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Anosmia associated with hearing loss and benign
Автор G. Ottaviano, G. Marioni, R. Marchese-Ragona, C.P. Trevisan1, C. de Filippis, A. Staffieri   

It is well known that head trauma may cause hearing loss, which can be either conductive or sensorineural. Benign paroxysmal positional

vertigo and olfactory dysfunction due to head trauma are also well known. The association between sensorineural hearing loss and anosmia,

following head trauma, is extremely rare.
Two rare cases of post-traumatic occurrence of hearing loss, olfactory dysfunction and benignpositional vertigo are reported and the pathophysiology of the association between sensorineural hearing loss, anosmia and benign paroxysmal

positional vertigo, after head injury, are briefly discussed. ENT specialists should, in the Authors’ opinion, be aware of the possible

association between anosmia, sensorineural hearing loss and benign paroxysmal positional vertigo after head injury, even in the absence of skull fracture.

Riassunto

I traumi cranici possono associarsi ad ipoacusia che puт essere sia neurosensoriale che trasmissiva. И noto che sia la vertigine parossistica

posizionale benigna che l’alterazione della capacitа olfattiva possono essere conseguenza di un trauma cranico. L’associazione

tra ipoacusia neurosensoriale ed anosmia dopo trauma cranico и molto rara. Descriviamo 2 casi in cui dopo trauma cranico entrambi

i pazienti hanno presentato ipoacusia neurosensoriale, alterazione olfattiva e vertigine posizionale benigna e discutiamo brevemente i

meccanismi fisiopatologici di tale associazione. Pensiamo sia giusto sottolineare la possibilitа che anosmia, ipoacusia neurosensoriale e

vertigine parossistica posizionale benigna possano presentarsi in associazione dopo trauma cranico anche senza frattura ossea.

Introduction

Post-traumatic hearing loss is a well known occurrence 1.

All head injuries, with or without skull base fracture, may

cause hearing loss which, in both instances, can be conductive

as well as sensorineural
2. The site of the hearing

impairment can be peripheral or central and the pathophysiology

of hearing loss, after skull trauma, may be

multiple. Benign paroxysmal positional vertigo due to

head trauma is a well-known occurrence. Head injury is

also a common cause of olfactory dysfunction.

The present report focuses on two cases of sensorineural

hearing loss (SNHL) with benign paroxysmal positional

vertigo and anosmia following traumatic head injury.

Case reports

Case 1

In September 2005, a 40-year-old male was referred to

our Department complaining of hearing loss and anosmia

following head trauma which had occurred nine days previously

on account of a pedestrian casualty. The patient

reported smelling loss, left ear tinnitus, vertigo after head

movements to the right, without hearing loss or earache.

Otoscopy revealed the external left auditory canal partially

covered by dry blood and mild hyperaemia of the left

tympanic membrane; the rest of the ear, nose and throat

(ENT) and neurovestibular examination was normal. The

neurological examination was also normal, apart from the

indicated alterations of the first and eighth cranial nerves.

Pure tone audiometry showed a severe left SNHL and a

moderate right SNHL (Fig. 1); pure tone average (PTA),

calculated for 0.5, 1, 2, 3 KHz, was 71.25 dB on the left

ear and 58.75 dB on the right ear. A previous pure tone

audiometry performed at the age of 25 years (routine

screening) was, bilaterally, within the normal range (right

and left PTAs: 20 dB). Middle ear impedance,

G. Ottaviano, et al.

EPUB

by tympanometry, showed Jerger type-A curves in both

ears. Controlateral stapedius reflexes were bilaterally absent.

Neither spontaneous nor positional nystagmus were

detected. The patient had undergone temporal bone computerized

tomography (CT) which did not show temporal

bone fractures and gadolinium-enhanced magnetic resonance

imaging (MRI) of the brain, brainstem, cerebellum-

pontine angles, internal auditory canals and olfactory

area that ruled out abnormalities. Oral steroid treatment

was prescribed but was refused by the patient who was

then treated with oral A, C, E vitamins, ginkgo biloba and

phospholipids twice a day (Otobrain
® Farmila-Thea Farmaceutici,

Settimo Milanese, Italy) for 3 months without

any improvement.

