INTRODUCTION
TINNITUS CAN ARISE IN ANY OF THE FOUR SECTIONS OF THE
HEARING SYSTEM:
THE OUTER EAR,
THE MIDDLE EAR,
THE INNER EAR,
THE BRAIN.
SOME TINNITUS OR "HEAD NOISE" IS NORMAL
A NUMBER OF TECHNIQUES AND TREATMENTS MAY BE OF HELP,
DEPENDING ON THE CAUSE.
TINNITUS
PERCEPTION OF SOUND WITHIN THE
HUMAN EAR IN ABSENCE OF
CORRESPONDING EXTERNAL SOUND
TYPES
 CLASSIFICATION 1:
 UNILATERAL
 BILATERAL
 CLASSIFICATION 2:
 SUBJECTIVE
 OBJECTIVE
 CLASSIFICATION 3:
 INTERMITTENT
 CONTINUOUS
 CLASSIFICATION 4:
 SLIGHT
 CATASTROPHIC
 CLASSIFICATION 5:
 VIBRATORY
 NON VIBRATORY
SUBJECTIVE TINNITUS: HEARD BY PATIENT ONLY.
OBJECTIVE TINNITUS: HEARD BY BOTH PATIENT & EXAMINER
INTERMITTENT TINNITUS: PRESENT SOMETIMES
CONTINUOUS TINNITUS: PRESENT CONTINUOUSLY
SLIGHT: NO INTERFERENCE WITH SLEEP, QUIET ACTIVITIES, AND NORMAL
DAILY ACTIVITIES.
CATASTROPHIC: INTERFERENCE WITH SLEEP, QUIET ACTIVITIES, AND
NORMAL DAILY ACTIVITIES
VIBRATORY TINNITUS: CAUSED BY TRANSMISSION TO THE COCHLEA OF
VIBRATIONS FROM ADJACENT TISSUES OR ORGANS.
NONVIBRATORY TINNITUS: PRODUCED BY BIOCHEMICAL CHANGES IN
THE NERVE MECHANISM OF HEARING.
COMMON CAUSES
 EAR:




EAR INFECTION
FB IN EAR
WAX IN EAR
INJURY FROM LOUD NOISES
 NOSE:
 NOSE ALLERGIES LEADING TO WAX BUILD UP IN EAR
 MEDICATIONS:
 ASPIRIN
 QUINIDINE ( CLASS IA ANTI ARRYTHMIC)
 OTHERS:
 LOW SEROTONIN LEVEL
 IDIOPATHIC
USUALLY DESCRIBED AS
"A RINGING NOISE”
BUT IN SOME PATIENTS IT TAKES THE FORM
OF







A HIGH PITCHED WHINING
BUZZING
HISSING
SCREAMING,
HUMMING
WHISTLING SOUND
TICKING
CLICKING
 ROARING
"CRICKETS" OR "TREE FROGS" OR “LOCUSTS”
 TUNES
 SONGS
 BEEPING
A "WOOSHING" SOUND (AS OF WIND OR WAVES)
DIAGNOSTIC APPROACH TO
TINNITUS
•
•
•
•
•
•
•
OTOLOGIC PROBLEMS, ESPECIALLY HEARING LOSS, ARE THE
MOST COMMON CAUSES OF SUBJECTIVE TINNITUS.
UNILATERAL HEARING LOSS PLUS TINNITUS SHOULD INCREASE
SUSPICION FOR ACOUSTIC NEUROMA.
SUBJECTIVE TINNITUS ALSO MAY BE CAUSED BY NEUROLOGIC,
METABOLIC, OR PSYCHOGENIC DISORDERS.
OBJECTIVE TINNITUS USUALLY IS CAUSED BY VASCULAR
ABNORMALITIES OF THE CAROTID ARTERY OR JUGULAR VENOUS
SYSTEMS.
INITIAL EVALUATION OF TINNITUS SHOULD INCLUDE A THOROUGH
HISTORY, HEAD AND NECK EXAMINATION, AND AUDIOMETRIC
TESTING TO IDENTIFY AN UNDERLYING ETIOLOGY.
UNILATERAL OR PULSATILE TINNITUS MAY BE CAUSED BY MORE
SERIOUS PATHOLOGY AND TYPICALLY MERITS SPECIALIZED
AUDIOMETRIC TESTING AND RADIOLOGIC STUDIES.
