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14.03.2016
MIXED HEARING LOSS Whenever the hearing loss of a patient includes a mixture of both conductive and sensorineural characteristics, is said to have a mixed hearing loss. Superior ventral cochlear nucleus (SVCN) Erythroblastosis typically causes hearing loss that centers around 3000–4000 Hz. Central Auditory Processing Disorders (CAPD) CAPD characterized by decreased understanding of speech in the presence of background noise.
FUNCTIONAL HEARING LOSS Functional or psychogenic hearing loss is the customary diagnosis when there is no organic basis for the patients apparent deafness. Functional Overlay It is entirely possible for hearing loss of functional origin to be superimposed on true organic hearing impairment. History: A 34-year-old woman with otosclerosis and hearing loss for over 10 years Refuse to use hearing aids She often says, What? Audiometric Patterns in Functional Hearing Loss There is no characteristic audiometric pattern in functional hearing loss, but the consistent inconsistencies serve to alert the physician. Malingering Malingering is the deliberate fabrication of symptoms that the patient knows do not exist.
Common ENT problemsOtitis externa (infection of the outer ear)Irritants, including cotton buds, can cause this common and very painful condition.
Chronic otitis media ("Glue ear")Persistent otitis media with bilateral effusions are the most common cause of hearing loss in children. Tympanic membrane perforation (hole in the ear drum)Infection, pressure changes or direct trauma to the ear canal may result in a hole in the ear drum.
If this does not heal of its own accord, patients may suffer from recurrent ear infections or a hearing loss, and surgical closure may be required (tympanoplasty). Acute otitis media (Acute middle ear infection)Middle ear inflammation may cause a facial nerve palsy, typically if the bony canal of the facial nerve is absent within the middle ear. If the infection persists the cartilage of the ear may die and patients can be left with an ugly a€?cauliflower eara€?. Acute sinusitisPatients usually complain of fever, purulent nasal discharge and facial pain. Regular bedside assessment of their visual acuity and colour vision should be carried out as these are the earliest signs of orbital compromise. Acute pharyngitisThis is most commonly due to a viral infection involving the tonsils and adenoids. Quinsy (peritonsillar abscess)Defined as a localized collection of pus between the tonsillar capsule and the superior constrictor muscle, this condition mainly occurs in young adults, either spontaneously or as a complication of acute tonsillitis. Unilateral tonsillar enlargement (one tonsil enlarged)In the absence of active infection a unilateral tonsillar enlargement should be treated with suspicion of malignancy. Acknowledgement: The illustarions included on these pages were generously donated to the author by Ms S Leighton. Hearing deficiency may have started originally as a conductive failure (otosclerosis) and later developed a superimposed sensorineural component.
In clinical practice, most cases with an original sensorineural etiology remain in that classification without an added conductive element. In chronic otitis media some toxic inflammatory metabolite produces a cochleitis or labyrinthitis. This example a warning to physicians to avoid assuring any patient that his hearing loss can be corrected merely by removing cerumen, because mixed hearing loss may be found subsequently. In every case of mixed hearing loss one should determine how much of the deficit is conductive and how much is sensorineural.
If the patient does not understand any better with a hearing aid or when the voice is raised, hearing is not improved even if the conductive portion of the mixed hearing loss is corrected. 17 The auditory pathway consists of a series of transducers that repeatedly change the speech stimulus so that it can be handled effectively by the cortex. Characteristic Features of central hearing loss : Hearing tests do not indicate peripheral hearing impairment.
This may be caused by injury to SVCN spheroid cells, the second-order neurons of the ascending auditory pathway, even in the presence of normal hair cells in the organ of Corti.
Common complaints include inability to study or read in the presence of noise, slowing of reading speed caused by noise(vacuum cleaners or air conditioners ) and suspicion by family members that the patient has a hearing loss.
