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Casepresentation
66y/F,Hxofhyperthyroidism20yrsagobutalreadycured
(detailedunknown).Annualseasonalinfluenzavaccineon
29/1/2012.
ConsultedERon12/6/2012duetobothupperlimbsweakness
for1week(since5/6/2012),graduallyinvolvedbothlowerlimbs.
BrainCT(12/6/2012):afewlacunarinfarction.
CXR(12/6/2012):lungmarkingincrease.
Lumbar+thoracicspineX-ray(12/6/2012):unremarkable.
InER,ptrefusedlumbarpunctureandsignpaperfordischarged.
On16/6/2012,ptcameERagain,c/olimbsweaknessdeteriorate
anddifficultyinswallowing,alsoeyesptosis.
Symptomsnofluctuatingfeature
LP,brainCTandCXRweredone.
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BrainCT(12/6/2012)
CXR
(12/6/2012)
Lungmarking
Increase.
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Compexam(12/6/2012)
Bloodtest:
Hemogram:unremarkable
CRP:0.27
Coagulationprofile:unremarkable.
Biochemistry:Glu:6.9,Normalliverandrenalfunction,
normalelectrolytelevel(K+:3.7mmol/L),normalCKand
LDHlevel.
Thyroidfunction:
T3:0.65ng/mL(0.80-2.00),T4:7.87ug/dL(5.10-14.10),
FT4:1.44ng/dL(0.93-1.70),TSH:3.33mIU/L(0.27-4.20)
Physicalexamination
BP142/87mmHg,P87/min,T36.9C,conscious,no
jaundice,AP(-),AC(-),ABD(-).
Neurologicalexamination:
Bothpupilsequal,3mmindiameter,reactivetolight,
necksoft,botheyesptosis,couldnotwhistle,slurred
speechanddifficultyinswallowing(bulbarpalsy)--
CNIII,VII,IXpalsy
Musclepoweroffourlimbsdecrease:bothupperlimbs:
1-2/5,bothlowerlimbs:0-1/5,DTR(-),painstimuli
feelingsymmetryandexistatbothlimbs,muscletone
decrease,bothBabinski''ssign(-).
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Diagnosis
1.Diagnosis:generalparalysisforstudy?
Localizationdiagnosis:“Where”
CentralorPeripheralneuropathy,myopathy?
Qualitativediagnosis:“What”
Differentialdiagnosis
Localizationdiagnosis:“Where”
“Quadriplegia”---Acutemotorweakness
UpperMotor
Neuron
disease
Lower
MotorNeuron
disease
Myopathy
DTR(Reflexes)Hyperactive↓orNoPreserved
Muscletone↑↓Normal
DistributionWholelimbDistal>ProximalProximal>Distal
Babinskisign(+)(-)(-)
AtrophyNo()PresentPresent
SensorydeficitMayMaypresentNo
FasciculationNoPresentNo
CKenzymenormalNormal↑
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Qualitativediagnosis:“What”
Clinicalfeature
Acuteonset+bilateralflaccidparalysis
DifferentiaDiagnosis
AcquiredNeuropathies:Guillain–BarréSyndrome?
Hx:progressivebilateralflaccidparalysiswithsensorypreserve
Lumbarpuncture,EMG,etc…
Hyperthyroidismhypokalemiaperiodicalparalysis
NormalK+andnormalthyroidfunction
NeuroMuscularJunction:MyastheniaGravis
Fatiguetest(+)atfourlimbs.
Neostigmintest:1st(+/-),2ndtime(-)
TryPiridostigmina60mgtidpo,noimproved.
Foodpoisoning(Botulism)
Hx,Pupilschangeandoculomotormuscleinjury
Myelitis
Nosensorydeficitlevelwasfound.
Poliomyelitis–rarely
LowerrMotorNeurondisease
Compexam:
LP/CSF(17/6/2012):
Glicose(LCR):H4.80mmol/l(2.20-4.20)
Protein(LCR):6.37g/l(<0.45g/L)
Aspect:Clear
Colour:Pinkish
Leukocytes:2/ul
Erythrocytes:Many(+/-100/μL)
BrainCT(16/6/2012):normal.
