**3. Hearing loss in head injury**

Deafness due to head injury is known since ancient times, the earliest account of which is the Edwin Smith papyrus, (Marc stiefel, 2006) the world's earliest known medical document, written around 1600 BC, but thought to be based on material from as early as 3000 BC. It is a textbook on trauma surgery, and describes anatomical observations physical examination, diagnosis, treatment, and prognosis of numerous injuries in exquisite detail. The symptoms and signs of head injury were given in considerable detail. It was noted that brain injuries were associated with changes in the function of other parts of the body. Feeble pulse and fever are associated with grievous injuries and deafness as well as aphasia are recognized in fractures of the temporal region.

Sushrutha who is known as "Father of Surgery" in India, even though he does not attach significance to the brain, however, considers head as the centre of all special senses and describes certain cranial nerves connected with specific sensory functions. He described two nerves lower down the back of the ear (vidhura), which, if cut, produce deafness; a pair of nerves (phana) situated inside the two nostrils, which if cut, cause anosmia. A pair of nerves below the outer end of the eye-brow, near the external corner of the eyeball (apanga) which if cut, cause total blindness.

Alexander and Scholl (Alexander AF and Scholl) as early as 1938 reported a 31% incidence of hearing loss in patients with head injury. In 1939 Grove (Grove W.E) reported an incidence of 32.6% of sensorineural hearing loss and suggested that bleeding in the inner ear was the cause whereas Uffenorde (Uffenorde W, 1924) stated that stretching of the fibers of the cochlear nerve in the internal auditory canal bought on the hearing loss after head injury. Similar results were reported by Gurdijan,( Gurdijan ES 1933) Fradis and Podoshin (Podoshin .L&,Fradis.M,1975) and M R Abd al Hady ( M.R.Abd AL-HADY et al,1990). Griffiths ( M.V.Griffiths )in 1979 reported an incidence of 56% of sensorineural deafness in cases of mild head injury . He stated that there may be difference in outcome depending on the type of violence. A blow to the head with a soft object seems to cause less damage to the hearing system than a blow to the head with a hard object with the same power at impact. The greater hearing loss according to him is due to an acoustic component.

Hearing Loss in Minor Head Injury 139

longitudinal fracture of the temporal bone, secondly in an ear opposite a temporal bone fracture and thirdly in a head injury with no evidence of skull fracture. According to them to produce labyrinthine concussion a head injury must be severe enough to cause loss of

Hearing loss is worst in the high frequency range and the peak loss is usually at 4000 Hz. The vertigo attacks are of postural type as described for patients having longitudinal

Experiments on animals show that the deafness is due to injury of the organ of corti, identical with that which results from a shock pulse in the air as a bomb blast or a pistol shot. They found that it results in violent displacement of the basilar membrane and organ of corti, that both reversible and irreversible cellular injuries result. They estimated hearing loss in animals, cats subjected to head injury. The hearing loss was estimated by audiogram and compared with a cochlear chart and found that the primary effect of trauma is to the organ of corti and the nerve degeneration is secondary. It is in fact the presence of damage to the organ of corti which ruled out nerve injury as a primary effect. The slightest detectable histological changes consisted of anatomical derangement of outer hair cells and their supporting cells. In mild injuries the outer hair cells which are normally tall and rectangular appeared shorter and wider and the nuclei were smaller and the chromatin was condensed. In severe lesions there was a loss of external hair cells and the beginning of cytological changes in the Dieters cells and the supporting cells, further progressive stages of injury consisted of flattening of the organ of corti and finally its complete disappearance. In labyrinthine concussion histological examination of the auditory system revealed the significant pathological changes to lie in the cochlea, when there was damage to the organ of corti severest in the upper basal turn, the region serving 4000Hz frequency. Thus according to them partial permanent deafness occurs in about 50% of patients who sustain a blow to the head to produce unconsciousness. Even a mild head blow without loss of consciousness

According to Makashima and Snow (Kazumi Makashima & James .B. snow, 1975) experimental findings by means of assessment of preyer reflex and cochlear potentials in guinea pigs after stimulating head injury by shaking them in a padded cage till they became unconscious showed that in animals which did not have fracture of the skull showed hemorrhage in and laceration of the 8th nerve where it exits from the medulla oblongata. Animals killed after 6 days and 30 days showed slight to moderate degeneration of outer hair cells and Hensens cells in the apical and middle turns of the cochlea, changes in the

The oto-neurological manifestations vary from patient to patient with head injury. Variability exists in type, severity and mode of onset of symptoms and signs. In some patients deterioration of hearing and vestibular functions occurs immediately after head injury and it may be transient or permanent. In other patients the symptoms may not manifest until later and deterioration of function may continue. According to them these facts suggest that there are various forms of trauma in the temporal bone and central

In a study done by E B Dorman (E.B Dorman et al 1982) the hearing loss was noted to be due to cochlear dysfunction. No 8th nerve or central abnormalities were detected. Various

pathways could be responsible for the deterioration of function.

consciousness.

can occasionally result in deafness.