In February 2006, as the patient continued to complain of

loss of smell, rhinological evaluation was performed. Direct

nasal endoscopy did not show any anatomical alteration

which could explain anosmia. Peak nasal inspiratory

flow showed flows of 170 l/min which were normal for

the patient’s age, height and sex, according to Ottaviano

et al.
3. A basal anterior active rhinomanometry showed

no abnormal nasal resistences. Le Nez du Vin was thenperformed according to McMahon and Scadding

4, which

we normally use as a quick test of olfaction. As the patient

gave more than one wrong answer, the University

of Pennsylvania Smell Identification Test was performed.

Since the patient gave only 9 correct answers, we concluded

that the patient was affected by anosmia according

to Doty et al.
5.

Eighteen months after the occurrence of the head trauma,

the patient, who still complained of a clear-cut loss of

smell, with hearing loss, was re-evaluated: the otological

and neurological examinations did not show any clinical

modifications, pure tone audiometry was unchanged, the

auditory brainstem response test (ABR) (120 dB nHL bilateral

click stimulation) showed a wave-form consistent

with cochlear hearing loss. Speech audiometry (speech

material: two-syllabic words) was performed. The left

and right speech-reception threshold (SRT) were 40 dB

and 30 dB, respectively. The video-nystagmographic gaze

test did not show spontaneous nystagmus. Apogeotropic

positional nystagmus was detected at the Dix-Hallpike

manoeuvre on the right side, compatible with benign

paroxysmal positional vertigo (BPV) of the right posterior

semicircular canal. Saccades were normal. Tracking

test was normal. A caloric test, performed by irrigating

each auditory external canal with cool (+30°C) and warm

(+44°C) water, showed a normal response.

Case 2

In March 2007, a 57-year-old female was referred to our

Department complaining of bilateral hearing loss, anosmia,

hypogeusia and vertigo following head trauma occurred

7 months before due to a pedestrian casualty. Otoscopy

was normal. Nasal endoscopy showed a slight deformity

of the septum and large inferior turbinates without abnormalities

in the olfactory area. Peak nasal inspiratory flow

showed flows of 120 l/min which were below normal values

for patient’s age, height and sex
3. The patient gave 3
wrong answers to Le Nez du Vin test. At the University of

Pennsylvania Smell Identification Test, the patient gave

only 10 correct answers and we concluded that the patient

was affected by anosmia. Neurological examination was

normal, apart from the indicated alterations of the first

and eighth cranial nerves. A post-traumatic CT brain scan

showed a bilateral contusion of the frontal cerebral region

(Fig. 2) and fracture of the occipital squama. Pure tone

audiometry, performed 1 month earlier, in another Institution

showed a moderate bilateral SNHL [PTA was 45 dB

bilaterally].

As trauma had occurred 7 months earlier, no therapy

was suggested to the patient. The patient was submit-

Fig. 1. Case 1. Pure tone audiometry (left PTA 71.25 dB, right PTA 58.75 dB).

Fig. 2. Post-traumatic CT scan of brain showing bilateral contusion of frontal cerebral region.

ted to further pure tone audiometry, speech audiometry,

ABR, videonystagmography, temporal bone CT scan and

gadolinium-enhanced MRI of brain, brainstem, cerebellum-

pontine angles, internal auditory canals and olfactory

area. The pure tone audiometry showed a bilateral SNHL.

The right ear PTA was 40 dB, the left ear 43.75 dB (Fig.

