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The Power is in Your Hands

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1 Introduction

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2 MuscularDisorders

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3 BoneDisorders

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4 JointDisorders

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5 GeneticMusculoskeletal

Disorders click here

6Other

ConnectiveTissue

Disorders click here

7 NeuromuscularDisorders

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Musculoskeletal System Conditions

Injuries to muscles, bones, joints, ligaments, tendons, tendinoussheaths, bursae are hard to see on radiographs and MRI

Massage therapists are wellequipped to assess these

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Bones

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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MusclesSpecialized thread like cells that with electrical and chemicalstimulation have the power contract while bearing weight

Massage moves fresh, highlyoxygenated blood, while flushing

old, toxic and stagnantinterstitial fluid out

Function: pull bony attachments together______________

Aerobic combustion: work with adequate supply ofoxygen; clean burning energy

______________Anaerobic combustion: without adequate supply ofoxygen; produces lactic acid, a nerve irritant

______________Delayed Muscle Soreness (DOMS) caused by increase oflactic acid; and/or calcium leakage from sarcomeres

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JointsAllows movement between bones, providing the fulcrum that bones canuse ; constructed so that no rough surfaces ever touch

Other ConnectiveTissue:

Tendons, tendinoussheaths, ligaments, bursae

________________

General ConnectiveTissue Problems:

overuse, stress, cortisol,poor sleep: everything is

interrelated

Organized into three classes: Synarthroses (immovable, i.e. cranial)

______________Amphiarthroses (slightly movable, i.e. between vertabrae)

______________Diarthroses (freely movable, i.e. knee); most vulnerable toinjury

Copyright 2009 Walters Kluwers Health l Lippincott Williams & Wilkins

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Muscular Disorders

Fibromyalgia

Myofascial Pain Syndrome

Myositis Ossificans

Shin Splints

Spasms, cramps

Strains

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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


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

__________________

Other issues: oxidative stress, freeradicals, inefficient hypothalamic-pituitary-adrenal (HPA) axis,aspartame use, others

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more Fibromyalgia

Signs andSymptoms Diagnosis Complications Treatments Massage

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

Education

Patient controls nutrition, sleep, exercise, stress

Medications

Guaifenesin

Tricyclic antidepressants

Drugs for restless leg syndrome (?)

Can be safeandappropriatewithintolerance ofclient Avoid ice Avoidovertreatment Don’t treattender pointslike triggerpoints

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Myofascial Pain SyndromeThe development of trigger points Demographics

Affects men and women aboutequally

May be more prevalent with agePrecise incidence is not known

Copyright 2009 Walters Kluwers Health l Lippincott Williams &Wilkins

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)

Satellite points form

Points may be active or latent

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more Myofascial Pain Syndrome

Signs and Symptoms Diagnosis Treatments Massage

Taut bands or nodules Predictable trigger pointmap Referred pain pattern Regional pain

No consistent criteria;most people have sometrigger points

Eradicate trigger points:

Vapo-coolantspray Injections ofanesthetic Dry needling Botox tointerfere withacetylcholinerelease Acupuncture

Indicates massage

Sustainedischemicpressure istraditional Short,pulsingpressuremay bemoreeffective

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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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more Myositis Ossificans

Signs and Symptoms Treatments Massage

Bruised sensation, then areafeels hard and tender Range of motion is limited Pain subsides, leaving ahardened mass (body eventuallyreabsorbs it)

Rest and isolate injury to preventexcessive bleeding Stretch to improve range ofmotion (ROM) post acute stage Surgical removal if necessary;can recur

Local contraindication Work within tolerance aroundedges

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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





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more Shin Splints


Mild or severe pain Worse with muscle activity

Lower leg injuries

Tibialis anterior, tibialis posteriorinjury Medial tibial stress syndrome Periostitis Stress fractures Chronic compartment syndrome Acute compartment syndrome

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

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Spasms, CrampsInvoluntary contraction of voluntary muscle; Cramps arestrong, painful, acute (charleyhorse); Spasms may bechronic

MassageIndicated, with caution

Watch for contraindicating conditionsRespect splinting mechanism

EtiologyFour main contributing factors:

NutritionIschemiaExercise-associated muscle crampingSplinting

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StrainsInjury to muscle-tendon unit, with emphasis on muscledamage

