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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2821_Библиотеки_им_академика_М_И_Перельмана
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FIGURE9-2.Angiosomesofthelowerextremity.Thefootandanklecanbedividedintosixterritoriescalled
angiosomes,basedonthearterysupplyingthem.Theconceptcanhelpinlocatingtheobstructioninthespecific
arteryinpatientswithlowerextremityischemiculcersandinplanningrevascularization.(Reproducedfrom
ShishehborMH.Acuteandcriticallimbischemia:whentimeislimb.CleveClinJMed.2014;81:209–216,with
permissionfromTheClevelandClinicFoundation©2014.TheClevelandClinicFoundation.Allrightsreserved.)
CONCLUSION
PAD is a pandemic disease with multiple facets. It confers a high risk for significant
cardiovascular and cerebrovascular morbidity and mortality. A multidisciplinary approach,
involving an interventional cardiologist, vascular surgeon, radiologist, infectious disease
specialist,andpodiatristisabsolutelycrucial.Podiatristsplayacriticalroleastheyareinthe
forefrontofthisbattleagainstPADandcanbeconsideredthe“footsoldiers.”Podiatristssee
andmanagetheentirespectrumofthediseaseandthusareinacriticalposition,whereinthey
cancreateasignificantpositiveimpactonthisdisease.Thegoalsofthetreatmentshouldbe
symptomrelief,improvement inthe qualityoflife,preventionofcardiovascularevents,and
limbsalvage.
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G
aitis themomentary loss andregaining ofbalancethat takes place with each step.Of
course most people never think aboutthis complex, rhythmic process that takes place
thousands of times each day which is dependent upon a myriad of three systems working
interdependently to allow for a smooth-in-form bipedal gait. The visual, vestibular, and
proprioceptive senses comprise the afferentsensorysystem. Nerves, muscles,bones, joints,
and tendons comprise the locomotor efferent system, and all are monitored and under the
controlofthecentralnervoussystem(CNS).1Itisonlywhenoneofthesesystemsbeginsto
faltereitherasaresultofsystemicdiseaseorasaresultoftheinevitableagingprocessthatthe
individualandthoseclosesttothembegintonoticethesechanges.
Most children take their first steps at approximately 1 year of age; however, complete
adultlikecoordination is not achieved until 6 years of age. Itis atthis timethat the lower
extremitynervoussystemreceivesitsfullmyelincoatingmakingiteasierfortheneuromotor
systemtoorchestrateamaturegaitpattern.2Theactofadultwalkingbeginswithaconfidence
inherentinthehumanorganismthatinstillsintheindividualthebeliefthatifheorshethinks
theycanwalkfrompointAtopointBtheyautomaticallywillbeabletodoso.Theythinkthey
canbecausetheyhavedoneitbeforeandthereforeshouldbeabletodoitagainuntiloneday
thatprocessisinterruptedandtheirfeetdonotrespondinthesamecoordinatedmannerasthey
once did. They begintonoticetheir gaitis notasgraceful,smooth,or spryasitoncewas.
Theremaybe anirregularity inarm–legcoordinationandsymmetry,increasedsway, shorter
steps, slower speed, trips, slips and falls, rigidity with motion, and an overall loss of
confidence in being able to accomplish basic locomotor tasks. Compensatory adjustments
madebytheindividualinanattempttoimprovestabilitymayresultinfurtherdisassociation
fromanormal-appearinggaitpattern.Itisatthispointthatprofessionalconsultationisusually
soughttodetermine whether or notthisalterationinfunctionisduetosystemicdisease, the
manifestationofidiopathicgaitchangesassociatedwiththeagingprocessorassimpleasan
improperlyfittingshoe.
Locomotionistheactofgettingfromoneplacetoanotherandinvolvesnotonlythelower
extremitybutthearm/handcomplexaswell.Gaitisthemeansofachievingthisaction.Balance
andgaitareintimatelyconnected.Walkingisaformofgaitwithaparticularpatternoffootfalls
andspecificrequirements(Table10-1).Itisacomplexprocessinvolvingthemusculoskeletal
and nervous systems, which represents the sum total of all the functional and structural
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capabilitiesoftheindividual.Walkingistheresponseoftheindividualwhoisactivelysolving
aspecificmotorproblem.Itisdictatedbyindividualconstraintsandtaskenvironment,thatis,
walkingonawet,slopedcobblestonestreetisamuchmoredifficulttaskthanwalkingona
dry, flat,level sidewalk.Gaitsolutionstolocomotorchallengesemerge,whicharetaskand
individualneuromotorcapabilityappropriate.
