27 Tinnitus: There Is Something You Can Do About It!

It is estimated that approximately 1 in 1000 adults experience tinnitus. The prevalence increases up to approximately 20% in the population over the age of 50 years.1

These estimates depend heavily on the precise definition. As a subjective symptom, the research design might have a direct influence on the results. For example, the definition and duration of tinnitus, sample age and also the differentiation between the perception of a sound, (tinnitus sensation) and the impact of tinnitus on a person (tinnitus suffering).

Tinnitus Etiology

There are many causes of tinnitus and in the majority of the cases result from the same conditions that cause hearing loss (HL), the most common being noise exposure and aging, but many are unknown.

Tinnitus is a common side effect of many classes of medications, particularly those used to treat cancer (Table 27.1).

Epidemiological studies have attempted to find links to other contributing factors, such as coffee, red wine, and temporal mandibular joint dysfunction. Although some of these studies find significant relationships, such findings are weak effects and often not replicated.

Strategies and Evidence

Middle Ear or Sensorineural Tinnitus

Broadly speaking, there are two sites of origin for tinnitus; the middle ear and the sensorineural system. Middle-ear tinnitus usually results from either the perception of blood flow (pulsatile) or muscle twitching (myoclonus) in the middle ear. In some cases either can be surgically treated.² Pulsatile tinnitus is often reported by the patient as “pulsing” or “humming.” It can reflect perception of normal blood flow in patients with a conductive HL or abnormal blood flow through tumors or vascular malformations. Auscultation of blood vessels interacting with the middle ear can be helpful, as having the patient tap their finger with each pulse of their tinnitus, while the pulse is palpated to check for synchrony with blood flow.

Stapedial and palatal myoclonus might be perceived as a twitching, and, in the case of stapedial myoclonus, often results in a periodic movement of the eardrum which can often be seen with an otoscope or with measures of middle-ear impedance. In severe cases the muscle can be severed. However, this reduces the effectiveness of the protection of these muscles to loud sounds. Similarly, injection of botulinum toxin can be used to treat palatal myoclonus.

Far more common is sensorineural tinnitus, which likely results from an abnormality of the spontaneous activity of neurons. This change in spontaneous activity might originate anywhere from the cochlea to the auditory cortex. Wherever the origination, the auditory cortex must have some abnormal representation of neural activity in order for the tinnitus to be heard.

Although early psychoacoustical data appreciated the importance of central coding,³ numerous imaging studies have documented a variety of brainstem and central sites that might be involved.^4–11

The precise way that tinnitus is coded in the auditory system is unknown, and there may be many subgroups and different mechanisms.¹² Three likely cortical representations are:

1. An increase in spontaneous activity¹³

2. Synchronous activity across neurons^14,15

3. Reorganization of tonotopic maps following peripheral HL¹⁶

Unexpected observations in some patients where muscle contractions of head, neck and limbs,^17,18 pressure of myofascial trigger points,^19,20 cutaneous stimulation of the hand or fingerprint region and face,²¹ electrical stimulation of the medial nerve and hand,²² finger movements,²³ orofacial movements,²⁴ and pressure applied to the temporomandibular joint or lateral pterygoid muscle^25,26 can change a person’s tinnitus indicate that nonauditory neural pathways are involved in some cases and tinnitus is not only the result of changes in the auditory pathway.

Cross-modal interactions between the somatic and auditory system in the midbrain and brainstem have been described,²⁷ including projections from the trigeminal nuclear complex to the cochlear nucleus.²⁸ All these studies suggest that tinnitus is complex and multimodal.

Table 27.1 Medications That Might Cause Tinnitus62,78

Adapted from references 62 and 78.

Tinnitus Patient

We have categorized patients as “curious,” “concerned” or “distressed.²⁹” Curious patients are those who are not bothered by there tinnitus, but are considering the implications of general health, hearing and likelihood it will go away. Some will benefit from reassurance and an information brochure.²⁹ Concerned patients are more worried about coping. They might already have impacts on their emotional well-being, hearing, sleep, and concentration. They want to know what treatments are available and how successful they are. Self-help books^29,30 should help many, and provide a more accurate perspective than is available on the Internet. The American Tinnitus Association also provides information and can identify healthcare workers who have indicated they are willing to provide help for tinnitus patients. Distressed patients are having difficulty and are often overtly anxious or depressed. They are likely to have already tried several “treatments” and been to several health-care professionals. Most concerned and distressed patients will benefit from counseling and sound therapy. For the very distressed patients, that show signs of clinical depression, anxiety and/or suicide, a referral to a psychiatrist or psychologist is warranted.

