1. Tinnitus Alexandra D. Costlow, B.S.

2. According to Merriam-Webster From Latin, tinnire, to ring Of imitative origin First Known Use: 1843 http://www.merriam-webster.com/dictionary/tinnitus

3. The Many Sounds of Tinnitus Ringing Hissing Roaring Whistling Swishing Buzzing Chirping, crickets Clicking “It goes along with my heartbeat.”*

4. Hear, Neuromonics Will Show You http://www.neuromonics.com/patient/treatment/index.aspx?id=50

5. Common Audiological Causes Hearing loss Cerumen accumulation/occlusion Eustachian tube blockage Otitis media Exposure to loud noise Ototoxic chemicals* Otosclerosis - frequently Meniere’s Disease (episodic tinnitus along with hearing loss, dizziness, and aural fullness) Acoustic neuroma – Even when the tumor is removed, 50% of pts continue to experience tinnitus (Benson et al., 2009) http://www.emedicinehealth.com/tinnitus/page2_em.htm

6. …So Who’s Hearing Things Now? Subjective Tinnitus Only the patient perceives head noise This is the more common form Objective tinnitus Head noise is audible to the patient and to the professional Relatively rare Originates in the ear, head, or neck Muscular or vascular etiology Myoclonus is found in pts with degenerative diseases* Benson, A.G., McGuire, J.F., Djalilian, H.R., Hanks, K.M., Robbins, W.K. (2009)

7. Myoclonus The neuromuscular control over ear muscles deteriorates in an individual with good very good sensory perception. The stapedius and/ or tensor tympani muscles repeatedly contract and relax. This results in audible click noises arising from the ear. Can be unilateral or bilateral. Treatment is lysis of the muscle/s through tympanotomy incision. Benson, A.G., McGuire, J.F., Djalilian, H.R., Hanks, K.M., Robbins, W.K. (2009)

8. Other Causes of “Click” Tinnitus Jaw joint misalignment i.e. the tempero- mandibular joint (TMJ) http://www.emedicinehealth.com/tinnitus/page2_em.htm

9. Cardiological Etiology Carotid artery Injury due to aging or surgery Ectasia: Dilation, expansion, distentsion, bulging Blood flow through the artery is tumultuous Follows the pt’s heartbeat Can be ausculated by the examiner Jugular Vein and bulb More common than the 2 other objective etiologies Produces a “Venous hum” Pt describes a vibratory or low-pitched sound Benson, A.G., McGuire, J.F., Djalilian, H.R., Hanks, K.M., Robbins, W.K. (2009)

10. Anatomical Reference – Jugular Vein (External) http://www.frca.co.uk/article.aspx?articleid=100030

11. Anatomical Reference – Carotid Artery http://www.nlm.nih.gov/medlineplus/ency/presentations/100124_1.htm

12. Causes of Pulsatile Tinnitus Suggests involvement of blood flow through vessels near the ear May be normal or pathological Space-occupying lesions Anemia* (Contributing cause) Overactive thyroid Hypertension Benign intracranial pressure http://www.emedicinehealth.com/tinnitus/page2_em.htm

13. Red Flags Sudden onset tinnitus (with or without hearing loss) Sudden onset hearing loss and tinnitus Unilateral tinnitus Pulsatile tinnitus Report of tinnitus + symptoms of a stroke Sudden difficulty communicating, movement disorders, personality changes http://www.emedicinehealth.com/tinnitus/page4_em.htm

14. Getting to the Crux Tinnitus is a symptom, NOT a disease. The pathology causing tinnitus may be outside of the scope of audiologists. The actual “cause” of tinnitus depends on pathophysiology. Understanding the pathophysiology will help us (AuDs, PhDs, MDs, DOs, neurologists, neurosurgeons, etc…) to better treat people who experience tinnitus.

15. A Familiar Scenario Patient: I’ve had this ringing in my ears for years. My doctor told me that there’s no cure for it. Is that true? Audiologist:

16. Pathophysiology Nuerophysiologically, “ … Tinnitus is the consequence of the brain’s response to input deprivation from the auditory periphery” (Benson et al., 2009). Leaver et al. (2011) suggest that tinnitus occurs due to abnormal function of the limbic system, which controls emotion. Suggests link to depression, anxiety?