Speed is a key indicator of the functional status of the locomotor system. In fact,
observation of the unprompted speed at which an individual walks is a cost-effective
determinantused topredicttheoverall health oftheindividual—the speedier live longer.
3,4
Walking speed inversely correlates with the ability of theindividual to live independently,
performvariousactivitiesofdailylivingsuchasbeingabletocrossanintersectionbeforethe
lightchanges,andtheriskoffalling.5Aninevitableresultoflivingalongerlifeisthatatsome
point,usuallysomewhereinthesixthdecade,peoplestartslowingdown.6Thisprocesscanto
someextentbedelayedthroughexerciseandpropernutrition;however,no oneintheirlater
yearswalksasspritely,runsasfast,orbalancesaswellastheydidintheiryouth.
Central pattern generators (CPGs) are groupings of neurons or neural circuits that can
generateandcontrolcoordinatedmovements.Itisaninnateneuromotorandspinalreflexive
neuralnetwork.7CPGsaremodifiedbysensoryinput.Changesinneuraloutputaredependent
uponjointangle,interjointrelationships,centerofgravity(COG),andtheweightbearingstatus
ofthelimb andare recognized bymultisensorial afferent input or byperipheral receptors.
7
Activation patterns for the leg musculature and stance to swing phase transitions during
ambulationaredeterminedbylocalinformationreceivedthroughmechanicalreceptorsinthe
plantar aspect of the feet andfrom proprioceptive inputs inthe extensor foot musculature.
8
Locomotorcontrolisdistributedacrossneuralnetworksorganizedathigherandlowerlevels
withparallelascendinganddescendingpathwaysforintegrationamongdifferentsubsystems.
Age-resistant neurospinal circuits control limb movements and modulate antigravity muscle
tone and active propulsion.However,active propulsive power deteriorates withadvancing
age.Thechallengefortheagingindividualisthepreciseregulationoftheir musculoskeletal
systemfunctionwhilemaintainingbalanceandpropellingthebodyforward.Themaintenance
of dynamic neuromuscular equilibrium providing external stability essential for safe
locomotionisadverselyaffectedbyageandsystemicdisease.
It has been stated that gait and balance are intimately connected, and when stepping is
impairedthereisanincreasedriskforfalls.ThismaybeduetothedisplacedCOG,impaired
CNSregions,aninabilitytocorrectperturbationsorduetothemanifestationofagaitdisorder
affectingposturalstability.
1
Thereareanumberoffactorsthatinfluencegait(Table10-1).Mostindividualsexperience
anincreasingdifficultyinambulationwithincreasingage.9Gaitabnormalities increase with
ageeveninotherwisehealthyindividuals.In75%ofthecases theetiologyismultifactorial,
butifsolitaryitisprobablymusculoskeletalinnature.
9
Spielberg in his landmark study investigating the walking patterns of older people
classifiedgaitchangeswithadvancingageintothreestages(Table10-2).10Thechallengefor
healthpractitionersistobeabletoascertainwhetherornotalterationsingaitcanbeascribed
totheexpectedchangesaccompanyingthe aging process,resultinginanidiopathic geriatric
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Table10-1.
Table10-2.
gaitduetooraggravatedbyanunderlyingsystemicdisorder.Systemicdisordersaffectinggait
may be divided into the following etiologic categories: neurosensory, metabolic,
cardiovascular,musculoskeletal,andidiopathic.
WalkingRequisites
Uprightposture
Abilitytoalternatelyswingfromdoublelimbsupporttosinglelimbsupport
Singlelimbsupport
Lateralstability
Alternatelygenerateandresistself-producedforwardmomentum
Intactcentralpatterngenerators
GeriatricGaitStage(byAge)
Stage1:60–72y
Decreasedvelocity(>63y=1.6%/y)
Decreasecadence
Decreaseverticalexcursion(COG)
Decreasedsteplength
Disturbedcoordinationofupperandlowerextremities
Stage2:72–86y
Arm–legsynergyislost
Increasedunwantedmovements
Stage3:86–104y
Rapiddisintegrationofgaitpatterns
Arrhythmicsteppingpatterns
OBSERVATIONALGAITANALYSIS
Human gaitshould beeffortless andefficient with minimal energyexpenditure and minimal
shiftintheCOGfromitsprotected,balancedpositionanteriortothesecondsacralvertebrae
asitmovesforwardtoitsintendeddestination.11Thegreaterthenumberofcontactpointsin
the locomotor apparatus thesimplerthe effort.In thecaseofa wheel thenumber ofcontact
pointsisinfinite;however,inhumansthereareonlytwo.
