Tinnitus: A Proposed Rating System for Workers' Compensation Claimants

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By Ronald R. Ward, M.D., F.A.C.S. (OTO/HNS) & Robert Sweetow, Ph.D. (Audiology) 

The United States Dept. of Labor Occupational Safety and Health Administration estimates that nearly 250 million dollars are spent annually on workers' compensation for hearing loss disability. Tinnitus is a commonly reported symptom by claimants indicating industrial hearing loss and other related auditory and somatosensory anomalies. While there is a defined method for evaluating hearing loss, no such procedure currently exists for tinnitus, largely because of its subjective nature and lack of objective measures, but also as a result of the multiple other complaints that may be associated with tinnitus. In this paper, basic education regarding tinnitus, its causation, diagnosis, and related maladies are presented. This discussion is followed by a rationale and proposed rating system that may be used by qualified medical examiners. 

The majority of claimants in the Workers' Compensation (WC) system evaluated by otolaryngologists have complaints of hearing loss and/or tinnitus (While there are no published data on the subject, it is the experience of the authors in their role as Independent Medical Examiners, that more than 90% of claimants report symptomatic tinnitus). (1,4,5) Unfortunately, due to the subjective nature of tinnitus, a clear rationale and guidelines for rating this symptom have not been agreed upon and remain highly idiosyncratic. The purpose of this paper is two-fold. First, it will provide basic education regarding the nature, causation, and consequences of tinnitus. Second, it will propose a practical and specific rating system to convert the subjective nature of tinnitus to a more objective methodology. 

Claimants of tinnitus typically have been exposed to excessive industrial noise during the course of employment over a period of years. Some may have been continuously employed by one employer, others have histories of noise exposure at several employment venues. Some cases are caused by sudden, catastrophic events, e.g. explosions, however, most are of gradual onset. Workers exposed to high levels of industrial noise include, but are not limited to, firefighters, police officers, construction workers, airline maintenance employees, utility plant employees, truck drivers, heavy equipment operators, longshoremen, etc. Claimants may or may not have had consistent usage of hearing protective devices, i.e. earplugs or headsets, made available by their employers.

Moreover, many employers do not routinely supply or require the use of these protective devices in spite of Occupational Safety and Health Administration (OSHA) guidelines specifying protective measures for individuals exposed to workplace noise levels of 90dBA or greater. Some workers may obtain their own protective devices and use them when feasible for personal and co-worker safety. Unfortunately, the inherent necessity to hear well in many jobs that routinely have either sporadic or continuous high noise levels often precludes the use of indicated hearing protection for safety and job performance reasons. Furthermore, noise level testing often is not performed at many worksites. Thus, noise level testing may only be conducted upon request of the employee, the Qualified Medical Examiner (QME), or following a significant workplace event. Even if such testing is performed, the findings may not reflect all of the noise levels some workers, e.g. firefighters, police officers, and transportation employees, at varying work locations are exposed to. 

Definition of Tinnitus 

Tinnitus may be defined as the perception of noise or ringing in the ears or head in the absence of an associated external sound. It can be characterized as hissing, roaring, pulsing, whooshing, chirping, whistling, clicking, constant, intermittent, fluctuating, monotonal, or multitonal (Sweetow, 1986; 1996). (3) Hearing Health Foundation statistics and numerous other studies (Davis and El Refaie, 2000; Coles, 1996; McFadden, 1982), estimate that approximately 15% of the adult population report tinnitus, 10-20% of tinnitus sufferers seek medical attention, and 80-90% of tinnitus patients show some evidence of hearing loss. Aural-related tinnitus can be secondary to hair cell damage in the cochlea, lesions on the auditory nerve, a central (brain) origin, or a combination of these anatomic regions. 

