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IORIGINAL ARTICLE'

A Study of Congenital and Early AcquiredImpairment of Hearing

Parmod Kalsotra*, S. Kumar*, P. Gosh*, N. K. Mishra**, I. C. Verma***

Abstract

The present study included 261 patients (M:F=I.72: I) suffering from congenital and early acquiredhearing loss. The aetiological breakup of the hearing loss was: genetic factors 47.5%. non-geneticfactors 16.8%, congenital ear malfonnations 8.5% and cryptogenic factors in 27.2% cases. Autosomalrecessive mode of inheritance was seen most commonly (62%) followed by autosomal dominant(20%) in the genetic group of hearing loss. Maternal Rubella was most common cause of prenatalgroup of hearing loss while perinataly birth anoxia and prematurity were common. Postnatalymeningitis was most common aetiology ofhearing loss. Linkage analysis on SLINK 2 point autosomaldata yielded LOD score of more than 3 in an autosomal dominant family.

KeyWords

Congenital. Genetic. Non-genetic, Hearing loss.

Introduction

-

·d

).

,.;1

:1

Impairment of hearing is one of the major

disabilities occuring in India, affecting about 1.8%of ·the population. According to the National

Sample Survey (I), the prevalence of hearing

disability per 1000 population. were 5.53 in rural and

3.90 in urban areas. These rates are higher than those

for disability due to loss of vision and locomotor

problems.

There is virtually no data regarding prevalence

of congenital and early acquired hearing loss in

India except few regional surveys. Kameswaran and

Rajendra Kumar (lCMR) (2) reported 0.1 % of the

population to be suffering from congenital sensorineural'.

hearing loss and 0.02% of urban and rural population

suffering from congenital conductive hearing loss inTamil Nadu. Pat et. al. (3) reported 2 per 1000 children

under 5 years and 4.2 per 1000 children under 15 years

to have bilateral sensorineural hearing loss ofworse than

60 dB. This study was undertaken to find out the

prevalence ofcongenital and acquired hearing loss \\ 1111

analysis of various causes for the same.

Material and Methods

The present study was undertaken at ENT OPO, All

India Institute of Medical Sciences, New Delhi to study

the main aetiologcial factors causing congenital and early

acquired hearing loss.

'1

from the Deptls. of *ENT, **Ncuro-Radiology & ***Paediatrics. All India Institute of Medical Sciences, New Delhi, India.Correspondence to: Dr. Parmod Kalsotra, Lecturer, Department arENT, SMGS Hospital, Govt. Medical College. Jammu (J&K) India.

1'01. 4 No.3, July-September 2002 136

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I. Patient Selection

ta) InclUSion cntcna All those patients with

prelmgually 'mpaired hearing who have no history

of environmental factors to explain the hearing

loss dunng the pre lingual period were subjected'.

to further detailed work up.

Ib) ExclUSion cnteria The following cases were

excluded Irom the study.

(I) H,story of ear infections and trauma.

(il) IIlstory of Q!otoxic drug intake, mumps,

measles or men ingi tis after 6 months ofage.

(ill) Family history ofotospongiosis.

2. Work-up of an Individual Case

Detahed work-up of an mdividual case was carried

out mcludmg prenatal, perinatal and postnatal history to

find out vanous exog~nouscongenital causes.

Pedigree chart of the affected child was drawn at least

upto three generations and a detailed systemic

exammatlon of ophthalmology, cardiovascular system

and abdomen was performed to look for associated

anomahes. ENT examination with spec,al attenllon to

branchial arch system was performed. Mode of

IIlhentancc was ascertained whenever possible as per

the criteria used by RIJn and Cremers (4) for acceptance

ofherednary and acquired causes.

Spec,al l11\'esllgations were performed wherever

mdlcated and possible to establish the diagnosis. These

mcludcd :

I. Antibody tnres lor toxoplasmosis, rubella. CMY.

measles. mumps 111 cases when suspected and

feas,ble espcctally for Rubella within 4 years of

age (6) and CMY within 3 weeks of life (7).

2. EKG for suspcctcd Jervell and tange-Neilson

syndrome.

3. ERG for suspected Usher's syndrome.

4. Thyroid function test lor suspected pendred's

syndrome.