PEOPLE WITH SIMILAR PSYCHOACOUSTIC DESCRIPTIONS OF
TINNITUS DIFFER RADICALLY IN THEIR LEVEL OF ANNOYANCE AND
SENSE OF ITS IMPACT ON DAILY LIFE
SCREENING FOR EXPOSURE TO EXCESSIVE OR LOUD NOISES CAN BE
PERFORMED DURING ROUTINE HEALTH MAINTENANCE VISITS. CONTINUED
COUNSELING ABOUT THE RISK OF HEARING LOSS IS WARRANTED IF THE
PATIENT IS EXPOSED TO DAMAGING SOUNDS.
MENIERE'S DISEASE (EXCESSIVE ACCUMULATION OF ENDOLYMPH IN
THE MEMBRANOUS LABYRINTH) IS A DIAGNOSIS OF EXCLUSION THAT IS
CHARACTERIZED BY ONE OR MORE SYMPTOMS THAT INCLUDE
RECURRENT EPISODES OF VERTIGO, UNILATERAL AURAL FULLNESS,
TINNITUS, AND HEARING LOSS.TINNITUS CHARACTERISTICALLY AFFECTS A
PERSON IN TWO WAYS: BETWEEN ATTACKS IT IS A RINGING NOISE, WHILE
DURING AN ATTACK IT IS A ROARING NOISE. OVER TIME, THE HEARING
LOSS AND TINNITUS MAY BECOME PERMANENT OR ABATE.
ACOUSTIC NEUROMA, UNCOMMON, BENIGN TUMOR, ARISES FROM
SCHWANN CELLS COVERING VESTIBULAR BRANCH OF EIGHTH CRANIAL
NERVE. VESTIBULAR NERVE IS DESTROYED SO SLOWLY BY ACOUSTIC
NEUROMA THAT VESTIBULAR SYMPTOMS, SUCH AS DIZZINESS OR
VERTIGO, MAY BE MINIMAL OR TRANSIENT. THE FIRST SYMPTOM IS
USUALLY TINNITUS. TINNITUS MAY BE PRESENT FOR MONTHS OR YEARS
BEFORE HEARING LOSS OR VERTIGO IS NOTICED. THE TINNITUS IS
UNILATERAL IN 95 PERCENT OF CASES. IT IS CONTINUOUS AND LESS
DISTURBING THAN THE TINNITUS OF MENIERE'S DISEASE.
HISTORY
ONSET
COMMENTS
PROGRESSIVE HEARING LOSS WITH
TINNITUS & ADVANCING AGE
SUGGESTS PRESBYCUSIS.
PRECIPITOUS ONSET CAN BE
LINKED TO EXCESSIVE OR LOUD
NOISE EXPOSURE OR HEAD
TRAUMA.
LOCATION
UNILATERAL TINNITUS CAN BE
CAUSED BY CERUMEN IMPACTION,
OTITIS EXTERNA, AND OTITIS MEDIA.
TINNITUS WITH UNILATERAL
SENSORINEURAL HEARING LOSS IS
THE HALLMARK OF ACOUSTIC
NEUROMA.
PATTERN
CONTINUOUS TINNITUS
ACCOMPANIES HEARING LOSS.
EPISODIC TINNITUS SUGGESTS
MENIERE'S DISEASE. PULSATILE
TINNITUS SUGGESTS A VASCULAR
ORIGIN.
CHARACTERISTICS (I.E., PITCH,
COMPLEXITY)
LOW-PITCHED RUMBLING PATTERN
SUGGESTS MENIERE'S DISEASE,
HIGH-PITCHED PATTERN SUGGESTS
SENSORINEURAL HEARING LOSS
ASSOCIATED VERTIGO, AURAL
FULLNESS, HEARING LOSS
MENIERE'S DISEASE
EXPOSURE TO OTOTOXIC
MEDICATIONS/FACTORS
NOISE-INDUCED OR MEDICATIONINDUCED HEARING LOSS
EXACERBATING/ALLEVIATING
FACTORS
TINNITUS OF PATULOUS
EUSTACHIAN TUBE IS ALLEVIATED
BY LYING DOWN WITH HEAD IN
DEPENDENT POSITION.
HYPERLIPIDEMIA, THYROID
DISORDER, VITAMIN B12
DEFICIENCY, ANEMIA
CAN BE POTENTIAL CONTRIBUTING
CAUSES
PHYSICAL EXAMINATION
•
OTOLOGIC EXAMINATION-EXTERNAL CANAL AND TYMPANIC
MEMBRANE INSPECTED FOR SIGNS OF CERUMEN IMPACTION,
PERFORATION, OR INFECTION.
