Abstract. – OBJECTIVE: The aim of this studyis to develop a diagnostic-therapeutic algorithmfor those suffering from tinnitus who seek emer-gency aid.

MATERIALS AND METHODS: A literature re-view has been performed on articles from thelast 30 years.

RESULTS: It is important to activate medical orsurgical diagnostic and therapeutic strategies, inorder to safeguard and rehabilitate the variousfunctions affected. Psychiatric comorbidity is themost frequent pathological condition of thosewith serious or catastrophic tinnitus. In thesecases, mortality risk is linked to suicide, morbidi-ty to tinnitus-correlated distress.

CONCLUSIONS: Tinnitus, mainly linked toloss of hearing, is a frequent symptom amongthe population at large. About 7% of those af-fected by tinnitus turn to their doctor to solvetheir problem, while between 0.5 and 2% requesturgent medical assistance. Their cry for helpmay be the result of an acute onset of tinnitus orthe rapid impairment of an already chronic con-dition. Tinnitus is not considered an urgent ear,nose and throat (ENT) condition by the Associ-azione Otorinolaringologi Ospedalieri Italiani(AOOI) [Italian Association of Hospital ENT],even though there are many pathological condi-tions, sometimes serious, associated with tinni-tus and emergency action is necessary to re-duce the risk of morbidity and mortality.

Key words:Tinnitus, Decompensated tinnitus, Urgency, Emer-

gency, Psychiatric comorbidity, Suicide.

Introduction

Tinnitus can be defined as the perception of asound in the absence of an external stimulus1,2.The word comes from the Latin “tinnire” (toring)3,4 and is usually described by the patient asa “ringing in the ears”5.

Corresponding Author: Filippo Mazzei, MD; e-mail: filippo.mazzei@gmail.com 2955

Tinnitus is perceived as a subjective hearingsensation in one or both ears and/or in the head5,6,not produced by an external source, and can be re-ported as a simple (whistling, hissing, buzzing,etc.) or as a complex sound7. Tinnitus may be con-tinuous, discontinuous or intermittent and, accord-ing to its characteristics, pulsatile or non-pulsatile.

Tinnitus is a symptom, not a disease. Over theyears, various classifications have been pro-posed: the most common differentiates betweenobjective and subjective tinnitus.

Objective tinnitus is rare and is found in lessthan 1% of cases8. It is audible when a careful ex-amination is made of the ear and the temporal orcervical regions9,10. The sound generally comesfrom internal biological activity such as vascularturbulence: pulsation11; convulsion of the musclesin the middle ear, Eustachian tube and soft palate;and temporomandibular joint dysfunctions9.

Some authors claim that it is incorrect to termthese phenomena “tinnitus”, and prefer “so-matosounds”. For convenience, the term tinnituswill be used to include objective tinnitus in thisstudy.

Subjective or internal auditory tinnitus ismuch more common than external auditory tinni-tus and is found in approximately 20% of thepopulation. It is perceived as a sound or noise andcan be called true, intrinsic, auditory, non-vibrato-ry tinnitus, or phantom sounds1. Unlike objectivetinnitus, it originates in the acoustic pathways.

Depending on the time length, tinnitus may beacute, subacute or chronic. It is acute up to threemonths and subacute up to six months. If it per-sists for more than six months, it is chronic (eventhough some authors already consider it so afterthree months8). In 1999, Zenner and Pfister12 pro-posed an innovative and systematic classificationof tinnitus, based on knowledge of the anatomyand physiology of the hearing system. They made

European Review for Medical and Pharmacological Sciences

When alarm bells ring: emergency tinnitus

G. ALTISSIMI1, M. SALVIATI2, R. TURCHETTA1, M.P. ORLANDO1, A. GRECO1, M. DE VINCENTIIS1, A. CIOFALO1, C. MARINELLI1, V. TESTUGINI3, F. MAZZEI1, G. CIANFRONE1

1Department of Neurology and Psychiatry, Umberto I University Hospital, Sapienza University, Rome, Italy 2Department of Sensory Organs, Umberto I University Hospital, Sapienza University, Rome, Italy3AIRS onlus (Italian Association for Research on Deafness), Rome, Italy

2016; 20: 2955-2973

2956

a first distinction between subjective and objectivetinnitus, subsequently further distinguishing sub-jective tinnitus, based on its anatomical site, asconduction, sensorineural and central tinnitus12.

According to some authors7,13 and dependingon the patient’s sequelae, tinnitus can be dividedinto “clinical” (decompensated) or “nonclinical”(compensated).

Patients can cope with compensated tinnitusand suffer little or no psychological stress. Theirquality of life remains more or less the same.

Decompensated tinnitus, found prevalently in1-2.4% of the adult population7,12, causes a highlevel of psychological stress and emotional over-lay. Patients’ quality of life is seriously compro-mised.

Our group recently proposed a clinical-neuro-plastic classification of tinnitus, called TinnitusHolistic Simplified Classification (THoSC)14,which focuses on a more rational diagnostic andtherapeutic management that is, in our view,nearer to clinical reality.

We classified tinnitus as:• Audiologic or deafferentation tinnitus –

caused and sustained by hearing loss;• Somatosensory tinnitus – caused, sustained

and modulated by cross-modal somatosensorytinnitus in patients without a clear profile ofhearing loss, where a tinnitogenic trigger canbe recognized from non-auditory devices;

• Psychogenic tinnitus – caused, sustained andmodulated by psychological disorders or psy-chopathological conditions;

• Combined classes – tinnitus caused and sus-tained by at least two of the three previousfactors.Tinnitus is frequently triggered by conditions

that cause a reduction in auditory acuity (presbya-cusis, acute and chronic acoustic trauma, otosclero-sis, Ménière’s disease, chronic otitis, sudden deaf-ness, VIII cranial nerve schwannoma, etc.).

About 70% of hypoacusic patients are aware oftinnitus and about 95% of patients who suffer fromtinnitus are hypoacusic. These data support the hy-pothesis whereby the sensory deafferentation of theauditory cortex constitutes, in many cases, themain risk factor for the creation of tinnitus, a phe-nomenon activating the deafferented areas.

An ear without a brain is unable to transmitand transduce or perceive sounds; a brain with-out an ear can be devastated by the perception ofsounds.

Ten to fifteen% of the population is affectedby chronic tinnitus4,6, which may at times cause

great stress15, with anxiety, depression, difficultyin concentrating and sleep disorders16.

There is a significant link between more seri-ous tinnitus, anxiety and sleep disorders and gen-eral psychopathological level17,18.

Patients who complain higher discomfort thanthe average person affected by tinnitus are thevery ones who have a higher stress level.

Numerous studies highlight a link betweenthe gravity of the tinnitus and psychometric para-meters, particularly anxiety, depression and som-atization19,20.

Data from the literature highlight that be-tween 26.7021 and 77%22 of patients with tinnitusmanifest psychiatric comorbidity.

The risk of suicide in these patients is tentimes more than that of the average person23.

Psychiatric comorbidity and the risk of suicideare not the only elements that can lead patientswith tinnitus to seek emergency counselling.

Tinnitus is a frequent symptom, principallylinked to loss of hearing24. About 7% of patientsaffected by tinnitus ask for help in resolving theproblem; between 0.5 and 2% require urgentmedical assistance7,25.

This need for help may be the result of anacute onset of tinnitus or the rapid impairment ofan already chronic condition.

The aim of this study is to develop a diagnos-tic-therapeutic algorithm for those suffering fromtinnitus who seek emergency aid.

Materials and Methods

A literature review has been performed on ar-ticles retrieved from PubMed from the last 30years. Research was carried out using keywordssuch as “tinnitus and emergency”, “tinnitus as ur-gency”, “tinnitus and psychiatric comorbidity”,in a time span from 1984 to 2015.

Results

Pathologies associated with tinnitusThe medical pathologies exhibiting tinnitus in

their symptomatological characteristics are nu-merous, and are both of otological and non-oto-logical origin (see Table I for further details).When the cause of this phenomenon is unknown,the term “idiopathic tinnitus” is used.

G. Altissimi, M. Salviati, R. Turchetta, M.P. Orlando, A. Greco, M. De Vincentiis, et al.

Some of these pathologies may constitute ur-gent cases, and this is why it is particularly im-portant for a patient with acute tinnitus to bethoroughly assessed.

At times, the characteristics of tinnitus maydirect a clinician towards the possible underlyingpathology (see Table II for further details).

Tinnitus may be pulsatile or non-pulsatile.This differentiation is the one mainly adopted inthe literature or diagnostic-therapeutic algo-rithms. We have chosen to follow this model forits practical implications in a clinic.

Pulsatile tinnitusPulsatile tinnitus synchronized with heartbeat

is rare26, potentially disabling, and can have bothvascular and non-vascular aetiology. When it isvascular, it may be caused by turbulence in thebloodstream from increased volume or an irregu-lar vascular lumen.

Tinnitus is probably of arterial origin if it getsworse with light compression of the ipsilateraljugular vein while it is probably venous if it im-proves with compression or by rotating the headin the direction of the tinnitus – both these move-

2957

Emergency tinnitus

Aetiopathogenesis Pathological characteristics

Otological, infectious Otitis externa, Otitis media, labyrinthitis, mastoiditisOtological, neoplastic Vestibular schwannoma, meningioma, vascular tumoursOtological, labyrinthine Sensorineural hearing loss, Ménière’s disease, vestibular vertigoOtological, other Impacted cerumen, otosclerosis, presbyacusis, noise exposure, barotraumas,

genetic deafness, sudden hearing lossNeurological Meningitis, migraine, multiple sclerosis, epilepsyTraumatic Head or neck injury, loss of consciousnessOtofacial Temporomandibular joint disorderCardiovascular Hypertension, vascular disorders, cerebrovascular disordersRheumatological Rheumatoid arthritisImmune mediated Systemic lupus erythematosus, systemic sclerosisEndocrine and metabolic Diabetes mellitus, hyperinsulinaemia, hypothyroidism, hormonal changes

during pregnancyOtotoxic medications Analgesics, antibiotics, antineoplastic drugs, corticosteroids, diuretics,

immunosuppressive drugs, non-steroidal anti-inflammatory drugs, steroidal anti-inflammatory drug

Psychiatric disorders Depression, anxiety and somatization

Table I. Common systemic neuro-otological risk factors for developing tinnitus.

Otoneurological pathology Tinnitus characteristics

Tubal dysfunction Murmuring, synchronous with respirationMyoclonus of muscles in soft palate and middle ear Jerks, lasting several seconds or minutes

Congenital vascular malformation Throbbing, synchronous with heart beator malformation acquired through head and neck, reverberating circulation in vessel near ear

Ménière’s disease Less frequent tinnitus, preceding vertigo attacks, then giving way to moment of calm Otosclerosis Continuous tinnitus more often at low frequency, sometimes pulsatile and intermittentPresbyacusis, ototoxicity, Bilateral and high-frequency tinnitus noise trauma

Schwannoma VIII CN Unilateral and high-frequency tinnitusMiddle or outer ear Usually low-frequency or “white noise” tinnitus, associated with transmissive

hearing loss Cochlear Usually high-frequency tinnitus, often corresponding to damaged frequency,

associated with neurosensory hearing loss Central nervous system Tinnitus with varying frequencies, often with accompanying neurological signs

and symptoms

Table II. Characteristics of tinnitus in relation to pathologies.

