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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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FIGURE21-5.A:Imageofthespinewiththeduraopenshowingthecontentsofthespinalcanalbelowthespinal
cord.Onecanseethevariousnerverootscontinuingcaudallyformingthecaudaequinaorhorse’stail.B:Sagittal
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Table21-2.
viewofthespineshowingterminationofthespinalcordatL1/L2.(FromHainesDE.NeuroanatomyinClinical
Context.Philadelphia,PA:WoltersKluwer;2014,withpermission.)
Cervicalspondylosisreferstodegenerationofthecervicalspine.Thisprocessbeginswith
alossofintegrityoftheintervertebraldisk.1Thisprocesstypicallyoccurswithage,althougha
geneticpredispositiontowarddiskdegenerationmayexistinsomeindividuals.Thisprocessis
typicallyasymptomatic.Asthediskbreaksdown,itlosesheightandbulgesoutwardintothe
spinal canal. This disk bulge may also occur laterally impinging on the spinal roots.
Breakdown of thedisk then leads to increased loads on the vertebral bodies andjointsof
Luschka (uncinate joints). In response, the uncinate joints and vertebra form more bone in
ordertobettersupporttheincreasedloads.Bonefromthevertebralbodiescanprojectintothe
canaland restrictthespaceavailable for the cord, whereas uncinatehypertrophycan cause
lateralcompressionandnerverootimpingement(Fig.21-6A).Bulgingofthedisksandlossof
disk height can also lead to infolding of the posterior soft tissues such as the ligamentum
flavumandthePLL.Thesetissuescancausedynamiccompressionofthecordinflexionand
extension(Fig.21-6B). Ossificationof the PLL is most commonlyseeninan Asian patient
population and may lead to severe anterior cord compression (Fig. 21-7). Although the
“normal”spinalcanalhasapproximately7to8mmofspacetoaccommodateintrusionsfrom
osteophyte formation and ossification, some patients may present with congenitally narrow
spinalcanalsandbeathigherriskfordevelopingmyelopathy.
5
DifferencesintheClinicalPresentationofUpperversusLower
MotorNeuronDisease
ClinicalSign UpperMotorNeuron LowerMotorNeuron
Weakness Yes Yes
Atrophy Mildatrophypossible Yes
Fasciculations Notpresent Present
Reflexes Increased Decreased
Babinski/pathologicreflexes Present Absent
Tone Increased Decreased
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FIGURE21-6.A:Normalcervicalanatomy.B:Examplesofdegenerativechangesinthecervicalspinethatcan
causecompressionofthespinalcord.C:Exampleofdynamiccompressionofthespinalcordduetosofttissue
impingementfromtheposteriorlongitudinalligamentorligamentumflavum.(AandB:FromShenFH,SamartzisD,
FesslerRG.TextBookoftheSurgicalSpine.MarylandHeights,Missouri:Elsevier;2015.C:FromLawMDJr,
BernhardtM,WhiteAAIII.Cervicalspondyloticmyelopathy:areviewofsurgicalindicationsanddecisionmaking.
YaleJBiolMed.1993;66(3):165–177.)
Chronic compression of the spinal cord because of the static and dynamic factors
describedearlier leadstodamageofthespinal cord throughchronic distortionofthespinal
cord microvasculature. Chronic compressionof the cord leads to flattening, elongation,and
stretchingandeventuallossofthemicrovasculature.Ascompressionproceeds,changesoccur;
the majority of changes are seen in the lateral funiculi and the corticospinal tracts.5 More
severe cases are associated with changes inthemedial grayarea and ventral aspectof the
dorsalcolumns.Theanteriorcolumnsappeartoberelativelyprotectedevenincasesofsevere
compression.
