Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4693_Библиотеки_им_академика_М_И_Перельмана
.pdf
MostcliniciansrecognizetheexistenceofsecondaryBMS—painrelatedtoanorganiccausesuchasa
systemicdisease—andprimaryBMS,whichistheneuropathicphenomenon.
26
Aninterestingquestionis
whether thereis overlap betweenthetwo: is the developmentofneuropathicchangesassociated with
primaryBMSrelatedtoalocalorsystemicdisease?SuarezandClark
26
reportthatBMSismorefrequent
inwomenwithsystemicdiseases.RecentliteratureonSjögrensyndrome,acommonautoimmunedisease
affectingmorewomenthanmen,indicatesthatperipheralneuropathiesareamongthemostcommonnon-
glandmanifestations.
27
Theprevalenceofperipheralneuropathyisunknown,buthasbeenestimatedat5
to20%.
27
Althoughthegeneralprevalenceofsmall-fiberneuropathy,suchasthatdescribedbyLauria,
10
isunknown,onestudyassessingskinbiopsiesfoundthatmeanintraepidermalnervefiberinnervationwas
considerablylowerinpatientswithSjögrensyndromethanin age-andsex-matchedcontrols.
28
Thisis
similar to thefindings ofreduced epithelial nervedensity reported byLauria etal
10
Like treatment of
BMS,treatmentofneuropathyassociatedwithSjögrensyndromecanincludeantiepilepticdrugs(AED)
andantidepressantsusedasadjuvantanalgesics.
27
Recent literature has also suggested that BMS may be caused by mast-cell activation disorder.
29
However,itislikelythatthestudy,basedonthreecases,describessecondaryBMSratherthanprimary
BMS, given that these cases did not respond to AED and antidepressant medication but responded
dramaticallytononsteroidal anti-inflammatorydrugs andhistamineactingmedications.
29
Therefore,itis
morelikelythatmast-celldisordersarepartofthedifferentialdiagnosisforBMSratherthanacausefor
primaryBMS.
29
Anothersuggestionhasbeenanassociation betweenzincdeficiencyandthe pathogenesisofBMS.
30
Choetalreportedthatzincdeficiencywaspresentin~27%ofpatientswithBMS,andthatpainscoresin
suchpatients whoweretreatedwithzinc replacementimproved significantlycomparedwiththose ofa
controlgroup.
30
An animalmodelhassuggestedthat zincdeficiencycauseshistological changesinthe
tongue,butitisuncertainhowthisisassociatedwithneuropathy.
30
Ithasbeensuggestedthatneuropathicpainbeginsperipherallyandprogressestocentralsensitization.
Jääskeläinen, whohasdone much ofthe quantitative sensorytesting workinBMS,suggeststhatBMS
encompasses changes in both the peripheral trigeminal nerve and in central pathways.
18
While
conventionalimagingsuchasmagneticresonanceimagingmayfailtodetecttrigeminalpathology,itmay
beevidentonsensorytesting.
18
OntestingheatsensationthresholdsandpaininBMS,changeswerefound
inthemouthaswellasdistallocations,suggestingthatBMSmaybeassociatedwithdisseminatedsmall-
fibernervechanges.
18
Centrally,blink-reflextestingsuggestsaroleforthestriataldopaminergicsystem
inBMS pain.
18
Overall, sensory data suggest that both peripheral and central nervous system (CNS)
changesarepresent,butdonotpinpointthelocationofspecificchangesinthesomatosensorysystem.
18,26
TasteChanges
Bartoshuk’s group have demonstrated the convergence of taste sensation and pain both clinically and
experimentally.
30,31
Thechordatympaninerve(cranialnerveVII)leavesthetonguewiththelingualnerve
(cranial nerveV)andtravelsthroughthe pterygomandibularspace.Theinferioralveolarnerve(cranial
nerve V), which conveys sensation from the lower teeth, also passes through this same space. Often,
anesthesia of the inferior alveolar andlingual nerves required for dental procedures abolishes touch,
pain,andalsotastesensationsontheinjectedside.Thechordatympaniandlingualnervesseparateand
thechordatympanipassesthroughthemiddleear.Researchers
30,32–34
havedemonstratedthatanesthesia
ofthechordatympanibehind thetympanicmembrane intensifies tastesfrom thearea innervated bythe
glossopharyngeal nerve (cranial nerve IX)—the posterior aspect of thetongue onthe opposite side—
supporting a model of central inhibition between the chorda tympani and glossopharyngeal nerves.
