RESEARCH DISSERTATION TITLE: THE PATTERN OF HEARING LOSS AS SEEN AT THE UNIVERSITY OF BENIN TEACHING HOSPITAL, BENIN CITY.
BY
DR. PAUL R O C ADOBAMEN
ADDRESS: ENT UNIT, DEPARTMENT OF SURGERY, UBTH, BENIN CITY.
A RESEARCH DISSERTATION, SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENT FOR THE AWARD OF FMCORL OF THE NATIONAL POST GRADUATE MEDICAL COLLEGE OF NIGERIA.
MAY 2006.
1 CANDIDATE’S DECLARATION
I, Dr. Adobamen P R O C hereby declare that: “The pattern of hearing loss as seen at the University of Benin
Teaching Hospital, Benin City”;
- Is an original prospective work done by me as the sole author and assistance received is duly acknowledged.
- This work has not been previously submitted either in part or in full to any other College for a Fellowship nor has it been submitted elsewhere for publication.
SIGNATURE------
DATE------
2 CERTIFICATION
This study titled: “The pattern of hearing loss as seen at the University of Benin Teaching Hospital (UBTH), Benin City” was done by Dr. Adobamen P R O C under our supervision. We also supervised the writing of this dissertation.
1. NAME: Prof. F O Ogisi. FRCS, FICS, FWACS, FMCORL,
DLO.
STATUS: CONSULTANT OTORHINOLARYNGOLOGIST, HEAD
AND NECK SURGEON, PROFESSOR.
ADDRESS: DEPARTMENT OF SURGERY, U. B. T. H.,
BENIN CITY, NIGERIA.
SIGNATURE:------
DATE:------
2. NAME: PROF B C EZEANOLUE. FMCORL, FWACS, FICS
STATUS: CONSULTANT OTORHINOLARYNGOLOGIST,
HEAD AND NECK SURGEON, ASSOCIATE. PROFESSOR.
ADDRESS: DEPARTMENT OF OTOLARYNGOLOGY, U.N.T.H.,
ENUGU, NIGERIA.
SIGNATURE:------
DATE:------
3 DEDICATION
This book is dedicated to the bride of Jesus Christ; for their gallant stand for the Word of God.
4 5 6 ACKNOWLEDGEMENT
I express my profound gratitude to Jesus Christ; Who directed me during this project. I also thank Him for giving me the grace to successfully complete the project against all odds, especially at the data analysis stage, which was so burdensome and painstaking.
I express my sincere thanks to the dynamic, indefatigable and charismatic Prof. FO Ogisi and the energetic, prudent and meticulous Prof. BC Ezeanolue for the materials and hints they gave to me, that helped in this work. I also appreciate their patience in reading through and correcting the manuscript several times despite their hectic daily schedule. I also thank them for their constructive criticisms and encouragement throughout the period of this work.
I express my sincere gratitude to my wife; Oluchukwu and my children who had to be alone during my long stay on outside postings. I thank Miss Jennifer Ehizibue for the secretarial assistance of this project. I also express my deep respect and thanks to Mr. Clifford Ogiugo, the audiology
7 technician who did the pure tone audiometry for the patients in this study.
Lastly, I express my sincere appreciation to Professor
B A Oyejola of Statistics Department, University of Ilorin, for the statistical analysis of the data of this project.
8 TABLE OF CONTENTS
Contents Page
Candidate’s declaration i
Certification ii
Formative assessment of dissertation proposal iii
Ethical clearance certificate iv
Dedication v
Acknowledgement vi
Table of contents vii
Summary ix
CHAPTER ONE
Introduction 1
Research problem 3
Scope and limitations of the study 4
Justification/significance of the study 5
CHAPTER TWO
Aims and objectives of the study 6
CHAPTER THREE
Review of literature 7
3.1 Normal ear anatomy and conduction of sound waves 7
9 3.2 Measurement of hearing 11
3.3 Diagnosis of hearing loss 14
3.4 Types of hearing loss 17
3.5 Causes of hearing loss 18
3.6 Prevalence of hearing loss in Nigeria 21
3.7 Hearing loss in specific conditions 24
CHAPTER FOUR
Patients and method 36
4.1 Patients 36
4.2 Study method 37
4.3 Data analysis 39
CHAPTER FIVE
Results 40
CHAPTER SIX
Discussion 62
Conclusion 85
Recommendation 87
References 89
Appendix I (Consent form) 103 Appendix II (Questionnaire) 104 Appendix III (Registration of title of dissertation) 106
10
SUMMARY
Background- Deafness and hearing impairment are major causes of disability in developing countries. In Nigeria the magnitude of the problem of hearing impairment is enormous.
Aims and objectives- The aim of the study was to determine the pattern of hearing loss, the types of hearing loss and the clinical profile of patients presenting with hearing loss, at the University of Benin Teaching Hospital
(UBTH), Benin City.
Methodology- This study was a 12-month prospective clinical and audiological, hospital based study. Patients who presented with hearing loss at the Ear. Nose and Throat
(ENT) clinic of University of Benin Teaching Hospital, Benin
City, between September 2004 and August 2005 were recruited into the study. Pure tone air conduction thresholds of these patients were measured for the frequencies 250Hz, 500Hz, 1000Hz, 2000Hz, 4000Hz and
8000Hz. Bone conduction thresholds were measured at
500Hz, 1000Hz, 2000Hz and 4,000Hz.
11 Results- There were 257 patients, aged between 10years and 100 years in this study. There were 139 males and 118 females. Eighty-two patients had unilateral hearing loss while 175 patients had bilateral hearing loss; giving a total of 432 ears with hearing loss that were studied. The main causes of hearing loss were ototoxicity (15.7%), chronic suppurative otitis media (14.9%), presbyacusis (13.2%), wax impaction (8.9%) and rhinosinusitis (7.4%). In 10.6% of cases, the cause of the hearing loss was unknown. Multiple aetiological factors were identified for some ears. Different pure tone thresholds and types of hearing loss were encountered in this study, depending on the aetiological factor responsible for the hearing loss. Tinnitus was the commonest symptom that was complained of by patients with hearing loss. Hypertension was the commonest co- morbid medical condition associated with hearing loss in this study. The mean duration of hearing loss before presentation at ENT clinic was 5.1years 9.2SD in the right ear and 5.4years 9.5SD in the left ear.
Conclusion: The pattern of hearing loss as seen in UBTH,
Benin City, is not significantly different from that obtained
12 in other parts of Nigeria. The need for prophylactic measures to be put in place to prevent these aetiological factors, the provision of modern facilities for early detection, treatment and rehabilitation of patients with hearing loss were highlighted.
Keywords- Hearing loss, Benin City, Ototoxicity, Chronic suppurative otitis media, Presbyacusis, Pattern.
13 CHAPTER ONE
INTRODUCTION
The World Health Organization (WHO) applies the term
“deaf” to persons whose hearing impairment is so severe that they cannot benefit from amplification1. It will be difficult for this definition to find relevance in the context of a developing country, like Nigeria; where hearing aid facilities are not widely available and the few available ones cannot be adequately maintained2,3. Those persons who are
“deaf,” according to the above definition, are either totally without hearing or have profound hearing impairment
(>90dB).
It was projected that there would be 562 million people with hearing impairment in the world by 2005 by the World
Health Organization4. A 1985 World Health Organization
(WHO) resolution in relation to the prevention of deafness and hearing impairment, pointed out that much deafness and hearing impairment is avoidable or remediable and that developing countries had the greatest need for the prevention and remediation of hearing problems5. A 1995
WHO resolution estimated that there were 120 million
14 people with ‘disabling hearing difficulties’ worldwide and urged member states to set up national programmes for the prevention of deafness and hearing impairment5. It was envisaged that technical assistance to such countries would be provided by the WHO.
Deafness and hearing impairment are major causes of disability in developing countries. Unfortunately, they are generally neglected in comparison with other disabling conditions. The reasons for this neglect are many.
Principally, this is because deafness and hearing impairment produce unseen disability. There is also ignorance of the true size and nature of the problems and a conspicuous lack of resources to tackle these problems, particularly in developing countries.
Lastly, lack of awareness of the possibilities for prevention as well as uncertainty about the most appropriate methods for treatment and rehabilitation especially in developing countries is another reason for this neglect.
Although many countries do not have the wherewithal to mount their own national studies of hearing impairment,
15 they can rely on data from other countries. However, the extrapolations from such data are usually filled with uncertainties. Each country should therefore continue to aspire for the epidemiological studies that are required to provide the accurate, population-based data on which the extent of the problem can be determined. Accurate data are needed for governments to determine priorities within health programmes, to select and monitor preventive strategies and to predict treatment and rehabilitation needs.
Accurate data is also needed to determine the individual and societal costs of hearing impairment as well as the benefits of prevention.
Accordingly, the significance of the challenge of deafness is made more painful when we realize that the deaf have great problems in communicating and that these problems affect all aspects of their existence6.
RESEARCH PROBLEM
A high proportion of patients presenting at the Ear,
Nose and Throat (ENT) clinic of UBTH, have hearing loss. It will be necessary to scientifically document the incidence of hearing loss as seen in UBTH, Benin City. Also to find out
16 the actual pattern in terms of the types, the severity, the age and sex distribution and other associated conditions.
SCOPE AND LIMITATIONS OF THE STUDY
This study is based on patients seen at the ENT clinic of UBTH, Benin City.
UBTH is the main tertiary hospital/referral centre of
Edo and Delta States of Nigeria and neighbouring States
(Kogi, Ondo). However, the absence of specialist E.N.T services in some parts of Nigeria, has extended the catchment area of UBTH beyond the hospital’s designated catchment area.
This is a hospital based study which may not be truly representative of the pattern as in a community based study.
The non-availability of Oto-acoustic emission, cortical evoked response and brain-stem evoked response audiometer (instruments for objective assessment of hearing) is also a limitation of this study.
JUSTIFICATION/SIGNIFICANCE OF THE STUDY
A study on the pattern of hearing loss as seen in
UBTH, Benin City has not been previously conducted. This
17 study is to establish a baseline for the formulation of policies for the prevention, treatment and rehabilitation of patients with hearing loss. At the end of this study, an approximate estimate of the incidence of the different types of hearing loss and their aetiological pattern as seen in
UBTH, Benin City, would have been determined.
It will also serve as a useful background study, for future work on deafness in this region.
18 CHAPTER TWO
AIMS AND OBJECTIVES OF THE STUDY
The general objective:
The study is to document the aetiological pattern and the types of hearing loss among patients as seen at UBTH,
Benin City.
Specific Objectives:
1. To determine the hearing threshold of patients
presenting with hearing loss, using the pure tone
audiometer.
2. To determine the type of hearing loss of patients
presenting at ENT clinic, UBTH, Benin City.
3. To determine the age and sex distribution of the
patients presenting with hearing loss.
19 CHAPTER THREE
REVIEW OF LITERATURE
3.1 NORMAL EAR ANATOMY AND CONDUCTION OF
SOUND WAVES.
The external ear consists of the auricle, the external auditory canal and the lateral surface of the tympanic membrane. The middle ear consists of the medial surface of the tympanic membrane, the tympanic cavity (containing the malleus, incus and stapes), the eustachian tube, the attic, aditus ad antrum, mastoid antrum and mastoid air cells. The inner ear consists of the cochlea and the semicircular canals. The cochlear branch of the vestibulocochlear nerve transmits impulses from the cochlea to the cochlear nuclei located in the brain stem.
Neural tracts then pass from the cochlear nuclei to the ipsilateral and contralateral superior-olivary complex. From the superior olivary complex tracts travel via the lateral lemniscus to the inferior colliculus and from this to the medial geniculate body. Finally, they leave the brainstem and terminate in the auditory cortex at the lateral or
Sylvian fissure7.
20 The healthy ear processes sound frequencies ranging from 20Hz to 20, 000Hz. It detects sounds as soft as 0.002 dynes/cm2 (OdB HI) and can tolerate sounds a million times more intense (200 dynes/cm or 120 dB HI). Sound frequencies between 500Hz and 4,000Hz are the frequencies most important for speech8.
Sound waves are first collected in the external ear through the external auditory canal, resulting in the vibration of the tympanic membrane. These vibrations are in turn transmitted to the inner ear by the ossicles of the middle ear. The inner ear plays a vital role in the transformation of these mechanical vibrations into electrical impulses or signals, which can be recognized and decoded by the brain as sound.
The external ear may provide a 10dB amplification of sounds at the upper range of speech processing frequencies. This is due to a resonance in the external auditory meatus, that changes the sound pressure at the tympanic membrane in a frequency-selective way. The middle ear, provides an additional 20-30 dB of mechanical amplification by a mechanism comprising three
21 components. First, the force collected over the larger surface area of the tympanic membrane is expressed over the much smaller area of the stapes foot plate, with a corresponding increase in pressure. The pressure therefore increases in inverse proportion to the ratio of the areas.
This ratio is known as the impedance transformer ratio.
Secondly, the ossicles act as a lever, with the malleus being longer than the incus. This gives rise to the so-called lever ratio. The displacement at the stapes is therefore decreased, while the force is increased by this lever ratio.
Lastly, the tympanic membrane buckles as it moves to and fro. The reduction in the movement of the malleus means that the tympanic membrane acts as a mechanical lever. It therefore again increases the force and decreases the displacement at the stapes. This therefore increases the impedance ratio9.