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BrainCT(16/6/2012)
CXR(16/6/2012):
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Exclusionofmalignantdisorders
Bloodtumormarker:
CEA,AFP,CA125,CA19.9,CA15.3,SCC(-)
ChestAbdomenPelvisCT:
-Rightpulmonaryembolismevoked.
-Bronchiectasisinrightupperandbilaterallowerpulmonary
lobessuggested.Somefibroticlesionsinbilaterallower
pulmonarylobeswithbilateralpleuralthickeningevoked.
LP-CSFcytology:nomalignantcellwasfound.
LowerlegDoppler:noDVTwasfound.
ChestAbdomenPelvisCT
Rightpulmonaryembolism
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Diagnosis:
1.Guillain–BarréSyndrome
2.Rightpulmonaryembolism
Treatment
LMWHwasgivenforthetreatmentofPE.
IVIG:0.4g/kg/dayfor5days
Patient’ssymptomsnoimproved
GiveanothercourseofIVIG:0.4g/kg/dayfor5days
Ptosisimproved,leftlimbsweaknessimproved.Now
patient’sMPofupperlimbs:1-23-4,MPoflower
limbs:0-12-3,
RepeatChestCT2weekslater,rightpulmonary
embolusdisappeared.
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Questions
1.Isitinfluenzavaccinetheetiologyofthispatient?
2.What’stherelationshipbetweenpulmonary
embolismandGBS?
3.HowtotreatthepatientwhofailuretoIVIG
treatment?Plasmaexchange?
Guillain–BarréSyndrome
Guillain-BarréSyndrome,ReviewArticle,NEnglJMed2012June;
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Index
Introduction
Epidemiology
Etiology
Clinicalpresentation
Diagnosis
Treatment
Prognosis
Introduction
Guillain-Barre′syndrome(GBS)isanacute
onset,immune-mediateddisorderofthe
peripheralnervoussystem.
TheclinicalfeaturesofGBSweredescribed
byLandryin1859.
In1916,threeFrenchneurologistsGeorges
Guillain,Barre′,andAndreStrohl
describedtwosoldierswithacute
areflexic(无反射)paralysisfollowedby
recovery.Theynotedaraisedconcentration
ofcerebrospinalfluidproteinbutanormal
cellcount.
GeorgesGuillain
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Classification
ThetermGBS~~synonymouswithAcuteInflammatoryDemyelinating
Polyradiculoneuropathy(AIDP),butwiththeincreasingrecognitionoverthe
pastfewdecadesofvariants,thenumberofdiseasesthatfallundertherubric
GBShasgrowntoincludeaxonalvariantsandmorerestrictedvariantssuchas
MillerFishersyndrome(MFS)
Classification
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GBS=heterogenoussyndromew/variantforms
ThinkofAIDPasthetraditionalformasdescribed
previously,accountsfor85-90%
MillerFisherSyndrome:ocularmuscleparalysis,
ataxia,andareflexia(5%).GQ1bantibody.Only
1/4thw/extremityweakness
AMAN:selectiveinvolveofmotornerves,DTRsare
preserved,morecommoninJapan/China,almost
allprecededbyCampylobacterinfxn
AMSAN:moresevereformofAMAN+sensory,
rapidprogresstoquadriplegiaandrespiratory
failure
InChina/Japan,Axonal:30-65%,demyelinating:22-46%.
MillerFisher’ssyndrome
In1956,CMillerFisherdescribeda
triadofacuteophthalmoplegia,
ataxia,andareflexia,nowknownas
Fisher’ssyndrome.
Mayhavefacialandlowercranial-
nerveinvolvement.
AcriticaldifferencebetweenMFSand
AIDPorAMANis:
Anti-GQ1b&Anti-GT1aAbinMFS
thattargetoculomotorandbulbar
nerves.