AccordingtoBartoshuk’sgroup,reducedinputintotheCNSfromonetastenervereleasesinhibitionof
othertastes,resultinginthesetastesbeingintensified.
30
Tie etal
35
foundthat anesthesia ofthe chorda tympani canintensify capsaicin-induced pain on the
contralateralanteriortongue,suggestingthepresenceofcentralinhibitoryinteractionsbetweentasteand
oral pain. Furthermore, the intensification of pain was found to be related to an individual’s genetic
ability to taste 6-n-propylthiouracil (PROP), an extremely bitter compound, with the greatest
intensificationfoundin“super-tasters”(mainlyfemales)whoreportthemostbittersensationfromPROP
testing.
36
Basedon thesetaste–paininteractions,itis believed thatsomecases ofBMScouldbetheresultof
tastedamage,toeitherthechordatympani,withreleaseofinhibitionintheglossopharyngealnerve(taste
alterations,alterationsintouchandpain),orthetrigeminalnerve(changesintouchandpain).Consistent
withthismodel,tastedamagehasbeenfoundinmanypatientswithBMS.Notably,theintensityofpeak
oral painwasfoundtocorrelatewiththe densityoffungiformpapillae, with thegreatestdensitybeing
foundinpatientswithBMSwhowereprimarilysupertasters.
31,37
AccordingtoBartoshuk’sgroup,
30
iftastedamageproducesasufficientlossoftheinhibitionnormally
exerted on central structures mediating oral pain, then centrally acting medications that are known to
impactonpain,suchaspregabalin,mayamelioratethelossofinhibitionandrelievethepainofBMS.
SpatialTasteTesting
Taste on the tongue is innervated by the branches of the facial nerve (cranial nerve VII) and the
glossopharyngealnerve(cranialnerveIX),whichservedifferentregionsofthetongue.Often,changesto
tasteinpatientswithBMSmayoccurinoneareabutnotanother.
7
Asaresult,tastedamagepresentsasa
regionalphenomenonandrarelyasawhole-mouthphenomenon.
38
Therefore,spatialtastetestingisperformedtoassessperceivedtasteintensityforsweet,sour,salty,
andbittersolutionsappliedwith cottonsswabs,filterpaper,or dropsattheanteriortonguetipandthe
circumvallatepapillae,onboth leftand rightsides. Patientsratethe qualityandintensityofthe stimuli
usingavalidatedpsychometricscale,thegenerallabeledmagnitudescale—amodifiednumericscale.
39
Treatment
TherapyforBMSinvolvestheuseofcentrallyactingmedicationsforneuropathicpain,suchastricyclic
antidepressants, benzodiazepines, or gabapentinoids,
40
and recently paroxetine.
41
To our knowledge,
pregabalin has yet to be studied in BMS, but, in view of its success in the treatment of neuropathic
conditions,thismedicationmightprovideanadditionalapproachtothetreatmentofbothpainandtaste
disturbancesassociatedwithBMS.Limitedtrialstodatesupporttheuseoflowdoseclonazepam(0.25to
0.75mg)ortricyclicanti-depressants(10to40mg),includingamitriptyline,desipramine,nortriptyline,
imipramine clomipramine, or the selective serotonin reuptake inhibitor paroxetine. Clonazepam is a
benzodiazepineusedeithertopicallyorsystemically,
2,42,43
whichappearstohaveexcellentefficacyinthe
relief of BMS symptoms. In view of only partial or lack of response in some patients with BMS,
gabapentin has been used in combinationwith clonazepam with apparent anecdotal success.
1
Topical
medications, including clonidine and capsaicin, may be considered for application to local sites.
Systemic use of capsaicin has also been suggested,
44
as has α-lipoic acid with or without
psychotherapy.
45
Zinc supplementation for patients with diagnosed zinc deficiency has also been
proposed,withsignificantreliefreported.
30
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
QualitativeTasteDisorder:Dysgeusia
Qualitative taste disorders result from similar causes to quantitative taste disorders. The major
differenceisthatdysgeusiasaredifficulttomeasure,althoughtheymayproduceseverediscomfortin
dailylife.Treatmentisproblematic.
Thetermdysgeusiaisusedtodescribecertaindistortionsintaste:eitherthatpatientsperceiveanytaste
asbitter,salty,sour,metallic, or astringent;or that patients suffer fromamore-or-less continuoustaste
sensation, such as the continuous presence of bitter taste. These taste distortions are also termed
qualitative taste disorders. Accordingly, these “colorful” cases may include patients with normal
gustatoryfunction froma quantitative pointofview, butthey canbe extremely distressingforpatients,
resulting in weight loss and symptoms of depression.