Stria vascularis were minimal.

fracture.

The site of injury is important, frontal injuries resulting in a comparatively low incidence of hearing loss as compared to temporal blows. The type of audiogram recorded is an important indicator in assessing prognosis. Vertigo according to them has its own separate etiology and should be assessed and treated separately and not as a part of the post concussion syndrome.

In the immediate post injury period the incidence of hearing loss is 56% and vertigo is 24% which is very high when compared to controls (8%).Hearing loss recovered within three months. Accordingly, the mechanism of low frequency hearing loss is seen in patients with hydrops and suggests a similar peripheral mechanism. He stated that the lesions lie in the peripheral labyrinth due to edema or hydrops both of which subside with excellent prognosis. High frequency hearing loss may be caused by concussion and intense acoustic stimulation, concussion being reversible. Griffiths study showed a residual hearing loss in 14% of patients even after six months in cases of head injury with concussion without fracture.Vartiannenn (E.Vartianen et al, 1985) reported that in children who suffered blunt head trauma, 30% were found to have hearing loss of whom 16.3% had CHL and 13% had SNHL. One third of them recovered normal hearing with in six months. Similar results were reported by Zimmerman (William D.Zimmerman et al, 1993) Ludwig podoshin, (Podoshin .L. & Fradis.M, 1975) reported that conductive hearing loss due to head injury usually disappears in two months, if it persists ossicular discontinuity must be suspected.

According to Andrew T Lyos (Andrew.T.Lyos et al, 1995) in case of temporal bone fracture, immediate profound hearing loss may be caused by avulsion of the nerve or severe damage to the membranous labyrinth. Concussion directly to the otic capsule or acoustic trauma via the ossicular chain is well described. If it is not severe, it produces transient cochlear hyperemia resulting in temporary threshold shift. Feldman (Feldman H, 1987) stated that, sudden hearing loss with delayed onset can also occur following head trauma, thus it may be due to the sequelae consisting of perilymph fistula in one of the windows or a fracture of the labyrinthine capsule, which may manifest for the first time after a period of years or even decades.

Allison M Scott (Allison.M.Scot et al, 1999) found that in addition to low and high frequency hearing loss, audiograms with single and double sensorineural notches in mid frequency region may be related to head trauma.

The site of hearing impairment can be peripheral or central although the peripheral structures i.e., the middle ear and cochlea represent the most common site of injury. Nassulphis (Nassulphis P et al, 1964) found damage in the Reissner membrane and degeneration of the organ of corti in the spiral ganglion and cochlear nerve in several patients suffering from hearing loss following head injury. According to Schuknecht and Davison (Harold F.Schuknecht & Roderick C.Davison, 1956) auditory symptoms following head injury can be grouped according to the classification of labyrinthine damages which are:(a). Longitudinal fracture of temporal bone (b). Transverse fracture of temporal bone (c). Labyrinthine concussion. Labyrinthine concussion may be described as perceptive deafness and vertigo resulting from a blow to the head without fracture of bony labyrinth capsule. The nystagmus is positional and may persist for several months. The underlying pathology was thought to be due to injury to the utricle and saccule. Histopathological evidence showed rupture of the membranous walls of the utricle and saccule and degenerative changes in the macula of the saccule. This injury is commonest in ear with

The site of injury is important, frontal injuries resulting in a comparatively low incidence of hearing loss as compared to temporal blows. The type of audiogram recorded is an important indicator in assessing prognosis. Vertigo according to them has its own separate etiology and should be assessed and treated separately and not as a part of the post