DiagnosisandLowerExtremityFindings
PhysicalexaminationofpatientswithCSMdemonstrateslowermotorneuronsignsatthelevel
ofthecervical lesions(i.e., intheupper extremity)and uppermotor neuron signsatlevels
below the lesions (i.e., in the lower extremity). As most cases of CSM have combined
compressionofboththenerverootandthespinalcord,symptomstypicallyinvolveweakness,
pain, andhyporeflexia in theupper extremity andspasticityand hyperreflexia inthe lower
extremities.
4
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Patientsmaypresentwithsubtle complaintsrelatedtogaitinstabilityandchangesingait
and balance. Although there are certainly numerous causes for changes in gait patterns,
difficultywithbalanceanddifficultywithfinemotortaskssuchastandemwalkshouldraise
the examiner’s suspicion for cervical pathology. In patients with these symptoms, it is
importanttoalsoillicitahistoryofupperextremityfunctionastheymaycomplainofalossof
dexteritywithfinemotortaskssuchasbuttoningashirtorhandwriting.
FIGURE21-7.A:SagittalCTscanofacervicalspineshowingdegenerativediscdiseaseatmultiplelevelsand
ossificationoftheposteriorlongitudinalligament.B:Axialimageshowinganossifiedposteriorlongitudinalligament
narrowingthespaceavailableforthecordanteriorly.C:AxialMRIimagesshowingalevelwithoutcordcompression.
D:AxialMRIthroughthesamelevelseenontheCTscaninB.Thisimageshowsandexampleofseverecord
compression.E:SagittalMRIimageshowingcompressionofthespinalcordatmultiplelevels.
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Onphysicalexamination,patientswithmyelopathypresentwithamixofupperandlower
motor neuron findings in one or both upper extremities and primarily upper motor neuron
symptomsinbothlowerextremities.Clinicalsignstypicallyincludehyperreflexia,clonus,and
other upper motor neuron signs such as a positive Babinski in the lower extremity.
6,7
The
Babinskisign refers todorsiflexionofthebigtoe whenthe sole ofthefootisstroked bya
sharp object (Fig.21-8A). The clinical exam in patients who are suspected to have CSM
should also include an exam of upper extremity reflexes; pathologic reflexes in the upper
extremitiesincludetheHoffmansign(Fig.21-8B)andtheinvertedradialreflex(Fig.21-8C).
Unfortunately, all physical exam maneuvers for CSMare limitedbylow sensitivity and
specificity and thesereflexescan sometimes be seeninhealthy individuals.8 However, gait
imbalance,hyperreflexia,andBabinski’ssigninpatientspresentingtoalowerextremityclinic
shouldraisesuspicionandinitiateaworkuptoruleoutcervicalcompressionasthecauseof
thepatients’complaints.
Treatment
There is no predetermined course of CSM, and progression can vary between patients.
However,itisgenerallyagreedthatoncesignsandsymptomsofCSMareevident,thereisno
neurologicimprovementwithoutsurgicalintervention.
8,9
Deterioration,however,mightfollow
a stepwise clinical course, withlong periods of stabilityinterruptedby periods ofmarked
decline.Conservativemanagement hasconsistedofimmobilization andcervical traction,but
evidencefortheroleofconservativemanagementinsymptomaticCSMislimited.
8
Thedecisionbetweenconservativeandsurgical managementismore difficultinpatients
withmildsymptomsorcervicalstenosiswithoutobviousclinicalsignsofmyelopathy.These
patientsmaybemanagedconservativelywithperiodicobservationforsigns ofdeterioration
that might necessitate surgical intervention. Proponents of surgery, however, point to the
progressive degenerative cascade of CSM and the risk of progressive (and potentially
irreversible)neurologicinjuryas therationaleforearlysurgical intervention.
8,9
Changeson
imagingthatmightencouragesurgicalchangeinclude:signalchangesinthespinalcordinT2weightedimagesandnerverootimpingementfoundonmagneticresonanceimaging.
