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CNS malignancy (see Chapter 16). Big space-occupying tumors can cause AMS because of
elevatedintracranialpressureinmuchthesamewayasanintracerebralhemorrhage.Paraneoplastic
encephalitistendstopresentwithsubacutechangesinmemory,behavior,and/orpersonality,isoften
diagnosedpriortocancerdiagnosis,andisfrequentlyassociatedwithseizures.
Dementia (see Chapter 7). Whetherthe resultof amyloid accumulation,repeated vascular insult,
communicatinghydrocephalus,long-standingHIVinfection,oradozenothercauses,dementiatends
to present with gradual-onset and progressive AMS that can take the form of disorientation and
forgetfulnessaswellaspersonalityandmoodchanges.
Hypertensive encephalopathy. Sudden and severe rises inblood pressure that exceed the upper
limit of cerebral autoregulation can cause cerebral edema and subsequent neurologic deficits.
Gradual-onsetheadache,nausea,vomiting,restlessness,andconfusionarecommon.AnMRIcanbe
normal or show posterior bilateral white matter edema (if this sounds familiar, you are right.
Posteriorreversibleencephalopathysyndrome[PRES]andhypertensiveencephalopathyexistalong
thesamespectrum;someevenarguethatthedistinctionbetweenthetwoisirrelevant.Seepage117
foradiscussionofPRES).Symptomsshouldimprovewithgradualloweringofthepatient’sblood
pressure.
Non-NeurologicCausesofAMS
Thislistisalongonebutmanyoftheseconditionscanbeeasilyruledoutwithasimplebloodtest,urine
toxicologyscreen,orelectrocardiogram(ECG).AllofthesedisorderscancausesomedegreeofAMS;
thekeytorememberingthemliesintheirotherkeydistinguishingfeatures(associatepontine
demyelinationwiththerapiddevelopmentofhypernatremia,forinstance,graylinesonthefingernails
witharsenicpoisoning,etc)
Metabolicderangements
Hypo- and hyperglycemia. Both hypo- andhyperglycemiacanpresentwithconfusion,lethargy,and agitation. Theycanboth
also present with focal neurologic deficits as well as seizures: hypoglycemic seizures tend to be generalized and are often
precededbydiaphoresisandtachycardia;hyperglycemicseizuresaremostoftenfocalmotorseizures.
Hypo-andhypernatremia. Ingeneral, AMSisassociatedwithabnormal sodiumlevels onlyinthesettingofrapidchangesin
sodium; patients with chronic hypo- or hypernatremia are often asymptomatic. The rapid development of hyponatremia can
cause diffuse cerebraledema, whereas therapiddevelopment ofhypernatremia cancause osmotic demyelination syndrome
(ODS;previouslycalledcentralpontinemyelinolysis).ODSusuallypresentsseveraldaysafterabruptcorrectionofhyponatremia
and can cause corticospinal dysfunction (including weakness and hyperreflexia), corticobulbar dysfunction (dysarthria,
pseudobulbar palsy), generalized confusion and, when severe, seizures and even coma. MRI can show both pontine and
extrapontinedemyelinatinglesions,butthesechangesmaynotappearforseveralweeks.
Hypo-andhypercalcemia.Tetany,aformofneuromuscularirritabilitythatischaracterizedbyperioralnumbness,paresthesias,
andmuscle spasms, isthehallmarkofhypocalcemia,which canalsocause nonspecificmental statuschangessuchaslethargy,
irritability,anxiety,anddepression.Bothgeneralizedandfocalseizures,aswellasQTprolongationon theECG,canalsooccur.
Hypercalcemia is also associated with anxiety, depression, and generalized cognitive dysfunction, as well as gastrointestinal
symptoms(nausea,anorexia,constipation)andrenaldysfunction(polyuria,nephrolithiasis).