•
THE CRANIAL NERVES SHOULD BE EXAMINED FOR EVIDENCE OF
BRAIN-STEM DAMAGE OR HEARING LOSS.
•
AUSCULTATION OVER NECK, PERIAURICULAR AREA, ORBITS, AND
MASTOID SHOULD BE PERFORMED.
•
TINNITUS OF VENOUS ORIGIN CAN BE SUPPRESSED BY
COMPRESSION OF THE IPSILATERAL JUGULAR VEIN
SPECIFIC TESTING
•
•
•
•
•
•
FOR SENSORINEURAL OR CONDUCTIVE HEARING LOSS USING A
512-HZ OR 1,024-HZ TUNING FORK.
THE WEBER AND RINNE TESTS ARE THE MOST WIDELY USED
TUNING FORK TESTS.
WEBERS TEST: SOUND LATERALIZES TO THE OPPOSITE EAR IN
PATIENTS WITH A SENSORINEURAL HEARING LOSS, BUT TO THE
SAME SIDE IN THOSE WITH A CONDUCTIVE HEARING LOSS.
PATIENTS WITH NORMAL HEARING OR EQUAL DEAFNESS IN BOTH
EARS HEAR THE SOUND AT THE SAME LEVEL IN BOTH EARS.
RINNE TEST: IF AC IS GREATER THAN BC, HEARING IS NORMAL OR
SNHL IS PRESENT.
IF BONE CONDUCTION IS GREATER THAN AIR CONDUCTION,
HEARING LOSS IS CONDUCTIVE.
DIAGNOSTIC TESTS
•
AUDIOMETRIC ASSESSMENT
AUDIOGRAPHY: PRIMARILY TESTS THE FUNCTION OF THE
PERIPHERAL PORTION OF THE HEARING APPARATUS
SPEECH DISCRIMINATION TESTING: SOUND MUST BE INTERPRETED IN
THE CENTRAL NERVOUS SYSTEM BEFORE IT CAN BE USEFUL TO
THE PATIENT. POOR PERFORMANCE ON THE SPEECH TEST
USUALLY REFLECTS PATHOLOGY IN THE CENTRAL NERVOUS
SYSTEM.
TYMPANOMETRY: IDENTIFY PREVIOUSLY UNDETECTED MIDDLE EAR
EFFUSIONS, CHANGES IN TYMPANIC MEMBRANE STIFFNESS
CAUSED BY A PATULOUS EUSTACHIAN TUBE, OR MYOCLONUS
OF THE STAPEDIAL MUSCLE OR THE MUSCLES OF THE PALATE.
OTHER AUDIOMETRIC MEASUREMENTS:
•
•
•
•
PITCH MASKING (MATCHING THE FREQUENCY OF THE TINNITUS
WITH A VARIETY OF STIMULI),
LOUDNESS MATCHING (ESTIMATING THE LOUDNESS OF TINNITUS
WITH A PURE TONE OR NOISE),
MINIMUM MASKING LEVEL (A TEST IN WHICH THE AMOUNT OF
SOUND REQUIRED TO COVER THE TINNITUS IS RECORDED),
RESIDUAL INHIBITION (ACHIEVING DECREASED OR ABSENT
TINNITUS AFTER EXPOSURE TO A MASKING TONE AT THE PITCH
AND INTENSITY OF THE TINNITUS).
THESE MEASUREMENTS PROVIDE SOME INFORMATION AS TO
WHETHER THE TINNITUS CAN BE MASKED BY AN EXTERNAL NOISE
(I.E., MASKING THERAPY)
DIAGNOSTIC APPROACH TO TINNITUS
OBJECTIVE TINNITUS
•
CLINICIAN CAN PERCEIVE AN ACTUAL SOUND (E.G., A BRUIT)
EMANATING FROM THE PATIENT'S EARS
•
CAN ARISE FROM MUSCLE SPASMS THAT CAUSE CLICKS OR
CRACKLING AROUND THE MIDDLE EAR
•
SOME EXPERIENCE A SOUND THAT BEATS IN TIME WITH THE
PULSE (PULSATILE TINNITUS)
CAUSES OF OBJECTIVE
TINNITUS
– PULSATILE TINNITUS IS USUALLY RELATED TO BLOOD FLOW,
EITHER THROUGH NORMAL OR ABNORMAL BLOOD VESSELS
NEAR THE EAR.
