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Disorder Description
Quantitativetaste disorders—measurable ,rare,notalwaysnotice dbythepatient
Ageusia Completelossoftaste
Hypogeusia Diminishedtastecapacity
Hypergeusia Increasedtastesensitivity
Qualitativetastedisorders—notmeasurable,fre quent,noticedbythepatient
Parageusia Triggeredtastedistortion(e.g.,metallictastewheneating)
Phantogeusia Permanenttastedistortion,gustatoryhallucination
Dysgeusia Tastedisorder,oftenusedforqualitativetastedisorders
Complextastedisorders
Tasteagnosia Difficultyclassifyingornamingatastealthoughitisproperlyperceived
Fig. 15.1 Peripheraland centraltaste pathways.Taste disorders can be classified into peripheral or central taste disorders. MS, multiple
sclerosis.
Table 15.2Tastedisordersclassifiedaccordingtotheirpresumedetiology
Vascularetiology Ischemicandhemorrhagicstroke
Traumatic Contusion,skull-basefractures,cranialnervedamage
Toxicity:chemical Toxins,drugs
Metabolic Diabetesmellitus
Toxicity:physical Heat,coldness,radiation,altitudesickness
Neoplastic Space-occupyinglesions
Inflammatory:infectious Borreliosis,HIV,hepatitisC,rabies
Inflammatory:autoimmune Multiplesclerosis,Guillain–Barrésyndrome
Systemicautoimmunedisorders Sjögrensyndrome,Wegenergranulomatosis
Paraneoplasticdisorders Autoimmunemechanisms(molecularmimicry)
Neurodegenerativedisorders Alzheimerdisease,Parkinsondisease,andrelateddisorders,Creutzfeldt–Jakobdisease
Geneticdisorders Machado–Josephdisease,familialdysautonomia
HIV,humanimmunodeficiencyvirus.
Acarefulpatienthistory,testingofeachmodality,andclinicalwork-upisimportantforpatientswith
tastedisorders.
Pathophysiology
Often,wedonotknowtheexactpathologicalmechanismunderlyingtastedisorders,whichisreflectedby
the classification systems. Two of the three classification systems presented here are clinical and
observational classifications without any explanation about the underlying mechanism. We observe
patients with medication side effects, but barely know any molecular details about the disorders. In
contrast,the pathologicalmechanismseemsclear in situationswherealesionisvisibleordocumented
(asseeninFig.15.1).Inthesecases,thetastepathwayisdirectlyinjured.
EtiologyofTasteDisorders
Todetermineetiologyoftastedisordersthefollowingdifferentialdiagnosticapproachhasbeenshownto
beuseful:
•Isthetastedisordercausedbydrugsortoxins?
• Is the taste disorder caused by local factors in theoral cavity, for instance atrophy of the mucosa,
physical or chemical injuries, alteration of the composition of saliva, or otorhinolaryngological or
dentaldiseases(e.g.,Candidaalbicans)?
•Isthetastedisordercausedbyadiseaseoftheperipheralnervoussystem?
•Isthetastedisordercausedbyadiseaseofthecentralnervoussystem?
•Isthetastedisordercausedbyasystemicdisease?
•Didthetastedisorderoccurafteranydistinctevent(e.g.,infection,surgery,etc.)?
TasteDisorderCausedbyLesionsofthePeripheralNervousSystem
Taste disorders caused by peripheral nervous system disease can occur because of an isolated or
combinedlesionofone of thecranial nerves VII,IX, or X,such as occur inpolyneuritis cranialis or
Guillain–Barrésyndrome.
18
Tastedisorderscanalsooccurinpolyneuropathy.
Tastedisorders affect31to46%ofpatients with acutefacialpalsy,withno differenceinincidence
betweenthe idiopathic form (Bell palsy) and borreliacaused palsy. Compared with clinical signs and
symptoms, and especiallyanalysis ofcerebrospinal fluid, taste resultswere of poor clinical valuein
differentiatingamongthecausesoffacialpalsy.
