abnormalities of taste smell after head trauma - … · anosmia inability to detect or recognize...

Journal of Neurology, Neurosurgery, and Psychiatry, 1974, 37, 802-810

Abnormalities of taste and smell after head trauma

PAUL J. SCHECHTER AND ROBERT I. HENKIN'

From the Section on Neuroendocrinology, National Heart and Lung Institute,- National Institutes of Health, Bethesda, Maryland 20014, U.S.A.

SYNOPSIS Abnormalities of taste and smell were studied in 29 patients after head trauma. Theseabnormalities included decreased taste acuity (hypogeusia), a distortion of taste acuity (dysgeusia),decreased smell acuity (hyposmia), and a distortion of smell acuity (dysosmia). This syndrome can

occur even after minimal head trauma and can begin months after the moment of injury. Thepatients exhibited a significant decrease in total serum zinc concentration (patients, 77 + 3 Vg/100 ml,mean + 1 SEM, vs controls, 99 + 2 jg/100 ml, P> 0-001) and a significant increase in total serum

copper concentrations (113 + 4 Cug/100 ml vs 100 + 2 [ug/100 ml, P <0-001) compared with controlsubjects. Symptoms of hypogeusia, dysgeusia, and dysosmia are frequent sequelae of head injuryand are important to the patients and to their care after trauma.

Loss of olfactory acuity after trauma to the headis a well-recognized phenomenon and has beenestimated to occur in 1.3% to 65% of all headinjuries (Laemmle, 1931; Sumner, 1964). Blowsto the occiput have been reported as more likelyto produce loss of smell, presumably by a contre-coup effect, than blows to the forehead or othersites on the head (Sumner, 1964) and even trivialinjuries have been shown to result in olfactorysensory deficits (Sumner, 1964). In addition,distortion of odours has been described afterhead trauma (Leigh, 1943; Sumner, 1964, 1967).Spontaneous recovery of olfactory acuity hasbeen claimed in 8% to 3900 of patients sufferingfrom post-traumatic loss of smell (Leigh, 1943;Sumner, 1964).On the other hand, abnormalities of taste

sensation after head injury have received muchless attention and have been reported to occurless frequently than do olfactory disorders. Thefirst description of taste loss after head traumawas made by Ogle in 1870. Since that time, addi-tional cases of post-traumatic taste loss havebeen described in the literature. The incidence ofthis condition has been estimated to be approxi-mately 0-40/o of all head injuries, a much lowerincidence than that for post-traumatic olfactoryI Address for correspondence: Dr Robert I. Henkin, Section onNeuroendocrinology, Experimental Therapeutics Branch, NationalHeart and Lung Institute, Bldg 10, Room 7N262, Bethesda, Maryland20014, U.S.A.

802

disturbances (Mifka, 1965). Usually decreasedtaste acuity has been reported to be accom-panied by decreased olfactory acuity. In themajority of cases return of taste acuity has beenreported in the course of time, suggesting thatthis abnormality is more amenable to correctionthan post-traumatic smell loss (Sumner, 1967).No relationship between severity of head injuryand the occurrence or duration of taste loss hasbeen previously reported (Sumner, 1967).

Distorted taste sensations have been reportedto accompany post-traumatic taste loss (Sumner,1967). The incidence of distortion of either tasteor smell or both in patients with post-traumatictaste loss has been estimated to be between 6%and 33%o (Leigh, 1943; Sumner, 1964, 1967).

However, the presumed diagnosis of 'anos-mia' or 'ageusia' has been made in these studieson the basis of clinical subjective reports, withoutquantitative measurements to specify the degreeor extent of the taste or smell losses.

In this paper we present data on 29 patientswho experienced abnormalities of taste andsmell after head trauma. Quantitative estimatesof the losses of taste and smell were made. Therelationship of the sensory losses to alterations intrace metal metabolism will be discussed.

METHODS

On the bases of careful evaluation of symptoms of

Protected by copyright.

on 4 October 2018 by guest.

http://jnnp.bmj.com

/J N

eurol Neurosurg P

sychiatry: first published as 10.1136/jnnp.37.7.802 on 1 July 1974. Dow

nloaded from

http://jnnp.bmj.com/

Taste and smell changes after head trauma

approximately 400 patients with taste and smell com-plaints we have described alterations in taste andsmell perception as follows (Henkin, 1971):ABNORMALITIES OF TASTE Hypogeusia Decreasedability to taste salt, sweet, sour and/or bitter tastants.