3). Left and right ear SRT were 20 dB. ABR confirmed

the cochlear origin of bilateral hearing loss. Videonystagmography

showed a left post-traumatic BPV. Temporal

bone CT scan disclosed a right petrous apex fracture with

involvement of the otic capsule (Fig. 4). Gadolinium-enhanced

MRI of the central nervous system confirmed the

bilateral contusion of the frontal lobes without other abnormalities

(Fig. 5).

Head injuries may cause hearing loss which can be either

conductive or sensorineural.

After these kinds of traumas, the middle ear or cochlea

appear to be the most frequently involved areas. In these

cases, the hearing loss is most commonly due to a temporal

bone fracture with involvement of the otic capsule or

with disruption of the ossicular chain. Nevertheless, the

forces created by the trauma may also force the stapedial

foot inwards through the oval window
6 and, in some

cases, may cause rupture of the round or oval window

membranes leading to perilymphatic fistula. It is also well

known that an increase in cerebrospinal fluid pressure

may be transmitted to the inner ear via the cochlear aqueduct

or through the internal auditory canal
7 or by way ofthe endolymphatic sac 6 leading to damage in the organ of

Corti. Elevated intra-cranial pressures together with direct

injuries to blood vessels and thrombosis may also reduce

the blood supply to the inner ear
8 9. The eighth cranial

nerve may also be damaged contributing to hearing impairment

10.

Post-mortem histopathological studies in patients who

have suffered head injury have shown abnormalities of

the internal auditory canal, inner ear tissues, eighth nerve

and brainstem. Considering a limited series of 8 autopsy

cases, Makishima and Snow, in 1976, described, in 3

cases, the presence of blood in the scala tympani and, in

1 case of nubeculae, in scala vestibuli. They also found

haemorrhage (6 cases), laceration (5 cases) and oedema

(1 case) of the eighth nerve. Herniation (2 cases), haemorrhage

(4 cases), softening (5 cases) and oedema (1 case)

of the brain stem have also been described
11.

Reviewing the clinical features of 240 cases of BPV, in

1987, Baloh et al.
12 found that the first diagnostic category

was post-traumatic: these patients presented the onset

Fig. 4. CT scan of temporal bone showing right petrous apex fracture with

involvement of otic capsule.

Fig. 3. Case 2. Pure tone audiometry (left PTA 43.75 dB, right PTA 40 dB).

Fig. 5. T2-weighted MRI of central nervous system showing bilateral contusion of frontal lobes

of BPV within 3 days of well-documented head trauma.

From a physiopathological viewpoint, it is easy to conceive

that head trauma could throw otoconial debris into

different canals and be frequently responsible for BPV of

the posterior semicircular canal.

Head injury is also a common cause of olfactory dysfunction.

In 1997, Doty et al., following revision of 268

patients who had suffered head trauma, reported that

anosmia occurred in about 66.8% of the cases and that

rarely olfactory function became normal again
5. During

the trauma, either shearing of olfactory filaments (as

they pass through the cribiform plate) or contusion to

the olfactory bulb may occur. Moreover, contusion or a

shearing injury to the cerebral cortex (frontal and temporal

lobes) may occur
5 13 14. According to Zusho 13, 55.2%

of post-traumatic anosmia are not associated with facial

or skull fractures.

The association between SNHL and anosmia, following

head trauma is extremely rare. Kittel, in 1961, and Khul

and Krauss, in 1969, reported, separately, two cases of bilateral

SNHL, anosmia and vertigo due to a bilateral vestibular

areflexia after head injury
15 16. From the ENT examination

and the clinical and radiological examinations,

it seems that, in our first case, the bilateral SNHL may

most probably be explained by bilateral cochlear damage,

as well as the left SNHL, in the second case. In the second

patient, the right SNHL may be due to the temporal

bone fracture with the involvement of the otic capsule. In

the first case, anosmia seems to be most probable consequence

of olfactory filament shearing while, in the second

one, it could be explained by the contusion of the olfactory

bulb as well as of the frontal lobes, revealed by imaging.

In both cases, clinical and videonystagmographic

evidence of post-traumatic BPV was found.

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