In the immediate post injury period the incidence of hearing loss is 56% and vertigo is 24% which is very high when compared to controls (8%).Hearing loss recovered within three months. Accordingly, the mechanism of low frequency hearing loss is seen in patients with hydrops and suggests a similar peripheral mechanism. He stated that the lesions lie in the peripheral labyrinth due to edema or hydrops both of which subside with excellent prognosis. High frequency hearing loss may be caused by concussion and intense acoustic stimulation, concussion being reversible. Griffiths study showed a residual hearing loss in 14% of patients even after six months in cases of head injury with concussion without fracture.Vartiannenn (E.Vartianen et al, 1985) reported that in children who suffered blunt head trauma, 30% were found to have hearing loss of whom 16.3% had CHL and 13% had SNHL. One third of them recovered normal hearing with in six months. Similar results were reported by Zimmerman (William D.Zimmerman et al, 1993) Ludwig podoshin, (Podoshin .L. & Fradis.M, 1975) reported that conductive hearing loss due to head injury usually

disappears in two months, if it persists ossicular discontinuity must be suspected.

According to Andrew T Lyos (Andrew.T.Lyos et al, 1995) in case of temporal bone fracture, immediate profound hearing loss may be caused by avulsion of the nerve or severe damage to the membranous labyrinth. Concussion directly to the otic capsule or acoustic trauma via the ossicular chain is well described. If it is not severe, it produces transient cochlear hyperemia resulting in temporary threshold shift. Feldman (Feldman H, 1987) stated that, sudden hearing loss with delayed onset can also occur following head trauma, thus it may be due to the sequelae consisting of perilymph fistula in one of the windows or a fracture of the labyrinthine capsule, which may manifest for the first time after a period of years or

Allison M Scott (Allison.M.Scot et al, 1999) found that in addition to low and high frequency hearing loss, audiograms with single and double sensorineural notches in mid frequency

The site of hearing impairment can be peripheral or central although the peripheral structures i.e., the middle ear and cochlea represent the most common site of injury. Nassulphis (Nassulphis P et al, 1964) found damage in the Reissner membrane and degeneration of the organ of corti in the spiral ganglion and cochlear nerve in several patients suffering from hearing loss following head injury. According to Schuknecht and Davison (Harold F.Schuknecht & Roderick C.Davison, 1956) auditory symptoms following head injury can be grouped according to the classification of labyrinthine damages which are:(a). Longitudinal fracture of temporal bone (b). Transverse fracture of temporal bone (c). Labyrinthine concussion. Labyrinthine concussion may be described as perceptive deafness and vertigo resulting from a blow to the head without fracture of bony labyrinth capsule. The nystagmus is positional and may persist for several months. The underlying pathology was thought to be due to injury to the utricle and saccule. Histopathological evidence showed rupture of the membranous walls of the utricle and saccule and degenerative changes in the macula of the saccule. This injury is commonest in ear with

concussion syndrome.

even decades.

region may be related to head trauma.

longitudinal fracture of the temporal bone, secondly in an ear opposite a temporal bone fracture and thirdly in a head injury with no evidence of skull fracture. According to them to produce labyrinthine concussion a head injury must be severe enough to cause loss of consciousness.

Hearing loss is worst in the high frequency range and the peak loss is usually at 4000 Hz. The vertigo attacks are of postural type as described for patients having longitudinal fracture.

Experiments on animals show that the deafness is due to injury of the organ of corti, identical with that which results from a shock pulse in the air as a bomb blast or a pistol shot. They found that it results in violent displacement of the basilar membrane and organ of corti, that both reversible and irreversible cellular injuries result. They estimated hearing loss in animals, cats subjected to head injury. The hearing loss was estimated by audiogram and compared with a cochlear chart and found that the primary effect of trauma is to the organ of corti and the nerve degeneration is secondary. It is in fact the presence of damage to the organ of corti which ruled out nerve injury as a primary effect. The slightest detectable histological changes consisted of anatomical derangement of outer hair cells and their supporting cells. In mild injuries the outer hair cells which are normally tall and rectangular appeared shorter and wider and the nuclei were smaller and the chromatin was condensed. In severe lesions there was a loss of external hair cells and the beginning of cytological changes in the Dieters cells and the supporting cells, further progressive stages of injury consisted of flattening of the organ of corti and finally its complete disappearance. In labyrinthine concussion histological examination of the auditory system revealed the significant pathological changes to lie in the cochlea, when there was damage to the organ of corti severest in the upper basal turn, the region serving 4000Hz frequency. Thus according to them partial permanent deafness occurs in about 50% of patients who sustain a blow to the head to produce unconsciousness. Even a mild head blow without loss of consciousness can occasionally result in deafness.

