The Power is in Your Hands http://www.handsonlineeducation.com/Classes/APath3/path3entry.htm[3/13/18, 12:46:41 PM] Main Menu 1 Introduction click here 2 Muscular Disorders click here 3 Bone Disorders click here 4 Joint Disorders click here 5 Genetic Musculoskeletal Disorders click here 6 Other Connective Tissue Disorders click here 7 Neuromuscular Disorders click here Copyright HandsOn Therapy Schools 2009 PATH.3
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Terrific resilience, support and weight bearing capacity combined with a lightweight construction that provides a boney framework that protects vulnerableorgans and provides leverage for movement
Wolff’s law____________
Bone is living tissue thatremodels according tothe stresses that are
placed upon it
StructureCalcium, phosphorus on collagen matrix: concentric circles withholes for blood vessels
______________Long bones are spiraled
______________Shaft is hollow
______________Resilience, efficiency, lightweight construction
______________Osteoblasts (bone builders) and osteoclasts (bone clearers)under hormonal control pt 1
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FibromyalgiaSyndrome involving chronic pain in muscles, tendons,ligaments, and other soft tissues, along with othersymptoms; frequently seen with chronic fatiguesyndrome, irritable bowel syndrome, S migraineheadaches, sleep disorders, and several other chronicconditions
Demographics2–3% of the U.S. population
85–90% of diagnoses are in women
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
Etiology
Not well understood. Consistent factors include…
Sleep disorder: little or no stage IVsleep
__________________
Fatigue: may be related to sleep;could also be mitochondrial inefficiency
__________________
Pain: may be related toneurotransmitters, esp. high substanceP and nerve growth factor levels
__________________
Tender points: Develop in all fourquadrants of the body
Widespread painin shiftinglocations; canrange from adeep ache toburning andtingling Tender points:nine predictablepairs of these aredistributedamong allquadrants of thebody Stiffness afterrest Poor stamina Sensitivityamplification andlow paintolerance
Rule out similardiseases(challenging!) Diagnosticcriteria: Chronic pain for aminimum of 3months 11/18 tenderpoints are active(elicit diffuse painwith digitalpressure of about4 kg) Tender pointsmust bedistributed allover body Persistent fatigue Sleep notrefreshing;awaken withmorning stiffness
Depression,difficulty withrelationships andjobs, poor qualityof life
Myofascial Pain SyndromeThe development of trigger points Demographics
Affects men and women aboutequally
May be more prevalent with agePrecise incidence is not known
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Etiology
Trigger points:
Microscopic injury leading to pain spasm cycle
Energy crisis: sustained involuntary contraction ofisolated group of sarcomeres
At neuromuscular junction (NMJ), central triggerpoint
At tenoperiosteal junction, attachment triggerpoint
May also involve folded, dehydrated collagen
Contraction causes a knot or taut band
Myofibers need more fuel
Ischemia prevents blood from flowing into area
This is adenosine triphosphate (ATP) energycrisis
Pain-sensitizing chemicals are released; muscletightens; more acetylcholine is released at NMJ;neutralizing enzymes can’t get near; this causes small,involuntary, painful contraction
Neurons become demyelinated, may contribute toreferred pain pattern (Fig. 3.4)
Myositis OssificansMuscle inflammation with bone formation; Heterotopic ossification is more accurate: formation of osseoustissue outside of normal areas
EtiologyMost common is myositis ossificanstraumatica: blunt injury with bleedingbetween muscle sheaths
May be connected by astalk to nearby bonetissue or periosteumHardens at periphery,stays soft insideMay involve osteoblastsreleased from damagedperiosteum
