Work Cited:
Brozoski TJ, Spires DJ, Bauer CA (2007). “Vigabatrin, a GABA Transaminase Inhibitor, Reversibly Eliminates Tinnitus in an Animal Model.” Journal of the Association for Research in Otolaryngology, 8, 105-118.
Summary:
Incorporation of vigabatrin (a GABA agonist) into the drinking water of rats with acoustic trauma induced chronic tinnitus eliminated the psychophysical evidence of chronic tinnitus. Present study also demonstrated that elevation of central GABA levels effectively counteracted tinnitus.
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Work Cited:
Zheng Y, Hamilton E, McNamara E, Smith PF, Darlington CL (2011). “The Effects of Chronic Tinnitus Caused by Acoustic Trauma on Social Behavior and Anxiety in Rats.” Neuroscience 193, 143-153.
Summary:
Investigation of the effects of tinnitus on social interaction and anxiety in animals with acoustic trauma induced tinnitus. Rats with tinnitus demonstrated more aggression (biting, kicking, nudging, sleeping with) towards both rats given a sham procedure (placebo) and other tinnitus rats. Sham rats also demonstrated more aggression towards tinnitus rats.
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Work Cited:
Krick CM, Argstatter H, Grapp M, Plinkert PK, Reith W (2017). “Heidelberg Neuro-Music Therapy Enhances Task-Negative Activity in Tinnitus Patients.” Frontiers in Neuroscience, Auditory Cognitive Neuroscience 11 (384).
Summary:
Evaluation (using fMRI) of the activity of the brain's default-mode network, following the improvements of tinnitus-related distress after the HNMT intervention. Tinnitus-related distress points to a diminished activity of the DMN -- study allows for evaluation of neural changes associated with improvements in tinnitus distress. Found that the HNMT triggers increased DMN activity in the posterior cingulate cortex, which underlies the improvements in tinnitus-related distress.
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Work Cited:
Teismann H, Okamoto H, Pantev C (2011). “Short and Intense Tailor-Made Notched Music Training against Tinnitus: The Tinnitus Frequency Matters.” PLoS ONE 6 (9).
Summary:
Present study developed and evaluated a short term ( 5 days) and intensive (6 hours/day) tailor-made notched music training for patients suffering from chronic, tonal tinnitus. 2 matched patient groups with either low (</= 8 kHz) or high (>8 kHz) tinnitus frequencies. Evaluated persistency of TMNMT effects over a 4-week post-training phase. TMNMT took effect in patients with low frequency tinnitus (reduced subjective tinnitus loudness, distress, and auditory cortex evoked activity), but no significant results were observed in patients with high frequency tinnitus. Induced changes as a result of the TMNMT were also not persistent.
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Work Cited:
Grapp M, Hutter E, Argstatter H, Plinkert PK, Bolay HV (2013). “Music therapy as an early intervention to prevent chronification of tinnitus.” Int J Clin Exp Med 6 (7), 589-593.
Summary:
Present study investigates whether intervening during an early stage of acute tinnitus would prevent symptoms from becoming chronic. Evaluated music therapeutic intervention according to the "Heidelberg Model;" treatment lasted 10 consecutive 50-minute sessions of individualized therapy, and tinnitus severity and distress assessed by Tinnitus Questionnaire at start and end of treatment. Results show score changes from beginning to end -- significant improvement in tinnitus impairment.
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Work Cited:
Yang S, Weiner BD, Zhang LS, Cho SJ, Bao S (2011). “Homeostatic plasticity drives tinnitus perception in an animal model.” PNAS 108 (36).
Summary:
Present study investigated hearing loss-induced cortical map reorganization, synaptic plasticity, and tinnitus behaviors. Sensory deprivation-induced homeostatic down-regulation of inhibitory synapses may contribute to tinnitus perception. Drugs that enhance GABA-mediated inhibition, not one that reduces excitation, reversibly abolished tinnitus behavior. Results suggest that tinnitus is likely caused by homeostatic down-regulation of inhibitory synapses in the high CF zone.
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Work Cited:
Llano DA, Turner J, Caspary DM (2012). “Diminished Cortical Inhibition in an Aging Mouse Model of Chronic Tinnitus.” The Journal of Neuroscience, Neurobiology of Disease 32 (46), 16141-16148.
Summary:
Evaluated auditory cortical synaptic responses in aged animals with behavioral evidence of tinnitus and hearing loss, using flavoprotein autofluorescence imaging. Mice were exposed to noise trauma and assessed for behavioral evidence of tinnitus and hearing loss immediately after trauma and again after 24-30 months. Noise exposed animals showed 68% increase in amplitude of cortical activation compared with controls. Strength of cortical activation was significantly correlated to the degree of tinnitus behavior. Data suggests that noise trauma can cause long-lasting changes in the auditory cortical physiology and may provide specific targets to ameliorate the effects of chronic tinnitus.