2958

ments cause a reduction in jugular flow. Casesdescribed in the literature usually pertain to be-nign buzzing in the veins, but sometimes severeconditions may be present, such as arteriovenousmalformations, glomus tumours and carotidstenosis (see Table III for further details).

Arteriovenous fistulae with pulsatile tinnitusare common27. In 2008, Ali et al28 described thecase of a 66-year old patient who not only had pul-satile tinnitus, but also pain in the left ear, exoph-thalmos, conjunctivitis, diplopia and decreased vi-sual acuity. Computed tomography (CT) and mag-netic resonance (MRI) showed a cavernous left fis-tula. The patient was treated with detachable plat-inum coils and n-butyl cyanoacrylate and symp-toms cleared up completely.

Pulsatile tinnitus may be the warning of pos-sible carotid dissection, for which an urgent diag-nosis is important in order to help long-termprognosis and prevent ischemic complications. Inthis case, symptoms normally are face and neckpain, headache, unilateral pulsatile tinnitus,amaurosis fugax, Horner’s syndrome, retinal in-farction and cerebral ischaemia of the anteriorcirculation29.

In 2007 Nakagawa et al30 described the caseof a 48-year old woman who, as a result of a roadaccident, suffered from diplopia and pulsatile tin-

nitus in the left ear. An angiogram revealed acavernous carotid fistula and an extracranial dis-section of the internal carotid artery. The patientunderwent endovascular stent angioplasty, withcomplete resolution of the symptoms.

An acute ischaemic stroke of the anterior in-ferior cerebellar artery can be associated withpulsatile tinnitus, hearing loss, ataxia, nystagmusand hypoalgesia.

In 2001 Lee et al31 described the case of a 66-year old man who, a week before the onset ofdysarthria, facial paralysis and ataxia had dis-played sudden bilateral hearing loss, unilateraltinnitus and vertigo. The severity and persistenceof the hearing loss caused the authors to con-clude that loss of hearing was probably due tohypoperfusion of the inner ear artery, with rela-tive labyrinthine infarction.

Kotan et al32 described the case of a 42-yearold stroke patient who came to the emergencyroom complaining of tinnitus and vertigo andwho, after magnetic resonance angiography, wasdiagnosed with bilateral vertebral stenosis. About25% of strokes are caused by posterior circula-tion or the vertebrobasilar system. The symptomsof a vertebrobasilar ischaemia may be clinicallyobserved as tinnitus, vertigo, diplopia, migraines,hypokinesis and hearing difficulties. Despite its

G. Altissimi, M. Salviati, R. Turchetta, M.P. Orlando, A. Greco, M. De Vincentiis, et al.

Correlated pathologies Symptoms

Arteriovenous fistulae Pulsatile tinnitus, earache, exophthalmos, conjunctivitis, diplopia, loss of visual acuityCarotid dissection Face and neck pain, headache, unilateral pulsatile tinnitus, amaurosis fugax, Horner’s

syndrome, retinal infarction, cerebral ischaemia in anterior circulation Acute ischaemic stroke of anterior Pulsatile tinnitus, hearing loss, ataxia, nystagmus, hypoalgesiainferior cerebellar artery

Aneurysms of dural venous sinuses Pulsatile tinnitus, homolateral pain above earAneurysm of intrapetrous carotid Pulsatile tinnitus, hypoalgesia, signs of obstruction in Eustachian tubeartery

Ruptured aneurysm of the Unilateral tinnitus, dyspnoea, palpitationsnoncoronary sinus of Valsalva in the right atrium

Duplicated internal carotid arteries Pulsatile tinnitus, loss of hearing(ICA)

Benign vascular tumours Pulsatile tinnitus, otorrhagia, unilateral hypoalgesia Glioneuronal tumour Pulsatile tinnitus, non-specific broad symptomatological spectrum, generally

depending on size and extent of tumour Cerebellopontine angle Pulsatile tinnitus, unilateral tinnitus, slight headache, hearing loss, hemiparesis, angiosarcoma numbness, ataxia

Bilateral vertebral stenosis Tinnitus, vertigo, diplopia, headache, hypokinesis, hearing disordersHypertensive crisis Tinnitus, vertigo and headache, or severe such as dyspnoea, chest pains,

coma or deathGlomus jugulare tumour Pulsatile tinnitus, unilateral paralysis of the accessory nerve palsy homolateral to

tumour

Table III. Pulsatile tinnitus.

low risk of morbidity and mortality, prompt diag-nosis and relative treatment are of fundamentalimportance.

Feitosa-Filho et al33 underline how hypertensivecrises and emergencies are the clinical situationsrepresenting more than 25% of all medical emer-gencies. Hypertensive crises are clinical situationsfollowed by clinical signs and symptoms. About3% of all visits to the emergency services are dueto significant increases in blood pressure. Conse-quently, a hypertensive emergency is the most crit-ical clinical situation, needing particular attentionand care. Signs and symptoms may be slight, suchas tinnitus, vertigo and migraine or severe, such asdyspnoea, chest pains, coma and/or death.

Aneurysms of dural venous sinuses may beconsidered rare. Only eight cases have been pub-lished, five of which were treated surgically andthree by endovascular approach. Notably,Mehanna et al34 described an additional case,treated successfully by endovascular coiling, of a46-year-old woman affected for six years by pul-satile tinnitus that started after physical exercise,associated with a sharp pain above her right ear.Her symptoms worsened progressively to thepoint that she needed to compress her right jugu-lar vein, ipsilateral to the tinnitus, or turn herhead to the right in order to follow a conversa-tion. The only sign noted was a murmur heard onauscultation over the right temporal bone. An an-giographic evaluation revealed a high right jugu-lar bulb, a dominant right lateral sinus with an ir-regular venous aneurysm at the proximal rightsigmoid sinus. Endovascular treatment led to an80% improvement in the patient’s tinnitus andcomplete resolution of the temporal murmur.

An internal carotid aneurysm in the petroustemporal bone is a rare lesion: there are but 54cases described in the literature. The most com-mon symptoms are pulsatile tinnitus, hearing lossand signs of obstruction in the Eustachian tubes.Rupture of an aneurysm may provoke bleedingso intense that the common carotid artery mayneed emergency ligature35. In the case of an in-trapetrous carotid artery aneurysm, it is neces-sary to intervene at the first ontological symp-toms such as hearing loss and tinnitus, in spite ofthe surgical complexity36. Guenther et al37 de-scribed the case of a 32-year-old woman withleft-sided tinnitus, dyspnoea and sudden onset ofpalpitations. At the Emergency Department,echocardiography revealed a ruptured aneurysmof the noncoronary sinus of Valsalva in the rightatrium. The patient subsequently underwent im-

mediate surgery with a patch repair of the rup-tured aneurysm, which enabled her to be dis-charged in good health after a few days.

Among vascular anomalies are duplicated in-ternal carotid arteries (ICAs). Gartrell et al38 pre-sented the case of a 15-year-old male with an un-usual ICA anomaly, where there was no evidenceof tinnitus, vertigo or aural pressure. The pa-tient’s medical history was marked by recurrentacute otitis media and subsequent bilateral tym-panostomy, with no consequent complications.He had been fitted with hearing aids since hispreschool years. CT and MRI angiography re-vealed bilateral masses in both middle earspaces, which could be visualized through theanterior inferior quadrant of the tympanic mem-brane, together with a long-standing mixed uni-lateral hearing loss. In these cases, establishing acorrect diagnosis is paramount to avoid possiblecatastrophic haemorrhagic complications such asbleeding, hearing loss, or neurologic deficits.

An aberrant ICA is rare: there are only ap-proximately 45 cases recorded to date. The ma-jority of these cases, presented as a unilateralanomaly without duplication, were associatedwith pulsatile tinnitus and hearing loss. Bilateralaberrant ICAs are extremely rare, with only 14existing reports. Only one of these cases waswith duplicated ICAs. The case described by theauthors represents the only example known of abilateral duplicated ICA not associated with per-sistent stapedial arteries.

Conservative management of an aberrant ICA isgenerally advised, seeking to avoid middle earsurgery where possible. The patient should be fol-lowed closely and if, despite conservative treatment,bleeding occurs, embolization may be attempted.This is preferable, where possible, over ligation ofthe ICA. Embolization is a definitive treatment forarteriovenous malformation, aneurysms and an-giomatous malformations. In inoperable tumours,embolization can relieve pain, bleeding, pulsatiletinnitus or discomfort due to mass effect39.

Topal et al40 report the case of two sisters inwhich they diagnosed fibromuscular dysplasia ofthe carotid artery at the same age and had thesame symptom: pulsatile tinnitus. This is a non-inflammatory atherosclerotic vascular disease thatcan affect the arteries of the cervix, kidney andgut. The family presentation of this rare disease isindicative of a possible genetic etiology, but, atthe moment, the exact pathophysiology is not yetknown. In both cases a conservative treatmentwith aspirin was proposed.

2959

Emergency tinnitus

2960

With regard to benign vascular tumours, Nouriet al41 describe the case of a 60-year-old womanwith a capillary haemangioma, with symptoms ofpulsatile tinnitus, otorrhagia and unilateral hearingloss. A clinical test revealed a reddish polypoidmass at the bottom of the ipsilateral external audi-tory canal, covered by a thin inflamed tympanicmembrane. Conductive unilateral hearing loss waspresent. CT and MRI tests showed a vascularmass in the middle ear. The tumour was subse-quently removed. Haemangiomas are benign vas-cular tumours that are relatively common in thehead and neck. Their occurrence in the temporalbone, especially in the middle ear, is exceptional;they represent less than 0.21% of all temporalbone tumours. The tumour is usually ipsilateral,and symptoms may vary from an asymptomaticmass to a tumour with pulsatile tinnitus, otorrha-gia, hearing loss, vertigo, recurrent otitis media, orparalysis of the facial nerve42-44. An otoscopy usu-ally shows a reddish mass at the back of the tym-panum or, more rarely, a polypoid mass in the ex-ternal auditory canal. The main differential diag-nosis is with paraganglioma of the middle ear43,44.Surgery is required for a complete resection of thetumour because of its destructive and haemorrhag-ic potential. The relatively high recurrence ratevaries from 16 to 23%. It depends directly on thequality of the surgical resection43 and demon-strates the importance of follow-up for these pa-tients. Surgical excision is not always necessary,as shown in the literature, since congenital hae-mangiomas can regress spontaneously43,45. Thesurgical technique depends on the size of the tu-mour, degree of hearing loss and position of thejugular bulb43,46,47. Laser CO2 treatment can be aninteresting alternative to conventional surgery, al-lowing a better visualization of the middle earstructures and reducing bleeding41,42,45.

The rosette-forming glioneuronal tumour(RGNT) of the fourth ventricle is considered rare.The symptomatological spectrum is wide, non-spe-cific and generally depends on the size of the tu-mour and its extent. Despite benign histologicalfeatures and favourable post-operative progress,there is still limited clinical experience with regardto this tumour, which needs careful differential di-agnosis of possible posterior cranial fossa masses inorder to avoid undue surgical aggressiveness48.