According to Makashima and Snow (Kazumi Makashima & James .B. snow, 1975) experimental findings by means of assessment of preyer reflex and cochlear potentials in guinea pigs after stimulating head injury by shaking them in a padded cage till they became unconscious showed that in animals which did not have fracture of the skull showed hemorrhage in and laceration of the 8th nerve where it exits from the medulla oblongata. Animals killed after 6 days and 30 days showed slight to moderate degeneration of outer hair cells and Hensens cells in the apical and middle turns of the cochlea, changes in the Stria vascularis were minimal.

The oto-neurological manifestations vary from patient to patient with head injury. Variability exists in type, severity and mode of onset of symptoms and signs. In some patients deterioration of hearing and vestibular functions occurs immediately after head injury and it may be transient or permanent. In other patients the symptoms may not manifest until later and deterioration of function may continue. According to them these facts suggest that there are various forms of trauma in the temporal bone and central pathways could be responsible for the deterioration of function.

In a study done by E B Dorman (E.B Dorman et al 1982) the hearing loss was noted to be due to cochlear dysfunction. No 8th nerve or central abnormalities were detected. Various

Hearing Loss in Minor Head Injury 141

The mastoid portion of temporal bone is the inferiorly extending projection seen on the lateral surface of the temporal bone. It is composed of a squamous portion laterally and petrous portion medially separated by korner's petro squamous septum. The petrous

The tegmen tympani is the bony roof of the tympanic cavity, and separates it from the dura of middle cranial fossa. It is formed in part by petrous and part by the squamous bone, and the petrosquamous suture line, unossified in the young does not close until adult life.

The floor consists of a thin plate of bone which separates the tympanic cavity from the dome of the jugular bulb, sometimes it is deficient. The anterior wall of tympanic cavity is narrow as the medial and lateral walls converge. The lower portion of the anterior wall is larger

The bony cochlea lies in front of the vestibule and has an external appearance rather like the shell of a snail. The shell has approximately two and one half turns and its height is about

(SOURCE: www.nap.edu/openbook. page=35 Modified from Davis and Associates (1953)

portion (Greek for 'rock like') guards the sensory organs of the inner ear.

than the upper and consists of a thin plate of bone covering the carotid artery.

5mm while the greatest distance across the base is about 9 mm.

**4.1 The cochlea** 

Fig. 1. Cross section of the cochlea

hypotheses have been put forward to explain the hearing loss that appears after brain concussion.

According to Per-Olof Bergemalm (Per-olof Bergemalm, 2003) in cases of closed head injury 74% of patients showed progression of > 15dB HL which was significantly greater than the spontaneous progression in the control group. Age and temporal bone fractures were risk factors for progression but not brain contusion or Swedish Reaction Level Scale (RLS) They found an association between early PTA (Pure tone Audiometry) and progression as well as regression i.e. poorer the initial PTA the greater the progression indicating the increased instability of the auditory system. The cause of progression is usually unknown. One of the possibilities is the development of perilymphatic fistula, other reasons may be secondary degenerative changes in the cochlea following inner ear concussion and hypoxia following disturbance of micro-circulation. It has also been speculated whether progression is due to pre-existing autoimmune disease or whether the trauma itself may initiate such a reaction towards specific inner ear proteins. There may also be synergistic interaction between trauma and the effects of noise exposure (Neuberger M Korpert K et al 1992) and the use of oto-toxic agents and medication (Jacobson CA&.Jacobson JT, 1989)

According to Vernon and Press (Vernon JA, & Press LS, 1994) only 8% of the patients who sustained head injury complained of tinnitus.

Dizziness is a frequent complication of head injury. Numerous studies have attempted to quantify the incidence of neuro-otological abnormalities in patients with post traumatic dizziness. Toglia (Toglia J U et al, 1970) found out that 61% of patients had vestibular dysfunction. Gannon (Gannon RP et al, 1978) reported 32% and Wilson reported 57% neurootological test abnormalities in patients who sustained minor or moderate head injury. In case of recurring case of dizziness an organic etiology must be suspected. Hearing loss in the higher frequencies is sometimes seen as early as by age 20(Rakel R E, 2005) It increases systematically to age 60 (and beyond) and is largest at 4 kHz and 6 kHz and is much larger in males than in females.

A small Sensorineural hearing loss of 25dB at the age of 25 has little medical or social relevance, however by the age of 70 a hearing loss as a result of ageing is added to the preexisting hearing loss. This results in a moderate to severe sensorineural hearing loss. In other words a seemingly minor hearing loss at a very young age may become severe when combined with other factors which affect hearing.

