Transcript Tinnitus - The Medical Post
Tinnitus Aurium
Dr. Vishal Sharma
History
“ Bewitched ear ” in Ebers papyrus (3000 BC)
Tinnire (to ring) used by Pliny Elder, 23-79 AD
Joseph Toynbee died in 1866 due to chloroform + prussic acid vapour inhalation as tx for tinnitus
Fowler (1941): performed frequency matching, loudness matching & tinnitus masking
Definition
Conscious experience of a sound that originates in an involuntary manner in owner’s head with no corresponding external acoustic or electrical stimulus ( McFadden, 1982 )
Must persist for > 5 min at a time (Scott-Brown)
Due to aberrant spontaneous activity arising from altered state of excitation or inhibition within auditory system
Incidence
6 - 17 % of people experience tinnitus
3 - 7 % of people seek help for their tinnitus
0.5 - 2.5 % report severe effects of tinnitus
Tinnitus present in: deafness (60-85%), sudden SNHL (50%), NIHL (50-90%), presbyacusis (70%), acoustic neuroma (70%), Meniere’s attack (100%)
Subjective vs. Objective tinnitus
Subjective (true) tinnitus: heard by patient only
Etiology = otological & non-otological
Objective (pseudo) tinnitus or somato-sounds: heard by patient & examiner with stethoscope
Etiology = vascular & non-vascular
Other associated Dysacusis
Hyperacusis = hypersensitivity to sound due to increased abnormal gain within auditory system
Phonophobia or Misophonia = hypersensitivity + fear toward sound stimulus due to abnormal excitation of limbic & autonomic nervous system
Otological subjective tinnitus
Conductive causes
Impacted wax
Impacted foreign body
Otitis externa
Otitis media
Otosclerosis Cochlear causes
Presbyacusis
Noise induced
Meniere’s disease
Ototoxicity
Temporal bone trauma
Labyrinthitis
Otological subjective tinnitus
Retro-cochlear causes
Acoustic neuroma
Other CPA lesions
Vascular compression of 8 th nerve Central causes
Multiple sclerosis
CVA
CNS tumors
Hydrocephalus
Non-Otologic Causes of Subjective Tinnitus
Temporo-mandibular joint disorders Cardiovascular:
anemia, hypertension, Hypotension
Metabolic:
hypoglycemia, hypothyroidism, hyperthyroidism, hyperlipidemia
Neurologic:
epilepsy, migraine, meningitis
Withdrawal:
alcohol, caffeine, anti-depressants, anti histamines
Psychogenic:
anxiety, depression
Vascular Causes of Objective Tinnitus
Arterio-venous shunts: congenital arterio-venous malformation, acquired AV shunt, carotico cavernous fistula Arterial bruits: aberrant ICA, aneurysm / stenosis of ICA, persistent stapedial artery Venous hum: dehiscent jugular bulb, Hypertension Paragangliomas: glomus jugulare / tympanicum
Objective Tinnitus (non-vascular causes)
Patulous Eustachian tube
Myoclonus: palatal, stapedial, tensor tympani
Clicking temporo-mandibular joint
Live foreign body in external auditory canal
Spontaneous oto-acoustic emissions
Models for Mechanisms of Tinnitus
Conductive tinnitus model
Lack of ambient noise masking leads to enhancement or revealing of:
Sensori-neural tinnitus
Non-otological subjective tinnitus
Somato-sounds or objective tinnitus
Cochlear tinnitus model
Cochlear pathology
abnormal spontaneous rate or rhythm of activity in cochlear nerve
Spontaneous oscillations of outer hair cells
Glutamate neuro-transmitter excito-toxicity
Enhanced sensitivity of receptors to glutamate & endogenous opioid peptides dynorphins
Neural Tinnitus Model
De-myelinization of cochlear nerve fibres
cross-talk b/w nerve fibres
distortion of resting state of discharge in nerve fibres
Lack of efferent auditory pathway inhibition (pathway dysfunction or GABA down regulation)
