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Table10-4.
reducedforcesintheheelandforefootresemblingthoseseeninthegeriatricpopulation.
29,30
Asthediseaseprogresseswithashufflingtypegait,onlyonenarrowpeakintheverticalGRF
isshown.
ParkinsonianGaitCharacteristics
Increasemuscletoneandtremor
Stiffarmsheldcloselytobody
Absentarmswing
Impairedposturalreflexes
Stifflystooped
Armsclosetosides
Reducedstridelength
Increaseddoublelimbsupport
Increasedcadence
Slow,shufflingsteps
Difficulttoinitiatestepsorturns(“freezing”)
Cogwheelrigidity
Pillrolling
Festination
Freezingofgaitisadisabling,episodicaffectationinwhichthefeetappeartobe“gluedto
thefloor.”Fallsandfreezingofgaithavebeenlinkedtogethersincefreezinginmanyinstances
mayleadtofalls.Botharemorecommoninthelatterstagesofthediseaseprocess.31Freezing
ofgaitisacommonanddisablingfeatureofPDandismostcommonlyexperiencedduringgait
initiation,turning,andnegotiatingobstaclesofothertasks.32Thepathophysiologyoffreezing
ofgaithasbeenlinkedtoasymmetriesinlegcoordination.
33,34
Fallsmayresultfromattempting
sudden movementsorchangesinposturalpositions.Theriskoffallsis increased inthePD
patientwhoattemptstoperformmorethanoneactivityatatimesuchascarryingashopping
bagwhileambulating.Mostofthesefallsareforward(45%)and20%laterally.
31
Postural sway is the ability to maintain balance during upright stance and locomotion.
Postural sway characteristicallyincreases in most UMN lesion disorders, creating balance
disorders.However,inPDitisdiminished.Thisfact,coupledwithaninabilitytomaintainthe
centerofmassoverthebaseofsupport,increasestheriskoffallsintheparkinsonianpatient.
21
EMGstudieshavedemonstratedasignificantreductionintibialisanticusmuscleactivationin
earlystanceandearlyandlateswingphasesofgaitandareductionintricepssuraeactionat
propulsion.35Thehamstringsandquadricepsshowprolonged activationduringstance.35The
passivestiffnessofanklejointsandco-contractionoflegmusclesinstanceresultinabnormal
posturalswayinPDpatients.
36
Subcortical arteriosclerotic encephalopathy (SAE) also referred to as lower-body
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parkinsonismandcerebralataxiaaregaitdisordersthatresemblethatofPDbuthavecommon
underlyingmechanismsdifferentfromthatofparkinsonism.
37
CerebralPalsy
CP is an idiopathic perinatal disorder with an incidence of 2 per 1,000 live births.13 The
underlyingneurologicpathologyisnonprogressive;however,thesecondaryeffectsincluding
muscularcontracturesandabnormalbonegrowthcontinueandcausedeteriorationinfunction.
Spasticityoccurs in 80% of CP patients. Only 20%are quadriplegic,30% hemiplegic,and
50%diplegic.38SeventypercentofthosewithCPareabletowalk.Thefundamentalproblems
inthisdisorderincludeweakness,spasticity,andlossofselectivemotorcontrolwithretention
ofprimitive reflexes andpostural reactions. These neurologic deficiencies resultinequinus
function with knee and hip contractures, premature heel off, foot drop, and excessive limb
flexion during swing. Foot deformities include hammer, claw, and mallet toe deformities;
hallux flexus; equinus; varus; valgus; planovalgus; and the most commonly occurring
equinovarus.38Inweakerpatients,excessivepronation,crouchgaitwithkneeandhipflexion,
andtoedragare observed.The crouchgaitpositiondeleteriouslyaffectsloading patternsof
thekneeandsurroundingstructures,leadingtoaloadthatistwoandonehalftimesgreaterthan
thatofthenormalpain-freeindividual.