MassageIndicated, with caution

Watch for contraindicating conditionsRespect splinting mechanism

EtiologyCan be specific trauma Chronic cumulative overuse Myofibers are torn, fibroblasts lay down scar tissue Graded by severity:

First degree: mildly painful, no functionallimitSecond degree: moderate injuryThird degree: rupture, possibly avulsionfracture

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more Strains


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

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Bone Disorders

Avascular Osteonecrosis

Fractures

Osteoporosis

Paget Disease

Postural Deviations

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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


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

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more Avascular Osteonecrosis

Signs and Symptoms Diagnosis Treatments Massage

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

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FracturesAny variety of broken bone: Simple, Incomplete or Compound; Alsostress, compression, march, greenstick, comminuted, impacted,compression, malunion, etc.

DemographicsChildren > adults (high-risk

behaviors)Elderly: brittle bones, easy

falls

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more Fractures


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

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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


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


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more Osteoporosis

Signs and Symptoms Diagnosis Treatment Massage

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

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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



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more Paget Disease

Signs and Symptoms Diagnosis Treatment Massage

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



Postural DeviationsOverdeveloped spinal curves: Hyperkyphosis (humpback),Hyperlordosis (“wayback), Scoliosis (S, C or reverse-C curve)

EtiologyDistortions happen in multipleplains (rotoscoliosis) Functional problem: soft tissuetension Structural problem: bonydistortion; Most cases areidiopathic; Some related tocongenital problems Cerebral palsy, polio, musculardystrophy, osteogenesisimperfecta, spina bifida


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more Postural Deviations

Signs and Symptoms Treatment Massage

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



swayback Usually muscular imbalance Can cause significant low backpain

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Joint Disorders

Ankylosing Spondylitis

Dislocations

Gout

Lyme Disease

Osteoarthritis

Patellofemoral Syndrome

Rheumatoid Arthritis

Spondylosis

Sprains

Temporomandibular Joint Disorders

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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


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




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more Ankylosing Spondylitis


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



esp. in women

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DislocationsBones in a joint are separated to that they no longerarticulate; Other soft tissue damage too


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




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more Dislocations


Swelling, discoloration, loss offunction, pain

Complications

Fibrosis, scar tissue Damage to blood vessels, otherstructures Ligament laxity Subluxation, spontaneousdislocation, osteoarthritis

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

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GoutChemistry-based inflammatory arthritis Demographics

Men > women 10:1Women tend to be postmenopausal

1 million + in the United States


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:

Binge eating, drinking, surgery, suddenweight loss, infection

Uric acid accumulates, crystallizes Usually around great toe Usually sudden onset Tophi may develop later (deposits of sodium urate)

Risk Factors

High-purine diet (red meat, organ meats, shellfish,alcohol, lentils, mushrooms, peas, asparagus, spinach) Obesity Sudden weight changes Alcohol consumption



Hypertension Some blood disorders One attack may be followed by others with increasingfrequency

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more Gout


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

DiagnosisPain profile Distinguish from pseudogout forchemical accuracy Aspirated fluid shows uric acidcrystals

Drugs:

Pain relief (not aspirin)Anti-inflammatories

Metabolism/uric acid management Hydration Losing weight Changing diet

At least local contraindication;no ice! Get information oncardiovascular/kidney health

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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


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

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more Lyme Disease


StagesEarly local disease

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



Diagnosis

Difficult to be accurate Blood tests identify exposure, notwhether symptoms are related tocurrent infection False negatives Other tick-borne diseases

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OsteoarthritisSynovial joints (especially weight bearing); Usually due toage, wear and tear; Also called degenerative joint disease

DemographicsMost common type of arthritis

20 million to 40 million in the United

States

Men about equal to women; womenhave it more severely

Leading risk factors:

AgeOverweight

Massage therapists: take care of

saddle joint!


Etiology

Precarious environment inside joints; once damageoccurs, it is difficult to reverse Cartilage

Articular cartilage: small number ofchondrocytes with proteoglycans thatattract water

Arrangement varies byregionsSuperficial (in joint space)IntermediateDeep (attaches to bone)

Resistance to shearing andcompressive forces

Chondrocytes are active all through life, replacingand rebuilding surface

Don’t migrate to areas of damageWhen cartilage is damaged,chondrocytes make less fluid andcollagen

Cartilage degradesOsteocytes in epiphysesbecome active: bone spurs,may be cystlike cavitiesunder cartilage

Causes

Age: dry, prone to injury Overweight: stress on knees, hips



Lax ligaments: unstable joints History of trauma, arthroscopic surgery Repetitive pounding stress Others: Hormonal imbalance, nutritionaldeficiency, trigger foods, etc.