Ageusia Inability to detect or recognize any tastant(operationally defined as inability to detect or recog-nize saturated solutions of NaCl or sucrose, 500 mMHCI, or 8 M urea).

Dysgeusia General description of any distortion ofnormal taste perception.

Cacogeusia Abhorrent, obnoxious taste producedby oral introduction or mastication of food ordrink. Foods most commonly eliciting this symptomare eggs, meats, poultry, fish, garlic, onions,tomatoes, coffee, chocolate, and most foods fried inoil or fat.

Phantogeusia Intermittent or persistent taste per-ceived in the oral cavity independent of externalstimuli. This taste may be salty, sweet, sour, bitter,metallic, or indescribably obnoxious.

Heterogeusia Inappropriate consistent taste qualityproduced by oral introduction or mastication of foodor drink. This quality is unusual and unexpected butnot necessarily obnoxious-for example, all foodtastes salty or sweet.

ABNORMALITIES OF SMELL Hyposmia General de-crease in olfactory acuity.

Anosmia Inability to detect or recognize anyvapour at primary or accessory areas of olfaction(Henkin, 1967b).

Type I hyposmia Inability to detect or recognizeany vapour at primary area of olfaction but main-tenance of acuity at accessory areas of olfaction(Henkin, 1967b).

Type II hyposmia Decreased acuity at primary areaof olfaction with maintenance of acuity at accessoryareas of olfaction (Henkin, 1967b).

Dysosmia General description of any distortion ofnormal smell perception.

Cacosmia Abhorrent, obnoxious smell producedby the inhalation of odorants. Odorants whichmost commonly elicit this symptom are from per-fumes, soaps, automobile exhaust, hair sprays, andfrom most foods which elicit cacogeusia.

Phantosmia Intermittent or persistent odour,pleasant or unpleasant, perceived when no apparentodorant is present.

Heterosmia Inappropriate smell of consistentnature associated with odorants. This smell isunusual and unexpected but not necessarily foul orobnoxious.

MEASUREMENT OF TASTE AND SMELL ACUITY Tasteacuity was measured by determining detection andrecognition thresholds for representatives of the salt,sweet, sour, and bitter taste qualities by a forced-choice, three-stimulus drop technique (Henkin et al.,1963; Henkin et al., 1971). Sodium chloride was usedas representative of the salt taste quality; sucrose, forsweet; HCl, for sour; and urea, for bitter. 'Detectionthreshold' was defined as the lowest concentration ofsolute consistently detected as different from water.'Recognition threshold' was defined as the lowestconcentration of solute consistently recognizedcorrectly as salty, sweet, sour, or bitter. Taste thresh-olds were measured on one to four separate occa-sions in each subject. The lowest detection andrecognition thresholds were used for analysis when-ever more than one measurement was obtained.

Olfactory acuity was measured by determiningdetection and recognition thresholds for the vapoursof pyridine in water and for nitrobenzene and thio-phene in mineral oil by a forced-choice, three-stimulus sniff technique (Henkin et al., 1971;Marshall and Henkin, 1971). Smell thresholds weremeasured on one to three separate occasions. Thelowest threshold was used for analysis whenevermore than one measurement was obtained.

MEASUREMENTS OF METAL METABOLISM Serum con-centrations of zinc and copper and 24 hour urinaryexcretion of these metals were determined. Blood andurine samples were collected in metal-free tubes andplastic containers, respectively, as previously de-scribed (Meret and Henkin, 1971). Measurements ofzinc and copper were carried out by atomic absorp-tion spectrophotometry on an IL Model 153 atomicabsorption spectrometer by a method describedpreviously (Meret and Henkin, 1971).

SUBJECTS The experimental subjects were 29patients, 17 males and 12 females, mean age 49years (range: 22 to 76 years), 28 Caucasians and oneNegro (Table 1). These patients were referred to theTaste and Smell Clinic at the Clinical Center of theNational Institutes of Health by their personalphysicians for evaluation of subjective complaintsreferable to taste and/or smell abnormalities. Themean duration of symptoms at the time these

803



http://jnnp.bmj.com

/J N

eurol Neurosurg P


nloaded from


Paul J. Schechter and Robert L Henkin

H [+1+1+1+1+l1+ +1 +1+1+! I

++ ++++++I*++++++ ++ + ++++++++

II I+++I I+I+++I + +1 +1+1+11+

+ + q

+1 I!

