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We investigated the effects of tinnitus on measures of arousal and attention at various levels of the neuraxis to derive a profile of the pathophysiology of tinnitus.
Subjective tinnitus, the perception of sound in the absence of acoustic stimulation, is a common phenomenon affecting approximately 17% of the general population in the United States [1-3].
Although many tinnitus sufferers complain of poor concentration, neuropsychological testing has revealed that the cognitive inefficiency appears to be associated with the control of attention, especially the inhibition of attention task-irrelevant activity [8-10]. In this study, the pathophysiology of tinnitus was investigated by assessing various levels of the neuraxis for arousal and attention. In an attempt to determine any association between deficits in arousal and attention and the magnitude of the tinnitus complaint, we correlated the findings of these tests with the perceived severity of tinnitus based on tinnitus severity and sleep disturbance questionnaires. We identified and recruited patients with tinnitus (n = 29) and controls without a history of tinnitus (n = 35) from the Otolaryngology Clinic at the University of Arkansas for Medical Sciences. All subjects completed a tinnitus severity index [22], which was a modification of the Colorado Otolaryngology Associates Severity Index (Fig. We carried out recordings of the P50 potential using a paired-stimulus paradigm as previously described [12-16,24,25]. We placed headphones on each study subject, and the test stimulus was a rarefaction click of 0.1-millisecond duration, set at 50 dB above hearing threshold. The PVT assesses simple RT by measuring the amount of time taken by a subject to respond to a visual or auditory stimulus.
A total of 64 subjects were enrolled in the study: 29 individuals with chronic tinnitus (14 male, 15 female) and 35 control subjects (14 male, 21 female).
We found no significant difference between controls and tinnitus patients with regard to the insomnia portion of the sleep disorders questionnaire (p = .5). Several theories concerning tinnitus generation have been proposed, such as the discordant damage theory [32], spontaneous otoacoustic emissions [11], thalamocortical dysrhythmia [33,34], and maladaptive cortical reorganization after peripheral injury, analogous to the model of chronic pain [5,7,35,36].
Individuals with tinnitus frequently report poor mental concentration, but neuropsychological testing reveals that the effect of tinnitus on cognitive processing is likely to manifest selectively in tasks involving the control of attention [8-10]. In this study, the P50 potential was used as a measure of arousal and habituation at the brainstem-thalamus level.
In our study, we saw no significant difference in the overall amplitude of the P50 potential or habituation between individuals with tinnitus and age-matched controls.
The main deficit that distinguished tinnitus patients from control subjects in our study was a failure to sustain optimal performance (vigilance) over time, as reflected by the duration of their slowest RTs during PVT testing. In this study, we noted no significant difference between controls and individuals with tinnitus in the 10% fastest RTs, lapses, fatigability, or false starts, but we did detect a significant difference in the 10% slowest RTs (p = .02). The reason individuals with tinnitus seem to be able to habituate to externally generated auditory signals and not to those signals internally generated remains unknown. Of interest, the pattern of reaction-time variability observed in our cohort of tinnitus patients is similar to that observed in other cohorts of subjects with asymmetrical cortical activation.
The asymmetrical activation observed in these studies seems to promote variability in performance, whether it be RT or sensory perception, by introducing a degree of neural "noise" into the system that might also interfere with the process of habituation. Whether interventions designed to treat tinnitus can restore symmetry and alleviate performance variability represents the next logical step in this research. Though no universally accepted theory of tinnitus generation exists, most believe that it is related to central nervous system dysfunction, such as thalamocortical dysrhythmia, even though peripheral injury is the inciting event. This study was supported by NIH National Center for Research Resources Centers of Biomedical Research Excellence (COBRE) grant number RR020146.
Figura 1.13 Otitis media en fase de supuracion El oido medio quedo completamente repleto del exudado purulento, cuya presion abomba lateralmente la membrana timpanica.
Because psychological aspects often are underscored in the generation of tinnitus, we assessed the neuropsychological status in our group of patients. Psychological aspects and emotional stress are often underscored in the generation and perception of tinnitus, but the mechanisms of tinnitus are still unknown [1,2]. The ENG tests were performed using a computerized four-channel ENG system (version 2.4 Toennies Nystagliner, Wiirzburg, Germany) with DC-coupled amplifiers. Depending on the degree of symptom severity, scores of tests (especially the BDI and HAD) were ranged in several subclasses-minimal, mild, moderate, or severe-as described in the literature [6-9].
The neurootological assessments showed that tinnitus was more frequently unilateral in 48 patients (69.6%), with unilateral sensorineural loss in 40 patients (58%). We also compared abnormal ENG outcomes with normal and maximum abnormal scores of each neuropsychological test, but these were not statistically significant either.
In comparing abnormal neuropsychological test scores with ENG test outcomes (normal and those indicating central vestibular dysfunction [n = 37], among which were 29 central and 8 mixed), we found a higher percentage of the signs of vestibular system impairment for only the BDI test (39% vs.
In tinnitus patients, both this and previous studies revealed a high percentage of abnormal recording results in the ENG tests, despite the fact that only a few patients had complained of vertigo or dizziness [3,5].
Psychological factors often are implicated as playing an important role in the processes of perception, interpretation, and treatment of tinnitus and other neurootological diseases. The psychological aspect is also mentioned in relation to vestibular symptom manifestation. We would like to study whether this psychological problem in our patients influenced the ENG outcome.
In both tinnitus patients and those with dizziness, many factors may contribute to the results of tests for vestibular and neuropsychological examination. In tinnitus patients, signs of vestibular dysfunction and abnormal neuropsychological test scores are frequently observed. This research was presented at the Thirtieth Neurootological and Equilibriometric Society Congress, Porto, Portugal, April 3-5,2003. Congenital atresia of the external ears and severe tinnitus has been reported by two patients to be contralateral to the atretic ear. Our clinical experience since 1977 with tinnitus of the severe disabling type (subjective idiopathic tinnitus [SIT]) in more than 10,000 patients leads us to consider the establishment of a clinical accuracy for the diagnosis of tinnitus as the "key" to achieving tinnitus relief with therapeutic modalities now available. The completion of a medical audiological tinnitus patient protocol (MATPP) for SIT patients, with extensive testing of the cochleovestibular system, both peripheral and central, has been recommended to establish (1) accuracy of diagnosis of tinnitus, (2) its medical significance, and (3) a rationale for treatment based on a correlation of structure and function [4-6]. Patients with congenital atresia of the external ear and SIT completed the MATPP to establish an accurate diagnosis for the clinical type of tinnitus, to identify and treat factors influencing the clinical course of the tinnitus, and to establish a rationale for attempting tinnitus relief. The patient's tinnitus was described as a noise in "spells of increased intensity of a constant rumble in the left ear," fluctuant intensity, and increasing annoyance within 1-2 months before his neurotological consultation on November 30, 2004. We informed the patient that although no cure was available for tinnitus at this time, the goals of the consultation were to attempt to establish a clinically accurate tinnitus diagnosis and the medical significance of the tinnitus and to attempt to provide tinnitus relief by medication alone or in combination with instrumentation. We recorded the left-ear tinnitus intensity reported by the patient on a tinnitus intensity index (TII) and a tinnitus annoyance index (TAI). Associated complaints included increased left-ear hearing loss, fluctuant left-ear blockage, and weight loss of approximately 20 pounds. Sudden-onset tinnitus in the left ear occurred while the patient was at work on May 5, 2004, in a standing position. Tinnitus originally was reported as an intermittent "highpitched ring" in the left ear at age 21-25 after exposure to loud music. The patient's significant history included congenital atresia of the right external ear, presence of allergies, presence of hearing loss following noise exposure (including to firearms), and reconstructive surgery to the external right ear at age 6-7 years, and hospitalization for kidney stones. The physical examination included evaluation of the patient's general appearance and an external inspection, both of which were found to be satisfactory. Site-of-lesion audiometry identified severe hearing loss, which was mixed and predominantly conductive, on the right. Electronystagmography (December 1, 2004) revealed no spontaneous nystagmus, positional nystagmus, or neck torsion.
A computed sinusoidal harmonic rotation test (December 1, 2004) revealed left labyrinthine asymmetry, normal saccadic eye movement, and normal OFS.
QEEG (December 1, 2004) demonstrated significant electrical dysfunction in the central nervous system (CNS)(Fig. Baseline SPECT of brain findings (November 2, 2004) included bilateral parietal lobes hypoperfusion, more dominant on the right than on the left side, and bilateral mesial temporal hypoperfusion, more prominent on the right (Fig. Neuroradiology suggested findings may represent vascular deficiency as opposed to cortical atrophy. An MRI of the brain with gadolinium (May 10, 2004) showed none of the following: acute infarct or intracranial mass lesion, cerebellopontine angle mass or abnormal enhancement within the IAC or inner ears bilaterally, or otomastoiditis.
MRI and MRA scans (December 16, 2004) demonstrated a small area of flow gap or narrowing in the proximal portion of the straight sinus. Tinnitus was diagnosed to be predominantly of a central type in the left ear but to be subclinical in the right ear and to have a bilateral cochlear component. Additional diagnoses included an anxiety syndrome and bilateral heterochromia of the irises. Arteriovenous (AV) fistula, dural fistula, bilateral SEH, autoimmune inner-ear disease, hereditary sensorineural hearing loss, anterior internal cerebral artery (AICA) syndrome (left-sided), and cerebrovascular disease all were recommended to be ruled out. The initial ear, nose, and throat (ENT) consultation took place 2 days later (May 8, 2004). The patient made an emergency room visit (May 9, 2004) for evaluation of recurrent and increased intensity of the rumble and with concern about left-ear hearing. Neurotological consultation and follow-up visits (November 30, 2004-December 7, 2004) clinically established the following diagnoses: tinnitus of a predominantly central type in the left ear, with a left cochlear component, and subclinical in the right ear. Neurotological recommendations (December 4, 2004) for attempting tinnitus control included general rules pertaining to diet, such as elimination of stimulants and caffeine, and use of ear protection from noise, and specific recommendations of a combined therapy via medication and instrumentation, differentiating between sensory and affect components. For the sensory component, we recommended medication initially, followed by introduction of instrumentation. For treatment of the affect component, we recommended follow-up with neuropsychiatry and psychology for the anxiety syndrome complaint and for fear.
Close observation was advised to include clinical consideration of gradual, progressive cerebrovascular disease. Neurological followup evaluation (December 9, 2004) reported the tinnitus to be associated with "pressure pulsations" in the left head area. Neurological follow-up on January 14, 2005, reported persistent pulsation tinnitus on the left side of the patient's head. A neurotological follow-up visit on January 25, 2005, reflected attempts of tinnitus relief from December 7, 2004, to January 25, 2005, as initially recommended and which, by cooperation between the neurologist and the patient, were completed. The patient reported overall improvement-"water sound in back of head" gone since December 14, 2004-and described the quality of tinnitus frequency as "midrange electric motor" and "80-90% gone." Location of the tinnitus-left ear and back of the head on the right side-was significant. During telephone communication with the neurology physician (February 4, 2005), the patient reported that he was "doing OK," although concern about steroid dependence persisted in order to maintain tinnitus relief.