– CAUSES OF PULSATILE TINNITUS INCLUDE PREGNANCY,
ANEMIA (LACK OF BLOOD CELLS), OVERACTIVE THYROID, OR
TUMORS INVOLVING BLOOD VESSELS NEAR THE EAR.
– PULSATILE TINNITUS CAN ALSO BE CAUSED BY A CONDITION
KNOWN AS BENIGN INTRACRANIAL HYPERTENSION-AN
INCREASE IN THE PRESSURE OF THE FLUID SURROUNDING THE
BRAIN.
– CLICKING TYPES OF OBJECTIVE TINNITUS CAN BE CAUSED BY
JAW JOINT MISALIGNMENT (TMJ) PROBLEMS OR MUSCLES OF
THE EAR OR THROAT "TWITCHING."
– PATULOUS EUSTACHIAN TUBE
– STAPEDIAL MUSCLE SPASM
PULSATILE TINNITUS
PULSATILE TINNITUS IS USUALLY OBJECTIVE IN NATURE,IT IS PULSATILE
BECAUSE THE NOISE IS RHYTHMIC AND IT BEATS ALONG WITH YOUR
HEARTBEAT, RESULTING FROM ALTERED BLOOD FLOW OR INCREASED
BLOOD TURBULENCE NEAR THE EAR (SUCH AS FROM ATHEROSCLEROSIS
OR VENOUS HUM), BUT IT CAN ALSO ARISE AS A SUBJECTIVE
PHENOMENON FROM AN INCREASED AWARENESS OF BLOOD FLOW IN THE
EAR.
CAUSES:CHANGES IN THE BLOOD FLOW OF THE BLOOD VESSELS NEAR
THE EARS
IT MAY HAPPEN WHEN A PERSON BECOMES MORE AWARE OF
THE
FLOW OF BLOOD NEAR THE EARS.
SYMPTOM OF POTENTIALLY LIFE-THREATENING CONDITIONS LIKE
CAROTID ARTERY ANEURYSM OR CAROTID ARTERY DISSECTION.
A PUNCTURED EAR DRUM CAN ALSO MAKE YOU MORE AWARE OF
THE SOUNDS IN YOUR BODY SINCE THE BRAIN IS NO LONGER
ABLE TO PICK UP EXTERNAL SOUNDS.
CHARACTERISTIC: A LOW PITCHED BOOMING OR THUMPING,
ALSO A ROUGH BLOWING SOUND WHICH
COINCIDES WITH RESPIRATION,
A CLICKING HIGH PITCH RHYTHMIC SOUND.
BEATING (SINGLE, RHYTHMIC OR MULTIPLE BIPHASIC)
CONTRACTIONS IN THE MIDDLE EAR MAY CAUSE A RAPID
CLICKING SENSATION.
LOW VOLUME EAR HUMS WHICH ARE INAUDIBLE TO THE
EXAMINER CAN BE DUE TO BLOOD FLOW IN THE VEINS
OR ASSOCIATED WITH MENIERE’S DISEASE
TREATMENT:MEDICAL EXAMINATION TO LOCATE CAUSES AND BASED ON
THAT TREATMENT.
AN ULTRASOUND, CT SCAN, MRI, MRA AND ANGIOGRAPHY
OBJECTIVE TINNITUS, HOWEVER, IS QUITE UNCOMMON.
OFTEN PATIENTS WITH PULSATILE TUMORS WILL REPORT OTHER
COEXISTENT SOUNDS, DISTINCT FROM THE PULSATILE NOISE, THAT
WILL PERSIST EVEN AFTER THEIR TUMOR HAS BEEN REMOVED.
THIS IS GENERALLY SUBJECTIVE TINNITUS, WHICH, UNLIKE THE
OBJECTIVE FORM, CANNOT BE TESTED BY COMPARATIVE METHODS
SUBJECTIVE TINNITUS
•
•
MOST COMMON TYPE OF TINNITUS
YOU HEAR A SOUND BUT IT CANNOT BE HEARD BY OTHERS.
CAUSES OF SUBJECTIVE
TINNITUS
•
•
•
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COMMON OTOLOGIC DISORDERS – THE SAME CONDITIONS THAT
CAUSE HEARING LOSS.
THE MOST COMMON CAUSE IS NOISE-INDUCED HEARING LOSS,
RESULTING FROM EXPOSURE TO EXCESSIVE OR LOUD NOISES.
