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.

ONSET 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. 

HISTORY COMMENTS

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 MEDICATION-INDUCED 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 TINNITUSPULSATILE 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

• 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 INFECTIONACOUSTIC SHOCK CERUMEN (EARWAX) IMPACTION MIDDLE EAR EFFUSION SUPERIOR CANAL DEHISENCE

SENSORINERAL HEARING LOSS:

EXCESSIVE OR LOUD NOISEPRESBYCUSIS (AGE-ASSOCIATED HEARING LOSS) MENIERE’S DISEASE ACOUSTIC NEUROMA MERCURY OR LEAD POISONING

-

OTOTOXIC MEDICATIONS

ANALGESICS:ASPIRINNON STEROIDAL ANTI INFLAMMATORY DRUGS

ANTIBIOTICS:AMINOGLYCOSIDESE.G. GENTAMICIN CHLORAMPHENICOLERYTHROMYCIN TETRACYCLINVANCOMYCINVIBRAMYCIN

CHEMOTHERAPY AND ANTIVIRAL DRUGS:BLEOMYCININTERFERONPEGYLATED INTERFERON ALPHA-2BCISPLATINMECHLORETHANINMETHOTREXATEVINCRISTINE

LOOP DIURETICS:BUMETIDEETHACRYNIC ACIDFUROSEMIDE

OTHERS:

CHLOROQUINE QUININE

PSYCHEDELIC DRUGS:

5-MEO-DET5-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 SCLEROSISHEAD INJURY

SKULL FRACTURE CLOSED HEAD INJURY WHIPLASH INJURY TEMPAROMANDIBULAR JOINT DISORDER

METABOLIC DISORDERS:

THYROID DISORDER HYPERLIPIDAEMIAVITAMIN B12 DEFICIENCY

PSYCHIATRIC DISORDERS:

DEPRESSIONANXIETY

OTHER CAUSES:

TENSION MYOSITIS SYNDROME FIBROMYALGIAHYPERTONIA(MUSCLE TENSION) THORACIC PUTLET SYNDROME LYME DISEASEHYPNOGONIASLEEP 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 SELF-OSCILLATION, 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 EMBRYOGENESISALTHOUGH MAMMALIAN DEITERS CELLS REPRODUCE AND POSITION THEMSELVES APPROPRIATELY FOR REGENERATION, THEY HAVE NOT BEEN OBSERVED TO TRANSDIFFERENTIATE INTO RECEPTOR CELLS EXCEPT IN TISSUE CULTURE EXPERIMENTSTHEREFORE, 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 STUDYBENZODIAZAPAM (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 TREATMENTZINC SUPPLEMENTATION (WHERE SERUM ZINC DEFICIENCY IS PRESENT)ETIDRONATE OR SODIUM FLUORIDE (OTOSCLEROSIS)LIGNOCAINE OR ANTICONVULSANTS (USUALLY IN PATIENTS RESPONSIVE TO WHITE NOISE MASKING)CARBAMAZEPINEMELATONIN (ESPECIALLY FOR THOSE WITH SLEEP DISTURBANCE) VITAMIN COMBINATIONS (LIPOFLAVONOID)

ELECTRICAL STIMULATION:

TRANSCRANIAL MAGNETIC STIMULATION OR TRANSCRANIAL DIRECT CURRENT STIMULATIONTRANSCUTANEOUS ELECTRICAL NERVE STIMULATION DIRECT STIMULATION OF AUDITORY CORTEX BY IMPLANTED ELECTRODESGERMAN 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 THERAPYAUDITIVE STIMULATION THERAPY (MUSIC THERAPY)COMPENSATION FOR LOST FREQUENCIES BY USE OF A HEARING AID. ULTRASONIC BONE-CONDUCTION EXTERNAL ACOUSTIC STIMULATIONAVOIDANCE 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• 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

• PANDU

• ADHIMANTHA

• SHIROROGA (VAATAJA)

CHIKITSA SHOULD BE DONE BASED ON THE UNDERLYING SAMPRAPTI & OTHER ASSOCIATED LAKSHANA.