In a telephone communication with the neurotology physician (February 15, 2005), the patient reported tinnitus relief was being maintained. At a follow-up visit with neurotology (March 8, 2005), the patient reported tinnitus relief of 15-20% and increasing periods of "ignoring the complaint," with associated reduction in anxiety. During telephone communications with the neurotologist (March 15, 2005-April 12, 2005), the patient reported continued increasing periods and degrees of tinnitus relief. In telephone communication between the neurotologist and the patient (September 13, 2005), the patient reported tinnitus relief in excess of 90%, absence of any spells, occasional ear blockage prior to or accompanying the tinnitus, no imbalance, and occasional hyperacusis with tinnitus. During further telephone communication with the neurotologist (December 20, 2005), the patient reported tinnitus "rumble" relief in excess of 90%.
The etiology of the symptom of tinnitus, as described at the time of and following completion of neurotological consultation (November 30, 2004-December 7, 2004), is considered to have a chiefly vascular basis, reflecting insufficiency of the anterior and posterior intracerebral circulation, and to be a predominantly "soft" sign of gradual, progressive cerebrovascular disease.
The clinical history of the original tinnitus, described as an intermittent high-pitched ring in the left ear, is traced to age 21-25 and occurred after exposure to loud music (TII: best = 0 [95%] and 7 [3 days in duration after noise exposure]). Within the limits of examination at this time, we hypothesized that the clinical course of the tinnitus as described is a reflection of a gradual alteration in the hemodynamics of the intracerebral circulation, highlighted at this time by SPECT of brain of hypoperfusion in regions of interest supplied by the right MCA.
We considered a presumptive left SEH to be clinically related to alteration in homeostatic mechanisms between the fluid compartments of the brain and inner ear, with the resultant accompanying imbalance and reported left-ear hearing loss (May 5, 2004).
Acknowledged was the clinical history of a sudden onset of the tinnitus and the clinical history of tinnitus described as an increase in left-ear ringing 3-4 years ago. We recommended SPECT of brain in an attempt to improve the accuracy of the tinnitus diagnosis, to monitor the efficacy of modalities of therapy attempting tinnitus relief, and to provide a basis for neuroprotective drug therapy.
In an attempt to establish a specific vascular etiology, to exclude AV dural fistula, AV malformations, and cisternal and venous sinus anomalies, we recommended MRI, MRA, and MRV, which were reported to be essentially normal. In summary, we considered the tinnitus complaint in the left ear (as described on November 30, 2004) and its clinical course predominantly to be a "soft" sign of CNS dysfunction, on a vascular basis, superimposed on a preexisting sensorineural hearing loss. Is the reported SPECT of brain finding of hypoperfusion of the MCA in patients with a congenital atresia of the external ear an anomaly or a coincidence of occurrence [10-12]? We consider to be clinically significant the objective demonstration of hypoperfusion in brain areas of distribution of the MCA on the side of the congenital atretic ear in two patients. Over the long term, the inclusion of nuclear medicine imaging of brain and follow-up in cases of congenital atretic ear wherein this finding was demonstrated will determine the significance of the clinical course of cerebrovascular disease and cochleovestibular complaints in atretic and nonatretic ears. Is brain plasticity altered in the patient with a congenital atretic ear for tinnitus therapies hypothesized to occur at brain cortex [13-20]? Electrical and air conduction UHF thresholds of hearing (10-20 kHz) in the two cases of congenital atresia of the external ear (in both the ipsilateral and contralateral ears) were greater than expected for the age of the patient. Is the identification of a UHF sensorineural hearing loss greater than expected for the age of a patient, particularly a tinnitus patient with a congenital atresia of the external ear, a sign of predisposition to the effects of noise exposure and gradually increasing sensorineural hearing loss?
Is the finding of hypoperfusion in brain areas of distribution of the MCA in congenital atresia of the external ear a predisposition or a factor (or both) in the development of SEH [27-31]?
We considered the SEH and tinnitus in the contralateral ear to be a sign of the effect or presence of a vascular anomaly or an alteration in the intracerebral circulatory pattern on the side of the brain contralateral and secondary to the hypoperfusion in brain areas of the MCA in the atretic ear. The diagnosis of a delayed SEH in patients with tinnitus of the severe disabling type has been reported to be frequent and to influence the clinical course of tinnitus [27]. Clinically, the tinnitus described as a ringing in the ear contralateral to the atresia is considered a soft sign of inner-ear dysfunction.
What pathology in this tinnitus patient is reflected in the action of the drugs selected for attempting tinnitus relief (i.e., specifically steroids)? In addition to therapy directed at factors identified as influencing the clinical course of the tinnitus, therapy directed to the GABA-A receptor is hypothesized to increase inhibition at the brain cortex and provide neuroprotection, with resultant increased tinnitus relief and reduction or elimination of the steroid.
What is the incidence of an autoimmune etiology in patients with sensorineural hearing loss? The clinical history of the tinnitus in association with an alteration in hearing in the nonatretic ear introduces the consideration of autoimmune inner-ear disease.
What is the incidence of occurrence of objective and subjective tinnitus in the tinnitus population and, in particular, in the tinnitus patient with an atretic ear?
In the patient in this report, the objective tinnitus was the rumble auscultated with the stethoscope at the left lateral neck overlying the external ear and left postauricular fold. Is the congenital atretic external ear part of a syndrome that includes the MCA and a loss in the UHFs (10-20 kHz)? SPECT of brain has demonstrated hypoperfusion in brain areas of distribution of the MCA on the side of an atretic ear. A neuroprotective drug therapy strategy targeting the GABA-A receptor (RTT-GABA), for treatment of a severe, disabling, predominantly central-type tinnitus, with a clinical diagnosis of brain cortical ischemia based on brain SPECT, resulted in significant longterm tinnitus relief.
The incidence of hypoperfusion in brain areas of distribution of the MCA on the side of the atretic ear in patients with congenital atresia of the external ear remains to be established. The authors gratefully express their appreciation to the Martha Entenmann Tinnitus Research Center, Inc., for support of this educational and research effort.
The Hum is a phenomenon, or collection of phenomena, involving a persistent and invasive low-frequency humming, rumbling, or droning noise not audible to all people. Those who can detect the Hum have been referred to as "hearers", "sensors", "hummers", and "humlings". Other elements seem to be significantly associated with the Hum, being reported by an important proportion of hearers, but not by all of them. Some people perceive the Hum continuously, but others perceive it only during certain periods. In the Unsolved Mysteries segment called 'Mystery Hum', a tape recreation of the Taos Hum was used for this segment. On November 15, 2006 Dr Tom Moir, of the University of Massey in Auckland, New Zealand, made a recording of the Auckland Hum and has published it on the university's website.
It is during the 1990s that the Hum phenomenon began to be reported in North America and to be known to the American public, when a study by the University of New Mexico and the complaints from many citizens living near the town of Taos, New Mexico, caught the attention of the media.
It is difficult to tell if the Hum reported in those earlier cases and the Hum that began to be increasingly reported in North America in the 1990s should be considered identical or of different natures. A suggested diagnosis of tinnitus, a disturbance of the auditory system, is used by some physicians in response to complaints about The Hum. While the Hum is hypothesized by some to be a form of low frequency tinnitus such as the venous hum, some sufferers claim it is not internal, being worse inside their homes than outside.
People who both suffer from tinnitus and hear the Hum describe them as qualitatively different, and many hum sufferers can find locations where they do not hear the hum at all. Human ears generate their own noises, called spontaneous otoacoustic emissions, which about 30% of people hear. Researchers from the USArray Earthscope have tracked down a series of infrasonic humming noises produced by waves crashing together and thence into the ocean floor, off the North-West coast of the USA.
Global tectonic plate movement is causing an increase in earthquake activity, especially in the Pacific Ring of Fire.
In the case of Kokomo, Indiana, a city with heavy industries, the origin of the hum was thought to have been traced to two sources. The positive medical history of sonovestibular symptoms was confirmed objectively by CDP with sound stimulation with a high statistical significance. The phenomenon of sound-induced vestibular symptoms and signs, termed the Tullio phenomenon (TP), has been known for six decades.
The effect of inducing nystagmus and vestibular symptoms by acoustic stimulation depends on the functional integrity of the vestibular labyrinth alone and is reproduced in animals when the cochlea has been ablated.
Subsequently, TP was studied in terms of its physiological mechanism [4-9], nystagmic eye movements produced in response to intense sound [6,10-12], and the performance on a force platform with an acoustically stimulated vestibular system [10,13-15]. The presence of the TP was noted also in normal subjects (guinea pigs, monkeys, and humans) [19,20] and later even was found to be ubiquitous in normal subjects [21]. Previous reports show that the TP is provoked by a wide range of acoustic stimuli in terms of modes of delivery, intensity, and frequency. Most authors agree that the middle frequencies are the most effective in producing the TP in patients with inner ear pathology (Table 1) [6,12,14,15,24-26]. Vestibular dysfunction has been characterized in terms of deficits in the vestibuloocular reflex system and the vestibulospinal reflex system.
Posturography is an approach to the assessment of vestibular dysfunction that uses a force platform and provides various measures that reflect postural stability, such as the amount of body sway. The TP has been studied only by nystagmographic methods and by static posturography, as mentioned.
The changes in postural stability were monitored by CDP when subjects attempted to maintain balance on the platform under stimulation with sound.
A pure-tone sound of 110 dB at 1,000 Hz generated by a portable audiometer was delivered by air conduction in continuous mode through earphones. The extent of otological disease was established and documented in every case by history, physical examination, and audiometry. In addition, most subjects with audiovestibular disorders (groups A and B) underwent ENG with sound stimulation for the detection of spontaneous nystagmus, as in the classic method for the detection of the TP. The three study groups were matched in terms of age; consequently, differences between ages were not significant when compared statistically, as shown in Table 3.
The subjects in this study were not matched in terms of quantitative results of diagnostic tests; therefore, the gravity of their disorder did not constitute a prerequisite for their selection.
The 40 patients investigated first were classified according to their clinical diagnosis (Table 4).
Patients' medical history focused on two pertinent symptoms: tinnitus and dizziness (Table 5), with special stress on severity, duration, and precipitating factors. Table 6 exhibits the results of audiological tests: pure-tone audiometry, speech reception thresholds, and performance intensity function for phonetically balanced words (speech discrimination scores). For the statistical approach of the results obtained in CDP before, during, and after acoustic stimulation, we calculated the means of the composite equilibrium scores and the mean individual sensory ratio scores for each study group in each trial. For purposes of simplicity and a better expression, we preferred to plot the mean composite score and mean vestibular ratio obtained by the three study groups, instead of the individual scores achieved by each subject. Because the composite score is an average of all sensory conditions, it reflects the overall on-feet stability of the subject. The variation among the three study groups was examined by means of one-way ANOVA followed by Bonferroni multiple range test (Table 9). Because in the study of the TP we were interested in both the overall equilibrium and the vestibular system in particular, the vestibular ratio score given by the CDP software was investigated next.