BUT TINNITUS, ALONG WITH SUDDEN ONSET HEARING LOSS, MAY
HAVE NO OBVIOUS EXTERNAL CAUSE.
OTOTOXIC DRUGS CAN CAUSE TINNITUS EITHER SECONDARY TO
HEARING LOSS OR WITHOUT HEARING LOSS, AND MAY INCREASE
THE DAMAGE DONE BY EXPOSURE TO LOUD NOISE, EVEN AT
DOSES THAT ARE NOT IN THEMSELVES OTOTOXIC
OTOLOGIC PROBLEMS AND HEARING LOSS:CONDUCTIVE HEARING LOSS:
EXTERNAL EAR INFECTION
ACOUSTIC SHOCK
CERUMEN (EARWAX) IMPACTION
MIDDLE EAR EFFUSION
SUPERIOR CANAL DEHISENCE
SENSORINERAL HEARING LOSS:
EXCESSIVE OR LOUD NOISE
PRESBYCUSIS (AGE-ASSOCIATED HEARING LOSS)
MENIERE’S DISEASE
ACOUSTIC NEUROMA
MERCURY OR LEAD POISONING
-
OTOTOXIC MEDICATIONS
ANALGESICS:
ASPIRIN
NON STEROIDAL ANTI INFLAMMATORY DRUGS
ANTIBIOTICS:
AMINOGLYCOSIDESE.G. GENTAMICIN
CHLORAMPHENICOL
ERYTHROMYCIN
TETRACYCLIN
VANCOMYCIN
VIBRAMYCIN
CHEMOTHERAPY AND ANTIVIRAL DRUGS:
BLEOMYCIN
INTERFERON
PEGYLATED INTERFERON ALPHA-2B
CISPLATIN
MECHLORETHANIN
METHOTREXATE
VINCRISTINE
LOOP DIURETICS:
BUMETIDE
ETHACRYNIC ACID
FUROSEMIDE
OTHERS:
CHLOROQUINE
QUININE
PSYCHEDELIC DRUGS:
5-MEO-DET
5-METHOXY MESOPROPYL TRYPTAMINE
DISOPROPYL TRYPTAMINE (CITATION NEEDED)
HARMALINE (CITATION NEEDED)
N,N DIMETHYL TRYPTAMINE (CITATION NEEDED)
PSILOCYBIN (CITATION NEEDED)
SALVINORIN A (CITATION NEEDED)
NEUROLOGIC DISORDERS:
MULTIPLE SCLEROSIS
HEAD INJURY
SKULL FRACTURE
CLOSED HEAD INJURY
WHIPLASH INJURY
TEMPAROMANDIBULAR JOINT DISORDER
METABOLIC DISORDERS:
THYROID DISORDER
HYPERLIPIDAEMIA
VITAMIN B12 DEFICIENCY
PSYCHIATRIC DISORDERS:
DEPRESSION
ANXIETY
OTHER CAUSES:
TENSION MYOSITIS SYNDROME
FIBROMYALGIA
HYPERTONIA(MUSCLE TENSION)
THORACIC PUTLET SYNDROME
LYME DISEASE
HYPNOGONIA
SLEEP PARALYSIS
GLOMUS TYMPANICUM
MECHANISMS OF SUBJECTIVE
TINNITUS
• MECHANISM 1:
RELIES IN THE OTOACOUSTIC EMISSIONS.INNER EAR CONTAINS
THOUSANDS OF MINUTE HAIRS, CALLED “STEREOCILIA”, WHICH
VIBRATE IN RESPONSE TO SOUND WAVES AND CELLS WHICH
CONVERT NEURAL SIGNALS BACK INTO ACOUSTICAL VIBRATIONS.
SENSING CELLS ARE CONNECTED WITH THE VIBRATORY CELLS
THROUGH A NEURAL FEEDBACK LOOP, WHOSE GAIN IS
REGULATED BY THE BRAIN.
THIS LOOP IS NORMALLY ADJUSTED JUST BELOW ONSET OF SELFOSCILLATION, WHICH GIVES THE EAR SPECTACULAR SENSITIVITY
AND SELECTIVITY.
IF SOMETHING CHANGES, IT'S EASY FOR THE DELICATE
ADJUSTMENT TO CROSS THE BARRIER OF OSCILLATION AND
TINNITUS RESULTS.