Evaluation of the Tinnitus Patient

Medical Evaluation

Medical investigation of tinnitus etiology or etiologies are mandatory to perform the differential diagnosis of underlying diseases, some of which can be treated or controlled, mitigating or curing tinnitus as well as excluding life-threatening diseases that are associated with the symptom.

Clinical History

Obtaining a detailed clinical history requires time, but will offer important clues about etiology and to select laboratory and radiologic examinations that will be required to investigate a particular case.

As an initial approach, we have to distinguish between the perception of a sound (tinnitus sensation) from the complaint of tinnitus (suffering) which suggests abnormality. Characteristics such as localization, if it is perceived on the ears (right, left, or both) or in the head; the duration and if it has changed its characteristics recently, if it is pulsatile or constant, intermittent or fluctuant, and single or multiple; situations where tinnitus gets worse, for example, ingestion of alcohol, noise exposure, and stress, and whether it is relieved by any specific condition. As well as the presence of associated symptoms such as HL, sound intolerance, vertigo, ear pressure or blockage should also be asked.

Medications and dietary supplements in use, caffeine abuse, dietary habits, for example, vegetarians might have vitamin B₁₂ deficiency, symptoms of food allergies, and lactose intolerance.

Patient’s and family’s medical history could also give some clues, and should focus on the cardiovascular system and in metabolic disturbances, such as diabetes and hypercholesterolemia as well as deafness. Changes on tinnitus after a period of fasting and compulsion for sweets might be associated with insulin resistance a prediabetes state.

Anxiety and depression, concentration and sleep problems are frequent comorbidities. Sometimes, you may not find any clue in the whole clinical history but the patient will refer that his or her tinnitus has appeared or changed after a traumatic emotional situation.

It is useful to have a questionnaire that can be filled by the patient covering all these topics.

Physical Examination

A complete neurotologic physical examination is required. We highlight the otoscopic evaluation, pneumatoscopy, determination of the mobility of the tympanic membrane and how this affects tinnitus, and the presence of a middle ear mass.

Manipulations of blood flow (by asking patients to perform a brief vigorous exercise or by partially constricting a blood vessel of the neck) to determine a possible change on the tinnitus pulsing sensation, a palpable thrill and auscultation to search for a bruit on the neck, over the ears and the head also are useful in the presence of pulsatile tinnitus. Oral cavity examination may demonstrate myoclonic activity (palatal myoclonus).

Areas of tenderness and trigger points on the head and neck musculature might be associated to tinnitus somatic modulation.19,31 This could be verified by performing some maneuvers³¹ while the patient notices if there are changes on tinnitus intensity, pitch, and location.

The presence of a clicking or popping sound during chewing, jaw locking and changes on the biting pattern and dental occlusion are likely to indicate the presence of temporomandibular dysfunction that could be related to tinnitus.

Laboratory Evaluation

Blood tests such as whole blood count, cholesterol levels, triglycerides, glucose-insulin curve,³² thyroid stimulating hormone, free thyroxine (T4), autoimmune diseases tests, zinc serum levels,³³ vitamins B₁ and B₁₂ levels,³⁴ folic acid, erythrocyte magnesium, and screening for ototoxic drugs, could be performed, according to the clinical hypothesis.

Imaging Tests

The clinical evaluation will provide hints to decide what would be the most appropriate imaging study to be performed.

A patient presenting pulsatile tinnitus in which the hypothesis is a vascular malformation, neoplasm or anomalies, the imaging study of choice is a contrasted computed tomography (CT) of the temporal bone, brain, and scalp. If a dural vascular malformation is suspected, angiography may be indicated. Carotid aneurysm might be evaluated by neck magnetic resonance imaging (MRI), CT angiography or MR angiography.^35,36

On those subjects presenting sudden onset or worsening tinnitus, asymmetrical signs, and diseases of the auditory system² it is necessary to exclude posterior fossa tumors (most often a vestibular schwannoma), a brain MRI is the study of choice.³⁶

Audiological Evaluation

Hearing Tests

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