Surgical intervention typically consists of decompression of the spine along with
immobilization and fusion. More recent studies have suggested that hypermobility of the
cervical spinemightbeakey factorin driving myelopathicchanges.There are a varietyof
approaches andtechniquesavailable to decompress andstabilize the spine, but an in-depth
discussionofthesetechniquesisbeyondthescopeofthischapter.
LumbarSpine
LumbarStenosis
Pathophysiology
Lumbar stenosis refers to thenarrowing of the space available for thespine in the lumbar
spine.Lumbar stenosis differs from cervical stenosis because it typically occurs below the
level of the spinal cord. This fact is clinicallyrelevant because compression of thecauda
equina,unlikethespinalcord,doesnotaffectthelateraldescendingandposteriorascending
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tracts.Asaresult,patientswithlumbarstenosis,unlikepatientswithcervicalstenosis,donot
presentwithuppermotorneuroncomplaints.
FIGURE21-8.A:ExampleoftheBabinskisign;strokingapenonthebottomofthefootshouldnormallyresultin
downgoingtoes;upgoingtoesissuggestiveofuppermotorneurondisease.B:Hoffmansign:theexaminerflicking
themiddlefingerasillustratedresultsinflexionoftheotherdigits.C:Invertedradialreflex:Tappingthe
brachioradialistendonleadstoflexionofthedigits(A:FromHouseEL,PanskyB.AFunctionalApproachto
Neuroanatomy.NewYork,NY:McGraw-Hill;1960[Publicdomain],viaWikimediaCommons.BandC:From
EmereySE.Cervicalspondyloticmyelopathy:diagnosisandtreatment.JAmAcadOrthopSurg.2001;9(6):376–
388,withpermission).
LikeCSM,lumbarstenosisisaprogressive,degenerativeprocessthattypicallymanifests
clinicallylaterinlife(60sand70s).Similartothecervicalspine,degenerationinthelumbar
spineis thought tobegininthedisk.As the structureof thediskchanges withage,there is
tearingofthediskcontributingtodiskdegeneration,herniation,andlossofheight.Thisagain
leads to abnormal spine biomechanics and abnormal loading of the spinal canal and
degenerationofthefacetjoints.
1
Lumbar facets are oriented approximately 90° in the sagittal plane. This orientation is
optimalforflexionandextensioninnormalindividuals.However,asthefacetjointsbecome
inflamed, synovitis can lead to laxity and subluxation of the facet joints. This can cause
instability of thevertebral column as one vertebra may“slip” forward, reducing thespace
available for the cord (Fig. 21-9A). This condition is referred to as degenerative
spondylolisthesis(spondy =vertebralbodyandolithesis=slipinGreek)andcontributesto
lumbarstenosis.
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In additiontolaxityof the facetjoints,degeneration andabnormal loading also lead to
hypertrophy,osteophyte,andcystformation.Asnotedintheanatomysection,thefacetjoints
formtheposteriorborderoftheintervertebralforamen.Hypertrophyofthesejointscanleadto
nerverootcompressionintheintervertebralforamenaswellascompressionofthethecalsac.
Similarly,facetcystscanleadtonerverootimpingement.
Degeneration of the diskalso creates abnormal spaces across thevertebral bodies and
vertebralendplates.Thiscanleadtoosteophyteformationandcancontributetocompression
ofthethecalsacaswellastheexitingnerverootsintheintervertebralforamen(Fig.21-9B).
Causes of lumbar stenosis without degeneration include various congenital or
developmental disorders such as congenital spondylolisthesis because of defect in the
vertebralpars,achondroplasia,andothersyndromessuchasankylosingspondylitisandPaget
disease.
5
DiagnosisandLowerExtremityFindings
Patients with lumbar stenosis most commonly present with lower extremity pain. Patients
describe a feeling of leg numbness, fatigue, heaviness, cramping, burning, or weakness.
Symptoms of stenosis are typically referred to as “neurogenic claudication” and typically
worsenwhenpatientsareupright.