The sound energy causes mechanical vibration of the perilymph and the endolymph, which sets up a mechanical travelling wave in the coclea. A normal travelling wave is therefore fundamental to normal auditory function and a pathological wave can cause severe deficit. The mechanical
22 travelling wave sets the basilar membrane into vibration.
The basilar membrane contains an active mechanical amplifier which uses biological energy to boost the mechanical vibration of the basilar membrane. The acoustic stimuli in the form of the mechanical vibration is converted to electric potential by three main mechanisms.
First, is the cochlear microphonic which is an alternating current response that follows the waveform of the stimulus.
Superimposed on that, a direct current shift in the baseline of the microphonic is often seen. This is the summating potential.
The third, is the neural potentials which arise from the massed action potentials in the auditory nerve. The neural potentials are produced at the onset of a stimulus. They depend on the sum of a large number of synchronous action potentials. The summed effect is thought to be realized as the action potentials emerge from the internal auditory meatus, which is transmitted via the auditory pathway to the auditory cortex and decoded by the brain as sound9.
23 3.2 MEASUREMENT OF HEARING
The initial assessment of hearing loss can be done by clinical methods. This involves the use of human voice and tuning fork.
Clinical voice tests are performed using whispered, conversational and loud voices at 60cm and 15cm respectively from the patient’s ear. The point at which the clinician’s voice is inaudible, gives a rough estimate of the severity of hearing loss.
Tuning fork tests are also used to measure hearing loss. The Rinne test is positive when air conduction is better than bone conduction and this is found in normal hearing or a sensorineural hearing loss. When bone conduction is better than air conduction, it is known as Rinne negative and it is indicative of a conductive hearing loss. It is reported that the crossover point at which the Rinne test is likely to become negative is at air-bone gap of around
18dBHL10.
The Weber test is to detect the better hearing cochlea.
A tuning fork (usually 512Hz) is activated and placed on the midline of the patient’s head. In a normally hearing patient
24 the sound is heard centrally. The sound is lateralized to the side of the better-hearing ear when there is sensorineural hearing loss. However, when there is a conductive component to the hearing impairment, the sound will appear louder on the side with the worse conductive hearing loss. Other tuning fork tests are the
Bing test; for detecting conductive hearing impairment and
Stenger test; for detecting non-organic hearing loss10.
Pure-tone audiometry (PTA) involves estimating the threshold of hearing for certain standardized stimuli, usually via air conduction and bone conduction. The standards are also specific to particular audiometric test frequencies. For air-conduction, frequencies of 0.25, 0.5,1
2,3,4,6 and 8kHz are tested. For bone-conduction frequencies of 0.5, 1,2, 3 and 4 kHz are tested11.
The acoustic environment when performing pure tone audiometry must be sufficiently quiet so as not to mask the stimuli. The procedure starts at a low stimuli intensity, which is raised gradually to determine the hearing threshold for a particular frequency. This is repeated until
25 all frequencies have been tested, initially for air conduction and then for bone conduction11.
Other types of audiometry that can be performed are speech and oto-admittance. Speech audiometry is another good method of hearing loss measurement; the main disadvantage is that the accuracy of its measurement depends on the intelligence quotient of the individual.
Hearing loss measurement using otoacoustic emission, cortical evoked response audiometry and brainstem evoked response audiometry will give more objective and accurate results. The absence of these facilities at the E.N.T. clinic of UBTH, is a limitation of this study.
Behavioural tests are used for paediatric hearing assessment. This method is based on the presentation of a loud sound and observation of the baby’s response. The possible responses include; a startle, blinking, crying or cessation of activity.
Other ways of assessing hearing in children include the use of distraction test, visual reinforcement audiometry,
26 conditioned reflex (performance testing) and speech discrimination tests12.
3.3 DIAGNOSIS OF HEARING LOSS
Pure tone audiometry, gives an objective measurement of hearing loss, when done over the speech frequencies. This information is used in determining the severity and type of hearing loss.
The clinical unit of measurement of hearing is the
“decibel hearing level” (dBHL). “Decibel” (dB) is a logarithmic ratio of sound pressure- level of reference energy quantity.
20Pa (20 x106 N/m2) (0.0002dynes/cm2). 1 bar=105Pa.
The reference point for sound pressure level was chosen to coincide approximately with the threshold of hearing of normal subjects at the 1KHZ level13,14. The zero value of the hearing level scale is not an absolute zero, but a relative one, taken as the modal value of hearing thresholds obtained from large numbers of otologically normal subjects aged between 18 and 30 years11. The hearing level scale was adjusted to take care of the variations that would
27 have occurred with frequencies, as human ear threshold of hearing varies with frequency14.
The severity scale in common use is13 Pure-tone average (dB) Severity 31-50 Mild 51-70 Moderate 71-90 Severe 91+ Profound (at 500, 1000, 2000 and 4000Hz)
Another scale is as below8 Pure-tone average (dB) Severity 27-40 Mild 41-55 Moderate 56-70 Moderately severe 71-90 Severe 91 and above Profound (average at 500, 1000, 2000Hz and 4000Hz)
Other authors3,15 consider the lower limit of normal hearing to be 20dB. Sensorineural hearing loss is said to exist when there is an average of 15dB or greater bone
28 conduction loss at 500-4000Hz in at least two frequencies16.
In conductive hearing loss; diagnosis is ordinarily made via observation of an “air-bone gap” in the hearing threshold on audiometry, showing that hearing is superior when sound is transmitted in such a way that it bypasses the middle ear ossicular chain. The air- bone gap (*ABG) should be 15 dB or above or if less than 15dB is confirmed with an equal
Rinne test or a negative one using a 512Hz tunning fork15.
Mixed hearing loss is defined to be when there is a mean air-bone gap of 15dB or greater and a mean bone conduction of 30dB HL (averages at 500, 1000, 2000Hz and 4000Hz) 11,13.
Non-organic hearing loss is the condition, where audiometric measurements give rise to doubts as to the presence of hearing loss. Patients’ communication abilities are inconsistent with the audiogram or their responses are erratic. The Stenger test is to detect patients who feign a unilateral hearing loss11.
29 3.4 TYPES OF HEARING LOSS
Clinical types of hearing loss are conductive, sensory, neural (peripheral neural and central neural), mixed, non- organic13. The term “Sensorineural” is used to indicate that there is either a lesion involving the hair-cells of the cochlea, cochlear nerve or the auditory pathway leading to hearing loss.
In conductive hearing loss, there is a lesion in the external or middle ear, which prevents effective transmission of sound through the middle ear to the inner ear. The sensory receptors and neural pathways are normal.
In mixed hearing loss, lesions causing both sensorineural and conductive hearing loss are present in the same ear of the individual.
Non-organic hearing loss is due to a psychogenic problem or deliberate feigning on the part of the individual.
In this type of hearing loss, there is no organic lesion causing the hearing loss.
Sudden hearing loss is defined as greater than
30dBHL hearing reduction, over at least three contiguous
30 frequencies, occurring over 72 hours or less. It can be conductive, sensorineural or mixed.
3.5 CAUSES OF HEARING LOSS
Common causes of sensorineural hearing loss include old age (presbyacusis), Meniere’s disease, ototoxic medications, immune disorders, viral infections and noise exposure. Twenty percent (20%) of patients that suffered from meningitis developed sensorineural hearing loss in a published study17.
Other rare causes of sensorineural hearing loss are acoustic neuroma, glomus tumour, hyperviscosity syndromes such as Von Waldenstroms macroglobulinaemia and superficial siderosis resulting from bleeding into the central nervous system. Radiation to the ear is often associated with a chronic progressive hearing loss18.
Excessive sound (noise) is also a cause of sensorineural hearing loss. It is one of the commonest causes of hearing loss in the world. It can be from military, industrial and recreational sources. Hazardous noise causes temporary threshold shift; which is a post-
31 stimulatory fatigue. It is usually a high frequency threshold shift and recovery usually occurs within the first two days.
The degree of temporary threshold shift increases progressively with the intensity and duration of the stimulus19.
Noise also causes permanent threshold shift which is a sensorineural hearing loss. This is an irreversible elevation of the auditory threshold produced by noise exposure, associated with permanent pathological changes in the cochlea19. Exposure to steady-state noise and indeed to much impulse noise is responsible for permanent threshold shift20. Exposure to noise of greater than 85 dB continuously for more than 8 hours, five days in a week can predispose to the permanent threshold shift, depending on the susceptibility of the individual19.
Another aspect of noise induced hearing loss, is that due to acute acoustic trauma. This type of noise can rupture the tympanic membrane and also cause ossicular discontinuity, in addition to damaging the inner ear hair cells. Hence both conductive and sensorineural hearing loss can result. It is commonly encountered in the military and
32 industry; rifle shots, bomb explosion, blast injuries and metal riveting21
Congenital hearing loss includes both hearing loss developed in-utero as well as genetically inherited hearing loss. Treatments are mainly aimed at preventing further damage and making do with what is left. If the loss is minor then avoidance of noise and ototoxic medications may be appropriate treatment.
Tumours such as acoustic neuromas or metastatic cancer to the ear can be a cause of hearing loss. Typically there is a combination of a hearing problem and either dizziness or imbalance. Audiometry, generally shows an asymmetrical sensorineural hearing loss.
Differential diagnosis of sudden hearing loss includes viral disease, vascular disease (1%), autoimmune phenomena, perilymph fistulae, Meniere’s disease and acoustic neuroma (about 4-6%)22.
Although some hold that sudden hearing loss is generally idiopathic, viral disease appears to be the basis for about 60% of all causes of sudden hearing loss. Although called “sudden”, it seems unlikely that hearing loss is
33 abrupt but rather it probably evolves over a few hours.
Viruses detected in a study at the Massachusetts Eye/Ear
Infirmary included influenza type B, cytomegalovirus, mumps, rubella and varicella-zoster23.
Bilateral sudden hearing loss can also be due to gastric carcinoma. In an article24, six temporal bones and a brain tissue sample removed at autopsy from four patients with bilateral sudden hearing loss related to gastric adenocarcinoma were histologically studied. The pathological findings suggested that the sudden hearing loss of these patients might have occurred via one of two different mechanisms: 1) Metastasis to the internal auditory meatus; damaging the auditory nerve or, 2) inner ear haemorrhage; damaging Corti’s organ. These two mechanisms may cause bilateral sudden deafness in patients with gastric adenocarcinoma.
Causes of conductive hearing loss include a build up of ear wax in the external auditory canal, foreign body in the ear canal, otosclerosis, tympanosclerosis, otitis externa, otitis media, otitis media with effusion, trauma to the ossicular chain, temporal bone fracture, tumours of the
34 middle ear such as glomus tumour, erosion of the ossicular chain by cholesteatoma and perforation of the tympanic membrane.
3.6 PREVALENCE OF HEARING LOSS IN NIGERIA
A study on hearing loss in uncomplicated chronic suppurative otitis media among Nigerians, at University of
Nigeria Teaching Hospital (UNTH), Enugu, concluded that mild conductive hearing loss was the predominant pattern in this category of patients25. There was no significant sensorineural hearing loss found. The weight of evidence of workers who found sensorineural hearing loss in their studies cannot however be ignored16,26-30. The mechanisms they postulated were toxins permeating through the round window, damaging the cochlear hair cells and nerve cells, and endolymphatic hydrops in the apical turns of the cochlea.
The aetiological factors in acquired sensorineural hearing loss in Jos has been studied31. Common aetiological factors in the study included typhoid fever
(15.4%), pyrexia of unknown origin (10.5%), meningitis,
35 hypertension, drug ototoxicity, noise induced hearing loss and presbyacusis. In 16.5% of cases, the cause of the hearing loss was not known. More than 40% of the causative factors were preventable , 69.5% of patients had severe to profound hearing loss and 78.9% of patients suffered bilateral hearing loss. A more detailed study of the unknown causes would have been of help to unveil the inapparent but significant unknown causes.
Another work at UNTH, Enugu, implicated febrile illness (41.3%) as the major cause of profound childhood deafness in Nigeria32. The unknown causes in this series accounted for 20.6%, while meningitis, measles, mumps and hereditary causes accounted for the rest. The possible causes of the febrile illness with special emphasis on the role of viral infections and malaria were highlighted. This study however did not implicate chloroquine ototoxicity and rubella which are other common causes of profound deafness in our environment33,34. The author attributed the inability of the mothers of the children to implicate rubella and chloroquine ototoxicity to the high level of ignorance and illiteracy in our environment.
36 A study on impedance screening for otitis media with effusion in Nigeria children, recorded a 1.2% of 814 ears studied with otitis media with effusion as a cause of conductive hearing loss35. It was concluded that the magnitude of the problem of deafness in young school age children and its aetiological factors in Nigeria and indeed tropical Africa still needs to be extensively investigated.
Audiometric screening at 500Hz, 1000Hz, 2000Hz and
4000Hz showed significant hearing loss in 17% of the 552 ears of 6 year- old school children that were tested in Benin
City36. However a study incorporating all age grades to reflect the average pattern in Benin-City has not yet been done.