11
Gait is virtuallyimpossible to measure through observational gaitanalysis (OGA), and
althoughit is an unreliable indicator ofthebody inmotion,significant deviations from the
normshouldberelativelyeasytodiscerneventotheuntrainedclinician.Thecorrelationofthe
biomechanical examinationfindings as well as knowledgeofmusculoskeletal constraints is
criticalintheevaluationofgaitobservations.Whenobservinggaitbeginbyobtainingagross
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Table10-3.
reviewoftheorganisminmotion,thatwillprovideasenseofflowtotheactiontakingplace.
Beginfromthefootupwardandcompareeachsegmentwithnormalandwiththecontralateral
side, paying particular attentiontolower extremity articulations.12 Note head tilt; shoulder,
spinal,orpelvicdeviations;armswing;orlimp.Theeyesshouldbeleveltothehorizonand
themouthparalleltotheeyes.Shouldersshouldbelevel.Thekneeshouldbestraightaheadat
heelcontactwithoutexcessiveadductionorabductionofthefemur.Thereshouldbeneutralto
inverted calcaneus at heel contactwithoutundue impact and normal sequencingofthe gait
cycle. The heel should not be seen to “bounce” up prematurelyduring propulsion, and all
observationsshouldbe symmetrical andexpected.Thegaitangleandbaseofgaitshouldbe
withinnormalrangesandsymmetrical.Duringswingphase,the footshouldclearthe ground
efficientlywithoutexcessiveactivityoftheextensorgroup(Table10-3).
GaitInfluences
Advancingage
Visiondisorders
Inactivity
Chronicdisease
Frailty
Medications
Alcohol
Balancedisturbances
Musculoskeletaldisease
Footdiscomfort
Footdysfunction
Footdeformity
Footwear
Idiopathicgaitdisturbances
PATHOLOGICGAITOBSERVATIONS
Duringheelcontactphaseofthegaitcycle,theheelshouldcontactthegroundbeforeanyother
partofthefoot.A toe–heel gaitwouldbeanindicatorofanterior legmusculatureweakness
and/or posterior group contracture with or without spasm. This may be observed in any
disorder resulting in an imbalance between dorsiflexors and plantarflexors with secondary
paralysisorweaknessofthecommonperonealnervewithtricepssuraecontractureresultingin
adropfoot(pesequinus)deformitysuchaspostcerebrovascularaccident.Theremayormay
not be an accompanying or prodromal forefoot slap or forefoot scuff early in the disease
evolution.Asteppagegait,wheretheentirefootcontactsthegroundatheelstrike,isseenin
lowermotorneurondiseasesuchascommonperonealorpoplitealnervedisease.Incommon
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peronealnervepathologygait,thereisanaccompanyingfootslapwiththesteppagegait,andin
popliteal involvement it is a more flaccid, exaggerated steppage gait that is observed.
Steppage gait is a prominent distinguishing feature seen in Charcot-Marie-Tooth disease
(CMT).Duringthemidstancephaseofgait,anearlyheelliftoffmaybeobservedandmaybe
due toequinus influencesonthe lowerextremity especiallyaffectingthe tricepssurae.This
maybeseenincongenitalspasticityasobservedincerebralpalsy(CP),congenitalcontracture
of the gastrocnemius-soleus musculature or bony block at the ankle. A scissor, ataxic, or
Trendelenburg gait is seen in upper motor neuron (UMN) disease disorders such as CP.
Propulsive phaseofgait disorders may be dueto cerebellar pathology, lower motorneuron
lesionsuchasdiabeticneuropathy,oranantalgicgaitduetoincreasedforefootpressuredueto
halluxvalgusorhammertoedeformities.Acalcaneusgaitduetogastroc/soleusparalysismay
be seen in lower motor neuron lesion diseases such as diabetes mellitus, Guillain-Barré,
porphyria,andothers.Patientswithdiabeticneuropathyexhibitreducedactivepropulsiondue
toadeficitofgastroc/soleusfunction.