39
MultipleSclerosis
MSisabilateralUMNautoimmunediseaseseeninyoungadultsfrom20to40yearsofage
thatcausesprogressive neurodegenerationwithsubsequentataxic,paraparetic,spastic,stiff-
leggedgait,whichmayormaynotbesymmetrical.7GaitchangesseeninMSisdependenton
areas ofinjuryinvolvedandneurologicfunction.Gaitchangesseeninspinalcordinjuryare
similartothoseseeninMSdependingontheinjurylevel,residualneurologicfunction,muscle
weakness, spasticity, and secondary instability due to impaired coordination and sensory
deficits.7A scissoringgaitmaybeobserved duetoincreasedactivityofthehip adductors.
7
Excessive hip adduction interferes with swing phase limb advancement, decreased base of
support,decreased posturalstability,andresultantincreased riskforfalls.MSpatientshave
decreasedmusclestrength,proprioceptionandbalanceallofwhichfurthernegativelyimpact
gait. Symptoms vary with the disease severity and include sensory disturbances, limb
weakness,awkwardgait,andcognitivedeficits.
40,41
Patients with MS walk more slowly, take shorter steps, and exhibit a broader base of
gait.41 Gait abnormalities include decreased stride length, increased double support, and
reducedjointtorqueandpower.Variabilityofsteplengthandsteptimeisdirectlycorrelated
with disease severity.41 Individuals whouse gaitassistive devices had significantly greater
steplengthvariabilitythandidMSpatientswhowereabletowalkindependently.
41
Peak ankle plantarflexory torque is significantly reduced in late stance as revealed by
loweredanklepowergenerationforpropulsion.Thisresultsinaninabilitytosupportforward
progressionofthetrunkandtoinitiatetheswingphaseofgait.42MSpatientsthatareableto
walkfasterareabletoovercomethisdeficitbyincreasingtheangularvelocityofthesegment
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Table10-5.
resultinginincreasedanklepowerduringlatestance.40MSpatientsareunabletoadaptother
compensatory strategies to overcome reduced power at one joint by increasing power at
another.40 As a result of the numerous gait disturbances associated with the disease, MS
patientsexhibitasignificantdegreeoffatigueoverthecourseoftheday.
43
LOWERMOTORNEURONGAITDISTURBANCES
Lowermotorlesiongaitdisturbancesmaybelinkedtosystemic disorderssuchasdiabetes,
amyotrophic lateral sclerosis (ALS), CMT, or Guillain-Barré syndrome or may be due to
spinaldiscorperipheralnervecompression(Table10-5).Gaitabnormalitiesaredependent
on the level of involvement. For example, with common peroneal nerve compression or
disease,thereisasteppagegaitwithfootslapanddifficultyclimbingstairs.Withsciaticnerve
pathology,thelimbmaybefunctionlesswithguardinganddraggingoftheextremityforward.
Popliteal nerve involvement produces a more flaccid, exaggerated steppage gait and
gastroc/soleusparalysisproducesacalcaneusgait.ATrendelenburggaitisseenwithgluteal
paralysis.
EtiologyofLowerMotorLesionGaitDisorders
Diabetesmellitus
Alcoholism
VitaminB12deficiency
Malignancy
Medications
Collagenvasculardisease
Guillain-Barrésyndrome
Porphyria
DiabeticNeuropathy
Diabeticperipheralneuropathyisoneofthemostseverecomplicationsofdiabetes,occurring
in 30% to as high as 70% of all diabetic patients.
44–48
Diabetic neuropathy impairs the
somatosensory and motor systems thereby affecting the quality and quantity of sensory
information that is essential for the complexities involved in gait generation and control.
Patientswithdiabetesfrequentlyexhibitaconservative gaitstrategy, whichincludesslower
speeds,decreasedanklerangeofmotion,widerbaseofgait,decreasedstepandstridelength,
increaseddouble limb support,differences inkineticpatternswithmodified groundreactive
forces and joint moments of force, as well as delayed activation.
49,50
Changes in gait
parametersthatappeartobespecifictodiabetesincludeshorterstridelength,reducedspeed,
and altered lower limb and trunk mobility.51 Diabetic neuropathy patients exhibit a
significantlylongerstancephaseofgaitandstridetime.
47,51
Thereisan increase incadence
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andswingphasewithincreasedsusceptibilitytojointkinematicchanges.