Guode et al49 describe the case of a 16-year-old girl with right-sided tinnitus, ipsilateral hear-ing loss and mild headache, which had gone onfor a year. These subsequently worsened and, to-gether with vomiting and other neurological

symptoms (hemiparesis, numbness, ataxia) led toa diagnosis of angiosarcoma in the cerebellopon-tine angle, with haemorrhaging and oedema. Thepatient underwent an emergency suboccipitalcraniectomy to remove the tumour and had subse-quent radiotherapy treatment. Primary intracranialangiosarcomas are rare and few cases are reportedin the literature, mostly located in the supratentor-ial areas. This case highlights how important it isfor clinicians to be aware of the characteristics ofthis type of tumour and the need to include it inthe differential diagnosis of rare lesions located inthe cerebellopontine angle49.

Glomus jugulare tumours are rare, hypervascu-lar tumours that are generally benign and, becauseof their slow and insidious clinical manifestation,are diagnosed late. They represent a significant di-agnostic and management challenge to the clini-cian50,51. Auscultation of the cervical and temporalregions can reveal murmurs that help to localizethe lesion. In these cases, MRI, CT or angiogra-phy are recommended, and the patient should bereferred immediately to an ear, nose and throatspecialist. Primary manifestations involve the earapparatus and the lower cranial nerves caused bymass effect. In this regard, Seymour, Lloyd andHarcourt51 describe the case of a subject with aglomus associated with a previous accessorynerve palsy on the same side as the tumour. Glo-mus tumours, as part of the chromaffin cell sys-tem, may also secrete catecholamines, with com-plications that may arise related to inappropriatecatecholamine release52. Treatment options can in-clude surgery, radiotherapy and embolization.Surgery, followed by radiotherapy53 if necessary,is the treatment of choice. However, it can haveserious potential complications linked with the po-sition and the vascular nature of the tumour.

The clinician should always suspect a vascu-lar lesion in patients with a retrotympanic mass;careful diagnostic imaging investigations shouldalways be carried out before any middle ear sur-gical exploration.

Non-pulsatile tinnitus Non-pulsatile tinnitus is usually caused by a

non-vascular tinnitogenic source: hearing impair-ment, palatal and middle ear myoclonus, dys-functions of the Eustachian tube, tympanic mem-brane, Temporo-Mandibular Joint (TMJ), cervi-cal spine, etc. In the majority of cases, it is bilat-eral, while unilaterality may indicate a more seri-ous clinical condition such as a vestibular oracoustic neuroma, or Menière’s syndrome.

G. Altissimi, M. Salviati, R. Turchetta, M.P. Orlando, A. Greco, M. De Vincentiis, et al.

Meningiomas and vestibular neuromas are themost common benign intracranial tumours, infirst and second place, respectively. In the cere-bellopontine angle, these tumours represent 6-15%54,55 and 80%54,56,57 respectively, of all tu-mours.

The simultaneous presence of two kinds of tu-mour in the cerebellopontine angle, in the ab-sence of neurofibromatosis type 2 or history ofcerebral irradiation, is extremely rare. In the liter-ature, there are few cases of intracranial menin-gioma combined with neuroma in the same pa-tient58,59 and only five cases of meningioma andvestibular neuroma in the same cerebellopontineangle.

Grauvogel et al60 report the case of a 46-year-old woman with sudden left hearing loss, tinnitusand homolateral ataxia, with coexistent menin-gioma and vestibular neuroma, which were notdistinguishable radiologically. The diagnosticprocess and imaging studies showed an intra-and extrameatal lesion. The neuroradiological di-agnosis was vestibular neuroma. The patient un-derwent surgery via retrosigmoid approach,

which showed up two distinct tumours: a smallintrameatal neuroma and a larger meningioma,originating from the dura of the petrous bone.The patient experienced no neurological deficitafter surgery: in particular, the facial nerve func-tion was completely preserved. The definitivehistopathological examination revealed “fibro-matous meningioma and neuroma”. It is thusclear that a careful interpretation of imagingstudies before surgery is crucial60. Radiosurgeryis an alternative treatment option, particularly forsmaller neuromas, which do not press on thebrainstem or cause hydrocephalus61. Various the-ories attempt to explain the coincidence of twoquite distinct primary brain tumours in the ab-sence of conditions such as phacomatosis (forexample, neurofibromatosis type 2) or a previouscerebral irradiation. Tumours may developthrough pure chance, or the first tumour may actas a stimulus on the surrounding brain parenchy-ma or brain tissue and induce a new tumour in adifferent tissue. Alternatively, a cancerogenousstimulus may develop tumours in different tis-sues at the same time, or a residual embryonic

2961

Emergency tinnitus

Correlated pathologies Symptoms

Meningioma and vestibular Non-pulsatile tinnitus, acute loss of hearing, ataxianeurinoma

Ménière’s disease Non-pulsatile tinnitus, vertigo, fullness, loss of hearingPetrous apex cholesterol granuloma Non-pulsatile tinnitus, loss of hearing, vertigo, headache, facial spasms, diplopiaOccipital neuralgia syndrome Non-pulsatile tinnitus, migraine, pain in the distribution of the occipital nerve,

vertigo, nausea, visual disturbances, scalp paraesthesia Lumbar puncture Non-pulsatile tinnitus, postural headache, nausea, vomiting, ocular disturbancesSubdural haematoma Non-pulsatile tinnitus, persistent headache in homolateral region behind ear Pneumolabyrinth Non-pulsatile tinnitus, neurological and/or somatic symptoms Idiopathic sudden sensorineural New onset unilateral non-pulsatile tinnitus, unilateral hearing loss

hearing loss (ISSNHL)Autoimmune vestibulo-cochlear Non-pulsatile tinnitus, vertigo, fullnessdisorders (AVCD)

Multiple sclerosis Persistent non-pulsatile tinnitus, associated with reversible loss of hearingLightning or electrical damage Non-pulsatile tinnitus, blindness, confusion, amnesia, cardiac arrhythmias,

vascular instability Myiasis of the external Non-pulsatile tinnitus, otalgia, otorrhea and middle ear

Acute quinine toxicity Non-pulsatile tinnitus, nausea, vomiting, prolungation of QT intervalCarbon monoxide (CO) poisoning Tinnitus, hearing loss, vestibular disorders, cognitive sequelae, anxiety,

depression, headache, insomnia, fatigue, visual acuity disturbance, peripheral neuropathies and Parkinsonian-like syndrome

Overdose of salicylates, Non-pulsatile tinnitus, dizziness, numbness of the tongue, visual disturbances,tricyclic antidepressants muscle spasms, convulsions, reduced consciousness, coma and respiratory arrest and benzodiazepine

Heart attacks (particularly anterior) Non-pulsatile tinnitus, dizziness, headache, weakness, coughAcute acoustic trauma (AAT) Non-pulsatile tinnitus, frequent selective hearing loss Auricular foreign body Unilateral non-pulsatile tinnitus, dysgeusiaAuricular trauma Non-pulsatile tinnitus, hearing loss, vertigo, pain

Table IV. Non-pulsatile tinnitus.

2962

structure may become the matrix for the subse-quent development of a multiple brain tumour62.Tsukamoto, Hikita and Takaki58 hypothesizedthat meningioma and neuroma association maybe determined genetically, given that the genesresponsible for these tumours are both found inchromosome 22. In the case described above, thecombination of the two tumours most probablyoccurred incidentally. Nevertheless, the influenceof some factor in tumour growth, which forcesthe second tumour to grow, is theoretically possi-ble since tumours were near each other in thesame anatomical region. Further studies are nec-essary for a better understanding of the mecha-nisms that cause multiple tumours to grow60,61.

All patients with unilateral tinnitus shouldhave, as soon as possible, a hearing test and anMRI, with particular attention paid to the cere-bellopontine angle and the internal auditorycanal, and even more so if an asymmetric hear-ing loss is present, in order to exclude a vestibu-lar neuroma. Although a benign tumour, the lattermay represent an emergency in some cases, de-termining adverse occurrences such as signifi-cant haemorrhages63.

Endolymphatic sac tumours, which originatefrom the ductal epithelium and endolymphaticsac, are slow-growing, locally aggressive, low-grade malignancy. They often arise with tinnitus,sensorineural hearing loss, dizziness, mimickingMeniere's disease. Large tumours may be accom-panied by neuropathies of the cranial nerves.These tumours may be associated to von Hippel-Lindau syndrome. Therapy consists of excisionmicrosurgery. Radiation therapy has a limitedrole, in recurrences and tumours that cannot betreated surgically. An early diagnosis can helppreserve hearing64.

Symptoms such as vertigo, fullness, feelingof aural pressure, hearing loss and tinnitus, prob-ably caused by the presence of endolymphatichydrops and osteitis of the otic capsule, are typi-cal of Ménière’s disease65,66 and Cogan’s dis-ease67, which has similar symptoms to Ménière’sdisease, and needs to be distinguished by carefuldiagnosis. Some authors believe that it is impor-tant to monitor these patients, since they mayhave fluctuating symptoms over time, whichcould compromise their quality of life68. In somepatients (6%), congenital or acquired syphilismay cause Ménière’s disease69, with initialsymptoms similar to those of other etiologies.Consequently, failure to establish the specificetiologic diagnosis could result in unnecessary

surgical treatment or inappropriate medical ther-apy. In certain cases, if steroids are not givenpromptly, rapid and permanent hearing loss willresult. Etiology may be confirmed in these casesby a fluorescent treponema antibody absorption(FTA-abs) test69. The clinical features and histo-ry of the disease, in these patients, are unique:symptoms begin in the fifth decade of life, firstin one ear and then, after a few years, in the oth-er; caloric vestibular responses are reduced orabsent. Prompt administration of steroids will benecessary, particularly in a medical emergencywith severe and sudden hearing loss, at times to-gether with an endolymphatic subarachnoidshunt operation. Long-term use of steroidsseems to maintain effective hearing for morethan 20 years69.

A petrous apex cholesterol granuloma is themost common lesion in this anatomical region.Patients have various symptoms such as tinnitus,hearing loss, headache, facial spasms and diplop-ia. Kim et al70 analyse the case of a 32-year-oldman, who was first diagnosed with Ménière’sdisease. Based on this diagnosis, he was placedfor several months on a low-salt diet and had rel-ative pharmacological treatment. However, thesymptoms persisted and grew worse. The patientsubsequently came to the emergency departmentcomplaining of unilateral facial twitching andnumbness. An MRI was performed to rule out acentral neurological lesion. The test found a le-sion at the petrous apex. Surgical excision wasinfralabyrinthine, with a middle cranial fossa ap-proach, using a computerized surgical device(Brain Lab). After the operation, hearing loss andvertigo were no longer present. It is likely thatthe patient's Ménière disease-like symptomswere due to compression of the endolymphaticsac by part of the granuloma.

For diagnostic purposes, CT and MRI scanson the petrous temporal bone are of great help,particularly in clinical manifestations. The loca-tion and size of the granuloma are decisive withregard to disease-specific symptoms or signs pre-sent. Consequently, the possibility of a petrousapex lesion should be considered in patients whohave the clinical characteristics of aggravated en-dolymphatic hydrops69.

Kuhn et al71 describe, in a prospective casestudy over a one-year period in an emergency de-partment, and through a review of the literature,the clinical characteristics (migraine, pain in thedistribution of the occipital nerve, Tinel’s sign,and partial or complete relief from pain after lo-

G. Altissimi, M. Salviati, R. Turchetta, M.P. Orlando, A. Greco, M. De Vincentiis, et al.

cal anaesthetic injection) that can aid in diagno-sis of the occipital neuralgia syndrome. The latteris often accompanied by tinnitus, vertigo, nausea,visual disturbances and scalp paraesthesia. Oc-cipital neuralgia is the benign extracranial causeof headache. After local anaesthetic injection,further aiding diagnosis, patients had more relieffrom both pain and other symptoms71.