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more Osteoarthritis


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

Goals: reduce inflammation, limitor reverse damage Nonsteroidal anti-inflammatorydrugs (carry some risks) Topical applications: camphor,menthol, capsaicin Exercise: within pain tolerance forthree goals:

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



Proliferant injectionsCorticosteroidinjectionsSynovial fluidwithdrawalJoint lavage anddebridement

Joint replacement surgery:256,000 knee replacements,117,000 hip replacements peryear Procedures in development:numerous strategies are indevelopment:

Cartilage pasteDrill into epiphyses tostimulate cartilagegrowthTransplantosteochondral plugsOthers

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Patellofemoral SyndromePatellar cartilage is damaged: precursor of osteoarthritis atthe knee; also called jumper’s knee; anterior knee painsyndrome; overuse syndrome

Etiology

Two main contributors

Overuse/overloading;Percussive activity withtwisting, jumping Poor alignment; Especially withoverweight, poorfootwear, unevensurfaces, muscularimbalance

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more Patellofemoral Syndrome


Pain at anterior aspect of knee Stiffness after immobility Difficulty with walking, especiallydown stairs Crepitus

Diagnosis Can be difficult; looks likepatellar tendinitis (whichresponds to massage)

Change activity Physical therapy: Quads, hams,tensor fascia latae (TFL), deeplateral rotators Ice Nonsteroidal anti-inflammatories(NSAIDs) Orthotics Knee brace, taping

Irritation is inside joint capsule;not in reach for massage; canaddress pain, stiffness, tension,alignment

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Rheumatoid ArthritisAutoimmune attack on synovial membranes; can involveinflammation elsewhere too

Demographics

3.1 million in the United States

Women > men, 3:1

Mostly 20–50 years old, can be inchildren


Etiology

Immune system attacks synovial membranes

Can affect other areas: blood vessels,serous membranes, skin, eyes, lungs, liver,heart)

B cells, T cells, antibodies, inflammatory chemicals arepresent in joint during flare

Synovial membrane thickens, swellsFluid accumulatesInflamed tissue releases enzymes thaterode cartilageDeformation of joints

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more Rheumatoid Arthritis


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

First-line drugs: NSAIDs,steroids, cyclo-oxygenase-2inhibitors (with exercise,hydrotherapy, PT,occupational therapy [OT]) Second-line drugs: biologicalresponse modifiers,immunosuppressant drugs Other: diet, exercise, stress-reduction Surgery if necessary

Avoid circulatory massagewhile acute Between flares work for painreduction, improved ROM,lower muscle tension



Collapse at C1-C2

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

Radiographic evidence

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SpondylosisOsteoarthritis at spine; Age-related changes of thevertebrae, discs, joints, and ligaments of the spine



Etiology

Osteophytes grow on vertebrae

Can be on vertebral bodies or facetsCan put pressure on nerve roots orspinal cord

Intervertebral joints analogy with synovial joints:

Vertebral bodies = articulating bonesAnnulus fibrosis = capsular ligamentNucleus pulposus = synovial fluidShearing and compressive forceswear on cartilage, disc thins, bonespurs develop

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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more Spondylosis


May be silent Painless progressive loss ofROM Pain if nerve roots arecompressed Spinal cord compression: pain,loss of bowel/bladder control

Complications

Spreading problems in the spine Nerve pain Secondary spasm Blood vessel pressure Spinal cord pressure

Diagnosis

Radiography, MRI

Anti-inflammatories, exercise,massage, acupuncture,hydrotherapy

Locally injectedsteroids, surgery

Caution for nerve irritation,positioning, muscle splinting

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SprainsTorn ligaments Distinguishing Features

Sprains are injured ligaments, notmuscles or tendons

Sprains are more serious than

strains and tendinosis

Sprains tend to swell

Etiology

Linearly arranged collagen fibers link bone to bone

Injured when some fibers are rippedFirst, second, third degree (rupture)

Repair: laying down new collagen fibers

Begins disorganized and weakAligns according to weight-bearing forceWithout stress during healing, scar tissueremains weak and disorganized

