Two categories based on whether observer can hear the tinnitus (objective) or not (subjective).

  • Objective—much less common than subjective

    1. Vascular—typically corresponds to pulse (aka, pulse synchronous tinnitus); may be venous, arterial, or combination (arteriovenous) source or secondary to high-output cardiac state, tumors, other; (pulse synchronous tinnitus may be subjective also)

      • Pathogenesis:

        • – Venous sources

          • Jugular bulb: high riding and large, turbulent flow, dehiscent jugular plate at level of middle ear

          • Sigmoid sinus: diverticulum, turbulent flow, dehiscent sigmoid plate

          • Other venous structures: aberrant condylar vein, superior petrosal sinus, inferior petrosal sinus; aberrant vein contacting labyrinthine structures

        • – Arterial sources

          • Carotid artery: cervical carotid dissection, aneurysm, or stenosis; aberrant carotid artery; carotid body tumor; dehiscent carotid plate within the middle ear

          • Persistent stapedial artery: derived from internal carotid artery, passes through obturator foramen of stapes superstructure

        • – Arteriovenous (AV) malformations and dural AV fistulas

          • May be associated with venous drainage leading to enlarged cortical veins (high rate of bleeding)

          • Often associated with sigmoid/transverse sinus and prior craniotomy

        • – Tumors

          • Paraganglioma, middle ear adenoma, choristoma, facial nerve neuroma, hemangioma

          • Any tumor (or encephalocele) contacting the ossicular chain or TM may lead to pulse synchronous tinnitus (subjective or objective)

        • – High cardiac output states: anemia, thyrotoxicosis, pregnancy, beriberi, etc.

      • Diagnosis: Auscultation with stethoscope, Toynbee tube, palpation of peri-auricular tissue

        • – CT angiography

        • – Magnetic resonance angiography (MRA)/magnetic resonance venography (MRV)

        • – Formal cerebral angiography (small risk of stroke)

      • Treatment: based on etiology and severity of symptoms

        • – Selective embolization, surgical resection/clipping, and radiosurgery are options for dural AV fistulas and malformations.

        • – Surgical excision or combination of surgery and radiosurgery may be used for tumors.

        • – High output states should be medically corrected.

        • – Anatomic vascular abnormalities may or may not be amenable to intervention.

    2. Nonvascular—typically presents as clicking sensation

      • Palatal myoclonus—rapid (50-200 beats/min) irregular clicking caused by eustachian tube opening and closing from palatal musculature contraction.

        • – Symptoms often worse during times of stress

        • – Diagnosed by prolonged tympanogram showing movement with palatal contraction; may visualize palate with nasopharyngoscope as well; Toynbee tube may be used to auscultate rhythmic sound

        • – Treated with muscle relaxants or botox in refractory cases

        • – Often associated with central nervous system disease; MRI of posterior fossa should be performed to assess

      • Stapedial or tensor tympani muscle spasm

        • – Can be heard as clicking or crackling noise

        • – Diagnosis similar to above, but without observed palatal muscle contractions

        • – Treated with muscle relaxants or sectioning of tendons if refractory

      • Patulous eustachian tube—symptoms worsen with respiration and are often described as roaring sensation; autophony

        • – Can be diagnosed by TM movement with respiration, but not always visualized. Prolonged tympanometry may also be helpful

        • – Placement of head in dependent position for relief of symptoms

      • May be associated with temporomandibular joint disorders, normal swallowing that leads to TM movement (latter may be heard as single click with Toynbee tube)

  • Subjective

    1. Incidence: 10% of population

    2. Can arise due to numerous conditions, many of which are poorly understood

    3. Most commonly occurs secondary to hearing loss

      • Presbycusis, noise-induced hearing loss, acoustic neuroma, and Meniere disease are common associated problems

    4. Most pharmacologic agents that induce tinnitus are reversible

      • Partial list includes aspirin, aminoglycosides, loop diuretics, caffeine, and alcohol

    5. Characteristics:

      • Buzzing, clicking, humming, chirping or hissing type sounds are commonly described.

      • Roaring quality may be associated with Meniere disease.

      • Pulsatile or pulse-synchronous sounds may be described, despite not being audible to observer.