Desai et al72 report the case of a 29-year-oldwho, after a lumbar puncture, presented classicsymptoms such as postural headache, nausea,vomiting and ocular disturbances. These compli-cations are well known and may be due to multi-ple factors: needle size, type and needle bevelorientation. In order to clear up the symptoms,conservative treatment is usually sufficient; rest-ing in bed, intravenous hydration, caffeine andanalgesics. An epidural blood patch may be nec-essary in extreme cases.

Doganay et al73 describe the case of a 24-year-old patient with a normal clinical historyand normal laboratory tests, who developed asubdural haematoma after spinal anaesthesia atL4-L5 level. This severe and rare complicationcan be fatal if not treated.

Puncture of the dura mater can cause cere-brospinal fluid losses and strained and rupturedmeningeal blood vessels with relative bleeding.The first day after spinal anaesthesia, the patientbegan to have a headache. A post-spinalheadache was diagnosed and conservative treat-ment undertaken. Since the pain behind the leftear persisted, associated with tinnitus, emergencyCT scan was performed and showed an acutefronto-temporo-parietal subdural haematoma.Thus, a continuous atypical headache, with tinni-tus, after spinal anaesthesia, may indicate a pos-sible underlying subdural haematoma. In thesecases, an urgent diagnosis needs to be made,based on the patient’s history and imaging tech-niques.

Sahin et al74 described the case of a 50 yearold woman who developed sudden bilateral hear-ing loss with tinnitus after spinal anesthesia per-formed for hallux valgus surgery. A sudden hear-ing loss with bilateral tinnitus after spinal anes-thesia has been reported only in a few cases. Thepatient's hearing improved almost fully in themorning of the 3rd day after surgery. No recur-rence of hearing loss, tinnitus or vertigo havebeen reported during the follow-up of sixmonths. Auditory complications after spinalanesthesia should be carefully evaluated by ENTspecialist for an early diagnosis and its treatment.

Achache et al75 presented a case of retardedpneumolabyrinth subsequent to undiagnosedtraumatic perilymphatic fistula. From a review ofthe literature, the authors indicated the systemat-ic management procedure to be followed in orderto prevent further complications. Labyrinth in-volvement is rare but there is a risk of perilym-phatic rupture that is often underestimated on ini-tial clinical examination due to the predominanceof neurological and/or somatic symptoms.

Idiopathic sudden sensorineural hearing loss(ISSNHL), often associated with the onset ofunilateral tinnitus, should be considered a properontological emergency. It is a clinical conditioncharacterized by the sudden onset of hearingloss, mainly unilateral76-79. When ISSNHL is sus-pected, an appointment with a specialist shouldbe made as quickly as possible, together with ahearing test, since the percentage recovery andprognosis can be improved by prompt diagnosisand subsequent therapy80-82.

Diao et al83 referred the case of a 31 years oldpatient presenting with tinnitus and unilateralsensorineural sudden hearing loss as the firstmanifestation of chronic myelogenous leukemia,a rare event in patients with leukemia. Pure-tonetone audiometry revealed a pantonal profoundhearing loss in the left ear. Subsequent investiga-tions led to a diagnosis of chronic myelogenousleukemia. The cases of sudden hearing lossshould, therefore, be carefully evaluated in con-sideration of the possible coexistence of anyhaematological disorders.

In the last few years, sudden deafness hasbeen frequently described in association with an-terior inferior cerebellar artery (AICA) infarc-tion, generally together with other brainstem andcerebellar signs such as ataxia, dysmetria and pe-ripheral facial palsy78. Martines et al78 describethe case of a 53-year-old man who suddenly de-veloped hearing loss and tinnitus without anybrainstem or cerebellar signs. CT of his ear andtemporal bones was normal, and the lesion visi-ble only by MRI test. This case represents thefifth described in the literature to date and con-firms the importance of neuroimaging in emer-gency assessments, in order to limit the extent ofthe lesion with immediate therapy78. Moreover,early hearing recovery, in the first four weeks af-ter the onset of hearing loss, is directly correlatedwith tinnitus handicap84.

Autoimmune vestibulo-cochlear disorders(AVCD) represent a group of syndromes proba-bly caused by an autoimmune mechanism with

2963

Emergency tinnitus

2964

overlapping clinical features, manifesting as sen-sorineural hearing loss, often associated with ver-tigo, tinnitus and fullness84,85. Definitive evidenceof a classic autoimmune process is still lacking,but inner ear inflammation progresses to severe,irreversible damage within three months of onset(and often much more quickly). Thus, patientswith rapidly progressive AVCD must be treatedurgently, since prompt treatment with corticos-teroids and other antirheumatic/immunosuppres-sive agents can preserve hearing and vestibularfunctions.

Among other pathologies, of probable au-toimmune origin, that present tinnitus is theVogt-Koyanagi-Harada syndrome86. Anothercondition to be considered is tinnitus associatedwith multiple sclerosis. Rarely, cases of hearingloss, with or without tinnitus, occur in adults,particularly during disease exacerbation, ratherthan as an isolated feature of the disease.

Rodriguez-Casero et al87, on the contrary, de-scribe the case of an 11-year-old girl in whompersistent tinnitus and reversible hearing losswere the sole manifestation of multiple sclerosisin the initial symptoms.

Another case in the literature of reversiblehearing loss is that reported by Granata et al88, thatobserve the reversible posterior encephalopathysyndrome, a rare radiographic clinical entity, char-acterized by typical findings in the occipital andparietal lobes, caused by a subcortical vasogenicedema. The etiopathogenesis is not clear, althoughit is known that it is a endotheliopathy the posteri-or cerebral circulation, leading to failure of thecerebral autoregulation, posterior edema and en-cephalopathy. Of note, a possible pathological ac-tivation of the immune system has been suggest-ed. Most common clinical manifestations areheadache, seizures and blurred vision. Also fre-quent are acute tinnitus and vertigo. The symp-toms can be reversible, but hemorrhage or cerebralischemia may occur. Diagnosis is based on MRI,in the presence of a development of acute neuro-logical symptoms and clinical signs, high bloodpressure and/or conditions associated with toxiceffects on the endothelium.

We will review other rare cases of acute tinni-tus, associated with other symptoms, which mayrepresent a genuine emergency.

Cooper89 describes cases where people arestruck by lightning or have electrical injuries.Lightning injuries affect 800 to 1000 persons peryear. High-voltage electrical injuries may be dev-astating, with extensive burns, cardiac arrest, am-

putations and long, complicated hospitalization.Low-voltage injuries tend to be benign, althoughthey may have significant long-term morbidity,including chronic pain syndromes. The maincause of death is cardiac arrest. Apart fromburns, patients may have tinnitus, blindness, con-fusion, amnesia, cardiac arrhythmias and vascu-lar instability. Other long-term problems aresleep disturbances, anxiety attacks, pain syn-dromes, damage to the peripheral nervous sys-tem, and diffuse neurologic and neuropsycholog-ic damage89. Other sequelae such as seizures orsevere brain damage from hypoxia, during car-diac arrest, and spinal artery syndrome from vas-cular spasms are indirect results of electrical andlightning injury. Desai et al90 describe the case ofa young woman struck by lightning as she wasplaying soccer, resulting in tinnitus, loss of con-sciousness, paraesthesias, muscle spasms and theonset of a speech impediment.

Hatten et al91 present the case of a healthywoman, who had no apparent risk factors for in-festation, affected by myiasis in the middle andexternal ear, requiring surgical intervention. Myi-asis is an otolaryngological disease that is rare indeveloping countries. It is linked with environ-mental conditions and typically seen in disabledpatients living in poor hygienic conditions. Prog-nosis is usually good. The patient’s symptoms oftinnitus, otalgia and otorrhea were resolved aftervarious attempts at extraction of the larvae, withtheir complete eradication. Tympanoplasty wassubsequently necessary to reconstruct the dam-aged external and middle ear. Another case de-scribed by González Poggioli et al92 is of a 65-year-old woman with pain and tinnitus, whichhad lasted for a week, in her left ear. An otoscopyin the emergency department showed numerousdipteran larvae totally occupying the external au-ditory canal. The larvae were removed and thepatient was discharged after 24 hours of medicalobservation. Diagnosis of otic myiasis is throughdirect visualization of the larvae in the ear cavi-ties. Treatment is by removal of larvae from theear. Otic myiasis should always be suspectedclinically in patients who travel widely and havean atypical presentation of acute otalgia associat-ed with otorrhea.

Wolf et al93 observe two cases of acute qui-nine toxicity, one from self-poisoning and theother from an unidentified source. Both patientshad acute bilateral blindness, associated with theclassic symptoms of cinchonism, including tinni-tus, nausea, vomiting and prolongation of the QT

G. Altissimi, M. Salviati, R. Turchetta, M.P. Orlando, A. Greco, M. De Vincentiis, et al.

interval. Another case reported in the literatureby Bodenhamer et al94 describes delayed car-diotoxicity (cardiac conduction defects, dys-rhythmias and cardiovascular collapse) eighthours after quinine ingestion. Smilkstein et al95

refer two cases of acute blindness caused by qui-nine poisoning, with an initial unsuspected diag-nosis. One patient presented tinnitus, hearingloss, vomiting, abdominal pain and mental con-fusion, while the other complained of hearingloss, headache, confusion, tachycardia, first-de-gree atrioventricular block and subsequentbradycardia. In both cases, the onset of blindnesswas delayed for more than 12 hours after inges-tion. Afterwards, one patient regained normal vi-sual acuity while the other developed markedconstriction of visual fields and decreased visualacuity.

Jammehdiabadi et al96 carried out a retrospec-tive review of 150 cases to determine the diagno-sis of overdose patients who took salicylates, tri-cyclic antidepressants and benzodiazepine. Apositive history of salicylate ingestion, tinnitusand hyperventilation were the best predictive in-dicators of salicylate ingestion. Considering thesalicylate abuse in the United States of America,Chyka et al97 established guidelines for outpa-tient management, which could potentially opti-mize outcomes, avoid unnecessary emergencydepartment visits, reduce health care costs andreduce life disruption for patients and caregivers.The presence of typical symptoms of salicylatetoxicity such as tinnitus, hearing loss, hemateme-sis, tachypnea, hyperpnoea, dyspnoea, lethargy,seizures and mental confusion indicate chronicsalicylate toxicity and are useful and sufficientelements for referral of the patient to an emer-gency department.

Van Donselaar-Van der Pant et al98 observedfour rare cases of acute intoxication from sys-temic toxicity after local use of lidocaine. Symp-toms included tinnitus, dizziness, paraesthesia ofthe tongue, visual disturbances, muscle spasms,convulsions, reduced consciousness, coma andrespiratory arrest.