3.7 HEARING LOSS IN SPECIFIC CONDITIONS
Sickle cell anaemia
Sensorineural hearing loss has been documented as a common complication of sickle cell anaemia (SCA). A prevalence of 66% of sensorineural hearing loss in SCA patients as against 47% in healthy haemoglobin AA adults was observed37. Eventhough other causes of sensorineural
37 hearing loss were not evaluated in the SCA patients, the significant number of the SCA patients with sensorineural hearing loss, compared with the healthy haemoglobin AA adults, attest to the fact that sensorineural hearing loss is closely associated with sickle cell anaemia.
Ulcerative colitis
The association of sensorineural hearing loss and ulcerative colitis is well documented38 and it is speculated that this is autoimmune in origin. Immunological tests may provide a clue as to the aetiology of suspected cases of autoimmune inner ear disease. Immediate treatment with steroids with or without immunosuppressive therapy is essential, as delay may lead to irreversible hearing loss.
Noise induced hearing loss
Noise is a common cause of hearing loss in the United
States of America (U.S.A). Twenty-five percent of U. S.A work force is regularly exposed to potentially damaging noise39. Due to the danger of occupational risk of noise induced hearing loss there are government standards regulating allowable noise exposure. People working before
38 the mid- 1960’s may have been exposed to higher levels of noise when there were no laws in the U.S.A mandating use of devices to protect hearing. Noise can also cause a reversible hearing loss called a temporary threshold shift.
This typically occurs in individuals who are exposed to gunfire, and have tinnitus after the event. Non- occupational noise is also regularly encountered during recreational activities and it is a source of premature hearing threshold reduction.
CONGENITAL
A study emphasizing the delay in detection of congenital and early onset bilateral hearing impairment in children was done with a retrospectve review of 168 consecutive children with congenital or early onset bilateral hearing impairment (>25dB, 0.5- 4KHz, in the better hearing ear)40. Only 39% of the hearing impaired children were diagnosed within the first two years of life. The age at diagnosis was related to the severity of hearing loss, with profound (>95dB) hearing losses being detected earlier than the other degrees. However 37% of children with severe to
39 profound (>70dB) hearing loss were still not diagnosed until after two years of age. Children with severe to profound hearing loss and with known risk factors were diagnosed earlier than children with the same hearing status but with no known risk factors. It was concluded that the behavioural hearing screening tests used in our well-baby clinics are insufficient. Therefore more reliable methods such as evoked otoacoustic emissions, should be used for universal hearing screening of infants and young children in spite of the great cost.
A paper was published on hearing loss and pigmentary disturbances in Waardenburg Syndrome (WS) with reference to WS type II41. Thirty families in which there were
149 individuals affected by the Waardenburg Syndrome were investigated for penetrance of hearing loss and pigmentary abnormalities. A bilateral symmetrical sensorineural hearing loss was found to be the commonest type of hearing loss. The most frequent degree of hearing loss category was a hearing loss of >100dBHL with no difference between syndrome types. They concluded that
40 the frequency of pigmentation disorders was not greater when the hearing loss was more severe in either type.
INTRA-CRANIAL TUMOURS
Merino Galvez E et al reported the case of a female patient who presented with sudden deafness as the first symptom of a cerebellar tumour. The tumour was not localized strictly in the cerebellopontine angle and did not show direct compression on the extrabulbar portion of the
V111th cranial nerve42. Surgical intervention restored the hearing and caused the symptoms to disappear.
Sensorineural hearing loss of sudden onset may be the presenting symptom in up to 14% of patients with acoustic neuroma43. They presented the first reported case of sudden hearing loss in an only hearing ear with recovery to normal levels after steroid therapy on four separate occasions.
Evaluation revealed a 1.5cm acoustic neuroma. After middle cranial fossa decompression, a fifth episode with recovery after steroid use was documented.
41
PRESBYACUSIS
Presbyacusis is defined as hearing loss associated with degenerative changes of aging. Presbyacusis is a common type of hearing loss seen at the ENT clinic of
UBTH, Benin City. This type of hearing loss is typically gradual, bilateral and characterized by difficulty hearing sounds of high frequencies44.
There are four types of presbyacusis; sensory presbyacusis is caused by loss of sensory elements in the basal end (high frequency end) of the cochlea with preservation of neurons. These patients have symmetrical, high frequency sensorineural hearing loss. The pathology in sensory presbyacusis is the loss of hair cells in the cochlea.
Neural presbyacusis is caused by loss of cochlea neurons. These patients have poorer discrimination than patients with sensory presbyacusis.
Strial presbyacusis is caused by loss of the stria vascularis. Patients have a flat or slightly sloping hearing loss with good speech discrimination.
42 A fourth type, is cochlear conductive presbyacusis.
This is a sensorineural hearing loss caused by thickening of the basilar membrane, caused by deposition of basophilic substance. This diagnosis is made at autopsy.
Mixed presbyacusis with combination of two or more of the above types of presbyacusis is also possible.
COLLAPSE OF THE EXTERNAL AUDITORY MEATUS
Collapse of the external auditory meatus during audiometry can lead to spuriously increased hearing thresholds being obtained particularly at high frequencies leading to a misdiagnosis45. This may simulate conditions such as noise-induced hearing loss, presbyacusis and retrocochlear pathology. Consequently, inappropriate investigations and management may be undertaken. The need to initially identify the true nature of patients’ hearing losses were highlighted in the article.
TRAUMA
A prospective study of hearing loss in 120 cases with non-explosive blast injury of the ear, gathered over a six – year period, showed that 27.5% had normal hearing, 47.5% conductive hearing loss, 24.2% mixed hearing loss and
43 0.8% had pure sensorineural loss. The severity of conductive hearing loss correlated with the size of the eardrum perforation. Of all locations, perforations involving the posterior inferior quadrant of the eardrum were associated with the largest air-bone gap. Audiometric assessment revealed that none of the patients suffered ossicular chain damage46.
Healing of the tympanic membrane perforation was always accompanied by closure of the air-bone gap in the audiogram, while the recovery of the sensorineural hearing loss was less favourable. This study did not however indicate whether there was associated temporal bone fracture and if there was, whether it was longitudinal or transverse. In that way the pattern of hearing loss in this study will be easy to reconcile with the previously known pattern47.
NASOPHARYNGEAL TUMOUR
The pattern of hearing disability before and after radiotherapy for nasopharyngeal carcinoma has been studied48. Twenty-three males and ten females completed
44 the study. Middle ear effusions resulted in 39.3% of patients and 33.3% of patients had hearing disability pre- and post-irradiation respectively. No patient had hearing disability as a result of a sensorineural hearing loss. It was recommended that future reporting of post-irradiation hearing changes in patients with nasopharyngeal carcinoma, as in middle ear surgery, be considered from a disability–orientated approach. The conductive hearing loss in nasopharyngeal carcinoma, has been confirmed by other workers49,50.
NEUROSURGICAL PROCEDURES
The effect of neuro–surgery on hearing has been investigated51. In a neurosurgical group of thirty patients who underwent surgery, a significant loss of hearing was observed in the immediate post-operative period, with recovery over one week. It was suggested that following neurosurgery, the mechanism of hearing loss results directly from a decrease in pressure and/or volume of the cerebrospinal fluid, which is reflected within the
45 perilymphatic fluid, comparable to a transitory endolymphatic hydrops.
DISTAL RENAL TUBULAR ACIDOSIS
Hearing impairment has been reported in association with distal renal tubular acidosis among Saudi Arabia chidren52. In a study in which five patients were diagnosed as having primary distal renal tubular acidosis and rickets, four were found to have severe sensorineural hearing loss of over 80dB; two of which are brothers. Two patients were diagnosed as having secondary distal renal acidosis due to a genetic disorder called osteopetrosis. They are brothers and their audiograms showed a mild conductive hearing loss of an average of 35dB bilaterally. The tribal tradition in
Saudi Arabia fosters consanguineous marriages for cultural and social reasons and pre-arranged marriages are still seen.
OTOTOXICITY
The place of drugs as an aetiological factor for hearing loss has been extensively studied. Ogisi F O studying
46 chloramphenicol induced hearing loss, out of 49 causes of drug ototoxicity showed 43% to be due to the use of chloramphenicol53. The hearing impairment was found to be bilateral and severe to profound at onset in 66% of cases, with no improvement noticed even after cessation of drug use. The need to prevent this grave iatrogenic tragedy by limiting the use of the drug was stressed.
OTHERS
In an epidemiological study on relevant demographic factors and hearing impairment in 6421 Saudi Arabia children <12 years, it was noted that of 1256 considered at risk for hearing impairment, 55% were males and 45% were females54. The reasons were identified as family history, perinatal infections, anatomical malformation of the ear, head and neck, birthweight <2500g, hyperbilirubinaemia and bacterial meningitis. Eight hundred and seventy-nine children received the auditory brainstem evoked response and 377 received the pure tone auditory test. There were
494 children with hearing impairment. One hundred and sixty eight children (2.6%) had sensorineural hearing loss,
47 295 (5.2%) had conductive hearing loss. There were 8.6% of boys and 6.5% of girls who were classified as hearing impaired, ranging from 2-7 years of age. The hereditary cause of deafness (1.7%) was found to be higher than the
0.6% incidence previously reported.
Whereas, a vast number of aetiological factors for the different types of hearing loss has been implicated, the pattern seen in UBTH, Benin- City needs to be conclusively studied.
48 CHAPTER FOUR
PATIENTS AND METHOD
4.1 PATIENTS
All patients with a complaint of hearing impairment presenting to the E.N.T clinic of UBTH, Benin-City, between
September 2004 and August 2005, were evaluated to be enrolled for the study.
The criteria used for determining hearing loss in this study were:
1. Those with hearing threshold greater than 30dB in at
least two of the frequencies (500Hz, 1kHz, 2kHz, 4kHz)
for either air or bone conduction or for both.
2. Those that had an air-bone gap that was above 15dB.
The patients with hearing loss, were then enrolled into the study, based on the following inclusion criteria:
1. Those who gave informed consent for this study.
2. Those that were up to and above ten years of age.
The following exclusion criteria were looked for and patients with one or more of them were excluded from the study. The exclusion criteria were:
49 (1) Those who refused to give informed consent for this study.
(2) Children who were less than ten years of age, to avoid inaccuracies in audiological testing.
(3) Patients who were very ill who might not have responded accurately to audiological testing.
(4) Suspected psychiatric patients who would have given inaccurate responses.
(5) Those who did not perform pure tone audiometry for any constraint.
4.2 STUDY METHOD:
The study is a prospective study of patients presenting with hearing loss at the UBTH, Benin City. Approval for the study was granted by the ethical review committee of UBTH,
Benin- City.
On attending the clinic, the patient is clerked by a doctor who then sends the patient to this author, if a diagnosis of hearing loss is made. However, most patients who were referred to the E.N.T. Clinic with complaint of hearing loss during this study period, were first seen by the
50 author. The patient is then thoroughly evaluated to ascertain their eligibility for inclusion in the study, according to the criteria stated above. If eligible, the study is explained to the patient in a language he or she understands and informed written consent is obtained
(Appendix I).
A general medical history was taken and a general examination was carried out with emphasis on the otorhinolaryngological aspects. The findings were recorded in the adopted format (Appendix II).
Audiological measurements were done by pure tone audiometry in a double-walled, sound-proof cabin using a duly calibrated ( B and K artificial mastoid Type-4930) diagnostic audiometer of Amplaid 132 model, manufactured by the Biomedical Division of Amplifon S.p.A, Milano, Italy.
It has well-fitting TDH49 earphones and RADIOEAR B-7 bone conductor. It was designed to meet all applicable specifications of ANSI S.3-6, 1969 and ISO 389 standards for medical equipment. PTA was done by employing standard procedures 55,56,57.
51 All the patients were tested by the same trained and experienced audiology technician of the ENT clinic, UBTH,
Benin City, who knew the details of the study.
Pure tone audiometry (PTA) threshold for each ear was determined at 250Hz, 500Hz, 1KHz, 2kHz, 4KHz and 8KHz by air conduction. Also bone conduction measurements were obtained at 500Hz, 1KHz, 2KHz and 4KHz with the appropriate bone vitrator placed on the respective mastoid bone to confirm the presence of hearing loss.
Other tests and investigations were done as deemed necessary for individual cases, to ascertain the aetiological factor responsible for the hearing loss. Tests like Xray of the mastoid temporal bone, Xray of the paranasal sinuses, blood film for malaria parasite, Widal haemagglutination test, X-ray and CT scan of the post nasal space, ear swab for microscopy, culture and sensitivity, biopsy and histology of ear tumour were sporadically done depending on the particular case, to ascertain the proper diagnosis.
Tympanometry which was initially included in the study proposal was later removed from the study after due consultation with and approval by the supervisors of this
52 project, because only an insignificant percentage of the patients with hearing loss were able to afford the exhorbitant cost of the procedure. Later, the only available tympanometer in the ENT clinic of UBTH, Benin City, got bad and was not repaired throughout the remaining period of the study .
Patients with impacted cerumen auris had PTA done before the cerumen was removed. Although these patients were told to repeat their PTA after the cerumen was removed, most of them declined, as they claimed that their hearing was much better after the cerumen was removed.
Patients with active chronic suppurative otitis media had aural toileting done before PTA was carried out, to avoid contamination of the only available pair of ear phones in the ENT clinic of UBTH, Benin City and subsequent transmission of infection.