17. Pathophysiology In a healthy cochlea, there is a tonotopic organization (peripheral). Signal travels from the cochlea to the midbrain to the auditory cortex. 

18. Pathophysiology In a damaged cochlea, cortical and subcortical pathways adapt to lack of stimulation (plasticity) and the tonotopic organization (not just of the cochlea, but rather of the projections from the cochlea mesencephalon cortex) is altered (Benson et al., 2009). Neuroplasticity may take the form of: Creation or elimination of synapses, including their axons and dendrites, causing changes in how effectively the electrical signal is transmitted (Moller).

19. Anatomical Reference - Synapse http://hshgp.genome.washington.edu/teacher_resources/modules-view.htm

20. Pathophysiology In the auditory cortex, the area that no longer receives stimulation due to cochlear injury is called the lesion projection zone (LPZ). Following cochlear injury, neurons in the LPZ change in two ways: Increase in spontaneous firing rate Neurons that are adjacent to the LPZ represent a larger frequency range (Benson et al., 2009)

21. Pathophysiology This mechanism is believed to be the neurophysiological correlate of tinnitus (Benson et al., 2009). A key understanding in tinnitus research over the years was that although tinnitus presents in the ear, it is a neurological phenomenon. As evidenced by the fact that if the auditory nerve was severed, tinnitus was yet able to persist (Moller).

22. How is Tinnitus Quantified? May use pitch and loudness mapping 90% of pts report tinnitus at an intensity level of <20 dB 84% of pts report tinnitus at an intensity level of <9 dB These measures are useful for masking devices Do these measures match subjective reports of tinnitus severity? (Benson et al., 2009)

23. How is Tinnitus Quantified? The Tinnitus Handicap Inventory Self-report measure Validated in 1996 Measures how tinnitus affects daily life Functional, Emotional, and Catastrophic subscales (Newman, Jacobson, & Spitzer, 1996)

24. Tinnitus’ Kissing Cousins If the patient has tinnitus: Sound may be distorted. Patient may also have hyperacusis and/or phonphobia (Moller). The patient may have anxiety, isolation, and/or depression.

25. Treatment May depend on etiology Glomus tumor: Surgical removal Meniere’s Disease: Endolymphatic shunt, labyrinthectomy, antibiotic injection Courtesy of Hood Labs www.earassociates.com

26. Treatment Let’s hear from Roger Miller, PhD, Director for Hearing and Balance at NIDCD http://ocplmedia.od.nih.gov/nihradio/20110113NIDCDtinnitus.mp3?utm_source=twitterfeed&utm_medium=twitter Behavioral: Tinnitus Feedback Retraining, Support Groups, Counseling (informational and affective) Masking Vagal Nerve Stimulation: Like pressing “Reset” button in the brain

27. Treatment Pharmacologic: Treat symptoms related to tinnitus, such as depression and anxiety. Nortriptyline (50 mg): Most effective drug, although it causes dry mouth and takes 3-4 weeks to build up summative effect for benefit. SSRIs Paroxetine (10 mg) AKA Paxil Sertraline (50 mg/d) AKA Zoloft: Reduced tinnitus severity, as well as symptoms of depression and anxiety Benzodiazepines: Treats tinnitus as an anxiety disorder BUT should not use these if depression is present (and often it is). (Benson et al., 2009)

28. Non-Traditional Treatment Electrical Stimulation Overall, mixed success Stimulation may only be effective during stimulus presentation First attempted by Volta in the 1800s Types: Cutaneous, brain stimulation, promontory stimulation New: Repetitive transcranial magnetic stimulation (rTMS) (Benson et al., 2009)

29. Repetitive Transcranial Magnetic Stimulation (rTMS) The Society for Neuroscience www.sfn.org

30. Non-Traditional Treatment Biofeedback Commonly used for the management of pain Pt monitors involuntary bodily processes such as heart rate, blood pressure, and muscle tension through electromyography (EMG) and electroencephalography (EEG) (UMMC, 2011). Goal is to reduce anxiety and/or stress that may aggravate tinnitus Conducted by a psychologist <80% of pts report reduction in tinnitus symptoms (Benson et al., 2009).

