Tinnitus

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2] Sabeeh Islam, MBBS[3]

Overview

Tinnitus is derived from the Latin word tinnire, meaning to ring. Tinnitus can be classified as subjective and objective.  This classification not only explains the underlying etiology but also directs the management of tinnitus. In the normal functioning auditory pathway, there is ordered tonotopic frequency mapping from the cochlea to the auditory cortex via midbrain.  Conditions associated with cochlear damage result in altered tonotopic organization and ultimately tinnitus. The pathophysiology of tinnitus can be explained by the tinnitus model. Common causes of tinnitus include Ototoxicity, Presbycusis, noise induced hearing loss, late onset congenital hearing loss, meniere's disease, and Loop diuretics. The incidence rate of tinnitus increases with age and is more prevalent in older people. Tinnitus is more prevalent in men compared to women and smokers compared to non-smokers. If left untreated, patients may progress to functional impairment, insomnia, anxiety, and depression. TSI is used to rank the patient's based upon their severity. The score ranges from 0-45. Symptoms and history include sounds such as ringing, buzzing, pulsatile, roaring and humming and progressive hearing loss. An extensive neurological examination may rule out underlying brainstem damage or hearing loss. The Weber and Rinne test are done to establish sensorineural or conductive hearing loss. They are usually abnormal. MRI with contrast is followed by CT/CTA and ultimately interventional angiography, if needed. Initial audiometric tests are done to identify asymmetries between the ears and to locate the site of abnormality such as middle ear, cochlea, and brainstem.  These tests include: pure-tone audiogram, tympanometry, auditory reflex testing, determination of speech discrimination abilities, otoacoustic emissions testing and auditory brainstem response testing (ABR). Tinnitus is a symptom and not a disease itself.  It is a chronic condition that can be managed by treating the underlying etiology. The treatment of tinnitus is usually directed towards improvement in the quality of life by decreasing awareness or desensitizing towards tinnitus.  It is usually achieved by identifying the underlying pathology or the associated disease. It is recommended to treat underlying insomnia and depression (Grade 1B). Cochlear implants may be considered for tinnitus associated with severe sensorineural hearing loss. Other therapies include: tinnitus retraining therapy (TRT) (Grade 1C), biofeedback (Grade 2C), and cognitive behavioral therapy (CBT) as an adjunct to TRT (Grade 2C). Acupuncture and electrical stimulation are considered equally effective as placebo, no significant role established so far.


Historical Perspective

  • In the early 19th century, Frenchman and Jean Marie Gaspard Itard introduced the concept of masking.  They were the first ones to differentiate between subjective and objective tinnitus.
  • Later in the 19th Century, with the introduction of germ theory and anesthesia, surgical therapy such as incudectomy was established.
  • Tinnitus is derived from the Latin word tinnire, meaning to ring.

Classification

Tinnitus can be classified as subjective and objective.  This classification not only explains the underlying etiology but also directs the management of tinnitus.

Subjective tinnitus:

  • It is only experienced by the affected individual in the absence of any auditory stimulation
  • More common, usually described as continuous ringing, high pitch sound

Objective tinnitus:

Pathophysiology

In the normal functioning auditory pathway, there is ordered tonotopic frequency mapping from the cochlea to the auditory cortex via midbrain.[1][2]  Conditions associated with cochlear damage result in altered tonotopic organization and ultimately tinnitus. The pathophysiology of tinnitus can be explained by the tinnitus model.[3][4]

Lesion projection zone (LPZ):

This zone is defined as the area in the auditory cortex that represents the damaged cochlear input.  The neurons in the LPZ zone show 2 main changes:

  • Accelerated spontaneous firing rate
  • Increased representation of neurons that represent the damaged cochlear region also known as lesion edge frequencies in the LPZ

Tinnitus model:

This model explains 2 major phenomena in the auditory cortex caused by lack of sensory peripheral auditory input (cochlea)

  • Hyperactivity in the lesion projections zone (LPZ)
  • Increased cortical representation of the lesion-edge frequencies in the LPZ

Causes of subjective tinnitus

Sensorineural hearing loss:

Cochlear injury:

Vascular causes:

CNS causes:

Infections:

Bone disease:

Metabolic disorders:

Autoimmune diseases:

Medications:

Differential Diagnosis of Tinnitus

Diseases Clinical manifestations Para-clinical findings Gold standard Additional findings
Symptoms Physical examination
Lab Findings Imaging
Acute onset Recurrency Nystagmus Hearing problems, tinnitus
Peripheral
HSV oticus
+ +/− +/− + VZV antibody titres
Meniere disease
+/− + +/− + (Progressive)
Labyrinthine concussion
+ +
Perilymphatic fistula
+/− + +
  • CT scan may show fluid around the round window recess
Semicircular canal

dehiscence syndrome

+/− + +

(air-bone gaps on audiometry)

