility: sx provocation and pain Special tests: prone lumbar instability test CPR: Success with Lumbar Stabilization +Prone instability test* Aberrant Motion* Average SLR >91° Age ligaments, joint capsule Control Subsystem Neural=>neural control Active Subsystem Spinal muscles=>global & local stabilizers Physiological Considerations Precision of mvmt is impaired Dominance of “global” vs “local” control muscles during mvmt Weakness of trunk flexors and extensors Poor endurance of spinal extensors (more important than strength) Loss of proprioception & balance associated w/ trunk mvmts Abnormal muscle recruitment patterns Organizational changes in motor cortex leading to loss of motor control Lumbar Muscle Stabilizers Local Stabilizers Global Stabilizers -Multifidus -Rectus abdominis -Transverse Abdominis -External abdominal oblique -Internal abdominal oblique -Quadratus Lumborum -Erector Spinae Lumbar Multifidus Fibers pass superomedially form vertebral arches to SP’s spanning 2 to 4 vertebrae Short triangular muscle bundles, thickest in lumbar region Deep and superficial divisions -DM spans one segmental level -SM spans multiple levels Multifidus Function Multifidi have larger % of type I vs type II fibers DM contraction thought to produce joint compression vs rotation or extension mvmts DM: feedforward function to prepare spine for loading conditions or limb mvmt Multifidus muscle fibers short and arranged in tightly packed bundles -creates a physiological cross-sectional greater than other paraspinal mm -enables large force generation over small excursion -consistent w/ contribution to stabilization rather than spine mvmt Internal Abdominal Obliques Origin Insertion Inguinal ligament, iliac crest and TL fascia Lower ribs, pubic crest, and linea alba Transverse Abdominis Origin Insertion TL fascia, lower 6 ribs, inguinal ligament and The linea alba and pubic crest iliac crest Lumbar Stabilization Programs Rehabilitation of motor aspects of muscle function Neutral spine postures Low level of continuous tonic contraction Co-contraction of trunk muscles Precise co-contraction of TA and Multifidus Independent function of segmental vs global muscles  Functional Benefits Co-contraction Protection of joint from unexpected loads Maximizing joint congruency Equalizing pressure distribution over articular surfaces Centering joint Stress absorption Signs of unwanted global muscle activity Aberrant Mvmt -Excessive posterior pelvic tilt -Flexion of TL junction -Rib cage depression Contours of Abdominal -No mvmt of abdomen Wall -Visible contraction of EAO -Increased lateral diameter of abdominal wall Aberrant Breathing -Breath holding, lack of diaphragmatic breathing Patterns -Loss of motor control during breathing Excessive back extensor In thoracic erector spinae activity Methods of detection Observation, palpation, EMG Progression of LSE Simple=====>Complex Short Lever=====>Long Lever Isolation=====>Integration Known=====>Unknown Static=====>Dynamic Neutral=====>Out of Neutral? Gluteus Medius Maximum % MVIC in… -side plank abduction (dominant leg bottom)=>103% -side plank abduction (dominant leg top)=>89% -single leg squat=>82% -sidelying hip abduction=>81% -front plank w/ hip extension=>75% Gluteus Maximus Maximum % MVIC in… -front plank w/ hip extension=>106% -lateral step up=>90% -gluteal set/squeeze=>81% -single leg squat w/ rotation=>78% Successful Management of LBP Depends On Individual examination of adaptation of back muscle structure and function (loss of motor control, decreased CSA, etc) Identification of psychosocial features to develop a tx strategy Consideration of time-dependent mechanisms to tailor intervention to an individual Paradoxical Effect of LBP Inhibition of intrinsic muscles (local stabilizers) Inhibition activation of global stabilizers Loss of “fine tuning” function of intrinsic stabilizers is sacrificed for increasing the stiffness of the spine (reflexive protective mechanism) in people w/ LBP Contraindications to LSE Serious pathology Severe acute pain Progressive neurological deficits Cardiovascular disease (unstable) C-Spine Muscles Deep Cervical Flexors Lower Cervical/Upper Thoracic Extensors -Longus capitis -Multifidus -Longus colli -Semispinalis -Rectus capitis anterior Craniocervical Flexion Test Motor Control Test Normal=26-30mmHg