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(A)AnMRIshowingsubtleFLAIRhyperintensityinthepons(arrow)consistentwithODS.Notethatthelesionis
centeredinthemiddleofthepons,helpingtodis tinguishitfrom(B)stroke(arrow),whichis typicallyunilateral
(sincethepontineperforatingarteries,whichcomeoffthebas ilar,supplyeithertherightorleftpons ).(A,modified
fromKleinJ,Vins onEN,BrantWE,Helm s CA.BrantandHelms’FundamentalsofDiagnosticRadiology.5thed.
WoltersKluwer;2018;andB,reprintedfromKataokaS,HoriA,ShirakawaT,Hiros eG.Paramedianpontine
infarction.Neurological/topographicalcorrelation.Stroke.1997;28(4):809-815.)
Box15.2
Ahelpfulmnem onicwelearnedinmedicalschoolandhavereliedoneversince:fromhigh(sodium )tolow(sodium),thebrainwillblow
(i.e.,cerebraledem a),fromlowtohigh,thepons willdie(ODS).
Box15.3ChvostekandTrousseauSigns
These are classic form s of tetanythatyoucan assess on your examination. Chvostek sign refers to contraction ofipsilateral facial
musclesinducedbytappingthefacialnervejus tinfrontoftheear.Trouss eaus igniscarpopedalspasm(i.e.,involuntarycontractionof
muscleswithinthefootor,morecom m only,thehand)inducedbyinflationofabloodpressurecuff.
Chvostek(A)andTrousseau(B)signs .
Box15.4
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Didyou notice thathypo-andhyperkalemiado notappear onthis listofm etabolicdisordersthatcan cause AMS? Althoughcertainly
dangerousintheirownright,changesinpotas s iumconcentrationdonotdirectlyaffectthebrain.
Hypo- and hyperthyroidism.Themanifestations of thyroiddisease are highlyvariableand dependentonthepatient’s ageas
wellastheacuityandseverityofthethyroiddisorder.Hypothyroidismistypicallyassociatedwithfatigueandlethargy(aswellas
cold intolerance,weight gain,constipation, dryskin,andbradycardia),whereas hyperthyroidismis associatedwithanxietyand
emotionallability(aswellasheatintolerance,weightloss,tremor,palpitations,andtachycardia).Bothhypo-andhyperthyroidism
cancauseanoninflammatorymyopathycharacterizedbythesubacute-onsetofpredominantlyproximalweakness.Interestingly,
from a neurologicstandpoint—if a bit beyondthe scopeofthis book—hyperthyroidism canalsocause a formof hypokalemic
periodic paralysis in which patients present with sudden attacks of painless muscle weakness, and hypothyroidism can be
associated with pseudomyotonia (defined as abnormally slow muscle relaxation following mechanical or electrical muscle
stimulation). Hypothyroidismisalsoa relatively common cause of carpaltunnelsyndrome,a result of accumulationof matrix
substanceonandaroundthemediannerve.
Hepaticencephalopathy.Hepaticencephalopathycanpresentacutelyinthesettingoffulminantliverfailure(inwhichcaseit
canbeassociatedwiththe rapidanddangerousdevelopment ofcerebraledema), oritcanwaxand wane,smolderingbeneath
thesurfaceuntiltriggeredbyastresssuchasdehydration,infection,narcotics,benzodiazepines,ormedicationnoncompliancein
patients with underlying chronic liver disease. Early symptoms include irritability, apathy, and altered sleep patterns; AMS,
agitation,andcomamaydevelopinmoreseverecases.Asterixis—aformofnegativemyoclonuscharacterizedbysudden,brief,
and involuntary loss of muscle tone in the hand when the wrist is extended—is the characteristic examination finding. The
diagnosis is clinical.Although the serumammonialevel can be andofteniselevated, the ammonia level does notnecessarily
correlatewiththeclinical pictureand,inmostcases,doesnotneedtobechecked.Treatmentinvolvesidentifyingandremoving
triggers,aswellastheuseofmedicationssuchaslactuloseandrifaximin.
As terixisis bynomeans pathognomonicofliverdiseas e;itcanals obeasignofrenalfailure,metabolic
derangements,andvarious medications.