46
Sweet dysgeusia deserves special mention
becauseithasoftenbeenreportedtooccurwithneoplasmsinthethoraxandalsowithmyastheniagravis
(e.g.,refs.47,48).Otherthanthat,causesofqualitativetastedisordersaresimilartothoseofquantitative
tasteloss.Manydrugs that can potentially causetasteproblemshavebeenidentified.
49,50
Among many
others,AEDs
51
andantihypertensives
52
shouldbeconsideredaspotentialcausesofgustatorydysfunction.
Lesionsofthe peripheral nervoussystemmayalso beresponsible,forexampleafterdentalsurgeryor
tonsillectomy; dysgeusia can also occur as part of syndromes affecting the facial (most frequent),
glossopharyngeal,orvagalnerves,e.g.,idiopathiccranialnerveVIIpalsy(Bellpalsy).
53
Othercausesof
cranial nerve lesions have to be considered (e.g., neuroborreliosis or zoster, processes in the
cerebellopontine angle,
49,53
or dissection of cervical arteries).
54
Central causes of dysgeusia include
lesionsalongthetastepathwayfromthebrainstemtoitscorticalrepresentation.Brainstemtastedisorders
(ipsilateral disturbance) may be due to demyelinating processes, ischemia or hemorrhage, or vascular
lesions.
55
Thalamiclesionsarealsoknowntoresultintastedisorders,
56
andcorticaltastedisordershave
beendescribedinepilepsy.
57
Therapeuticapproachesaresimilartothoseforquantitativetasteloss(see
p. 185). Studies of zinc in patients with idiopathic dysgeusia reported significant improvement
58,59
;
however,suchimprovementwasnotseenincancerpatientswithdysgeusiarelatedtoradiotherapyofthe
oropharynx.
60
QualitativeSmellDisorder:ParosmiaandPhantosmia
Parosmia and phantosmia are almostalwaysaccompanied bysmell loss. As withdysgeusia, they
cannotbequantified,whichemphasizesthesignificanceofthemedicalhistory.Asimpleassessment
relatestothefrequencyandintensityofthesymptomsandtheirconsequencesfordailylife.
Some patients not only suffer from quantitative olfactory disorders, but also experience qualitative
olfactory dysfunction. These odor distortions can be roughly divided into parosmias (also called
“troposmia”)andphantosmias.
61
Whenpatientsreportparosmia,theyperceiveinhaledodorantstohavea
differentsmellfromhowtheyrememberit.Phantosmia,ontheotherhand,indicatestheperceptionofan
odor when no odorous source is present. Both parosmic and phantosmic sensations are typically
described as unpleasant, e.g., “burned,” “foul,” “rotten,” “fecal,” or “chemical” smells.
61–63
While
phantosmia appears to be a relatively rare symptom, parosmia is a frequent finding in patients with
olfactorysystemsinastateofregenerationordegeneration.
64
Itsfrequencyhasbeenestimatedtorange
from10to60%amongpatientswitholfactorydysfunction.
62,64,65
Thepathogenesisofparosmiaandphantosmiaisunclear.Bothperipheralandcentralcauseshavebeen
discussed
61,66
that may be considered to lead to olfactory distortions.
63
Psychiatric causes need to be
excluded (e.g., olfactory reference syndrome).
67
One of the most attractive explanations of parosmia
relatestothelossofolfactoryreceptorneurons(ORNs),forexample,aftertraumaorupperrespiratory
tractinfection(URTI).If notallORNswere lost,patients wouldstillbeabletoperceive anodor,but
becauseofthelackofcertainneurons,theywouldbeunabletoencodeaspecificodorquality.Thus,they
wouldbeunabletoformacomplete“picture”oftheodorant.
61
Consequently,patientswouldmisinterpret
thesensoryinputintheformofparosmias.Ontheotherhand,parosmiacouldalsobeacentralnervous
problem.Specifically, because of unknownpathologies, theintegrative or interpretative centers inthe
braincouldform a distortedpicture.
61,68
Consistent withthisis the factthat inpatientswith parosmia,
graymattervolumelosshasbeendemonstratedintheleftanteriorinsulaandinotherareasinvolvedin
olfactory processing, such as the right anterior insula, the anterior cingulate cortex, the hippocampus
(bilaterally),andtheleftmedialorbitofrontalcortex.
69
With regard to phantosmia,
61
it has been hypothesized that abnormally active ORNs or a loss of
inhibitory neurons could lead to distorted sensations.