LISTENING TO LOUD MUSIC KILLS OUR HAIR CELLS, AS WE LOSE
HAIR CELLS, AFFERENT NEURONS ARE ACTIVATED, ACTIVATING
AUDITORY PARTS OF THE BRAIN AND GIVING THE PERCEPTION OF
SOUND.
MECHANISM 2:
DAMAGE TO THE RECEPTOR CELLS. ALTHOUGH RECEPTOR CELLS
CAN BE REGENERATED FROM THE ADJACENT SUPPORTING DEITERS
CELLSAFTER INJURY IN BIRDS, REPTILES, AND AMPHIBIANS,
IN MAMMALS IT IS BELIEVED THAT THEY CAN BE PRODUCED ONLY
DURING EMBRYOGENESIS
ALTHOUGH MAMMALIAN DEITERS CELLS REPRODUCE AND POSITION
THEMSELVES APPROPRIATELY FOR REGENERATION, THEY HAVE NOT
BEEN OBSERVED TO TRANSDIFFERENTIATE INTO RECEPTOR CELLS
EXCEPT IN TISSUE CULTURE EXPERIMENTS
THEREFORE, IF THESE HAIRS BECOME DAMAGED, THROUGH
PROLONGED EXPOSURE TO EXCESSIVE DECIBEL LEVELS, FOR
INSTANCE, THEN DEAFNESS TO CERTAIN FREQUENCIES OCCURS. IN
TINNITUS, THEY MAY FALSELY RELAY INFORMATION AT A CERTAIN
FREQUENCY THAT AN EXTERNALLY AUDIBLE SOUND IS PRESENT,
WHEN IT IS NOT.
MECHANISM 3:
INCREASED NEURAL ACTIVITY IN THE AUDITORY BRAINSTEM WHERE
THE BRAIN PROCESSES SOUNDS,
CAUSING SOME AUDITORY NERVE CELLS TO BECOME OVEREXCITED.
MENIERE’S DISEASE
•
MÉNIÈRE DISEASE IS A SYNDROME
•
EPISODES OF:
SPINNING VERTIGO(SENSE OF THE
ROOM SPINNING),
HEARING LOSS (SNHL)
TINNITUS (RINGING IN THE EAR).
•
BETWEEN UNPREDICTABLE ATTACKS, HEALTHY
•
FIRST DESCRIBED IN 1861 BY THE FRENCH PHYSICIAN PROSPER
MÉNIÈRE.
CAUSES:
UNKNOWN
AFFECTS PEOPLE OF ALL AGES, ESP MIDDLE AGE OR OLDER.
UNCOMMON IN CHILDREN.
VASOSPASM- REDUCED BLOOD SUPPLY TO LABRYNTH
ENDOLYMPHATICHYDROPS- INCREASED TENSION OF ENDOLYMPH IN
LABRYNTH DUE TO REDUCED ABSORPTION (DUE TO INCREASED
BLOOD SUPPLY)
EMOTIONAL FACTORS
SYMPATHETIC SYSTEM OVERACTIVITY- VASOSPASM
HORMONAL DISTURBACES-CAUSE WATER & ELECTROYTE IMBALANCE
VIT B COMPLEX DEFICIENCY
PATHOLOGY:
INCREASED VOLUME OF ENDOLYMPH
DISTENSION OF MEMBRANOUS LABRYNTH
DEGENERATIVE CHANGES IN LBRYNTH
POSSIBILITY OF RUPTURE OF MEMBRANOUS LABRYNTH
MIXING OF ENDOLYMPH & PERILYMPH
CLINICAL FEATTURES:
GIDDINESS
SNHL
TINNITUS- CONTINUOUS OR ONLY DURING ATTACK
NAUSEA & VOMMITING
PERSPIRATION, GASTRIC UPSET & DIARRHOEA
FULLNESS IN EAR
HEADACHE
ANXIETY
NYSTAGMUS
TREATMENT:
REASSURANCE
LABRYNTHINE SEDATIVES- PROCHLORPERAZIME (STEMETIL)
DIMENHYDRINATE(DRAMAMINE)
VASODILATORS- NICOTINIC ACID, BETAHISTAMINE
VIT B1,6, 12
TRANQUILIZERS
SURGICAL:
DECOMPRESSION & SHUNT OPERATION OF ENDOLYMPHATIC SAC
PARTIAL DESTRUCTION OF VESTIBULE BY ULTRASONICS OR
CRYOSURGERY
VESTIBULAR NERVE SECTION
LABRYNTHECTOMY –BUT LEADS TO PERMANENT LOSS OF HEARING
PREVENTION
 FOR MUSICIANS, DJS, SPECIAL “MUSICIANS' EARPLUGS” PLAY A
HUGE ROLE, CAN LOWER THE VOLUME OF THE MUSIC WITHOUT
DISTORTING THE SOUND
 FOR ANYONE OPERATING LOUD ELECTRICAL APPLIANCES, SUCH
AS VACUUM CLEANERS, HAIR DRYERS, AND LAWN MOWERS,
EARPLUGS ARE ALSO HELPFUL IN REDUCING NOISE EXPOSURE.