Uremic encephalopathy. Uremic encephalopathy presents similarly to hepatic encephalopathy and can be associated with
irritability, disorientation, seizures, tremor, and asterixis. The onset and severity generally parallel the degree of azotemia.
Treatmentiswithhemodialysis,butthereisoftenalagtimeofhourstoseveraldayspost-dialysisbeforementalstatusclears.
AlcoholUseDisorder
Long-standingalcoholabusecanresultinthiamine(B1)deficiency,whichcanpresentacutelyas We rnicke ence phalopathy
or chronically as Korsakoff syndrome. The classic triad of Wernicke encephalopathy consists of ophthalmoplegia
(nystagmus, oculomotor cranial nerve palsies),gait ataxia, and, yes,encephalopathy (often characterized by disorientation,
inattentiveness, andapathy) butisactually the exceptionrather thanthe rule:onlyabout one-thirdof patients presentwith all
threefindings.Thediagnosisispredominantlyclinical.Thiaminelevels are oftenlow (but theydon’t have tobe),andMRIcan
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show(butdoesn’thavetoshow)T2hyperintensityinvolvingthemammillarybodiesand/orbilateralthalami.Onequickpearlthat
comesupoften, especiallyintheemergencydepartment:Wernickeencephalopathycanbeprecipitatedin patientswithbaseline
low levels of thiamine by giving glucose prior to thiamine repletion, so be careful! Treatment is with immediate high-dose
intravenousthiamine.KorsakoffsyndromeusuallyoccursasaconsequenceofuntreatedWernickeencephalopathyandpresents
withdeficitsinbothanterogradeandretrogradememory.Confabulation—inwhichpatientsunconsciouslyfillingapsinmemory
withdistortedorentirelyfabricatedinformation—isaclassicfeature.
Box15.5ThiamineDeficiency
Othercauses ofthiamine(B1)deficiencythatcanres ultinWernickeencephalopathyandKors akoffsyndromeincludechronicallypoor
nutrition (e.g., patients with anorexia and patients receiving prolonged intravenous feeding without appropriate supplem entation),
hem odialysis (due to increasedlos s ofwater-s oluble vitamins ),and hyperem esis ofpregnancy.Remember, thiamine deficiencycan
als ocausealength-dependentsensorimotorpolyneuropathy(seepage282).
Box15.6AlcoholWithdrawal
Seizuresassociatedwithalcoholwithdrawaltendtooccurwithinthefirs t12to48hours afterthelas tdrink,whereasdelirium tremens
(or DTs, characterized by tachycardia, hypertens ion, and hallucinations ) presents later, within 48 to 96 hours. Long-acting
benzodiazepines ,includingdiazepam andchlordiazepoxide,arestandardtreatmentformildwithdrawalsymptom s andareusedtohelp
preventprogressiontoseizures andDTs .
Medicationoverdoseandwithdrawal
Benzodiazepines. Benzodiazepinesworkbyincreasingthefrequency of GABAa chloridechannel op ening.Commonsideeffectsinclude sedation,
amnesia, and delirium, especially in elderly p atients. Benzodiazepine overdose presents with depressed mental status, ataxia, dysarthria, and
nystagmus. Unlikeopioidintoxication, benzodiazepines do not causepupillary changes or significant resp iratory depression. Treatment is with
flumaz enil(aGABAantagonist),whichmustbeusedcarefullybecauseitcanrapidlylowert hethresholdforseizure.Benzodiazepinewithdrawal—
like alcohol withdrawal—can be life-t hreatening, and—again like alcohol withdrawal—presents with tachycardia, hy p ertension, hy p erpyrexia,
tremor,andseizures.Treatmentis,logically,withbenzodiazepines,followedbyaslowtaper.
Box15.7
Ahelpfulmnemonic:benZodiazepinesincreasethefrequenZofGABAachannel opening.Barbiturates,ontheother hand,increasethedurationofGABAachannel opening.
