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12.AUD-InnerEaDisord

Audiology SLP314

TermDefinition
Sensori-neural hearing loss (2) 1.Cochlear- damaged hair cells, nerve fibers (most cases) 2.Retrocochlear- aud. nerve beyond cochlea past modiolus (rarer)
Tonotopic organization predicts (3) 1.Basal region damage: high freq loss 2.Apical region damage: low freq loss 3.Entire length of cochlea damaged: loss across freqs.
CAUSES OF SNHL (3) Hereditary. Congenital infection. Ototoxicity.
Hereditary causes -50% of early childhood SNHL. -May occur in isolation or part of syndrome ("Hidden Handicap"). -Late ID and shock if parents unaware of family Hx. -Studies 15 yrs ago “mean ID of severe to profound HL“ 18 to 24 months -Incentive for newborn screening.
Congenital infection - TORCH (5) 1. Toxoplasmosis 2. Other (Syphilis) 3. Rubella (German measles) 4. Cytomegalovirus (CMV) 5 Herpes (Genital)
Cytomegalovirus (CMV) Most common of the TORCH infections. Mild symptoms in mother. Fetus: SNHL, visual impairment, mental handicap, CP. No vaccine. Health/day care workers at risk from contact with bodily fluids - WASH HANDS!
Rubella AKA, 3-day or German measles. If mother contracts during 1st trimester, baby may acquire: SNHL, brain damage, blindness, MR, heart defects. Used to be major cause of SNHL. Vaccines brought incidence very low (last rubella epidemic- 1960s)
Syphilis STD (baby gets from infected mother). If untreated, causes SNHL later (1st to 6th decade). Treat baby with penicillin in early stages.
Toxoplasmosis Parasite from undercooked meat, cat feces. Causes SNHL, neurological impairment.
Genital Herpes Baby may acquire during birth via contact with active lesions. SNHL, neurological impairment, high death rate. Prevent with C-section delivery.
HYPERBILIRUBINEMIA Rh incompatibility (Mom - ; Dad +). Maternal antibodies attack fetus’s RBCs, cause breakdown. Bilirubin is deposited in the brain. Toxic to CNS and auditory pathways. Can prevent antibody buildup with Rhogam. Incidence has decreased due to preventative.
 May cause mild SNHL FETAL ALCOHOL SYNDROME; ANOXIA (lack of oxygen at birth); PREMATURITY (Birth weight < 3.3 lb. Ear is formed by 25 weeks)
BACTERIAL MENINGITIS SNHL in 5-35% of cases  Severe-profound loss typic.al  Infection of the lining of the brain.  Vaccines. May see vestibular damage also.
CHILDHOOD VIRAL ILLNESSES  Measles (10-day)  Mumps  Chicken pox  Vaccines for all now- incidence declined.
OTOTOXICITY (drugs “toxic to the ear”) Typically destroy HCs, beginning in base, then progressing  1. Aminoglycoside antibiotics (mycins). 2. Loop diuretics 3. Chemotherapy drugs 4. Aspirin
Aminoglycoside antibiotics Aminoglycoside antibiotics (mycins)  Used in hospital lVs.  Safe unless high dosage or with kidney malfunction.
Loop diuretics e.g. Furosemide (Lasix – used for heart problems).  Loss is temporary or permanent (if very high doses).  Amino glycosides and Loop diuretics together: synergistic effect (e.g., babies with respiratory problems)
Chemotherapy drugs (e.g. Cisplatin) Destroys HCs in base to apex (can progress after the drug is stopped - stays in cochlea). Do baseline audio, monitor hearing regularly. Change drug/alter dose. Balance medical condition w HL. Ultra-high freq. testing (8000-20,000 Hz). Early warning sys.
Aspirin Can cause temporary hearing loss  Tinnitus  Usually with higher doses (12-20 pills of 325 mg dose)
NOISE-INDUCED HEARING LOSS (NIHL) 2nd most common cause of SNHL in adults 1.Temporary Threshold Shift (TTS)  2.Permanent Threshold Shift (PTS):  Repeated episodes of TTS- warning sign that PTS may result.