4.3 DATA ANALYSIS
The hearing threshold of each hearing impaired ear was analyzed separately by finding the average of the air conduction at 500Hz, 1KHz, 2kHz and 4KHz respectively.
The severity of the hearing loss was then assessed with the
53 air-conduction average according to the severity scale in page 1513. The hearing impaired ears were further sub- grouped and analyzed according to the aetiological factors responsible for the hearing loss by taking the mean of the air conduction thresholds of all the ears with that aetiological factor. Data analysis was done by a statistician using the Excel and SPSS computer software, presenting the results in tables, histogram and audiographic formats.
The air-bone gap for a particular ear was calculated by noting the difference between the pure tone threshold for air and bone conduction of that ear at 500Hz, 1KHz, 2KHz and
4KHz. The air-bone gap for a particular aetiological factor was calculated by taking the average of the air-bone gap of all the ears with the particular aetiological factor
. Ears with average air-bone gap of 15dB and air conduction <30dB were regarded as having conductive hearing loss 55,56. Ears with air-bone <15dB and air condition >30dB were regarded as having sensorineural hearing loss. Ears with air bone gap >15dB and air conduction >30dB were regarded as having mixed hearing
54 loss. Ears with air-bone gap <15dB and air conduction
<30dB were regarded as having normal hearing.
The type of hearing loss for a particular aetiological factor, was determined by calculating the average air-bone gap and air conduction threshold of all the ears with that aetiological factor and comparing the result with the format given above.
55 CHAPTER FIVE
RESULTS
(1) There were 281 patients who presented with hearing loss during the period of the study at the ENT clinic. Only 257 patients met the criteria for inclusion in the study.
Twenty four patients were excluded from the study because they did not undergo pure tone audiometry due to different constraints.
Eighty two patients had hearing loss in only one ear, while 175 patients had both ears involved, giving a total of
432 ears with hearing loss that were studied. During this study period a total of 980 new patients were seen in the
ENT clinic of UBTH, Benin City.
(2) Age distribution
Age ranged from 10.0years to 100.0years, with a mean age of 40.5 years 19.4SD (Table i and Figure1).
56 Table i: Age group distribution of patients with hearing loss (n=257) Serial Age group Number of Percentage number (in years) patients (%) 1 10-19 30 11.7 2 20-29 69 26.8 3 30-39 43 16.7 4 40-49 24 9.3 5 50-59 37 14.4 6 60-69 29 11.3 7 70-79 23 8.9 8 80 and > 2 0.8 Total 257 100.0
Mean age 40 5 years 19.4SD
57 Figure I: Histogram showing the age groups of patients with
hearing loss.
AGECODE 80
ent) ent) 60 Mean =40..5 years SD 19.4 40 N=257
(No of pati (No
20 Std. Dev = 1.92 Mean = 3.6 N = 257.00
Frequency 0 1.0 2.0 3.0 4.0 5.0 6.0 7.0 8.0 AGECODE 10-19 20-29 30-39 40-49 50-59 60-69 70-79 80 and above
AGE GROUP
(in years)
(3) Sex Distribution
There were 139 males (54.1%) and 118 females (45.9%)
giving a male to female ratio of 1.2:1
4) Pure-tone average at frequencies of 500Hz, 1000Hz, 2000Hz and 4000Hz for the patients with hearing loss ranged between 30.4dB and 100dB with a mean pure tone average of 59.3dB.
AETIOLOGICAL FACTORS FOR HEARING LOSS There were a total of 22 different aetiological factors implicated in the hearing impairment of the 432 ears studied. Some ears had more than one aetiological factor (Table ii).
58 Table ii: Frequency distribution of 22 aetiological factors for hearing loss.
Aetiological factors Number of times Percentage Serial implicated (%) No 1 Ototoxicity 74 15.7 2 CSOM 70 14.9 3 Unknown causes 50 10.6 4 Presbyacusis 62 13.2 5 Wax impaction 42 8.9 6 Rhinosinusitis 35 7.4 7 Trauma to ear 30 6.4 8 Febrile illness 32 6.8 9 Noise Induced 14 3.0 10 Otitis externa 11 2.3 11 Nasopharyngeal 10 2.1 carcinoma 12 Hereditary 9 1.9 13 ASOM 8 1.7 14 OME 5 1.1 15 Neonatal Jaundice 4 0.8 16 Meniere’s disease 4 0.8 17 Septicaemia 3 0.6 18 Miscellaneous 8 1.7 Insufflation of discharge 2 into the eustachian tube from the nasopharynx Guillain Barre syndrome 2 Convulsion 2 Tumour of the 1 ear/external auditory canal Redundant canal wall 1 Total 471 100.0
59 Table iii: Types Of hearing loss Type Number of ears Percentage (%) Conductive 155 35.9 SNHL 147 34.0 Mixed 130 30.1 Total 432 100.0
Table iv: Severity of hearing loss Severity Pure tone Number of ears Percentage audiogram hearing (%) threshold Mild 31-50dB 192 44.5 Moderate 51-70dB 103 23.8 Severe 71-90dB 71 16.4 Profound 91dB and above 66 15.3 Total 432 100.0 Table Va: Average hearing threshold of patients who had drug ototoxicity (Right ears n=37)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 37 78.6486 21.20170 PTARAC 50 37 80.0000 21.95323 PTARAC1K 37 78.6486 25.37630 PTARAC2K 37 77.9730 24.50792 PTARAC4K 37 79.8649 25.67117 PTARAC8K 37 83.6486 23.61875 PTARBC50 37 56.0811 15.94849 PTARBC1K 37 59.1892 18.00901 PTARBC2K 36 62.0833 14.60797 PTARBC4K 36 59.1667 15.92393 Valid N (listwise) 36
NB
60 PTARAC25 is PTA of right ear by air conduction at 250Hz PTARAC50 is PTA of right ear by air conduction at 500Hz PTARAC1K is PTA of right ear by air conduction at 1KHz PTARAC2K is PTA of right ear by air conduction at 2KHz PTARAC4K is PTA of right ear by air conduction at 4KHz PTARAC8K is PTA of right ear by air conduction at 8KHz PTARBC50K is PTA of right ear by bone conduction at 500Hz PTARBC1K is PTA of right ear by bone conduction at 1KHz PTARBC2K is PTA of right ear by bone conduction at 2KHz PTARBC4K is PTA of right ear by bone conduction at 4KHz
Audiogram Va: Average audiogram of patients who had drug ototoxicity (Right ears n=37).
Pure tone average audiogram of patients with ototoxicity(Right Ear)
0 10 20 30 40 Air conduction 50 Bone 60 conduction 70
HearingThreshold(dB) 80 90 100 .25 .5 1 2 4 8 Frequency(kHz)
61
Table Vb: Average hearing threshold of patients who had drug ototoxicity (left ears n=37).
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 37 78.2432 22.85875 PTALAC50 37 77.9730 24.36583 PTALAC1K 37 79.4595 24.51711 PTALAC2K 37 77.0270 26.36442 PTALAC4K 37 82.4324 22.96197 PTALAC8K 37 88.1081 21.09342 PTALBC50 37 54.5946 15.24697 PTALBC1K 37 56.7568 17.80357 PTALBC2K 37 60.5405 14.98999 PTALBC4K 37 60.8108 15.20752 Valid N (listwise) 37
NB
PTALAC25 is PTA of left ear by air conduction at 250Hz PTALAC50 is PTA of left ear by air conduction at 500Hz PTALAC1K is PTA of left ear by air conduction at 1KHz PTALAC2K is PTA of left ear by air conduction at 2KHz PTALAC4K is PTA of left ear by air conduction at 4KHz PTALAC8K is PTA of left ear by air conduction at 8KHz PTALBC50 is PTA of left ear by bone conduction at 500Hz PTALBC1K is PTA of left ear by bone conduction at 1KHz PTALBC2K is PTA of left ear by bone conduction at 2KHz PTALBC4K is PTA of left ear by bone conduction at 4KHz
62
Audiogram Vb: Average audiogram of patients who had drug ototoxicity (left ears n=37).
Pure tone average audiogram of patients with ototoxicity(left ear)
0 10 20
30
40 50 60 70 80 Hearingthresholds(dB) 90 100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
Table Vc: Frequency distribution of drugs that caused ototoxicity (n=74)
Drug Number of ears Percentage % Unknown 17 23.0 Amantadine 2 2.7 Maloxine 2 2.7 Fulcin 2 2.7 Crystapenicillin 2 2.7 Chloroquine 8 10.8 Ciprotab 2 2.7 Chloramphenicol 22 29.7
63 Unspecified antimalarial 1. 1.4 Quinine 10 13.5 Frusemide 2 2.7 Diatebem 2 2.7 Rifampicin 2 2.7 Total 74 100
Table via: Average hearing threshold of patients who had CSOM (Right ears n=33)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 33 64.2424 18.79666 PTARAC 50 33 65.0000 20.53960 PTARAC1K 33 62.8788 19.24474 PTARAC2K 33 58.1818 20.53268 PTARAC4K 33 64.2424 19.96564 PTARAC8K 33 68.0303 22.91081 PTARBC50 33 30.4545 13.19112 PTARBC1K 33 32.5758 14.31352 PTARBC2K 33 36.6667 15.89353 PTARBC4K 33 35.4545 15.42946 Valid N (listwise) 33
64
Audiogram via: Average audiogram of patients who had CSOM (right ears n=33).
Pure tone average audiogram of patients with chronic suppurative otitis media(right ear)
0 10 20 30 40 50
60 70 80
thresholds(dB) Hearing 90 100 .25 .5 1 2 4 8
Frequency(kHz)
Air conduction Bone conduction
Table vib: Average hearing threshold of patients who had CSOM (left ears n=36)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 36 61.6667 16.03567 PTALAC50 36 61.1111 18.32684 PTALAC1K 36 60.5556 19.63153 PTALAC2K 36 57.5000 21.36419 PTALAC4K 36 63.6111 21.89622 PTALAC8K 36 70.6944 22.10859 PTALBC50 36 31.9444 15.08442 PTALBC1K 36 32.6389 15.69741 PTALBC2K 36 36.3889 15.97369 PTALBC4K 36 37.0833 17.29471 Valid N (listwise) 36
65 Audiogram vib: Average audiogram of patients who had CSOM (left ears n=36).
Pure tone average audiogram of patients with chronic suppurative otitis media(left ear)
0
10 20
30
40
50
60 70
Hearingthresholds(dB) 80 90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
66 Table viia: Average hearing threshold of patients who had unknown cause of hearing loss (Right ears n=27)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 27 50.0000 18.70829 PTARAC 50 27 48.7037 21.77651 PTARAC1K 27 48.3333 23.77782 PTARAC2K 27 45.5556 23.71032 PTARAC4K 27 52.2222 25.99310 PTARAC8K 27 54.4444 28.02243 PTARBC50 27 37.2222 13.89060 PTARBC1K 27 38.1481 17.43935 PTARBC2K 27 39.4444 17.50458 PTARBC4K 27 40.0000 16.98416 Valid N (listwise) 27
Audiogram viia: Average audiogram of patients who had unknown cause of hearing loss (Right ears n=27).
Pure tone average audiogram of patients with hearing loss of unknown aetiology(right ear)
0 10
20 30
40 50
60 70
Hearingthresholds(dB) 80 90
100 .25 .5 1 2 4 8 Frequency(dB) 67 Air conduction Bone conduction Table viib: Average hearing threshold of patients who had unknown cause of hearing loss (left ears n=23)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 23 55.8696 21.82847 PTALAC50 23 54.5652 25.44660 PTALAC1K 23 56.9565 22.44889 PTALAC2K 23 57.3913 26.32272 PTALAC4K 23 57.1739 26.19100 PTALAC8K 23 61.9565 26.18722 PTALBC50 23 41.9565 16.70187 PTALBC1K 23 42.8261 18.20502 PTALBC2K 23 45.8696 18.19417 PTALBC4K 23 42.3913 17.89296 Valid N (listwise) 23
Audiogram viib: Average audiogram of patients who had unknown cause of hearing loss (left ears n=23).
Pure tone average audiogram of patients with hearing loss of unkown aetiology(left ear)
0
10 20
30 40
50
60
70 Hearing thresholds(dB) 80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction 68 Table viiia: Average hearing threshold of patients who had presbyacusis(Right ears n=31)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 31 54.1935 21.05931 PTARAC 50 31 54.1935 24.05192 PTARAC1K 31 55.9677 24.98064 PTARAC2K 31 56.2903 23.97804 PTARAC4K 31 67.2581 24.89440 PTARAC8K 31 76.4516 20.86439 PTARBC50 31 43.5484 16.69299 PTARBC1K 31 45.0000 17.74824 PTARBC2K 31 53.2258 15.30514 PTARBC4K 31 49.5161 16.09114 Valid N (listwise) 31
Audiogram viiia: Average audiogram of patients who had presbyacusis (Right ears n=31).