Opioids. Opioids act on opioid (or mu) recept ors. There areseveraltypes of opioids:natural opiates (which includemorphine and codeine),
semisyntheticop ioids(e.g.,dextromethorphan),andfully sy nt heticop ioids(e.g.,methadoneandfentanyl).Opioidoverdosecanbelife-threatening
andpresentswithpinpointp up ils,depressedmentalstatus,bradycardia,andresp iratory depression.Treatmentiswithnaloxone,anopioidreceptor
antagonist .Opioidwithdrawal—althoughmiserableforthep atient—israrely(butnotnever)life-threatening;sy mptoms,whichtendtopeakwithin
about72hoursofthelastdose,includedilat edp up ils,fever,yawning,rhinorrhea,lacrimation,nausea,vomiting,anddiarrhea.Opioidagonists(such
as methadone and buprenorphine) are standard t reatment. Clonidine (an alpha-2adrenergicreceptor agonist) can also help mitigatethepatient’s
symptoms.
Recreationaldrugs
Marijuana.Marijuanaisderivedfromt hecannabisplantandcontainsinvaryingratiostwonaturalcomp ounds:tetrahy drocannabinol(THC),which
isthep rimarypsychoactivecomponent,andcannabidiol(CBD),whichhaslessp sychoactiveactivityandisnowsoldsep aratelythroughout much
oftheworldintheformofsupplement s,gummies,oils,bubblebath,lotions,andmore.Activityismediatedviathecannabinoidreceptors,CB1and
CB2,inthecentralandperipheralnervoussystems.Conjunctivalinject ion,socialwithdrawal,paranoia,drymouth,tachycardia,increasedappetite
(colloquiallyknownas“themunchies”),andevenp sychosiscanbecharacteristicofmarijuanaintoxication.Sympt omsofwithdrawalcanlastuptoa
weekandincludedepressedmood,irritabilit y,anorexia,nausea,andinsomnia.
Hallucinogens.Hallucinogens,includingmescaline,p silocybin,andlysergicaciddiethylamide(LSD),actasserotoninagonistsandcancausealtered
percep tion (in t he form of visual hallucinations, dist ortions of time and sp ace, and sy nest hesias [see Box 15.8]), eup horia, anxiety, panic,and
paranoia.M ilddysautonomia—tachycardia,hy pertension,andmydriasis—oftenaccompaniesthesesy mp toms.Therearenowithdrawalsy mptoms
(hallucinogens are not addictive drugs) although p eople can experience “flashbacks” later in life, characterized by a recurrence of symptoms
mimickingp riorhallucinogenuse.
Box15.8Synesthesia
Synesthesiaisaphenomenonin whichstimulati onofonesensory pathwayresultsinactivationofanother.For peoplewithsynesthesia,lettersornumbersmaybeperceivedasinher entl ycolored:“a”mightbered,
“2”blue,etc.Synesthetes,aspeoplewith synesthesia arecalled, maytastemusic,hearpain, orvisual izespecificconcepts—like mathematicaleq uati onsoruni tsoftime—asshapesfloating aroundthem.The
conditionisnotwellunder stoodbutmorecommonthanpreviouslythought;i thasbeensug g estedthatupto1inevery300peoplehassome form ofit.Vladimi rNabokov1,authorofLoli ta,Ada,andPaleFire, and
physicistRichardFeynmanar ebothbelievedtohavebeensynesthetes.
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Twosynesthetes:(A)VladimirNabokovand(B)RichardFeynman.
1
Hiswifeandsonalsoweresynesthetes!