Antalgic gait is a compensatory gait in whichthe gait alteration is an alteration in gait
designed to relieve pain. It ceases when the pain is absent. This is frequently seen in
musculoskeletaldisordersaffectingthelowerextremitysuchasinflammatoryofdegenerative
diseasedisordersaffectingthespine,hip,knee,ankle,orfoot.Disordersaffectingpostureor
balance may result in either a cautious or reckless gait. Cautious gait is caused by an
overresponsivenesstogaitinstabilityandfeaturesslowershorterstepswithincreaseddouble
support. Patients walkwith armsoutstretched as ifon ice andis linked to “fear offalling”
syndrome or “fall phobia.”1 Reckless or careless gait is seen in individuals with poor
assessment of their own fallingrisk. Ataxic gaitfrom the Greekfor “without order” is an
exampleofrecklessgaitwithwidebaseofsupporttoneutralizemedialtolateralinstability
commonlyseeninCNSdisorders.
NEUROSENSORYDISORDERSAFFECTINGGAIT
Normalfunctionofthefootanditsabilitytosupportanormallocomotorpatternisdependent
on intact neural pathways. Neurosensory gait disorders include myopathy, neuromuscular
junction disease, and upper or lower motor neuron lesions. Myopathic gait disorders are
causedbyimpairmentoftheconductionofmuscleimpulsessuchasseeninDuchennemuscular
dystrophy or alcoholic myopathy. The gait is described as dystrophic or atrophic with
exaggerated lateral trunk movements resulting in a penguin- or duck-like gait. Commonly
observed gait deviations include Trendelenburg, toe-walking, hyperlumbar lordosis, knee
instability,recurvatum,andbalancedisorders.13Gowerssign,namedbytherenownedBritish
neurologistSirWilliamRichardGowersinthelate19thcentury,isaninabilitytostandfroma
kneelingpositionduetolowerlimbmuscularweakness.Thepatientisforcedto“walk”over
hisownbodytoachievetheuprightposition.AlthoughclassicallyaclassicsignofDuchenne
muscular dystrophy, it is also seen in centronuclear myopathy and myotonic dystrophy.
Individualswithmyopathicdiseaserequirearmassistancetorisefromachair.
Myastheniagravisisanexampleofaneuromuscularjunctiondiseaseinwhichthegaitis
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laboredasaresultoftheirabilitytoeasilyfatigue.Thereisdifficultymaintainingtheupright
posture as well as inclimbing stairs. The accompanying double vision disorder magnifies
thesedeficits.
UMNGAITDISTURBANCES
UMNlesionpathologyisassociatedwithmuscleparesis,overactivity-spasticity,andstiffness.
CPGsmaybeintactintheseindividuals;however, dueto dysfunctional spinal reflexes and
supraspinalinputsmotorcontrolandgaitpatternsarepathologicallyaffected.7UMN-induced
gait disturbances are seen in cerebellar dysfunction secondary to tumor, abscess,
cardiovascular accident, CP, multiple sclerosis (MS), or Parkinson disease (PD). There is
axialinstabilitywithfewfocalneurologicsigns.Awidebase,slowandsmallsteps,shuffling,
unsteadiness,andlurchingtowardtheaffectedside(vestibularataxia)characterizethetypical
ataxic gait seen in these conditions. The patient has difficulty turning with severe truncal
instability. Attimes,the individual mayappear “frozen” with aninability toinitiateastep.
Sensoryataxia is duetoproprioceptive sensorydeficitsandis exemplified bya staggering
gait,whichmayincludestomping,slapping,orheavyheelstriketoincreasesensoryfeedback
asanaidetoambulation.7PatientswithsensoryataxiaexhibitapositiveRombergsign.UMN
lesionpatientsmaybeunabletoaccomplishunsupportedstance.
Cerebellar ataxia is caused by cerebellar dysfunction involved in limb movement and
dynamic balance control. Cerebellar gait has been described as a “drunken” gait that is
unstable,veering,andirregular.Studieshavedemonstratedthatthemainfeatureofataxicgait
isincreasedintrasubjectperformancevariability.
14,15
Tandemwalking,theactofplacingone
foot directly in front of the other while walking, is a sensitive clinical test for cerebellar
dysfunction.