Other forms associated withimmobility or bone abnormalities:
Spinal cord injury, Pagetdisease, hip replacementsurgery
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Shin SplintsUmbrella term for variety of lower leg problems
EtiologyAnatomy review
Lower leg muscles attach whole lengthof the bones Muscles are contained in four tightcompartments If feet don’t absorb, shock is translatedinto the lower leg Chronic overuse or misalignment Exercise without cooling down period Lower leg trauma All lead to edema inside compartments
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
Reduce activity Improve equipment (shoes,running surfaces, etc.) andtraining practices Hydrotherapy Steroid injection For acute compartmentsyndrome: surgery to split fascialsheaths
May indicate massage if noacute inflammation is present Can stretch lower leg musclesbetter than other interventions:good preventative Stress fractures, compartmentsyndrome need medical attention
Mild to intense local pain Pain exacerbated by resistedmovement or passive stretching Usually no palpable heat orswelling Scar tissue may accumulate,leading to Impaired contractility Adhesions
Get an accurate diagnosis Control inflammation: RICE,PRICES Rehabilitate damaged tissues Prevent further injury
Can be extremely useful toshorten recovery time, improvequality of healing tissue
Avascular OsteonecrosisBlood supply to bone is impeded; bone and blood vesselsdisintegrate, not replaced; high risk of fractures, arthritis,joint collapse
Demographics30–50 years old
10,000–20,000 diagnoses/year inUnited States
Leads to 50,000 hip replacementsurgeries/year
Legg-Calve-Perthes disease is inboys 3–12 years old
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Etiology
Head of femur is most vulnerable
Emboli of blood clots, fat cells, nitrogenbubbles block arterioles Venous congestion also causes damage
Often a complication of other disorders
Decompression sickness Lupus or other autoimmune disease(steroids) Pancreatitis Hemophilia Sickle cell disease Alcoholism
Joint pain duringmovement Becomes present atrest Looks like osteoarthritis
Joint collapse
Radiography, bonescans, computedtomography not usefulearly Magnetic resonanceimaging (MRI), biopsy,bone stress test forearly detection
Depends of age, causeNonsurgical: braces,crutches; electricalstimulation of bone Surgery: decompressmedullary canal;remove dead tissue;reshape or rebuild joint
Locally contraindicatesmassage May be helpful forpostural, movementcompensations
Usually obvious, may have to befound with radiography or bonescan
Usually heal well withimmobilization, relief fromweight-bearing or percussivestress Casts, pins or plates, reparativesurgery if necessary Grafting with various substances
Common sense: locally avoidwhile acute; work withcirculation, compensationpatterns
OsteoporosisPorous bones: calcium is removed faster than replaced Demographics
8 million women, 2 million men in theUnited States
34 million have precursor, osteopenia
(may be silent)
Women more at risk
Lower density to start with Childbearing
Hormone fluctuations at menopause
Most common in white and Asianwomen; other races can have it too
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
EtiologyBone density increases until about age 30Then bone density remains stable or decreases Calcium consumption may have influence onbone density, but so do other factors:
Other vitamins, minerals
Exercise habits
Blood pH
Other diseases
Medications
Mood
Calcium absorption
Requires acidic environment instomach Requires vitamins D, K (Too much vitamin A can impedecalcium uptake)
Calcium loss
Sweat, urine Meat-based proteins cause morecalcium to be excreted with urine Caffeine (coffee, soda) Medications