Causation of Tinnitus 

A partial list of causational factors (3,6) for tinnitus includes Hearing loss, Meniere's disease, loud noise exposure (Negri and Schorn, 1991), migraines (Guichard et al, 2016), head injury, drugs or medications that can be toxic to hearing, anemia, hypertension (Figueiredo et al, 2015), stress (Mazurek et al, 2015; Hoffman et al, 2013). cerumen impaction, auditory nerve tumors, excessive caffeine ingestion, diabetes mellitus (Kakarlapudi et al 2003; Somogyi, et al, 2013), hyperlipidemia ((Jhang, et al, 1989; Doosti, et al., 2016; Hang, et al, 2007) smoking (Palmer et al, 2004), temporomandibular joint (TMJ) disorders (Myers, 1988), cervical injury (Shore et al, 2007), and aging. (17, 24, 25, 26, 27) In the Workers' Compensation system, tinnitus is rarely the primary complaint.

Generally, it is evaluated as a symptom secondary to the primary complaint of industrial-related hearing loss. Tinnitus is frequently more noticeable in the absence of normal everyday distractions. Background noise can exacerbate it, but tinnitus is usually more noticeable in a quiet environment where there is no ambient masking. Tinnitus can result in interference with conversations, difficulty concentrating (Stevens et al, 2007; Rossiter et al, 2006; Hallum et al, 2004), and sleep disturbance (Folmer and Greist, 2000), leading to the need to take sedative medication at bedtime. In addition, emotional and psychiatric complications can occur (Marciano et al, 2003). A brief discussion of the most common factors causing tinnitus follows. 

Excessive noise exposure: OSHA standards require that workers not be exposed to sound levels greater than 85dBA averaged over an eight-hour period, with a 5 dB exchange rate (that is, 4 hours permissible exposure is 90 dBA, 2 hours is 95 dBA, etc.). The presenting complaint in industrial noise exposure is typically hearing loss and tinnitus. (7) Hearing loss: Hearing loss may be congenital, hereditary (familial), post-traumatic, or acquired (infectious, physiologic, allergic). Congenital implies a condition existing at or before birth regardless of cause. Congenital disorders may be the result of genetic or environmental factors. Hereditary implies a genetic disorder caused by one or more abnormalities in the genome, especially a condition that is present from birth. Genetic disorders may be hereditary, i.e. passed down from the parent's genes. In other genetic disorders, defects may be caused by new mutations or changes to the DNA. In such cases, the defect will only be passed down if it occurs in the germline. Post-traumatic implies loss related to an injury. Injuries that can result in hearing loss include, but are not limited to, temporal bone fracture, traumatic brain injury (TBI), tympanic membrane perforation, ossicular chain disruption, oval or round window rupture. Acquired implies that the aural system was intact and functioning normally prior to infectious, physiologic, or allergic events. Acquired factors include Eustachian tube disease, inflammatory middle ear disease, middle ear infections, and mastoiditis. Any of these hearing losses may be exacerbated by industrial injury. 

Patulous Eustachian tube: Associated with weight loss and pregnancy. Symptoms change with respiration. Lying down relieves symptoms. Somatosensory involvement: While the vast majority of people with tinnitus have hearing loss, a person with a cervical injury or bruxism, i.e. teeth grinding, may report tinnitus. (17,18) Some of these patients can change the perception of their tinnitus by moving their jaw or neck, or by even moving their eyes to one side or the other. This is possible because there is crosstalk between nerves (ephaptic transmission). In the case of cervical injury, some of the signals that ought to be shunted to the somatosensory cortex can actually get short-circuited over to the auditory cortex. If it reaches the auditory cortex, regardless of where it originates, it will be perceived as an acoustic event. Therefore, the signal that ought to be perceived as a somatosensory event or something that the patient actually feels can become something that the patient thinks they hear. Palatal myoclonus: Characterized by clicking sounds and spasms in tensor palatini, levator palatini, or levator veli palatini spasm. This condition is associated with multiple sclerosis, vascular disease, tumors, and other degenerative disorders. Idiopathic spasm (myoclonus) of stapedial muscle or tensor tympani muscle: Rare. Head injury: Temporal bone fracture/concussion, traumatic brain injury (TBI), and acoustic blast injury can result in hearing loss and/or tinnitus. 