 CHECK MEDICATIONS FOR POTENTIAL OTOTOXICITY. DOSE AND
DOSAGE INTERVAL, CAN REDUCE THE DAMAGE DONE.
 PROLONGED EXPOSURE TO NOISE LEVELS AS LOW AS 70 dB CAN
RESULT IN DAMAGE TO HEARING,SO AVOID IT.
 PARENTS SHOULD BE ENCOURAGED TO PROVIDE ADEQUATE
HEARING PROTECTION, SUCH AS SILICONE EAR PLUGS, FOR THEIR
CHILDREN.
TREATMENT
• OBJECTIVE TINNITUS:
•
•
•
•
•
GAMMA KNIFE RADIOSURGERY(GLOMUS JUGULARE)
SHIELDING OF COCHLEA BY TEFLON IMPLANT
BOTULINUM TOXIN (PALATAL TREMOR)
PROPRANOLOL AND CLONAZEPAM (ARTERIAL ANATOMIC
VARIATION)
CLEARING EAR CANAL (IN THE CASE OF EARWAX PLUG)
SUBJECTIVE TINNITUS:
DRUGS AND NUTRIENTS:
LIDOCAINE, INJECTION INTO THE INNER EAR FOUND TO SUPPRESS THE
TINNITUS FOR 20 MINUTES, ACCORDING TO A SWEDISH STUDY
BENZODIAZAPAM (LOREZAPAM, CLONAZAPAM) IN SMALL DOSES
TRICYCLICS(AMITRIPTYLINE, NORTRYPTILINE IN SMALL DOSES
AVOIDANCE OF CAFFEINE, NICOTINE, SALT)
CONSUMPTION OF ALCOHOL HAS BEEN FOUND TO BOTH INCREASE
AND DECREASE THE SEVERITY OF TINNITUS. BUT CANNOT BE
CONSIDERED A TREATMENT
ZINC SUPPLEMENTATION (WHERE SERUM ZINC DEFICIENCY IS PRESENT)
ETIDRONATE OR SODIUM FLUORIDE (OTOSCLEROSIS)
LIGNOCAINE OR ANTICONVULSANTS (USUALLY IN PATIENTS RESPONSIVE
TO WHITE NOISE MASKING)
CARBAMAZEPINE
MELATONIN (ESPECIALLY FOR THOSE WITH SLEEP DISTURBANCE)
VITAMIN COMBINATIONS (LIPOFLAVONOID)
ELECTRICAL STIMULATION:
TRANSCRANIAL MAGNETIC STIMULATION OR TRANSCRANIAL DIRECT
CURRENT STIMULATION
TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION
DIRECT STIMULATION OF AUDITORY CORTEX BY IMPLANTED
ELECTRODES
GERMAN NEUROLOGIST WOULD APPLY AN ELECTRIC OR MAGNETIC
CURRENT FOR STIMULATION OVER THE HEAD OF THE PATIENT TO
REDUCE RINGING SOUND.
BELGIAN NEUROSURGEON IMPLANTED ELECTRODES TO BRAIN OF
SUFFERERS TO NORMALISE OVERACTIVE NEURONES.
CAMBRIDGE SCIENTISTS ALSO FOUND THAT LIDOCAINE, AN
ANAESTHETIC REDUCES SOUND IN 2/3 OF PATIENTS FOR 5 MINUTES,
SURGERY:
REPAIR OF PERILYMPH FISTULA
EXTERNAL SOUND:
THE NEUROMONICS TINNITUS TREATMENT, INTRODUCED FIRST IN
AUSTRALIA NOW IN THE US.[CITATION NEEDED]
LOW-PITCHED SOUND TREATMENT HAS SHOWN SOME POSITIVE,
ENCOURAGING RESULTS)
TINNITUS MASKING (WHITE HOUSE, OR BETTER 'SHAPED' OR FILTERED
NOISE
TINNITUS RETAINING THERAPY
AUDITIVE STIMULATION THERAPY (MUSIC THERAPY)
COMPENSATION FOR LOST FREQUENCIES BY USE OF A HEARING AID.