19
Isolatedperipheralcranialnervelesionswithresulting
tastedisorderhaveawidedifferentialdiagnosis,includingdissectionofthebrain-supplyingarteriesand
local or systemic diseases affecting peripheral nerves. Further, lesions of the skull base or
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cerebellopontineangle,aswellastraumaticskullfractures,mightleadtotastedisorders.
20
However,the
most frequentcause ofisolated peripheral tastedisorder is surgical (iatrogenic) damagetooneof the
tastenerves(Fig.15.1). Theprocedures mostfrequently associatedwithtastedisorders are otological
surgerywithdamagetothechordatympani,
21
tonsillectomyandmicrolaryngoscopy
22
withdamagetothe
lingual branch of the glossopharyngeal nerve, and oral or dental surgery with damage to the lingual
nerve.
23
Unless the nerve is accidentallysevered, mostcasesofsurgically induced tastedisordersare
transientbecauseperipheralnervesregenerate.Thisprocess takesa longtimeandpatientsoftensuffer
fromdysgeusiaformanymonthsoryears.
Inpolyneuropathy,prominenttastedisorderscanoccurandhavebeenreportedincasesofdiphtheria,
porphyries,systemiclupuserythematosus,oramyloidosis.
13
Inarecentobservationalstudyof53patients
withpolyneuropathy,43%demonstratedsignificanttastedisorderontastestriptesting.Thedisorderwas
more severe inpatients withdiabeticpolyneuropathy.
24
Therearealso reportsofsome degreeoftaste
disorderinpatientswith trigeminalneuropathy,basedonthefactthatgustatorynervefibersrunviathe
trigeminal nerve.
25
This raises an interesting issue aboutinteraction between thechemical senses. As
mentioned,trigeminallesionsseemtoinfluencetastefunctionsubclinically.Theconversealsoseemsto
betrue,withtastelossaffectinglingualtrigeminalfunction.
26
Likewise,olfactoryimpairmentinfluences
taste function subclinically.
27
Taken together, these observations make interpretation of selective
chemosensorydisordersdifficult.
Generally,tastedisordersduetoperipheralnerve disease are accompaniedbyadditionalsignsand
symptomssuchaspain,alteredoralperceptions,andforeignbodyfeelingsinthepharynxororalcavity;
swallowingdisorders;palpablemasses;orpalatalorfacialpalsy.Tastedisorderscanoccurafterdental
procedures,
28
after surgical treatment of vestibular Schwannoma,
29
or following manipulation of the
lingualnerve.Inthecaseofcarotidgustatorysyndrome,atransientmetallictasteperceptionemergesafter
compressionofthe carotidartery, probably duetoa misconnectionwithin the glossopharyngeal nerve
betweenafferentimpulsesfromcarotidbaroreceptorsandsensoryimpulsesfromtastefibers.
30
TasteDisordersCausedbyLesionsoftheCentralNervousSystem
Centraltastedisorders are caused bylesionsalong the tastepathway, which startsatthe solitarytract
nucleus(NTS)andendsatthecorticaltaste-representingzones(Fig.15.1).Anisolatedoccurrenceofa
gustatorysymptomalone,however,israre,andadditionalclinicalsignsareusuallypresentanddominant
inthe acutephase of disease. For this reason, taste disorders are notoften reported by patients with
centrallesions,andareonlydetectedifcliniciansseekthemspecifically.
31
Differentapproachescanbetakentocentrallycausedtastedisorders.Fromatopographicalpointof
view, tastedisorders can be attributed to lesions of the brainstem, the thalamus, or cortical areas. In
brainstemlesions,thetastedisorderismainlyipsilateral(hemihypogeusiaorhemiageusia)andisduetoa
lesion of the NTS or pons.
32
Taste disorders caused by thalamic lesions manifest contralaterally,
ipsilaterally, or evenbilaterally.