5%USA,20%inTaiwan,25%Japan
CNSvariant:Bickerstaff’sbrain-
stemencephalitis
alterationofconsciousnessor
conticospinaltractsigns
据“HKChannel”微博透露，杜汶泽被医
生诊断患上香港极罕见的“米勒费雪症候
群”(MillerFisher)，严重者会四肢瘫痪、
窒息致死！由于患上该病，阿泽急需停止
所有工作，被迫留在家中养病，单单两个
月他已损失七位数酬劳！阿泽接受电话访
问时谈及现时病况：医生将其血液送去美
国化验，检查严重程度，康复时间应该是
两个星期至半年不等。虽然视觉重影、四
肢麻痺，但阿泽乐观地说：虽然会致命，
但好少去想个情况！
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CIDP
CIDP-ChronicInflammatoryDemyelinating
Polyradiculoneuropathy(CIDP)
SometimescalledchronicGBS
Twoconditiondifferintimecourseandinresponseto
steroid
CIDPinsidiousonsetandprogressionoveratleast8
weeks(AIDP4weeks)
CIDP90%improveswithsteroidsalthough50%will
relapseafterwards.
Epidemiology
TheincidenceoftypicalGBS:0.6~2cases/100,000/year
ThemostrecentEuropeincidencereport1.2-1.9/100,000
ThelifetimelikelihoodofanyindividualacquiringGBSis
1:1000.
AtypicalcasessuchasFisher’ssyndromearemuchless
common;incidenceof0.1per100000
Menareabout1.5timesmorelikelytobeaffectedthan
areWomen
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Etiology
Guillain-Barrésyndromehasbeenreportedtofollow
vaccinations(influenzavaccine?)
epiduralanesthesia
thrombolyticagents
Ithasbeenassociatedwithsomesystemicprocesses,
suchas
Hodgkin''sdisease
SLE
Sarcoidosis,and
infectionwithCampylobacter,Lymedisease,EBV,CMV,HSV,
mycoplasma,andrecentlyacquiredHIVinfection
Campylobacterinfection
Campylobacterinfectionisthemostcommonlyidentified
precipitantofGuillain-Barrésyndrome
Acase-controlstudyinvolving103patientswiththedisease
foundthat26%ofaffectedindividualshadevidenceof
recentC.jejuniinfectioncomparedwith2%ofhousehold
and1%ofage-matchedcontrols
SeventypercentofthoseinfectedwithC.jejunireporteda
diarrhealillnesswithin12weeksbeforetheonsetofthe
neurologicillness
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InfluenzavaccineandGBS?
Duringa1976massimmunizationagainstA/New
Jersey/1976/H1N1“swineflu”intheUnitedStates,peoplewho
receivedthevaccinewereatincreasedriskforthedevelopment
oftheGuillain–Barrésyndrome.(Rare:<1/1millionvaccine
recipients).
Bycontrast,influenza-likeillnessesseemtoberelevant
triggeringeventsforGBS.
Otherseasonalinfluenzavaccineshavenotbeenassociatedwith
thesameincreaseinrisk.
WiththepandemicinfluenzaA(H1N1)outbreakin2009,there
wasgreatconcernthatvaccinationagainstH1N1mightalso
triggertheGuillain–Barrésyndrome,butthatdidnotoccur.
Etiology
Themainlesionsareacuteinflammatorydemyelinating
neuropathyand,particularlyinpatientswith
Campylobacter-associateddisease,acuteaxonal
degeneration
Thesechangesmaybecausedbycross-reactingantibodies
toGM1ganglioside(presentinhighconcentrationsin
peripheralnervemyelin)formedinresponsetosimilar
epitopesexpressedbytheinfectingCampylobacterstrain
However,mechanismsotherthanmolecularmimicrymay
beassociatedwiththeproductionofantibodiestoGM1
ganglioside
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Pathogenesis
Peripheralnervedemyelinationbelievedtobeimmunene--
mediated
Usuallypost-infectious:molecularmimicrybetween
gangliosidesandantecedentinfectiousagents
Lymphocyticinfiltrationofspinalroots/peripheralnerves&
thenmacrophage-mediated,multifocalstrippingofmyelin
Result:defectsinthepropagationofelectricalnerve
impulses,witheventualconductionblockandflaccid
paralysis
Pathogenesis
PanelAshowstheimmunopathogenesisof
AcuteInflammatoryDemyelinatingPolyneuropathy(AIDP).
