**5.3 Oto-acoustic emissions**

As early as 1948, Gold (Gold.T,1948) discovered that the outer hair cells of the cochlea could produce energy by an active mechanical process. However it was not until 1978 that Kemp (Kemp 1978) by a series of basic and clinical experiments demonstrated that the cochlea was capable of producing low intensity recordable sounds called oto-acoustic emissions (Fig-3). Oto-acoustic emissions (OAEs) can be defined as the audio frequency energy which originates in and is released from the cochlea, transmitted through the ossicular chain and tympanic membrane and measured in the external auditory meatus. They can occur either spontaneous or in response to acoustic stimulation. OAEs are believed to reflect the active biomechanical movement of the basilar membrane of the cochlea (Fig-4). This retrograde traveling wave is thought to be responsible for the sensitivity, frequency selectivity and wide dynamic range of the normal auditory system. Oto-acoustic emissions (OAEs) are believed to be the by product of pre-neural mechanisms of the cochlear amplifier and in particular, to be linked to the normal functioning of the outer hair cells. Oto-acoustic emissions are vulnerable to a variety of agents such as acoustic trauma (Hamernik RP, 1996) hypoxia, (Rebillard.G Lavigne& Rebillard.M) and oto-toxic medications (Ress .B D et al, 1999) that cause hearing loss by damaging outer hair cells.

Hearing Loss in Minor Head Injury 145

It has been established that DPOAEs are reduced or eliminated by compromise of middle ear conduction pathway. Normal middle ear functioning is pre-requisite for measuring DPOAE and it is therefore important to include immitance measurements while recording DPOAEs.

In the study done in the ENT department of Christian Medical College India, 60 patients with history suggestive of mild head injury were evaluated over a period of six months.

INCLUSION CRITERIA: All patients with (a) history suggestive of Mild Head injury (MHI) Glasgow coma scale scoring system [GCS] 13 – 15 and improving (b) age between 6 – 60 years,(c) Patients discharged from casualty after observation period of 24 hours,(d) History

EXCLUSION CRITERIA: Patients with past history of ear disease, previous head injury or noise trauma. and patients having family history suggestive of autoimmune disease and

A detailed evaluation of the severity of injury using Glasgow coma scale scoring was done. Radiological investigations like X-Ray of skull (antero-posterior and lateral) and CT scan

The external auditory canal and tympanic membrane were assessed to rule out any signs of temporal bone fracture like bleeding from external auditory canal, palpable step deformity, tympanic membrane perforation or haemotympanum. If the external auditory canal was filled with clotted blood patient was called for assessment after a period of one week. Eyes were checked for nystagmus and conjugate deviation. Facial nerve function tests were done and when the patient was cooperative facial nerve function was graded according to House

*Pure tone audiometry was done and Hearing thresholds of 15-25 dB across the frequencies were considered to be as normal.* Tympanometry was done using a probe tone frequency of 226Hz. An ipsilateral stapedial reflex at 1000 Hz was elicited. The ipsilateral acoustic reflex threshold was seen as normal if the level at which it is elicited falls between 70db and 100db.

Repeat evaluation was done after a period of three and six months. A detailed otoneurological evaluation was done in all three visits and patients were specifically asked for

Road traffic accidents (RTA) were the most common cause of Minor head injury as seen in all studies. The incidence of road traffic accidents in age groups 20-50 years, in our study, (Fig-5) was similar to the study done by Ludwig podoshin and M R Abd AL-Hady. A vast majority (75%) of the RTA's (Road traffic accidents) (Fig-6) were two wheeler accidents and

DPOAE testing was done at 1000Hz, 2000Hz, 3000Hz, 4000Hz, and 6000Hz.

Majority (83%) were males and 66% were between ages of 20-50 years.

This means is also used to confirm the presence of any middle ear pathology in MHI.

**6. Study** 

hearing loss.

of loss of consciousness of less than 20 minutes.

Brackmann scale (House JW, &Brackmann DE 1985)

symptoms of hearing loss tinnitus and vertigo

none wore helmets at the time of accident.

**6.1 Results and analysis** 

were used to detect skull fractures.

Taking into account estimates of amplification provided by outer hair cells, complete destruction of OHC'S alone could result theoretically, in a hearing loss of 60 dB. Early investigations in to OAE'S proved that they are not present when the sensorineural hearing loss exceeds 40-50dB (Collet L, 1989), (Gorga, Michael P, 1997).

DPOAEs measures have shown excellent intra-subject test reliability which allows monitoring of dynamic changes of cochlear function (V.Rupa, 2001)

Fig. 3. Basilar membrane displacements produced in cadaveric human cochlea in response to 200Hz at 4 separate points of time. Envelope of travelling wave is also noted

Fig. 4. Schematic representation of travelling wave along basement membrane

It has been established that DPOAEs are reduced or eliminated by compromise of middle ear conduction pathway. Normal middle ear functioning is pre-requisite for measuring DPOAE and it is therefore important to include immitance measurements while recording DPOAEs. This means is also used to confirm the presence of any middle ear pathology in MHI.