Once again the one-way ANOVA followed by the Bonferroni mUltiple range test (Table 11) analyzed the variation among the three study groups.
The vision preference is one of the sensory ratios provided by the sensory analysis of the CDP's software. The sensory analysis revealed a variety of disequilibrium types or sensory organization patterns according to the specific sensory system responsible for imbalance (Table 13). A more intriguing pattern-the combined vestibular and vision dysfunction-was observed in some group A patients on trials 2 and 3 (20% and 25%, respectively).
A last sensory organization pattern observed on sound delivery in two patients in group A was a vestibular dysfunction combined with vision preference.
The current study focused on the postural stability of normal subjects and patients with otological impairments and on a third group of patients with similar otological disorders accompanied by a history of sonovestibular symptoms.
Hadj-Djilani [14,15] studied the performance on the force-plate under sound stimulation with exactly the same sound stimulus that we delivered in our work (1,000 Hz, 110 dB SPL). Our normal subjects and the patients with inner ear impairments without a medical history of Tullio symptoms showed no significant change in postural stability.
The occurrence of vestibular disturbance complicated by vision dysfunction during exposure to strong acoustic stimuli in patients suffering from Tullio symptoms is not surprising, given the exposure of the hyperirritable "Tullio" ears to intense noise as a general excitation and discomfort. The diagnosis of vestibular malfunction related to sound exposure may be of crucial clinical significance, beyond the obvious medicolegal implications. An additional goal of this study had been to evaluate and compare the sensitivities of CDP and ENG in detecting vestibular impairment in the study participants. CDP and ENG were compared in a retrospective study of a mixed population of 375 patients with complaints of dizziness and imbalance [34]. Two additional retrospective studies [35,36] compared CDP and ENG results in patients with confirmed vestibular system deficits. Because of the nonoverlapping nature of the two tests, the foregoing three studies concluded that both vestibuloocular and vestibulospinal tests were essential components in the diagnostic workup.
We have managed to learn since the inception of this study that many patients who experience attacks of vertigo when exposed to loud noise complain of these symptoms solely in circumstances of noisy environment. A 43-year-old active ambulance driver was referred to the Otolaryngology Department of Bnai-Zion Medical Center 2 years before his admission to the current study. A constant, very disturbing tinnitus of alternately low and high pitch had been complicating his condition ever since.
The pure-tone audiogram exhibited a bilateral hearing loss of notched configuration in the higher frequencies, typical of NIHL (Fig. Prior to his admission to this study, the patient underwent ENG that revealed neither spontaneous nor gaze nor positional nystagmus, with no evidence of any vestibular pathology.
His temporary unsteadiness provoked by sound occurred because of an underlying vestibular dysfunction, as indicated by sensory analysis: The vestibular ratio is very low (Fig 6). This work constitutes the final wrap-up of the preliminary study presented at the Twenty-Fourth Neurootological and Equilibriometric Society Congress, 1997, and subsequently published in the International Tinnitus Journal 3:2, 1997. SoundCure ® Quote “For the tinnitus patient, living with this persistent condition requires changing the way he or she thinks about health care and daily life. How to cite this article Zeigelboim BS, Teive HAG, Carvalho HAS, Abdulmassih EMS, Marques JM, Cardoso RC. OBJECTIVE: This study aims to examine vestibular disorders in patients with recessive spinocerebellar ataxia. CONCLUSION: The most evident neurotological symptoms were dizziness, lack of coordination of movement, and imbalance when walking. Keywords: ataxia, spinocerebellar ataxias, spinocerebellar degenerations, vertigo, vestibular function tests.
Hereditary ataxias correspond to roughly 10% of genetic diseases that affect the nervous system. The mutation responsible for this disease is found on chromosome nine where an expansion of a GAA trinucleotide repeat in the X25 gene occurs. The first symptoms are usually observed in childhood or the early teen years, however, in some cases, the diagnosis can be made before the age of two or after twenty. The spinocerebellar ataxias (SCAs) are part of a list of diseases that, by their manifestations and areas of impairment, may cause vestibular alterations, with labyrinth exams being an important tool in confirming vestibular disorders and their relationship with the central nervous system. A questionnaire to obtain otoneurological symptoms and personal and family information was applied. Patients undertook a special diet, starting 72 hours before the otoneurological exams (abstaining from the intake of coffee, any kind of soda or caffeinated tea, chocolate, smoke, or alcohol). The search for positional nystagmus and vertigo was verified through Brandt and Daroff's maneuver16. The search for spontaneous nystagmus occurred without specific stimulation, with open and closed eyes.
We performed ENG with three-channel equipment (Berger Eletromedicina, model VN316, made in Sao Paulo, Sao Paulo, Brazil). We performed tests with a rotatingchair (Ferrante, model COD 14200, made in Sao Paulo, SP, Brazil), a visual stimulator (Neurograff Eletromedicina, model EV VEC, Sao Paulo, SP, Brazil), and air caloric stimulator (Neurograff Eletromedicina, model NGR 05, Sao Paulo, SP, Brazil). Calibration of the ocular and saccadic movements is based on the capture of the variations of electric potential between the cornea and the retina. The normal velocity range for spontaneous nystagmus search is less than 7 degrees per second with closed eyes. For the oscillatory tracking test, we requested patients to visually track oscillatory targets in the visual stimulator, and we registered the ocular movements.
In the optokinetic nystagmus search, we requested that patients track multiple targets (three horizontal streams of lighted dots) moving forward and backward. In the rotation test, patients' heads were laterally tilted 30 degrees to stimulate lateral semicircular ducts (right anterior and left posterior), in which the variations of angular acceleration are sensed. The caloric test requires patients to be positioned with head and body tilted 60 degrees backward (Brunning's position I) for proper stimulation of the lateral semicircular canals18. We compared results with normal standards, obtained from epidemiological studies for the Brazilian population19-21. The diagnosis of peripheral vestibulopathy is achieved by comparison with normal standards and the absence of pathognomonic signs of central vestibular alterations.
We applied the Difference of Proportions Test for the purpose of comparing the vestibular examination results (analyzing normal and abnormal results) and correlating the type of recessive ataxia with the most abnormal results in the vestibular examination (caloric, rotational, optokinetic, and gaze nystagmus) and then, with symptoms of dizziness, lack of coordination of movement with imbalance when walking. For vestibular function, in testing for spontaneous, gaze, optokinetic, rotational, caloric, and oscillatory tracking nystagmus, results were altered in both SCA groups, as shown in Table 3. Regarding the result of vestibular examination, we observed a higher incidence of central vestibular dysfunction (57.9%), as shown in Table 4. The application of the Difference of Proportions Test proves that there was a significant difference between the proportions of normal and abnormal tests (p = 0.0000).
The correlation between Friedereich and undetermined ataxias with the three most evident neurotological symptoms can be seen in Table 5.
The combination of vestibular dysfunction with the presence of cerebellar atrophy may contribute significantly to the onset of gait instability, which is one of the initial symptoms of SCAs26. Prim-Espada et al.28 performed an electrooculography exam (EOG) on 51 patients genetically diagnosed with FA and observed saccadic movements, for those with positional, optokinetic, and spontaneous nystagmus. Zeigelboim et al.11 reported that the loss of hair cells in the cristae ampullaris and maculae, the decline in the number of nerve cells in the vestibular ganglion (Scarpa), the degeneration of the otoliths, reduced labyrinthine blood flow, progressive depression of neural stability, and the reduction in the ability to compensate for vestibulo-ocular and vestibule-spinal reflexes all contribute to reducing the speed of tracking movements and for rotational and caloric hyporeactivity of both the peripheral and central vestibular systems, which is present in SCAs. In the present study, when comparing the result of vestibular evaluations with recessive SCAs, this differ ence became significant for central vestibular dysfunction. In the present study, no significance was observed in correlation with the most obvious neurotological symptoms (dizziness, lack of coordination of movement and imbalance when walking) with recessive SCAs. It was evident that changes in the ENG are related to the severity of SCAs or the clinical stage of the disease. The most evident neurotological symptoms were dizziness, lack of coordination of movement and imbalance when walking. Alterations in vestibular examinations occurred in 89.5% of patients, being found in the caloric test, with a predominance of central vestibular system dysfunction deficiency. This underscores the importance of the contribution of the labyrinthine evaluation for topodiagnosis of neurodegenerative diseases since in most cases the initial symptoms are neurotological, and also in the choice of procedures to be performed in clinical and therapeutic monitoring. The authors gladly acknowledge the financial support from the National Council of Scientific and Technological Development (CNPq) - Process n. Paper submitted to the RBCMS-SGP (Publishing Management System) on September 29, 2014; and accepted on October 2, 2010. This simple technique recently discovered by scientists at leading medical universities is the best way to permanently silence the noise blaring inside your ears.
Individuals with tinnitus of at least 6 months' duration (14 male, 15 female) and healthy controls (14 male, 21 female) were tested for arousal and habituation to repetitive stimulation at the brainstemthalamus level by measuring the P50 potential, a scalp-recorded, auditory-evoked response, using pairs of click stimuli. Approximately one-fourth of these individuals seek professional help owing to associated mood, sleep, and concentration disturbances [1-3].
This is believed to be related to difficulties in habituation to the perceived tinnitus sound, with a resulting sensory gating deficit.Habituation can be defined as the reduction of perception after repeated exposure to a repetitive stimulus, but whether the mechanism of auditory habituation resides in the primary auditory pathway, in subcortical areas, or at higher cognitive levels is not known [11]. The P50 potential, a scalprecorded, auditory-evoked response that occurs at a latency of 40-70 milliseconds in humans, was used to assess arousal and habituation at the brainstem-thalamus level of the neuraxis.
Assessment of simple reaction time (RT) is the most commonly used measure of thalamocortically mediated attentional systems related to vigilance or sustained attention [17-19]: Arousal falls as vigilance continues, and attention is required to boost arousal and support performance [20]. All tinnitus patients reported experiencing the presence of their phantom auditory perception for at least 6 months.
Briefly, we recorded the P50 potential at the vertex referenced to a frontal electrode using gold-plated surface electrodes. The auditory stimulus was a >90-dB sound pressure level tone of 1,000 Hz; no patient complained of discomfort at this level. One tinnitus subject was excluded owing to an inability to obtain replicable waveforms, leaving 28 tinnitus patients for assessment. Table 3 shows the correlations between the total score on the tinnitus questionnaire, the score on the sleep disorders questionnaire, and the results for the PVT. Though none of these theories is universally accepted, most propose that the development of chronic tinnitus is related to central nervous system dysfunction, even though peripheral injury in the cochlea is the inciting event. External noise has been demonstrated to have a negative impact on performance during dual tasks involving sustained attention, especially when the stimulus is varied. Orienting involves arousal systems the function of which was reflected by the initial P50 potential amplitude; habituation was reflected by a reduction of the P50 amplitude to the second stimulus.