轴突髓鞘Schwanncell
Membrane-attack
Complex
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Pathogenesis
AIDP:immune
attackdirectedat
schwanncell
plasmalemmaesp.at
nerverootswithIgG
&complement
depositspreceding
demyelination
Pathogenesis
PanelBshowstheimmunopathogenesisof
AcuteMotorAxonalNeuropathy(AMAN).
Raniernodes
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ClinicalPresentation
Firstsymptoms:numbness,paresthesia,weakness,
paininthelimbs,orsomecombination.
Themainfeatureisprogressivebilateraland
relativelysymmetricweaknessofthelimbs
(Period:12hr~28daysbeforeaplateauisreached)
TypicallygeneralizeHyporeflexiaorareflexia
Prodromehistory:URTIordiarrhea3daysto6
weeksbeforetheonset
PhysicalExamination
Symmetriclimbweaknesswithdiminishedorabsentreflexes
Minimallossofsensationdespiteparesthesias
Signsofautonomicdysfunctionarepresentin50%pts,including
Cardiacdysrhythmias(asystole,bradycardia,sinus
tachycardia,andatrial/ventriculartachyarrhythmias)
Orthostatichypotension
Transientorpersistenthypertension
Paralyticileus
Bladderdysfunction
Abnormalsweating
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DiagnosticStudies
CSFanalysis
Afterthefirstweekofsymptoms,analysisofthecerebrospinal
fluid(CSF)typicallyreveals(albuminocytologicicdissociation)(80-
90%pts)
normalpressures
fewcells(typicallymononuclear)(<50cells/ul)
anelevatedproteinconc.(greaterthan50mg/dL)
Earlyinthecourse(lessthanoneweek),proteinlevelsmaynotyet
beelevated(<50%),butonlyrarelydotheyremainpersistently
normal,andincreaseto75%inthethirdweek.
IfCSFpleocytosisisnoted,otherdiseasesassociatedwith
GBSeg,HIVinfection,Lymedisease,malignancy,and
sarcoidosisshouldbeconsidered
DiagnosticStudies
Electrophysiologicstudies
Themostspecificandsensitivetestsfordiagnosisofthe
disease,alsoclassifythepatternandseverityofGBS
Theydemonstrateavarietyofabnormalitiesindicating
evolvingmultifocaldemyelination
Slowednerveconductionvelocities
Partialmotorconductionblock
Abnormaltemporaldispersion
Prolongeddistallatencies
EMG:prolongedorabsentFwaves
Anormalstudyafterseveraldaysofsymptoms,makesthe
diagnosisofGuillain-Barrésyndromeunlikely
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Neurophysiologytesting
Diagnosis
BilateralANDflaccidweaknessofthelimbs
DecreasedorabsentDTRinweaklimbs(10%normal)
MonophasicillnesspatternANDintervalbetween
onsetandnadirofweaknessbetween12hand28days
andsubsequentplateau
CSF:Cytoalbuminologicdissociation
Electrophysiologic(EMG)findingsconsistentwithGBS
Absenceofanidentifiedalternativediagnosisfor
weakness.
BrightonCollaborationGBSWorkingGroup,
Vaccine,2011Jan10
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Differentialdiagnosis
Wide
Localizestoperipheralnerves
ratherthanbrainstem,spinal
cord,caudaequina,orNMJ,or
muscle.
presenceofdistalparesthesia
increasethelikelihoodof
correctdiagnosis
Ifsensoryinvolveisabsent,
shouldexcludepoliomyelitis,
MG,hyokalemia,botulismor
acutemyopathy.
Treatment
Monitoringofcardiacandpulmonarydysfunction
ECG,BP,SPO2,vitalcapacity,swallowingmonitored,
q2-4hrifprogressing,q6-12hrifstable
Insertionoftemporalcardiacpacemaker,useof
Mechanicalventilator,NGT
Preventionofpulmonaryembolism
Prophylacticuseofsubcutaneousheparin
Compressionstockings
Immunotherapy
NEngljmed366;24nejm.orgjune14,2012
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PulmonaryembolismandGBS?