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Work Cited:
Krick CM, Argstatter H, Grapp M, Plinkert PK, Reith W (2017). “Heidelberg Neuro-Music Therapy Restores Attention-Related Activity in the Angular Gyrus in Chronic Tinnitus Patients.” Frontiers in Neuroscience, Auditory Cognitive Neuroscience 11.
Summary:
Present study aims to evaluate the role of the angular gyrus during visual attention tasks in tinnitus sufferers treated with HNMT. Visual attention was evaluated using fMRI during a visual continuous performance task (CPT). CPT results revealed a relationship between error rates and tinnitus duration at baseline. Patients with chronic tinnitus who were treated with HNMT had decreasing error rates compared with recent-onset patients. fMRI analyses confirmed greater activation of the AG during CPT in chronic patients after HNMT treatment compared to recent-onset patients. Findings suggest that HNMT treatment helps shift the attention from the auditory phantom percept toward visual cues in chronic tinnitus patients, and this shift may involve the AG.
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Work Cited:
Argstatter H, Grapp M, Hutter E, Plinkert P, Bolay HV (2012). “Long-term effects of the ‘Heidelberg Model of Music Therapy’ in patients with chronic tinnitus.” Int J Clin Exp Med 5 (4), 273-288.
Summary:
Present study aims to explore the long-term impact of the HNMT treatment after 5.4 years. 107 complete questionnaires entered analysis for the study, and 76% of patients achieved a reliable reduction in their tinnitus scores. Overall tinnitus distress diminished. Evaluation of therapeutic elements displays that only music therapy specific interventions were rated helpful by the patients. Results demonstrate that the HNMT for chronic tinnitus seems to be effective in the long run. (HNMT as a 9 session 50 minute intervention across 5 days)
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Work Cited:
Argstatter H, Grapp M, Plinkert PK, Bolay HV (2012). “ ‘Heidelberg Neuro-Music Therapy’ for chronic-tonal tinnitus – treatment outline and psychometric evaluation.” International Tinnitus Journal 17 (1), 34-44.
Summary:
Present study investigates HNMT treatment (compact and standard). 135 patients with chronic, tonal tinnitus attended a standardized protocol for neuro-music therapy. Results were compared to a cognitive behavioral placebo music therapy procedure. Tinnitus distress was assessed using the German version of the tinnitus questionnaire at admission, discharge, and 6 months after therapy. Results showed that TQ scores significantly improved: over 80% of music therapy patients (standard and compact) revealed a reliable improvement compared to 44% in the placebo group. Therapy impact seems long lasting, since TQ scores remained stable until follow up at 6 months. Demonstrated that HNMT has fast onset and long-lasting effects for patients with "tonal" tinnitus, likely because it's more individualized and active in musical training directly for the patient's tinnitus sound.
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Work Cited:
Bauer CA, Brozoski TJ, Rojas R, Boley J, Wyder M (1999). “Behavioral model of chronic tinnitus in rats.” Otolaryngology – Head and Neck Surgery, 121 (4), 457-462.
Summary:
Present study induced tinnitus in rats with salicylate (known to produce tinnitus in humans). Given sodium salicylate in their water and conditioned to press a lever for food in the presence of continuous white noise. Results indicated that the experimental subjects could detect the tone stimuli and weren't hearing impaired. Conclude that rats, under the proper condition, perform in an auditory discrimination task as though they had tinnitus.
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Work Cited:
Jones A, May BJ (2018). “Effects of Acoustic Environment on Tinnitus Behavior in Sound-Exposed Rats.” Journal of the Association for Research in Otolaryngology, 19, 133-146.
Summary:
Present study tested sound exposed rats for tinnitus while housing them in either noisy or quiet conditions. Results showed that those housed in quiet conditions developed behavioral signs of tinnitus, while those housed in noisy conditions didn't. This suggests that sustained patterns of noise-driven activity may prevent injury-induced changes in central auditory processing. This could be applied clinically as early intervention with sound therapy, helping to reduce the risk of tinnitus in individuals that experienced acute cochlear injury.
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Work Cited:
Xia C, Yin M, Wu C, Ji Y, Zhou Y (2020). “Neuroglial activation in the auditory cortex and medial geniculate body of salicylate-induced tinnitus rats.” Am J Transl Res, 12 (10), 6043-6059.