16
CerebrovascularAccident
In an average year, 0.2% of the population will suffer a stroke.13 It is the most common
neurologic deficit and leading cause of gait impairmentinrehabilitation facilities.13 Stroke
results in a hemiparetic gait with marked asymmetry and increased stance time on the
unaffected limb,decreased stance anddecreased swing onthe affected side, andincreased
doublesupporttime,7allinessenceincreasingstabilitybydecreasingdemandsplacedonthe
affectedlimb.Speed ofambulationinstrokepatientsis alsonegativelyaffected.17 This has
beenshownto be duetoweakankle plantarflexors, hipflexors, andkneeextensors.18 Arm
swingmaybe absentordiminishedontheaffectedside.Initially, thearm maybeflaccidor
held inadductionandflexion.7 The affected limb is held stiff-legged in extension,internal
rotation,and equinovarusof thefootand ankle.This createsdifficultyinachieving forefoot
clearance during swing phase with compensatory adjustments including hip elevation,
increased trunk sway, circumduction, and occasionally contralateral vaulting.7 Swing phase
initiationisdifficult,delayed,andprolonged.Electromyogram(EMG)studieshaverevealed
prolongedtibialisanteriorfunctioninanattempttodorsiflextheforefoottocleartheground.
19
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Inpatientswithtransientbrainischemia(TBI),thezoneofneurologicinsultisnotaswell
circumscribed. Therefore, the range of neurologic deficits is wider. TBI patients generate
increasedsteplengthandnormalstancetimeonaffectedlimbcomparedwithstrokepatientsin
spiteofincreasedstancetimeontheunaffectedextremity.
7
ParkinsonDisease
PDisaprogressiveasymmetricaldisordercausedbyabasalgangliadopaminedeficiencyand
isresponsiblefor10%ofgaitdisturbancesinadults.20Duetoneurotransmitterimbalances,PD
patientsprogressivelyloseflexibilityandadaptabilityinlocomotorresponsesandwalkwitha
stereotypical shortened-step, narrow-base, shuffling gait. The ability to respond to gait
challenges including cognitive demands made during ambulation and gait perturbations are
significantlycompromisedinthePDpatient.
21
Althoughinitiallyasymmetrical,thecontralaterallimbeventuallybecomesaffectedin80%
ofcasesthoughnotasseverelyasthesideofinception.20Approximately1%ofthoseover50
yearsofagehavePD.13Inacommunitydwelling,15%ofthose65to74yearsofageexhibit
gaitabnormalityandoneormoresignsofPD.Thisnumberrisesto30%forthe75-to-84-year
groupand50%inthoseover85yearsofage.22Therehasbeenreporteda35%incidencein
gaitdisordersincommunitydwellersover70yearsofage.
23
Like other UMNdisease disorders, parkinsonian gait is ataxic innature withdistinctly
different and distinguishing “hallmark of the disease” characteristics. These include pill
rolling,tremor,festination,rigidity,posturalinstability,andanoverallslownessofgaitknown
as hypo- or bradykinesia (Table 10-4). In some severe cases, there may be akinesia or
completeloss ofmobility.Unlikepyramidaldisorders, strengthispreservedwith the lower
extremitythatisrigidinnature.Festinationistheinabilityoftheparkinsonianpatienttoslow
downoncegaithasbeeninitiated.Thisisduetomuscularhypertonicitymanifestedbyankle
andkneestiffnessalongwithpelvisandtrunkflexion.
24
Asymmetricarmswingandaccompanyingtremoraswellasstaggeringanden-blocturning
aresuggestiveofearlyPD.25Asthediseaseprogresses,thereispronouncedtendencytodrag
theipsilateralleganddecreasedfootclearanceandreducedsteplengthmaybemoreclearly
evident.25 Patients with PD typically increase cadence in an attempt to compensatefor the
shorter step length and reducedvelocity.1 In additiontothe above-mentioned deficits, it is
significanttonotethatbalancecontrolisasymmetricalinabout75%ofpatientswithPD.
20
Parkinsoniangaitischaracterizedbyafootflatstrikeplacingtheentirefootontheground
atthesametime.26Inadvancedstages,atoe–heelgaitmaybeobserved.Patientshavereduced
footliftduringswingphaseofgaitwithresultantreducedtoeclearancebetweenthefootand
the ground.27Thereis reducedimpactatheel strikeinparkinsonianpatientswithadditional
decreasesasthediseaseprogresses.28Theloadonthe forefootisincreasedwithatendency
towardmedialdisplacement.Theinterpatientgaitvariabilityinfootstrikepatternislessthan
inthe normal population.28 Thevertical ground reactionforce (GRF) has two peaks in the
normalindividual:oneatheelcontactandoneatpropulsion.InearlystagesofPD,thereare
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