31. Non-Traditional Treatment Homeopathic Therapy GinkoBiloba: Antioxidant that inhibits platelet aggregation  promotes circulation to small blood vessels such as those that supply the cochlea. Niacin: May provide smooth muscle relaxation and promote circulation to small blood vessels. Pts may report that Niacin reduces severity of tinnitus (Benson et al., 2009).

32. Pediatrics Prevalence varies Shetye and Kennedy (2010) noted it occurs in 12 - 36% of children with normal hearing and in <66% of children with hearing loss. Shetye and Kennedy (2010) noted that 3 – 10% of children are significantly affected by it. May be more difficult to identify in children Might pediatric tinnitus become more prevalent due to environment? (Shetye & Kennedy, 2010).

33. Areas of Further Research – Moving from Anecdotal to Evidence-Based Practice Caffeine: Anecdotal evidence tells us that caffeine consumption exacerbates tinnitus. St. Claire et al. (2010) found that caffeine consumption had no effect on tinnitus severity but that caffeine withdrawal symptoms were observed. Heritability: Anecdotally, tinnitus may “Run in families.” Kvestad et al. (2010) found low heritability of tinnitus.

34. Works Cited American Tinnitus Association (ATA). What you should know about tinnitus. Retrieved from http://www.ata.org/sites/ata.org/files/pdf/ATA%20Facts% 20About%20Tinnitus.pdf AnaesthesiaUK. (2010). Cannulation of the internal jugular vein. [Graphic]. Benson, A.G., McGuire, J.F., Djalilian, H.R., Hanks, K.M., Robbins, W.K. (2009). Inner Ear, tinnitus. MedScape online encyclopedia. Retrieved from http://emedicine. medscape.com/article/856916-overview Gurr, P., Owen, G. Reid, A. & Canter, R. (1993). Tinnitus in pregnancy. Clinical Otolaryngology, 18(4), 294-297. Kvestad, E., Czajkowski, N., Engdahl, B., Hoffman, H., & Tambs, K. (2010). Low heritability of tinnitus: Results from the second Nord-Trandelag study. Archives of Otolaryngology, Head and Neck Suergery, 136(2), 178-182. Leaver, A.M., Renier, L., Chevillet, M.A., Morgan, S., Kim, H.J., Rauschecker, J.P. (2011). Dysregulation of limbic and auditory networks in tinnitus. Neuron, 69(1), 33-43. Moller, A. R. Pathophysiology of tinnitus. [Powerpoint slides] presented at the University of Texas at Dallas, School of Behavioral and Brain Sciences. Retrieved from http://www.slideworld.org/slideshow.aspx/Pathophysiology-of-tinnitus-ppt-4329

35. Works Cited Neuromonics Inc. (2011). What tinnitus sounds like. Retrieved from http://www.neuromonics.com/patient/treatment/index.aspx?id=50 Newman, C.W., Jacobson, G.P., & Spitzer, J.B. (1996). Development of the tinnitus handicap inventory. Archives of Otolaryngology, Head and Neck Surgery, 122(2), 143-8. Shetye, A., & Kennedy, V. (2010). Tinnitus in children: An uncommon symptom? Archives in disease in childhood, 95(8), 645-648. St. Claire, L., Stothart, G., McKenna, L., & Rogers, P.J. (2010) Caffeine abstinence: An ineffective and potentially distressing tinnitus therapy. International Journal of Audiology, 49(1), 24–29. The Society for Neuroscience. (2011). Obsessive-compulsive disorder. Retrieved from http://www.sfn.org/index.aspx?pagename=brainbriefings_obsessivecompulsivedisorder University of Maryland Medical Center. (2011). Biofeedback. Retrieved from http://www.umm.edu/altmed/articles/biofeedback-000349.htm U.S. Department of Health and Human Services National Institutes of Health. (2011). Carotid artery surgery – series. In MedLine Plus. Retrieved from http:// www.nlm.nih.gov/medlineplus/ency/presentations/100124_1.htm