This suggests that tinnitus patients have no impairment in their level of tonic arousal and that, though tinnitus represents a fundamental deficit in habituation, the deficit appears not to be at the brainstem-thalamus level.
One fundamental difference between the two stimuli could be represented by differences in thalamocortical activation. In a group of patients with stroke accompanied by neglect, variability in RT was observed [46] and was likely a consequence of the asymmetrical hemisphere activation known to characterize patients with right hemisphere stroke and neglect [47,48]. Neural noise resulting from asymmetrical cortical activation could also disrupt sustained attention over time. One new intervention, neuronavigated low-frequency repetitive transcranial magnetic stimulation (rTMS), has been shown to exert sustained therapeutic effects on tinnitus sensation when targeting asymmetrically active areas of the primary auditory cortex [45]. Results of reaction-time testing in a particular tinnitus subject before and after repetitive transcranial magnetic stimulation as compared to a series of tinnitus patients and controls.
Use of the P50 auditory-evoked response amplitude and paired-stimulus paradigm revealed no impairment in arousal, with a normal ability to habituate to external auditory stimuli in the tinnitus patients as com-pared to controls. We found an increased number of abnormal electronystagmography (ENG) recordings in tinnitus patients.
Tinnitus is frequently associated with sensorineural hearing loss but rarely with dizziness or vertigo.
We compared the scores of neuropsychological evaluation with normative data prepared for each test and matched for age, gender, and socioeducational level of patients. Only 21 tinnitus patients (30.4%) had remote episodes of vertigo and dizziness in anamnesis. Percentage of abnormal electronystagmography test results in all tinnitus patients (n = 69) and control group subjects (n = 43).
Comparison of abnormal electronystagmography outcomes (n = 46) with neuropsychological test results.
In the group of tinnitus patients with abnormal neuropsychological test scores, a percentage of normal and abnormal ENG outcomes was nearly the same, without any statistical correlation (Fig. Comparison of abnormal neuropsychological test scores with normal and abnormal electronystagmography outcomes.
Comparison of abnormal neuropsychological test scores with electronystagmography outcomes indicating central vestibular impairment. This finding coincides with the results of Hallam and Stephens [10], who reported no correlation between objective assessment of balance and the complaint of dizziness. In patients affected with anxiety, some authors reported enhanced vestibular responses [14-16]. Our preliminary study showed that abnormal results of visuooculomotor tests were more correlated with neuropsychological tests measuring cognitive functioning than with emotional distress [19]. Mechanisms of psychological aspects in tinnitus and vestibular dysfunction are still unclear [20], so conclusions should be drawn very carefully to avoid overestimation of ENG outcomes. In such patients, abnormal ENG results did not correlate with neuropsychological tests measuring cognitive function and emotional status. The use of the nuclear medicine imaging technique of single-photon emission computed tomography (SPECT) of brain has demonstrated hypoperfusion in brain areas supplied by the middle cerebral artery on the side of the atretic ear.
Multifactorial elements influence the clinical course of SIT and attempts for establishing tinnitus relief [1-3]. We present these findings to support previous recommendations of extensive cochleovestibular and brain function testing to be completed in SIT patients. As far as we can determine, these findings, highlighted by brain SPECT, have not previously been reported in patients with congenital atresia of the external ear.
Also demonstrated were memory interference and increased tinnitus intensity reported with increasing left-ear blockage. The TII at that time was reported as best (0; 95%) and worst (7) for 3 days after noise exposure. Ocular examination revealed symmetrical eyelids, clear conjunctivae, heterochromic irises, and equally reactive pupils without sign of spontaneous labyrinthine irritation.
SPECT of brain: bilateral parietal lobes hypoperfusion, more dominant on the right than on the left side, and bilateral mesial temporal hypoperfusion, more prominent on the right. Sinusitis was seen bilaterally, although it was more pronounced in the maxillary than the ethmoid sinus.
A partial obstruction in this area was suspected, although artifact may have accounted for this finding. Hearing loss was mixed moderate-severe and predominantly of the conductive type in the right ear and of a mild sensorineural type in the left, with a bilateral cochlear component and involvement of the central auditory pathways bilaterally (see Fig. An objective tinnitus and presumptive secondary endolymphatic hydrops (SEH) was diagnosed in the left ear. SPECT of brain (December 2, 2004) reported hypoperfusion in regions of interest in brain consistent with distribution of the right MCA (see Fig. The diagnoses included atypical left-ear tinnitus, congenital right-ear deafness, structural anatomy of the seventh and eighth nerve complexes to be normal right as reported on the MRI obtained on May 10, 2004.
Instrumentation recommendations were deferred pending tinnitus relief results and would include (if necessary) a trial tinnitus masker and UHF acoustic stimulation and external electrical stimulation and tinnitus retraining therapy. Follow-up with an internist was recommended to maintain stable blood pressure and to complete a metabolic battery with appropriate treatment as necessary. We further advised that the patient consider Klonopin use if no medical contraindication existed. Progression complaints of hearing loss, tinnitus, vertigo, and ear blockage, alone and or in combination, were to be clinically considered a "soft" sign of gradual, progressive CNS disease. We hypothesized this original tinnitus to have been clinically predominantly a cochlear type before May 2004 and considered it to have become since age 21-25 years subclinical in the left ear. We further conjectured a resultant ischemia at brain cortex with noisy spells at the brain cortex owing to left cortical activation and a cochlear tone (as previously outlined), reflecting activation of a subclinical left-ear tinnitus, due to possible interference in AICA blood flow to the left cochlea.
Alteration in aeration of the middle ears secondary to Eustachian tube dysfunction or SEH (or both) identified in the left ear may result in fluctuation in hearing or progressive sensorineural hearing loss (or both).
The hearing in the left ear has been stable clinically and confirmed by audiometric testing since November 30, 2004, and when the patient was last seen (September 13, 2005).
When seen in initial neurotological consultation (November 30, 2004), the ear blockage had been predominantly located in the left ear and clinically related to left inner-ear SEH. The report of interference in memory 3 months before November 30, 2004, was considered significant. The report of SPECT perfusion asymmetries in the brain was the basis for recommending a neuroprotective receptor-targeted therapy directed at the GABA-A receptor, in an attempt to treat a presumptive ischemia of the affected cortical areas. We considered the medical significance of the tinnitus symptom to be gradual, progressive cerebrovascular disease. What is the incidence of the hypoperfusion in brain areas of distribution of the MCA in patients with a congenital atresia of the external ear?
Follow-up nuclear medicine imaging studies in the atretic ear population with and without tinnitus will determine its incidence of occurrence. Nuclear medicine positron emission tomography imaging of brain before and after UHF stimulation revealed a correlation of metabolism of brain at the cortex, with residual neuronal function in the 10- to 20-kHz range of hearing [25]. Additional considerations to explain differences in UHF thresholds include exposure to loud noise and a hereditary sensorineural hearing loss.

Follow-up studies by hearing conservation programs in general and specifically for the population of tinnitus patients with a congenital atresia of the external ear will provide answers to this question.
It is considered to be a reflection of the SEH: the result of failure to reestablish "normal" homeostatic mechanisms controlling the hemodynamics of the intracerebral vascular and spinal fluid systems in response to hypoperfusion in the areas of distribution of the right MCA.
Within the limits of examination and supported by blood testing, we did not identify any evidence of autoimmune inner-ear disease.
Correlation of the findings of the neurotological workup with extensive testing of the cochleovestibular system (both central and peripheral and objective testing of CNS metabolic and electrophysiological responses) provided for accuracy of the tinnitus diagnosis and a rationale for achieving significant tinnitus relief. The medical significance of an objective and subjective tinnitus of the severe disabling type, as demonstrated with SPECT of brain, may be a soft sign of gradual, progressive cerebrovascular disease. We suggest that the findings of hypoperfusion in brain areas of distribution of the MCA on the side of the atretic ear and hearing UHF thresholds in the ear contralateral to the atresia are part of a syndrome in patients with congenital atresia of the external ear. Robert Stack reported that one of the "Hum sufferers" created the audio tape, mainly for the purpose in that particular segment. However, in the 1970s and 1980s, a similar phenomenon had been the object of complaints from citizens, of media reports and of studies, mostly in the United Kingdom but also in other countries such as New Zealand. Tinnitus is generated internally by the auditory and nervous systems, with no external stimulus. An investigation by a team of scientists in Taos dismissed the possibility that the Hum was tinnitus as highly unlikely. The people that hear these sounds typically hear a faint buzzing or ringing, especially if they are otherwise in complete silence, but most people don't notice them at all. The first was a pair of fans in a cooling tower at the local Daimler-Chrysler casting plant emitting a 36 Hz tone. The Tullio phenomenon evaluated by computed dynamic posturography (CDP) under acoustic stimulation is reflected in postural unsteadiness, rather than in the classic nystagmus. This establishes the described method as a sensitive testing technique for validating the existence of the Tullio phenomenon in patients with a variety of disorders of the inner ear, especially chronic noise-induced hearing loss and acute acoustic trauma. In his early works on labyrinthine physiology, Pietro Tullio [1-3] described how sound stimuli caused pigeons to sway in the plane of the horizontal semicircular canals when minute holes were created in these canals. Blecker and deVries [4] showed that a microphonic, analogous to the cochlear microphonic, can be recorded from the cristae of the fenestrated semicircular canal of the pigeon and that the frequency response of this crystal microphonic parallels the frequency response curve for the TP.
No difference in body sway was observed according to whether sound was delivered with monaural or binaural stimulation [13]. Lowfrequency noise (50-400 Hz) was shown also to induce responses in the vestibular neurons [9] by direct influence on vestibular end organs [3,9], and its influence on vestibular function was studied with infrasound stimuli of 25, 50, and 63 Hz at 130-132 dB [13,17]. Tests of the vestibuloocular reflex system-caloric irrigation, vertical axis rotation of the entire body, and ENG evaluations of spontaneous and positional nystagmus -provide information about the symmetry of a vestibular lesion affecting the horizontal semicircular canals. One of the latest versions, computed dynamic posturography (CDP) (Equitest), attempts to ferret out the effects of various sensory inputs to the brain and to relate them to overall on-feet balance and stability [27-29]. We could not find any study of vestibular responsiveness to acoustic stimulation evaluated by CDP in the literature. Mean composite equilibrium scores in three consecutive sensory organization tests; the second trial was carried out with acoustic stimulation In conditions 5 and 6.
From the wide range of acoustic stimuli used to provoke a sonovestibular response, we favored one of low intensity that efficiently, yet safely, elicits a Tullio response. Some patients were investigated by imaging studies (computed tomography or magnetic resonance imaging). Informed consent was obtained from the subjects, and the experimental protocol was approved by the local Ethics (Helsinki) Committee and the Israeli Ministry of Health. The only criteria in our choice were the established diagnosis of an audiovestibular disease and an accurate medical history concerning the presence or absence of sonovestibular complaints. The two dominating categories in this study, comprising a majority of 80% (70% in group A and 90% in group B), were patients demonstrating hearing loss caused by noise.