5. Mucopolysaccharide and amimo ac,ds screenmg

in the urine in suspected metabolic aetIOlogy.

6. Renal function test for Alport 's and other otorenal

syndromes.

7. Serum uric acid. pyrophosphates ctc to exclude

metabolic causes.

8. Chromosomal studies: In the presence of mul11ple

malformations in a case ""th heanng loss not

suspected to be due to a single gene d,sroder were

subjects for chromosomal studies.

3. Hearing Evaluation

Included the pure tone audiometry. free flllJd testlOg

(FFT) inpedence and acoustic reflex and bramstem

evoked response audiometry (BERA).

4. Radiology

High resolution CT Scan (1.5 mm sect,ons through

temporal bone in 30 degrees aXial plane) "as done In

selected cases particularly whcrc cochlear dysgenesIs

was suspected.

Results

The present study group included 261 cases 01

congenital and early acquired heanng Impalrmen

attending ENT outpatients department. All pat,enls wllh

a hearing loss conductive. mixed or senson-neural.

averaging 25 dB HL or more m the beller ear by at,conduction. within the frequency range of500-2000 HI

were included in the study.

Aetiology

The aetiology of 261 children stud'ed. was elassdied

into f<;lur main groups as shown in Table I. Congemla!

ear malformations were considered separately beeauM

they d,d not fall into any defill1tl\'e group (5).

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TableNo. I

Aetiology of Hear"jog Loss

\ctiolog) No. or eases Percentage

Genetic 124 47.5

AuIOS0Il1.11 Recessive 77 29.5

Autosomal Dominant 26 10.0

X-Rcccssl\c 1 0.4

Multifactorial 15 5.7

Chromosomal 2 0.8

UnclasSified <ISS0Cialion 3 1.1

~ on-Genetic 44 16.8

Prenatal 6 2.3

Pennatal 12 4.6

Neonatal Jaundice 3 1.1

Smh anax l<l & prematurity 9· 3.5

Postnatal 26 99

MClllgltlS 18 6.9

OIOIO\; IClt) 5 1.8

Typhoid 2 0.8

Inf<Jlllilc Measles I 0.4

J. Cryptogenic 71 27.2

~ Congcnitltl Ear \Ialformation 22 85

External c::tr 1l1<llformatlon 19 7.3

Middle car malformation 3 1.2

Total 261 100.00

I. Non-genetic group (n=44) was further sub­

classified into 3 main categories depending upon time

ofexogenous msult to auditory apparatus which may be

anlenata!. pennatal or Immediate post natal period

extending till 6 months of age.

la) Prenatal group (n=6) : This included 5 cases of

congenItal rubella and in one case, Ihe mother had

uncontrolled tuberculosis during pregnancy. Serology

lias possible 10 only two cases, while in resl of three

cases. no serology was advised due to late presentation.

'<0 case of congennal CMV could be diagnosed because

oflaler presentation of cases as serology in diagnostic

only," first 3 weeks of life (7).

Vol. 4 No.3. July-Seplember 2002

(b) Perinatal group (n= 12) : It mcluded three cases

of neonatal jaundice, nine cases of birth anOXia and

prematurity (Birth weight < 1500 gm.) BOlh the factors

i.e. birth anoxia and prematurity, were grouped logether

because of small sample and both are known to

supplement each other in causation of hcaring

impairment (8).

(c) Immediate postnatal causes (n=26) : This group

included cases ofpostnatal causes which were presumcd

to have acted upon during firsl 6 months of hfc. These

included one case of infan:ile measles. IwO cases of

typhoid fever. five cases of ototOXIC drug

(aminoglycosides) intake and remaming 18 cases with

history of neonatal meningitis. The causallve organIsm

was tubercular bacilli in t patient, pneumococcal 10 3

patients, while in remaining 14 pallents no defi11lte

causative organism was found.

2. Genetic factors (n=24) were further subclassi eied

as shown in Table I.