Meniere's disease: Meniere's syndrome is a disorder of the inner ear characterized by episodes in which the patient may experience dizziness, vertigo, tinnitus, hearing loss, and/or fullness in the ear. Usually, only one ear is initially affected; however, over time both ears may become involved. Episodes generally last from 20 minutes to a few hours. The time between episodes varies. The hearing loss and ringing in the ears may become constant. The cause of Meniere's disease is unclear but likely involves both genetic and environmental factors. The common element is excessive endolymphatic fluid in the inner ear system. Factors include heredity, post-infectious, post-traumatic, toxic exposure, allergy, and idiopathic. 

Migraine: Vestibular and/or otic migraine may or may not present with classic symptoms of migraine, i.e. severe throbbing headache on one side of the head, nausea and vomiting, extreme sensitivity to light and noise, and the need to go to a dark, quiet room to sleep. Vestibular symptoms include vertigo, imbalance, dizziness, unsteadiness, and extreme sensitivity to motion. Hearing symptoms include muffled hearing, ear fullness, and tinnitus or ringing in the ear. The cause of migraine headaches is probably related to both abnormal discharges in cells within the brain and to the constriction of the wall of the blood vessels in and around the brain. Factors that have been associated with migraine include hypoglycemia, stress and altered sleep patterns, diet, chocolate, red wine, caffeinated beverages, cheeses, monosodium glutamate (MSG), female gender, menstruation, and familial propensity. 

Drugs or medicines that are toxic to hearing: There are more than 200 medications and chemicals that are known to cause hearing and balance problems. Examples include aminoglycoside antibiotics (e.g. gentamycin), cancer chemotherapy drugs (e.g. cisplatin and carboplatin), salicylates (e.g. aspirin), other non-steroidal anti-inflammatory drugs, e.g. Motrin, Naprosyn, quinine, and loop diuretics, ACE inhibitors, and calcium antagonists. Loud noise exposure while taking ototoxic medications may increase their damaging effects. Smoking is considered a drug as well. (16) 

Vascular (pulsatile) tinnitus: Pulsatile tinnitus can be classified by its site of generation as arterial, arteriovenous, or venous. Typical arterial causes are arteriosclerosis and fibromuscular dysplasia. Common causes at the arteriovenous junction include arteriovenous fistulae and highly vascularized skull base tumors. Common venous causes are benign intracranial hypertension, and, as predisposing factors, anomalies and normal variants of basal veins and sinuses e.g. jugular bulb anomalies. 

There are two plausible causes of pulsatile tinnitus:

1) Blood flow accelerates, or changes in blood flow disrupt the laminar flow, and the resulting local turbulence is audible. 

2) Normal blood flow sounds within the body are perceived more intensely, either as a result of alterations in the inner ear with increased bone conduction or as a result of disturbance of sound conduction leading to loss of the masking effect of external sounds.

Pulsatile tinnitus is usually unilateral unless the underlying vascular pathology is bilateral. Somatosensory pulsatile tinnitus is bilateral tinnitus with no vascular cause. Diagnostic vascular imaging studies include CTA (computer tomography angiography), MRA (magnetic resonance angiography), and DSA (digital subtraction angiography). Full Doppler ultrasound of the head and neck is essential. A lumbar puncture measuring CSF (cerebrospinal fluid) pressure may be indicated. 

Hypertension: There is evidence of an association between tinnitus and hypertension, although a cause-and-effect relationship is uncertain. (9) 

Stress: Emotional stress is a frequent co-factor in tinnitus patients. (2, 19, 20, 21, 22, 23) Fear and anxiety regarding tinnitus can increase subjective severity. The mechanism of stress contributes to the onset of or progression of tinnitus remains unknown. Pathways induced by emotional stress and the outcome of their induction include corticosteroid-dependent changes in gene expression, epigenetic modulations, and the impact of stress on neuronal plasticity and neurotransmission. (8,10) 

Cerumen impaction: Cerumen impaction, epithelial impaction, and epithelial hyperkeratosis on the tympanic membrane can result in tinnitus by direct contact with and stimulation of tympanic membrane activity. 