Hyperthyroidism Heavy alcohol use Smoking Inflammatory bowel disease Hormonal imbalances Eating disorders
Maintaining bone density
Osteoblasts and osteoclasts, underhormonal control Most activity in trabecular bone(epiphyses and vertebral bodies) Loss of key struts increases risk ofcollapse Calcium is used outside of bones too Blood clotting Nerve transmission Buffer for pH balance in blood Osteoporosis develops when calciumabsorption/loss/maintenance balanceis lost Vertebrae and femur especiallyvulnerable
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
Silent while early Later: thinned,collapsed vertebrae,loss of height, widow’shump, back pain
Complications
Spontaneous fractures Hip fracture refers tohead of femur Slow healing: < 1/3return to previousactivity levels
DEXA: dual X-rayabsorptiometry Maybe ultrasound, CTPresence of fractures
Hormone replacementtherapy can slowprogression; these carryother possible risks Bisphosphates SERMS (selectiveestrogen receptormodulators) Exercise Diet, calciumsupplements
Prevention
Four main steps:
Get dietary calciumfrom absorbablesources Exercise Get vitamin D Avoid substances andbehaviors that pullcalcium off bone
Depends on resiliencyof client Adjust for fragility, etc. Can offer important painrelief
Paget DiseaseBone is reabsorbed 50x faster than normal; replaced withdisorganized fibrous connective tissue; also called osteitisdeformans
DemographicsAbout 1 million in the United States
Men > women
Especially common in whites from
northwestern Europe
Family predisposition
EtiologyOsteoclasts become huge (5x larger than normal)and hyperactive Osteoclasts are also busy but can’t keep up Bone tissue is broken down/replaced ataccelerated pace Usually in one bone only Skull, vertebrae, pelvis, legs most often Doesn’t appear to progress from one bone toanother Cause is unknown; may involve slow-acting virusalong with genetic predisposition
No early symptoms Later: deep bone pain,palpable heat, problemsrelated to bone changes Loss of hearing Chronic headache Pinched nerves Change in leg shape
Complications
Fractures Arthritis Central nervous system(CNS) problems if skullbones are affected Loose teeth withmandible Heart failure 1% develop rare butaggressive form of bonecancer
Radiography or bonescan Blood test for alkalinephosphatase indicatesoveractive osteoblasts
Similar to osteoporosis Exercise, physicaltherapy Aspirin, pain relievers Calcitonin,bisphosphates Surgery if necessary
Requires caution butprobably safe for activeclients Work with health careteam
Can be subtle or extreme Can lead to breathing problems,lung infections, heart problems
Scoliosis
1–2% of teenagers Girls > boys, 7:1, usually bend toright Mild is 30°–40°, treated withexercise, chiropractic, brace, etc. Severe is 40°+, will probablyprogress about 1° per year;candidate for surgery
Hyperkyphosis Overdeveloped thoracic curve May be congenital in young men:Scheuermann disease In older people may be related toosteoporosis, ankylosingspondylitis Surgery for 75°+ curvature
Hyperlordosis
Overpronounced lumbar curve:
Depends on type, age, severity
Can be especially effective forfunctional problems Even for others, can offer painrelief
Ankylosing SpondylitisProgressive inflammatory arthritis of the spine; alsocalled rheumatoid spondylitis
DemographicsInherited disorder; Usually appears in
men 16–35 years old
1% of U.S. population
Men > women 3:1
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EtiologyProbably autoimmune, maybe triggered bybacterial infection No antinuclear antibodies: seronegativespondyloarthropathy Goes with Crohn disease, ulcerative colitis,psoriasis Usually begins with chronic inflammation atsacroiliac (SI) joint on one or both sides
Progresses up spine Joints become inflamed, cartilagedegenerates, discs ossify, vertebralbodies square off Vertebrae fuse in flexion Fusions are called syndesmophytes Can fuse at vertebral costal joints too
