Tinnitus also represents a common symptom among children with hearing loss.
Tinnitus is a subjective phenomenon that is difficult to evaluate
objectively, with it being measured, quantified, and described only
based on the responses of patients. Although tinnitus can have many
different causes, it most commonly results from otologic disorders,
with the most common cause believed to be noise-induced hearing loss.
The various therapeutic approaches to tinnitus have produced mixed
results, and hence it is generally assumed that tinnitus has diverse
CHARACTERISTICS OF TINNITUS
The sounds associated with most cases of tinnitus have been described as being analogous to cicadas, crickets, winds, falling tap water, grinding steel, escaping steam, fluorescent lights, running engines, and so on. It is believed that these types of perception result from abnormal neuronal activity at a subcortical level of the auditory pathway.
Most patients with both tinnitus and hearing loss report that the frequency of the tinnitus correlates with the severity and frequency characteristics of their hearing loss, and that the intensity of the tinnitus is usually less than 10 dB above the patient's hearing threshold at that frequency. Some patients who have central auditory processing disorders and have difficulties understanding speech in noise report experiencing tinnitus even though their pure-tone audiometric thresholds are normal.
Somatic tinnitus is a type of subjective tinnitus in which the frequency or intensity is altered by body movements such as clenching the jaw, turning the eyes, or applying pressure to the head and neck.Reports that tinnitus is louder upon awakening suggest the involvement of somatic factors, such as bruxism. Reports that tinnitus vanishes during sleep but returns within a few hours further suggest that psychosomatic factors, such as neck muscle contractions occurring in an upright position or jaw clenching, play etiological roles.
Because objective tinnitus (which is audible to another person) represents the semantic opposite of subjective tinnitus, a better nosological approach might be to use the term somatosound instead of objective tinnitus irrespective of whether the sounds are audible to others, reserving the term tinnitus for the perception of sound in the absence of any acoustic source. Thus, "tinnitus" would describe cases previously diagnosed as subjective tinnitus. Objective tinnitus might be vascular or mechanical in origin. Objective tinnitus of vascular origin could be a referred bruit from stenosis in the carotid or vertebrobasilar system. Objective mechanical tinnitus is due to abnormal muscular contraction of the nasopharynx or middle ear, as can occur in palatal myoclonus. Pulsatile tinnitus can also manifest subjectively as an increased awareness of blood flow in the ear. Indeed, the cause of somatosensory pulsatile tinnitus syndrome is not vascular, with the syndrome deriving from cardiac-synchronous somatosensory activation of the central auditory pathway or the failure of somatosensory-auditory central nervous system (CNS) interactions to suppress cardiac somatosounds. Pulsatile tinnitus superimposed on steady tinnitus could result from the pulsation of blow flow with the spiral capillary of the basilar membrane.
There is pronounced neuronal activity in the auditory pathways during sleep due to the auditory system continuously monitoring the sound environment. Common detrimental activities and/or conditions include noise exposure, being located in a quiet place, emotional stress, loss of sleep, and physical exhaustion. Annoyance, depression, and interference with sleep are more common and the tinnitus is louder in patients with Meniere's disease than in those with tinnitus deriving from other etiologies.Furthermore, the successful control of vertigo in patients with Meniere's disease can lead to them focusing more on their tinnitus and hence becoming more distressed by this condition.
The strength of the reaction to tinnitus is therefore determined by its significance and by past experience-the actual intensity and characteristics of the sound are of secondary importance.
Noise-induced tinnitus can be acute or chronic. Acute tinnitus can last from a few minutes to a few weeks after noise exposure. In some cases, tinnitus has a gradual onset and several years can pass before an intermittent, low-intensity tinnitus becomes bothersome. Spontaneous remission by natural habituation is experienced by more than three-quarters of sufferers. Habituation occurs within the CNS, whereas adaptation involves a peripheral sensory organ. For those in whom the condition worsens, the tinnitus intensity increases over time but its pitch tends to remain stable. If tinnitus persists for more than 2 years, it is considered permanent and irreversible. However, chronicity is not associated with a favorable response to treatment.
CAUSES AND PATHOPHYSIOLOGY
Peripheral auditory system
Spontaneous otoacoustic emissions (SOAEs), first discovered by Kemp, are small acoustic signals presumed to be generated by the electromotile activity of the OHCs of the cochlea and propagated into the external auditory canal. SOAEs produced by the cochlea can be perceived as tinnitus. SOAEs are usually inaudible, but they can become audible due to instability. These atypical SOAEs are much more prevalent in the higher frequency range and can appear at sound pressure levels up to 55 dB SPL in the ear canal. Tinnitus due to SOAEs is mild and is more common in subjects with normal hearing and in those with only middle ear disorders. SOAEs decrease as hearing loss progresses, and hence these otoacoustic emissions are not likely to cause tinnitus when a hearing loss of 35 dB or more is present. However, SOAEs cannot fully explain the mechanism of tinnitus since aspirin largely abolishes SOAEs without improving tinnitus.
Central auditory system
The dorsal cochlear nucleus
Auditory plasticity theory
Limbic and autonomic nervous systems
The aforementioned theories cannot explain why some people suffer from tinnitus while others do not. More than 80% of those perceiving tinnitus for the first time do not associate the sound with any negative meaning and experience spontaneous habituation. However, if the first perception of tinnitus induces high levels of annoyance or anxiety by association with unpleasant stimuli or with periods of stress and anxiety, tinnitus mightlead to high levels of annoyance or anxiety. At the unconscious level, tinnitus can increase progressively without the patient being aware, resulting in enhanced activity in the limbic and autonomic nervous systems. In such situations, tinnitus emerges as a clinically significant problem.
COGNITIVE AND BEHAVIORAL THERAPY
Electrical stimulation of the cochlea with trains of pulses at 5,000 pulses per second can substantially or completely suppress tinnitus with either no perception or only a transient perception of the stimulus. Stimulus with electrical pulses at such a high rate restores spontaneous-like patterns of spike activity in the auditory nerve, which could explain how it suppresses tinnitus.Transcutaneous electrical nerve stimulation of areas of skin close to the ear increases the activation of the DCN via the somatosensory pathway and could augment the inhibitory role played by this nucleus on the CNS, thereby ameliorating tinnitus.
Nevertheless, counseling represents an essential part of treatment, regardless of the management approach adopted for a particular patient. An informed explanation of tinnitus, together with reassurance, improves the condition of most patients over time. For those with persistent tinnitus, cognitive and behavioral therapy, augmented by pharmacologic intervention, might represent the most promising treatment regimen. Most importantly, a strong doctor-patient relationship underpins successful management and high levels of satisfaction among patients.
Source: Han, B, Lee, H, Kim, T, Lim, J, Shin, K. Tinnitus: Characteristics, Causes, Mechanisms, & Treatments. Journal of Clinical Neurology. 2009, March 31.