The inability to hear results entirely or mainly from psychological or emotional factors, and the peripheral hearing mechanism may be essentially normal. Psychogenically induced hearing loss usually is a uniform flat- tone loss in all frequencies, suggestive of a well-marked conductive impairment. Usually, the hearing impairment is bilateral, and the bone conduction level is the same as the air conduction level. This may cause speech delay, language problems and even behavioural issues (children often feel isolated or frustrated).Removing the "glue" in addition to grommet insertion allows air to re-enter the middle ear to restore hearing. Causes include labyrinthine viral infection, labyrinthine vascular compromise, intracochlear membrane ruptures, and immune-mediated inner ear disease. Orbital cellulitis is an acute sinus infection that spreads to involve the eye lids and eye. These patients will require intravenous antibiotics and surgery to decompress the orbit if there is an abscess in order to save the eye. This condition is extremely painful and is treated by aspirating the abscess under local anaesthetic. It may be caused by voice strain but any patient who is hoarse for three weeks or longer must have their throats examined to make certain that a vocal cord tumour is not the cause of the voice change. Acid can rise up into the throat and cause a caustic burn that leaves a feeling of a lump in the throat.
The difficulty may have been sensorineural in the beginning ( presbycusis ), and a conductive defect (middle-ear infection ) may have developed subsequently. In contrast, most cases that start as conductive hearing impairment later develop some sensorineural involvement. The sensorineural deficit may be caused by penetration of the oval window with exposure of the perilymph. Prognosis: In mixed hearing loss the prognosis depends on the relative proportion of conductive and sensorineural pathology. There is no characteristic audiometric pattern, except that the disparity between the hearing level and the speech interpretation is quite marked.
Central pathology must be included in the differential diagnosis of the hearing loss producing a 4000-cycle dip on the audiogram.


If people talk to a person with CAPD while he or she is involved in auditory concentration such as listening to a television program, the person will often not hear. The basis for functional hearing loss in most patients is psychogenic, the product of emotional conflict, ( neurotic anxiety ). Hysterical blindness and paralysis are other examples of the same type of somatization or conversion reaction. In a patient with unilateral functional deafness there may be complete absence of bone conduction on the side of the bad ear, though the good ear has normal acuity. If the patient claims he has one good and one bad ear, and the examiner obstructs his good ear with a finger, then shouts into it loudly enough to be heard easily by bone conduction alone, the malingerer claims he hears nothing. Cogan, “Syndrome of nonsyphilitic interstitial keratitis and vestibuloauditory symptoms,” Archives of Ophthalmology, vol. Treatment requires regular suctioning of debris from the ear canal (microsuction) combined with appropriate ear drops (commonly a steroid and antibiotic combination). The grommets usually fall out after 18 months in this age group.Adults with a persistent middle fluid ear should undergo examination of the postnasal space under general anaesthesia. The infection is usually bacterial, Pseudomonas is often involved and requires treatment with a combination of oral and intravenous antibiotics. Treatment is by surgical incision and drainage with pressure dressing or quilting sutures to prevent recollection. Patients develop swelling and redness of the eye lids and the globe of the eye is pushed forwards. Treatment consists of supportive measures and antibiotics if a secondary bacterial infection is present. Patients find it difficult to swallow and may need admission to hospital for intravenous antibiotics. It is essential to formally examine the throat with a flexible nasolaryngoscope to make certain that a cancer is not the underlying cause.
In some cases the conductive and the sensorineural elements may have started simultaneously ( severe head injury affecting both the inner ear and the middle ear ). Despite meticulous surgical care, the inner ear also can be traumatized readily and made more susceptible to infection. The best way to approximate the conductive and the sensorineural components of a hearing loss is to perform all possible tests for estimating the patients sensorineural potential or cochlear reserve. If the sensorineural component is slight, the surgical prognosis is good, and under favorable circumstances the hearing may approximate the level of the bone conduction. In certain cases, central hearing loss may mimic peripheral causes of deafness, including occupational deafness.
However, if one gets the persons attention by calling his or her name before speaking, the first sentence will not be missed, and hearing is normal.
Tinnitus is a characteristic feature of hysterical deafness, and patients often claim that the noise is unbearable. Too spectacular an improvement with a hearing aid, especially when the patient has set the controls at minimal amplification, or a sudden disproportionate improvement in hearing after a simple procedure such as drum massage or insufflating the eustachian tube.
Such a patient even may deny hearing shouts directed at the bad ear in spite of the good hearing in the opposite ear. If there is no clinical improvement after 24-48 hours, surgery may be required to release the pus within the middle ear and restore the function to the nerve. Oral antibiotics should be prescribed while sutures are in place.Nasal traumaA fractured nose should be seen approximately 5 to 7 days after injury when the swelling has decreased. Patients who suffer 4-5 episodes of tonsillitis over 12 months are likely to benefit from removal of the tonsils.