Pure tone average audiogram of patients with presbyacusis(right ear)
0
10 20
30 40
50 60
70
Hearing thresholds(dB) 80
90 100 .25 .5 1 2 4 8 Frequency(kHz) 69 Air conduction Bone conduction Table viiib: Average hearing threshold of patients who had presbyacusis(left ears n=31)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 31 54.3548 20.72607 PTALAC50 31 53.8710 22.01173 PTALAC1K 31 54.6774 22.20869 PTALAC2K 31 57.4194 20.77141 PTALAC4K 31 71.1290 20.15398 PTALAC8K 30 80.5000 20.01508 PTALBC50 31 42.9032 16.62198 PTALBC1K 31 42.9032 17.01833 PTALBC2K 31 51.2903 16.01914 PTALBC4K 31 52.5806 16.32335 Valid N (listwise) 30
Audiogram viiib: Average audiogram of patients who had presbyacusis (Left ears n=31).
Pure tone average audiogram of patients with presbyacusis(left ear)
0
10
20 30
40
50
60
70 Hearingthresholds(dB) 80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction70 Bone conduction Table ixa: Average hearing threshold of patients who had wax impaction (Right ears n=27)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 27 44.6296 19.36124 PTARAC 50 27 43.1481 20.57576 PTARAC1K 27 44.6296 17.20498 PTARAC2K 27 47.0370 20.01246 PTARAC4K 27 50.9259 21.16951 PTARAC8K 27 59.6296 20.98195 PTARBC50 27 27.9630 9.32936 PTARBC1K 27 29.0741 11.01023 PTARBC2K 27 32.5926 12.27649 PTARBC4K 27 31.4815 13.28785 Valid N (listwise) 27
Audiogram ixa: Average audiogram of patients who had wax impaction (Right ears n=27).
Pure tone average audiogram of patients with wax
impaction(right ear)
0
10
20
30
40
50
60
Hearing thresholds(dB) 70
80
90
100 .25 .5 1 2 4 8 Frequency(kHz) 71 Air conduction Bone conduction Table ixb: Average hearing threshold of patients who had wax impaction (Left ears n=14)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 14 45.3571 13.36820 PTALAC50 14 43.5714 13.36306 PTALAC1K 14 45.3571 14.06910 PTALAC2K 14 49.2857 16.15515 PTALAC4K 14 60.7143 20.08225 PTALAC8K 14 68.5714 22.31148 PTALBC50 14 27.1429 6.71230 PTALBC1K 14 26.0714 2.89467 PTALBC2K 14 32.1429 10.32441 PTALBC4K 14 35.0000 14.67599 Valid N (listwise) 14
Audiogram ixb: Average audiogram of patients who had wax impaction (Left ears n=14).
Pure tone average audiogram of patients with wax impaction(left ear)
0
10
20
30
40
50
60
Hearing thresholds(dB) 70
80
90
100 .25 .5 1 2 4 8 Frequency(kHz) 72 Air conduction Bone conduction Table xa: Average hearing threshold of patients who had rhinosinusitis ( Right ears n=20)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 20 50.2500 18.17133 PTARAC 50 20 47.7500 19.36322 PTARAC1K 20 50.0000 16.85854 PTARAC2K 20 45.5000 16.53545 PTARAC4K 20 51.2500 20.18826 PTARAC8K 19 56.3158 23.79555 PTARBC50 20 30.0000 12.97771 PTARBC1K 20 29.5000 10.74832 PTARBC2K 20 35.5000 12.86570 PTARBC4K 20 31.7500 11.95111 Valid N (listwise) 19
Audiogram xa: Average audiogram of patients who had rhinosinusitis (Right ears n=20).
Pure tone average audiogram of patients with chronic rhinosinusitis(right ear)
0
10
20
30
40
50
60
Hearing thresholds(dB) 70
80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
73
Table xb: Average hearing threshold of patients who had rhinosinusitis ( Left ears n=14)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 14 54.2857 17.85165 PTALAC50 14 46.7857 20.34388 PTALAC1K 14 49.6429 21.25525 PTALAC2K 14 48.5714 20.32700 PTALAC4K 14 50.7143 22.00150 PTALAC8K 14 52.1429 23.18108 PTALBC50 14 35.0000 17.75907 PTALBC1K 14 31.4286 15.37087 PTALBC2K 14 34.2857 15.54858 PTALBC4K 14 31.7857 13.53161 Valid N (listwise) 14
Audiogram xb: Average audiogram of patients who had rhinosinusitis (Left ears n=14).
Pure tone average audiogram of patients with chronic rhinosinusitis(left ear)
0
10
20
30
40
50
60
70 Hearing thresholds(dB) 80 90 100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction74 Bone conduction
Table xia: Frequency distribution of causes of trauma to the ear (n =30) Cause Number of ears Percentage (%) Slap 21 70.0 RTA 8 26.7 Fire burn to ear canal 1 3.3 Total 30 100.0
Table xib: Average hearing threshold of patients who had trauma to the ear ( Right ears n=12)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 12 50.4167 19.59340 PTARAC 50 12 47.0833 24.35144 PTARAC1K 12 51.2500 24.59906 PTARAC2K 12 51.6667 24.15229 PTARAC4K 12 65.8333 22.94592 PTARAC8K 12 65.4167 23.78486 PTARBC50 12 31.2500 14.16221 PTARBC1K 12 34.1667 17.29862 PTARBC2K 12 37.5000 19.82881 PTARBC4K 12 40.0000 20.56033 Valid N (listwise) 12
75 Audiogram xib: Average audiogram of patients who had trauma to the ear (Right ears n=12).
Pure tone average audiogram in patients with trauma to the ear(right ear)
0
10
20
30
40
50 60
70 thresholds(dB) Hearing 80
90
100 .25 .5 1 2 4 8
Frequency(kHz)
Air conduction Bone conduction
76 Table xic: Average hearing threshold of patients who had trauma to the ear ( Left ears n=17)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 17 46.1765 20.04132 PTALAC50 17 43.8235 23.88314 PTALAC1K 17 47.3529 24.18145 PTALAC2K 17 49.7059 24.46110 PTALAC4K 17 58.2353 25.30694 PTALAC8K 17 67.3529 28.23549 PTALBC50 17 31.1765 13.86649 PTALBC1K 17 31.4706 13.78005 PTALBC2K 17 36.7647 17.22473 PTALBC4K 17 38.8235 18.50079 Valid N (listwise) 17
Audiogram xic: Average audiogram of patients who had trauma to the ear (Left ears n=17).
Pure tone average audiogram of patients with trauma to the ear(left ear)
0
10
20 30
40
50
60 70
Hearing thresholds(dB) Hearing
80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
77 Table xiia: Frequency distribution of causes of febrile illness
(n=32)
Cause Number of ears Percentage (%)
Meningitis 10 31.2
Measles 8 25.0
German measles 2 6.3
Lassa fever 2 6.3
Mumps 1 3.1
Unspecified febrile illness 9 28.1
Total 32 100.0
Table xiib: Average hearing threshold of patients who had febrile illness (Right ears n=16)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 16 89.0625 12.67790 PTARAC 50 16 91.8750 13.40087 PTARAC1K 16 92.5000 13.16561 PTARAC2K 16 89.6875 20.28700 PTARAC4K 16 91.5625 21.19109 PTARAC8K 16 90.6250 22.12653 PTARBC50 16 63.1250 7.93200 PTARBC1K 16 65.9375 11.72160 PTARBC2K 15 66.6667 7.48013 PTARBC4K 15 63.6667 13.94718 Valid N (listwise) 15
78 Audiogram xiib: Average audiogram of patients who had febrile illness (Right ears n=16).
Pure tone average audiogram of patients with febrile illness(right ear)
0
10
20
30
40
50
60
Hearingthresholds(dB) 70
80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
79 Table xiic: Average hearing threshold of patients who had febrile illness (Left ears n=16)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 16 88.4375 13.99032 PTALAC50 16 86.2500 18.30301 PTALAC1K 16 84.0625 21.92554 PTALAC2K 16 79.6875 27.77701 PTALAC4K 16 82.8125 28.57556 PTALAC8K 16 87.8125 26.45554 PTALBC50 16 55.6250 14.12740 PTALBC1K 16 57.8125 16.82941 PTALBC2K 16 61.2500 16.17611 PTALBC4K 16 60.6250 17.59498 Valid N (listwise) 16
Audiogram xiic: Average audiogram of patients who had febrile illness (Left ears n=16).
Pure tone average audiogram of patients with febrile illness(left ear)
0
10
20 30
40
50
60
70
Hearing thresholds(dB) Hearing
80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction 80 Table xiiia: Average hearing threshold of patients who had noise-induced hearing loss (Right ears n=8)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 8 55.6250 12.93873 PTARAC 50 8 55.0000 13.62770 PTARAC1K 8 56.2500 15.97990 PTARAC2K 8 50.6250 16.35270 PTARAC4K 8 62.5000 13.09307 PTARAC8K 8 62.5000 21.54729 PTARBC50 8 43.7500 14.33029 PTARBC1K 8 43.7500 10.60660 PTARBC2K 8 45.6250 12.37437 PTARBC4K 8 48.7500 15.75482 Valid N (listwise) 8
Audiogram xiiia: Average audiogram of patients who had noise- induced hearing loss (Right ears n=8).
Pure tone average audiogram in patients with noise induced hearing loss(right ear)
0
10
20
30
40
50
60
70 thresholds(dB) Hearing 80
90
100 .25 .5 1 2 4 8 Frequency(kHz) 81 Air conduction Bone conduction Table xiiib: Average hearing threshold of patients who had noise-induced hearing loss (Left ears n=6)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 6 50.0000 11.83216 PTALAC50 6 47.5000 18.64135 PTALAC1K 6 45.0000 19.74842 PTALAC2K 6 44.1667 18.81932 PTALAC4K 6 53.3333 22.73030 PTALAC8K 6 62.5000 22.74863 PTALBC50 6 45.8333 14.97220 PTALBC1K 6 40.0000 14.83240 PTALBC2K 6 43.3333 15.70563 PTALBC4K 6 50.8333 15.30251 Valid N (listwise) 6
Audiogram xiiib: Average audiogram of patients who had noise- induced hearing loss (Left ears n=6).
Pure tone average audiogram of patients with noise induced hearing loss(left ear)
0
10
20
30
40 Air conduction 50 Bone conduction 60
70
Hearing thresholds(dB) Hearing
80
90
100 82 .25 .5 1 2 4 8 Frequency(kHz) Table xiva: Frequency distribution of causes of otitis externa (n= 11) Causes Number of ears Percentage (%) Bacterial infection 4 36.4 Chemical otitis external 1 9.1 Otomycocsis 6 54.5 Total 11 100.0 Table xivb: Average hearing threshold of patients who had otitis externa (Right ears n=6)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 6 35.0000 15.81139 PTARAC 50 6 35.8333 14.97220 PTARAC1K 6 46.6667 14.71960 PTARAC2K 6 44.1667 26.34704 PTARAC4K 6 48.3333 26.20433 PTARAC8K 6 55.0000 30.33150 PTARBC50 6 31.6667 16.32993 PTARBC1K 6 32.5000 18.37117 PTARBC2K 6 34.1667 17.72475 PTARBC4K 6 32.5000 18.37117 Valid N (listwise) 6
83 Audiogram xivb: Average audiogram of patients who had otitis externa (Right ears n=6).
Pure tone average audiogram of patients with
otitis externa(right ear)
0 10
20
30
40
50
60
70 thresholds(dB) Hearing 80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
84 Table xivc: Average hearing threshold of patients who had otitis externa (Left ears n=5)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 5 47.0000 19.55761 PTALAC50 5 49.0000 28.80972 PTALAC1K 5 52.0000 37.34970 PTALAC2K 5 53.0000 34.74910 PTALAC4K 5 64.0000 23.82226 PTALAC8K 5 73.0000 17.53568 PTALBC50 5 40.0000 21.21320 PTALBC1K 5 43.0000 24.64752 PTALBC2K 5 43.0000 24.64752 PTALBC4K 5 43.0000 24.64752 Valid N (listwise) 5
Audiogram xivc: Average audiogram of patients who had otitis externa (Left ears n=5).
Pure tone average audiogram of patients with otitis externa(left ear)
0 10 20
30
40
50
60
70
Hearing thresholds(dB) Hearing
80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction 85 Table xva: Average hearing threshold of patients who had nasopharyngeal carcinoma (Right ears n=5)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 5 46.0000 8.94427 PTARAC 50 5 47.0000 13.96424 PTARAC1K 5 42.0000 9.08295 PTARAC2K 5 41.0000 10.83974 PTARAC4K 5 49.0000 16.35543 PTARAC8K 5 59.0000 21.33073 PTARBC50 5 28.0000 6.70820 PTARBC1K 5 26.0000 2.23607 PTARBC2K 5 28.0000 4.47214 PTARBC4K 5 26.0000 2.23607 Valid N (listwise) 5
Audiogram xva: Average audiogram of patients who had nasopharyngeal carcinoma (Right ears n=5).