(a) Auto~omal dominant (n=26) : It mcluded 4 cases

ofnon-syndromal inheritance and 22 cases with specilic

syndromes. It included 7 cases or Waardenburg's

syndrome, 6 cases of Treacher-collms syndrome. 4 or

Alport's syndrome, 2 of Crollzon 's syndrome and one

with Apert's syndrome. Two patients had associated

malformations not fittmg mto any known syndrome. It

included one remale patient with associated upper limb

malfornlation and bilateral conductive heating loss. while

in another patient. bilateral conductive heaCing

Impairment was associated with OptiC atrophy and

velopharyngeaI incompetence, both showmg autosomal

dommant pattern of inheritance.

(b) Autosomal recessive (n=77) : It Included

two cases of Usher's Type I syndrome and rest 75 of

non-syndrome hearing loss. No case or Pendred's

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syndrome or Jervell and Lange Nielson syndrome was

detected.

(c) X-linked inheritance (n=l) : The present study

included one case ofHunter's syndrome with moderately

severe mixed hearing impainnent.

(d) Multi Factorial inheritance (polygenic group)

(n=15) : It included II cases ofcraniofacial microsomia,

one ofCharge association and 3 patients ofKlippel-Feil

syndrome.

(e) Chromosomal group (n=2) : Included one case

of Turner's syndrome (moderately severe conductive

hearing impainnent) and one case ofDown's syndrome

with severe sensory hearing loss.

(I) Unclassified association (n=3) : It included two

female patients with associated congenital heart defects,

one had atrial septal defect and pulmonary stenosis with

moderate conductive bilateral hearing impainnent. The

other had ventricular septal defect with severe SNHL

and an epileptic focus on EEG. The third case had

associated microcephaly, syndactyly and mental

retardation with severe hearing impainnent.

3. Congenital Ear Malformations (n=22) :

It included 19 cases ofexternal ear malfonnation and

3 cases of isolated middle ear malfonnations. External

ear anomalies included 9 cases ';;ith bilateral and 10 with

unilateral involvement (7 with right side and 3 with left

side involvement). The 3 cases of isolated middle ear

malfonnation were taken up for middle ear exploration

and the findings were:

~ Body ankylosis of Malleus and Incus in first case.

- Absence oflong process of Incus withabsent stapes

suprastructure and narrow oval window niche in

the second case.

139

In third case, stapedius tendon was absent with

malfonned stapedial crura.

4. Unknown aetiology (crypotogenic group)

(n=71) :

There were 71 cases where the history. laboratory

and other evidence could not identify the precise

cause of the hearing impairment to any of the

preceding aetiological factors. In this group. 5 cases

which had more that two possible causes of hearing

impainnent, were included as per Rijn and Cremer's (4)

guidelines, while in rest 66, possible aetiology could be

ascribed.

Sex Ratio

The present study of 261 cases consisted of 165

males (63.2%) and 96 females (36.8%) with male

preponderance of 1.72 : I. Table 2 shows a marked

preponderance of males in the postnatal, Mendelian

single gene inheritance group and cryptogenic group

while preponderance of females in multifactorial and

chromosome abnonnalities group.

Audiological Assessment of the Study Group

Two hundred and ten children cooperated for pure

tone audiometry. Results from free-field tests

supplemented by BERA were available in 44 children.

In remaining 7 children: results were inconsistent and

till the tennination of our study, no consistent response

was found ever on BERA te.ting. Four patients had blank

audiograms (no response to any frequency). It included

3 cases ofgenetic deafness (Waardenberg' s syndrome =

I and craniofacial microsomia"" 2) and one case of

cryptogenic deafness.

Air conduction threshold of these patients were

categorised according to severity of hearing impairment

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mto 5 groups as per Kemker's (9) criteria. The results

were as per Table 3. There was an overall male

preponderance in all categories of hearing loss.

The degree of hearing impairment in each category

,elalive to the aetiology of hearing' impairment was.

observed as shown in Fig. I. With maximum number of

cryptogenic and genetic cases with severe to profound

,earing loss.

\ge of Diagnosis of Hearing impairment:

In the present study, the age of presentation

"d subsequent diagnosis was variable, the range

being from less than I month to 22 years (mean age =

6.73 years) as shown in Fig. 2. 40.5% of

cases presented before 4 years of age with peak at

fourth year (16%). The range of age group when the

parents suspected the hearing impairment was right from

birth due to presence of congeni)al external ear

malformations to as late as 16 years (mainly in females

of marriageable age desirous ofearly tTeatment). In 242

cases the mean was 2.54 years (insufficient data In

19 cases).