Starts as low back pain May refer into buttocks, legs:looks like disc problem Immobility at spine, hips Flare and remission During flare: general malaise,iritis, fever
Complications
Vertebral fracture Peripheral nerve pressure,cauda equina syndrome Loss of lung capacity,pneumonia, other lung infections Inflammation of eyes, heart,kidneys, other organs
Diagnosis
Observable symptoms Blood tests Radiography May take a long time to confirm,
Exercise to maintain function Physical therapy (PT) for spinestrength, posture Painkillers, anti-inflammatories Immune-suppressants(DMARDS: disease-modifyingantirheumatic drugs) Surgery
Work with caution aroundinflammation Work with health care team,while subacute Work to help maintain spinefunction
DislocationsBones in a joint are separated to that they no longerarticulate; Other soft tissue damage too
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EtiologyUsually significant force Shoulder most often Fingers Congenital weakness in connective tissues(Marfan, Ehlers-Danlos) Hip dysplasia may be present at childbirth, canlead to osteoarthritis in adulthood
For large joints: immediatereduction Radiography to rule out fracture Splinting, exercise, PT Other interventions: ligament-shortening surgery, thermalcapsulorrhaphy, proliferantinjections
Avoid while acute; in subacutestage work for scar tissueresolution, improved ROM Be careful about positioning oflax joints
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
EtiologyUric acid is not extracted Metabolic gout: kidney function is normal; uric acidlevels are high Renal gout: uric acid is normal; kidneys are impaired Both: Kidneys are compromised and uric acid levelsare high May be triggered by:
Sudden onset, usually at feet Extremely painful inflammation May cause fever May cause punched-outformation in bone Kidney stones, renal failure,high blood pressure,cardiovascular disease: allinterrelated
Lyme DiseaseInfection with spirochete Borrelia burgdorferi; Twospecies of deer ticks: Ixodes scapularis, Ixodespacificus
DemographicsMontana is only state with no Lyme
disease reported
90% cases in Northeast and mid-Atlantic, Wisconsin, Minnesota
At risk: work and play in grassy or
wooded areas
20,000 diagnoses/year in the UnitedStates; also in Europe and Asia
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
Etiology
Ticks live about 2 years In spring/summer of first year they crawl ontobushes and stems to find a warm-blooded host Pick up B. burgdorferi from deer or othermammals; pass on to humans Slow-growing bacterium that invades severaltypes of tissues
Symptoms appear 7–30 days aftertick bite. Bull’s-eye rash , highfever, fatigue, night sweats, stiffneck, headache. (Often no rash ispresent; looks like flu,mononucleosis)
Early disseminated disease
Systemic symptoms develop:
Cardiovascular:irregular heart beat,dizziness Neurological:headaches, Bell palsy,numbness, tingling,forgetfulness General: debilitatingfatigue
Late diseaseInfection of one or more joints:knee, elbow, shoulder. Usuallythree joints or fewer. Can causepermanent damage. Looks likerheumatoid arthritis. Symptoms usually last weeks tomonths, then subside Some get progressively worse
Antibiotics, long course for slow-growing bacteria (up to 12months)
Prevention
Long sleeves, pants Light-colored clothing Insect repellants Examine skin Remove ticks with tweezers,take to doctor (if removed within24 hours, risk of infection is verylow)
Contraindicated when joints areacutely inflamed Be careful aboutneurological/circulatorycomplications Know what ticks look like ifworking in endemic area
Lax ligaments: unstable joints History of trauma, arthroscopic surgery Repetitive pounding stress Others: Hormonal imbalance, nutritionaldeficiency, trigger foods, etc.