Pure tone average audiogram of patients with nasopharyngeal carcinoma(right ear)
0
10
20
30
40
50 60
70 thresholds(dB) Hearing 80
90
100 86 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction Table xvb: Average hearing threshold of patients who had nasopharyngeal carcinoma (Left ears n=5)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 5 46.0000 9.61769 PTALAC50 5 44.0000 8.21584 PTALAC1K 5 49.0000 6.51920 PTALAC2K 5 50.0000 20.31010 PTALAC4K 5 71.0000 8.21584 PTALAC8K 5 64.0000 12.44990 PTALBC50 5 25.0000 .00000 PTALBC1K 5 25.0000 .00000 PTALBC2K 5 25.0000 .00000 PTALBC4K 5 27.0000 4.47214 Valid N (listwise) 5
Audiogram xvb: Average audiogram of patients who had nasopharyngeal carcinoma (Left ears n=5).
Pure tone average audiogram of patients with nasopharyngeal carcinoma(left ear)
0
10
20
30
40
50
60
70 thresholds(dB) Hearing 80
90
100 87 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
Table xvia. Frequency distribution of hereditary hearing loss. (n=9)
Relation Number of ears Percentage %
Maternal uncle 4 44.5
Paternal uncle 2 22.2
Younger brother 3 33.3
Total 9 100.0
Table xvib: Average hearing threshold of patients with hereditary hearing loss (Right ears n=5)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 5 85.0000 17.32051 PTARAC 50 5 87.0000 14.83240 PTARAC1K 5 83.0000 24.89980 PTARAC2K 5 78.0000 33.27912 PTARAC4K 5 93.0000 10.95445 PTARAC8K 5 90.0000 15.41104 PTARBC50 5 61.0000 12.44990 PTARBC1K 5 64.0000 8.94427 PTARBC2K 5 64.0000 13.41641 PTARBC4K 5 69.0000 5.47723 Valid N (listwise) 5
88 Audiogram xvib: Average audiogram of patients with hereditary hearing loss (Right ears n=5).
Pure tone average audiograms of patients with hereditary hearing loss(right ear)
0
10 20
30 40
50 60
70 thresholds(dB) Hearing 80
90 100 .25 .5 1 2 4 8 Frequency(kHz) d Air conduction Bone conduction
89 Table xvic: Average hearing threshold of patients with hereditary hearing loss (Left ears n=4)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 4 80.0000 20.41241 PTALAC50 4 73.7500 22.86737 PTALAC1K 4 76.2500 6.29153 PTALAC2K 4 67.5000 18.48423 PTALAC4K 4 61.2500 12.50000 PTALAC8K 4 68.7500 11.81454 PTALBC50 4 63.7500 9.46485 PTALBC1K 4 63.7500 9.46485 PTALBC2K 4 63.7500 12.50000 PTALBC4K 4 67.5000 5.00000 Valid N (listwise) 4
Audiogram xvic: Average audiogram of patients with hereditary hearing loss (Left ears n=4).
Pure tone average audiogram of patients with hereditary hearing loss(left ear)
0
10
20
30
40
50
60
70
Hearing thresholds(dB) Hearing
80
90
100 .25 .5 901 2 4 8 Frequency(kHz)
Air conduction Bone conduction Table xviia: Average hearing threshold of patients who had acute suppurative otitis media (ASOM) (Right ears n=6)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 6 34.1667 9.17424 PTARAC 50 6 34.1667 9.70395 PTARAC1K 6 38.3333 14.71960 PTARAC2K 6 33.3333 7.52773 PTARAC4K 6 40.8333 11.58303 PTARAC8K 6 44.1667 14.97220 PTARBC50 6 25.8333 2.04124 PTARBC1K 6 25.8333 2.04124 PTARBC2K 6 27.5000 6.12372 PTARBC4K 6 27.5000 6.12372 Valid N (listwise) 6
Audiogram xviia: Average audiogram of patients who had ASOM (Right ears n=6).
Pure tone average audiogram of patients with acute suppurative otitis media(right ear)
0 10 20 30 40 50 60 70
Hearing thresholds(dB) Hearing 80 90 100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
91 Table xviib: Average hearing threshold of patients who had acute suppurative otitis media (ASOM) (Left ears n=2)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 2 37.5000 3.53553 PTALAC50 2 35.0000 7.07107 PTALAC1K 2 35.0000 7.07107 PTALAC2K 2 32.5000 10.60660 PTALAC4K 2 55.0000 14.14214 PTALAC8K 2 65.0000 7.07107 PTALBC50 2 25.0000 .00000 PTALBC1K 2 25.0000 .00000 PTALBC2K 2 25.0000 .00000 PTALBC4K 2 32.5000 10.60660 Valid N (listwise) 2
Audiogram xviib: Average audiogram of patients who had ASOM (Left ears n=2).
Pure tone average audiogram of patients with acute suppurative otitis media(left ear)
0
10
20 30
40
50
60
70 thresholds(dB) Hearing 80
90
100 .25 .5 1 2 4 8 Frequency(kHz)92
Air conduction Bone conduction
Table xviiia: Average hearing threshold of patients who had otitis media with effusion (OME) (Right ears n=2)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 2 52.5000 17.67767 PTARAC 50 2 42.5000 10.60660 PTARAC1K 2 45.0000 7.07107 PTARAC2K 2 45.0000 7.07107 PTARAC4K 2 55.0000 14.14214 PTARAC8K 2 47.5000 17.67767 PTARBC50 2 25.0000 .00000 PTARBC1K 2 25.0000 .00000 PTARBC2K 2 25.0000 .00000 PTARBC4K 2 32.5000 10.60660 Valid N (listwise) 2
Audiogram xviiia: Average audiogram of patients who had OME (Right ears n=2).
Pure tone average audiogram of patients having otitis media with effusion(right ear)
0
10
20 30
40
50 60
70 thresholds(dB) Hearing 80 90
100 .25 .5 1 2 4 8 93 Frequency(kHz)
Air conduction Bone conduction
Table xviiib: Average hearing threshold of patients who had otitis media with effusion (OME) (Left ears n=3)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 3 48.3333 23.62908 PTALAC50 3 45.0000 13.22876 PTALAC1K 3 55.0000 20.00000 PTALAC2K 3 60.0000 18.02776 PTALAC4K 3 68.3333 20.81666 PTALAC8K 3 58.3333 31.75426 PTALBC50 3 25.0000 .00000 PTALBC1K 3 25.0000 .00000 PTALBC2K 3 36.6667 12.58306 PTALBC4K 3 30.0000 8.66025 Valid N (listwise) 3
Audiogram xviiib: Average audiogram of patients who had OME (Left ears n=3).
Pure tone average audiogram of patients having
otitis media with effusion(left ear)
0
10 20 30
40
50 60 70 thresholds(dB) Hearing 80
90
100 .25 .5 1 2 4 8 Frequency(kHz)94
Air conduction Bone conduction Table xixa: Average hearing threshold of patients who had neonatal jaundice ( Right ears n=2)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 2 52.5000 10.60660 PTARAC 50 2 67.5000 17.67767 PTARAC1K 2 80.0000 28.28427 PTARAC2K 2 87.5000 17.67767 PTARAC4K 2 85.0000 21.21320 PTARAC8K 2 80.0000 28.28427 PTARBC50 2 52.5000 3.53553 PTARBC1K 2 72.5000 17.67767 PTARBC2K 1 60.0000 . PTARBC4K 1 60.0000 . Valid N (listwise) 1
Audiogram xixa: Average audiogram of patients with neonatal jaundice (right ear n=2)
Pure tone average audiogram of patients with neonatal jaundice (right ear)
0
10
20 30
40 50
60
70 (dB) thresholds Hearing 80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
95
Table xixb: Average hearing threshold of patients who had neonatal jaundice ( Left ears n=2)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 2 67.5000 17.67767 PTALAC50 2 75.0000 7.07107 PTALAC1K 2 85.0000 21.21320 PTALAC2K 2 82.5000 24.74874 PTALAC4K 2 85.0000 21.21320 PTALAC8K 2 80.0000 28.28427 PTALBC50 2 55.0000 7.07107 PTALBC1K 2 65.0000 7.07107 PTALBC2K 2 67.5000 3.53553 PTALBC4K 2 62.5000 10.60660 Valid N (listwise) 2
Audiogram xixb: Average audiogram of patients with neonatal jaundice (Left ears n=2)
Pure tone average audiogram of patients with
neonatal jaundice(left ear)
0
10
20
30 40
50
60
70
Hearing thresholds(dB) Hearing
80 90
100 .25 .5 1 2 4 8 Frequency(kHz)96
Air conduction Bone conduction
Table xxa: Average hearing threshold of patients who had Meniere’s disease. (Right ears n=3)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 3 63.3333 34.03430 PTARAC 50 3 65.0000 26.45751 PTARAC1K 3 68.3333 17.55942 PTARAC2K 3 60.0000 21.79449 PTARAC4K 3 65.0000 26.45751 PTARAC8K 3 81.6667 20.20726 PTARBC50 3 46.6667 20.81666 PTARBC1K 3 58.3333 12.58306 PTARBC2K 3 60.0000 13.22876 PTARBC4K 3 51.6667 20.20726 Valid N (listwise) 3
Audiogram xxa: Average audiogram of patients who had Meniere’s disease (Right ears n=3).
Pure tone average audiogram of patients with menieres' disease(right ear)
0
10
20 30
40 50
60 70
Hearing thresholds(dB) Hearing
80
90 97 100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
Table xxb: Average hearing threshold of the patient who had Meniere’s disease. (Left ear n=1)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 1 40.0000 . PTALAC50 1 40.0000 . PTALAC1K 1 50.0000 . PTALAC2K 1 40.0000 . PTALAC4K 1 40.0000 . PTALAC8K 1 45.0000 . PTALBC50 1 45.0000 . PTALBC1K 1 45.0000 . PTALBC2K 1 45.0000 . PTALBC4K 1 40.0000 . Valid N (listwise) 1
Audiogram xxb: Average audiogram of patients who had Meniere’s disease (Left ear n=1).
Pure tone average audigram of patients with mennieres' disease
0
10
20
30
40
50
60
70 thresholds(dB) Hearing 80
90
100 .25 .5 1 2 4 8 98 Frequency(kHz)
Air conduction Bone conduction Table xxia: Average hearing threshold of the patients who had Septicaemia (Right ears n=2)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 2 87.5000 17.67767 PTARAC 50 2 95.0000 7.07107 PTARAC1K 2 95.0000 7.07107 PTARAC2K 2 92.5000 10.60660 PTARAC4K 2 100.0000 .00000 PTARAC8K 2 100.0000 .00000 PTARBC50 2 70.0000 .00000 PTARBC1K 2 70.0000 .00000 PTARBC2K 2 70.0000 .00000 PTARBC4K 2 70.0000 .00000 Valid N (listwise) 2
Audiogram xxia: Average audiogram of the patients who had septicaemia (Right ears n=2).
Pure tone average audiogram of patients with septicaemia(right ear)
0
10
20
30 40 50 60
70
Hearing thresholds(dB) Hearing
80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
99 Table xxib: Average hearing threshold of the patient who had Septicaemia (Left ear n=1)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 1 100.0000 . PTALAC50 1 100.0000 . PTALAC1K 1 100.0000 . PTALAC2K 1 85.0000 . PTALAC4K 1 95.0000 . PTALAC8K 1 100.0000 . PTALBC50 1 70.0000 . PTALBC1K 1 70.0000 . PTALBC2K 1 70.0000 . PTALBC4K 1 70.0000 . Valid N (listwise) 1
Audiogram xxib: Average audiogram of the patient who had septicaemia (Left ear n=1).
Pure tone average audiogram of patients with septicaemia(left ear)
0
10
20 30
40
50 60
70
thresholds(dB) Hearing 80 90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction 100
Table xxiia: Frequency distribution of miscellaneous causes of hearing loss (n=8) causes Number of ears Percentage % Insufflation of discharge into the eustachian tube from the nasopharynx 2 25.0 (from forceful nose blowing) Guillain Barre syndrome 2 25.0 Convulsion 2 25.0 Redundant canal wall 1 12.5 Tumour of the ear/external Auditory canal 1 12.5 Total 8 100.0
Table xxiib: Average hearing threshold of the patients with miscellaneous causes of hearing loss. (Right ear n=3)
Descriptive Statistics
N Mean Std. Dev iation PTARAC 25 3 60.0000 35.00000 PTARAC 50 3 68.3333 27.53785 PTARAC1K 3 70.0000 17.32051 PTARAC2K 3 71.6667 15.27525 PTARAC4K 3 80.0000 17.32051 PTARAC8K 3 83.3333 20.81666 PTARBC50 3 48.3333 22.54625 PTARBC1K 3 51.6667 23.62908 PTARBC2K 3 56.6667 15.27525 PTARBC4K 3 58.3333 12.58306 Valid N (listwise) 3
101 Audiogram xxiib: Average audiogram of patients with miscellaneous causes of hearing loss (Right ear n=3)
Pure tone average audiogram of patients with miscellaneous causes of hearing loss(right ear)
0
10 20 30
40
50
60
70 threshold(dB) Hearing 80
90
100 .25 .5 1 2 4 8 Frequency(kHz)
Air conduction Bone conduction
102 Table xxiic: Average hearing threshold of the patients with miscellaneous causes of hearing loss. (Left ear n=5)
Descriptive Statistics
N Mean Std. Dev iation PTALAC25 5 67.0000 24.13504 PTALAC50 5 68.0000 30.12474 PTALAC1K 5 63.0000 28.85308 PTALAC2K 5 58.0000 23.34524 PTALAC4K 5 72.0000 20.79663 PTALAC8K 5 73.0000 16.43168 PTALBC50 5 44.0000 20.43282 PTALBC1K 5 42.0000 21.38925 PTALBC2K 5 51.0000 17.81853 PTALBC4K 5 41.0000 20.43282 Valid N (listwise) 5
Audiogram xxiic: Average audiogram of patients with miscellaneous causes of hearing loss (Left ear n=5)
Pure tone average audiogram of patients with miscellaneous causes of hearing loss(left ear)
0
10 20 30
40 50 60
70
Hearing thresholds(dB) Hearing
80
90 100 .25 .5 1 2 4 8 Frequency(kHz) Air conduction Bone conduction
103 Symptoms associated with hearing loss
A total of 828 instances of symptoms were associated with hearing loss in the 432 ears studied. Some ears had more than one associated symptom. Table xxiii: Frequency distribution of symptoms associated with hearing loss (n=828) Symptom Frequency Percentage % Tinnitus 222 26.8 Itching 102 12.3 Fullness in ear 92 11.1 Otalgia 81 9.8 Catarrh 112 13.5 Nasal obstruction 112 13.5 Otorrhoea 56 6.8 Vertigo 51 6.2 Total 828 100.0
MEDICAL HISTORY
Fifty patients with hearing loss, presented with co- morbid medical conditions. Some patients had more than one co-morbid medical condition. The medical conditions and their frequency of distribution are as shown. (Table xxiv).