31,33
This phenomenon indicates that there are ascending crossing and
noncrossingfibersfromthebrainstemtothethalamus.Inbilateralthalamiclesions,anhedonicaspectscan
beprominent,leadingtogustatoryindifferenceandchangesineatingbehavior.
20
Tastedisordersduetocorticallesionsaredifficulttoidentifyfromthehistoryorclinicalneurological
examination. Recent studies have shown that gustatoryfunction is represented in the parietal, insular,
anteromedialtemporal,andorbitofrontalcortex.
34
Lesionsintheseregionscanleadtoepilepticgustatory
sensations(phantogeusia,gustatoryaura)ortogeneraltastedisorderswithimpairmentofthetotaltaste
perception.
Intermsofetiology,tastedisordersduetocerebrovascularandneurodegenerativediseasesaremost
frequent. In an observational study in cooperative stroke patients, 30% revealed significant taste
impairmentand6%hadalateralizedtastedisorder.Predictorsforsuchimpairmentaremalegender,high
NationalInstitutes ofHealth StrokeScalescore, coexistent swallowingdisorder,anda partial anterior
circulationinfarct.
31
Similarresultswereobtainedinastudyof120consecutivepost-menopausalwomen
withacutestroke,21 to40% ofwhomdemonstratedimpairmentofgustatorycapacity withoutsignsof
lateralization.
35
Inbothstudies,asubstantialremissionwasobserved.Evenincasesofminorstroke,taste
disorderscanoccurandleadtoachangeinfoodintakebehavior.
36
Inneurodegenerativediseases,tastedisordersaremorefrequentandsevere.Tastetestingshouldbe
performed on patients with Parkinson disease, in particular, because taste, like olfaction, might be
diminished.
37–39
Atastedisorderwasrecentlyreportedeveninpatientswithmildcognitiveimpairment
andgradedassevereasthatinAlzheimerpatients.
40
Tastedisorders inpatients with multiple sclerosis have been reported,
41,42
and circumscribed taste
abnormalities can be seen in patients with brainstem plaques.
43,44
Recently, it was emphasized that
inflammationanddemyelinationalongthegustatorypathwaycancausesignificanttastedisorders,which
fortunatelyremitcompletelyfollowingsteroidtherapy.
45
Anecdotalevidencealsosuggeststhatamyotrophiclateralsclerosis,
46
myastheniagravis,
47
orcentral
nervousdermoid cystsmaybe preceded bydysgeusia.
48
In some cases, dysgeusia as a paraneoplastic
symptomhasbeenreportedasthefirstsignoflungcancer.
49
Otherprominenttastedisordershavebeen
reportedinsinglecasesofaltitudedisease,familialdysautonomia,Machado–Josephdisease,newvariant
Creutzfeldt–Jakobdisease,andevenrabies.
13
TasteDisordersinNeurologicalDiseaseswithnoDistinctLocalization
Taste disorders can occur in neurological conditions that cannot be precisely classified as central or
peripheral,asinmostcasesofsystemicormetabolicdiseasesordeficiencysyndromes.Thus,indiabetes
—asystemicdiseasewithseveralneurologicalcomplications—ageneralreductionintastecapacityhas
beenreported.
50,51
Cancerpatients often revealseveretastedisorders withastrong negativeimpacton
qualityoflife.Etiologically,cytotoxictherapyisthemostcommoncause.
52
Inimmunologicalconnective
tissue diseases (e.g., Morbus Wegener or Sicca syndrome), chemosensory disturbances are often
encountered.
53,54
Phantogeusia is predominantly seen in patients with psychotic disorders, whereas
anorexiapatients show ageneral taste impairmentthatis associatedwith food unpleasantness.
55
Taste
disorders after allogeneic stem cell transplantation are associated with the cytotoxic drugs that are
necessaryinthiscomplextreatmentregimen,whereaschronicgraft-versus-hostdiseaseorhyposalivation
areoflessimportance.
56
Further,anykindofmetabolicdisorder(e.g.,kidneyorliverinsufficiency)may
initiallypresentastastedisorder.