Tumors: Acoustic neuroma of the 8th cranial nerve (auditory) can generate tinnitus. Tinnitus is a frequent post-radiation therapy complication in head and neck tumors. 

Age: The aging process usually results in outer hair cell loss or impaired function of these cells. These cells are in the area of high-frequency perception, thus damage can result in the form of high-frequency tinnitus. 

Diabetes mellitus: Several clinical studies have concluded that both sensorineural hearing loss and tinnitus (and vertigo) have a higher prevalence in patients with type 2 diabetes than non-diabetic patients. These impairments develop at an earlier age in diabetic individuals. The reason for this finding is postulated to be cochlear microangiopathy. (12, 13)

Hyperlipidemia: Postulated mechanism for cochlear hearing loss and tinnitus is decreased blood supply to the inner ear during hyperlipidemia secondary to increased platelet aggregation and blood viscosity or high lipid peroxide level in the serum and inner ear. (14,15) Thyroid disorders: Tinnitus and hearing impairment have been associated with hypothyroidism. Hyperthyroidism produces tinnitus due to turbulent blood flow. 

Infantile hypothyroidism must be diagnosed and treated expeditiously to avoid long-term hearing impairment. Treatment of these disorders with medical and/or surgical means may improve tinnitus outcomes. The most accepted theory is that tinnitus is a result of a disruption in auditory input (Roberts, et al, 2010; Salvi et al, 2000). 6 When there is damage to the peripheral auditory system, there is a subsequent change in the central nervous system. This has been demonstrated via functional imaging studies, e.g. PET and fMRI. (11) Studies have shown that when the central system is not receiving the expected input, rather than shutting itself down and becoming less active, it increases its activity. This is particularly true in areas of the dorsal cochlear nucleus, the inferior colliculus, and the auditory cortex. In addition, peripheral hearing loss typically occurs from damage to the outer hair cells which have an efferent function. This may produce a decrease in the inhibitory function of the auditory system. Cortical plasticity is affected by the tonotopic arrangements of both the cochlea and the auditory cortex (Muhlnickel et al, 1998). (25)

Certain areas of the primary auditory area respond to high frequencies, and other areas respond to lower frequencies. When there is damage to the basal turn of the cochlea, (the region that processes high frequencies), the intact cortical neurons responsible for processing the high frequencies change their function, that is, they respond to other frequencies, such as the mid frequencies. The fortunate individual with tinnitus undergoes a natural process of habituation, to the extent that the tinnitus may become less noticeable or even not bothersome at all. Importantly, there is a major association between fear and threat and tinnitus disturbance. If a person does not perceive tinnitus as being of any importance, the natural habituation process is more likely to take place than when a person has negative emotions and cognitions regarding their tinnitus. 

Fortunately, this occurs for most, though clearly not all, people experiencing tinnitus. The longer the person has the symptom, more areas of the brain become activated. This is important because it has now been clearly demonstrated that the limbic system, particularly the hippocampus and amygdala, the brain regions most responsible for managing emotions, are strongly associated with tinnitus suffering (Eggermont and Roberts, 2004). (10, 19, 20,21, 22, 23) 

Diagnosis and Treatment of Tinnitus 

The first step to be taken in evaluation is an appointment with an otolaryngologist (ear specialist) for a complete history and physical examination. Some physicians ask that a tinnitus questionnaire be filled out. This is followed by a diagnostic audiogram performed by a licensed audiologist. The audiologist may perform tinnitus pitch and loudness matching levels at the same visit. Depending on the findings of these examinations, further testing may be indicated, i.e. blood work, imaging studies, etc. Diagnosis is made based upon all available or indicated data. 