+ m

++ ++II+I+I++III+ I+ + ++I+I+++

-;;E E E110 0 C40.. . .

-;. m=e

4-0

40

m0o mo X voooo o t!o om

-.+ I +e..++±N+ ++ ++ ++ + +++ +++ + 4'.

1 1 $'' I I I I I I I I II1 1 Q 1 1 1 M 1 -LI'

.*4Y* ) .

0. ~ .'0E E E E E E E EE E E E E E E E E E E E E E EE- E E E EEN.EE.E E EE- EE EE E4 _ " _N 0-4 _-. o.- " _" _- 0- " _-- " _* _ __4 0- 0- 0.

-41 --41 4-4 -411 -+4~C4lmOe ~NM - --- o-~el N

a o 00o o m C o N't t o NW) n It In'I tnv" N " - It It 1t " \D 't

Cd Yd

-t064jttm L4 " x2244~ ..i

.4-j 6-u -~ 2ci: em~0 ~.004.

14t-4~! -41 -lmol e4 iN.: encl

'ICO 00 w0N 'I4 'O0 mO 0o

i Cj~~~" a;E HoM0;w

804

t3

O

Q'

0i

In02

:sIAbo

6.6L

4t0

0Cqsz1.

-*40

-

c

t-

3 3 ;

vi 6 F2



http://jnnp.bmj.com

/J N

eurol Neurosurg P


nloaded from



patients were first seen was 2- years (range: 3months to 23 years). All patients had suffered headtrauma before the onset of their symptoms and allclaimed to have had normal senses of taste and smellbefore the trauma.

Twenty-four of the patients (83%) noted the onsetof changes in taste or smell immediately after thetrauma or as soon as their mental state becameclear. The other five patients noted onset ofsymptomsfrom three weeks to four months after trauma.

Seven of the 29 patients (24%) suffered variousfractures of the skull after trauma (documented byradiographs of the skull): occipital fractures (two),parietal (one), basilar (two), temporal (one), and bothbasilar and parietal (one). The site of trauma to theremaining 22 patients varied; however, eight of 11who could specifically localize a site reported thattrauma occurred in the occipital area. Two patientshad a subdural haematoma (one right temporalregion, one left temporoparietal region) which weresurgically evacuated; one had an epidural haema-toma in the parasagittal area.Of the 25 patients in whom this information could

be obtained, 20 reported a period of unconsciousnessafter trauma which lasted an extended period oftime. In three patients the trauma was considered tobe so trivial by the patient that medical treatment wasnot sought. In two cases head trauma was severeenough to produce other permanent neurologicaldeficits.The control subjects were 35 normal volunteers

without disease and 60 patients with various diseasesbut without any subjective abnormality of taste orsmell. These subjects were 44 Caucasian males and51 Caucasian females, aged 15 to 77 (mean: 39) years.The patients had diseases in which zinc and coppermetabolism was not altered.

EVALUATION OF PATIENTS Each patient underwentan extensive examination of the head and neckregion which revealed no pathology related to thehead trauma. Fungiform, circumvallate, and palatalpapillae were present in each patient and bilateralparotid salivary flow rates and pharyngeal andlaryngeal movements were normal. The followinglaboratory tests were performed in each patient: ahaematological examination including haemoglobin,haematocrit, red blood cell indices, total whiteblood cell count with a differential count, reticulo-cyte and platelet counts, and erythrocyte sedimenta-tion rate; serum sodium, potassium, chloride,carbon dioxide, calcium, phosphorus, magnesium,blood sugar, urea nitrogen, creatinine, uric acid,alkaline phosphatase, glutamic oxalacetic andglutamic pyruvic transaminases, total protein,albumin, electrophoresis and cholesterol; urin-

analysis including specific gravity, pH, evaluation ofpresence of glucose and bilirubin, and a micro-scopic examination of the sediment. Radiographs ofthe chest, skull, including measurement of thevolume of the sella turcica (DiChiro and Nelson,1962), and sinuses were carried out. A brain scanafter intravenous injection of 99m Technetium wasalso obtained. Results of these tests did not relate thesensory loss of any patient to any underlying patho-logical aetiology other than the trauma sustained.