57
Tastedisordershavebeendetectedinsewageandtoxicwasteworkers,probablyduetotoxicagentsin
theirworkingenvironment.
58
Itisknownthatammonia,isodecane,hairdressingchemicals,andgasoline
canleadtotoxicallymediatedtastedisturbances.
59
Smokingsignificantlyincreasestheriskofolfactory
dysfunctionbutdoesnotaffecttheriskoftastedisorder.
60
Overall,itshouldberememberedthattastedisordersaremorefrequentinthesegeneralizeddiseases,
even if there is noknown underlying mechanism. These systemic diseases—as well as age per se—
increasesusceptibilitytotastedisorders.
61
Interestingly, therearerecentreportsontastephenomena in
patients withsynesthesia.Some individualswith synesthesia perceive specific tasteimpressionswhile
listeningtocertainpiecesofmusic.
62,63
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The tastefibers from three cranial nerves converge from the peripherytoa single nucleusinthe
brainstem.Largepartsofthetastepathwayareipsilateral,butthereispartialcrossingandbilateral
projectionatthelevelofthethalamusandinsula.Tastedisorderscanbeclassifiedintothosewith
peripheralcausesorthosewithcentralnervoussystemcauses.
Drug-inducedTasteDisorders
One major cause of taste disorders is medication side effects. Patients often perceive a relationship
betweenanewtastedisorderandthe intake ofa drug.IntheDrugInteractionsandSideEffectsIndex,
morethan200drugsarelistedascapableofcausingchemosensorytastedisturbances.Arecentreviewof
drug-inducedtastedisorders, basedondatafrom thePhysician’sDeskReference,summarizes22 drug
classesthatcausealtered tasteorsmell perceptions.
64
Table 15.3 lists drug classes andtypical agents
capableofcausingtastedisorders.
The mechanisms thatcontributetotaste disordersare not wellunderstood. Onetheoryis thatdrugs
affectthephysiologicalprocessoftastingbyalteringreceptoraffinityorsignaltransduction.Furthermore,
achangeinsalivaflowratemayplayarole.Also,theexcretion ofthedrugoritsmetabolitesintothe
saliva may cause an unpleasant or distorted taste. Other proposed mechanisms of drug-induced taste
disorders include the following: the accumulation of silver in nerve fibers; a change in the influx of
calciumandotherions;ionchelationandthelossoftissue-boundzinc;alteredbradykininmetabolism;
disturbedsecond-messenger synthesis;general catabolism; and altered metabolism ofprostaglandins.
65
Mostofthesehypothesesremainspeculation,supportedbylittlebiochemicalorphysiologicalevidence.
Finally,itisimportanttonotethatdrug-inducedtastedisordersarenotlimitedtomedication.Somefruits
havethecapacitytoinduceatransienttastedistortion,
66
and,veryrecently,pinenutshavebeenclaimed
toinducedysgeusialastingforseveralweeks.
67
Any kind of drug—and also some foods—can cause dysgeusia. The onset and disappearance of
symptomsmaybeconsiderablydelayedinrelationtodrug/foodintakeanddiscontinuation.
PostviralandIdiopathicTasteDisorders
Mosttastedisordersseeninspecializedcenterseitherfollowanupperrespiratorytractinfectionorare
ofunknownetiology.Thesearegenerallydescribedasidiopathictastedisordersandprobablyconstitute
ahighlyheterogeneousgroup.Idiopathictastedisordersareusuallyqualitativebutcanalsopresentwith
quantitative complaints. Fortunately, most idiopathic taste disorders—and especially qualitative
disorders—seemtoimproveovertheyears.Moodstateseemstoberelatedtoresolutionrates,
68
which
suggeststhatsomeoftheseidiopathicdysgeusiacasesmaybeinducedbydepressivestates.