Types of noise (2)  Continuous- steady, on for long time  HL from long-term exposure (e.g., industrial)  Impulse- intense, short duration  HL may result from one exposure (e.g., gunshot, explosion)  Estimated 235 dB at 10 ft.; 199 dB at 100 ft.
Damage to Cochlea:  TTS Swollen hair cells, bent stereocilia
Damage to Cochlea: PTS- continuous noise  Loss of HCs, nerve fibers, damage to stria vascularis
Damage to Cochlea: PTS- impulse noise Organ of Corti blown off basilar membrane.  Rupture of Reissner’s membrane  Interference of current flow.  Can occur in response to one episode
Impulse noise: *Organ of Corti may be floating around in the endolymph * Rupture of Reissner’s membrane – disrupt chemical composition of the endolymph and result in hearing loss
Characteristic NIHL audiogram (PTS) 4000 Hz “notch” May also have tinnitus (high-pitched ringing). Impulse cause would be even more extensive.
OSHA: Damage Risk Criteria (DRCs) 85 dB: 8 hours (max allowable time)  90 dB: 4 hours  95 dB: 2 hours  100 dB:1 hour  105 dB: 30 min  110 dB: 15 min  115 dB: 7.5 min  > 115 dB: forbidden  (120 dB: rock concert, jet engine  >120 dB: jack hammer)
Industry: Hearing Conservation Programs Programs required at > 85 dB for 8 hours. 1.Reduce noise (modify equipment) 2.Require use of hearing protection. 3.Monitor hearing of employees (annually). Industrial Audiology – specialty area. Use mobile vans, monitor worker’s hearing, advise.
MENIERE’S DISEASE (endolymphatic hydrops) symptoms (3) 1. Unilateral hearing loss (may progress to bilat.)  2. Tinnitus (low frequency, roaring)  3. Vertigo (spinning)
MENIERE’S DISEASE characteristics Occurs episodically- attacks, remission  May feel fullness in the ear prior to an attack.  During remission- usually fluctuating hearing loss is the only symptom.
MENIERE’S DISEASE physiology Abnormal build-up of endolymph in scala media and vestibular organs.  Pressure of fluid on HCs produces HL and tinnitus.  Pressure overstimulates the vestibular system.  Cause unknown.  Usually begins between age 40-60, rare in children.
MENIERE’S DISEASE audiometric findings Early stage: low freq SNHL (fluctuates). Later stage: flat, permanent SNHL.
MENIERE’S DISEASE treatments -Limit fluid retention (Diuretics, reduced salt). -Sedatives, tranquilizers (anxiety may precipitate attack). -Vestibular suppressants (e.g., antivert). -Antihistamines (one theory – due to allergies). -Surgery (for incapacitating vertigo – 10%)
PRESBYCUSIS Most common cause of SNHL in adults (aging)
Types of presbycusis (4) 1.Sensory 2.Neural 3.Metabolic 4.Mechanical (#3 and 4- less common). Can occur singly or in combination
Sensory Presbycusis degeneration of HCs and supporting cells
Neural Presbicusis degeneration of AN fibers
Metabolic Presbicusis atrophy of stria vascularis (wasting away, dec in size)
Mechanical Presbicusis impaired mobility of basilar mem.
Central changes in age-related HL Neural degeneration throughout auditory pathways in brain  ~15% of elderly have these central auditory deficits.  Further interferes with speech processing. Central changes compound symptoms of Presbycusis.
Symptoms of Presbycusis Slow progressive, bilat SNHL, symmetrical (high freq slope) -High pitched, tinnitus -Progressive decline in speech understanding (especially in noise) .
Presbycusis data (2011) The same nutrients that maintain vascular health by antioxidant activity may also influence susceptibility to hearing loss:  Lycopene, Vitamins C and E, Magnesium.  No cure: treat with hearing aids, aural rehabilitation, counseling
Otoacoustic Emissions -Spontaneous. -Evoked
Created by: ashea01