49
Patients with diabetic neuropathy walk slower and more cautiously than healthy
individuals and employ different knee and ankle adjustments with increasing speeds.
Increasing cadenceleads to loss of gait cycle stabilitydue to a diminutionofmotor skills
adaptiveresponsivemechanisms.Diabetesreducestheabilitytoaccomplishshockabsorption
duringgait.51Atheelcontactinthediabeticpatient,thelackofsensoryafferentinputleadsto
delayedactivationofankleandkneemusculature.52Muscle atrophyandweaknesscombined
with fat pad degeneration and increased stiffness affect shock absorption.53 The premature
plantarflexionatheelcontactobservedindiabeticneuropathypatientsresultsinincreasedfoot
flat phase and increased forefoot loading predisposing to ulcer production. Studies have
demonstratedmoderatelyhigherplantarpressuresindiabeticperipheralneuropathypatientsat
therearfoot,midfoot,andforefootcomparedwithcontrols.47Thisisprobablyduetoincreased
timespentinthestancephaseofgaitandnotsolelyduetoincreasedgroundreactiveforces.
47
Increased dermal thickness and inelasticity coupled with fatpad atrophy affect braking
forceatheelcontact.
54–56
Thesechangesaffecttheabilityofthefirstrockermechanisminthe
foot from functioningproperly.50 Lack of sensory afferent input with muscle weakness and
limitedjoint mobility affect single limb supportand gaitinstability.
50,57
There is a delayed
peak activation of the gastroc/soleus group during stance phase of gait thereby extending
midstance and delaying active propulsion. The tibialis anticus is also delayed in stance,
affecting forthcoming swing and toe clearance and thereby compromising the entire gait
cycle.49Limitedjointmobilityaffectsthesecondrockermechanismnecessaryfornormalgait.
Thethirdrockermechanismisnegativelyaffectedbecauseofaninabilitytogenerateadequate
ankle plantarflexory torquenecessary for propulsion. As a result, hip flexors may be used
insteadofankleplantarflexorstoassistinpropulsion.Abnormalanklemechanicsfurtheradd
toabnormalhipmechanics.Awiderbaseofgaitcombinedwithskinandfatpaddegeneration
affectmedial–lateralshearandpushingforce.
57
Looser extremitystiffnessassociatedwithdiabetesnegativelyaffectstheswingphaseof
gait.Lackofafferentsensoryinput,muscleweaknessanddiminishedjointmobilityincreases
gaitinstabilityandimpactssinglelimbsupport.
50,57
Diabetes produces physiologic changes in the organism that in turn result in decreased
lower extremity function. Additional comorbidities associated with elevated blood glucose
levels,suchascardiovasculardisease,may also contributeto,andmagnify,disturbedlower
extremityfunction.45Theexistenceofapreexistingpathologicfoottypeinthediabeticpatient
determinesthebiomechanicalbehaviorandfunctionalityofthefootandhasbeenshowntobe
clinicallyrelevant.
51,58
Itisthisintrinsicdeficiencyinstructureoralignmentthatistheprimary
underlyingcauseofhyperkeratosesandsubsequentplantarulcerationinthediabeticespecially
onewithneuropathy,whichnegativelyalterstheindividual’sresponsetoeffectivelymanage
elevatedplantarpressure.
58–61
Charcot-Marie-ToothDisease
CMT, also known as peroneal muscle atrophy, refers to a group of inherited autosomal
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dominant, and in some cases recessive, disorders resulting in symmetrical, progressive
peripheral neuropathy,whichtypicallybeginsinthefeet.There isprogressiveloss ofmotor
function withresultantweakness, muscleatrophy, andlimbdeformitiessecondarytomuscle
imbalance.Theseincludea“hallmarkofthedisease”cavovarusfoottypeandclawtoeswith
plantarflexedfirstrayandcompensatoryforefootvalgus.Thisiscausedbyperonealweakness
especiallyinthebrevissegment alongwithweaktibialisanteriorandsparingofthetibialis
posterior.39Theperonealmuscle atrophy evidenced inthelowersegmentsofthelegsgives
rise tothe“stork leg”or “invertedchampagne bottle” appearance. Thecavovarusfoot type
predisposes the patient to increased plantar pressures on the calcaneus, first, and fifth
metatarsalheads.There isasequentialprogressionofweaknessandatrophybeginning with
the peroneus brevis, toe extensors, and tibialis anticus and ending with the intrinsic
musculature.39Asaresult,thereisclawingofthedigitsthroughoutswingphaseduetoextensor
musculaturesubstitutionforaweakenedtibialisanticus.Thismayresultinfootslaporifmore
severe footdrop.Duringstancephaseduetogastroc/soleusweakness,theanklemaybuckle
forwardwithanteriortibialmigrationonthetalus.Inmoreseverecases,a“crouch”gaitmay
beobserved.39 As the disease progresses, theremaybe a progressive inabilityto ambulate
fromweakness,balance,and/orassociateddeformities.