Summary:
Present study examined markers associated with astrocytes and microglia in the primary auditory (A1) cortex and medial geniculate body (MGB) of rats with salicylate-induced tinnitus. Results demonstrated that acute and chronic administrations of salicylate could cause reversible tinnitus-like behavior. There was increased astrocyte activation and microglia proliferation in the central auditory system of rats experiencing tinnitus. This potentially implicates a glial regulation in tinnitus development.
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Work Cited:
Brozoski TJ, Wisner KW, Sybert LT, Bauer CA (2012). “Bilateral Dorsal Cochlear Nucleus Lesions Prevent Acoustic-Trauma Induced Tinnitus in an Animal Model.” Journal of the Association for Research in Otolaryngology, 13, 55-66.
Summary:
Present study investigated DCN (dorsal cochlear nucleus) ablation to reduce tinnitus in animal models. DCN presents with abnormally elevated spontaneous neural activity of animals with tinnitus. Present study failed to decrease pre-existing tinnitus and believes DCN may serve as a trigger zone rather than a chronic generator of tinnitus. This trigger mechanism may involve plastic circuits that increase spontaneous neural output to rostral areas like the inferior colliculus. This increased drive could produce persistent pathological changes in the rostral areas that comprise the tinnitus signal.
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Work Cited:
Zheng Y, Reid P, Smith PF (2015). “Cannabinoid CB1 receptor agonists do not decrease, but may increase acoustic trauma-induced tinnitus in rats.” Frontiers in Neurology, 6 (60), 1-9.
Summary:
Present study investigated the use of cannabinoids as treatment for tinnitus in acoustic trauma-induced rats. Cannabinoids significantly increased the number of tinnitus animals in the exposed-tinnitus group, but not in the sham group. Results suggest that cannabinoids may promote the development of tinnitus, especially when there is pre-existing hearing damage.
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Work Cited:
Zheng Y, McNamara E, Stiles L, Darlington CL, Smith PF (2012). “Evidence that memantine reduces chronic tinnitus caused by acoustic trauma in rats.” Frontiers in Neurology, 3 (127), 1-10
Summary:
Present study investigates the use of memantine (an uncompetitive NMDA receptor) as treatment for acoustic trauma-induced tinnitus. Results suggest that memantine may reduce tinnitus caused by acoustic trauma, shown by significantly decreased proportion of rats that exhibited tinnitus behavior.
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Work Cited:
Ralli M, Lobarinas E, Fetoni AR, Stolzberg D, Paludetti G, Salvi R (2010). “Comparison of salicylate and quinine induced tinnitus in rats; development, time course and evalution of audiological correlates.” Otol Neurotol, 31 (5), 823-831.
Summary:
Present study examined the similarities and differences between the frequency and time course of tinnitus and hypoacusis induced by salicylate and quinine. Compared salicylate and quinine induced tinnitus in rats using the gap prepulse inhibition of acoustic startle (GPIAS). Results were not statistically significant and were variable among animal subjects.
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Work Cited:
Zheng Y, Stiles L, Chien YT, Darlington CL, Smith PF (2014). “The Effects of Acute Stress-Induced Sleep Disturbance on Acoustic Trauma-Induced Tinnitus in Rats.” BioMed Research International, 1-8.
Summary:
Present study examined whether acute stress-induced sleep disturbance could increase the susceptibility to acoustic trauma-induced tinnitus in rats. Sleep disturbance didn't exacerbate the perception of tinnitus in rats. Neither tinnitus alone nor tinnitus plus sleep disturbance altered the number of orexin-expressing neurons in the hypothalamus. Results suggest that acute sleep disturbance doesn't cause long term changes in the number of orexin neurons and doesn't change the perception of tinnitus induced by acoustic trauma in rats.
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Work Cited:
Ralli M, Troiani D, Podda MV, Paciello F, Eramo SLM, Corso ED, Salvi R, Paludetti G, Fetoni AR (2014). “The effect of the NMDA channel blocker memantine on salicylate-induced tinnitus in rats.” Basic Research in Otolaryngology, 34, 198-204.
Summary:
Present study aims to determine whether systemic treatment with memantine (NMDA channel blocker) prevents salicylate-induced tinnitus in animals. Tinnitus-like behavior was assessed with the GPIAS. Memantine didn't cause a significant change in GPIAS. Results indicate the role of NMDA receptors in the induction of salicylate-induced tinnitus.
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Work Cited:
Zheng Y, Smithies H, Aitken P, Gliddon C, Stiles L, Darlington CL, Smith PF (2015). “Cell proliferation in the cochlear nucleus following acoustic trauma in rat.” Neuroscience 303, 524-534.