ULTRASONIC BONE-CONDUCTION EXTERNAL ACOUSTIC STIMULATION
AVOIDANCE OF OUTSIDE NOISE (EXOGENOUS TINNITUS
PSYCHOLOGICAL:
COGNITIVE BEHAVIORAL THERAPY
LIGHT-BASED:
PHOTOBIOMODULATION (A.K.A. LOW LEVEL LASER THERAPY)
OTHERS:
PATIENTS DISCOMFORTED BY TINNITUS AND HAVE NO REMEDIABLE
CAUSE, AUDITORY MASKING MAY PROVIDE SOME RELIEF.
KARNANAAD &
KARNAKSHWEDA
TWO DISEASE AMONG 28 KARNAROGAS ACCORDING TO
SUSHRUTACHARYA.
THIS ARE TWO SPECIFIC DISEASE IN WHICH SOME ABNORMAL
EXTERNAL SOUND IS HEARD IN THE EAR. BUT IN BOTH THE
DISEASE THE TYPE OF SOUND DIFFERS.
KARNANAAD
“KEVALA VAATARABDHO NANAVIDHASHABDANVITA”
DOSHA: VAAT
CAUSES:
VAATPRAKOPAK AHAR
RUKSHA KASHAY ANNAPAN
ATICHINTA
SHRAVANENDRIYA ATIYOG/ MITHYAYOG
ATISHRAMA
RATRIJAGARAN
KSHAYA
RECURRENT PRATISHYAY
SAMPRAPTI: HETUSEVAN
VAATPRAKOP
VAAT BECOMES PURIT IN SHABDAVAHA NADI
VAAT BECOMES VIMARGAG (VIRUDDHA MARGA PRAPTA)
VIVIDHA SHABDA PRODUCED
KARNANAAD
KARNANAAD IF IGNORED & NO TREATMENT IS TAKEN THEN IT FURTHER
PROCEEDS TO BAADHIRATVA (A H 17/10)
KARNAKSHWEDA
“SHWEDANAM VENUGHOSHAVAT”
DOSHA: DOSHA SANSRUSHTA VAATARABDHO
KAPHAVAATABHYAM SANSRUSHTA SHONITEN (VIDEHA)
CAUSES: ATISHRAMA
VIRECHANA ATIYOG PASCHAT ATI SHEETA SEVA
ATIRUKSHAKASHAY ANNAPAN
ATICHINTA
KSHAYA
RATRIJAGARAN
ATISHEETA ANNAPAN
SAMPRAPTI: HETUSEVAN
VAATPRAKOP
SHABDAPATHE PRATISHTHATI
CHIKITSA OF KARNANAAD &
KARNAKSHWEDA
SAAMANYA KARNAROGA CHIKITSA IS: GHRITAPAN
(Su U 21/3)
RASAYAN SEVAN
AVYAYAM
SHIRASNANA AVOIDED
BRAMHACHARYA
AKATHANAM
SAME CHIKITSA TOLD FOR ALL 4:
(Su U 21/4)
KARNANAAD
KARNAKSHWEDA
KARNASHULA
BAADHIRYA
IT IS: SNEHAPAN
ABHYANGA
PASCHAT VIRECHAN (ERANDATAILADI)
VAATHARA SWEDA- NADISWEDA OR PINDASWEDA
BHOJAN PASCHAT GHRITAPAN
PASCHAT DUGDHAPAN
BASTIKARMA
MURDHABASTI (BALATAILA)
CHIKITSA
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NIDAN PARIVARJAN
BILWA TAILA KARNAPURAN
DASHAMULA TAILA KARNAPURAN
SHALYA NIRHARAN
NASYADIK CHIKITSA
SHIROBHYANGA
TRIPHALA GUGGULA
VACHA, PIPPALI (PRATISHYAY JANYA SAMPRAPTI)
KARNAGUTHAK NIRHARAN
PATHYA PAALAN
SNIDHA-MADHUR BHOJAN
AVOID ATIBHASHYA
AVOID ATISHRAMA
KARNANAAD ALSO SEEN IN
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PANDU
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ADHIMANTHA
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SHIROROGA (VAATAJA)
CHIKITSA SHOULD BE DONE BASED ON THE UNDERLYING SAMPRAPTI
& OTHER ASSOCIATED LAKSHANA.