70
A central cause is also hypothesized for
phantosmia, where hyperactive braincells mightcreate theimpression of anodorous sensation.Some
patientswithqualitativeolfactorydisordersdonotreportahistoryofURTIorheadtrauma,butindicate
spontaneous onset of the symptoms.
61
Qualitative olfactory dysfunction is typically, but not always,
associatedwithquantitativeolfactoryloss.Whilethedebateisfarfromover,parosmiamaybeseenasan
indicatorofachangingolfactorysystem.Phantosmiamaybeasignofdeafferentation.
It is known that most qualitative olfactory impairments gradually improve.
61,64
Patients therefore
appreciateknowing that thereis ahighchance that the condition will improveordisappear withtime.
Appropriate counseling and watchful waiting is therefore recommended. In extremely severe cases,
endoscopic surgical excision of olfactory epithelium has been suggested as a possible therapeutic
approach.
61,71
Although other treatments have been reported, none has yet been established in routine
clinical practice. For example, excellent results have been reported by Zilstorff using local cocaine
treatment.
63
Othertreatmentapproachesaresimilartothosedescribedforquantitativeolfactoryloss.
References
1.GrushkaM,EpsteinJB,GorskyM.Burningmouthsyndrome.AmFamPhysician2002;65(4):615–620
2. Woda A, Navez ML, Picard P, Gremeau C, Pichard-Leandri E. A possible therapeutic solution for stomatodynia (burning mouth
syndrome).JOrofacPain1998;12(4):272–278
3.DanhauerSC,MillerCS,RhodusNL,CarlsonCR.Impactofcriteria-baseddiagnosisofburningmouthsyndromeontreatmentoutcome.J
OrofacPain2002;16(4):305–311
4.GrushkaM.Clinicalfeaturesofburningmouthsyndrome.OralSurgOralMedOralPathol1987;63(1):30–36
5.EguiaDelValleA,Aguirre-UrizarJM,Martinez-CondeR,Echebarria-GoikouriaMA,Sagasta-PujanaO.Burningmouthsyndromeinthe
BasqueCountry:apreliminarystudyof30cases.MedOral2003;8(2):84–90
6.KlausnerJJ.Epidemiologyofchronicfacialpain:diagnosticusefulnessinpatientcare.JAmDentAssoc1994;125(12):1604–1611
7.GrushkaM,SessleBJ.Burningmouthsyndrome.DentClinNorthAm1991;35(1):171–184
8. Basker RM, Sturdee DW, Davenport JC. Patients with burning mouths. A clinical investigation of causative factors, including the
climactericanddiabetes.BrDentJ1978;145(1):9–16
9.ZakrzewskaJM.Theburningmouthsyndromeremainsanenigma.Pain1995;62(3):253–257
10. Lauria G, Majorana A, Borgna M, et al. Trigeminal small-fiber sensory neuropathy causes burning mouth syndrome. Pain
2005;115(3):332–337
11.BergdahlM,BergdahlJ.Burningmouthsyndrome:prevalenceandassociatedfactors.JOralPatholMed1999;28(8):350–354
12. Tammiala-Salonen T, Hiidenkari T, Parvinen T. Burning mouth in a Finnish adult population. Community Dent Oral Epidemiol
1993;21(2):67–71
13.WardropRW,HailesJ,BurgerH,ReadePC.Oraldiscomfortatmenopause.OralSurgOralMedOralPathol1989;67(5):535–540
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
14.BenAryehH,GottliebI,Ish-ShalomS,DavidA,SzargelH,LauferD.Oralcomplaintsrelatedtomenopause.Maturitas1996;24(3):185–
189
15.CairnsBE.Theinfluenceofgenderandsexsteroidsoncraniofacialnociception.Headache2007;47(2):319–324
16. Patton LL, Siegel MA, Benoliel R, De Laat A. Management of burning mouth syndrome: systematic review and management