By definition, all patients with sonovestibular complaints (clustered in group A) had to be suffering from either lightheadedness, true vertigo, or plain disequilibrium, with or without nausea and vomiting.
The binaural hearing loss percentage was based on the pure-tone thresholds at the speech frequencies of SOO, 1,000, 2,000, and 3,000 Hz and were calculated according to the formula used by the American Medical Association [32].
For a more accurate evaluation of hearing loss, basic statistical tests were run on several audiometric parameters. This was accomplished by the alternate binaural balance test administered to patients with a difference of 2S dB or more between the hearing thresholds of the two ears at the test frequency. As we have seen, this presumption about the nonsimilarity of the two sets of subjects with otological disorders eventually was proved partially correct. Vestibular ratios scores obtained in computed dynamic posturography in three consecutive sensory organization tests, the second under stimulation with sound.
Switching to this representation is correct as long as the mean follows the trend of most individual values in the group. The trend over repeated trials of SOT was studied by ANOVA for repeated measurements, followed by the Bonferroni test for repeated measurements, applied to the average composite score (Tables 7,8). The trend over repeated trials of SOT was again studied by making use of the ANOVA for repeated measurements, followed by the Bonferroni test for repeated measurements (Table 10; see also Table 8). It reflects the degree to which affected patients rely on visual information to maintain balance, even when the information is incorrect. In this pattern, the sensory ratio of condition 4 to condition 1 is abnormal, whereas those of the remaining pairs are within the normal range (the equilibrium scores for condition 4 are abnormally low relative to the scores on condition 1). In this pattern, the sensory ratios on both SOT condition 5 to condition 1 and condition 4 to condition 1 are abnormal, with normal 2 to 1 and 3 and 6 to 2 and 5 ratios. Our two sets of pathological patients were picked by definition with regard to the medical history of inner ear disease and to the exclusion of neurological (somatosensory), orthopedic, and vision dysfunction.
Both the ratio for conditions 5 and 1 and the paired analysis of conditions 3 and 6 relative to conditions 2 and 5 were abnormal.
Accomplishing that would have enabled a correct parallel and eventual contrast between the results and effectiveness of the two vestibular tests in evaluating the TP. The postural responses were monitored on the Equitest (the CDP) in three consecutive sensory organization tests, with the second performed partially under binaural delivery of sound (1 IO dB at 1,000 Hz).
This establishes the described method as a sensitive testing technique for validating the existence of the TP in patients with a variety of disorders of the inner ear, especially chronic noise-induced hearing loss and phonal trauma, even when employing stimuli of harmless intensities (110 dB) and short durations (6 × 20 sec). Three sensory systems are involved in the maintenance of balance: vestibular, visual, and somatosensory. As mentioned, ENG recordings were not made in some cases for a multitude of reasons, and the testing protocols were not identical in the remaining subjects. CDP abnormalities were documented in 55% of the cases, whereas ENG revealed abnormality in only 26% of the patients.
In these more homogenous groups of 46 and 52 patients, ENG and CDP abnormalities were equally prevalent and occurred in approximately 50% of the cases. The contrast between ENG findings and CDP findings in the particular case of patients with sonovestibular symptoms, however, is an interesting aspect and remains one of our objectives for the future.
Others may suffer anyway, but their symptoms are significantly exacerbated during sound stimulation.
He presented with a history of dizziness attacks triggered suddenly by noise, such as loud music or at weddings, or the whine of jet engines on aircraft flying at low altitude.
He had been an otherwise healthy person, except for a peptic ulcer, silent at the time of our investigation, for which he had been administered antacids and H2-receptor blockers in the past. ENG with acoustic stimulation included a 60-second continuous recording of ocular movements during binaural stimulation with the pure tone of 110 dB at 1,000 Hz. Individual and composite scores obtained from a patient with noise-induced hearing loss and the Tullio phenomenon in the sequence of three consecutive computed dynamic posturography sensory organization tests (SOTs). Sensory ratio scores obtained from the same patient as in Figure 5 (with noise-induced hearing loss and the Tullio phenomenon) in the sequence of three consecutive computed dynamic posturography sensory organization tests . Remind patients that tinnitus is different for every individual and that there is much we are still learning about tinnitus.
The patients underwent the following procedures: case history, ENT and vestibular evaluations. Alterations in vestibular examinations occurred in 89.5% of patients, mostly in the caloric test, with a predominance of deficient central vestibular system dysfunction. Currently there are over 20 different types of autosomal recessive ataxias that have been mapped and classified according to their pathogenesis1. Subjects without this mutation have 17-22 repetitions, whereas those affected by this disease have, on average, 700-1000 GAA trinucleotide repeats5. The main features of the disease are: ataxia (impaired coordination) which initially affects the lower limbs and subsequently the higher limbs, absence of tendon reflexes, and weakness in the lower limbs, dysarthria, loss of deep distal sensitivity and bilateral Babinski sign. The tests that make up the vestibular examination permit the assessment of the relationship between balance and the function of the posterior labyrinth, vestibular branches of the eighth cranial nerve, vestibular nuclei of the floor of the fourth ventricle, the vestibular pathways, and, especially, vestibuloocular, vestibulocerebellar, vestibulospinal, and vestibuloproprioceptive-cervical interrelationships11.
We evaluated 19 patients (7 females and 12 males) who were referred from the Neurology Service, Department of Clinical Medical from the Clinical Hospital for review at the Otoneurology Research Center, a teaching institution in the same city, with a diagnosis of recessive SCA. Otorhinolaryngological evaluation was performed to exclude any alteration that could interfere with the exams. Analgesics, tranquilizers, and antihistaminic and antivertigo medications were suppressed during this period to minimize possible interferences with the test results. The first part of our patients' evaluation was simply clinical and consisted of a systematic search for spontaneous, gaze, and positional nystagmus. Patients were requested to remain seated with the head and neck bent and the body tilted to the side, which evokes the vertigo; the head was then positioned 45 degrees in the opposite direction, and the neck rested on a horizontal plane at the final position. We searched for horizontal and vertical gaze nystagmus with 30-degree deviations (right, left, up, and down). We cleaned the periorbital region with alcohol and placed the electrodes with electrolytic paste at the lateral angle of each eye and in the midpoint of the frontal line, forming a triangle and enabling the register of horizontal, vertical, and oblique ocular movements. We requested patients to keep the head still while visually tracking a light target moving in horizontal direction and then in vertical direction.
After that, patients' heads were positioned 60 degrees backward and 45 degrees to the right and left sides so that the vertical semicircular canals were stimulated.
Table 1 shows the criteria used to analyze each test as well as to distinguish central from peripheral vestibulopathy. Because of its multidisciplinary clinical form, various events may occur with disease progression. Lesions of the cerebellar vermis cause ataxia of the upper limbs, head titubation, dysmetria, and tremors in eye movements, and it is this anatomical part that expresses the extent electrical activity of the eye and neck muscles (Cogan et al., 1982). Ito et al.25 showed involvement of the central vestibular system and stressed the importance of vestibular evaluation in diseases that involve the posterior fossa. We emphasize the importance of studying the concomitant vestibular system in clinical and genetic tracking. We used the psychomotor vigilance task, a reaction-time test, to assess attentional processes mediated by thalamocortical functions.
The exact mechanisms of tinnitus generation and the related central nervous system dysfunction are unknown, rendering diagnosis and treatment difficult and often empirical. Positron emission tomography (PET) has revealed that habituation to auditory stimuli probably occurs in subcortical structures, perhaps at the level of the thalamus, suggesting the importance of the lower levels of the neuraxis (brainstem and thalamus) in this process [11]. The P50 potential is sleep state- dependent, habituates at low frequencies of stimulation, and is blocked by the muscarinic antagonist scopolamine [12-14] (and thus is thought to be generated, at least in part, by the reticular activating system).
The PVT is a test of behavioral alertness and involves a simple (not choice) reaction-time test designed to evaluate the ability to sustain attention and to respond in a timely manner to salient signals [21]. Patients or controls with significant neurological disease, acoustic neuromas or glomus tumors, active Meniere's disease, or profound hearing loss ( > 90 dB at 4,000 Hz) were excluded from the study. The measures included a numerical scoring system for questions related to the perceived evaluation of tinnitus discomfort, which could then be used in the statistical evaluation of this parameter. We monitored eye movements (electrodes placed diagonally across one eye) and jaw movements (electrodes placed on the masseter muscle and chin) for interference with the P50 potential waveform. We delivered pairs of clicks once every 5 seconds until 64 pairs of evoked potentials were acquired, averaged, and stored by the computer. The visual cue comprised blinking numbers, and subjects were asked to press with the thumb or forefinger of the dominant hand a response button on a remote control as soon as the stimulus was perceived, hence stopping the counter and displaying the RT in milliseconds.
Control subjects and tinnitus patients showed no difference in level of arousal, as measured by the amplitude of the P50. A working model that appears to explain many of the findings in tinnitus suggests that tinnitus is generated by lack of inhibition of auditory nuclei in the thalamus, which occurs when thalamic relay cells are hyperpolarized by a lack of normal depolarizing sensory input. A consequence of habituation is the process of sensory gating, which represents a critical function to focus attention and filter out extraneous information, and can be derived from the use of paired stimuli to test the level of habituation in the system being studied.
Our findings also indicate that patients with tinnitus have a normal ability to habituate to externally generated repetitive stimuli. RT during a vigilance task is a classic measure of attentional influences on intrinsic alertness [17-19]: Arousal falls as vigilance continues, and attention is required to boost arousal and support performance [20]. Real sounds presented to an ear activate bilateral auditory cortical sites, whereas tinnitus almost always results in asymmetrical activation of the auditory cortex [41]. Our study documents poor sustained attention to auditory stimulation in patients with tinnitus in the absence of any deficits in responding to externally generated sounds.
Tinnitus, by report, was worse in the left ear, which correlated with 20-30% greater activation of the right primary auditory cortex versus the left on PET-CT.
Slowest 10% response time in this patient improved, with the posttreatment results becoming similar to those of the control group in our study.
However, a significant deficit in sustained attention occurred, as measured by the slowest responses on the PVT, suggesting a failure of cortical modulation of the thalamocortical processes related to attention.
Midlatency auditory evoked responses: Differential effects of a cholinergic agonist and antagonist. Neurophysiological evidence for a defect in neuronal mechanisms involved in sensory gating in schizophrenia. Neurophysiological evidence for a defect in inhibitory pathways in schizophrenia: Comparison of medicated and drug-free patients.
Neural correlates of attention and arousal: Insights from electrophysiology, functional neuroimaging and psychopharmacology.
Microcomputer analyses of performance on a portable, simple visual RT task during sustained operations. Midlatency auditory evoked responses: Differential abnormality of P1 in Alzheimer's disease. A comparative study of visuospatial memory and learning in Alzheimertype dementia and Parkinson's disease. Disinhibition of the sleep state-dependent p1 potential in Parkinson's disease-improvement after pallidotomy. The P50 midlatency auditory evoked potential in patients with chronic low back pain (CLBP). Focal metabolic activation in the predominant left auditory cortex in patients suffering from tinnitus: A PET study with [18F]deoxyglucose.