Weaver stated that about 50,000 people in theUnited States of America each year are admittedto emergency departments for carbon monoxide(CO) poisoning, which can occur either frombrief exposures to high levels of CO or fromlonger exposures to lower levels. Symptoms in-clude headaches, nausea, vomiting, dizziness,general malaise, blunting, chest pain and dysp-noea. Neurological problems may often also be

associated, such as tinnitus, hearing loss, vestibu-lar disorders, cognitive sequelae, anxiety, depres-sion, headaches, insomnia, fatigue, visual acuitydisturbance, peripheral neuropathies and Parkin-sonian-like syndrome. While breathing oxygenhastens the removal of carboxyhaemoglobin(COHb), hyperbaric oxygen (HBO2) hastens CO-Hb elimination and favourably modulates the in-flammatory processes caused by CO poisoning,improving the mitochondrial function, transientlyinhibiting lipid peroxidation, impairing leukocyteadhesion to injured microvasculature, and reduc-ing cerebral inflammation caused by CO-inducedformation of myelin basic protein99.

Culić et al100 suggested a possible linkage be-tween different myocardial infarction sites andspecific symptoms. Anterior infarctions, with re-spect to inferior and lateral ones, presented tinni-tus in association with headaches, asthenia, dysp-noea, coughs and dizziness.

An acute acoustic trauma (AAT) may be treat-ed as an otological emergency. Vavrina et al101

presented a retrospective study on the therapeuticeffect of hyperbaric oxygenation in patients withunilateral or bilateral acute acoustic trauma. Twogroups of patients were treated in the same phar-macological way (dextran [Rheomacodrex]),ginkgo extracts (Tebonin) and prednisone, butonly one group underwent additional hyperbaricoxygenation at a pressure of 2 atmospheres ab-solute for 60 minutes, once a day. Both treatmentgroups were comparable as far as age, gender,initial hearing loss and prednisone dose are con-cerned. The delay at the beginning of therapywas 15 hours in both groups and treatment wasstarted within 72 hours in all cases. Control au-diometry, performed after about one week oftherapy, showed a significant hearing gain in thegroup exposed to hyperbaric oxygenation.Ylikoski et al102 further indicated how, inacoustic trauma cases, hyperbaric oxygen thera-py has a positive effect on both loss of hearingand tinnitus. The therapeutic rationale of admin-istering positive pressure oxygen is based on ex-perimental studies showing how noise exposureresults in cochlear hypoxia. Hyperbaric oxygena-tion is the only method of increasing concentra-tion of oxygen in the inner ear fluids, which thusfacilitates the cellular regeneration processes103.

Foreign bodies in the external auditory canalcan cause unilateral tinnitus. Auricular foreignbodies can be easily identified at an emergencydepartment. Ness et al104 report the case of a 16-year-old patient, who came to the emergency de-

2965

Emergency tinnitus

2966

partment complaining of unilateral tinnitus anddysgeusia. The only history of injury was an inci-dent that had occurred in the past few days. Awooden foreign body was found by otoscopy inthe auditory canal. A CT scan revealed it to beabout 3 cm. It had pierced the middle ear, disrupt-ing the ossicles. Subsequent otomicroscopy inves-tigation in the operating theatre showed a severedchorda tympani nerve with ossicle rupture. This iscertainly an unusual presentation for an aural for-eign body but, in consideration of possible lesionsto the middle and inner ear, it is important for acareful clinical evaluation to be carried out beforeand after removal of foreign bodies.

Fang et al105 described the case of a 48-year-old woman who had worn a hearing aid in her leftear for many years and who came to the emer-gency department complaining of severe otalgia,with otorrhagia, that had lasted for one day. Anotomicroscopy revealed a fruit-fly larva movingin the external auditory canal. The skin over thefloor of the canal, close to the eardrum, was erod-ed. The larva was removed and the patient re-ceived topical antibiotic treatment with ofloxacin,which resolved the otalgia immediately. Twoweeks later, the erosion was completely healed.

Ear trauma is a common problem in emer-gency medicine. Although injuries of the ear arenot usually life threatening, they can account forsignificant morbidity. Patients may experiencetinnitus, hearing loss, vertigo and pain. Injuriesto the ear may occur because of penetrating orblunt traumas, loud noises, chemical exposure,explosions and thermal injury106. Chukuezi etal107 analyse ear trauma with regard to etiology,presentation and influencing factors. In the ma-jority of cases, the trauma affects the tympanicmembrane because of the sudden increase inpressure to which is it exposed. Slaps are themost common aetiology, while bleeding from theear, hearing loss and tympanic membrane perfo-ration are the most frequent presentations.

Reitsma et al108 observe a rare case of a nineyears old patient with idiopathic intracranial hy-pertension, which presented tinnitus, bilateralprogressive sensorineural hearing loss, headache,ear pain and dizziness. This is the second casedescribed in the literature of pediatric idiopathicintracranial hypertension that occurs with hear-ing loss. The patient underwent physical exami-nation, audiometry, MRI, CT scans, lumbarpuncture. Fundus examination and imaging tech-niques showed no particular anomalies. At firstobservation pure-tone audiometry revealed a

hearing threshold of 30 dB HL in both sides. Twomonths later the threshold lowered to 35 dB HL.Lumbar puncture revealed an increased intracra-nial pressure: an idiopathic intracranial hyperten-sion was therefore diagnosed. After the lumbarpuncture problems were gradually solved andhearing returned to normal.

Syed et al109 observe two cases of primary epi-dermoid cysts of the mastoid. One presented withheadache and progressive imbalance, the otherwith unilateral hearing loss and tinnitus. Epider-moid cyst of the temporal bone are extremely rare:such lesions that arise in isolation within the mas-toid have never been reported previously in the lit-erature. In both cases surgical treatment was nec-essary. The diagnosis of an epidermoid cyst isbased on clinical history, physical examination theradiological, histological and intraoperative fea-tures. Complete removal of the lesion with its cap-sule is recommended to prevent recurrence and toenable a good long-term prognosis.

Tinnitus and emergency psychiatric comorbidity

Tinnitus is a clinical symptom of disorders inthe auditory system. It often does not have an or-ganic origin and is correlated with stress. Expo-sure to noise can be, in these cases, a triggeringfactor110. Severe tinnitus can have a significantimpact on the quality of life of the affected per-son111. Approximately half of adults and one-third of children affected with tinnitus and seek-ing help suffer from anxiety and/or depressivedisorders, with epidemiological peaks reaching77%21. Consequently, it is important to identifythese disorders promptly and refer suitable treat-ment112. In the literature and in the clinical envi-ronment, the comorbid disorders most frequentlypresent in people needing specialist assistancefor tinnitus are those of a psychological nature.The definition itself of “decompensated tinni-tus”13 refers to concomitant emotional conditionsand stress. The tinnitus “discomfort” level seemsto be correlated mainly with the compresence ofa psychological disorder, rather than with the au-diologic characteristics of the symptom113.

Mortality of patients with decompensatedtinnitus appears substantially linked to the riskof suicide: data in the literature estimate that therisk of suicide in tinnitus patients is ten timeshigher than the general population23. As regardsmorbidity, or the result of tinnitus handicap,concomitant psychiatric symptoms represent the

G. Altissimi, M. Salviati, R. Turchetta, M.P. Orlando, A. Greco, M. De Vincentiis, et al.

most reliable measure of compromised qualityof life114.

Somatic symptoms such as tinnitus are fre-quent in patients with distress from post-traumaticstress disorder (PTSD)115. Fagelson116 has con-firmed that 34% of 300 patients with tinnitus en-rolled in his clinic carried a diagnosis of PTSD. In2006, Hinton et al117 reported that 50% of Cambo-dian refugee patients with a history of PTSD suf-fered from disturbing tinnitus. Somatic symptomsare correlated with greater PTSD severity. Tinni-tus has also been considered to be a trigger ofmemories of the specific trauma. Hinton et al117

describe the possibility that the memory of thetraumatic episode could be connected and/orcaused by tinnitus. Some authors maintain thatflashbacks and intrusive memories contribute toexacerbation of the tinnitus itself. Henry et al118

suggested that exacerbation of tinnitus in some pa-tients, in the presence of particular environmentalsounds, depended, at least in part, from the factthat the sound triggered a memory of past events,which produced a distressing emotional state.These associations would be particularly evidentin those patients where the onset of tinnitus can betraced back to a specific episode of exposure to asound or a traumatic event, like that which causedthe PTSD.

Besides acute PTSD, psychiatric urgency isrepresented by the risk of suicide or by a psychi-atric comorbidity, which makes the tinnitus so de-bilitating that urgent consultation is necessary.Conflicting reports emerge from the literature:some studies affirm that there is no direct correla-tion between tinnitus and suicide119, while othersuphold the contrary120. In both cases, comorbidityshould be carefully assessed. Or rather, if some au-thors attribute the risk of suicide to the copresenceof depressive disorders117, the latter, besides beingextremely frequent121 are, in each case, directlycorrelated with the severity of the tinnitus itself122.Consequently it is reasonable to consider comor-bidity therapy urgent, both with regard to the riskof suicide or attempted suicide and in terms ofacute decompensation. In a 2006 study, Langguthet al123, in support of these considerations, surmisea complex interaction between tinnitus and depres-sion, based on a common physiopathology, orcompromise of hippocampus neurogenesis. More-over, from genetic research, tests show how a vari-ant of the brain derived neutrophic factor (BDNF)can act as a common susceptibility factor in bothdisorders123. Various studies have also been under-taken on the serotonin transporter gene124.

A 1992 study by Lewis et al125 on a group oftinnitus sufferers suggest that the suicide risk was118 per 100000 people a year (more than tentimes the general rate). These estimates shouldbe interpreted with care, given the methodologi-cal weaknesses present and the limited numberof cases taken into consideration. In anotherstudy in 1994, Lewis et al126 found 28 cases ofsuicide in tinnitus sufferers. These authors alsoidentified a series of common suicide risk factors– male, elderly, socially isolated, history of psy-chiatric illness – particularly depression (70%),problems of alcohol abuse and previous historyof attempted suicide. Although the sample evalu-ated is small, the study produced interesting re-sults. In a study in 1996, Johnston et al127 drewattention to the significance of concomitant de-pression and risk of suicide in the geriatric popu-lation. The elderly may often have atypicalsymptoms such as an impaired ability to commu-nicate, feelings of helplessness and tinnitus.

Lewis et al128, in a study over a short three-month period of 184 patients in South Glamor-gan hospital in Wales, United Kingdom, evaluat-ed the percentage of people who had attemptedsuicide by poison, pointing out that patients withtinnitus were under-represented (1.6%), with re-spect to the general population (7%). The resultsobtained should be interpreted bearing in mindthat: (1) the three-month study period enabledonly a somewhat limited sample to be consid-ered; (2) only one hospital was studied, and (3)suicide modalities are numerous.

Contrasting data emerge from the literature. Arelationship between tinnitus and the risk of sui-cide has been shown, particularly in the elderly,and is frequently correlated with depression. Fewstudies111 have been carried out to date on acutedecompensated tinnitus, which is perceived as achronic problem in the majority of cases. Basedon our case series, there may be exacerbation of“chronic decompensation”, in correlation withparticularly stressful or significant events in aperson’s life, followed by adjustment distur-bances, which require urgent consultation. It isimportant, therefore, to carry out early treatmentto prevent decompensation129. In 2004, a studyby D’Amelio et al130 on patients with severe tin-nitus showed the importance of early interven-tion in the acute stage of tinnitus, since the pa-tient’s immediate reaction to the manifestation oftinnitus could be of prognostic value for the levelof emotional stress to be experienced with chron-ic tinnitus.