3,4-methylenedioxyamphetamine(MDMA). M DM Ais a p sychostimulantthatcombines t hedopaminergicandadrenergiceffectsofamphetamines
withtheserotonergiceffectsofhallucinogens.EcstasyandM ollyarecolloquialtermsforM DM A.Thesearepopularrecreat ionaldrugs—they are
usedascommonly asamphetaminesandcocaine—inpartbecauseofthemisapp rehensionthatM DM Aisrelatively safe.Euphoria,empathy toward
others, sexual arousal,disinhibition,andpsychedelicmanifestationsaret hemain effects. However,sideeffectsarecommon, andthedrugaccounts
forover20,000emergencyroomvisitsannually.M inorsideeffectsarepredictable andinclude anxiety,insomnia,excessivethirst ,lossofapp etite,
fever, and teeth grinding (bruxism). Overdose can cause dramatic increases in blood pressure (hypertensive crisis) and body temperature
(hyperthermia),hyponatremia,cardiacarrhythmias,seizures,p sy chosis,anddeath.Inaddition,becauseMDM Aiscurrentlyillegalandunregulated,
thesepopulardrugsmaybelacedwith otherdrugs.It isunclearexactly howaddictiveM DM Ais,but currentliteraturesuggest s thatrepeateduse
canleadt o tolerance and dependence,andwithdrawal canbeassociatedwith fatigue, insomnia,depression, suicidalthoughts,andexacerbationof
underlyingmooddisorders.
Phencyclidine. Phencyclidine(PCP) acts as an NMDAreceptor antagonist. PCP intoxication canpresent with aggressive or belligerent behavior,
ataxia,verticalorrotatory nystagmus,mydriasis,t achycardia,andhypertension.Thereisnospecifictreatment,butplacingpatientsinaquiet,dark
roomcanhelp. Benzodiazepinesandantipsychoticscanbeusedto help managebehavioralsy mptoms. PCP,like LSD,is notanaddictivedrug,so
thereareno associatedwithdrawalsympt oms. Ketamine isaPCP analogue that is nowusedas bothananestheticandat reatment for refractory
depression.
Box15.9ChasingtheDragon
“Chasingthedr agon”isaspecificmethodof heroin usethatinvolvesvaporizingandtheninhal ingthedrug.Thistechniq uecancauseararebutpotentiallydevastating formof spong iformleukoencephalopathy
(i.e.,whitematter—leuko—inthebr ain—encephalo—isdamaged—pathy).Initialsymptomsincludeconfusionandrestlessnessandcanprogr essto muscl espasms,general izedparesis,centralfevers,andeven
death.
Heavymetalpoisoning
Lead.Theeffectsofacuteleadp oisoningdependonboththeageofthep atientandthedegreeofleadabsorpt ion.Sourcesofleadincludeoldhouses
(the U.S.banned lead-basedp aint in 1978) andceramic dishes with chippedpaint, as wellas battery andcarfactories. T he mnemonic LEAD is
helpfultorememberthecharacteristicfeaturesofleadpoisoning:Leadlinesont hegingivaandmet aphysesoflongbones,Encep halopathy(memory
loss, confusion, headaches), Abdominal discomfort (as well as Anemia and Arthralgias), and Drops (wrist or foot drops, due t o ext ensor muscle
weakness).Childrencanpresentwithp icabehaviors(eatingitemsnotnormallyconsideredfood,suchasdirtorgrass)andlearningdelays.Long-term
consequences includerenal, cardiovascular,andcognitivedysfunction.Treatmentincludesremoval ofthesourceand/orremovalofthep atientfrom
exp osure,aswellaschelationtherapy (EDTA,DM SA,dimercap rol).
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Leadlines(whitearrows)visibleonx-rayonthebonesofthelowerextremities.(Modi fiedfromHenr etigFM.Atoddlerinstatusepilepticus.In:Oster houdtKC,Perr oneJ,DeRoos
F,etal.,eds.Toxicologypearls.Hanley&Belfus;2004:S2-S5.)
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Mercury.Sourcesofmercury exp osureincludemet alrefineries,goldmining,batteryfactories,papermanufacturing,anddentistry (amalgamfillings,
whicharestillusedworldwide,canreleasesmallamountsofelementalmercury,particularly inp atientswho grindtheirt eeth).M ercuryp oisoning
presents acutely withshortness ofbreath,cough, chest p ain,nausea,vomiting,dy sp nea,guminflammation,dermatitis,andconjunctivitis.Chronic
exp osure cancause p ersonality changes and memory loss. Treatment consists of supportive care, removalof exposure, and—incertaincases—
chelatingagents.