Longterm effects of repetitive transcranial magnetic stimulation (rTMS) in patients with chronic tinnitus. The aim of this study was to compare the ENG outcome with the patients' neuropsychological status. In our previous study, we found in tinnitus patients an increased number of abnormal recordings of visuooculomotor tests, which implies central vestibular system impairment [3].
The patients received their diagnoses at the Ear, Nose, and Throat Department of the Medical University of Lodz from 1999 to 2001.
We used both computerized quantitative analysis and individual morphology assessment of all test recordings. They found that 36% of tinnitus patients had signs of vestibular imbalance in postural tests, although they did not have vestibular symptoms. In that study, we did not find a correlation between the results of vestibular evaluation based on ENG outcome and neuropsychological status. Poor efficacy of the Hospital Anxiety and Depression Scale in the diagnosis of major depressive disorder in both medical and psychiatric patients.
Anxiety and depression in an older research population and their impact on clinical outcomes in a randomized controlled trial.
Psychological manifestations of vertigo: A pilot prospective observational study in a Portuguese population. Results of Visual Ocular-Motor Tests and Neuropsychological Evaluation in Tinnitus Patients.
Ultrahigh-frequency audiometry (UHFA) has revealed a bilateral loss of hearing greater than expected for the age of affected patients.
The clinical course of two cases of congenital atresia of the external ear and tinnitus supports this clinical experience. In addition, the patient experienced an occasional perception of "water rushing" 4-5 days after a reduction in the rumble intensity and a "ring" in the left ear.
The patient reported an increased frequency of occurrence within the last 3-4 years and an increased intensity (average TII, 3) after left-ear rumble. A review of symptoms revealed anxiety, memory interference of 3 months' duration, and kidney stone. During otoscopic examination, the external leftear canal was found to be satisfactory, whereas signs of reconstructive external right-ear surgery and right external canal atresia were seen. Among the tuning-fork evaluations, the Weber test showed right lateralization, whereas the Rinne test was positive on the left and negative on the right. Rightsided gaze testing showed a right-beating nystagmus with ocular fixation suppression (OFS), downward gaze testing resulted in vertical up-beating nystagmus with OFS, and left-sided gaze testing revealed dysrhythmia with no OFS. We considered magnetic resonance imaging (MRI) or magnetic resonance angiography (MRA) for further evaluation. A Diamox stress test could differentiate between the two but was deferred due to allergy to sulfa. An audiometric test (May 8, 2004) reported no response in the right ear but left-ear hearing within normal limits for language and speech and a mild sensorineural hearing loss at 4 kHz. Intramuscular Decadron (10 mg) and continued Medrol Dosepak and Ativan (1 mg) for anxiety were recommended. Hearing loss in the right ear was predominantly mixed and involved a cochlear component, whereas there was a predominantly cochlear-type hearing loss in the left ear within normal limits for language and speech (see Fig.
A neuroprotective drug protocol was recommended of a receptor-targeted therapy, gabapentin (100-mg tablet in one dose to be titrated based on the TII), and clonazepam (Klonopin, 25 mg at bedtime), if not medically contraindicated, the dose to be titrated based on the TAI.
Any deterioration in the patient's condition was to be assessed by an internist, a neurologist, or an ENT specialist, and should include audiometry in an attempt to maintain hearing. Neuroradiological follow-up including CT scan of the temporal bones confirmed right external-ear canal atresia, a dilated right IAC, and a normal left temporal bone. The complaint of ear blockage was reduced in the left ear, and no vertigo or balance complaint remained.
The rumble sound was objectively auscultated over the left external ear (November 30, 2004).
We further hypothesized that a cerebrovascular factor, gradual in onset, "triggered" the subclinical left-ear tinnitus to manifest itself as spells of noise at the brain cortex, located in the head, and as a "tone" in the left-ear cochlea. Alteration in underlying homeostatic mechanisms maintaining normal function of the fluid compartments of the blood-brain and bloodlabyrinth barriers are hypothesized to have contributed to the left-ear SEH. The UHFA findings of a loss of hearing greater than expected for the age of the patient may be a reflection not only of noise exposure in the past but, more significantly, together with the heterochromia of the irises, of a hereditary sensorineural hearing loss. To be considered at this time was a left-ear AICA syndrome associated with gradual, progressive cerebrovascular disease.
Recommendations included replacing the antiseizure medication topiramate (Topamax) with gabapentin (Neurontin) in combination with clonazepam (Klonopin).
We advised the patient to enter into this decision-making process if the tinnitus complaint persisted and the significance of the tinnitus complaint outweighed the incidence of potential complications of angiography.
Accurate tinnitus diagnosis by inclusion of peripheral and central tests of cochleovestibular function or dysfunction combined with tests of brain function (SPECT, QEEG) provided a rationale for tinnitus treatment that resulted in significant tinnitus relief, maintenance of hearing, and control of balance. Specifically, brain plasticity at the cortex was most effective with UHF acoustic stimulation when the integrity of the brain at the cortex was intact and the residual neuronal function in the 10- to 14-kHz range of hearing did not exceed audiometric thresholds (30-40 dB). For the future, routine hearing testing, including establishment of UHF audiometric thresholds in all patients with congenital atresia of the external ear, will provide an answer to the question of whether this observation is special for patients with congenital atresia of the external ear and will assist in the determination of its medical significance for hearing conservation in general. It is considered clinically significant that the diagnosis of a secondary (delayed) endolymphatic hydrops was identified in two cases of congenital atresia of the external ear, in the tinnitus ear contralateral to the side of the atresia. We recommend conducting a complete evaluation of the cochleovestibular system, both peripheral and central, including nuclear medicine imaging (SPECT of brain, UHFA, and QEEG), in an MATPP for SIT patients to improve the accuracy of the tinnitus diagnosis, to provide a rationale for treatment, and to monitor the clinical course of the tinnitus complaint. As far as we know, the finding of hypoperfusion in brain areas of distribution of the MCA on the side of the atretic ear has not been previously reported. GABA-A-benzodiazepine- chloride receptor-targeted therapy for tinnitus control: Preliminary report.
A Hum on the Big Island of Hawaii, typically related to volcanic action, is heard in locations dozens of miles apart. Data from the Taos Hum study suggests that 2% to 5% of the general population can detect the Hum, with individuals 50 years of age or older being particularly prone to sensing it.
Common consequences include a lack of sleep, as the Hum can keep some people awake or wake them in the middle of the night.
This was done since their audio equipment didn't pick up low-frequency sounds very well, and so that the show's viewers and other non-"Hum sufferers" would get an idea of what the actual auditory phenomenon sounded like.
However, the theory that the Hum is actually tinnitus fails to explain why the Hum can be heard only at certain geographical locations, to the degree those reports are accurate.
The second was an air compressor intake at the Haynes International plant emitting a 10 Hz tone. Bristol, England, Aukland, New Zealand and Bondi, Australia have all been plagued by unexplained booming, buzzing or droning noises. With such a method, the dangerous effects of noise-induced instability can be assessed and prevented. This vestibular microphonic can be recorded from any of the vestibular end organs and has been observed in many species.
A scan of the literature for the different stimuli used in different studies reveals that the sound pressure levels used to elicit a TP in healthy subjects were higher than those used in subjects with pathologies of the ear. These vestibular tests, however, do not characterize the vestibular deficit in terms of patients' functional status (the ability to stand and walk) because such patients are evaluated in "passive" positions in which balance is not required.
CDP includes test conditions in which the platform and visual environment are moved to reduce subjects' ability to use visual and proprioceptive information for balance. Static posturography falls short of revealing pure vestibular malfunction, manifested clinically as unsteadiness when standing or walking. This SPL is well within safety limits (Table 2) in accordance with the Illinois Occupational Diseases Act [30] and the Occupational Safety and Health Administration Regulation [31]. All patients with abnormal visual, orthopedic, and neurological function (other than audiovestibular disorders) were excluded from the study.
Therefore, patients in group A were intrinsically a "dizzier" and (as demonstrated later) a more "unstable" set of subjects than were those in group B.
Single-factor analysis of variance (ANOVA) revealed insignificant differences among hearing loss percentages, speech reception thresholds, and speech discrimination scores of the two pathological groups (see Table 6). These study groups harbor a discrepancy with regard to symptomatology, whereas objective audiometry revealed a similar degree of hearing impairment. In this way, excessive clutter in the illustration is avoided without generating any statistical error in this case.
Thus, the severity of dizziness in these patients (as indicated by history) found a confirmation in terms of posturography by showing a worse balance even in the absence of sound. In group A, the vestibular component of the equilibrium again demonstrates a decrease on stimulation with sound (see Fig 3). Thus, we got a confirmation of what theoretically was expected; the impaired on-feet stability is (at least in part) explained by a flawed vestibular system in patients with TP.
The vision preference scores did not show a large variation, either over consecutive trials or across study groups (Table 12).
The initial proportion of vestibular dysfunction increased on acoustic stimulation to 55% in group A but subsequently decreased in the third trial. As we know from the literature, this pattern is not observed commonly in patients with impairment limited to the vestibular system but rather are suggestive of central nervous system pathology, possibly in addition to that of the vestibular system. CDP performances demonstrated that 90% of the 40 subjects (groups A and B) showed either normal balance or vestibular dysfunction solely. In these cases, the average equilibrium scores for conditions 3, 5, and 6 were not only below the normal limits but were abnormally low relative to the scores on conditions 1 and 2.
Regrettably, not all 60 study subjects underwent ENG recording under stimulation with sound, and some of those who did were not evaluated identically in terms of duration of exposure to the acoustic stimulus for various reasons. In comparing our results to those found in previous works in which static posturography methods were used, we must take note of the controversy surrounding the subject in the literature.
In these works, they studied the TP using low-frequency sound (25-63 Hz, 130 dB SPL) and observing the change in stability on a static posturograph.
This stimulus is well within the noise exposure standards and therefore is safe, with a temporary threshold shift the only unwanted effect it produces. When vestibular damage occurs and remains undiagnosed, the overall function of balance relies only on the other two systems.
Conclusions based on such a methodological incongruity of the two diagnostic tests could be erroneous.
Hence, CDP provided the only documented evidence of pathology in approximately 30% of the cases.
Both categories, especially the former, undergo extensive and protracted workup as the usual diagnostic tests fail to reveal the gravity of their otoneurological disease. He described these attacks as short (minutes), mainly lasting through the duration of the noise but sometimes beyond that, and always accompanied by nausea.
As compared to relatively good overall equilibrium (composite score, 78) and competent sensory systems on the first trial (see Fig. The second trial was performed with acoustic stimulation during conditions 5 and 6, whereas the other two were quiet SOTs in the regular mode.
Responses of squirrel monkey vestibular neurons to audiofrequency sound and head vibration. Influence of pressure loading to the external auditory canal on standing posture in normal and pathological subjects.
