Specialist ENT TINNITUS

TINNITUS

Definition: Tinnitus is defined as a sound perceived more than five minutes at a time in the absence of any external acoustic or electrical stimulus to the ear and not occurring immediately after exposure to loud noise, phantom auditory perception, or head noise. Types: There are two types of tinnitus- Subjective tinnitus– Here tinnitus audible only to the patient. May be due to sensorineural hearing loss due to any cause. Objective tinnitus– Here tinnitus audible not only to patient, but also to the examiner. It usually caused by arteriovenous malformations, glomus tumors, palatal or tympanic myoclonus. Aetiology: I. Vascular somatosounds– Vascular lesions, either arterial or venous, can produce turbulent blood flow, leading to pulsatile somatosounds. They include: a) Vascular tumors- Glomus tympanicum or jugular, Hemangioma. b) Vascular malformations- Arteriovenous malformations, aneurysms, fistulae, carotid artery stenosis, transverse sinus stenosis. c) Increased intracranial pressure- venous hum. d) Transmitted cardiac murmurs. e) Different hyperdynamic vascular states- pregnancy, hyperthyroidism, anaemia. II. Myogenic somatosounds- The most common forms are palatal and less common middle ear muscles, tensor tympani and stapedial myoclonus. III. Patulous eustachian tube- It leads to to-and-fro movements of the tympanic membrane, synchronous with nasal respiration which can be perceived as ‘blowing’ sound or their own voice reverberation. IV. Temporomandibular joint abnormalityIt causes audible vibratory sound arising from jaw clenching. V. Spontaneous otoacoustic emissions can be the reason of tinnitus.
Pathophysiology of Tinnitus: The auditory system consists of two pathways:
  1. Afferent pathway-This provides input to the proximal structure of auditory system. This is predominantly excitatory.  
  2. Efferent pathway-This modulates acoustic information. It is predominantly inhibitory.

Any pathological alteration at any one level may have functional consequence at the other levels of the auditory system. Tinnitus is the consequence of the aberrant spontaneous neuronal activity within the auditory system. It can be due to lesion or dysfunction at the level of cochlea to the uppermost level of the auditory system. Tinnitus related neuronal activity triggers feedback mechanism in order to balance between excitation and inhibition and preserve the homeostasis.

Tinnitus is characterized by process of habituation, so in most cases the tinnitus gradually attenuates. However, some fail to adopt to habituation leading to persistent tinnitus.

Mechanism of Tinnitus:
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Mechanical tinnitus based on spontaneous cochlear (OHC) oscillations
Specialist ENT Screenshot 2020 11 20 Ear final book document
Mechanism of tinnitus by Glutamate: 1.Glutamate is a potent excitatory and highly neurotoxic on cochlear afferent. It is released at inner hair cell synaptic region.
Specialist ENT Screenshot 2020 11 20 Ear final book document
2. Glutamate receptor (NMDA   N-Methyl-D-aspartate) can be selectively blocked by antagonist caroverine resulting in reduced tinnitus. Mechanism of tinnitus by NMDA, Non-NMDA receptor modulation:
  1. Lateral olivocochlear efferent release endogenous opoid (Dysnorphins) in response to stress, at the inner hair cell synaptic region. This increases the sensitivity of Glutamate receptors (NMDA and Non-NMDA receptors) resulting in Stress induced tinnitus.
  2. Dopamine agonist (Piribedil) decreases the sensitivity of NMDA and Non-NMDA receptors resulting in reduced tinnitus.
Mechanism of tinnitus by abnormal calcium ion channel conductance:
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Nimodipine (L-type calcium channel blocker) reduce the sensitivity of calcium channel results in reduced tinnitus. Mechanism of tinnitus due to abnormal Peripheral and Central Auditory activation:
  1. Irritative central lesions like tumors, vascular loop, stimulate tinnitus.
  2. Treatment by antiepileptics reduces tinnitus.
  3. Peripheral activation of somatosensory, somatomotor and visual motor system stimulates activation of extralemniscal polysensory pathway, resulting in tinnitus. Patient have a gaze evoked tinnitus, jaw clinching, electrical stimulation of median nerve.
Mechanism of tinnitus due to efferent dysfunction or reduction of GABA effect: Noise trauma, ototoxicity, ageing results in downregulation of inhibitory activity of GABA on neurotransmitter receptor in central auditory pathway (mostly at cochlear nucleus and inferior colliculus), resulting in increased damage to the auditory system, expressed in form of tinnitus. Mechanism of spontaneous activity and tonotopic reorganization:
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Treatment with hearing aids and cochlear implant will establish the afferent input, thus reducing tinnitus. Tinnitus due to Stress and Psychological disorder:
  1. Stress results in increase in Catecholamines (adrenalin and nor adrenalin) by stimulating synaptic adrenocortical system.
  2. Stress results in increase glucocorticoids (cortisol) by stimulating hypothalamopituitory- adrenocortical system. Increased level of cortisol is related to tinnitus.
  3. Lateral olivocochlear efferent release endogenous opoid (Dysnorphins) in response to stress, at the inner hair cell synaptic region. This increases the sensitivity of Glutamate receptors (NMDA and Non-NMDA receptors) resulting in Stress induced tinnitus.
  4. Dopamine agonist (Piribedil) decreases the sensitivity of NMDA and Non-NMDA receptors resulting in reduced tinnitus.
Diagnosis and Treatment:
Specialist ENT Screenshot 2020 11 20 Ear final book document
Specialist ENT Screenshot 2020 11 20 Ear final book document
  1. Treatment of underlying disorders– In the majority of cases of pulsatile tinnitus underlying pathology can be identified thus allowing a direct treatment of the underlying cause.
  2. Surgical treatment of tinnitus– auditory nerve section, or cochlear destruction, have provided little evidence of effectiveness and may even make tinnitus worse.
  3. Tinnitus retraining therapy– The TRT implements a habituation-based protocol which includes sound therapy and cognitive-behavioral techniques (CBT).
  4. Instrumentations-a. Hearing aids are the first line in management for patients with tinnitus and hearing loss. Hearing aids may reduce awareness of tinnitus by amplification of external sounds.b. Cochlear implants in patients with profound hearing loss have been found useful in abolishing/reducing tinnitus in a significant number of cases.
  5. Noise generators– Sound therapy is currently an essential part of treatment of tinnitus. Tinnitus maskers are wearable behind-the ear or in the-ear devices, used for presentation of sounds in a controlled manner in order to reduce or eliminate the perception of tinnitus.
  6. Pharmacological treatments– pharmacological treatment has a limited contribution to the treatment of tinnitus. Pharmacological treatment on hypothetical underlying mechanisms includes:a) Antidepressants like Tricyclic antidepressants, nortriptyline and amitriptyline.

    b) GABA analogues- GABA A (benzodiazepines and gabapentin) and GABA B (baclofen) analogues.

    c) Ca ++ channel antagonists like Nimodipine, Flunarizine.

    d) Antiepileptics like Carbamazepine.

    e) Selective glutamate receptor antagonist like Caroverine.

    f) Prostaglandin analogues. Prostaglandins act as neuromodulators of the afferent pathway within the cochlea.

    g) Lidocaine- Lidocaine is one of the most intriguing drugs used in controlling tinnitus and, probably, the most effective one. Lidocaine is known to be a sodium channel blocker which operates most efficiently in nerves with the high discharge rates, through its capacity to reduce the maximum firing rate of the nerve. The trans-tympanic application has been reported to be successful with less systemic side effect.

  7. Supplementary treatments include electrical or magnetic stimulation, Ginkgo biloba, Vitamin B12, acupuncture or zinc.

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