AmyotrophicLateralSclerosis
ALSalsoreferredtoasLouGehrigdiseasenamedafterthefamedYankeefirstbasemanwhose
careerwasendedduetothisdebilitatingprogressiveneurodegenerativedisorder.ALSaffects
CNS motor neurons that directly or indirectly control muscular contractions during
ambulation.
62–64
Neurologicdysfunction iscausedbydeteriorationofmotorneuronsortheir
myelin sheath disrupting normal pathways of transmission to target muscle fibers.
62,63
The
motorneuronsarereplacedbyfibrousastrocytescausingmuscletissueatrophy,weakness,and
ultimatelyparalysis.62 Due to this interruption of cerebellum-to-muscle pathway, the lower
limbs cannot properly perform voluntary movements thereby pathologically impacting gait.
This resultsinslower walkingspeeds in ALSpatients with an increased variability in gait
rhythmtimeseriescomparedwithhealthyindividuals.65InfactgaitvariabilitypatternsinALS
ismorepronouncedthaninPDandHuntingtondisease.
66
OnsetofALSissubtlesothatearlydetectionofthediseaseisuncommon.Thepatientmay
experienceawkwardnessingaitcausedbydifficultyinsymmetricaluseofthelimbsthereby
alteringstrideandswingphaseintervals.67Stridetimeislongerandthemagnitudeofstride-tostridevariabilityisincreased.
66,68
Stridetimeisdefinedasthetimebetweeninitialcontactof
onefoottothesuccessivecontactofthatsamefoot.69Gaitasymmetryisaprominentfeaturein
allALSpatients.
METABOLICDISORDERSAFFECTINGGAIT
Endocrine disorders affecting gait include hypothyroidosis and vitamin B12 deficiency.
Medications, notably CNS depressant, antianxiety, antihypertensive, hypnotics, and so forth,
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will unfavorably affect gait, decreasing ability to balance and to resist gait perturbations.
Psychologicalissuesaffectinggaitincludepsychogenicgait,fearoffalling,andgaitassociated
withseniledementia.
SenileDementia
Deteriorationinspatial cognitive abilities with advancing age is compounded by disorders
suchasseniledementiapresentinatleast9%ofolderpersons.Evenmildformsmayrestrict
travelinfamiliarenvironmentsinspiteofanotherwisehealthylocomotorsystem.Intheolder
individual, lower extremity function involves intention and integration of higher cortical
sensoryinformation.Impairmentincognitionimpairsgaitandthesesamegaitimpairmentsmay
be able topredictfuture decline anddementia.70 Therefore,identificationofthe underlying
disease process accompanying the gait abnormality may allow earlier treatment to be
instituted.Alzheimerdiseaseisthe mostcommontypeofdementia withconcomitantlossof
independent andsafe mobility due tobalance and gaitdysfunction. Eventhose in theearly
stagesofthediseasehavebeenshowntohavegaitandbalancedeficitsincluding decreased
speed, shorten step length, and increased time in double support.71 Recovery from a gait
perturbationortheabilitytocompletesimplecognitivetaskswhilewalkingisdifficultforthe
early Alzheimer disease patient therebynegativelyaffectinggait.72 This is accomplishedby
slower speeds, decreased step andstridelengths,decreased cadence,and increased double
support.73 In fact, Eggermont et al.70 in their study suggest that walking speed could be
evaluated as a predictor of gait impairment and falls in older individuals. Gait instability
increases the risk of falls in the Alzheimer disease patient.