recommendations.OralSurgOralMedOralPatholOralRadiolEndod2007;103Suppl:S39.e1–13
17. Jääskeläinen SK, Rinne JO, Forssell H, et al. Role of the dopaminergic system in chronic pain—a fluorodopa-PET study. Pain
2001;90(3):257–260
18. JääskeläinenSK. Clinical neurophysiologyandquantitative sensorytesting inthe investigationoforofacialpain andsensory function.J
OrofacPain2004;18(2):85–107
19.HagelbergN,ForssellH,AaltoS,etal.AltereddopamineD2receptorbindinginatypicalfacialpain.Pain2003;106(1–2):43–48
20.ForssellH,JääskeläinenS,TenovuoO,HinkkaS.Sensorydysfunctioninburningmouthsyndrome.Pain2002;99(1–2):41–47
21.HeckmannSM,HeckmannJG,HiIzMJ,etal.Oralmucosalbloodflowinpatientswithburningmouthsyndrome.Pain2001;90(3):281–286
22.Formaker BK,MottAE,FrankME.The effectsoftopicalanesthesiaonoralburninginburningmouthsyndrome. AnnNYAcadSci
1998;855:776–780
23.NaglerRM,HershkovichO.Sialochemicalandgustatoryanalysisinpatientswithoralsensorycomplaints.JPain2004;5(1):56–63
24. Lim J,GreenBG. Thepsychophysicalrelationshipbetween bitter taste andburning sensation:evidence of qualitative similarity.Chem
Senses2007;32(1):31–39
25.LindenRW.Taste.BrDentJ1993;175(7):243–253
26.SuarezP,ClarkGT.Burningmouthsyndrome:anupdateondiagnosisandtreatmentmethods.JCalifDentAssoc2006;34(8):611–622
27.BirnbaumJ.PeripheralnervoussystemmanifestationsofSjögrensyndrome:clinicalpatterns,diagnosticparadigms,etiopathogenesis,and
therapeuticstrategies.Neurologist2010;16(5):287–297
28. GøranssonLG, Brun JG, Harboe E, Mellgren SI, Omdal R. Intraepidermal nerve fiber densities inchronicinflammatory autoimmune
diseases.ArchNeurol2006;63(10):1410–1413
29.AfrinLB.Burningmouthsyndromeandmastcellactivationdisorder.OralSurgOralMedOralPatholOralRadiolEndod2011;111(4):465–
472
30.ChoGS,HanMW,LeeB,etal.Zincdeficiencymaybeacauseofburningmouthsyndromeaszincreplacementtherapyhastherapeutic
effects.JOralPatholMed2010;39(9):722–727
31.BartoshukLM,SnyderDJ,GrushkaM,BergerAM,DuffyVB,KvetonJF.Tastedamage:previouslyunsuspectedconsequences.Chem
Senses2005;30(Suppl1):i218–i219
32.GrushkaM,BartoshukL.Burningmouthsyndromeandoraldysesthesias.CanJDiagnosis2000;99–109
33. Lehman CD, Bartoshuk LM, Catalanotto FC, Kveton JF, Lowlicht RA. Effect of anesthesia of the chorda tympani nerve on taste
perceptioninhumans.PhysiolBehav1995;57(5):943–951
34. Yanagisawa K, Bartoshuk LM,Catalanotto FA, Karrer TA,Kveton JF. Anesthesia ofthe chordatympaninerve andtaste phantoms.
PhysiolBehav1998;63(3):329–335
35.TieK,FastK,KvetonJ,etal.Anesthesiaofchordatympaninerveandeffectonoralpain.ChemSenses1999;24:609
36.BartoshukLM,DuffyVB,MillerIJ.PTC/PROPtasting:anatomy,psychophysics,andsexeffects.PhysiolBehav1994;56(6):1165–1171
37.EliavE,KamranB,SchahamR,CzerninskiR,GracelyRH,BenolielR.Evidenceofchordatympanidysfunctioninpatientswithburning
mouthsyndrome.JAmDentAssoc2007;138(5):628–633
38. Snyder DJ, Prescott J, Bartoshuk LM. Modern psychophysics and the assessment of human oral sensation. Adv Otorhinolaryngol
2006;63:221–241
39.BartoshukLM,Duffy VB,GreenBG,etal.Validacross-groupcomparisons withlabeledscales: thegLMSversusmagnitudematching.