Study:30casesofGBSreviewedinamedicalcenter,3
casesautopsy-provedPE,7additionalptsfulfilled
clinicaldiagnosisofPE.Conclusion:incidenceofPE
inGBS:33%.
PErecognizedafrequentcomplicationofGBS.
AdverseeffectsassociatedwithIVIGadministration
includedDVT/pulmonaryembolism,feverandrenal
failure,etc.
RamanTK,BlakeJA,HarrisTM.Chest.1971Dec;60(6):555-7.
PulmonaryembolisminLandry-Guillain-Barre-Strohlsyndrome.
Immunotherapy
ThemainmodalitiesoftherapyforGBSisImmunotherapy
include
PlasmaExchange(Plasmapheresis,PE)
Intravenousimmuneglobulin(IVIG)
Glucocorticoids:NOROLE!!
InaCochranesystematicreviewof6trialswith587ptshad
showncorticosteroidtherapyisineffectivefortreatingGBS.
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PlasmaExchange(PE)
Plasmaexchangewasthefirsttreatmentthatwasfoundto
beeffectiveinhasteningrecoveryinpatientswiththe
Guillain–Barrésyndrome.
Mosteffectivewhenitwasstartedwithinthefirst2weeks
afterdiseaseonsetinpatientswhowereunabletowalk.
Mechanism:plasmaexchangenonspecificallyremovesAbs
andcomplementandappearstobeassociatedwith
reducednervedamageandfasterclinicalimprovement
Theusualempiricalregimenis5exchangesoveraperiodof
2weeks,withatotalexchangeof5plasmavolumes.
PlasmaExchange(PE)
Plasmaexchangeisrecommendedforpatientswho
Unabletowalkunaided
Demonstrateworseningvitalcapacities
Requiremechanicalventilation
Havesignificantbulbarweakness
Asaresultofthecost,risk,anddiscomforttothepatient,
plasmaexchangeisgenerallynotusedforambulatory
patientswithmilddiseaseorforpatientswhosesymptoms
arenolongerprogressingafterthreeweeks
Thechoiceb/wplasmaexchangeandIVIGisdepon
availability,ptcontraindications,etc.Becauseofeaseof
administration,IVIGisfrequentlypreferred.Thecostand
efficacyofthe2treatmentsarecomparable.
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Intravenousimmuneglobulin(IVIG)
IVIGinitiatedwithin2weeksafterdiseaseonset,is
reportedtobeaboutaseffectiveasplasmaexchangein
patientswiththeGBSwhocannotwalkindependently
IVIghasreplacedplasmaexchangeasthepreferred
treatmentforsevereGBSinmosthospitalsbecauseof
itsgreaterconvenienceandavailability
Nodifferencebetweenthetwotreatmentsinthe
improvementindisabilityafter4weeks
Nosignificantdifferencebetweenthetwotreatmentswith
respecttodurationofmechanicalventilation,death,or
residualdisability
IVIG
Mechanism:immuneglobulinmayactbyneutralizing
pathogenicantibodiesandinhibitingautoantibody-
mediatedcomplementactivation,resultinginreduced
nerveinjuryandfasterclinicalimprovement.
TheregimenofIVIgalmostalwaysusedhasbeen0.4
g/kgperdayfor5days.
Trialsofcombiningtreatments,givingIVIgaftereither
plasmaexchangeorimmunoabsorptionhavefailedto
showextrabenefitcomparedwitheitheralone.
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Questions:
1.PEvsIVIg?Howtochoice?
2.DoesSequentialtreatmentwithPEfollowed
byIVIghaveasuperioreffecttoeitherRxalone?
3.What’sthetreatmentinthosewhodeteriorate
inspiteoftherapy?