RESULTS

SUBJECTIVE RESPONSES Subjective changes intaste and smell are shown in Table 2. Seventeenpatients (590%) complained of decreased tasteacuity and 13 (450%) complained of dysgeusia.Ten (340%) noted cacogeusia, six (210%) reportedphantogeusia, and seven (24%) experiencedheterogeusia. Seven patients experienced morethan one specific symptom of dysgeusia andthree reported the presence of cacogeusia,phantogeusia, and heterogeusia.

TABLE 2SUBJECTIVE ABNORMALITIES OF TASTE AND SMELL IN

PATIENTS AFTER HEAD TRAUMA

Taste

Hypogeusia (Y) Dysgeusia (Y.)

Cacogeusia Phantogeusia Heterogeusia

59 34 21 24

Snmell

Hyposmia (%) Dysosmia (%0)

Cacos,nia Phantosmia Heterosmia

90 38 14 17

Twenty-six patients (900%) complained ofdecreased olfactory acuity. One patient reporteddecreased olfactory acuity immediately aftertrauma but noted a spontaneous and gradualreturn to normal. The two other patients deniedany decreased olfactory acuity. Twelve patients(41%) complained of dysosmia. Of these, 11(38%) reported cacosmia, four (14%) reportedphantosmia, and five (170%) reported heterosmia.Five patients experienced more than one specific

805



http://jnnp.bmj.com

/J N

eurol Neurosurg P


nloaded from



TABLE 3MEDIAN DETECTION AND RECOGNMON THRESHOLDS FOR FOUR TASTE QUALITIES IN 29 PATIENTS

WITH HYPOGEUSIA AFTER HEAD INJURY

Taste quality Patients Normal subjects

MDT/MRT Range MDT/MRT Range

NaCl 75/150 6-650/30-* 12/30 6-60/6-60Sucrose 60/90 12-800/30-* 12/30 6-60/6-60HCI 15/90 0 8-> 500/3-> 500 3/6 0 5-6/0 8-6Urea 650/800 90-> 8,000/90-> 8,000 120/150 90-150/90-150

MDT: median detection threshold in mM. MRT: median recognition threshold in mM.* Inability to recognize saturated solutions of NaCl or sucrose.

symptom of dysosmia and three reported thepresence of all three.Because of decreased palatability of food, par-

ticularly associated with dysgeusia and dysosmia,nine patients (310%) sustained weight losses of 4to 25 pounds (2 to 5 kg). Of these nine, sixexperienced symptoms of cacogeusia and/orcacosmia. Sixteen patients (55%) reported thatthey had noticeably increased the addition ofNaCl to food to obtain the preferred salty tasteand six (21 %) noted that they had to increase theamount of sugar they normally added to theirfood or drink to produce the preferred sweettaste.

Six of the 17 patients questioned (35%0)reported a decrease in libido which was directlyrelated in time to the trauma. Whether thisrelated to the trauma, per se, or to the sensoryloss resulting therefrom, or both is unclear.However, patients with the syndrome of idio-pathic hypogeusia, without a history of trauma,often reported a similar loss of libido (Henkin etal., 1971; Schechter et al., 1972).

OBJECTIVE MEASUREMENTS Taste Median de-tection and median recognition thresholds forfour taste qualities in the patients are comparedwith those of control subjects in Table 3; in thepatients seven of eight threshold measurementswere elevated above the upper limit of the normalrange; the median detection threshold for sucrosewas the only one which was within the normalrange. Four patients exhibited ageusia forspecific tastants; for NaCl (one patient), HCI(two patients), and urea (four patients). Ninepatients exhibited elevated detection and recog-

nition thresholds for all four tastants. Fifteenhad elevated detection and recognition thresholdsfor sucrose; 22 for NaCl; 27 for HCI; and 25 forurea.Each patient studied exhibited elevated detec-

tion or recognition thresholds for at least one

taste quality. In four patients threshold eleva-tions were minimal, the major abnormality con-

sisting of a confusion in the recognition of sourand bitter. These latter patients complainedprimarily of dysgeusia. Eleven patients who

TABLE 4MEDIAN DETECTION AND RECOGNITION THRESHOLDS FOR THREE VAPOURS IN 28 PATIENTS WITH HYPOSMIA AFTER

HEAD INJURY

Vapour Patients Normal subjects

MDT/MRT Range MDT/MRT Range

Pyridine 10-1/102 10- 3_*/10 - 3-* 10 - 7/10- 3 10-8-10- 5/10 - 4-10 - 2Nitrobenzene 10-1/A 10-3-*/10-2_* 10-6/10-3 10-7-10-5/10--01-2Thiophene A/A 10 4-*/1 -3-* 10 - 7/10- 3 10- 8_10 - 5/10- 4-10 - 2

MDT: median detection threshold in mole/I. MRT: median recognition threshold in mole/I. A: ability to detector recognize an absolute solution.* Inability to detect or recognize an absolute solution.