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more Sprains


Acute Stage

Pain, heat, redness, swelling,loss of function

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

RICE (rest, ice, compression,elevation) PRICEMMM (protection, rest,ice, compression, elevation,medicine, mobility, modalities)

Indicated when subacute forimproved circulation, scar tissueformation, stiffness

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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


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

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more Temporomandibular Joint Disorders


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

Nonsurgical: Hot/cold; PT,ultrasound, massage, anti-inflammatories, localanesthetics, splints, proliferantinjections Surgical: dissolve adhesionsand scar with injections;arthroscopic surgery; jointreplacement

Can be useful to interrupt theprocess before permanentdamage occurs

Reduce muscletension, improveawareness, addressreferred painpatterns



on cartilage damage, musclefunction, subluxation

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Genetic Musculoskeletal Disorders

Ehlers-Danlos Syndrome

Margan Syndrome

Muscular Dystrophy

Osteogenesis Imperfecta

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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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more Ehlers-Danlos Syndrome


Depends on genetic anomaly

Easy bruising; poorwound healing; frequentjoint dislocations; eyeproblems (detachedretina, myopia); mitralvalve prolapseRarely: extremepostural deviations,baggy skin

Several types:

Classic EDSHypermobility EDSVascular EDSKyphoscoliosis EDSArthrochalasia EDSDermatosparaxis EDS

Diagnosis

Genetic testing not alwaysconclusive

Family history with signsand symptoms

Mild EDS may not be identified, butchildren can have it in moreextreme form: genetic counseling isimportant

Treated by symptom

Education topreserve jointfunctionSkin careSpecial care withdental workHigh-risk pregnancy

High doses of vitamin C mayimprove some connectivetissue strength

Appropriate if heart is healthyand joints not stretched too far

Delicate skin, easybruising

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Marfan SyndromeGenetic mutation causes production of dysfunctionalfibrillin

Demographics

200,000 in the United States haveMarfan or a related disorder

Usually passed from parent to child

25% = spontaneous mutation


Etiology

Faulty protein fibers → connective tissues areweak Musculoskeletal system, meninges, heart, aorta,eyes most at risk

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more Marfan Syndrome


Ranges from mild to severe

Musculoskeletal systemanomalies: long fingersand toes, arms and legs;protruding or sunkensternum; posturaldeviationsCardiovascular systemanomalies: aortic andmitral valves maycollapse → heartproblems; risk ofaneurysm, aorticdissectionEye disorders: myopia,dislocated lens,detached retinaNervous systemanomalies: stretched,weakened dura mater:dural ectasiaOther symptoms: stretchmarks, hernias, flat feet,spondylolisthesis, andhammertoes

DiagnosisNo simple genetic test

Clinical examination,family history,observation

By symptom

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

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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

Congenital muscular dystrophyFacioscapulohumeral dystrophyLimb-girdle dystrophyEmery-Dreifuss muscular dystrophyOculopharyngeal muscular dystrophy

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more Muscular Dystrophy


Vary by type

Duchenne and Beckerare similar

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

Work with health care team

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Osteogenesis ImperfectaGroup of genetic disorders that changes the quality of type Icollagen fibers; Four main subtypes; (other, much rarer types)

Demographics

Type I most common: 1 in 30,000births

Type II: 1 in 60,000 births

Type III: 1 in 70,000 births

Type IV and others: very rare

20,000–50,000 in United States

have OI

Males = females

Autosomal dominant: if one parenthas the gene, each child has a 50%

chance of having OI

About 25% of cases spontaneouswith no family history

Etiology

Type I collagen is a triple helix of intertwiningprocollagen fibers OI is shortage or faulty production of type I collagen

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Other Connective Tissue Disorders

Baker Cyst

Bunions

Bursitis

Dupuytren Contracture

Ganglion Cysts

Hernia

Osgood-Schlatter Disease

Pes Planus, Pes Cavus

Plantar Fascitis

Scleroderma

Tendinopathies

Tenosynovitis

Whiplash

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Baker CystSynovial cysts at the popliteal fossa, usually on medialside; also called popliteal cysts


Etiology

Joint capsule at knee develops a pouch

Common in children

In adults, may be related to other joint problems:

Osteoarthritis, rheumatoid arthritis,cruciate ligament tears, meniscus tears

Complications

Could impair blood flow

Risk of thrombophlebitis, deep veinthrombosis (DVT)