Table 15.3Drug-inducedtastedisorders(modifiedaccordingDotyetal
64
)
Druggroup Class oragent
Antihypertensives
andcardiac
medications
Amiodarone,propafenone,ACEinhibitors,diuretics,losartan,spironolactone,β-blockers,calciumantagonists,lipid-
loweringagents(atorvastatin,fluvastatin,lovastatin,pravastatin)
Psychiatric
medications
Benzodiazepines,tricyclicantidepressants,lithium,antipsychotics(clozapine,trifluoperazine),hypnotics(zolpidem,
eszopiclone),CNSstimulants(amphetamine,dexamphetamine,methylphenidate)
Neurological
medications
Antiepilepticdrugs(carbamazepine,phenytoin,lamotrigine,topiramate),antimigrainedrugs(sumatriptan,
naratriptan,rizatriptan),antiparkinsonianagents(levodopa),anticholinergics,acetazolamide,baclofen,dantrolene
Anti-infectious
agents
Antibacterials(ampicillin,ciprofloxacin,azithromycin,metronidazole,tetracycline),antifungals(griseofulvin,
terbinafine),antivirals(aciclovir,ganciclovir,pirodavir,oseltamivir)
Antineoplastics Platinderivatives,alkylatingdrugs,vincristine,methotrexate
Anti-inflammatory
agents
Dexa-andbeclometasone,budesonide,gold,penicillamine
Thyroiddrugs Carbimazole,levothyroxine,thiamazole,propylthiouracil
CNS,centralnervoussystem;ACE,angiotensin-convertingenzyme.
Idiopathic taste disorders are the most commonly diagnosed causes of dysgeusia. This probably
reflectsthepoorclinicalknowledgewecurrentlyhaveoftastedisorders.
Diagnosis
Asforall medicaldisciplines,the firststeptoward therapy is the diagnosis.As discussed,a detailed
history, extensive testing (see Chapter 14), and thorough neurological, dental, and otolaryngological
examinationisrequired.
Afterthesesteps,mostdiagnosesareclear.However,howdoweproceedwiththeremainingpatients,
inwhomnosuspectedcausecanbeisolated?Thereiscurrentlynoevidence-basedschemeforhowthese
patientsshouldbemanaged.Wedonotclaimourproposedapproachtofurtherdiagnosticproceduresto
betheonlyvalidone,butwehopetogivesomeusefulclinicalrecommendations.First,imaging,ideally
head and brain magnetic resonance imaging, should at least rule out the possibility of any neoplasia.
Bloodscreeningforliver,renal,andthyroidfunction,immuneandinflammatorymarkers,hematological
parameters, and glucose metabolism may suggest if further investigation of any systemic disorders is
required. The necessity for vitaminandmetal analysis is debatable ina population highlyunlikelyto
sufferfrommalnourishment.DrugdiscontinuationandoralswabsforCandidascreeningmightbehelpful,
although there is nopublishedevidencetosupportthis. Follow-upsometimes revealsnewfactorsthat
helpidentifytheunderlyingcause.
Itisimportanttoseekadiagnosis.Afterahistoryandappropriatetesting,bloodteststoscreenfor
deficiencies,andimagingofthebrain/cranialnerves,maybehelpful.
TherapyofTasteDisorders
Aspecifictherapyfortastedisorderisnotavailable.Insomesmallrandomizedstudies,zinchasshown
significantbenefitinpatients withidiopathictastedisorders.Patientstreatedwithzincdemonstrateda
significant improvement in taste capacity accompanied by a significant improvement in general well-
beingandadecreaseindepression.
69
Inanotherstudy,theintakeofzincledtoanimprovementintasting
in both patients with zinc deficiency and patients with normal zinc levels.
70
The ratio of apo:holo-
activitiesofangiotensin-convertingenzymemaybeapredictorofimprovementinthesecases.Inafurther
study, a zinc-containing drug (polaprezinc), administered at 68 mg daily for 12 weeks, led to an
improvementintastingcomparedwithplacebo.Thenotedsideeffectsweremild.
71
There are therapeutic recommendations for steroids and vitamin A, although their efficacy is not
proven.