Assuming there is no surgical lesion or medical condition to be addressed as the underlying cause of tinnitus, non-invasive treatment modalities (Sweetow and Sabes, 2010) include hearing aids, cognitive behavior therapy, tinnitus retraining therapy, relaxation exercises, counseling, habituation approaches, and tinnitus masking devices, including home devices such as sound-producing machines (e.g. aquariums, low-level music, indoor waterfalls and portable media players (iPod or MP3). These options can be discussed with one's audiologist or otolaryngologist. In addition, there are some reports of benefits with biofeedback, hypnosis, and electrical stimulation. (28) 

Whole Person Impairment Rating for Tinnitus 

If an impairment based on an objective medical condition is not addressed by the AMA Guides, physicians are instructed to use clinical judgment, comparing measurable impairment resulting from the unlisted, objective medical condition to measurable impairment resulting from similar objective medical conditions with similar impairment of function in performing activities of daily living.

Hearing loss and tinnitus are conditions addressed in the AMA Guides to the Evaluation of Permanent Impairment, 5th Edition, Chapter 11, pp, 246-251. If there is a ratable hearing impairment per the Guides' reference tables, a Whole Person Impairment (WPI) can be assigned for tinnitus in accordance with the claimant's symptoms and degree of severity. (29, 30) Lacking ratable hearing impairment, tinnitus can be assigned a WPI rating only if the evaluator evokes Almarez/Guzman by analogy. It must be clearly stated that the degree of impairment secondary to tinnitus is not truly represented by the rating of the hearing impairment. (31) The symptoms related to tinnitus must be clearly stated, i.e. effects on sleep, conversations, concentration, cognition, etc. Section 11.2a is used for the analogy as it concerns tinnitus. Ratings of 1 to 5 are allowable. In Workers Compensation cases, tinnitus does not usually warrant a WPI rating or compensation, if there is no ratable hearing loss. The exception can be made if the examiner uses an Almaraz/Guzman analogy and clearly states that the tinnitus is in itself the industrial injury and thus should be compensated for.

Referral for further assessment by a psychologist may be appropriate. Whether this appeal works depends on who is reviewing the case. Any rating scale for objectifying tinnitus should be based on Activities of Daily Living (McCombe et al, 1999). (32) Tyler et al, 2014, proposed that the primary effects related to tinnitus impacting emotional well-being (including depression and anxiety), sleep, and understanding speech (either because of difficulty concentrating or hearing loss) can produce secondary effects on social, work, leisure activities. (33) In addition, it is important to consider whether the worker's current noise environment or profession is still viable and whether there is an impact on the claimant's ability to work anywhere. A final permanent disability rating is obtained only after the impairment rating obtained from an evaluating physician is adjusted for diminished future earning capacity, occupation, and age at the time of injury. 

The secondary conditions related to, or caused by the person's reaction to tinnitus are difficult to quantify due to their subjective nature. Therefore, a number of subjective rating scales have been proposed. Among the most popular and well-researched scales used in the United States are the Tinnitus Functional Index (TFI) (Meikle et al, 2012) and the Tinnitus Handicap Index (THI) (Newman et al, 1996). 35 Either of these short (requiring less than 10 minutes to administer and score) surveys can be utilized to establish baseline subjective reaction, measure progress, and assist in establishing a rating classification. For the purpose of the proposed guidelines below, the TFI will be employed due to the extensive research and statistical validation associated with it. The TFlis a questionnaire consisting of 25 items designed to address eight important domains of negative tinnitus impact: intrusiveness, reduced sense of control, cognitive interference, sleep disturbance, auditory difficulties attributed to tinnitus, interference with relaxation, quality of life reduction, and emotional distress. Each of the 8 subscales consists of 3 items except for the quality of life subscale which consists of 4 items. All items are scored using a percentage score or a 0-10 scale giving a maximum possible score of 250. The overall TFI score can be defined by dividing the total score by the number of answered questions and by multiplying by 10. Performing this calculation, the overall score will be within a 0-100 range. In lieu of the TFI, the examiner may use the THI, as both the TFI and THI have maximum scores of 100 (most adverse reaction). 