Tullio phenomenon and postural stability: experimental study in normal subjects and patients with vertigo. Effects of increasing intensity levels of intermittent and continuous 1000 Hz tones on human equilibrium. Adaptation to alter support and visual conditions during stance: patients with vestibular deficits. Effect of visual support surface references upon postural control in vestibular deficit subjects. Computerized dynamic posturography: its place in the evaluation of patients with dizziness and imbalance. Comparison between dynamic posturography and ENG recordings in patients with peripheral vestibular disorders. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.Designations used by companies to distinguish their products are often claimed as trademarks. This underscores the importance of the contribution of topodiagnostic labyrinthine evaluations for neurodegenerative diseases.
In this group of diseases, some are very rare, being observed only in isolated populations, whereas others are found worldwide2.
The affected gene's function is to encode mitochondrial protein, frataxin, which is involved in iron metabolism2-5. Lesions to the cerebellum cause ataxia of the upper limbs, head titubation, dysmetria, and tremors in eye movements, which is the part of the anatomy that shows electrical activity along the ocular muscles and neck. The second part consisted of interpretation of the ENG test results, which is the objective register of the variations in the corneoretinal potentials, captured by sensitive electrodes. Patients returned to the first position and repeated the procedure toward the opposite side. The equipment is adjusted so that the eyes' movement performs an angle of 10 degrees (standard calibration). Occurrence, direction, inhibiting effect of ocular fixation (IEOF), and maximum slow component angular velocity of nystagmus (MSCAV) were registered. The test is used to evaluate the integrity of the oculomotor system in controlling the slow movements of the eyes. Occurrence, directional preponderance, and measurements of the MSCAV of nystagmus were evaluated.
Records were registered with open and closed eyes to note IEOF, direction, MSCAV absolute values, and correlation between directional preponderance and post caloric nystagmus direction. The most evident changes in other studies11,12,25 were the presence of positional nystagmus, irregular eye movement calibration, spontaneous rebound nystagmus, bidirectional and multiple gaze nystagmus, and the abolition of optokinetic nystagmus, pendular tracking type IV, vestibular hypofunction, the absence of the inhibitory effect for ocular fixation, and signs of Aubry for proof of Barany. Fahey et al.29evaluated 20 patients with FA and observed that despite the presence of normal saccadic velocity, latency was shown to be essentially extended. Studies in human vestibular function I: Observations on the directional preponderance ("nystagmusbereitschaft") of caloric nystagmus resulting from cerebral lesions. Normal limits of evaluation parameters of neurograff digital vectonystagmography [in Portuguese]. Vestibular, saccadic and fixation abnormalities in genetically confirmed Friedreich ataxia.
We then correlated deficits in arousal and attention, as measured by these tests, with perceived tinnitus severity.
Most believe that the inciting event for tinnitus generation lies in cochlear or auditory nerve dysfunction, but the per-ception of tinnitus is traced back to central mechanisms in most cases [2,4-7]. Though the amplitude of the P50 potential is a measure of the level of arousal, a paired-stimulus paradigm can be used to measure habituation, which is part of the process of sensory gating [15,16]. The PVT was designed to be simple to perform, free of a learning curve or influence from acquired skills (aptitude, education), and highly sensitive to an attentional process that is fundamental to normal behavioral awareness. Individuals on psychotropic medicines, including antidepressants, anticonvulsants, or sleep aids, also were excluded.
We also administered the insomnia portion of the sleep disorders questionnaire to both tinnitus and control groups to assess functional impairment in sleep function [23].
The P50 potential was identified as the largestamplitude positive wave occurring between 40 and 70 milliseconds. Control subjects and tinnitus patients likewise did not show significant differences in habituation as measured by the ability to suppress a second, closely paired stimulus, regardless of ISI. As shown, we found no significant correlation between sleep disturbance and the PVT but did note a significant association with irritability and discomfort with tinnitus and the number of false starts. The action potentials generated by this hyperpolarizing mechanism usually occur in rhythmic bursts, which can lead to the establishment of a reverberating loop between the thalamus and the auditory cortex, where tinnitus is perceived. Sustained attention, or vigilance, as measured by the PVT, is an extremely useful measure of the thalamocortically mediated attentional system. Although sleep pressure is known to reduce performance, no difference was seen in sleep disturbance in the tinnitus patients versus controls, and no correlation was seen with tinnitus severity or sleep disturbance and the PVT results, with the exception of the number of false starts seen in individuals reporting increased irritability. Numerous studies that have been published concerning functional imaging (PET scans) in tinnitus patients have shown increased activity consistently in one hemisphere, primarily the left, regardless of tinnitus laterality or bilaterality [42-45]. These results might be integrated with current findings on the central mechanisms of tinnitus if brought in line with asymmetrical cortical activation. One week after completion of the treatment, the patient reported a 50% reduction of tinnitus using a visual analog loudness scale. These findings were not related to sleep disturbance or tinnitus severity, suggesting that the functional deficits may be linked to the pathophysiology of the patients' tinnitus and not to any associated comorbidities. The ENG outcomes were evaluated by obvious established criteria, and we classified the site of lesion when two or more abnormal recording results occurred in tests. The majority of the ENG outcomes in our patients imply central vestibular system dysfunction, which was also pointed out by Seabra et al. Their study showed that psychological care was necessary in 64% of patients in their dizziness group, in 45% of patients in their tinnitus group, and in 27% of patients in their hearing loss group. The only tendency was a prevalence of abnormal scores in one of the tests measuring levels of depression (the BDI test) in patients with a central type of vestibular impairment. Quantitative electroencephalography (QEEG) has shown a significant central nervous system electrical dysfunction correlated with the SPECT of brain findings.
A sensation of "vertigo" of approximately 24-hour duration described as a "drunk feeling" followed the rumble sensation.
Clinically, an ischemia was presumed to be present based on our past SPECT of brain experiences with tinnitus patients of the severe disabling type [10].
Physical examination was consistent with the diagnosis of chronic vasomotor rhinosinusitis, chronic catarrhal otitis media, and Eustachian tube dysfunction on the left. The patient reported an improvement, which included elimination of the vertigo and left-ear blockage and a reduction in the tinnitus intensity.
Initial neurological recommendations included continuation of the steroids in a tapered dosage and a trial of Topamax and verapamil if the tinnitus complaint persisted or recurred. The patient reported no associated complaint of hearing loss, vertigo, ear blockage, nausea, headache, drowsiness, or blurring of vision. Our advice was to follow the neurological recommendation of Mobic, 7.5 mg bid, to assist in prednisone reduction, which was reported by the patient to be effective. The clinical history of spells of this tinnitus, which are influenced by steroids, is considered to be mainly cortical in location. We considered both auditory percepts to be a clinical reflection of altered hemodynamics in cerebrovascular circulation. Normal Eustachian tube function control has been maintained with decongestant nasal steroid spray.
We recommended neurological consultation follow-up to establish the neurological significance of these complaints and correlation with SPECT results, MRI reports, and central cochleovestibular test findings. The MRA results (December 16, 2004) showed a small area of flow gap or narrowing in the proximal portion of the straight sinus, leading to suspicion of a partial obstruction or artifact in this area.
Clinically, such tinnitus patients reported tinnitus relief as most effective and demonstrated hypometabolism at the cortex. The diagnosis of SEH was supported by the subjective complaint of ear blockage in the tinnitus ear and its reduction with diuretic therapy.
A maintenance dose of Klonopin and a gradually increasing dosage of the antiseizure drug gabapentin replaced the Topamax.
Presented at the Thirty-First Congress of the Neurootological and Equilibriometric Society, Bad Kissingen, Germany, March 24-27, 2004. Proceedings of the Fifth International Symposium on Meniere's Disease and Inner Ear Homeostasis Disorders. There may exist individual differences as to the threshold of perception of acoustic or non-acoustic stimuli, or other normal individual variations that could contribute to the perception of the Hum by some people in the population and not by others. This should be carried out preferably by means of CDP with acoustic stimulation for an objective corroboration of their complaint before continuing activity in a noisy environment, thus preventing dangerous loss of balance when exposed to noise.
Tullio observed the currents created in the labyrinthine fluids in response to sound by watching the motion of dye particles introduced into the endolymph and perilymph.
Furthermore, information gathered from these studies may indicate that the vestibular response-evoking threshold intensity varies with the frequency of the stimulus: Normal subjects evidence sonovestibular responses at midfrequency range (l,000 Hz) over 120 dB [23].
CDP constitutes a comprehensive sensorial function test of the equilibrium by virtue of its inherent feature of isolating the vestibular, visual, and somatosensory contribution to overall balance, unlike older posturography techniques that served as mere systemic balance tests. We deem CDP a very appropriate technique for investigating the interaction between balance and sound within the labyrinth. According to these noise exposure safety standards, subjects can be exposed safely to 110 dB for a half-hour daily before any otological damage would occur.
Subsequently, we summarized all the relevant medical information supplied by history and the battery of audiological tests. The findings were not suggestive of any correlation between recruitment and the presence or absence of sonovestibular symptoms. This is not surprising, considering that abnormal sensory preference is, in essence, the effect of a central pathology (arising from the vestibular nuclei or their higher connections), whereas all the subjects in this study were patients suffering from peripheral disease exclusively (arising from the labyrinth or vestibular nerve). The vestibular dysfunction percentages remained constant in the other two groups on repeated trials. The significance of this disclosure of a disturbance in the central connections responsible for equilibrium, triggered by acoustic stimulation in the patients with sonovestibular symptoms, has yet to be interpreted. Only 10% (two subjects in group A on trial 1 and two in group B on trial 3) revealed an inability to use input from the visual system to maintain balance. In general, patients with this kind of pattern are unable to use vestibular system inputs and are abnormally destabilized by orientationally inaccurate visual stimuli.
Not only did the intense sound have no deleterious effect on the balance of normal subjects but they improved their postural stability during sound stimulation, probably through the alerting response. Thus, it can be used routinely for detecting this disturbing and potentially dangerous phenomenon in patients who complain of sudden dizziness or report protean descriptions of feeling bad when they happen to be exposed to intense noise at a concert hall, discotheque, airfield, or work. Even though the functional impact of vestibular and vision dysfunction is limited to noise exposure in such patients, they require a stable support surface reference to maintain balance (somatosensory-dependent) in those instances. When, in addition, other sudden sensory deprivation occurs or if new relationships develop between the sensory systems involved in balance, spatial disorientation may transpire under these circumstances. Among the cases with history of head injury, 100% had CDP abnormalities, whereas ENG results were normal in all of them.
Among patients with abnormal ENG and normal SOT results, the majority had compensated unilateral lesions.
Such patients' symptoms seldom improve, because the underlying damage is by and large permanent regardless of etiology. Additionally, he mentioned occasional vertiginous attacks caused by bending forward, always quite suddenly relieved by straightening out.
Speech audiometry found binaural speech reception thresholds and speech discrimination scores of 20 dB and 100% at 55 dB, respectively.

5A), our patient demonstrated a sharp decrease in his overall balance when exposed to the pure tone of 110 dB at 1,000 Hz (composite score, 52) (see Fig. Cited by Erlich MA, Lawson W, The incidence and significance of the Tullio phenomenon in man. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. Among them, is Friedreich's ataxia (FA) initially described by Nicholaus Friedreich in 1863, however only becoming known around 1882.