5,10
Inanuprightposition,thelumbarspineassumesitsmost
lordotic posture, which reduces the space available for the cord and contributes to
compression. As a result, patients will typically complain of leg pain that is worst with
standingorwalkingbutrelievedbysittingorbendingforward.
Becauseoftheexertionalnatureofthepatients’complaintsandthefactthatlumbarstenosis
typicallyaffectsan older population, itis important to differentiateneurogenic claudication
fromvascularclaudication.Oneimportantdifferenceisthatvascularclaudicationistypically
relievedassoonaspatientsstoptheirexertionalactivities,whereaslumbarstenosisrequires
thatpatientschangetheirpostureinsomewaytoreducelumbarlordosis.Forexample,patients
with vascularclaudicationmightreportanimprovementinpain after they stopwalkingand
standforafewminutes,whereaslumbarstenosispatientswillhavethesamepainevenwhen
standingbecausethespineremainsextended.Sittingorleaningforwardwillresultinreliefof
their symptoms. The “shopping cart sign” refers to the fact that many patients report an
improvementinsymptomsand mobility whenleaningforwardontoashoppingcart.Walking
uphillis easierforpatientswithlumbarstenosis asthe spineisrelativelyflexedduringthis
activity while walking downhill is harder asthe spineis extended.Theoppositeappliesto
patients with vascular claudication. Another common activity that might be elicited in the
historyisthestationarybike.Becausethisactivityisperformedinaseatedpositionbutstill
increases lower extremityoxygendemand,patientswithvascularclaudicationwilltypically
report increased pain after certain distances, whereas spinal stenosis patients are typically
morecomfortablewiththeseactivities.
Sometimes,patientswithspinalstenosismaypresentwithnolegpainbutwithlowback
pain radiating into the bilateral buttocks. In these cases, it can sometimes be difficult to
differentiate pathology from the spine from pathology from the hip joint.2 Although it is
difficulttodifferentiatehippathologyfromspinepathologyonthehistory,thepresenceofa
limp,limited hipinternalrotation,and groinpain allsuggesthip pathology insteadof spine
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pathology.
Finally,patientswithstenosismayalsocomplainofradicularsymptoms,thatis,painalong
a specified dermatome because of compression of a nerve in the lateral recess or
intervertebral foramen.Low backpainis alsoacommon complaint butin casesofisolated
back pain, caution must be used to ensure that the patients’ symptoms are consistent with
stenosis(improveswithsitting,flexingforward,etc.).
Examinationofapatientwithlumbarstenosisbeginswithathoroughhistorycoveringthe
points mentioned earlier. The history must also elicit any complaints of bowel or bladder
dysfunction, progressive weight loss, fevers, chills, and history of cancer. Because lower
extremitycomplaintsmaybe thesignof a number ofsystemic diseases, a thorough medical
history must also be obtained. The examination in the clinic begins with inspection and
observationofpostural changes(e.g.,leaning forward whensitting). Examination of gaitis
importantaspatientswithseverestenosiswillwalkorflexforwardtoreducespineextension.
Thepresenceofalimp,however,shouldraisesuspicionforaprocesslocalizedtothelower
extremity.Acompletereflexexamshouldalsobeperformed.Itisnotuncommonforpatients
with lumbar stenosis tohave diminished reflexes, although thiscanbedifficulttoascertain
because reflexes tendtobe diminished in older patients.Asymmetric reflexes should raise
suspicionforspinalpathology.Completestrengthtestingofbothlowerextremitiesshouldbe
performed.Althoughlowerextremityweaknessisnotclassicallydescribedinspinalstenosis,
theremaybesomeweaknessfoundifthereisaradicularcomponenttothepatients’disease.
Specialteststhatmaybeperformed includehyperextensionofthespineto determineifthis
maneuver recreates the patients’ pain. Upper motor neuron findings (such as hyperreflexia,
clonus,Babinski,etc.)mustberuledout.