Arsenic.Sources include contaminated water (arseniccan seep out of soil and rocks into water and wells) and workp laceexp osure (p rimarily
inhalation of arsenic dust in refining factories). Acute poisoning can present with abdominal pain, nausea, and diarrhea which can lead to
hypovolemia. Cardiac arrhythmias and shock can occur in severe cases. Chronic sy mp toms include a sy mmetricsensorimotor p olyneuropathy,
cognitivedysfunction,andseizures,as well as theap p earance ofgray lineson thefingernailsandp igmentationaroundtheaxilla.Arsenicexp osure
also p redisp oses t o various types of cancer, including skin, bladder, lung, liver, and renal cancer. Acute p oisoningoften requires advanced life
support;chelationwithdimercap rolorDM SAcanbeusefulforbothacuteandchronicexposure.
OtherCauses
Hypoxiaandhypercapnea.Bothhypoxiaandhypercapneacancauseencephalopathy,oftenintheformoflethargy,confusion,
andmemory lossthatare most likely the result of cerebralvasodilationandincreasedcerebralblood flow leadingtoelevated
intracranialpressure.ThedegreeofCO2retentionseemstocorrelatebestwiththedegreeofneurologicdysfunction.
Cardiaccauses.Confusionordepressedmentalstatuscanbetheinitialpresentationofmyocardialinfarctionordecompensated
heart failure, particularly in elderly patients. A careful physical examination and an ECG can quickly assess any underlying
cardiacdisease.
Systemicinfection. Anysystemic infection(pneumonia,urinarytract infection, cellulitis, etc.) cancause AMS,particularly in
theelderlyorotherwisefragilepatients.
Primary psychiatric causes. In patients with established diagnoses of psychiatric conditions such as bipolar depression or
schizophrenia,it canbe relativelystraightforwardto attributeAMStoa primarypsychiatriccause. In patients presentingwith
newpsychoticsymptoms,however,thedifferentialshouldremainbroad;itisoftenonlyafteracomprehensiveworkup(including
basicbloodtests,urinetoxicologyscreen,lumbarpuncture,brainimaging,andsoforth,dependingonpresentation)thataprimary
psychiatricdiagnosiscanbeconvincinglyestablished.
SummaryofNon-NeurologicCausesofAMS
Category Examples
Metabolic
derangement
hypo-andhyperglycemia,hypo-andhypernatremia,hypo-andhypercalcemia,
hypo-andhyperthyroidism,hepaticanduremicencephalopathy
Alcoholuse
disorder
Medicationoverdose
andwithdrawal
benzodiazepines,
opioids
Recreational
drugs
marijuana,hallucinogens,MDMA,PCP
Heavymetal
poisoning
lead,mercury,arsenic
Other
causes
hypoxiaandhypercapnea,cardiaccauses,systemicinfection,primarypsychiatric
causes
AMS:EvaluationinaNutshell
Wewarnedyou:itisalongdifferential.Butmanyofthesepotentialcausescanbequicklyandeasily
ruledout.ThekeyistofilethislistawayandrefertoitwheneveryouareevaluatingapatientwithAMS.
Thebiggestmistakeyoucanmakeistoarrivetooquicklyorcarelesslyatananswer.Beawareof
inherentbias:justbecauseapatienthasahistoryofdrugusedoesnotmeanthatheorshecannotalso
haveanunderlyingmalignancyorastroke.Approacheachcasesystematically:takeacarefulhistory
(gettingasolidsenseofthepatient’sbaselinecognitivefunctioniscrucial!),performadetailed
examinationandreviewofpertinentlaboratorydata,andaskforrelevantimagingforpatientswithnew
focalityontheirexamination.Involveotherservicesandphysicians:theworkupofthesepatientsoften
requiresteamworkacrosssubspecialties.Pushyourselftothinkthroughthefulldifferential.Finally,
understandthatyoudonotalwaysneedtoarriveatanimmediateandspecificanswer.Oftenthebestthing
thatneurologistscandoforpatientswithAMSistocomprehensivelyruleoutthebigdo-not-miss
neurologicdiagnoses.