Cogan syndrome
+ +/− + Increased ESR and cryoglobulins
  • CT scan may show calcification or soft tissue attenuation obliterating the intralabyrinthine fluid spaces
Vestibular schwannoma
+ +/− +
Otitis media
+ +/− Increased acute phase reactants
Aminoglycoside toxicity
+ +
Central
Vestibular migraine
+ +/− +/−
  • ICHD-3 criteria
Multiple sclerosis
+ +/− +/− Elevated concentration of CSF oligoclonal bands
  • CT scan shows brain atrophy and contrast enhanced demyelinating plaques
  • MRI showing cerebral plaques disseminating in time and space.
  • MS is twice as prevalent in women as compared to men
  • The onset of symptoms is mostly between the age of fifteen to forty years and rarely before the age of fifteen or after the age of sixty years
Brain tumors
+/− + + + Cerebral spinal fluid (CSF) may show cancerous cells
  • On CT scan most of the brain tumors appears as a hypodense mass lesions
  • On T1- weighted MRI most of the brain tumors appears as a hypointense or Isointense whereas on T2-weighted MRI they appear as hyperintense lesions
Cerebellar infarction/hemorrhage + ++/− +/−
  • Based on the time interval lapsed between the onset of stroke and imaging performed there may be different presentations
Brain stem ischemia + +/− +/−
  • Based on the time interval lapsed between the onset of stroke and imaging performed there may be different presentations
  • For more information click here

ABBREVIATIONS

VZV= Varicella zoster virus, MRI= Magnetic resonance imaging, ESR= Erythrocyte sedimentation rate, EEG= Electroencephalogram, CSF= Cerebrospinal fluid, GPe= Globus pallidus externa, ICHD= International Classification of Headache Disorders

Epidemiology and Demographics

  • Tinnitus affects 10 to 15% of the population.
  • 85% of the population presenting with ear symptoms/disorders report tinnitus as an associated symptom.[7]
  • The incidence rate of tinnitus increases with age and is more prevalent in older people.[8]
  • Tinnitus is more prevalent in men compared to women and smokers compared to non-smokers.[9][10]

Risk Factors

Natural History, Complications and Prognosis

  • Early clinical features may include ear fullness, huming or ringing sensations in the ear
  • If left untreated, patients may progress to functional impairment, insomnia, anxiety, and depression.[11]

Diagnosis

Diagnostic criteria:

Tinnitus severity index (TSI)

  • TSI is used to rank the patient's based upon their severity
  • The score ranges from 0-45

Tinnitus handicap questionnaire:

  • This questionnaire includes 27 questions and is used to estimate the social, physical and emotional handicap severity

Tinnitus handicap inventory:

  • This questionnaire has 4 categories to classify severity
  • None, mild,  moderate, and severe.

History and Symptoms:

  • Sounds such as ringing, buzzing, pulsatile, roaring and humming
  • Progressive hearing loss
  • Recent exposure to excessive or loud noise or head trauma
  • Poor hygiene leading to cerumen impaction
  • Ear pain
  • History of certain medication exposure

Physical Examination:

  • The ear examination may show signs of cerumen impaction, underlying infection or tympanic membrane perforation.
  • Auscultation of neck, orbits and periauricular areas as helpful in establishing the diagnosis of vascular causes
  • An extensive neurological examination may rule out underlying brainstem damage or hearing loss
  • The Weber and Rinne test are done to establish sensorineural or conductive hearing loss. They are usually abnormal.

Laboratory Findings:

  • There are no specific lab findings associated with tinnitis.

Imaging:

  • MRA and CTA are the gold standard diagnostic tests for arteriovenous fistula related tinnitus.
  • MRI with contrast is the initial preferred diagnostic test of choice for suspected vascular tinnitus.
  • MRI with contrast is followed by CT/CTA and ultimately interventional angiography, if needed.[12]

Other Diagnostic Testing:

  • Initial audiometric tests[13] are done to identify asymmetries between the ears and to locate the site of abnormality such as middle ear, cochlea, and brainstem.  These tests include:
    • Pure-tone audiogram
    • Tympanometry
    • Auditory reflex testing
    • Determination of speech discrimination abilities
    • Otoacoustic emissions testing
    • Auditory brainstem response testing (ABR)

Treatment

  • Tinnitus is a symptom and not a disease itself.  It is a chronic condition that can be managed by treating the underlying etiology.
  • The treatment of tinnitus is usually directed towards improvement in the quality of life by decreasing awareness or desensitizing towards tinnitus.  It is usually achieved by identifying the underlying pathology or the associated disease.
  • It is recommended to treat underlying insomnia and depression. (Grade 1B)

Medical Therapy

Following medications have minimal to modest role in relieving tinnitus.