Risk of rupture, bleeding in joint, infection,posterior compartment syndrome




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more Baker Cyst


Usually silent; knee may bepainful from underlying problem May feel full or tight on medialaspect of calf

Ice, NSAIDs Aspiration, cortisone shots

May recur

Local contraindication; calfsymptoms may be a red flag forDVT

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BunionsAlso called hallux valgus: laterally deviated big toe;at little toe: bunionette

Demographics

Women > men, 10:1

High-heeled, narrow-toed shoes

Genetic predisposition


Etiology

Factors that lead to misalignment betweenfirst metatarsal and proximal phalanx of greattoe:

Pes cavus, pes planusShape of the bonesMuscle imbalanceFootwear

Joint is distorted, bunion on top is irritated May develop bone spurs, osteoarthritis

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more Bunions


Lump on medial side ofmetatarsophalangeal (MTP) jointof great toe

May be hot andpainful

Remove irritants, improvefootwear Massage and exercise for foothealth ROM, traction, gentle friction Cortisone injection

Surgical correction

Locally contraindicated wheninflamed, otherwise appropriate

Work with othercompensationpatterns, intrinsic footmuscles

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BursitisSynovial sacs outside joint capsules becomeinflamed



Etiology

Bursae act as shock absorbers and reducefriction where tendons cross over bones Repetitive stress irritates bursae

Pain, limited ROM, muscletightness

Accompanies general inflammation, gout,rheumatoid arthritis, etc. Can be from infection, especially at knee orolecranon

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more Bursitis


Pain on passive and activemovement Limited ROM (muscle splinting) Often no heat is palpable

Diagnosis

Patient history: consider otherlocal injuries

NSAIDs, warm packs Aspiration, cortisone injection Bursectomy (may grow back) New movement patterns!

Local contraindication whileacute Otherwise appropriate: work todecompress surroundingmuscles

Avoid infection

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Dupuytren ContractureIdiopathic shrinking and thickening of palmar fascia; alsocalled palmar fasciitis

DemographicsMen > women

Middle-aged, Northern European

descent

Some genetic predisposition

Other risk factors:Smoking, alcohol use, seizure

disorders, type 1 and 2 diabetes


Etiology

Idiopathic

Looks like excessive posttrauma scartissue: type III collagen in palmar fascia andfingers

Collagen thickens and gets denser; living cells recede

Flexion may be normal; extension is limited

Similar connective tissue phenomena:

Plantar fibromatosis (Ledderhose disease)on sole of footPeyronie disease under skin on shaft ofpenisKnuckle pads (Garrod nodes) at DIPs ofhands

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more Dupuytren Contracture


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

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Ganglion CystsPouches on joint capsules or tendinous sheaths


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

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more Ganglion Cysts


Range from tiny to large Not usually painful unlessirritated

Usually resolve spontaneously Cortisone injection, aspiration,surgical removal (often growback)

Don’t smash with aBible!

Local contraindication May be irritated with friction Untreated bumps need diagnosis

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HerniaHole in abdominal wall, diaphragm Demographics

5 million diagnosed per year

700,000 surgeries

Men with abdominal hernias >

women: 7:1


Etiology

Several factors

Weakness of abdominal wall; straining;childbirthSmall intestines can protrude, get caughtand damagedWeak spot at inguinal canal for men

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more Hernia


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



Osgood-Schlatter DiseaseIrritation and inflammation at quadriceps attachment ontibia; also called tibial tuberosity apophysitis

Demographics

Usually adolescent athletes Running, jumping sports

Boys > girls


Etiology

Rapid bone growth, especially at tibia and femurduring adolescence

Soft tissues may not keep up Quads are taxed with athletics

Stress at attachment leads to pain andinflammation Tibial tuberosity enlarges; microscopic fractures,possible avulsion

Usually unilateral

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more Osgood-Schlatter Disease


Acute: tibial tuberosity is hot,swollen, painful

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

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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

Underlying diseases that affectfeet

Charcot-Marie-Tooth syndrome; musculardystrophy; polio, cerebral palsy; neurologicaldamage

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more Pes Planus, Pes Cavus


Complications

Loss of shock absorption →

Change in footalignment Heel spurs Plantar fasciitis Neuromas Osteoarthritis at foot,knee, hip, SI, spine,TMJ, headaches, etc.

Especially an issue with poorperipheral circulation: diabetes,etc.