806



http://jnnp.bmj.com

/J N

eurol Neurosurg P


nloaded from



exhibited elevations in detection and recognitionthresholds were subjectively unaware of anyhypogeusia, complaining only of loss of smell.No correlations could be made between taste

qualities affected, extent of taste impairment andseverity of injury, presence or absence of skullfracture, locus of blow to the head, or whether aperiod of amnesia followed the trauma.

Smell Median detection and recognition thresh-olds for three vapours in 28 of the patients areshown in Table 4. Each patient exhibited elevateddetection or recognition thresholds for at leastone vapour, even though three patients statedthat they had no loss of smell acuity at the timeof study. These latter patients subjectively com-plained only of taste loss. All patients exhibiteddetection thresholds for the three vapours testedwhich were elevated above the upper limit of thenormal range. Nine patients exhibited at leastone recognition threshold within the normalrange. One demonstrated anosmia. Thirteenpatients demonstrated an inability to detect orrecognize at least one vapour. Five patientsexhibited type I hyposmia; 23 patients exhibitedtype II hyposmia.As with taste acuity, no correlations could be

made between extent of olfactory loss andseverity of injury, presence or absence of skullfracture, locus of blow to the head, whether ornot a period of unconsciousness followed thetrauma, or to the variability in time after injuryat which the symptoms occurred.

DISCUSSION

The present study describes alterations in tasteand smell in 29 patients after head trauma. These29 comprise the single largest reported series ofpatients with post-traumatic loss of taste and theonly group in whom quantitative measurementsof taste acuity have been determined. Althoughit is not possible to estimate prospectively theincidence of taste disturbances after head trauma,careful attention to the patients' complaints andquantitative taste testing revealed a greater inci-dence of taste abnormalities than the 0 4°/ pre-viously estimated (Sumner, 1967). In addition,although taste and smell abnormalities usuallyoccur immediately after head injury, theseresults emphasize that symptoms can commence

several months after trauma. These observationssuggest that patients should be observed atintervals subsequent to their injury in spite of theabsence of other signs or symptoms of neuro-logical dysfunction at the time of injury.

Differentiation between delayed onset of tasteand smell abnormalities in patients after headinjury and some forms of 'idiopathic' impair-ment of taste and smell can be difficult. Aetio-logical factors such as the sudden onset of theimpairment after an influenza-like illness or somesurgical procedure (Henkin et al., 1971) or theadministration of a drug (Henkin, 1971a) areuseful sources of information to help in thisregard. The presence of acute or chronic localnasal pathology such as polyps, sinusitis, rhinitis,or nasal allergies is also useful. However, inthose patients who note only a gradual, pro-gressive diminution in acuity in taste and smell,the history of a specific incident of head traumamay be the only aetiological factor which can beused to differentiate these patients from thoseaffected by the myriad of other causes of tasteand smell abnormalities (Henkin, 1967a, b).Quantitative measurement of taste and smellloss, presence or absence of dysgeusia, andmeasurement of serum and urinary zinc levelsmay also be useful to differentiate post-traumaticfrom some types of 'idiopathic' impairment(Henkin et al., 1971).No relationship between severity of head

injury, presence or absence of amnesia or skullfracture, specific locus of injury, and severity ofsensory loss could be made. However, the highincidence of occipital trauma in these patientssuggests that a blow to this area of the skull maypredispose to taste and smell alterations. Evenminimal trauma may be sufficient to precipitatesensory symptoms.

In all cases olfactory symptoms invariablyaccompany gustatory complaints. Objectivemeasurements of taste and smell acuity revealedthat elevated smell thresholds invariably accom-panied elevated taste thresholds even if patientsdid not complain of loss of smell.