In surgical trauma to the inner ear, high-frequency hearing loss often falls below the preoperative level, and the patient may complain of reduced discrimination though his pure-tone threshold is improved. However, the discrimination is not improved much, even after correction of the conductive defect. The chief function of the auditory cortex is to interpret and to integrate these impulses and to provide the listener with the exact meaningful information intended by the speaker, or to permit the listener to react appropriately to the actual implication of the sound. The spheroid cells of the superior ventral cochlear nucleus (SVCN) show an anatomical frequency gradient, low ventral to high dorsal. Treatment : altering the listening environment to obtain the best possible signal-to-noise ratio.
Hearing acuity usually varies, depending on the patients emotional state at the time of testing. In complete deafness the presence of cochlear nerve reflexes with loud noises indicates either malingering or hysteria. The diagnosis of CS is based upon presence of characteristic inflammatory eye disease and vestibuloauditory dysfunction. Children develop symptoms of irritability, have a raised temperature and often pull at their ears. Children will need to be held by a parent or nurse; the first attempt at removal is the best.
If the patient hears and discriminates well when speech is made louder, then the conductive element probably is a major cause of the hearing difficulty, and there is a good chance that surgery will improve the hearing.
A similar adverse effect is noted in the ear opposite the tumor when certain words are interrupted periodically or accelerated. However, if the foreign body cannot be removed, patients require a short general anaesthetic to allow removal.
All contact sports and alcohol must be avoided in the first few weeks after the onset of symptoms.
The patient was admitted with headache, vertigo, nausea, vomiting, right leg claudication, musculoskeletal pains, bilateral hearing loss, and blindness for the past two months. Labyrinthitis Otosclerosis was at one time thought to retain its purely conductive character for years; today it is recognized that this condition develops sensorineural impairment in same cases. Conjunctival hyperemia, bilateral cataract, and interstitial keratitis were detected with a slit lamp examination. Pure tone audiogram (PTA) and auditory brain stem response (ABR) showed bilateral sensorineural hearing loss. Fauci, “Cogan syndrome: studies in thirteen patients, long-term follow-up, and a review of the literature,” Medicine, vol. IntroductionCogan’s syndrome (CS) is a rare chronic inflammatory disorder characterized by nonsyphilitic interstitial keratitis and vestibuloauditory dysfunction [1].


Associations between CS and systemic vasculitis as well as aortitis also exist [2–4].
In the two largest series to date, the median age of onset was 22 years (range 5 to 63 years) [2, 3].
In these cases, the diagnosis of CS can only be established after the development of eye or inner ear disease [8]. The predominant ocular feature of CS is interstitial keratitis (IK), which typically causes eye redness, pain, photophobia, and blurred vision. On examination of patients with IK, an irregular, granular corneal infiltration is observed, affecting particularly the posterior part of the cornea, near the limbus. Ocular inflammation may involve other parts of the eye and lead to iridocyclitis, conjunctivitis, episcleritis, anterior or posterior scleritis, or retinal vasculitis [3, 8–10]. Most patients do not develop features of more widespread systemic vasculitis, with the exception of aortitis and aneurysm or aortic insufficiency, occurring in about 12% of patients [8].
Presentation CaseA 47-year-old female was hospitalized due to headache, vertigo, nausea, vomiting, right leg claudication, musculoskeletal pains, progressive bilateral hearing loss, and blindness for the past two months. On biomicroscopy, bilateral ciliary hyperemia, cataract, and interstitial keratitis with marginal infiltrates were noticed (Figure 1).
The fundus examination revealed mild hyperemia of both optic discs, with blurred borders, and no signs of vitreous or retinal inflammation. She tested negative for autoimmune tests (anti-nuclear antibody, anti-neutrophil cytoplasmic antibody rheumatoid factors, anti-phospholipid antibodies, complements, and cryoglobulins) and negative for syphilis serology tests (VDRL, FTA-Abs). Laboratory tests and cerebrospinal fluid (CSF) analysis were all negative for an infection (antibodies IgG and IgM against Epstein-Barr virus, herpes zoster virus, herpes simplex virus, Cytomegalovirus, chlamydia, hepatitis viruses B and C, HIV, Toxoplasma gondii, and Mycobacterium tuberculosis).