#### **4. Anatomy of the ear and temporal bone**

From the point of view of injury to the ear the anatomy can be divided into preauricular pinna, post auricular region, tympanic membrane, external auditory canal, middle ear and inner ear. Preauricular region is the region of the ear in front of the auricle. Post auricular region is the region behind the auricle. The temporal bone is a composite structure and cconsists of tympanic bone, mastoid process, squamous and petrous parts. The tympanic bone forms the anterior, inferior and parts of the posterior wall of the external auditory canal. Laterally the tympanic bone borders the cartilaginous external auditory canal. The sqamous portion of the temporal bone serves as the lateral wall of middle cranial fossa and interfaces with the parietal bone superiorly and with the zygomatic process and the sphenoid anteriorly.

hypotheses have been put forward to explain the hearing loss that appears after brain

According to Per-Olof Bergemalm (Per-olof Bergemalm, 2003) in cases of closed head injury 74% of patients showed progression of > 15dB HL which was significantly greater than the spontaneous progression in the control group. Age and temporal bone fractures were risk factors for progression but not brain contusion or Swedish Reaction Level Scale (RLS) They found an association between early PTA (Pure tone Audiometry) and progression as well as regression i.e. poorer the initial PTA the greater the progression indicating the increased instability of the auditory system. The cause of progression is usually unknown. One of the possibilities is the development of perilymphatic fistula, other reasons may be secondary degenerative changes in the cochlea following inner ear concussion and hypoxia following disturbance of micro-circulation. It has also been speculated whether progression is due to pre-existing autoimmune disease or whether the trauma itself may initiate such a reaction towards specific inner ear proteins. There may also be synergistic interaction between trauma and the effects of noise exposure (Neuberger M Korpert K et al 1992) and the use of

According to Vernon and Press (Vernon JA, & Press LS, 1994) only 8% of the patients who

Dizziness is a frequent complication of head injury. Numerous studies have attempted to quantify the incidence of neuro-otological abnormalities in patients with post traumatic dizziness. Toglia (Toglia J U et al, 1970) found out that 61% of patients had vestibular dysfunction. Gannon (Gannon RP et al, 1978) reported 32% and Wilson reported 57% neurootological test abnormalities in patients who sustained minor or moderate head injury. In case of recurring case of dizziness an organic etiology must be suspected. Hearing loss in the higher frequencies is sometimes seen as early as by age 20(Rakel R E, 2005) It increases systematically to age 60 (and beyond) and is largest at 4 kHz and 6 kHz and is much larger

A small Sensorineural hearing loss of 25dB at the age of 25 has little medical or social relevance, however by the age of 70 a hearing loss as a result of ageing is added to the preexisting hearing loss. This results in a moderate to severe sensorineural hearing loss. In other words a seemingly minor hearing loss at a very young age may become severe when

From the point of view of injury to the ear the anatomy can be divided into preauricular pinna, post auricular region, tympanic membrane, external auditory canal, middle ear and inner ear. Preauricular region is the region of the ear in front of the auricle. Post auricular region is the region behind the auricle. The temporal bone is a composite structure and cconsists of tympanic bone, mastoid process, squamous and petrous parts. The tympanic bone forms the anterior, inferior and parts of the posterior wall of the external auditory canal. Laterally the tympanic bone borders the cartilaginous external auditory canal. The sqamous portion of the temporal bone serves as the lateral wall of middle cranial fossa and interfaces with the parietal bone superiorly and with the zygomatic process and the

oto-toxic agents and medication (Jacobson CA&.Jacobson JT, 1989)

sustained head injury complained of tinnitus.

combined with other factors which affect hearing.

**4. Anatomy of the ear and temporal bone** 

in males than in females.

sphenoid anteriorly.

concussion.

The mastoid portion of temporal bone is the inferiorly extending projection seen on the lateral surface of the temporal bone. It is composed of a squamous portion laterally and petrous portion medially separated by korner's petro squamous septum. The petrous portion (Greek for 'rock like') guards the sensory organs of the inner ear.

The tegmen tympani is the bony roof of the tympanic cavity, and separates it from the dura of middle cranial fossa. It is formed in part by petrous and part by the squamous bone, and the petrosquamous suture line, unossified in the young does not close until adult life.

The floor consists of a thin plate of bone which separates the tympanic cavity from the dome of the jugular bulb, sometimes it is deficient. The anterior wall of tympanic cavity is narrow as the medial and lateral walls converge. The lower portion of the anterior wall is larger than the upper and consists of a thin plate of bone covering the carotid artery.