104 Table xxiv: Frequency distribution of co-morbid medical conditions. Medical conditions Number of patients Percentage % Hypertension 36 14.0 Diabetes mellitus 10 3.9 Haemoglobin AS 1 0.4 Retroviral infection 1 0.4 Parkinson’s disease 1 0.4 Total 49 100.0
DURATION OF HEARING LOSS
Duration of hearing loss ranged from 6hrs to 50 years. The mean duration of hearing loss in the right ears before presentation at the ENT clinic was 5.1 years 9.2SD, while that of the left ears was 5.4years 9.5SD.
105 CHAPTER SIX
DISCUSSION
Out of the 257 patients enrolled for the study, 82 patients had hearing loss in one ear, while 175 patients had bilateral hearing loss. This is to be expected, as both ears are often commonly exposed to the same systemic aetiological factors.
Whereas hearing impairment accounted for 48.7%
(875 cases out of 1797) of the new cases, seen at the ENT clinic, of Jos University Teaching Hospital, between 1982 to
1983,58 it accounted for only 28.7% (281 out of 980) of the new cases during the study period in UBTH, Benin City.
The difference in the percentage of patients with hearing loss in the study at Jos, may be due to the methodology employed. No clear diagnostic criteria for ascertaining hearing loss was mentioned in the study at
Jos. It is very likely that a rather subjective assessment of hearing loss, gave rise to a relatively high percentage of patients with hearing loss, compared to this study in Benin
City.
106 The age distribution (Table i), shows a preponderance of patients (67.2%) between 20-59 years of age. This is similar to other findings; Lagos in 200259 and Jos.31 This age group, is the working active group that hearing loss is more likely to be a challenge to and they are likely to seek medical attention.
The sex distribution shows a male preponderance, with a male to female ratio of 1.2 to 1. This agrees with previous works by Ijaduola,60 Mcpherson and Holborow 61,
Holborow, Martinson and Anger62 and O B Da Lily Tariah31.
This is however at variance with the study by Olusesi AD59 which showed a slight female preponderance and Billings and Keena that noted almost equal male and female distribution of sensorineural hearing loss63.
The average pure tone threshold at frequencies of
500Hz, 1000Hz, 2000Hz and 4000Hz ranged from 30. 4dB
(when the patient is likely to benefit from intervention) to
100dB (when the patient’s response to intervention is likely to be slow, minimal or absent). The overall average pure tone threshold at the above frequencies was 59.3dB. This gives an overall impression of a moderate hearing loss. It is
107 hoped that with the right preventive and therapeutic measures aimed at the aetiological factors, the outcome is likely to be favourable.
Twenty two aetiological factors were found for hearing loss in this study (Table ii). Ototoxicity, chronic suppurative
Otitis media (CSOM), presbyacusis, impacted ear wax, rhinosinusitis, febrile illness and ear trauma were the commonest causes of hearing loss in Benin City in decreasing order of frequency. However in 10.6% of cases of hearing loss, the aetiology was unknown. As also noted by other authors, some patients had multiple aetiological factors responsible for the hearing loss in a particular ear
59,31.
Drug ototoxicity accounted for 74 cases (15.7%) of the aetiological factors with profound sensorineural hearing loss been the main variety of hearing loss. The average pure tone threshold and audiogram of patients who had drug ototoxicity, show a severe mixed hearing loss worse at high frequency. (Table va,b and Audiogram va,b). Of this number, in 17 ears(23.0%) the particular drug responsible for the hearing loss was not known. The common causes of
108 drug ototoxicity in the study were; chloramphenicol 22 ears
(29.7%), Quinine 10 ears (13.5%), chloroquine 8 ears
(10.8%). Olusesi AD, Ibekwe AO and OB Da lily Tariah also noted the role of these drugs in the causation of hearing loss in their studies 28,28,54. A study at UNTH, Enugu, had earlier implicated chloroquine (21%), native herbs (21%), streptomycin (16%), Quinine (13%) and clopamide (8%) 60 as causes of hearing loss.
Quinine intoxication occurs in the stria vascularis and outer cochlear hair cells 65. Most of the native herbs used for malaria fever are also likely to contain quinine. Chloroquine ototoxicity is fairly common in our environment and has been found to be more commonly associated with parenteral administration33,66,67.
In an earlier study on drug ototoxicity in Benin City, ototoxicity was attributed to overdose of drugs, renal dysfunction, idiosyncracy and rapid build up of high blood levels of the drugs68. The study was the first to highlight the high incidence of chloramphenicol ototoxicity in Benin City which was found to be severe and associated with poor prognosis. The role of a good history in ascertaining the
109 causative agents, health education, caution in the use of potentially ototoxic drugs and where possible avoidance of their use were emphasized. The incidence of chloramphenicol ototoxicity, however appears to be increasing with 22 cases seen in this 1 year study, compared to the 21 cases in his three year study in Benin
City53.
Chronic suppurative otitis media (CSOM) accounted for the next commonest cause of hearing loss with 70 ears
(14.9%). Conductive hearing loss was the main type of hearing loss encountered for CSOM in this study; 39ears
(55.7%). Some cases of CSOM also presented with sensorineural hearing loss; 10 ears (14.3%) and mixed hearing loss; 21 ears (30.0%). The average pure tone threshold and audiogram of patients who had CSOM show a moderate mixed hearing loss (Table via,b and audiogram via,b).
There is a very high incidence of CSOM in our environment69,70. Environmental conditions, socio-economic circumstances, racial and ethnic susceptibilities are the identified factors 71,72,73,74. The clinical management of many
110 patients with chronic discharging ear is difficult because of malnutrition, severe infections and low follow-up compliance rate70, hence the high incidence of hearing loss in our environment.
Other researchers had similar findings with regard to
CSOM in Jos with conductive hearing loss seen in 714 cases (81.6%) and sensorineural hearing loss in 161 cases(18.1%)58.
Whereas O B Da Lily-Tariah had only 4 out of 474 cases (0.8%) with sensorineural hearing loss31, Ezeanolue
BC studying uncomplicated chronic suppurative otitis media among Nigerians did not find sensorineural hearing loss in his series of patients with CSOM25. His finding in
144 diseased ears was mild conductive hearing loss. He however concluded that the weight of evidence of workers who found sensorineural hearing loss in their studies cannot be ignored 16,26-30.
Unknown causes accounted for 10.6% of the aetiological factors. The average pure tone threshold and audiogram of patients who had unknown aetiological factors, show a mild to moderate sensorineural hearing
111 loss. (Table viia,b and Audiogram viia,b). In this group definite clinical causative factors could not be established.
Physical examination revealed no important finding. There was also no family history of hearing loss. Vascular malformations, haematological disorders, systemic diseases and genetic disorders75 may be contributory factors in this unknown group. Further investigations like computerized axial tomography, magnetic resonance imaging, serological and genetic studies may identify definitive causes of deafness in this category of patients 31. The unknown causes in this study (10.6%) is small, compared to O B Da lily- Tariah (16.5%)31, Ibekwe AO (20.6%)32, Bergstrom
(30%)76, sellars and Beighton from south Africa (46%),77
Obiako (30.3%)78 and Holborow (36%)62. High index of suspicion, detailed clinical history, examination by the same examiner and better diagnostic facilities compared to previous studies are probably responsible for the lower percentage of unknown causes in this study.
Presbyacusis accounted for 13.2% of the aetiological factors. The average pure tone threshold and audiogram of patients who had presbyacusis show a moderate
112 sensorineural hearing loss worse at high frequency (Table viiia,b and Audiogram viiia,b). The hearing loss was more of sensorineural hearing loss and mixed hearing loss especially at high frequencies. It is also possible that the mixed variety might be due to other multiple aetiological factors in the same ear as reported by Olusesi AD59. He recorded 15 out of 105 ears (14.29%) as having presbyacusis, although 3 out of the 15 occurred with other factors as multiple aetiological factors. Bhatia PL recorded 9 cases of presbyacusis out of 875 cases of hearing impairment (1.03%) between 1982 and 1983. OB Da lily-
Tariah working at Jos between 1989 to 1994 recorded 7 out of 474 cases (1.48%) of presbacusis31. It is possible that increase in life expectancy due to increase in the level of societal education, better standard of living and access to improved health facilities contributed to this recent increase in presbyacusis as seen in this study in Benin City and in
Olusesi’s series. This is substantiated by recent studies at
U C H Ibadan recorded a high incidence of presbyacusis; 35 out of 114 (30.70%) of geriatric patients with otological complaints79 and at Enugu which recorded 71 cases of
113 presbyacusis out of 210 geriatric patients (35.3%) with otological disorders80. It is hoped that with the rapid growth of the elderly population, presbyacusis will become a larger percentage of patients with hearing loss in the future and otolaryngologists would need to be prepared to take care of this category of patients adequately.
Impacted wax accounted for 8.9% of the causes of hearing loss. Out of 42 cases of wax impaction, conductive hearing loss was seen in 34 cases and mixed hearing loss in
8 cases. It is very likely that the mixed hearing loss might be due to the presence of wax causing a conductive hearing loss and an unknown aetiological factor presenting as sensorineural hearing loss; both giving a picture of mixed hearing loss.
The average pure tone threshold and audiogram of patients who had impacted wax show a mild conductive hearing loss (Table ixa,b and Audiogram ixa,b). Wax was a common feature in the Jos series58, while it was the third commonest ear condition in UNTH’s pattern of diseases of the ear 81.
114 Rhinosinusitis leading to eustachian tube dysfunction caused conductive hearing loss in 68.6% of cases of rhinosinusitis. The average pure tone threshold and audiogram of patients who had rhinosinusitis show a mild conductive hearing loss (Table xa,b and Audiogram xa,b).
There were 30 cases of trauma to the ear. Slap to the ear accounted for 70.0%, road traffic accident for 26.7% and fire-burn to the external auditory canal 3.3% (Table xia). Most slaps were on the left ear, as this is the ear facing the right hand (most active) of most assaulters. Conductive hearing loss was the dominant type of hearing loss (56.7%) in cases of trauma to the ear in this study. The average pure tone threshold and audiogram of patients who had trauma to the ear show a mild to moderate mixed hearing loss worse at high frequency (Table xib,c and Audiogram xib,c).
A research at Sagamu found faulty attempts at removal of foreign bodies from the ear to be responsible for
79% of ear trauma, assaults 5.5% and road traffic accident
6.9%82. This was correlated by a study at Enugu where foreign bodies were also found to be responsible for a high
115 percentage (82%) of ear trauma. Only a few cases of slaps to the ear resulting in perforations of the tympanic membrane were encountered at Enugu81. The pattern of hearing loss in ear trauma in Benin City correlates with that of researchers at Tel-Aviv Israel, where an assessment of hearing status among 120 patients with ear slaps had conductive hearing loss accounting for 47.5%, mixed hearing loss 24.2% and pure sensorineural hearing loss
(0.8%)46
In this study febrile illness was accounted for by meningitis 31.2%, measles 25.0%, unspecified febrile illness
28.1% etc. (Table xiia). Febrile illness resulted in sensorineural hearing loss; (71.9%) and mixed hearing loss;
28.1%. The average pure tone threshold and audiogram of patients who had febrile illness show a severe to profound mixed hearing loss. (Table xiib,c and Audiogram xiib,c). The deafness following meningitis if believed to result from labyrinthitis83.
Ibekwe AO found that febrile illness accounted for
41.03% of profound deafness in children in Nigeria. Febrile illness include malaria, mumps, measles, whooping cough,
116 poliomyelitis and bacterial infections like meningitis and pneumonia.32 The commonest cause of febrile illness in a tropical country like Nigeria is malaria fever. These febrile illnesses also cause convulsion. The abuse of chloroquine in the treatment of malaria fever with its ototoxic effect also contribute to profound deafness.78
In this study, febrile illness accounted for 6.8% of hearing loss. This reduced percentage compared to Ibekwe’s series may be due to renewed preventive measures against viral infections, the roll-back malarial initiative and improved access to quality health-care.