Fifty-two percent (15 of 29) of the patientshad symptoms of one or more forms of dysgeusiaor dysosmia. This incidence is considerablyhigher than that estimated by previous investiga-tors (Leigh, 1943; Sumner, 1964, 1967). In somepatients these symptoms were much more

807



http://jnnp.bmj.com

/J N

eurol Neurosurg P


nloaded from


Paul J. Schechter and Robert I. Henkin

FIGURE. Total serum concen-tration of zinc in 27 patientswith hypogeusia and hyposmiaafter head injury (Lii) and in95 control subjects (U). Theper cent of total individuals ineach category is plotted on theordinate, serum zinc concentra-tion in 1ig/100 ml on theabscissa. Note the shift of thedistribution of the serum zincconcentrations of the patientstoward the direction of lowerthan normal concentrations ofzinc.

i

.I

disturbing than the hypogeusia or hyposmia andnot uncommonly obscured the actual loss ofsensory acuity. Indeed, because of the intensityof these obnoxious taste and smells somepatients with dysgeusia and/or dysosmia con-sidered their taste and smell acuity to be moreacute than before their trauma.

TABLE 5SERUM CONCENTRATION AND URINARY EXCRETION OF ZINCAND COPPER IN PATIENTS AFTER HEAD INJURY AND IN

CONTROLS

Serum (g/100 ml) Urinary (p.g/24 hr)

Zn++ Cu+ + No. Zn+ + Cu+ + No.

METAL MEASUREMENTS Total serum zinc andcopper concentrations and 24 hour urinaryexcretion of zinc and copper in the patients werecompared with those from control subjects(Table 5). The patients exhibited a significantdecrease in total serum zinc concentrations (P <0-001) and a significant increase in total serumcopper concentration (P < 0-001) compared withcontrols. Urinary zinc excretion was also slightlybut not significantly higher in the patients whileno differences in the urinary excretion of copperwere observed.The Figure illustrates the differences between

the distribution of concentration of total serumzinc in 95 control subjects and in 27 patientswith hypogeusia and hyposmia after headtrauma. There is a shift of the distribution ofserum zinc levels of the patients toward thedirection of lower than normal zinc concentra-tions. No control subject had a total serum zincconcentration below 61 ,ug/l00 ml whereas 18%of the patients had serum zinc levels below this

Post-traumapatients 77±3*t 113±4* 27 482±54 31±2 22

Controls 99 ± 2 100± 2 95 419 ± 25 34 ± 3 67

* P< 0-001. t Mean ± ISEm

value. On the other hand, no patient had a totalserum zinc concentration greater than 110 ,ug/100 ml, whereas 22% of the control subjects hadserum zinc levels above this concentration.The aetiology of dysgeusia and dysosmia after

head trauma is obscure. Paskind (1935) sug-gested that dysosmia was a symptom of nerveirritation which preceded anosmia or nervedestruction. On the other hand, Leigh (1943)suggested that dysosmia represented a stage ofrecovery from anosmia. Since dysosmia cancommence long after the appearance of hypos-mia, Paskind's hypothesis is not tenable. Leigh'ssuggestion also does not adequately explain thecausation of these symptoms, since many cases

808

zi!ii*.Iz



http://jnnp.bmj.com

/J N

eurol Neurosurg P


nloaded from



of dysosmia and dysgeusia have been observedwithout any subjective loss of taste or smell orwithout objective threshold elevations of tasteand smell (Schechter et al., 1972).The magnitude of the subjective complaints of

loss of smell in these patients is of interest be-cause the majority of these patients exhibitedtype IL hyposmia, a quantitative defect inolfactory acuity. This differs from type I hypos-mia, which characteristically follows surgicalinterruption of the olfactory nerves, extirpationof the olfactory epithelium in maxillofacial pro-cedures to treat carcinoma of the sinuses (Hoyeet al., 1970), or after total surgical laryngectomy(Henkin et al., 1968). Many patients with type IIhyposmia are unaware of their sensory loss(Henkin and Marshall, 1971). However, thesuddenness of the loss of olfactory acuity whichusually follows the head trauma may be thestimulus for the complaints of the patients.The mechanism whereby a single blow to the

head produces abnormalities of taste as well assmell is unclear. Post-traumatic hyposmia hasbeen thought to be produced by a shearing ofolfactory nerve filaments as they pass throughthe rigid cribiform plate (Ogle, 1870; Sumner,1967). Although this hypothesis may explain thehyposmia resulting from trauma, it does notexplain the accompanying abnormalities oftaste, since simultaneous bilateral damage to theolfactory, lingual, glossopharyngeal, and vagusnerves does not occur in these injuries. Indeed,each patient in this study exhibited normal oralpapillae, salivary flow, and pharyngeal andlaryngeal function, observations which are in-compatible with intact sensory function of theseventh and ninth cranial nerves. Further evi-dence against such a neurological lesion pro-ducing both taste and smell abnormalities is thatthis entire syndrome can occur after head traumaof such a mild degree that medical assistance isnot sought. In addition, this syndrome occurredwithout any other residual neurological deficitsincluding those of cranial nerves seven and ninein most patients studied.