Apportionment is a method of determining the degree of permanent disability. It means that the employer is allowed to assign the disability, in terms of percentages, to a previous workers' compensation injury to the same body part. Apportionment can also be assigned to causation factors of prior non-industrial injury or illness involving the same body part. Apportionment of tinnitus impairment (disability) per current medical-legal standards, the AMA Guides, Fifth Edition, and by analogy and evocation of Alvaraz-Guzman Il must be based on documented historical facts and patient symptoms. For example, if the claimant has a ratable hearing impairment in the 500Hz to 3000Hz range on audiometric testing, a further, separate rating for tinnitus can be assigned for the claimant's tinnitus symptoms. 

The tinnitus rating must be based on symptoms that have documented factors of causation, e.g. excessive noise exposure, head injury, industrially acquired illness, etc. Although other potential causations are present, e.g. diabetes mellitus, hyperlipidemia, Meniere's disease, these factors for tinnitus cannot be utilized in the determination of apportionment lacking specific documentation of industrially related cause and effect. These latter factors remain theoretical, can be mentioned in a QME report, however generally will not be accepted in a Workers' Compensation claim as fact-based evidence. In the case of a claimant failing to have ratable hearing impairment in the 500Hz to 3000Hz audiometric range, Almaraz-Guzman Il can be evoked by analogy as a separate compensable industrially-acquired impairment. The tinnitus can be claimed as the actual industrial injury with justification based on Almaraz/Guzman. The QME must state in clear language why Almaraz-Guzman applies in cases where tinnitus is present in the absence of ratable hearing impairment, i.e. if a claimant indicates tinnitus affects his activities of daily living, a rating for tinnitus should most accurately reflect the degree of impairment. 

 

References: 

1. AMA Guides to the Evaluation of Permanent Impairment, 5th Edition, Chapter 11, pp. 246-251. 

2. AMA WPI: http://www.dir.ca.gov/dwc/pdr.pdf. 

3. Coles RRA. 1996. Epidemiology, aetiology and classification. 1995. In: Vernon JA, Reich G, editors. Proceedings of the Fifth International Tinnitus Seminar, Portland, OR: American Tinnitus Association. pp. 25-30. 

4. Davis A, El Refaie A. 2000. Epidemiology of tinnitus. In: Tyler RS, editor. Tinnitus Handbook. San Diego: Singular Thomas Learning. p 1–23. 

5. Doosti A, Lofti Y, Bakhshi E. 2016. Effects of Hyperlipidemia on Noise Induced hearing loss, Indian J Otolaryngol Head Neck Surg 68(2): 211-3. 

6. Eggermont JJ, Roberts LE. 2004. The neuroscience of tinnitus. Trends Neurosci 27:676–682. 

7. Figueiredo RR, de Azevedo AA, de Oliveira Pinedo N. 2015. Tinnitus and arterial hypertension: systematic review, European Archives of Oto-Rhino-Laryngology 272, (11), 3089-3094. 

8. Folmer RL, Griest SE. 2000. Tinnitus and insomnia, Am J Otolaryngol 21(5): 287-93. 

9. Guichard, E., Montagni, I., Tzourio, C. et al, 2016. Association between headaches and tinnitus in young adults: Cross-sectional study. Headache 56: 987–994. 

10. Hallam RS, McKenna L, Shurlock L. 2004. Tinnitus impairs cognitive efficiency. Int J Audiol 43(4): 218-26. 

11. Hang NC, Yu ML, HO KY, et al. 2007. Hyperlipidemia in noise-induced hearing loss. Otolaryngol Head Neck Surg 137(4): 603-6. 

12. Hearing Health Foundation statistics: http://hearinghealthfoundation.org/statistics. 

13. Hoffman E, Behr R, Neumann-Haefelin T et al, 2013. Pulsatile tinnitus, imaging and differential diagnosis, Dtsch Arztebi Int: 110(26): 451-458.

14. Kakarlapudi V, Sawyer R, Staecker H. 2003. The effect of diabetes on sensorineural hearing loss. Otol Neurol 24(3): 382-6. 