Summary:
Present study aims to further investigate the nature of cell proliferation in the CN (cochlear nucleus) following acoustic trauma-induced tinnitus in rats. Bromodeoxyuridine (BrdU) immunohistochemistry was used to measure cell proliferation and newborn cell survival. Double immunolabeling for BrdU and Ki-67, BrdU and CD-11b, and BrdU and doublecortin (DCX) was used to investigate the origin of the proliferating cells. Results suggest that DCX-expressing cells in the CN may proliferate in response to acoustic trauma. But the proportion of cells proliferating, and the survival rate of the newborn cells may not support functional neurogenesis in the CN.
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Work Cited:
Yang G, Lobarinas E, Zhang L, Turner J, Stolzberg D, Salvi R, Sun W (2007). “Salicylate induced tinnitus: Behavioral measures and neural activity in auditory cortex of awake rats.” Hearing Research, 226, 244-253.
Summary:
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Work Cited:
Ruttiger L, Ciuffani J, Zenner HP, Knipper M (2003). “A behavioral paradigm to judge acute sodium salicylate-induced sound experience in rats: a new approach for an animal model on tinnitus.” Hearing Research, 180, 39-50.
Summary:
Rats conditioned to access a liquid feeder whenever a constant white noise was played. No reward was given during silence. Feeder access was increased after tinnitus was induced in rats using 350 mg/kg of sodium salicylate, indicating the presence of tinnitus.
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Work Cited:
Brozoski TJ, Caspary DM, Bauer CA, Richardson BD (2010). “The effect of supplemental dietary Taurine on tinnitus and auditory discrimination in an animal model.” Hearing Research, 270, 71-80
Summary:
Present study adds taurine (partial agonist at inhibitory glycine and y-amino butyric acid receptors) to the daily diet of rats to examine its effects on chronic tinnitus and normal auditory discrimination. Rats were trained and tested in an operant task shown to be sensitive to tinnitus. Results show that high taurine dose significantly attenuated tinnitus, which returned to near pre-treatment levels following washout. Results were consistent with hypothesis that taurine attenuates tinnitus and improves auditory discrimination by increasing inhibitory tone and decreasing noise in the auditory pathway.
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Work Cited:
Wang H, Brozoski TJ, Caspary DM (2011). “Inhibitory neurotransmission in animal models of tinnitus: Maladaptive plasticity.” Hearing Research, 279, 111-117.
Summary:
Review examines evidence for chronic plastic neuropathic changes in the central auditory system of animals with psychophysically defined tinnitus.
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Work Cited:
Zheng Y. Hamilton E, Begum S, Smith PF, Darlington CL (2011). “The effects of acoustic trauma that can cause tinnitus on spatial performance in rats.” Neuroscience, 186, 48-56.
Summary:
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Work Cited:
Bauer CA, Kurt W, Sybert LT, Brozoski TJ (2013). “The cerebellum as a novel tinnitus generator.” Hearing Research, 295, 130-139.
Summary:
A series of experiments examining the role of the cerebellum in trauma-induced tinnitus. PFL (paraflocculus of the cerebellum) was surgically ablated in animals before the induction of tinnitus. It was found that PFL ablation eliminated established tinnitus without altering auditory discrimination. However, PFL ablation before tinnitus induction attenuated, but didn't completely eliminate tinnitus.
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Work Cited:
Brozoski TJ, Ciobanu L, Bauer CA (2007). “Central neural activity in rats with tinnitus evaluated with manganese-enhanced magnetic resonance imaging (MEMRI).” Hearing Research, 228, 168-179.
Summary:
Incorporation of vigabatrin (a GABA agonist) into the drinking water of rats with acoustic trauma induced chronic tinnitus eliminated the psychophysical evidence of chronic tinnitus. Present study also demonstrated that elevation of central GABA levels effectively counteracted tinnitus.
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Work Cited:
Zheng Y, McPherson, Smith PF (2014). “Effects of early and late treatment with L-Baclofen on the development and maintenance of tinnitus caused by acoustic trauma in rats.” Neuroscience, 258, 410-421.
Summary:
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Work Cited:
Brozoski TJ, Bauer CA (2005). “The effect of dorsal cochlear nucleus ablation on tinnitus in rats.” Hearing Research, 206, 227-236.
Summary:
Present study investigates the hypothesis that the rostral output of the DCN is necessary for the experience of chronic tinnitus by ablating the dorsal DCN and the dorsal acoustic stria of rats with psychophysical evidence of tinnitus. Ablating the DCN should decrease the evidence of tinnitus, if the DCN plays a role in chronic tinnitus. However, bilateral dorsal DCN ablation didn't significantly affect the psychophysical evidence of tinnitus, and ipsilateral dorsal DCN ablation appeared to increase the evidence of tinnitus. Results showed that the DCN doesn't act as a simple feed forward source of chronic tinnitus.
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