Randomisedtrialof
plasmaexchange,
IVIG,andcombined
treatmentsin
Guillain-Barré
syndrome
Lancet1997;349:225–30
IntreatmentofsevereGBS
duringthefirst2weeks
afteronsetofneuropathic
symptoms,PEandIVIghad
equivalentefficacy.The
combinationofPEwith
IVIgdidnotconfera
significantadvantage.
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AmericanAcademyofNeurology(AAN)guideline
1.Treatmentwithplasmaexchange(PE)orintravenous
immunoglobulin(IVIg)hastensrecoveryfromGBS.
2.PEandIVIgareequallyeffectiveinpatientswithadvance
GBSsymptoms.
3.PEmaycarryagreaterriskofsideeffectsandismore
difficulttoadminister.
4.Combiningthetwotreatmentsisnotrecommended.
5.Steroidtreatmentisnotbeneficial.
AAN,2003
Studies
Thecombinationofplasmaexchangefollowedbyacourse
ofIVIGisnotsignificantlybetterthanPEorIVIGalone.
AlsothesubsequentPEfollowedIVIGisnotrecommended
,maywashouttheplasmaIVIGlevel.
AsecondcourseofIVIGinseverelyunresponsivepatients
wasreportedtobebeneficialinonestudy.
Emergingdrugs:
adaptedIVIgdosagesbasedonprognosticfactors
Specificimmunomodulation,includingcomplementinhibitors.
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Prognosis
65%canwalkindependently@6mos
Overall,80%usuallyrecovercompletely
5-10%haveprolongedcoursew/incompleterecovery,
~3%wheelchairbound
causingrespiratoryfailurerequiringventilationin
about25%,
Approx5%diedespiteICU(sepsis,PE,cardiacarrest)
85%haveresidualsymptoms,suchasfatigueandpain
2%willdevelopchronicrelapsingChronic
InflammatoryDemyelinatingPolyradiculoneuropathy
(CIDP)
AgeSexTreatmentPrognosis
132yFIVIG5dCompleterecovery
225yFIVIG5d+SteroidNearlycompleterecovery
350yMICUMV+IVIG+Steroid+PEDischargewithSequela
(4limbsMP:0)
458yMIVIG5dNearlycompleterecovery
559yFIVIG5dNearlycompleterecovery
624yFICUMV+IVIG+SteroidDischargewithsequela
(4limbsMP:4)
719yMIVIG5dCompleterecovery.
866yFIVIGImproved
Ourdepartment,inlast10years(2002~2012)
Age:19~66y66ySexex--M:F=3:525%needMV,75%completerecovery25%ismillerfishersyndrome
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Takehomemessage
1.GBSisanacuteimmunemediatedneuropathy,still
carriesagraveprognosis.
2.GBShasaclinicalfeatureofacuteflaccidparalysis.
3.Earlytreatmentisimportantfortheprognosisof
GBSalthoughearlydiagnosisisnoteasy.
4.IVIGandplasmaexchangehastensrecoveryfrom
GBS.
5.SecondcourseofIVIGcanbetryinseverely
unresponsivepatients.
6.SteroidisnotroleinAIDPbutusefulinCIDP.
References
NobuhiroYuki,Guillain–BarréSyndrome.nengljmed366;24
PlasmapheresisandacuteGuillain-Barresyndrome.TheGuillain-BarreSyndrome
StudyGroup.Neurology1984;2:1296.
Ropper,AH.TheGuillain-BarreSyndrome.NEnglJMed1992;326:1130.
Sumner,AJ.ThephysiologicbasisforsymptomsinGuillain-BarreSyndrome.Ann
Neurol1981;9Suppl:28.
FarcasP,AvnunL,FrisherS,HerishanuYO,WirguinI.Efficacyofrepeated
intravenousimmunoglobulininsevereunresponsiveGuillain-Barrésyndrome.
Lancet1997;350:1747.
PlasmaExchange/SandoglobulinGuillain-BarréSyndromeTrialGroup.
Randomisedtrialofplasmaexchange,intravenousimmunoglobulin,and
combinedtreatmentsinGuillain-Barrésyndrome.Lancet1997;349:225-30.
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Thankyouforyourattention!
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