pt 4
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Deep pain, stiffness; especiallywithout warmup or with overuse At fingers: phalangeal epiphyseswiden At distal interphalangeal joints(DIPs): Heberden nodes At proximal interphalangealjoints (PIPs): Bouchard nodes
Diagnosis
Physical examination, patienthistory Rule out other causes of jointinflammation; radiography notconclusive
Improve and maintainhealthy range ofmotionIncrease stamina andlose weightImprove the strengthof musclessurrounding affectedjoints
Nutritional supplements:Glucosamine and chondroitinsulfate
Popular and showresults for mild tomoderate arthritisGlucosamine mayaffect insulin levels indiabetic patientsMade from the shellsof shellfish (watch forallergies)Chondroitin may affectblood clotting
Arthroscopic procedures:
Can be useful to reduce pain,ease muscle tension; Doesn’trebuild damaged cartilage
Patellofemoral SyndromePatellar cartilage is damaged: precursor of osteoarthritis atthe knee; also called jumper’s knee; anterior knee painsyndrome; overuse syndrome
Flare and remission Prodrome: malaise precedes sharp,specific joint pain Rheumatic nodules Joints are hot, painful, stiff
May improve with gentlemovementKnuckles in hands, toes,ankles, wrists
Bilateral, may not be symmetrical
Complications
During flares
Rheumatic nodules on thescleraSjögren syndromePleuritisCarditis or pericarditisHepatitisVasculitisRaynaud syndrome, skinulcers, bleeding intestinalulcers, and internalhemorrhaging.Bursitis and anemia, esp.with childhood onset
Between flares:
DislocationsRuptured tendons
Goals
Reduce painLimit inflammationStop damageImprove function
Diagnosis History, radiography, blood test forrheumatoid factor At least four of these:
Morning stiffness that lastsat least 1 hourArthritis in three or morejointsInvolvement of PIPs,metacarpophalangeal joints(MCPs), DIPsBilateralPositive serum rheumatoidfactorRheumatoid nodules
Not all osteophytes cause pain (radiography notdefinitive for cause of pain) Age contributes to ossification of anteriorlongitudinal ligament, posterior longitudinalligament, ligamentum flavum
DISH (diffuse idiopathic skeletalhyperostosis) may cause gradualpainless loss of ROM
More typical development of arthritis at facets, SIjoint, costovertebral joints
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Significant swelling,esp. if connected tojoint capsuleAnterior talofibularligament is mostcommonly sprained
Subacute Stage
Inflammation subsides
24–48 hours later,depending onseveritySome injuries goback and forth,depending on usage
Complications
Masking symptoms especially ofminor fractures Repeated injury, with poor-quality healing Ligament laxity collagen haspoor rebound; can lead toosteoarthritis
Temporomandibular Joint DisordersCollection of signs and symptoms associated with jawproblems; also called TMD: temporomandibular jointdisorders
Demographics
An estimated 10 million in the UnitedStates (not all seek help)
Women > men
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
Etiology
TMJ has huge mobility:
Elevation, depression, retraction,protraction, side flexionJoint capsule stretches
Fibrocartilage disc can get injured (video clip 1) Muscles develop trigger points
Causes May be initiated by fall or motor vehicle accident(MVA): jawlash Can be spontaneous, connected to stress, bruxism Symptoms and causes can be circ Other factors
Misalignment at jaw, biteHormonal sensitivity?High overlap between ligament laxityand heart valve problems: connectivetissue quality issues?Frequently seen with fibromyalgia,chronic myofascial pain syndrome,irritable bowel syndrome
Jaw, neck, and shoulder pain Limited range of motion Popping in the jaw Locking of the joint Grinding teeth (bruxism) Ear pain Headaches Chronic misalignment of cervicalvertebrae
Diagnosis
Differentiate from myofascial painsyndrome, other tension patternsthat cause pain in face and head
Sprain of ligament thatattachesstylomandibular joint tobase of the skull: alsocalled Ernest syndromeTrigeminal neuralgiaOccipital neuralgiaOsteomyelitis
MRI, radiography,electromyography, clinicalexamination can yield information
Ehlers-Danlos SyndromeGroup of genetic disorders leading to connective tissueweakness
Demographics
Rare: about 50,000 in the UnitedStates, but many with mild form
Men = women
No racial predisposition
Etiology