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Follow-uponYourPatient:Onyourwaytotheemergencydepartmentyou’vequickly
thoughtthroughtheAMSdifferential,sowhenyoumeetDonaldandhiswifeyouareready.
YoudoaquickexaminationasyouwaitfortheCTscanner—heis,indeed,unresponsiveto
voicebutperksupwithstrongnailbedpressure.Younotethathisgazeismidline,hetracks
youasyouspeak,andheismovingallfourextremitiesequally.Withinaminuteortwo,and
withrepeatedprompting,heisabletotellyouhisname,recognizehiswife,andnameafew
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simpleobjects.Hecanfollowone-stepcommandsbuthastroublewithtwo-stepcommands.
Asheispositionedinthescanner,youtaketheopportunitytotalktohiswife.Shetellsyou
heis“fine”atbaseline,althoughshedoesn’tliketoleavehimhomealoneforextended
periodsoftimebecauseonceortwicehehasforgottentoturnoffthestove.Hetakesa
beta-blockerandantibioticsforhisUTI.Hewasalsorecentlygivena“sleepingpill”byhis
friendandtookoneortwolastnightforthefirsttimebecausehecouldn’tfallasleep.TheCT
showsgeneralizedatrophybutisotherwiseunremarkable.Whenyoureexaminehim,heis
evenmoreawakeandisnowabletotellyouwhereheisandcancountbackward—slowly
butcorrectly—from20.
Yourassessmentatthispointisthatheisagraduallyimprovingencephalopathicpatient:hehas
nothingfocalonexamination,andyoususpectthatthesleepingpill(probablyabenzodiazepineor
nonbenzodiazepinesedativehypnoticlikezolpidem)hastriggeredthisevent,itseffectssuperimposed
onanalreadyvulnerablecognitivebaseline(hisage,suspectedunderlyingcognitiveimpairment,
recentinfection,andantibiotictreatmentallputhimatrisk).Withinafewhours,hehasreturnedfully
tohiscognitivebaseline,andhisurinetoxicologyscreencomesbackpositiveforbenzodiazepines.
Youdiscusstherisksofsleepingmedicationswithhimandhiswife,andheisdischargedhome.
Younowknow:
1. Themostcommonanddo-not-misscausesofAMS.
2. Thataphasiaandencephalopathyareeasilyconfusedbutcriticaltodistinguishfromeachother.Encephalopathygenerallypresentswith
globalconfusionandinattentiononexamination,whereasaphasiaisafocaldeficitthatpresentswithdifficultyunderstanding,producing,
and/orrepeatinglanguage.Aphasicpatientsarenottypicallyinattentiveandoftenappearfrustratedbytheirdeficits.
3. Howtoevaluatea patientwithAMS. Acareful historyandexaminationare crucial,andbasiclaboratorytests andimagingcanhelp
diagnose—or,justasimportantly—helpcrossthingsoffyourdifferential,whenindicated.
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16Neuro-Oncology
Inthischapter,youwilllearn:
1. All about the most common primary brain tumors, including glial tumors (such as
glioblastomas),neuronaltumors(suchasneuroblastomas),andprimaryCNSlymphoma
2. How to differentiateamong colloid, dermoid,epidermoid, and arachnoidcysts, and when
andhowtheseotherwisebenigncystscancausetrouble
3. Aboutparaneoplasticsyndromes,theirassociatedantibodies,andtreatments
4. About immune checkpoint inhibitors: how they work, and how they can causepotentially
dangerousneurologictoxicity
CASE16
YourPatient:Zhara,a58-year-oldhumanresourcesspecialistwithnopastmedicalhistory,
presentstotheemergencydepartmentwithsudden-onsetleftarmweaknessthatbegan
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