Calcium channel dysfunction
ed intracellular calcium
ed activity in cochlear nerve
Central tinnitus model
Abnormal central processing of peripheral neural activity mediated by neuro-transmitters glutamate, glycine & acetylcholine
Extra-lemniscal auditory activation by somato sensory, somato-motor & visual-motor systems
Tonotopic reorganization of auditory cortex
Trigger factors for tinnitus
Psychological stress (serotonin & adrenaline)
Noise exposure
Head injury, TM joint injury, neck injury
Ear syringing
Changes in atmospheric pressure
Surgical operations
Neuro-physiological model for tinnitus
Proposed by Pawel Jastreboff in 1990
Conditioned reflex loops
Conditioned reflex loops
CRL develop b/w limbic system, ANS, subcortical pathways & auditory cortex
Concern & fear toward tinnitus
negative reinforcement
make CRLs strong
Once strong CRLs develop, peripheral auditory signals not necessary for tinnitus perception
Role of tinnitus retraining therapy: break these CRLs by natural habituation
Points in favour of Neuro-physiological model
1. Significant damage to auditory system not required for tinnitus to develop as 30% pt with tinnitus have normal hearing 2. 30% pt with hearing loss don’t have tinnitus 3. Tinnitus associated with emotional distress, sleep problems, anxiety & negative emotions, suggesting involvement of limbic system & ANS
History taking in Tinnitus patient
Sleep disturbance / emotional upset
Pulsatile or persistent tinnitus
Does tinnitus get masked by ambient noise?
Deafness / vertigo / hyperacusis / phonophobia
Trauma: head / cervical spine / noise
Ototoxicity / withdrawal from drugs
Anxiety / depression
DM / HTN / thyroid disease / epilepsy / migraine
General Examination
Auscultation: for objective tinnitus
Pallor / hypertension / hypotension
Effect of neck turning on tinnitus
Effect of jugular vein compression on tinnitus
Temporo-mandibular joint mobility for clicks
E.N.T. examination
1. Otoscopy:
for EAC pathology
for spontaneous movement of T.M.
Synchronous with pulse: vascular somatosound
Synchronous with breathing: patulous E.T.
Synchronous with soft palate twitch: myoclonus 2. Tuning Fork Tests: conductive vs. SNHL
Investigations
Pure Tone Audiometry: to assess hearing threshold & rule out hyperacusis
S.I.S.I. & A.B.L.B.: for cochlear deafness
T.D.T.: for retro-cochlear deafness
Impedance audiometry: Rule out otosclerosis Large fluctuations in compliance with respiration = patulous Eustachian tube
Otoacoustic emissions: for cochlear function
B.E.R.A.: for retro-cochlear pathology
CT scan with contrast: for CPA & CNS tumours in unilateral tinnitus
Angiography: for vascular malformations, glomus tumours
Functional MRI & PET scan: tinnitus activates primary auditory (temporal) cortex, associative auditory (temporo-parietal) cortex, hippocampus, prefrontal-temporal network & limbic system
Psycho-acoustical measurement
Pitch or frequency matching of tinnitus
Loudness matching of tinnitus
Minimal masking level for tinnitus
Residual inhibition: temporary suppression or elimination of tinnitus following its masking
Other Investigations
CBP with ESR
Sugar profile: FBS, PPBS, RBS
Thyroid profile: T3, T4, TSH
Lipid profile: TG, LDL, HDL
Circulating auto-antibodies
Syphilis serology
Treatment Protocols
Prevention
Pathological conditions to be treated
Psychotherapy
Prosthetic:
H.A., C.I., T.R.T., tinnitus maskers (?)
Pharmacological (?)
Surgery (?)
Stimulation ?:
electrical, magnetic, electromagnetic
Others:
Ginkgo biloba ?, acupuncture ?, yoga ?