        • – Encephalocele against ossicles may cause pulsatile tinnitus

        • – Idiopathic intracranial hypertension

          • Common in obese, middle-aged females

          • Associated visual disturbances and headache

      • Sounds may be intermittent or continuous

        • – SBUTT: Sudden, brief, unilateral, tapering tinnitus; common in normal individuals

    6. Pathogenesis

      • Most likely occurs due to functional abnormalities of the auditory portion of the central nervous system (CNS)

      • Neural plasticity may cause reorganization in the auditory nuclei in response to a more peripheral event. This may then induce a hyperactive state causing tinnitus. Possible peripheral events include

        • – Decreased or abnormal peripheral input (hair cell loss, etc.).

        • – A pathological insult may lead to decreased or abnormal spontaneous time pattern firing of auditory nerve fiber

          • This may be the cause in cases of nerve compression in acoustic neuromas and vascular loops

      • Other CNS centers likely play a role in the perception of tinnitus

        • – Cranial nerve centers (trigeminal) influence the auditory system.

        • – Amygdala, the limbic system, and other centers dealing with emotion may play a role as well.

        • – May explain why some individuals with normal audiograms may develop tinnitus.

    7. Diagnosis

      • Complete history to evaluate for potential sources of trauma, ototoxicity, noise exposure, etc.

      • Otomicroscopy to evaluate the ear canal, tympanic membrane, and middle ear space

        • – Debris, wax, hair, foreign body, other materials may cause tinnitus.

      • Standard audiometric testing should be done to evaluate hearing thresholds and word recognition scores.

      • Otoacoustic emission testing may be performed to document outer hair cell function.

      • Tinnitus matching may be performed in contralateral ear to characterize frequency and volume of tinnitus.

        • – No correlation between tinnitus characteristics and patient aggravation level.

        • – Approximately 50% of patients studied have tinnitus amplitude of 5 dB.

      • If vascular etiology is considered, work up as above.

    8. Treatment

      • Avoidance of noise/medication/other source of potential injury.

      • Counseling patients plays a major role in tinnitus treatment.

        • – Patients should be screened for anxiety and depression as these often exacerbate tinnitus symptoms.

        • – All medications should be reviewed.

        • – Dietary triggers such as high-salt diet, alcohol intake, and caffeine should be discussed.

      • Over time, approximately 25% of patients have near symptom resolution, 50% report significant improvement, and 25% remain stable.

      • Bedside masking (whether actual masking device versus fan or radio between stations) should be used in those bothered by bedtime symptoms.

      • Hearing aid—first line of treatment in patients with associated hearing loss.

        • – Return of previously lost sounds may mask tinnitus.

        • – If tinnitus refractory, can use masking device (or tinnitus instrument) in hearing aids.

          • Creates sound stimulus in hopes of masking tinnitus

          • Can also be used independent of hearing aids

        • – Use of masking device in hearing aid increases likelihood of tinnitus control from 25% to 55%.

      • Tinnitus retraining therapy—combination of counseling and broadband sound exposure habituate patient to tinnitus.

        • – Patients are exposed to 16 hours of broad-band noise per day.

        • – Noise is initially presented low but slowly increased to a level where the tinnitus is just still audible to the patient.

        • – Ideally over a year a patient will either no longer hear tinnitus or be undisturbed by it.

      • Biofeedback therapy—requires patient cooperation in undergoing therapy with psychologist

        • – Uses various triggers such as increased temperature or pulse for patient to recognize increased focus on tinnitus. Using these triggers patients can learn to focus attention away from tinnitus.

        • – Significant overlap with stress reduction.

      • Neuromodulators—special auditory devices that deliver a combination of tones, music, and other sounds, based on a patient’s unique tinnitus characteristics, in an effort to effect change in auditory neural pathways

      • Transcranial magnetic stimulation—repetitive treatments, designed to alter perception of tinnitus; still investigational with little supportive data in terms of efficacy

      • Cochlear implant placement—unilateral placement is being offered in some centers for disabling tinnitus; in conjunction with single-sided deafness, may represent emerging treatment option; still investigational with limited data

      • Medication

        • – Treatment of underlying anxiety and depression can help patients contend with tinnitus

        • – Various supplements, such as melatonin, lipoflavinoids, niacin, among others, have been suggested for tinnitus treatment

        • – Psychotropic medications, including low-dose anti-depressants, antianxiety medications, selective serotonin reuptake inhibitors (SSRIs), and benzodiazepines, have also been used for tinnitus treatment

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Apr 30, 2020 | Posted by in OTOLARYNGOLOGY | Comments Off on Tinnitus

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