PhysiolBehav2004;82(1):109–114
40.WhiteTL,KentPF,KurtzDB,EmkoP.Effectivenessofgabapentinfortreatment ofburningmouthsyndrome. ArchOtolaryngolHead
NeckSurg2004;130(6):786–788
41.YamazakiY,Hata H,KitamoriS, OnoderaM,Kitagawa Y.Anopen-label, noncomparative,doseescalationpilotstudyoftheeffectof
paroxetineintreatmentofburningmouthsyndrome.OralSurgOralMedOralPatholOralRadiolEndod2009;107(1):e6–e11
42.Grushka M,EpsteinJ,MottA.Anopen-label, doseescalationpilotstudyoftheeffectofclonazepaminburning mouth syndrome.Oral
SurgOralMedOralPatholOralRadiolEndod1998;86(5):557–561
43. Gremeau-Richard C, Woda A, Navez ML, et al. Topical clonazepam in stomatodynia: a randomised placebo-controlled study. Pain
2004;108(1–2):51–57
44.PetruzziM,LauritanoD,DeBenedittisM,BaldoniM,SerpicoR.Systemiccapsaicinforburningmouthsyndrome:short-termresultsofa
pilotstudy.JOralPatholMed2004;33(2):111–114
45. FemianoF,LanzaA, BuonaiutoC,et al.Burningmouthsyndrome andburningmouthin hypothyroidism:proposal foradiagnosticand
therapeuticprotocol.OralSurgOralMedOralPatholOralRadiolEndod2008;105(1):e22–e27
46. Cowart B, Klock CV, Pribitkin E, Breslin P. Relative impact of taste versus smell dysfunctions on quality of life. Chem Senses
2007;32:A16
47.PanayiotouH,SmallSC,HunterJH,CulpepperRM.Sweettaste(dysgeusia).Thefirstsymptomofhyponatremiainsmallcellcarcinoma
ofthelung.ArchInternMed1995;155(12):1325–1328
48.NakazatoY,ItoY,NaitoS,TamuraN,ShimazuK.Dysgeusialimitedtosweettasteinmyastheniagravis.InternMed2008;47(9):877–878
49.SchiffmanSS.Tasteandsmellindisease(firstoftwoparts).NEnglJMed1983;308(21):1275–1279
50.AckermanBH,KasbekarN.Disturbancesoftasteandsmellinducedbydrugs.Pharmacotherapy1997;17(3):482–496
51.AvoniP,ContinM,RivaR,AlbaniF,LiguoriR,BaruzziA.Dysgeusiainepilepticpatientstreatedwithlamotrigine:reportofthreecases.
Neurology2001;57(8):1521
52.OhkoshiN,ShojiS.Reversibleageusiainducedbylosartan:acasereport.EurJNeurol2002;9(3):315
53.RoobG,FazekasF,HartungHP.Peripheralfacialpalsy:etiology,diagnosisandtreatment.EurNeurol1999;41(1):3–9
54.TaillibertS,BazinB,Pierrot-DeseillignyC.Dysgeusiaresultingfrominternalcarotiddissection.Alimitedglossopharyngealnervepalsy.J
NeurolNeurosurgPsychiatry1998;64(5):691–692
55.LeeBC,HwangSH,RisonR,ChangGY.Centralpathwayoftaste:clinicalandMRIstudy.EurNeurol1998;39(4):200–203
56. Adler A. Zur Topik des Verlaufes der Geschmackssinnsfasern und anderer afferenter Bahnen im Thalamus. [Article in German] Z
GesamteNeurolPsychiatr1934;149:208–220
57.Hausser-HauwC,BancaudJ.Gustatoryhallucinationsinepilepticseizures.Electrophysiological,clinicalandanatomicalcorrelates.Brain
1987;110(Pt2):339–359
58.ChoGS,HanMW,LeeB,etal.Zincdeficiencymaybeacauseofburningmouthsyndromeaszincreplacementtherapyhastherapeutic
effects.JOralPatholMed2010;39(9):722–727
59. Heckmann SM, Hujoel P, Habiger S, et al. Zinc gluconate in the treatment of dysgeusia—a randomized clinical trial. J Dent Res
2005;84(1):35–38
60. HalyardMY,Jatoi A,SloanJA, et al.Does zinc sul-fatepreventtherapy-induced taste alterations inhead andneckcancer patients?