2967

Emergency tinnitus

2968

In accordance with data from the literature,we consider early intervention to be important toprevent decompensation, which influences thetinnitus handicap131, particularly in terms ofseverity132.

Results

Writings in the literature are based on small-sized samples or case reports, given the rarity ofsome conditions that are implicit in tinnitus inthe acute stage, and the few available studies onthe matter. In our opinion, this further highlightsthe importance for a clinician to have a “diagnos-tic instrument” available to assess the tinnitus pa-tient, particularly when tinnitus is “decompensat-ed”. In light of the above, we have elaborated analgorithm that could be useful in the “manage-ment of tinnitus in the acute stage”. Clinicians, toassess decompensation, lacking instrumentalsymptomatology that can digitalize and registerthe symptom with pathology and associated risk,may now take advantage of an instrument widelyused in first assessment of the tinnitus handicap:the Tinnitus Handicap Inventory (THI). Thisquestionnaire constitutes a first-level screeningtest to determine psychiatric comorbidity114. THIhas gained widespread acceptance as a “self-re-port” measure of tinnitus handicap. At this point,it is used widely in the literature; it assesses theimpact of tinnitus on the activities of daily life.THI consists of 25 multiple-choice questions,which assess various areas – functional, emotion-al and catastrophic. The test enables grading ofthe tinnitus handicap based on scores (very mildwith score of 0-16, mild 18-36, moderate 38-56,severe 58-76, catastrophic 78-100). When thetest score is greater than 36133, psychiatric inves-tigation is needed, to evaluate possible psychi-atric comorbidities, by category (Diagnostic andstatistical manual of mental disorders, fourth edi-tion – DSM IV), and with probable further suit-able psychotropic treatment, since there is a cor-relation between psychopathological conditionsand THI score133.

The algorithm we have presented, based onour experience and on cases in the literature,makes a first distinction between pulsatile andnon-pulsatile tinnitus, leaving prominent spacefor an evaluation of the patient’s psycho-emo-tional state.

The most probable underlying pathologiescausing the symptom are listed in Figure 1.

Based on the characteristics of the tinnitus, itsonset, model, any associated symptoms, impactof the patient’s attitude on the tinnitus, examina-tion of the temporomandibular joint and the cer-vical spine, it will be possible to target any un-derlying pathology and diagnostic-therapeutictreatment.

Conclusions

To date, there are no clinical standards andguidelines for better management of patientswith tinnitus in emergency situations134. Whatemerges from our work is the realization that amultidisciplinary approach is the most appropri-ate way of dealing with the “tinnitus problem”and avoiding decompensation. In management oftinnitus at the acute stage, it will be necessary inthe first place to consider the medical urgency,since multiple, even severe, pathologies may un-derlie the tinnitus symptom, which will need im-mediate medical or surgical treatment. It will beimportant as well to recognize, assess and man-age any concomitant psychiatric urgency, in or-der to rationalize therapeutic intervention.

At present, tinnitus is not regarded by the Ital-ian Hospital Otology Association (AssociazioneOtorinolaringologi Ospedalieri Italiani [AOOI])as an urgency135, but as a symptom associatedwith internal medicine, surgery and otorhino-laryngology.

When we speak of tinnitus, a question arisesspontaneously: “… are we faced with a simplesymptom or a threat?” Tinnitus is too often anunderestimated symptom, even when urgent. Atpresent, we still see a somewhat superficial man-agement of tinnitus patients on the part of doc-tors, where the clinical case is often underesti-mated. This cannot be justified, particularly inthe case of sudden or rapid decompensation tin-nitus. We could be faced with a real emergency.In fact, tinnitus could be the sign of an ominouspathological process, hiding even severe psycho-logical effects that can lead to suicide. For thisreason, clinical cases presenting tinnitus shouldbe analysed with particular attention.

The main objective, in assessing tinnitus in anemergency department, is to identify life-threat-ening causes, preserve hearing, identify curablecauses and provide appropriate data and sympto-matic treatment in order to avoid reaching achronic condition or, even worse, decompensa-tion of the symptom.

G. Altissimi, M. Salviati, R. Turchetta, M.P. Orlando, A. Greco, M. De Vincentiis, et al.

Other diagnostic-therapeutic algorithms havealready been described in the literature but, inour opinion, the algorithm presented in our workhas the merit of being simple and easy to use byall doctors, whether specialists or not. It also hasthe exclusive feature of allowing a primary as-sessment of the patient’s psychological aspectthrough a questionnaire that can highlight possi-ble psychiatric comorbidity, particularly whenthe underlying pathology is underestimated.

At present, since a positive universal and con-clusive therapy for tinnitus is lacking, an in-depthstudy of the patient serves as an essential basis forsubsequent more targeted and effective treatment.

————————————CONFLICT OF INTERESTS

The Authors declare that they have no conflict of interests.

References

1. JASTREBOFF PJ. Phantom auditory perception (tinni-tus): mechanisms of generation and perception.Neurosci Res 1990; 8: 221-254.

2. LANGGUTH B, KREUZER PM, KLEINJUNG T, DE RIDDER D.Tinnitus: causes and clinical management.Lancet Neurol 2013; 12: 920-930.

3. HELLER AJ. Classification and epidemiology of tinni-tus. Otolaryngol Clin North Am 2003; 36: 239-248.

4. BAGULEY D, MCFERRAN D, HALL D. Tinnitus. Lancet2013; 382: 1600-1607.

5. MORGENSTERN, L. The bells are ringing: tinnitus intheir own words. Perspect Biol Med 2005; 48:396-407.

6. BAGULEY DM. Mechanisms of tinnitus. Br Med Bull2002; 63: 195-212.

7. AXELSSON A, RINGDAHL A. Tinnitus – a study of itsprevalence and characteristics. Br J Audiol 1989;23: 53-62.

8. GEORGIEWA P, KLAPP BF, FISCHER F, REISSHAUER A,JUCKEL G, FROMMER J, MAZUREK B. An integrativemodel of developing tinnitus based on recentneurobiological findings. Med Hypotheses 2006;66: 592-600.

9. LOCKWOOD AH, SALVI RJ, BURKARD RF. Tinnitus. NEngl J Med 2002; 19: 347: 904-910.

10. FOLMER RL, MARTIN WH, SHI Y. Tinnitus: questionsto reveal the cause, answers to provide relief. JFam Pract 2004; 53: 532-540.

11. MØLLER AR. Neural plasticity in tinnitus. Prog BrainRes 2006; 157: 365-372.

12. ZENNER HP, PFISTER M. Systematic classification oftinnitus. Proceedings of the Sixth International Tin-nitus Seminar. Special edition, 2002; pp. 17-19.

2969

Emergency tinnitus

Figure I.

2970

13. DUCKRO PN, POLLARD CA, BRAY HD, SCHEITER L.Comprehensive behavioral management of com-plex tinnitus: a case illustration. Biofeedback SelfRegul 1984; 9: 459-469.

14. CIANFRONE G, MAZZEI F, SALVIATI M, TURCHETTA R, OR-LANDO MP, TESTUGINI V, CARCHIOLO L, CIANFRONE F, AL-TISSIMI G. Tinnitus Holistic Simplified Classification(THoSC). A new assessment for subjective tinni-tus, with diagnostic and therapeutic implications.Ann Otol Rhinol Laryngol 2015; 124: 550-560.

15. SCHUTTE NS, NOBLE W, MALOUFF JM, BHULLAR N.Evaluation of a model of distress related to tinni-tus. Int J Audiol 2009; 48: 428-432.

16. GOPINATH B, MCMAHON CM, ROCHTCHINA E, KARPAMJ, MITCHELL P. Risk factors and impacts of inci-dent tinnitus in older adults. Ann Epidemiol 2010;20: 129-135.

17. FOLMER RL, GRIEST SE, MARTIN WH. Obsessive-com-pulsiveness in a population of tinnitus patients. IntTinnitus J 2008; 14: 127-130.

18. SALVIATI M, BERSANI FS, TERLIZZI S, MELCORE C, PANICOR, ROMANO GF, VALERIANI G, MACRÌ F, ALTISSIMI G,MAZZEI F, TESTUGINI V, LATINI L, DELLE CHIAIE R, BION-DI M, CIANFRONE G. Tinnitus: clinical experience ofthe psychosomatic connection. NeuropsychiatrDis Treat 2014; 10: 267-275.

19. KHEDR EM, AHMED MA, SHAWKY OA, MOHAMED ES,EL ATTAR GS, MOHAMMAD KA. Epidemiological studyof chronic tinnitus in Assiut, Egypt. Neuroepidemi-ology 2010; 35: 45-52.

20. BAUCH CD, LYNN SG, WILLIAMS DE, MELLON MW,WEAVER AL. Tinnitus impact: three different mea-surement tools. J Am Acad Audio 2003; 14: 181-187.

21. BELLI S, BELLI H, BAHCEBASI T, OZCETIN A, ALPAY E,ERTEM U. Assessment of psychopathological as-pects and psychiatric comorbidities in patients af-fected by tinnitus. Eur Arch Otorhinolaryngol2008; 265: 279-285.

22. TURNER O, WINDFUHR K, KAPUR N. Suicide in deafpopulations: a literature review. Ann Gen Psychi-atry 2007; 6: 26.

23. MARCIANO E, CARRABBA L, GIANNINI P, SEMENTINA C,VERDE P, BRUNO C, DI PIETRO G, PONSILLO NG. Psy-chiatric comorbidity in a population of outpatientsaffected by tinnitus. Int J Audiol 2003; 42: 4-9.

24. GOLDMAN DR, HOLME R. Hearing loss and tinnitus-the hidden healthcare time bomb. Drug DiscovToday 2010; 15: 253-255.

25. SAVAGE J, WADDELL A. Tinnitus. BMJ Clin Evid2012; 2012: 0506.

26. SISMANIS A. Pulsatile tinnitus. Otolaryngol ClinNorth Am 2003; 36: 389-402.

27. CHEN YJ, HOW CK, CHERN CH. Cerebral dural arte-riovenous fistulas presenting as pulsatile tinnitus.Intern Med J 2007; 37: 503.

28. ALI S, RADAIDEH MM, SHAIBANI A, RUSSELL EJ, WALKER

MT. Persistent trigeminal artery terminating in theposterior inferior cerebellar artery: case report.Neurosurgery 2008; 62: 746-748.

29. SCHELFAUT D, DHONDT E, DE RAEDT S, NIEBOER K,HUBLOUE I. Carotid artery dissection: three casesand a review of the literature. Eur J Emerg Med2012; 19: 181-187.

30. NAKAGAWA N, AKAI F, FUKAWA N, YUGAMI H, KIMOTOA, MAJIMA S, TANEDA M. Endovascular stent place-ment of cervical internal carotid artery dissectionrelated to a seat-belt injury: a case report. MinimInvasive Neurosurg 2007; 50: 115-119.

31. LEE H, WHITMAN GT, LIM JG, LEE SD, PARK YC. Bilat-eral sudden deafness as a prodrome of anteriorinferior cerebellar artery infarction. Arch Neurol2001; 58: 1287-1289.

32. KOTAN D, SAYAN S, ACAR BA, POLAT P. Bilateral ver-tebral artery stenosis present with vertigo. BMJCase Rep 2013; 2013. doi: 10.1136/bcr-2012-007544.