Measles is a widespread infection, causing deafness by destruction of neuroepithelium of endolymphatic system
(endolymphatic labyrinthitis) by the viral particles carried into the inner ear via the bloodstream. It is presently experiencing a markedly reduced incidence, due to the effective measles vaccination that has gained wide acceptance and coverage in the country.
Noise exposure accounted for 3.0% of cases of hearing loss in this study. Most of the cases were due to noise exposure at work. The average pure tone threshold and
117 audiogram of patients who had noise-induced hearing loss, show a mild to moderate sensorineural hearing loss. (Table xiiia,b and Audiogram xiiia,b).
O B Da lily-Tariah found noise-induced deafness to be responsible for 3.6% of SNHL in Jos, while Olusesi AD recorded 7.6% of noise-induced hearing loss. Seven out of eight of Olusesi’s cases were due to brief impulse noise from fireworks called “Banga” and “Knockouts” which are often displayed during celebrations in cosmopolitan urban areas like Lagos. Although most of the previous works on noise- induced deafness focused on occupational noise 84,85,86, a recent study noted sensorineural hearing loss in only one out of 120 cases (0.8%) with non explosive blast injury to the ear46.
Otitis externa accounted for 2.3% of hearing loss. Of this number otomycosis accounted for 54.5% and bacterial infection of the external auditory canal accounted for 36.4%
(Table xiva). Majority of the hearing loss from otitis externa were of the conductive variety (81.8%). The average pure tone threshold and audiogram of patients who had otitis
118 externa show a mild to moderate mixed hearing loss. (Table xivb,c and Audiogram xivb,c).
Okafor B C recorded a high incidence of otitis externa between July 1973 and June 1978 (587 cases), ranking second to CSOM among diseases of the ears. Thirty-five (35) of the 587 cases [5.96%] were clinically diagnosed as otomycosis. The average of seven cases of otomycosis seen yearly at Enugu, is comparable to the finding of 6 cases ( 1 year period) in this study in Benin City.
Nasopharyngeal carcinoma accounted for 2.1% (10) of hearing loss; 90% of this number was conductive and 10% was sensorineural hearing loss. The average pure tone threshold and audiogram of patients who had nasopharyngeal carcinoma show a mild to moderate conductive hearing loss (Table xva,b and Audiogram xva,b).
Okeowo PA in an earlier study on cancer in Nigeria did not document any case of hearing loss in nasopharyngeal carcinoma (NPC)87. However in a second study on NPC, hearing loss was documented in 16 out of 98 patients
(16.3%)88. However the pattern of the hearing loss was not commented on. But Mezue and Ezeanolue B C identified 3
119 cases of hearing loss out of 6 cases reported in an article on nasopharyngeal carcinoma. They however classified one of the cases as been conductive but were silent on the nature of the other two89.
Obiako had pointed out that the time lag in arriving at a proper diagnosis remains a sore point about NPC in developing countries90. However, it is commonly believed among practicing otorhinolaryngologists that with a unilateral conductive hearing loss in a patient with cervical lymphadenopathy, nasal symptoms, unilateral facial headache and paralysis of the soft palate on the same side there should be a high index of suspicion for nasopharyngeal carcinoma. Nasopharyngeal carcinoma causes conductive hearing loss by obstructing the eustachian tube, while the sensorineural hearing loss, is likely due to the infiltrative nature of a pathological type of nasopharyngeal carcinoma 91.
Hereditary factors accounted for 9 cases (1.9%)of hearing loss. Seven of these had SNHL, while 2 had mixed hearing loss. The average pure tone threshold and audiogram of patients who had hereditary hearing loss
120 show a moderate to severe mixed hearing loss. (Table xvib,c and Audiogram xvib,c). Thirty three percent of the patients had 1st degree relative (sibling), while 66.6% had second degree relative (uncles) with similar hearing loss. 77.8% of the hearing loss was severe to profound, while 22.2% was of moderate severity. Olusesi AD found 50% of the hereditary hearing loss in his series in first degree relative and 35% in second degree relative. His study identified 1.9% incidence of hereditary SNHL in Lagos59 as against 1.9% in this study in Benin City. Sellars, Napier and Beighton had hereditary causes of 20%92, Ijaduola 13.2%60, McPherson and
Holborow 8%61 and Holborow, Martinson and Anger 3.2%62.
Current research on the genetics of inherited deafness by
Kelsell et al, showed that the deafness at DFNBI locus is due to mutations in the gene GJB2, encoding the protein connexin 2693. Mutations in the GJB2 gene cause deafness by altering the function of connexin 26 situated in the inner ear94.
Acute suppurative otitis media (ASOM) accounted for only 1.7% of hearing loss. The average pure tone threshold and audiogram of patients who had ASOM show a mild
121 conductive hearing loss (Table xviia,b and Audiogram xviia,b).
Considering the fact that unresolved ASOM is what often leads to CSOM, which has a high incidence of 14.9% in this study, one may like to find out the reason for this low incidence of ASOM. First, it might be due to the use of antibiotics; either by self medication or from the advice of patent medicine store dealers. Inadequate dose of antibiotics suppress the acute symptoms until they become chronic. Secondly, it is not far fetched from BC Okafor’s conclusion that the main factors are socio economic; as most patients lived in outlying distant communities with poor transport facilities and often came to the unit as a last resort. Therefore, acute problems were delayed whilst trying around locally for a remedy. Persistent or recurrent otorrhoea over many years was usually the signal for seeking the help of the otolaryngologists70.
Otitis media with effusion (OME) accounted for only
1.1% of hearing loss. The average pure tone threshold and audiogram of patients who had otitis media with effusion
122 show a mild to moderate conductive hearing loss (Table xviiia,b and audiogram xviiia,b).
Okeowo in 1981 reported a prevalence of 6.6% of OME amongst school children in Lagos95, while Ogisi reported
5.2% prevalence in Benin City in 198836. However, only
2.5% of the screened children in Benin City had hearing loss. The lower prevalence of 1.1% in this study compared to the 2.5% of hearing loss in Ogisi’s study is due to the fact that his work was restricted to children (6yrs old); an age with the highest incidence of adenoids and upper respiratory tract infection.
Meniere’s disease accounted for 0.8% of hearing loss and this diagnosis was made in patients with episodic vertigo, tinnitus and fluctuating sensorineural hearing loss.
This incidence is low compared to some countries96. It is however higher than the very low incidence in the Indian population in south western America97. The average hearing threshold and audiogram of patients who had Meniere’s disease show a mild to moderate sensorineural hearing loss
(Table xxa,b and Audiogram xxa,b).
123 Only 1 case of tumour of the ear/external auditory canal (liposarcoma) was seen in this study. This agrees with the finding of Okafor that neoplasms of the ear are rare in any population group81. The pure tone threshold and audiogram of the patient who had a tumour in the external auditory canal show severe to profound mixed hearing loss.
Other causes of hearing loss during this study included neonatal jaundice (0.8%), septicaemia (0.6%),
Guillain Barre syndrome, insufflation of discharge into the eustachian tube from the nasopharynx, convulsion and redundant external auditory canal wall (Table xxiia).
Hearing loss due to ear canal collapse that can be overcome by the placement of an insert into the ear canal has been reported45 and is probably the cause of hearing loss in the case with redundant collapsible external auditory canal wall. Neonatal jaundice, septicaemia and convulsion are usually encountered during childhood period. Although they reflect poor obstetrical and paediatric practices, we are gradually having fewer cases of hearing loss due to these aetiological factors because of improved quality of health care.
124 Table iv shows that 68.3% of hearing loss are of the mild to moderate category. This portends good prognosis as there is still residual hearing which is likely to improve with appropriate rehabilitative intervention.
Table xxiii shows the symptoms associated with hearing loss, with tinnitus being the commonest (26.8%).
This is also similar to the report of Olusesi AD in Lagos with tinnitus being the commonest otologic symptom associated with sensorineural hearing loss (27.6%). Obiako similarly reported tinnitus as the commonest symptom associated with noise induced hearing loss among miners in Zambia copper belt. Although various mechanisms are responsible for the persistent tinnitus in sensorineural hearing loss98, cochlear tinnitus generation results from discordant damage of outer and inner hair cells99.
Thirty-five (35) patients with hearing loss gave a history of hypertension. This is a co-morbid medical condition. But it is also possible that arteriosclerosis secondary to hypertension resulted in ischaemia of labyrinthine blood vessels resulting in SNHL. It is also likely that anti-hypertensives especially those containing thiazide
125 diuretics contributed to the hearing loss by their ototoxic actions31.
Ten patients with hearing loss also had diabetes mellitus in this study. Reports on the relationship between diabetes mellitus and hearing loss have been controversial.
However in a study, diabetics were found to have a higher mean hearing threshold at a frequency of 500Hz than non- diabetic Mexican American adults100. Future studies of the relationship between diabetic control and hearing loss are needed.
One patient with hearing loss had haemoglobin AS genotype on haemoglobin electrophoresis. Hearing loss has not been documented as a complication of haemoglobin AS abnormality. This may therefore be an incidental finding.
Todd’s study in which 22% incidence of SNHL was found in sickle cell disease patients compared with a 4% incidence in a control group is worth mentioning101. Sickle cell disease causes vaso-occlusive episodes, either acute or chronic, leading to ischaemic damage of the inner and outer hair cells and the stria vascularis. Onakoya PA, Nwaorgu OGB and Shokunbi WA concluded in their article that SNHL is a
126 common complication of sickle cell anaemia in our environment. They hoped that this will serve as a guide towards a more focused approach to their comprehensive management37.
Although only 1 patient with hearing loss had retroviral infection in this study, the incidence of otologic symptoms in patients with human immunodeficiency virus
(HIV) infection has been reported to be as high as 56%.
Sensorineural hearing loss, otitis externa, serous and acute otitis media are the commonest otologic diagnosis in HIV infected population102. In another study by Nwaorgu and
Osowole at Ibadan fifty percent of the patients presented with varying otological diseases including otomycosis, SNHL and otitis media103. A similar study at Kaduna also recorded
3.1% of HIV patients with sensorineural hearing loss104.
The duration of hearing loss before presentation ranged from 6hours to 50 years, with a mean duration of
5.1years 9.2SDin the right ear and 5.4years 9.5SD in the left ear. This is short, compared to Olusesi’s study where the mean duration of hearing loss before presentation at ENT clinic was 10.0 years59.
127 This is however a reflection of the fact that patients went to patent medicine stores, consulted primary care physicians without consulting a specialist otorhinolaryngologist. Low socio-economic status, superstitious beliefs, low level of education and probably long distance from UBTH due to the unavailability of otorhinolaryngologist in their immediate community are the reasons for this late presentation. It is therefore possible that with this long duration before presentation, patients that could have been treated and their hearing loss remedied, might now become difficult to be remedied or even become irreversible due to loss of neural plasticity31.
128 CONCLUSION
1. A total of 28.7% of the patients that presented at the
ENT clinic of UBTH, Benin City, during the study
period had hearing loss.
2. A total of 67.2% of the patients with hearing loss in
this study, belonged to the young active age group.
3. Ototoxicity, CSOM, presbyacusis, wax impaction and
rhinosinusitis are the commonest causes of hearing
loss in Benin City. However 10.6% of the cases of
hearing loss had unknown aetiology. Some patients
had multiple aetiological factors in the same ear.
4. The overall pattern of hearing loss in Benin City is not
different from what is obtainable in other parts of
Nigeria.
5. Two hundred and ninty five ears (66.3%) with hearing
loss in Benin City were mild to moderate in severity.
6. Tinnitus is the commonest symptom and hypertension
the commonest co-morbid medical condition
associated with hearing loss in Benin City.
7. The mean duration before patients with hearing loss
present at the ENT clinic in Benin City is 5.1 years
129 9.2 SD in the right ear and 5.4 years 9.5 SD in the
left ear.
8. The hearing loss of patients in Benin City may still be
remedied with appropriate therapeutic and
prophylactic measures.
130 RECOMMENDATIONS
1. Provision of appropriate diagnostic facilities for the
early detection and evaluation of hearing impairment
in our community, (including Otoacoustic emission,
Brain stem evoked response audiometer,
Tympanometer).
2. Avoiding drug abuse to reduce the level of drug
ototoxicity.
3. Early and appropriate referral to specialist otologists
when hearing loss is suspected to avoid
mismanagement and delay in instituting proper
treatment.
4. Avoiding overcrowding, provision of clean portable
water and maintenance of good environmental
sanitation to prevent chronic suppurative otitis media,
meningitis, measles infection, mumps, lassa fever and
German measles which are aetiological factors for
hearing loss.
5. Proper evaluation of hearing loss patients to identify
the various aetiological factors, in cases of multiple
aetiological factors.
131 6. Provision of hearing aid facilities and training of more
ENT Surgeons, ENT nurses, audiologists and
audiology technicians.
7. Health education campaigns to enlighten the public on
the aetiology, prevention, treatment and rehabilitation
of hearing loss to decrease its incidence.
8. In this study 10.6% of aetiological factors were
grouped as unknown. The need for more research and
the provision of equipment to identify these specific
aetiological factors is being highlighted.
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