Results ofphaseIII double-blind,placebo-controlledtrial fromtheNorth Central CancerTreatmentGroup(N01C4). IntJ RadiatOncol
BiolPhys2007;67(5):1318–1322
61.LeopoldD.Distortionofolfactoryperception:diagnosisandtreatment.ChemSenses2002;27(7):611–615
62.ZarinkoK.ÜberKakosmiasubjectiva.In:FestschriftzurFeierdes80-jährigenStiftungsfestesdesärztlichenVereinszuHamburg.Leipzig:
Langkammer;1896:339–342
63.ZilstorffK.Parosmia.JLaryngolOtol1966;80:(11)1102–1104
64.RedenJ,MaroldtH,FritzA,ZahnertT,HummelT.Astudyontheprognosticsignificanceofqualitativeolfactorydysfunction.EurArch
Otorhinolaryngol2007;264(2):139–144
65.DeemsDA,DotyRL,SettleRG,etal.Smellandtastedisorders,astudyof750patientsfromtheUniversityofPennsylvaniaSmelland
TasteCenter.ArchOtolaryngolHeadNeckSurg1991;117(5):519–528
66. Holbrook EH,Leopold DA,SchwobJE. Abnormalitiesof axon growthin human olfactory mucosa.Laryngoscope2005;115(12):2144–
2154
67.BegumM,McKennaPJ.Olfactoryreferencesyndrome:asystematicreviewoftheworldliterature.PsycholMed2011;41(3):453–461
68. Frasnelli J, Landis BN, Heilmann S, et al. Clinical presentation of qualitative olfactory dysfunction. Eur Arch Otorhinolaryngol
2004;261(7):411–415
69.BitterT,SiegertF,GudziolH,etal.Graymatteralterationsinparosmia.Neuroscience2011;177:177–182
70. Muller A, Rodewald A, Reden J, Gerber J,vonKummer R, Hummel T. Reduced olfactory bulb volume in post-traumatic and post-
infectiousolfactorydysfunction.Neuroreport2005;16(5):475–478
71. Leopold DA, Loehrl TA, Schwob JE. Long-term follow-up of surgically treated phantosmia. Arch Otolaryngol Head Neck Surg
2002;128(6):642–647
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
17StructuralImaginginChemosensoryDysfunction
NasreddinAbolmaali
Summary
Structural imaging in chemosensory dysfunction can visualize the morphological anatomy and
pathology of the entire chemosensory pathway, from the oral and nasal mucosa and adjacent
structures(e.g.,paranasal sinuses),alongthe particularcranial nerves, and throughthe respective
ganglia to the brain. While some of these structures display only subtle and mainly size-related
changesduring life,the olfactory system contains highlyplastic structures. For example, research
indicates that smell deficitsleading toa reduced sensoryinput resultinstructural changes at the
leveloftheolfactorybulb.Therefore,certaincasesrequire highlyspecificand optimizedimaging
with quantitative image analysis. However, in most patients, structural imaging in chemosensory
dysfunctionisacomparativelynonspecificdiagnostictoolusedmainlytoexcludemalignancyinthe
brain and the head and neck region. Clinical symptoms prompting imaging of the chemosensory
system typically occur onlyifboth sides of therespective structures are affected, which is more
frequent in olfaction than in gustation. If only one side is affected, most patients will neither
experienceanychemosensorydysfunctionnorbeabletolateralizethelossofchemosensoryinput.
This chapter discusses some of the radiological basics for the assessment of chemosensory
structures, results of quantitative imaging, and major pathologies in which imaging is clinically
relevant.
ImagingTechnique
Magneticresonanceimagingisthemodalityofchoiceforimagingchemosensorydysfunction.
TechnicalConsiderations:MagneticResonanceImaging
FieldStrength
Magnetic resonance imaging (MRI) is the major imaging modality used to visualize the anatomy and
pathologyofchemosensorydysfunction,mainlybecauseofitsinherenthighsofttissuecontrast.Itrelies
on signals from hydrogen atoms. The number of hydrogen atoms contributing to the MRI signal is
increasedathigherfieldstrengths.Therefore,itmayseemthatsmallstructures,suchastheolfactorybulb
(OB)(Fig.17.1)andtheolfactorytract(OT),arebestvisualizedat3to7T.However,certainartifacts
thatincreasewithfieldstrengthreducetheapplicabilityofthesesystems.Forexample,themainpartsof
theOTarenoteasilyvisualizedatafieldstrengthatorabove3T,asso-calledsusceptibilityartifacts,
occurring at the posterior frontobasis between cerebrospinal fluid (CSF) and the air-filled paranasal
sinuses,maydeterioratesignal(Fig.17.2).Furthermore,thesesystemsarestillnotavailableeverywhere.
Therefore, the imaging technique was optimized at 1.5 T, using advanced receiver-coil techniques or
selectedimagingsequences.Thetechniquesdiscussedhereinwereperformedat1.5T,whichremainsthe
referencestandardformanyapplications.Mostoftheimagesinthischapterwereacquiredat1.5T.
Fig.17.1CoronalT2-weightedturbospin-echomagnetic resonanceimaging.Theolfactorybulbs(arrows)are surroundedbycerebrospinal
fluidandlocatedabovethecribriformplateandbelowtheolfactorysulci(arrowheads)ofthefrontallobes.
ReceiverCoils
When MRI was first used to visualize the OB, mostly small-loop coils were employed, which were
placedonthenasion,andenabledcomparativelyhigh-resolutionimagesoftheOBtobeobtained.