It has been reported that in most cases oftaste loss after head trauma there is a spontane-ous return of normal taste acuity with time(Sumner, 1967). This had not occurred in any ofthe patients observed in this study even thoughintervals as long as 23 years had elapsed between

the time of head injury and the time they wereobserved in our clinic.We have previously demonstrated that altera-

tions in the metabolism of trace metals eitherdrug induced (Henkin et al., 1967; Henkin andBradley, 1969; Henkin et al., 1972) or secondaryto various disease states (Henkin and Bradley,1969; Henkin et al., 1971; Schechter et al., 1972;Cohen et al., 1973) are associated with altera-tions in taste and smell acuity. Patients with thesyndrome of idiopathic hypogeusia with dys-geusia, hyposmia, and dysosmia exhibit de-creased concentrations of total serum zinc andincreased concentrations of total serum copper(Schechter et al., 1972), the values beingnumerically quite similar to those observed inpatients after head trauma. The oral administra-tion of Zn + + to patients with the former syn-drome resulted in a decrease in symptoms andreturn of taste acuity towards or to normal in asignificant number of patients (Schechter et al.,1972). Patients with hypogeusia after thermalinjury exhibited decreased serum zinc concentra-tions and increased 24 hour urinary excretion ofzinc (Cohen et al., 1973). Administration of theamino acid, L-histidine, associated with a signifi-cant zincuria and subsequent hypozincaemiawith a loss of total body zinc produces hypo-geusia, hyposmia, anorexia and, not un-commonly, dysgeusia and dysosmia (Henkin etal., 1972). Administration ofZn+ +, in the face ofcontinued L-histidine administration, was associ-ated with the rapid return of serum zinc tonormal and the correction of the abnormalitiesof taste and smell to normal (Henkin et al., 1972).The relationship between altered sensory percep-tion and abnormalities of zinc metabolism hasbeen documented in various forms of liverdisease (Henkin and Smith, 1971, 1972), growthretardation (Hambidge et al., 1972), malabsorp-tive processes of several types (Henkin, unpub-lished observations), and malignancies of severaltypes (Henkin, unpublished observations).

Since patients with hypogeusia and hyposmiaafter head injuries exhibit serum zinc concentra-tions similar to those observed in patients withhypogeusia subsequent to zinc loss some aspectsof the altered taste and smell perception inpatients after head trauma may be secondary toalterations in zinc metabolism. If these patientswere to respond to oral zinc administration in a

809



http://jnnp.bmj.com

/J N

eurol Neurosurg P


nloaded from



similar manner to that observed in patients withidiopathic hypogeusia, then improvement inthese taste and smell abnormalities might beexpected. Studies are currently in progress todetermine if this hypothesis be correct.

The authors wish to thank Mrs Carol J. Franklinand Mrs Diane A. Bronzert for their assistanceduring this study.

REFERENCES

Cohen, I. K., Schechter, P. J., and Henkin, R. I. (1973).Hypogeusia, anorexia, and altered zinc metabolismfollowing thermal burn. Journal of the American MedicalAssociation, 223, 914-916.

Di Chiro, G., and Nelson, K. B. (1962). The volume of thesella turcica. American Journal of Roentgenology, 87, 989-1008.

Hambidge, K. M., Hambidge, C., Jacobs, M., and Baum,J. D. (1972). Low levels of zinc in hair, anorexia, poorgrowth, and hypogeusia in children. Pediatric Research, 6,868-874.

Henkin, R. I. (1967). Abnormalities of taste and olfaction inpatients with chromatin negative gonadal dysgenesis.Journal of Clinical Endocrinology and Metabolism, 27,1436-1440.

Henkin, R. I. (1967a). The definition of primary and acces-sory areas of olfaction as the basis for a classification ofdecreased olfactory acuity. In Olfaction and Taste. 2, pp.235-252. Edited by T. Hayashi. Pergamon Press: Oxford.