Improved footwear, orthotics PT to work with peroneuslongus, tibialis posterior If very extreme: surgical repair

Indicated

Can improve nutritionto ligaments, relievepain, work withcompensation

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Plantar FascitisPain at plantar fascia; could be inflammatory ordegenerative

Demographics

2 million/year seek treatment

Men = women

Two groups more than others:Runners (up to 10%)

Older adults who are overweight

Etiology

Plantar fascia is vulnerable to damage

OverweightWorn-down shoesUnequal leg lengthFlat or pronated feet, jammed archesTight calf muscles

Secondary to

Gout, diabetes, rheumatoid arthritis

Fibers fray, become disorganized

Probably not usually inflamedDegeneration of collagen matrix(changes treatment options)

Radiography shows bone spurs (secondary,probably not causative of pain)

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more Plantar Fascitis


Acutely painful after periods ofrest, immobility

Sharp, bruisedfeeling at anteriorcalcaneus or deep inarch Pain subsides withwarming up, returnswith fatigue

Remove tensions that reinjureplantar fascia

Warm, massagefoot/leg beforestandingOrthoticsNight splint to hold footin dorsiflexionNSAIDs, topical anti-inflammatories,massage, iceCortisone injections: Conservative;otherwise plantarfascia may ruptureShockwave lithotripsySurgery to divide,release damagedfasciaLong-lasting condition:6–18 months forresolution

Indicated to decrease tension incalf muscles, organize collagenwithin

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SclerodermaAutoimmune disease leading to production of abnormalamounts of collagen, often in skin: hard skin; Othertissues may be affected

Demographics

About 300,000 in the United States

Women > men, 3–4:1


Etiology

Immune system attacks lining of small bloodvessels

Local edema, fibroblast stimulation Lots of type III collagen (basis for scartissue)

Local scleroderma: only skin is involved; mayaccumulate over years, then stabilize or reverse

Morphea scleroderma: oval patcheson trunk, face, extremities

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

Causes

Unknown; some factors:

Abnormal immune responses andchronic inflammation → excess



collagen production Chimeric cells (genes of anotherperson) Chemical exposures Viral infections

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more Scleroderma


CREST syndrome

C: Calcinosis:accumulation ofcalcium deposits in theskin, especially in thefingers R: Raynaudphenomenon E: Esophagealdysmotility S: Sclerodactyly:hardening of thefingers T: Telangiectasia

Other symptoms/complications:

Skin ulcers, changesin pigment, hair loss,weak muscles, swollenconnective tissues,lung damage, heartpain, arrhythmia, heartfailure, renal failure,trigeminal neuralgia,carpal tunnelsyndrome, Sjögrensyndrome

Manage symptoms,complications:

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

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TendinopathiesInjury, damage to tendons

Etiology

Tendons are made of type I collagen in liquid groundsubstance

Some elastin fibers are woven in for stretchand rebound (limited) Looks hard, shiny, white

With injury:

Collagen degenerates Tendon becomes weak: tendinosis

CausesIntrinsic factors

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



Fibroblasts produce type III fibers: thinner,weaker

Pro-inflammatory white blood cells not present: notusually inflammatory Tenoperiosteal junction, musculotendinous junctionmost at risk

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more Tendinopathies


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

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TenosynovitisTendons that pass through a synovialsheath become irritated and inflamed

Etiology

Tenosynovial sheath (also calledepitenon) becomes inflamed,shrinks around inner tendons

Usually related tooveruse At the thumb: DeQuervain tenosynovitis

Can occur as a complication ofother diseases, especiallyrheumatoid arthritis, gout, diabetes

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more Tenosynovitis


Local pain, sometimes with heatand a palpable nodule, at baseof fingers

Flexion is difficult;extension even moreso Crepitus, pop whenjoint extends

Anti-inflammatories, steroidinjection, surgery to splitsynovium

Avoid while acute Otherwise can help improveproduction of synovial fluid,freedom of movement

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WhiplashAlso called cervical acceleration-deceleration(CAD); Mixture of injuries with MVAs or othertrauma

Demographics85% of neck pain from injury (?)

1 million cases of CAD/year from MVA

15.5 million people in the United States have

had whiplash


Etiology

Damage depends on variables: direction onimpact, speed, weight of vehicles, seatbelt,etc.