15. Marciano E, Carrabba L, Giannini P, et al. 2003. Psychiatric comorbidity in a population of outpatients affected by tinnitus, Int J Audiol 42(1): 4-9. 

16. Mazurek B, Szczepek AJ, Hebert S. 2015. Stress and tinnitus, HNO 63(4): 258-65. 

17. McCombe A, Baguley D, Coles R., et al. 1999. Guidelines for the grading of tinnitus severity: the results of a working group commissioned by the British Association of Otolaryngologists, Head and Neck Surgeons. Clin. Otolaryng 26, 388-393. 

18. McFadden D. 1982. Tinnitus: Facts, Theories, and Treatments. Washington, DC: National Academy Press. 

19. Meikle MB, Henry JA, Sweetow R, et al 2012. The Tinnitus Functional Index: Development of a New Clinical Measure for Chronic, Intrusive Tinnitus. Ear Hear. 33(2):153-76. 

20. Muhlnickel W, Elbert T, Taub E, et al. 1998. Reorganization of auditory cortex. In tinnitus. Proc Natl Acad Sci USA 95:10340-10343. 

21. Myers LJ. 1988. Possible inflammatory pathways relating temporomandibular joint dysfunction to otic symptoms. J Craniomandib Pract 6 (1): 65-70. 

22. Negri B, Schorn K. 1991. Noise-induced hearing loss and tinnitus. HNO 39(5): 192-4. 

23. Newman CW, Jacobson GP, Spitzer JB. 1996. Development of the Tinnitus Handicap Inventory. Arch Otolaryngol Head Neck Surg 122:143–148. 

24. Occupational Noise Exposure. In https://www.osha.gov/SLTC/noisehearingconservation/. 

25. Palmer KT, Griffin MJ, Syddall HE, et al. 2004. Cigarette smoking, occupational exposure to noise, and self-reported hearing difficulties. Occupational and Environmental Medicine 61:340-344. 

26. Roberts LE, Eggermont JJ, Caspary DM, et al. 2010. Ringing Ears: The Neuroscience of  Tinnitus. The Journal of neuroscience : the official journal of the Society for Neuroscience 30(45):14972-14979. 

27. Rossiter S, Stevens C, Walker G. 2006. Tinnitus and its effect on working memory and attention, J Speech Lang Hear Res 49(1): 150-60. 

28. Salvi RJ, Wang J, Ding D. Auditory plasticity and hyperactivity following cochlear damage. 2000. Hear Res. 147:261-274. 

29. Shore S, Zhou J, Koehler S. 2007. Neural mechanisms underlying somatic tinnitus. Prog Brain Res 166:107–23. 

30. Somogyi A, Rosta K, Vaszi T. 2013. Hearing impairment and tinnitus in patients with type 2 diabetes. Orv hetil 154(10): 363-8. 

31. Stevens C, Walker G, Boyer M, et al. 2007. Severe tinnitus and its effect on selective and divided attention, Int j Audiol 46(5): 208-16. 

32. Sweetow R. 1996. Tinnitus. In Hearing Disorders; 3rd Edition. Northern, J.L. Editor. Allyn and Bacon, Boston, MA. 299-309. 

33. Sweetow R. 1986 Cognitive Aspects of Tinnitus Patient Management. Ear Hear 7:390-396. 

34. Sweetow, R, Sabes, JH. 2010. An overview of common procedures for the management of tinnitus patients. Hearing Journal 63(11), 9-10. 

35. Tyler, R., Ji, H., Perreau, H., et al. 2014. Development and validation of the Tinnitus Primary Function Questionnaire. Am J Audiol 23, 260–272. 

36. Zhang Q, Zhonghua Er, Bi Yan Houu, et al. 1989. Mechanism of inner ear damage due to hyperlipidemia 24(2): 75-8. 

37. Almaraz-Guzman II WCAB En Banc Decision: Providing a WPI that is the most accurate reflection of the impairment, Workers' Compensation Law, Steven D. Feinberg, M.D., 09/27/2009.