71,72
Advancing age further
magnifies the effects ofAlzheimerdisease ongait byadversely affecting spatial knowledge
requiredfortravelingtogoalsnotvisiblefromthestart.
CardiovascularDisordersAffectingGait
Anintactcardiovascularsystemprovidesthehemodynamicrequisitesnecessarytomaintainan
upright posture without collapsing. Peripheral arterial disease (PAD) especially when
accompaniedbyintermittentclaudicationmayseverelyrestrictatindividual’sabilitytowalk
longerdistances. Inaddition,calfpainsecondarytothediminishedbloodsupplyassociated
withPADmayresultinanantalgicgaitwithdiminishedpropulsiveactivityduetoincreased
demandsplaced onthismuscle.Theindividualwalksmore slowlyandless propulsivelyto
reduce muscle oxygen requirements, thereby lessening the likelihood of cramping and the
abilitytowalklongerdistances.Orthostatichypotension,aprecipitousdropinpressureupon
standing, disrupts gait stability by affecting one’s ability to balance well. Vertebrobasilar
insufficiencymayresultinthesame setofcircumstances.Chronic edemamayaffectgaitby
limitinganklejointmotiontherebyincreasingdorsiflexorydemands,extendingthemidstance
phaseofgaitandreducingpropulsion.
MusculoskeletalDiseaseandGait
Arthritisaffectsapproximatelyoneinsixindividualsandistheleadingcauseofdisabilityin
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Table10-6.
the United States. Any condition affecting the musculoskeletal or neuromotor systems
negativelyaffectsgait.Ithasbeenestimatedthat75%ofindividualsover65yearsofagehave
some arthritis of the weightbearing joints with the knee and hip being the most commonly
affected13(Table10-6).
Theenergycostforlocomotionincreasesintheelderlyinthepresenceofcardiopulmonary
andmusculoskeletal system changes, reduced tissue tolerance, and the use of gait assistive
devices. When systemic musculoskeletal disease is coupled with age-related degeneration,
thereisacompoundeddecreaseinthemaximummanageablestresswitharesultantincreased
chanceoffailure.Itisunlikelythatage-relatedmusculoskeletalsystemdegenerativechanges
alonewillimmobilizetheindividual;however,theycananddoinfluencethedistanceableto
betraveled,thetimeittakes,andthetypesofterrainthatcanbetraversed.
Musculoskeletalstrengthdecreaseswithadvancingage.By60yearsofage,thereisa25%
to30%loss,andafter70yearsofagethereisa30%additionallossofstrengthperdecade.
74
Walkingdoesnotrequirefullstrength;infact,thegastroc/soleusrequiresthegreateststrength
for propulsion but other muscles may substitute. Cardiopulmonary deterioration negatively
affectsmuscle function.Tendonandligamentchanges asaresultofmusculoskeletal disease
and/orcompoundedbytheagingprocessresultsinjointstiffnesswithaccompanyingdecrease
inrangeofmotiontherebynegativelyalteringgait.Thesechangeslimittheabilityofotherwise
intact muscles to generate power at various speeds and over varying terrains. Changes in
musculoskeletal mass distributionwithadvancing agepresentachallengetobalancecontrol
systemsandincreaseloadontheposteriormusculature.Theseindividualshavelimitedability
tosustainlocomotionforextendedperiodsoftime.
MusculoskeletalDisordersAffectingGait
Osteoarthritis
Rheumatoidarthritis
Psoriaticarthritis
Ankylosingspondylitis
Polyarteritisnodosum
Polymyositisrheumatica
Musculardystrophy
Systemiclupuserythematosis
Rheumaticfever
Pagetdisease
Lymedisease
Gout
Reitersyndrome
RheumatoidArthritis
Rheumatoid arthritis (RA) affects thefeet in 20% of cases atthe time of diagnosis, which
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progresses to 80% with a disease duration of 5 years.75 The disease leads to functional
disabilityandpathologicgaitalterationsthatsubstantiallyandnegativelyimpactthequalityof
life.76Footpainmayhavethestrongestinfluenceonfunctionalabilityregardlessofthedisease
duration.77Theforefootis affectedin90%to97% ofpatientsand themidfootandankle in
50%.