33. FEITOSA-FILHO GS, LOPES RD, POPPI NT, GUIMARÃESHP. Hypertensive emergencies. Rev Bras Ter In-tensiva 2008; 20: 305-312.

34. MEHANNA R, SHALTONI H, MORSI H, MAWAD M. En-dovascular treatment of sigmoid sinus aneurysmpresenting as devastating pulsatile tinnitus. Acase report and review of literature. Interv Neuro-radiol 2010; 16: 451-454.

35. FALCIONI M, PICCIRILLO E, TAIBAH A, DE DONATO G, CARU-SO A, RUSSO A. Intrapetrous carotid arteryaneurysm.Acta Otorhinolaryngol Ital 1999; 19: 36-41.

36. MOONIS G, HWANG CJ, AHMED, T, WEIGELE JB, HURSTRW. Otologic manifestations of petrous carotidaneurysms. AJNR Am J Neuroradiol 2005; 26:1324-1327.

37. GUENTHER F, VON ZUR MUHLEN C, LOHRMANN J, BODEC, GEIBEL A. Rupture of an aneurysm of the non-coronary sinus of Valsalva into the right atrium.Eur J Echocardiogr 2008; 9: 186-187.

38. GARTRELL BC, KENNEDY TA, GUBBELS SP. Bilateral du-plicated internal carotid arteries presenting asmiddle ear masses: a case report and review ofthe literature. Ann Otol Rhinol Laryngol 2012;121: 521-524.

39. KENDALL B. Embolisation techniques in neuroradi-ology. J Neurol 1986; 233: 323-335.

40. TOPAL H, LEMMENS R, FOURNEAU I. Possible famil-ial presentation in two siblings with carotid fibro-muscular dysplasia. Acta Chir Belg 2015;115:83-86.

41. NOURI H, HARKANI A, ELOUALI IDRISSI M, ROCHDI Y,ADERDOUR L, OUSSEHAL A, RAJI A. Capillary heman-gioma of the middle ear: one case report and re-view of the literature. Case Rep Otolaryngol2012; 2012: 305172.

42. KOJIMA H, YAGUCHI Y, MORIYAMA H. Middle ear he-mangioma: a case report. Auris Nasus Larynx2008; 35: 255-259.

43. HECHT DA, JACKSON CG, GRUNDFAST KM. Manage-ment of middle ear hemangiomas. Am J Otolaryn-gol 2001; 22: 362-366.

44. HSUEH PJ, CHEN, WY, CHIANG YC, LEE FP. Capillaryhemangioma of the middle ear. Otolaryngol HeadNeck Surg 2007; 136: 666-667.

45. ALOBID I, GASTÓN F, MORELLO A, MENENDEZ LM, BENITEZP. Cavernous haemangioma of the internal auditorycanal. Acta Otolaryngol 2002; 122: 501-503.

46. KOSTRZEWA JP, BOWMAN MK, WOOLLEY AL. Middleear hemangioma: a novel treatment for a rareproblem. Int J Pediatr Otorhinolaryngol Extra2010; 5: 50-52.

G. Altissimi, M. Salviati, R. Turchetta, M.P. Orlando, A. Greco, M. De Vincentiis, et al.

47. RUTHERFORD KD, LEONARD G. Hemangiomas of theexternal auditory canal. Am J Otolaryngol 2010;31: 384-386.

48. MARHOLD F, PREUSSER M, DIETRICH W, PRAYER D,CZECH T. Clinicoradiological features of rosette-forming glioneuronal tumor (RGNT) of the fourthventricle: report of four cases and literature re-view. J Neurooncol 2008; 90: 301-308.

49. GUODE Z, QI P, HUA G, SHANGCHEN X, HANBIN W.Primary cerebellopontine angle angiosarcoma. JClin Neurosci 2008; 15: 942-946.

50. BLACKBURN W, LEUNG G, MORASH C. Brain TumourFoundation Award 2007. Glomus jugulare tu-mours: are they really so benign? Can J NeurosciNurs 2007; 29: 21-28.

51. SEYMOUR FK, LLOYD S, HARCOURT JP. Glomus jugu-lare tumour presenting with isolated accessorynerve palsy. J Laryngol Otol 2004; 118: 234-236.

52. COLES MC. Glomus jugulare tumor presentationand management: a case study. J Neurosci Nurs2004; 36: 221-223, 235.

53. LIU JF. NI DF, GAO ZQ, XU CX, LI WY, CHEN XM. Di-agnosis and therapy of glomus tympanicum andglomus jugulare tumors. Zhonghua Er Bi Yan HouKe Za Zhi 2004; 39: 543-545.

54. BONNEVILLE F, SARRAZIN JL, MARSOT-DUPUCH K, IFFE-NECKER C, CORDOLIANI YS, DOYON D, BONNEVILLE JF.Unusual lesions of the cerebellopontine angle: asegmental approach. Radiographics 2001; 21:419-438.

55. SCHALLER B, HEILBRONNER R, PFALTZ CR, PROBST RR,GRATZL O. Preoperative and postoperative audito-ry and facial nerve function in cerebellopontineangle meningiomas. Otolaryngol Head Neck Surg1995; 112: 228-234.

56. CHEN AF, SAMY RN, GANTZ BJ. Cerebellopontineangle tumor composed of Schwann andmeningeal proliferations. Arch Otolaryngol HeadNeck Surg 2001; 127: 1385-1389.

57. EVANS DG, HUSON SM, DONNAI D, NEARY W, BLAIR V,TEARE D, NEWTON V, STRACHAN T, RAMSDEN R, HARRISR. A genetic study of type 2 neurofibromatosis inthe United Kingdom. I. Prevalence, mutation rate,fitness, and confirmation of maternal transmissioneffect on severity. J Med Genet 1992; 29: 841-846.

58. TSUKAMOTO H, HIKITA T, TAKAKI T. Cerebellopontineangle meningioma associated with cranial acces-sory nerve neurinoma-case report. Neurol MedChir 1994; 34: 225-229.

59. MAIURI F, CAPPABIANCA P, IACONETTA G, ESPOSITO F,MESSINA A. Simultaneous presentation of menin-giomas with other intracranial tumours. Br J Neu-rosurg 2005; 9: 368-375.

60. GRAUVOGEL J, GRAUVOGEL TD, TASCHNER C, BAUM-GARTNER S, MAIER W, KAMINSKY J. A rare case of radi-ologically not distinguishable coexistent menin-gioma and vestibular schwannoma in the cerebel-lopontine angle-Case report and literature review.Case Rep Neurol 2010; 2: 111-117. 27.

61. KONDZIOLKA D, FLICKINGER JC, LUNSFORD LD. Theprinciples of skull base radiosurgery. NeurosurgFocus 2008; 24: E11.

62. TOKUNAGA T, SHIGEMORI M, HIROHATA M, SUGITA Y,MIYAGI J, KURAMOTO, S. Multiple primary brain tu-mors of different histological types-report of twocases. Neurol Med Chir 1991; 31: 141-145.

63. YATES CW, WEINBERG M, PACKER MJ, JACOB A. Fatalcase of tumor-associated hemorrhage in a largevestibular schwannoma. Ann Otol Rhinol Laryn-gol 2010; 119: 402-405.

64. WICK CC, MANZOOR NF, SEMAAN MT, MEGERIAN CA.Endolymphatic sac tumors. Otolaryngol ClinNorth Am 2015; 48: 317-330.

65. GRECO A, GALLO A, FUSCONI M, MARINELLI C, MACRIGF, DE VINCENTIIS M. Ménière's disease might bean autoimmune condition? Autoimmun Rev 2012;11: 731-738.

66. SAJJADI H, PAPARELLA MM. Ménière's disease.Lancet 2008; 372: 406-414.

67. GRECO A, GALLO A, FUSCONI M, MAGLIULO G,TURCHETTA R, MARINELLI C, MACRI GF, DE VIRGILIO A,DE VINCENTIIS M. Cogan's syndrome: an autoim-mune inner ear disease. Autoimmun Rev 2013;12: 396-400.

68. DE SOUSA LC, PIZA MR, DA COSTA SS. Diagnosis ofMénière's disease: routine and extended tests.Otolaryngol Clin North Am 2002; 35: 547-564.

69. PULEC JL. Ménière's disease of syphilitic etiology.Ear Nose Throat J 1997; 76: 508-510, 512-514.

70. KIM HC, AN YS, AHN JH. Petrous apex cholesterolgranuloma presenting as endolymphatic hydrops:a case report. Clin Exp Otorhinolaryngol 2009;2:151-154.

71. KUHN WF, KUHN SC, GILBERSTADT H. Occipital neu-ralgias: clinical cognition of a complicatedheadache. A case series and literature review. JOrofac Pain 1997; 11:158-165.

72. DESAI MJ, DAVE AP, MARTIN MB. Delayed radicularpain following two large volume epidural bloodpatches for post-lumbar puncture headache: acase report. Pain Physician 2010; 13: 257-262.

73. DOğANAY F, PIRBUDAK L, GÜL R, ALPTEKIN M, KAPLANN. Postspinal subacute subdural hematoma:case report. Agri 2013; 25:129-132.

74. SAHIN C, TERZIOGLU U, YIGIT G. Sudden bilateralhearing loss after spinal anaesthesia. J LaryngolOtol 2015; 129:395-397.

75. ACHACHE M, SANJUAN PUCHOL M, SANTINI L, LAFONT B,CIHANEK M, LAVIEILLE JP, DEVÈZE A. Late pneumo-labyrinth after undiagnosed post-traumatic peri-lymphatic fistula. Case report illustrating the im-portance of systematic emergency management.Eur Ann Otorhinolaryngol Head Neck Dis 2013;130: 283-287.

76. FODEN N, MEHTA N, JOSEPH T. Sudden onset hear-ing loss-causes, investigations and management.Aust Fam Physician 2013; 42: 641-644.

77. VIJAYENDRA H, BUGGAVEETI G, PARIKH B, SANGITHA R.Sudden sensorineural hearing loss: an otologicemergency. Indian J Otolaryngol Head Neck Surg2012; 64: 1-4.

78. MARTINES F, DISPENZA F, GAGLIARDO C, MARTINES E,BENTIVEGNA D. Sudden sensorineural hearing lossas prodromal symptom of anterior inferior cere-bellar artery infarction. ORL J OtorhinolaryngolRelat Spec 2011; 73: 137-140.

2971

Emergency tinnitus

2972

79. GRECO A. FUSCONI M, GALLO A, MARINELLI C, MACRIGF, DE VINCENTIIS M. Sudden sensorineural hear-ing loss: an autoimmune disease? AutoimmunRev 2011; 10:756-761.

78. HAMID M, TRUNE D. Issues, indications, and con-troversies regarding intratympanic steroid perfu-sion. Curr Opin Otolaryngol Head Neck Surg2008; 16: 434-440.

81. SCHREIBER BE, AGRUP C, HASKARD DO, LUXON LM.Sudden sensorineural hearing loss. Lancet 2010;375: 1203-1211.

82. CHIOSSOINE-KERDEL JA, BAGULEY DM, STODDART RL,MOFFAT DA. An investigation of the audiologichandicap associated with unilateral sudden sen-sorineural hearing loss. Am J Otol 2000; 21: 645-651.