Following medications have been studied for tinnitus but are not found to be effective and have no role in the treatment of tinnitus

Surgery

Other therapies:

Prevention

  • Tinnitus may be been prevented by limiting the exposure to loud noise.

References

  1. Minen MT, Camprodon J, Nehme R, Chemali Z (October 2014). "The neuropsychiatry of tinnitus: a circuit-based approach to the causes and treatments available". J. Neurol. Neurosurg. Psychiatry. 85 (10): 1138–44. doi:10.1136/jnnp-2013-307339. PMID 24744443.
  2. Qiu C, Salvi R, Ding D, Burkard R (January 2000). "Inner hair cell loss leads to enhanced response amplitudes in auditory cortex of unanesthetized chinchillas: evidence for increased system gain". Hear. Res. 139 (1–2): 153–71. doi:10.1016/s0378-5955(99)00171-9. PMID 10601720.
  3. Melcher JR, Sigalovsky IS, Guinan JJ, Levine RA (February 2000). "Lateralized tinnitus studied with functional magnetic resonance imaging: abnormal inferior colliculus activation". J. Neurophysiol. 83 (2): 1058–72. doi:10.1152/jn.2000.83.2.1058. PMID 10669517.
  4. Lockwood AH, Salvi RJ, Coad ML, Towsley ML, Wack DS, Murphy BW (January 1998). "The functional neuroanatomy of tinnitus: evidence for limbic system links and neural plasticity". Neurology. 50 (1): 114–20. doi:10.1212/wnl.50.1.114. PMID 9443467.
  5. Fortune DS, Haynes DS, Hall JW (January 1999). "Tinnitus. Current evaluation and management". Med. Clin. North Am. 83 (1): 153–62, x. doi:10.1016/s0025-7125(05)70094-8. PMID 9927967.
  6. Levine RA (1999). "Somatic (craniocervical) tinnitus and the dorsal cochlear nucleus hypothesis". Am J Otolaryngol. 20 (6): 351–62. doi:10.1016/s0196-0709(99)90074-1. PMID 10609479.
  7. Shargorodsky J, Curhan GC, Farwell WR (August 2010). "Prevalence and characteristics of tinnitus among US adults". Am. J. Med. 123 (8): 711–8. doi:10.1016/j.amjmed.2010.02.015. PMID 20670725.
  8. Shetye A, Kennedy V (August 2010). "Tinnitus in children: an uncommon symptom?". Arch. Dis. Child. 95 (8): 645–8. doi:10.1136/adc.2009.168252. PMID 20371585.
  9. Adams PF, Hendershot GE, Marano MA (October 1999). "Current estimates from the National Health Interview Survey, 1996". Vital Health Stat 10 (200): 1–203. PMID 15782448.
  10. Ahmad N, Seidman M (2004). "Tinnitus in the older adult: epidemiology, pathophysiology and treatment options". Drugs Aging. 21 (5): 297–305. doi:10.2165/00002512-200421050-00002. PMID 15040757.
  11. Stouffer JL, Tyler RS (August 1990). "Characterization of tinnitus by tinnitus patients". J Speech Hear Disord. 55 (3): 439–53. doi:10.1044/jshd.5503.439. PMID 2381186.
  12. Dietz RR, Davis WL, Harnsberger HR, Jacobs JM, Blatter DD (May 1994). "MR imaging and MR angiography in the evaluation of pulsatile tinnitus". AJNR Am J Neuroradiol. 15 (5): 879–89. PMID 8059655.
  13. Tunkel DE, Bauer CA, Sun GH, Rosenfeld RM, Chandrasekhar SS, Cunningham ER, Archer SM, Blakley BW, Carter JM, Granieri EC, Henry JA, Hollingsworth D, Khan FA, Mitchell S, Monfared A, Newman CW, Omole FS, Phillips CD, Robinson SK, Taw MB, Tyler RS, Waguespack R, Whamond EJ (October 2014). "Clinical practice guideline: tinnitus executive summary". Otolaryngol Head Neck Surg. 151 (4): 533–41. doi:10.1177/0194599814547475. PMID 25274374.

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