Linkage Analysis:

18 family pedigrees were studied out of which

four were selected for linkage analysis (3 of

autosomal recessive and one of autosomal

dominant inheritance). Only the pedigree of autosomal

dominant inheritance generated LOD (log of odds)

score of 3 or greater 72.8% of the times (Fig. 3)

while 3 autosomal recessive families were not

good enough to generate signi ficant linkage data.

This analysis was done at National Institue of

Deafness and other Communication Disroders

(NIH), USA on SLINK programme for Linkage

Analysis (10, II).

Table No. 2

Sex distribution in relation to aetiology of hearing impairment

Sex

\tale

Female

\1F Ratio

In Genetic Group:

Genetic

. 73

51

1.43 : 1

Non genetic Cryptogenic Congenital Earmalformations

29 45 t 8

15 26 4

1.93 : I 1.73: I 4.5 :

Sex

Male

Female

MF Ratio

AutosomalDominant

19

7

2.71 :

AutosomalRecessive

48

29

2,52: I

Multifactorial

4

11

0.36: 1

X-linked Chromosomal

2

Unknownassociation

2

0.5 : I

In non-genetic group:

\1alc

Female

MF Ratio

Prenatal

3

3

I: I

Perinatal

6

6

I: I

Postnatal

20

6

3.3 :

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Tablr No.3 Fig. 3

Audiologic:'lJ assessment (Kemker-'s Criteria)

Number Male Female

\111d 25--10 dB il\1odcralc ~1-55 dB 15 9 6

\ 1odcrarcl\-sc\ CIT 56-70 dB 30 19 IISC\ ere '1-90 dB 84 50 34

'Profound <)0 dB 125 84 41

Inconsistent 7 3 4 '

"umber of children of (':!ell sex in hearing impairment category 11

MJTOSOMAl OOMINAHl

LOO SCORE.) 1

50r,--

\* Results In J Males and ~ Females were inconsistent)

Discussion

In Ihe present study. the age of presentatIOn and

subsequent diagnosis is quiellate (6.73 yem) as comparedto western literature (13-15). The part of delayed

d,agnosls rests upon community practices lor dclayed

speech and the social awareness and partly due to absence

of any active health surveillance In th,s aspect In many

places and absence of any high risk reg'stry.

Consanguinity

In the present study, 10 families were plckcd up.

who had consanguineous marnage wlthll] three

generations. Eighteen children born to thesc pallcnts were

included in the study accounling for 6.9% of all cases.

In the literature, the incidence reported ranges from 5°'0

to 9% (13, 16). Consanguinity in India IS seen mainly In

South India, 60 to 70% as reported by Ganga el al. (J 7)

Age of Diagn·osis of Deafness

M ale Preponderance ill Sex Ratio

There is an overall preponderance of male, 10 the

present sample which is consistent with the literature

(12-14). Male children appear to be more suseepllble to

adverse factors acting in the prenatal. natal and posl­

natal lifc. but the reason for this has not been proYcd

satisfactorily. The present study had female

preponderance in chromosomal and multi factorial

inheritance which has been well documented by Newton

(13) and Oas (14).

Prols••

• Gene'" ~ Non Genel"; _ C'Ylllooen,c

Fi~. I : Uegrec of IIcal"ing Loss (n -= 261)

Fig 2: \gc of Di~lgnosis of Hearing Loss(11~261)

70-

'0,

50FRC '0ENT 30A

201GE

10

0MOd

_ Con, I loA

'o-

N 30·UM

~ /BE

20___..../ ~R ,

V'lOt-

,0-- ~ -'---'0-' '-2 2-3 3-' .-. 6-6 . 6-7 7-8 a-. ,HO "0

YEARS •

Sex ~ 70db HL 70 db HL

\Ialc 28 134

Female 17 75

\IF- RJtlO I 65 I I. 78 I

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and RajInder Kumar (18) and in Muslims. Our study

sample maInly had cases from North and West India

thereby It had relaltvely small sample ofconsanguinity.