Henkin, R. I. (1967b). The role of taste in disease andnutrition. Borden's Review ofNutrition Research, 28, 71-87.

Henkin, R. I. (1971). Disorders of taste and smell. Journal ofthe American Medical Association, 218, 1946.

Henkin, R. I. (1971a). Griseofulvin and dysgeusia: implica-tions ? Annals of Internal Medicine, 74, 975-796.

Henkin, R. I., and Bradley, D. F. (1969). Regulation of tasteacuity by thiols and metal ions. Proceedings of the NationalAcademy of Science of the United States of America, 62,30-37.

Henkin, R. I., Gill, J. R., Jr, and Bartter, F. C. (1963).Studies on taste thresholds in normal man and in patientswith adrenal cortical insufficiency: the role of adrenalcortical steroids and of serum sodium concentration.Journal of Clinical Investigation, 42, 727-735.

Henkin, R. I., Hoye, R. C., Ketcham, A. S., and Gould,

W. J. (1968). Hyposmia following laryngectomy. Lancet,2, 479-481.

Henkin, R. I., Keiser, H. R., and Bronzert, D. (1972).Histidine-dependent zinc loss, hypogeusia, anorexia, andhyposmia. (Abstract.) Journal of Clinical Investigation, 51,44a.

Henkin, R. I., Keiser, H. R., Jaffe, I. A., Sternlieb, I., andScheinberg, I. H. (1967). Decreased taste sensitivity afterD-penicillamine reversed by copper administration.Lancet, 2, 1268-1271.

Henkin, R. I., Schechter, P. J., Hoye, R., and Mattern,C. F. T. (1971). Idiopathic hypogeusia with dysgeusia,hyposmia, and dysosmia. A new syndrome. Journal of theAmerican Medical Association, 217, 434-440.

Henkin, R. I., and Smith, F. R. (1971). Hyposmia in acuteviral hepatitis. Lancet, 1, 823-826.

Henkin, R. I., and Smith, F. R. (1972). Zinc and coppermetabolism in acute viral hepatitis. American Journal ofMedical Science, 264, 401-409.

Hoye, R. C., Ketcham, A. S., and Henkin, R. I. (1970).Hyposmia after paranasal sinus exenteration or laryngec-tomy. American Journal of Surgery, 120, 485-491.

Laemmle, H. (1931). Ueber Geruchsstorungen und ihreklinische Bedeutung. Archiv fur Ohren-, Nasen- undKehlkopfheilkunde, 130, 22-42.

Leigh, A. D. (1943). Defects of smell after head injury.Lancet, 1, 38-40.

Marshall, J. R., and Henkin, R. 1. (1971). Olfactory acuity,menstrual abnormalities, and oocyte status. Annals ofInternal Medicine, 75, 207-211.

Meret, S., and Henkin, R. I. (1971). Simultaneous directestimation by atomic absorption spectrophotometry ofcopper and zinc in serum, urine, and cerebrospinal fluid.Clinical Chemistry, 17, 369-373.

Mifka, P. (1965). Der traumatisch verursachte Verlust desGeruchs und Geschmackssinnes. In Late Sequelae of HeadInjuries. 8th International Congress of Neurology, Vienna,1965, Proceedings, Vol. 1, pp. 379-388. Wiener Medizi-nischen Akademie: Vienna.

Ogle, W. (1870). Anosmia; cases illustrating the physiologyand pathology of the sense of smell. Lancet, 1, 230-231.

Paskind, H. A. (1935). Parosmia in tumorous involvement ofolfactory bulbs and nerves. Archives of Neurology andPsychiatry (Chic.), 33, 835-838.

Schechter, P. J., Friedewald, W. T., Bronzert, D. A., Raff,M. S., and Henkin, R. I. (1972). Idiopathic hypogeusia: adescription of the syndrome and a single-blind study withzinc sulfate. International Review ofNeurobiology, Suppl. 1,125-140.

Sumner, D. (1964). Post-traumatic anosmia. Brain, 87, 107-120.

Sumner, D. (1967). Post-traumatic ageusia. Brain, 90, 187-202.

810



http://jnnp.bmj.com

/J N

eurol Neurosurg P


nloaded from


abnormalities of taste smell after head trauma - … · anosmia inability to detect or recognize...

Documents