DiscussionCogan’s syndrome (CS) was first described in 1945 by an ophthalmologist, Dr. Cogan, who reported on a syndrome of nonsyphilitic interstitial keratitis (IK) and vestibuloauditory symptoms that resembled Meniere’s disease [1]. In addition to the ocular and audiovestibular involvement, numerous systemic manifestations were reported in 1960 by Cody and Williams in patients with CS [12].
More than 200 cases of CS have been reported in the literature, despite being a rare condition that mostly affects Caucasian young adults [11, 13].In 1980, Haynes et al. In atypical CS, where the ocular manifestation is episcleritis, scleritis, iritis, uveitis, or chorioretinitis rather than interstitial keratitis, there is a worse prognosis and a higher frequency of aortic and other systemic manifestations [11].Recurrent episodes of inner ear disease frequently result in profound hearing loss.
In a retrospective series of 60 patients from one center, hearing loss was typically sudden, bilateral, fluctuating, and progressive, resulting in complete hearing loss in 73 of 120 ears [8]. Two smaller studies both found bilateral deafness in approximately two-thirds of patients [2, 3].
Typically, audiometry testing demonstrates a sensorineural hearing loss, preferentially involving the low and high range frequencies; poor speech discrimination is also observed.
In one preliminary study, at least 30 percent of patients had a pure tone audiometry threshold of greater than or equal to 60 dB, a threshold value indicative of moderately severe hearing loss [4].
Hearing loss is often bilateral from onset but in some patients it may be unilateral initially, becoming bilateral later. Aortitis, which may develop within weeks to years of disease onset, has been described in approximately 10 percent of patients [2, 3, 11].
It may cause proximal aorta dilation, aortic valvular regurgitation, ostial coronary artery disease, and thoracoabdominal aortic aneurysms [11, 14–18]. A small- or medium-sized vessel arteritis has been described in some cases [23].Nonspecific systemic manifestations of CS include fever, fatigue, weight loss, lymphadenopathy, hepatomegaly, hepatitis, splenomegaly, pulmonary nodules, pericarditis, abdominal pain, arthralgia, arthritis, myalgia, and urticaria [4, 8, 10, 11]. Driscoll, “Cogan syndrome: a retrospective review of 60 patients throughout a half century,” Mayo Clinic Proceedings, vol. Systemic corticosteroids are always the most widely used and successful therapy in Cogan’s syndrome.
For patients requiring high and prolonged doses, additional immunosuppression is appropriate. However, patients without systemic disease or severe eye disease unmanageable by topical corticosteroids should not be subjected to protracted courses of corticosteroids or immunosuppressive agents, particularly when little gain in hearing is obtained with their use [19]. Infliximab might be an alternative therapy in cases of failure of corticosteroids and immunosuppressive therapy [28, 29]. However, treatment might be more effective when started at an early stage of the disease, when the lesions are still reversible.
Surgical bypass grafting or aortic valve replacement may be required in some patients [20].4.
ConclusionOur case report of CS demonstrates objective, simultaneous deterioration of hearing and vestibular function, which partially improved and stabilized after the introduction of immunosuppressive medication. The diagnosis of CS is largely based on clinical features, supported by the histologic abnormalities and exclusion of other conditions. Tatoulis, “Cogan's syndrome with aortitis, aortic regurgitation, and aortic arch vessel stenoses,” Annals of Thoracic Surgery, vol. Heublein, “A case of coronary stenosis developing after successful aortic valve repair in Cogan's syndrome,” Thoracic and Cardiovascular Surgeon, vol.
Brewster, “Thoracoabdominal aortic aneurysm in Cogan's syndrome,” Journal of Vascular Surgery, vol.
Haynes, “Use of immunosuppressive agents in the treatment of severe ocular and vascular manifestations of Cogan's syndrome,” The American Journal of Medicine, vol. Walshe, “Renal artery stenosis complicating Cogan's syndrome,” Clinical Nephrology, vol. Vollertsen, “Vasculitis and Cogan's syndrome,” Rheumatic Disease Clinics of North America, vol. Ford, “Ulcerative colitis and giant cell arteritis associated with sensorineural deafness,” Journal of Laryngology and Otology, vol. Berrettini, “Efficacy of methotrexate in Cogan's syndrome,” Journal of Rheumatology, vol.



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