Genetic mutation affects collagen, elastin,other extracellular matrix of connectivetissues
Hypermobility of jointsChronic joint painDelicate skinPoor wound healing
Most common form passed throughautosomal dominant genes: if one parent is acarrier, each child has a 50% chance ofdeveloping EDS Other types are recessive: both parents mustcarry the gene
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Beta blockers toreduce force onaortaBlood pressuremedicationProphylacticantibiotics to protectheart valvesSurgery to correctspine, thorax, heartvalves if necessary
Can be appropriate with carefor delicate tissues, high risk ofheart/aorta problems Work with health care team
Muscular DystrophyGroup of related diseases with genetic anomalies; Degeneration, wasting of muscle tissue
Demographics
Duchenne and Becker are X-linked
Carried by mother, passed tosons
400–600 born each year
Other types not gender specific:
males = females
Etiology
Normal muscles use a protein, dystrophin, to helpconvert fat or glycogen into fuel
The most common forms of MD involveinadequate production dystrophinMuscle cells atrophy and die, replaced by fatand connective tissueContractures develop
Duchenne muscular dystrophy: most common: 1:3500male babies. No dystrophin is produced Becker muscular dystrophy: less common, less severe:1:30,000 boys, some dystrophin is produced Myotonic muscular dystrophy: most common adult-onset MD; myotonia, cataracts, GI dysfunction, heartproblems Other varieties
A toddler hasdifficultywalkingLeg pain,waddling gait,lumbar curve,walks on toesCan also affectspine, joints,heart, lungs
Most Becker MD patients die youngwith cardiac or respiratory failure
Diagnosis
Much easier to find now
Blood test for creatinekinaseLook for neurologicalproblemsBiopsy
Interventions to prolongactivity, life expectancy Massage, PT to minimizecontractures Surgery to release tighttendons, correct spine Steroids Assistive devices asnecessary
Sensation is intact: massage issafe
Check forcirculatory health,other complicationsof lost movement
Ring and little fingers affectedmost Begins as mildly tender bump;cord extends into palm, towardfinger Bilateral about 50% of time Can be slow or fast, mild orsevere Constricted nerve, blood supplymay lead to amputation
Without treatment, can lead toloss of function in affectedfingers Injections with cortisone,collagenase, needleaponeurotomy Surgery if necessary Recurs about one-third of time
As long as sensation is present,massage is safe; may not makesignificant changes May be useful post surgery tohelp recover function
Ganglion CystsPouches on joint capsules or tendinous sheaths
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
Etiology
May grow with trauma or overuse; many arespontaneous Filled with viscous fluid, may have multiple lobes May grow in a place to interfere with movement or limitfunction
Mucous cysts grow on DIPs, may distortgrowth of fingernail
Inguinal hernia: most commonvariety; occur at inguinal ring Epigastric hernia: aboveumbilicus; linea alba splits Paraumbilical hernia: linea albasplits at umbilicus Umbilical hernia: most commonin newborn babies; usuallycloses by age 2 Femoral hernia: Most common inwomen; bulge at femoral ringbelow inguinal ligament. Risk ofstrangulation is high Hiatal hernia: Diaphragmatichiatus is stretched; stomachbulges into thorax Other hernias: at incisions,obturator, lateral aspect of rectusabdominus
Complications Bigger = safer for short term(less risk of strangulation) Strangulation can lead toinfection
Surgical repair
Truss is temporarysolution
Local contraindication at herniaand for recent surgery For past surgery, no cautions
Subacute: permanentremodeling of tibial tuberosity
Goals: reduce pain, limit damageto quad attachment Careful heating, warming upbefore activity Cooling down and stretching Rest if necessary Brace or cast followed byrehabilitative exercises Surgery if necessary
Locally contraindicated forcirculatory massage while acute Later, work to reduce pain atknee, stretch soft tissues,promote good quality healing
Pes Planus, Pes CavusPes planus = flat feet; Pes cavus = caved feet(jammed arches); Feet lack medial and lateralarches or arches don’t flatten and rebound
Etiology
Imbalance in forces at feet has repercussionsthrough the rest of the body Pes planus, cavus can be from congenitalproblems in bone shape; strength of footligaments; muscle imbalance; poor footwear