78,79
Typicalforefootdeformitiesincludeseverehalluxabductovalgus,hammerandclaw
toedeformities,subluxatedmetatarsalandphalangealarticulationswithanteriordisplacement,
andatrophyoftheplantarfatpad.Forefootdeformityisassociatedwithreducedtoecontact,
increasedforefoot pressures,anddelayedheellift.80RApatientsdemonstratehigher plantar
pressures, and this is especially true in theforefoot region.81 This fact has been linked to
increase joint destruction in these regions thereby creating an additional negative gait
impact.
79,82
Forefoot pressure increases with disease in duration.80 Rear and midfoot
deformities include classic pesvalgoplanus, with or without peroneal spasm.77 Navicular
heightwasnormalinRApatientswithforefootdeformitiesbutwasmarkedlyreducedinthose
withrearfootandforefootdeformities.77A50%reductioninhalluxdorsiflexionwasobserved
duringterminalstanceinallRApatientgroupsstudied.77Thisfindingisconsistentwithhallux
abductovalgus (HAV)productionand attendantjointdamage.77 Studies indicateacomplete
breakdownofsagittalrockerfunctionandwindlassmechanismnecessaryforloadacceptance
andstabilitythroughmidstanceandpropulsion.
77
Pathomechanical stresses through the genicular region are dependent on mechanical
alignmentnotsolelyduetothediseaseprocessitself.Valgusdeformityofthekneeisoftenseen
in RA patients and is frequently the result of RA in the hip thereby increasing pathologic
medialgenicularstressesandinfluencinglateraltibialsubluxationtherebynegativelyaffecting
gait.Accompanyingthisprocessareincreasedpathologicforcesonthemedialsegmentofthe
foot,increasingpronation,valguspositionoftherearfoot,andeventualsubluxation.
83
ItisnosurprisethatRApatientstendtowalkslowerwithalongergaitcycle,shorterstep
length,longer double support, stance phase, time,and lower cadence when compared with
normalsubjects.
75,84
Theclassicpatternofmorningstiffnesswithitsattendantpathologicgait
manifestations improves during the day and has been linked to circadian variation in proinflammatorycytokines.
85–87
Absolutewalkingspeedcorrelatesdirectlywithdiseaseactivityandcharacteristics.
77,80,88
Lowered walking speed results in significantly reduced ankle plantarflexion, medial arch
flattening, hallux dorsiflexion, and hallux abduction atpropulsion.
87,89
Although it has been
reported thattemporal andspatial characteristics inRAsimilarlycorrelatewiththe disease
process,thishasbeendemonstratedtobemorelinkedtoaccumulateddamageoverthecourse
ofthediseaseratherthantocurrentdiseaseactivity.
88,90
TheRApatienthassmallerrangesof
motionandreducedjointmomentsandworkacrossthelargejointsofthelowerlimbsduring
walking than in normal individuals.91 There is reduced joint moments and power of
hip/flexion/extension, hip adduction/abduction, knee flexion/extension, and ankle
plantarflexion.75 In fact, the most evident difference between RA patients and normal
individuals is the reduced positive work at the ankle, which may be due to decreased
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plantarflexor moments during preswing. This may be attributed to decreased speed and
decreasedplantarflexorpower.91RAsubjectstendtowalkwithaTrendelenburggait.91There
isincreasedinternaltibialrotation,delayedheelrise,decreasedplantarflexionattoeoff,and
marked eversion of the rearfoot all contributing to a loss of normal rocker function of the
foot.75Lossoffunctionalbalanceaccompaniesthesechangesandimposesanotherobstaclefor
the RA patient to contend with duringambulation.91 It is the rearfoot pathomechanics with
resultant marked calcaneal eversion that affects gait more severely in RA than in those
individualswithsevereforefootdeformityalone.91Chronicpainisoneofthemaincausesof
disabilityandlossoffunction.91GaitinRAisdeterminedbyavoidingpain.Therefore,these
patientswalkslowertocontrolthespeedandforcesassociatedwithheelstrikeandtoeoff.