1
Owing
to the limited field of view (“depth penetration”) of these coils, the OT and posterior parts of the
olfactorysystemcouldnotbevisualized,andstandardheadcoilswereapplied,allowingimagingofthe
wholebrainatsomewhatlowerspatialresolution.Newheadcoils(e.g.,multichannelheadarraycoils)
allow similaror evenbetterspatialresolutionthansmall-loop coilsandprovide informationfrom the
entirebrain.
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Fig.17.2CoronalT2-weightedturbospin-echomagneticresonanceimagingat3T.Theolfactorytracts(posteriortotheolfactorybulbs)are
notvisibleasalargesusceptibilityartifacthasdestroyedtheimagedataset(arrows).Theseartifactsdonotlimitvisualizationofthisregionat
1.5T.
SequenceTechniques
Basically, two different tissue characteristics may be assessed: the T1 time, using T1-weighted
sequences;andtheT2time, usingT2-weightedsequences.Different sequencetypes (mainlyturbospin
echo[TSE], constructive interferenceinsteady-state precession[CISS],turbofastlow-angle shot)are
capable ofgenerating different contrastsbetweentissues.Additionally,andindependentofthe desired
tissuecontrast,sequencesmaybeoptimizedforthree-dimensional(3D)imagingortwo-dimensional(2D)
imaging.
Forhigh-resolutionimaging,2DdataacquisitionispreferablyperformedusingTSEtechniques,which
generateavoxelsizeof0.405mm
3
.Avoxelisa3Dpictureelement(volumeelement)consistingofthe
slicethickness(mm)multipliedbythein-planeresolution(mm×mm).Withsuchsmallvoxels,accurate
volumetry of theOB is feasible. To accuratelyassess this, 2D TSE sequences should be acquired in
coronalsliceorientation(perpendiculartothefrontobasis;maximumslicethickness2mm)coveringthe
entirefrontalskullbaseandthepituitarygland.TovisualizepathologyalongtheOBorwithintheMeckel
cave, a sequencewith strongerT2-weighting (e.g., CISS
2
) appears to be advantageous.Thistechnique
generates brightsignals fromCSFandverylow signal intensities fromall other tissuesand structures
(i.e., high contrast for the sensitive visualization of structures surrounded by CSF [Fig. 17.3]). The
disadvantageofthissequenceisthepoorcontrastamongnerves,brain,air,andbone.
If the entire afferent olfactory or gustatory system, including nasal and oral cavity and posterior
structures,needstobeinvestigated,3Dimagingwithisotropicvoxels(whichrevealidenticallengthsof
themarginsofeveryvoxelinallthreespatialorientations)coveringtheentirecraniumispreferred.The
acquireddatasetsallowformulti-planarreformationinanyorientationandmaybeacquiredbeforeand
after intravenous administration of contrast material. For such large volume acquisitions, imaging is
preferably performed at 3 T to keep the acquisition time short whilst providing adequate spatial
resolution.
Fig. 17.3 Coronal, heavily T2-weighted, constructive interference in steady-state precession (CISS) magnetic resonance imaging. High
contrastis providedbetweencerebrospinal fluidandotherstructures.Therefore,subtleliquidstructures,e.g.,smallfluid-filledspaceswithin
theolfactorybulbs(arrows),canbeappreciated,whilethecontrastbetweenotherstructuresistoolowfordetailedanalysis.
Forclinicalpurposes,andmainlytoexcludefrontal,prepontine,orintra-axialtumorsorinfections,the
imaging protocol includes T1-weighted 2D imaging before and after intravenous administration of
contrast material. Imaging should be performed using axial, coronal, and sagittal planes to provide
sufficient information for preoperative planning. The use of fat suppression techniques improves the
delineationofextracranialtumorsgrowingalongcranialnervesandinvadingsubcutaneousfat.Fortumor
detectionintheheadandneck region,so-calledTIRM(turboinversionrecovery magnitude)sequences
withstrongfatsuppression(inversiontimeabove160milliseconds)arepreferablyperformed,asthese
imaging techniques are highly sensitive at detecting pathologies surrounded by normal soft tissues,
especiallyfat.
Table17.1showsimportanttechnicalparametersofrecommendedsequencedesigns.
NewDevelopments
As the signal in MRI relies on hydrogen, the contrast between cortical bone and air is low. New
techniques,suchassequencesdeliveringultrashortechotimes,allowforenhancedcontrastbetweenair
andbone,andmaybeappliedtoMRIoftheparanasalsinusesinthenearfuture.
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Соседние файлы в папке Библиотека им академика М.И. Перельмана