13
In a small cohort, branchedchain amino acid supplementation improved taste capacity in
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patientswithhepatitisC,accompaniedbyanincreaseofthelevelofzinc.
72
Incasesofburning-mouthsyndromeanddysgeusia,supportivemeasures,suchasstimulationwithan
ice cube and medication for the treatment of neuropathic pain (e.g., antidepressants, gabapentin,
pregabalin),can be tried.
13,73–76
In patients withtastedisorders afterchemotherapyor radio-therapy,a
self-careprogramcanbeofvalue,forexampleomittingstronglysmellingortastingmeals,drinkingmore
water,optimizingoralhygiene,andeatingsmallmealsmorefrequently.
77
Therapyfortastedisordersdependsonthediagnosedcauseofthedysgeusia.Mostcasesimprove
spontaneously.
Acknowledgments
WethankDr.HergenFriedrichforthedrawingofFig.15.1.
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16BurningMouthSyndromeandQualitativeTasteandSmell
Disorders
MiriamGrushka,VictorChing,JoelEpstein,AntjeWelge-Luessen,ThomasHummel
BurningMouthSyndrome
Burning mouth syndrome can be extremely disturbing. Causes are multiple. Treatment is not
established.Itisoftenassociatedwithtasteloss.
Introduction
Burning mouth syndrome (BMS) is characterized by a burning sensation in the intraoral mucosal
membranesandperioralareasintheabsenceofclinicalandlaboratoryfindingstoaccountforthepain.
1–3
Diagnosis is often made on a clinical basis. Sensations associated with BMS have been variously
describedas“burning,”“annoying,”“granularorsandy,”or“drynessandswelling.”
2
Frequently,patients
donotreportpainwheneating,sleeping,oronwaking,butthesensationgraduallyincreasesthroughout
the day to peak in late afternoon and early evening.
1,2
Up to two-thirds of patients with BMS also
complainofdysgeusia,
4,5
describedasthepresenceofaconstant“foul,”bitter,ormetallictastesensation,
whichmaybeatleastasdisturbingastheburningpainitself.
1
Prevalence
TheprevalenceofBMShasbeenreportedtobebetween0.7and5%inthegeneralpopulation(including
Canadian studies
1,6
), with the variation probably due to study methodology (survey or clinical
assessment)andlocation.
1,6–8
BMSismostcommonlyreportedbyfemalepatientsinthefifthtoseventh
decade of life,
4,9,10
and investigations have often focused on menopausal and post-menopausal
populations.
11–14
ThehighproportionofpostmenopausalpatientswithBMShasledtointerestintherole
ofestrogeninchronicorofacialpain,
15
andwhetherchangesinestrogenlevelscanprecipitateBMS.
Etiology
ThereisanincreasingconsensusthatBMSisanidiopathicneuropathicpaincondition.
9,16
However,there
is noconsensusonthe etiologyor whether developing BMScanbeattributed to a single precipitating
event.
4,12
Recentevidencehassuggestedthatbothcentral
17–20
andperipheralneuropathicchanges
10,21–23
arepresentinpatientswithBMS.ArecentstudybyLauriaetal
10
assessedsuperficialnervechangeson
biopsyoftheanteriortwo-thirdsofthetonguein12patientsdiagnosedwithBMS.Comparedwithcontrol
subjects,patientswithBMSdemonstratedasignificantlylowerdensityofunmyelinatedepithelialnerve
fibers and subpapillarynerve fibers, withevidenceofdiffuse axonal derangementinthepatientswith
BMS.
10
Thechangeswerecausedbyaprimaryaxonopathyratherthananeuronopathy.Likeothersmall-
fiber neuropathies, the severity of thesymptoms did not correlate withthe density ofepithelial nerve
fibers.
10
Previousstudieshaveshownthattheseepithelialnervefiberssynapsewiththetastebudsinthe
fungiformpapillae,andsuchchangesmaybethebasisforboththedysgeusiaandthepainexperiencedby
somepatientswithBMS.
22,24,25
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