Linear scleroderma: discolored line or band on aleg, arm, or over the forehead Systemic scleroderma: blood vessel damage inskin and other organs: digestive tract, heart,circulatory system, kidneys, lungs, synovialmembranes, tenosynovial sheaths
Limited systemic scleroderma: slowonset, may infiltrate other organs Diffuse scleroderma: sudden onset,earlier involvement of internal organs Sine scleroderma: internal organs only
C: Calcinosis:accumulation ofcalcium deposits in theskin, especially in thefingers R: Raynaudphenomenon E: Esophagealdysmotility S: Sclerodactyly:hardening of thefingers T: Telangiectasia
Drugs to manageRaynaud syndrome,kidney function,GERD, muscle andjoint pain, immunesystem overactivity PT, OT for flexibility,especially in hands Avoid smoking, coldtemperature, spicyfood
Depends on resiliency of client
Be careful ofcirculatory, kidneyhealth Bodywork thatdoesn’t challengefluid flow may bebeneficial
Direct, shearing forces through tendonOveruse without recovery timePoor flexibilityUnderlying diseaseCortisone injection
Extrinsic factors:
Training errorsPoor equipmentFall or trauma
Damaged tendon looks dull gray or brown, soft More liquid ground substance Fibers are disrupted and not continuous Fibroblasts and extra blood vessels are active
Looks like muscle strain: pain onresisted contraction, passivestretching Usually not palpably hot
Use of anti-inflammatories underquestion Steroids may give short-termrelief, but with long-term risks Rest, ice, stretching,rehabilitative exercise, patience
Respect acute injury (lymphaticwork may be beneficial) In postacute or chronic condition,can speed healing, help organizescar tissue, improve localnutrition
MRI, CT, nerve conduction tests(hard to evaluate soft tissuedamage with these)
Radicular painindicates nerve rootirritation General painsuggests referral fromsoft tissue injury
Neck collar (as short a time aspossible) Pain relievers, anti-inflammatories, muscle relaxants PT, massage to strengtheninjured muscles, reduce spasm,resolve trigger points, improvequality of healing tissue, etc.
Avoid mechanical massage whileacute Reflexive, energetic work maysupport autonomic recovery Rule out contraindicating injuries Then, look for progressiverelease of muscle spasm,improved connective tissuehealth
Disc DiseaseCollection of problems with nucleus pulposus orannulus fibrosis
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins
EtiologyOuter layer of discs = 3 layers of annulusfibrosis Inner center = nucleus pulposus (spherical) Annulus fibers are strongest when tight,weakest when slack
Nucleus needs annulus to bestrong
Annulus begins to degenerate around age20–30; nucleus begins to shrink
Annulus can develop cracks,fissures; connecting vertebraedevelop osteophytes, →spondylosis
Nucleus breaks through annulus or annuluscracks Damaged discs leak highly inflammatorypain-sensitizing chemicals Discs usually protrude posterolaterally; someother forms are possible Bulging directly posteriorly: cauda equinasyndrome (medical emergency)
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From pressure on nerve tissue,inflammatory response May be intermittent Local and radicular pain Specific muscle weakness Parasthesia Reduced sensation Numbness
Complications
Spinal cord compression
Cauda equinasyndrome
Diagnosis
Damaged discs can look likeligament injury, bone spurs,tumors, infection Radiography, CT, myelogram,MRI
Goal: to allow bulgingnucleus/cracked annulus to recede Chiropractic, osteopathy:manipulation to create space Bed rest, traction PT: posture, good body mechanics Medication: muscle relaxants,painkillers Other interventions:
Chemonucleolysis Various types ofdiskectomy
Avoid while pain is acute(comes and goes)
Work to createspace in spine Adjust positioning,bolsters, supportcushions Work with otherhealth careproviders for bestoutcome
Often around eyesand lower face:ptosis, problemswith eating,drinking Symptoms worsein morning,evening Slowly progressive,can affect arms,legs, respiratorymuscles (this isnow rare)
Goals: boost nervetransmission, suppressimmune system activity atNMJ Meds keep ACh active, steroidsuppress immune system Surgery may remove thymus Plasmapheresis in crisis(removes antibodies)
MG involves motor loss but notsensory deficit: massage is safe