75
Osteoarthritis
Osteoarthritis(degenerativejointdisease)ofthelowerextremityisthemostcommoncauseof
gaitdisordersinolderindividuals.Itaffectsover60%ofthoseover65yearsofage,andasa
resultover50%becomedisabled.Whendegenerativejointdiseaseaffectsthefootorankleas
itfrequentlydoesintheelderly,anantalgicgaitensue.92Thisisaresultofcompensatorygait
changesinanattempttorelievepainandcontinuetoallowforwardmovementofthebodyover
the supporting limb. The difficulty pain and difficulty in ambulation are most noticeable
poststatically especially upon arising. Gait characteristics include decreased velocity and
stride length inan attempttolessenpathologic pressures. Patients experience difficulty and
exacerbation of symptomatology when ambulating on uneven surfaces or climbing or
descendingstairs.Reducedrangesoffoot,ankle,andkneearticulationsoccurinanattemptto
limitmotionandlessenpressures,whichleadtosecondarysofttissuecontractures,including
equinusfunction.
93
Musculoskeletal gait disorders may be caused postsurgically as following knee or hip
replacement. Gait may be affected following prolonged periods of immobility because it
occursafter lowerextremity fracture care, illness,or surgical intervention.Musculoskeletal
dysfunctioncausedbydisuseordisabilityresultsincompensatorysmallmodificationsofthe
locomotor pattern until the most efficient pattern for the individual is obtained. Foot
discomfort, deformity, or dysfunction as a result of lower extremity systemic disease
especiallymusculoskeletalwillnegativelyinfluencegaitpatterns.
IdiopathicGeriatricGait
Alifetimeofweightbearinginevitablytakesitstollonthefeetevenintheabsenceofsystemic
disease.Changesmaybeduetogradualrelaxationofligamentscontributingtolongitudinaland
transversemetatarsalarchcollapse,anteriorfatpaddisplacementandatrophywithsecondary
increased metatarsal head pressure, progressive contractures and stiffness, increased
talonavicular lowering, and increased talocalcaneal angle, increasing early degenerative
changes.Idiopathicgeriatricgaitaccountfor16%ofgaitdisordersandmaymanifestitselfas
earlyas60yearsofage.Itisalsoreferredtoasessentialgaitdisorderoftheelderly,senile
gait,marcheà petitpas, or theelderlyshuffle. Itisaguardedgaitwhosediagnosis maybe
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Table10-7.
madeby excluding thepresenceofsystemic disease asits etiology. Gaitcharacteristics are
commensuratewithdecreasedstrengthanddiminishedabilitytoprocesssensoryinformation
(Table10-7).Visiondisordersfurtherexaggeratethesefindings.Visionplaysaprimaryrolein
initialadjustmentforchangesinsurfaceshapeorslope.Over65%ofthepopulationisaffected
with macular degeneration, which causes a loss of center field vision, which affects
environmentalinputinformationtherebynegativelyaffectinggait.Theincidencerisesrapidly
inolderindividualsaffecting10%ofthoseinthe70-to-74-year-oldagerange,14%inthe75to-79-year-oldcategory,andalmost24%areaffectedwithmaculardegenerationover80years
ofage.
94
IdiopathicGeriatricGaitCharacteristics
Decreased
Activepropulsionandpropulsivepower
Ankleextension
Verticalcenterofpressureexcursions
Amplitudeofsagittalplanerotations
Abilitytore-center
Abilitytosolvemovementproblems
Velocity
Stepandstridelength
Cadence
Pelvicrotation
Swingphase
Limbexcursions
Jointrangeofmotion
Increased
Doublelimbsupport
Stance
Midstance
Horizontalheadexcursion
Baseofgait
COPmovement
SUMMARY
Abnormalities in gaitmaybe a manifestationofsystemic disease or part of idiopathic gait
changes associated with the agingprocess. Observation of gait abnormalities by the astute
clinicianmay enable early diagnosis of its associated underlying disorder in turn allowing
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