83. DIAO M, TIAN F, SUN J. Sudden sensorineural hear-ing loss as the first manifestation of chronicmyeloid leukaemia: case report. J Laryngol Otol2014; 128:1015-1017.

84. RAHMAN MU, POE DS, CHOI HK. Autoimmunevestibulo-cochlear disorders. Curr Opin Rheuma-tol 2001; 13: 84-189.

85. GRECO A, DE VIRGILIO A, GALLO A, FUSCONI M, RUOP-POLO G, TURCHETTA R, PAGLIUCA G, DE VINCENTIIS M.Idiopathic bilateral vestibulopathy: an autoim-mune disease? Autoimmun Rev 2014; 13: 1042-1047.

86. GRECO A, FUSCONI M, GALLO A, TURCHETTA R,MARINELLI C, MACRI GF, DE VIRGILIO A, DE VINCENTIISM. Vogt-Koyanagi-Harada syndrome. AutoimmunRev 2013; 12: 1033-1038.

87. RODRIGUEZ-CASERO MV, MANDELSTAM S, KORNBERGAJ, BERKOWITZ RG. Acute tinnitus and hearingloss as the initial symptom of multiple sclerosisin a child. Int J Pediatr Otorhinolaryngol 2005;69:123-126.

88. GRANATA G, GRECO A, IANNELLA G, MASSIMO G, MAN-NO A, SAVASTANO E, MAGLIULO G. Posterior re-versible encephalopathy syndrome-Insight intopathogenesis, clinical variants and treatment ap-proaches. Autoimmun Rev 2015; S1568-9972:114-117.

89. COOPER MA. Emergent care of lightning and elec-trical injuries. Semin Neurol 1995; 15: 268-278.

90. DESAI BK, FAIRCLOUGH R. A case of a speech imped-iment following a near lightning strike. Int JEmerg Med 2011; 4: 60. 19

91. HATTEN K, GULLETH Y, MEYER T, EISENMAN DJ. Myia-sis of the external and middle ear. Ann Otol Rhi-nol Laryngol 2010; 119: 436-438.

92. GONZÁLEZ POGGIOLI N, VÁZQUEZ BARRO JC. Otic myi-asis. Case report. Acta Otorrinolaringol Esp 2009;60: 213-214.

93. WOLF LR, OTTEN EJ, SPADAFORA MP. Cinchonism:two case reports and review of acute quinine toxi-city and treatment. J Emerg Med 1992; 10: 295-301.

94. BODENHAMER JE, SMILKSTEIN MJ. Delayed cardiotoxi-city following quinine overdose: a case report. JEmerg Med 1993; 11: 279-285.

95. SMILKSTEIN MJ, KULIG KW, RUMACK BH. Acute toxicblindness: unrecognized quinine poisoning. AnnEmerg Med 1987; 16: 98-101.

96. JAMMEHDIABADI M, TIERNEY M. Impact of toxicologyscreens in the diagnosis of a suspected over-dose: salicylates, tricyclic antidepressants, andbenzodiazepines. Vet Hum Toxicol 1991; 33: 40-43.

97. CHYKA PA, ERDMAN AR, CHRISTIANSON G, WAX PM,BOOZE LL, MANOGUERRA AS, CARAVATI, EM, NELSON LS.OLSON KR, COBAUGH DJ, SCHARMAN EJ, WOOLF AD,TROUTMAN WG. Salicylate poisoning: an evidence-based consensus guideline for out-of-hospital man-agement. Clin Toxicol (Phila) 2007; 45: 95-131.

98. VAN DONSELAAR-VAN DER PANT KA, BUWALDA M, VANLEEUWEN HJ. Lidocaine: local anaesthetic with sys-temic toxicity. Ned Tijdschr Geneeskd 2008; 152:1-5.

99. WEAVER LK. Hyperbaric oxygen therapy for carbonmonoxide poisoning. Undersea Hyperb Med2014; 41: 339-354.

100. CULIć V, MIRIć D, ETEROVIć D. Correlation betweensymptomatology and site of acute myocardial in-farction. Int J Cardiol 2001; 77: 163-168.

101. VAVRINA J, MÜLLER W. Therapeutic effect of hyper-baric oxygenation in acute acoustic trauma. RevLaryngol Otol Rhinol 1995; 116: 377-380.

102. YLIKOSKI J, MRENA R, MAKITIE A, KUOKKANEN J, PIRVOLAU, SAVOLAINEN S. Hyperbaric oxygen therapyseems to enhance recovery from acute acoustictrauma. Acta Otolaryngol 2008; 128: 1110-1115.

103. WINIARSKI M, KANTOR I, SMEREKA J, JURKIEWICZ D. Ef-fectiveness of pharmacologic therapy combinedwith hyperbaric oxygen in sensorineural hearingloss following acute acoustic trauma. Prelimi-nary report. Pol Merkur Lekarski 2005; 19: 348-350.

104. NESS B, STEGER J, DELLA-GIUSTINA D. "I can't taste icecream": an unusual case of tinnitus and dysgeu-sia. Pediatr Emerg Care 2004; 20: 832-834.

105. FENG HM, SHIH CP. Images in clinical medicine: anunusual auricular foreign body. N Engl J Med2014; 370: e11.

106. TURBIAK TW. Ear trauma. Emerg Med Clin NorthAm 1987; 5: 243-251.

107. CHUKUEZI AB, NWOSU JN. Ear trauma in Orlu, Nige-ria: a five-year review. Indian J Otolaryngol HeadNeck Surg 2012; 64: 42-45.

108. REITSMA S, STOKROOS R, WEBER JW, VAN TONGEREN J.Pediatric Idiopathic Intracranial Hypertension Pre-senting With Sensorineural Hearing Loss. AnnOtol Rhinol Laryngol 2015; 124: 996-1001.

109. SYED MI, PLODPAI Y, KHOO SG, RUTKA JA. Primaryepidermoid cysts of the mastoid: clinical andtreatment implications. Eur Arch Otorhinolaryngol2016; 273: 1055-1059.

110. MAZUREK B, OLZE H, HAUPT H, SZCZEPEK AJ. The morethe worse: the grade of noise-induced hearing lossassociates with the severity of tinnitus. Int J Envi-ron Res Public Health 2010; 7:3071-3079.

111. HÄRTER M, MAURISCHAT C, WESKE G, LASZIG R, BERG-ER M. Psychological stress an impaired quality oflife in patients with tinnitus. HNO 2004; 52: 125-131.

112. HOLGERS KM. Tinnitus treatment is guided by etiol-ogy. Noise, stress or anxiety/depression plausiblecauses. Lakartidningen 2003; 100: 3744-3749.

G. Altissimi, M. Salviati, R. Turchetta, M.P. Orlando, A. Greco, M. De Vincentiis, et al.

113. BASKILL JL, COLES RR, LUTMAN ME, AXELSSON A. Tinni-tus severity grading: longitudinal studies. Bord,France, Fourth International Tinnitus Seminar1991; pp. 457-460.

114. NEWMAN CW, JACOBSON GP, SPITZER JB. Develop-ment of the tinnitus handicap inventory. ArchOtolaryngol Head Neck Surg 1996; 122:143-148.

115. GUPTA MA. Review of somatic symptoms in post-traumatic stress disorder. Int Rev Psychiatry2013; 25:86-99.

116. FAGELSON MA. The association between tinnitusand posttraumatic stress disorder. Am J Audiol2007; 16:107-117.

117. HINTON DE, CHHEAN D, PICH V, HOFMANN SG, BAR-LOW DH. Tinnitus among Cambodian refugees:relationship to PTSD severity. J Trauma Stress2006; 19: 541-546.

118. HENRY JL, KANGAS M, WILSON PH. Development ofthe psychological impact of tinnitus interview: aclinician-administered measure of tinnitus-relateddistress. Int Tinnitus J 2001; 7: 20-26.

119. JACOBSON GP, MCCASLIN DL. A search for evidenceof a direct relationship between tinnitus and sui-cide. J Am Acad Audiol 2001; 12:493-496.

120. SCHAAF H, EIPP C, DEUBNER R, HESSE G, VASA R, GIEL-ER U. Psychosocial aspects of coping with tinnitusand psoriasis patients. A comparative study ofsuicidal tendencies, anxiety and depression.HNO 2009; 57: 57-63.

121. GEOCZE L, MUCCI S, ABRANCHES DC, MARCO MA,PENIDO NDE O. Systematic review on the evi-dences of an association between tinnitus anddepression. Braz J Otorhinolaryngol 2013; 79:106-111.

122. ZÖGER S, SVEDLUND J, HOLGERS KM. Relationshipbetween tinnitus severity and psychiatric disor-ders. Psychosomatics 2006; 47: 282-288.

123. LANGGUTH B, LANDGREBE M, KLEINJUNG T, SAND GP,HAJAK G. Tinnitus and depression. World J BiolPsychiatry 2011; 12: 489-500.

124. DENIZ M, BAYAZIT YA, CELENK F, KARABULUT H, YILMAZA, GUNDUZ B, SARIDOGAN C, DAGLI M, ERDAL E,MENEVSE A. Significance of serotonin transportergene polymorphism in tinnitus. Otol Neurotol2010; 31: 19-24.

125. LEWIS JE, STEPHENS SDG, HUWS D. Suicide in tinni-tus sufferers. J Audiologic Med 1992; 1: 30-37.

126. LEWIS JE, STEPHENS SDG, MCKENNA L. Tinnitus andsuicide. Clin Otolaryngol Allied Sci 1994; 19: 50-54.

127. JOHNSTON M, WALKER M. Suicide in the elderly.Recognizing the signs. Gen Hosp Psychiatry1996; 18: 257-260.

128. LEWIS JE, STEPHENS SDG. Parasuicide and tinnitus. JAudiologic Med 1995; 4: 34-43.

129. OLDEROG M, LANGENBACH M, MICHEL O, BRUSIS T,KÖHLE K. Predictors and mechanisms of tinnitusdistress--a longitudinal analysis. Laryngorhi-nootologie 2004; 83: 5-13.

130. D’AMELIO R, ARCHONTI C, SCHOLZ S, FALKAI P, PLINKERTPK, DELB W. Psychological distress associatedwith acute tinnitus. HNO 2004; 52: 599-603.

131. ANDERSSON G, FREIJD A, BAGULEY DM, IDRIZBEGOVIC E.Tinnitus distress, anxiety, depression, and hear-ing problems among cochlear implant patientswith tinnitus. J Am Acad Audiol 2009; 20: 315-319.

132. FOLMER RL, GRIEST SE, MEIKLE MB, MARTIN WH. Tin-nitus severity, loudness, and depression. Oto-laryngol Head Neck Surg 1999; 121: 48-51.

133. SALVIATI M, MACRÌ F, TERLIZZI S, MELCORE C, PROVEN-ZANO A, CAPPARELLI E, ALTISSIMI G, CIANFRONE G. TheTinnitus Handicap Inventory as a screening testfor psychiatric comorbidity in patients with tinni-tus. Psychosomatics 2013; 54: 248-256.

134. HENRY JA, ZAUGG TL, MYERS PJ, KENDALL CJ,MICHAELIDES EM. A triage guide for tinnitus. J Fam.Pract 2010; 59: 389-393.

135) LAUDADIO (ed.). Urgenze ed emergenze in ORL.Bologna, Italy. Associazione OtorinolaringoiatriOspedalieri Italiani; 2001.

2973

Emergency tinnitus