Aetiology

(a) Genetic Group

The modcs of Inherited deafness in the present

study are comparable to the various studies in the

literature like Rijn and Cremers (4), Elango (7),

Felnmesser (16) and Fraser (19), all revealing

predomInance ofautosomal recessive inheritance except

studies by ParvIng (20) and Ruben and Ruzycki (21)

with significant autosomal dominant inheritance.

(b) :"on-Genetic Group (n=44)

I. Prenatal group (n=6) : There were five cases

ofcongcnital rubella in the present study. In the Western

literature, It vanes li-olll < 7% in non-epidemic years

( 19) lO about 60",,, 111 epidemic years (22).

2. Periuatal causes ('1=12): (a) Neonataljaundice

(n=3. 1.1'5%): The proportion of neonatal jaundice in

the present study "as very small as compared to the

western literature which varies from 4.5% to 15% (13,

14: 16.23.24).

(b) Birth anoxia and prematurity (n=9): There were

nme cases (3.5%) ofbirth anoxia and prematurity group.

In the literature. \'anous studies have shown different

tigures "arylng from 1'10 to IS"!., (5-7,16.25).

3. Postnatal causes (n=26) : The present study

re\t~aledmeningitis as 1110St common calise of postnatal

hearIng loss whIch IS well documented In the literature

by varIOUS authors (4.7. 12, 13. 15).

In the Iilerature the percentage of non-genelic

group vanes from 17 lYo to 75% (maximum studies have

quoted 30°,,, to 40%) (5. 13. 16. 26). 'In this study the

relaltvely few cascs of nongenetic congenital and early

acquIred group (16.8%) as compared to genetic and

cryplOgeolc group IS not m agreement with the literature.

ThIS may be due to 1I1cluSlon of the congemtal and early

acquired group (within 6 months postanatal) excluding

Vol. -l '\'0. 3. JlIly~Scplclllbcr 2002

all other acquired causes in this study. Also other possible

explanation in the referral system \\ here multiple

handicapped dcaf children are rcferrcd directly to

rehabilitation departments and special c1illlcs tor mentally

retarded. Also due lO lack of "High RIsk Registry", lh~

cases are not referred for subsequent screen1l1g and

. management. Due to lack of good Infrastructure at

peripheral level. increased mortality in acquired group

results in less number ofsurvivals to present subscquentl,

seeking advice for deafness. Also large number ofstud Ie,

in the literature havc included maInly the posllmgual

deafness and therefore the subsequcl1l Increase In the

percentage of nongenetlc acqll1red causes as compared

to the present study.

Cryptogenic Group (unknown cause) (n=71) (27.2'Yo,)

In various studies in literature. thc cryptogenic

group has been reported from as 10\\ as 10% 10 ahout

60% (average 400/0) whIch 15 well III accordance \\'Ith

the present study (5. 13. 15.26,27).

Congenital Ear Malformations

The present study included 22 (8.5"'0) cases 01

external ear malformations with 19 cases or ntemal

auditory canal atresia and thrce cases of lsolat~d

congenital middle ear pathology which IS driTerent li'om

the figures reported in literature Val) IIlg li'om 211II to -lu."

(19.23.28.29).

Conclusion

In this study. the mcan age 01' prcs~n,"llon and

diagnosis of hearing loss was 6.73 years. [hc ~encllc

aetiology was found to be most C0I111110n calise (-17.5 11n I

followed by cryptogcnic (27.2",,) and nOll-genctlc

(16.8%) of the congenital and early acqUired dcali,c".

Autosomal recessive mode of InhcrJlanCl' \\ a") ..... l'1'1l 1110 ..... 1

commonly (62%) followed by autosomal domll1ant (2()""j

in the gcnetic group. Maternal rubella lIlJectlnn \\as the

most common cause of prenatal de3fl1es~ \\-hllt'

perinatally birth anOXia and prematuntv \\cre common

Post natally the menlllgitis and OlOlO'IClt) '\ere morc

common.

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The pre,cnt siudy being a preliminary study

conducted at a tertiary centre. has its own bias. merits

and dement' bUI docs reflect the need of 'Higb risk'

registry mamtenance at alilhe peripheral hcalth centres

\\ nh active sun edlance and subsequent screening for

early detection ofheanng loss.

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Vol. 4 1\0 J. Jllly-Scplcmbcr ~(~