With 20 mph rear impact, force ismagnified at neck; Head ispropelled into flexion at 12g

Cervical muscles and ligaments can bestrained

Anterior and posterior longitudinalligaments also at risk:unreachable

Other structures:

Joint capsules at facetsSoft tissues of neck and throatIntervertebral discsSubluxation at vertebraeTMJSpinal cord, brain, nerves

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more Whiplash


Symptoms and complicationsinterrelated

Often a delay in onsetof symptoms

Ligament sprains Damaged facet joint capsules Misaligned cervical vertebrae Damaged discs Spasm Trigger points Neurological symptoms TMJ disorders Headaches

Diagnosis

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

pt 6



Neuromuscular Disorders

Carpal Tunnel Syndrome

Disc Disease

Myasthenia Gravis

Thoracic Outlet Syndrome

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Carpal Tunnel SyndromeEntrapment of median nerve at carpal tunnelleading to symptoms in the hand

Demographics

Affects up to 10% adults at some time

Women > men, 3:1

Etiology

Pain may be from

Pressure directly on nerve Pressure impeding blood flowto nerve

Aggravating factors

EdemaSubluxation of carpal bonesFibrotic buildup

Underlying conditions

Diabetes, hypothyroidism,lymphedema, acromegaly,rheumatoid



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more Carpal Tunnel Syndrome


Nerve signs

Tingling, pins and needles,burning, shooting pain,intermittentnumbness/weakness Thenar pad may atrophy May be worse at night(sleeping position)

Diagnosis

Description of symptoms; Tinel test,Phalen maneuver Nerve conduction test,electromyogram

Wrist splint Anti-inflammatories Cortisone injection Exercises Proliferants to tighten looseligaments Surgery: open or endoscopic

Depends on cause Work conservatively, monitorresults If work exacerbatessymptoms, stop!!

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Disc DiseaseCollection of problems with nucleus pulposus orannulus fibrosis



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

Types of Disc Problems

Herniated nucleus pulposusBulgeProtrusionExtrusionRuptureDegenerative disc diseaseInternal disc disruption

Progression

Person goes into flexion Person jerks upright, forcing nucleus intoposterior space



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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more Disc Disease


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

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Myasthenia GravisGrave muscle weakness—W. Erb, 1890; Autoimmunedisease → degeneration/destruction of receptor sites atneuromuscular junctions

Demographics

Usually women in 20s, men in 50s

14 in 100,000 in the United States

Affects 36,000 people in the UnitedStates

EtiologyMotor neurons contact muscles at NMJ

Acetylcholine crosses synapse, beginsmuscle contraction

In MG the acetylcholine (ACh) receptor sites don’tfunction

ACh is released; muscle doesn’trespond Autoantibodies attack receptor sites

Thymus is involved

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more Myasthenia Gravis


Weakness, fatigue in affectedmuscles

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

Excessive heat mayaggravate symptoms;avoid Immunosuppressant drugshave risks

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Thoracic Outlet SyndromeNeurovascular entrapment; Between anteriorand medial scalene; Between clavicle and firstrib; Under coracoid process


EtiologyBrachial plexus is spinal nerves C5–T1

Any impingement between neckand destination makessymptoms C8 and T1 contribute to ulnarand median nerves; these aremost vulnerable

Axillary and subclavian veins/arteries alsoget pinched

Neurological TOS (nerveimpingement) Vascular TOS (vascularimpingement) Disputed TOS: symptoms arepresent, no impingement

Contributing Factors

Cervical ribs Muscle imbalance Connective tissue bands

Differential Diagnosis

Cervical misalignment



Spondylosis Rib misalignment Other injuries

Rotator cuff, elbow, wrist, carpaltunnel syndrome, double crush,disc disease, cervical sprain

Other factors

Lung cancer, thrombosis

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more Thoracic Outlet Syndrome


Nerve pain: shooting, electricalpain, numbness, reducedsensation, parasthesia

Vascular symptoms: feeling offullness, cold, weakness,asymmetrical color

Often worse at night,depending on sleep position

Diagnosis

Not all tests are accurate for allpeople

EAST (elevated arm stresstest)Wright hyperabduction testAdson testNerve velocity conduction,electromyogram, radiography,MRI, etc.

Depends on cause (need foraccurate diagnosis)

Muscleatrophy/tightness:exercise, stretching(massage)

Surgery for cervical rib,bone spurs

Indicated for muscle imbalance

Focus on balancearound the rib cageand shoulder

pt 7 Back to Lesson Home


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