Prevention / Avoidance of:
Viral infections
Noise induced hearing loss
Ototoxic drugs
Chocolate, cheese, tea, coffee, red wine
Rapid withdrawal of addictive substances
Tx of causative factors
Impacted wax
Otitis media
Meniere’s disease
Anemia
Hypertension & hypotension
Diabetes mellitus & hypoglycemia
Hypothyroidism & hyperthyroidism
Psychotherapy
Cognitive behavioral therapy aims at removing negative emotions due to tinnitus perception ( cognitive therapy ) & modification of tinnitus motivated avoidance behavior ( behavior therapy )
Bio-feedback displays electro-myographic evidence of frontalis muscle tension due to tinnitus. Awareness helps in its removal.
Hearing aids & Cochlear Implants They help in pt with deafness + tinnitus by:
Reducing awareness of tinnitus by amplification of ambient sounds
Improved auditory input enhances central mechanism of habituation & promotes central adaptive plasticity
Tinnitus Maskers
Synonym: white noise generators
Complete masking: tinnitus becomes inaudible due to higher intensity of masking noise. Not used. Partial masking: provides low intensity background noise against which loudness of tinnitus gets reduced. Preferred technique.
Tinnitus masker + hearing aid = tinnitus instrument
Facts about tinnitus masking
total suppression (total masking) of tinnitus prevents tinnitus habituation
partial suppression (partial masking) does not prevent tinnitus habituation
activation of limbic & autonomic nervous systems by too loud or unpleasant sounds, enhances tinnitus & prevents habituation
Facts about tinnitus masking
low-level noise masking also enhances tinnitus ( stochastic resonance )
stochastic resonance range = 20 dB, beginning from –5 dB below threshold of tinnitus detection
Ideal masking intensity = b/w stochastic resonance & total masking called “ mixing point ”
Ideal masking intensity
Tinnitus characteristics
Conductive: low-pitch, masked at auditory threshold
Cochlear: high pitch (except Meniere’s disease), masked at auditory threshold
Retro-cochlear: high-pitch, masked well above auditory threshold
Central: high-pitch, resistant to masking
Based on
neuro-physiological model of tinnitus
Blocks tinnitus-related neuronal activity from reaching cerebral cortex (where it is perceived) & from activating
limbic & autonomic nervous systems
Uses combination of
low level, broad-band sound therapy & psychological counseling
to achieve
habituation of tinnitus
. Tinnitus never masked in TRT. Retraining takes
12 -18 months . Success rate = 80%
Conditioned reflex loops
Effect of habituation by TRT
Pharmacological Treatment
Anti-depressants:
Amitryptiline = 25 mg TID for 3 weeks
Fluoxetine = 20 mg BD for 3 weeks G.A.B.A. analogues:
Alprazolam = 0.25 – 0.5 mg OD
BD for 3 weeks
Clonazepam = 0.5 – 1.0 mg OD
BD for 3 weeks
Gabapentin = 300 mg OD
TID for 3 weeks
Baclofen = 10 mg BD
25 mg BD for 3 weeks
Calcium blocker: Nimodipine = 30 mg BD X 3 wk Glutamate blocker: Caroverine infusion Antiepileptics:
Carbamazepine = 100 mg BD
200 mg TID (3 wk)
Na Valproate = 200 mg TID
500 mg TID X 3 wk
Lamotrigine = 50 mg OD
100 mg BD X 3 wk Prostaglandin: Misoprostol = 200 μg QID X 3 wk Lignocaine: IV & trans-tympanic application
Surgical treatment
Surgical removal of vascular malformations
Surgical division of cochlear nerve
Micro-vascular decompression of anterior inferior cerebellar artery loop around auditory nerve Results of surgery for tx of tinnitus are poor & may actually worsen tinnitus
Stimulation of cochlea (?)
Electrical: by round window or cochlear implant
Magnetic: by magnet placed in E.A.C.
Electro-magnetic: increases blood flow Spontaneous OAE suppression (?)
Aspirin
Quinine
Treatment of Hyperacusis & Misophonia
Hyperacusis treatment
Attenuation of environmental sounds by ear plugs:
temporary solution only for anticipated NIHL. Persistent use enhances hyperacusis
Hyperacusis desensitization therapy:
using sound with higher frequencies removed (pink noise) give short exposures to moderately loud sound
Sound retraining therapy:
like TRT
Misophonia treatment: listening to music