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FIGURE21-9.A:CTscanshowingdegenerativelisthesis,thatis,forwardslippageofL4onL5.B:ImageofL2/L3
diskspaceshowingnoevidenceofcanalnarrowing.C:Incontrast,withaxialimageofL4/L5showingfluidinthe
facetjoints(pinkarrows)thatislikelyresponsibleforthelaxityandlisthesis,athickenedligamentumflavum(green
arrow)leadsthecentralstenosis(yellowarrow).
Diagnostic studies include plain radiographs, computed tomography, and magnetic
resonanceimaging.
Treatment
TheNorthAmericanSpineSocietyhasreleasedevidence-basedguidelinesforthediagnosis
and treatment of lumbar stenosis.11 These guidelines recognize that the natural history of
lumbar stenosis is largelyunknown. Multiple prospective observational studies haveshown
thatbetween30%and50%oflumbarstenosispatientshaveafavorablenaturalhistorywithno
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significantprogressionoftheirsymptomsandnolimitationsinactivitiesofdailyliving.This
seems to be the case regardless of the medical intervention used. Additionally, this group
recognized that patients with stenosis do not suffer from rapid or catastrophic decline but,
rather, a progressive worsening of symptoms. Conservative management may include
analgesics, physical therapy, epidural steroid injections, andbracing. Nonsurgical treatment
optionscanprovidelong-termrelief,althoughthereareonlyweakdatatosupportthisclaim.
Severalstudies haveshownimprovedoutcomes inpatientswith stenosis following surgical
interventions; however, these are generally only recommended in cases with moderate or
severesymptomsofstenosis.TheSpinePatientOutcomesResearchTrial(SPORT)indicated
patients with lumbar stenosis for surgery if they met the following criteria: (1) history of
neurogenic claudication or radicular symptoms for at least 12 weeks and (2) confirmatory
cross-sectionalimagingatoneormorelevels.Thisstudydemonstratedimprovedoutcomesin
thesurgicallytreatedcohortthathavebeenshowntobemaintainedatupto4-yearfollow-up,
12
althoughmorerecentinvestigationhasshownadiminishingtreatmenteffectat8-yearfollowup.
13
LumbarRadiculopathy
Pathophysiology
As noted intheanatomysection, the intervertebral disk sits betweenthe adjacent vertebral
bodies.Itconsistsofthreedistinctparts:thevertebralendplates,thenucleuspulposus,andthe
annulus fibrosus (Fig. 21-10). The nucleus pulposus consists of aggrecan and other
proteoglycansandtypeIIcollagen.1Thisenvironmentishighlyhydrophilicandretainswater.
Approximately80%ofthenucleusconsistsofwater.Asaresult,thenucleuspulposusserves
assomethingofa shockabsorberfortheintervertebraldisk.Thenucleusissurroundedbya
lamellatedlayerofsheetscalledtheannulusfibrosus.TheannulusconsistsoftypeIcollagen
andservesto“contain”thenucleus;thestructureoftheannulusisbestsuitedtoresistingaxial
loads.Diskdegenerationbeginswithlossofwaterinthenucleuspulposus;thisisfollowedby
biomechanicalchangesthatleadtomoreforcesbeingplacedontheannulus.Theannuluscan
thenexperiencecircumferentialfissuresthatleadtodiskherniation.
1
Inthelumbarspine,thelumbardiskisboundedposteriorlybythePLLinthemidline.In
effect,thisrenderstheposterolateralpartofthediskbare,makingthisthemostlikelylocation
for disk herniation (Fig. 21-1D). Lumbar disk herniations may be classified as central,
posterolateral,foraminal,orextraforaminal.Thelocationofthediskherniationisimportantas
it guides localizationof symptoms and allows for correlationwith cross-sectional imaging.
Ideally,thepatients’symptomsshouldmatchthefindingsonimaging.
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