The deficit of this protein causes the accumulation of iron in mitochondria compromising the mitochondrial respiratory chain and increasing oxidative stress2,6,7. Other characteristics that can be attributed to cases are: nystagmus, optic atrophy, hearing loss (may be present), atrophy in the hands and distally in the lower limbs, scoliosis, pes cavus, and claw toes2-8. Some evidence suggests that lesions in the cerebellar vermis cause vertical dysmetria while more lateral or paravermian lesions cause horizontal dysmetria. The diagnosis of ataxia was performed by means of genetic testing using the Polymerase Chain Reaction (PCR) technique13-15. The ENG test is composed of: calibration of the ocular movements, search for spontaneous and gaze nystagmus, the oscillatory tracking test, optokinetic nystagmus search, and rotatory and caloric tests.
As these movements are registered, we adjust the gain of the graphic needle to 10-mm amplitude (first channel) and to 5-mm amplitude (second and third channels).
We observed the presence, directional preponderance, and frequency of the ocular movements, using the same formula for optokinetic nystagmus search.
Normal absolute values are within 2 degrees and 24 degrees per second, whereas normal relative values are lower than 41% for labyrinth preponderance and less than 36% for nystagmus directional preponderance. Among the damaged neuronal structures, the occurrence of vestibular hypofunction is known, but little is known about when and why it occurs. In addition, vestibular abnormalities were observed with a sharp reduction in the gain of the VOR. Fahey et al.29 emphasized that the range of alterations in eye movements suggest changes in the brainstem, as well as cortical and vestibular pathways. Results showed no difference between tinnitus patients and controls in level of arousal or habituation to repetitive sensory stimulation, as measured by the amplitude of the P50 potential and the ability to suppress a second, closely paired stimulus, respectively. This study was approved by the Institutional Review Board at the University of Arkansas for Medical Sciences. We measured the amplitude of the P50 potential as previously described [12-14,24-31], and we determined habituation by calculating the ratio of the P50 potential induced by the second stimulus of a pair to the P50 potential induced by the first stimulus of a pair, expressed as a percentage.
These thalamocortical dysrhythmias then lead to or facilitate maladaptive cortical reorganization and the phantom perception of sound in a chronic fashion [4,5,33-36]. Second, it is blocked by the muscarinic cholinergic antagonist scopolamine and, therefore, may be mediated, at least in part, by cholinergic neurons [14]. Although significant sleep deprivation leads to a global reduction in the reaction-time parameters of the PVT, the lapses (RTs >500 msec) and the 10% slowest RTs are the most sensitive measures of vigilance. These findings suggest that the vigilance deficit observed in patients with tinnitus may be linked to the pathophysiology of their tinnitus and not to any associated comorbidities, such as sleep disturbance or diminished quality of life. Interestingly, the man likewise showed an improvement in slowest 10% RT, with the posttreatment results becoming similar to those of the control group in our study (Fig.
The performance variability and perhaps the inability to habituate to the internally generated sounds are hypothesized to be related to asymmetrical cortical activation that is known to characterize this condition. We also decided to assess the neuropsychological status in our group of patients because it contributes to diagnosis and treatment strategies. In our patients, we found a high percentage of abnormal scores in neuropsychological tests measuring both emotional distress and cognitive functioning. Otherwise, patients with vestibular symptoms are found to exhibit abnormal scores in neuropsychological examination.
Our present study did not confirm previous findings, although we conducted it on a larger group of patients and took into consideration all ENG test batteries, not merely the results of visuooculomotor tests. The annoyance included interference in communication, concentration, performance, and participation in social activities. A screening test revealed mixed moderate-severe right-sided hearing loss and mild left sensorineural hearing loss.
Cranial nerve examination showed the eighth cranial nerve on both sides to be abnormal and the remaining nerves normal. The GABA-A receptor, with its inhibitory activity in brain function, exerts a neuroprotective action [8,11].
MRI of the IACs and brain (May 10, 2004) demonstrated no cerebellopontine or IAC angle tumor and no mass, otomastoiditis, acute infarct, or intracranial mass lesion. The air conduction UHFA identified thresholds of sensorineural hearing loss greater than expected for the age of the patient (Fig.
We also recommended discussion with a neurologist of an angiogram to rule out AV malformation or dural fistula if the tinnitus complaint persisted or progressed. The subjective tinnitus described as an occasional ringing is thought to be mostly cochlear in location.
The complaint of ear blockage will be recurrent in this patient, and accurate diagnosis will determine the selection of treatment. Also recommended was that complaints of progressing or deteriorating hearing loss, tinnitus, vertigo, and ear blockage, alone or in combination, be followed up by repeat ENT and neurological consultation in an attempt to maintain hearing and to maximize attempts at tinnitus relief. We hypothesized that the original left-ear bruit was an objective tinnitus found on auscultation, reflecting predominance of the left vascular drainage. The etiology of the SEH (delayed) in both cases of congenital atresia of the external ear is considered to be cerebrovascular. However, in the late 1990s, seismologists discovered that the world also constantly vibrates at very low frequencies even when there are no quakes.
And the Earth itself is known to make a hum, generated by a number of events including the rumbling of storm-driven ocean waves. He noted that these currents were in perfect correspondence with the frequency of the applied tone.
At low frequencies (25-63 Hz), the minimal intensity would be 145 dB [13], whereas at frequencies up to 2,500 Hz, the vestibular responses occur only at a sound pressure level (SPL) exceeding 120-160 dB [19]. This was followed 20 minutes later by a test carried out in quiet stance in SOTs I through 4 and with acoustic stimulation in SOT 5 and SOT 6 (Fig. This duration is more than an order of magnitude larger than the total of 120 seconds for which our subjects were exposed during the sequence of two SOTs (5 and 6) repeated three times each. In vestibular dysfunction, the sensory ratio of condition 5 to condition 1 is abnormal, whereas those of the remaining pairs are within the normal range.
This pattern was observed neither in those in group B nor in normal controls, whether stimulated acoustically or not.
None of the patients demonstrated somatosensory or central pathology, except for the "central" pattern exhibited by those in group A during and after exposure to sound, as discussed in the previous paragraph. As both the lack of visual and support surface inputs and conflicting visual inputs are destabilizing, these patients are more impaired functionally than are those with either vestibular dysfunction or vision preference alone. In the absence of a stable surface, they do not make effective use of either vestibular or visual inputs [33]. Exposure to intense noise in unusual environmental settings (during flying under changing gravitational forces, diving, physical activity in darkness, or night driving) might produce conditions that in certain circumstances could even be life-threatening. In contrast, patients with normal ENG and abnormal SOT results had clear positive symptoms of vestibular system disorder.
By the nature of his trade, he had been constantly exposed to the wail of the ambulance siren for almost two decades, and this had turned his everyday life for the last 7 years into a desperate condition.
Capelli, 1929.) Cited by Erlich MA, Lawson W, The incidence and significance of the Tullio phenomenon in man. It is a neurodegenerative disease that is progressive in nature, and has autosomal recessive heredity, with early onset in most cases2-4. Diabetes may be present in 10% of cases, and cardiomyopathy occurs in approximately two thirds of patients being the leading cause of death7-9. Moreover, the more anterior the lesion, the more intense the dysmetria will appear in the upper eye, whereas the more posterior the lesion, the more intense the dysmetria will appear in the lower eye12.
Thirteen patients are currently undergoing genetic research to know what type of recessive SCA they have and, therefore, belong to the undetermined SCA group.
Takegoshi & Murofushi27 note that spinocerebellar degeneration is one of the clinical entities for disorders of the vestibular system. However, reaction-time assessments showed that patients with tinnitus have attentional deficits relative to controls (p = .02).
Each channel was led to a Grass Instruments P511 amplifier (Quincy, MA) with a high-resistance input stage. Third, it undergoes rapid habituation at stimulation rates greater than 2 Hz; therefore, it is not manifested by a primary afferent pathway but perhaps by multisynaptic, low-security synaptic elements of the reticular activating system relayed to the cortex through the intralaminar thalamus [14]. Neuropsychological evaluation was conducted by means of the Beck Depression Inventory (BDI), the Hospital Anxiety and Depression (HAD) test, the Mini Mental Status (MMS) test, and the Trail- Making Test (TMT). The aim of this study was to compare the electronystagmography (ENG) outcome in tinnitus patients with their neuropsychological status. In all subjects, we performed neurootological, ophthalmological, and audiological examination, including pure-tone and speech audiometry, tympanometry, auditory brainstem response, and neuroradiological imaging if necessary. Hallam and others [10,17] noticed in a group of tinnitus patients that those with additional dizziness complaints obtained higher scores on an anxiety scale. Completion of the medical audiological tinnitus patient protocol, including SPECT of brain, UHFA, and QEEG, accurately established the clinical tinnitus diagnosis of predominantly a central-type tinnitus, a clinical hypothesis that the medical significance of the tinnitus is a "soft" sign of cerebrovascular disease, and provided a rationale for treatment directed to a presumed ischemia of brain based on a receptor-targeted therapy targeted to the GABA-A receptor, resulting in significant tinnitus relief.
Steroid therapy and a low-sodium diet received prior to November 30, 2004, resulted in a reduction of spells of the rumble.
The findings of SPECT of brain in areas of distribution of the MCA were the basis for recommending various tests. Factors that are identified in the clinical history and can influence (and have influenced) the clinical course of the ringing tinnitus included fluctuation in bilateral aeration of the middle ears, SEH identified in the left ear, noise exposure, and stress. We considered this vascular hypothesis to be supported by the central cochleovestibular test findings (auditory brainstem response, QEEG), the SPECT of brain report (December 2, 2004), and the clinical response of the patient to treatment with steroids and antiseizure medication.
Close attention by patient and ENT specialists will improve the ability to maintain hearing and balance.
In addition, the alteration in the hemodynamics of the cere-brovascular circulation has been hypothesized also to involve the AICA, a long-term effect that may include SEH. The introduction of Mobic-a nonsteroidal antiinflammatory agent, on a neurologist's recommendation-in combination with gabapentin and Klonopin, was accompanied by elimination of the steroid and an increase in and maintenance of long-term tinnitus relief. Researchers now believe the Earth's hum can help them analyze the composition of our planet's interior. The second group (B) included 20 neurootological patients without a history of Tullio phenomenon. He also noted that at higher sound intensities, a nystagmus was produced, the frequency of which corresponded to the oscillations of the internal current. Bearing in mind that acoustic stimuli in unusual environmental conditions always affect both ears, we preferred to employ a binaural stimulation in the attempt to prove the hypothesized correlations in accordance to the hazards of quotidian reality. Thus, the equilibrium scores for condition 5 only, or for conditions 5 and 6, are abnormally low relative to the scores on condition 1.
This abnormal pattern is described as occurring in patients with balance disorders secondary to traumatic head injuries but also was reported in other patient populations. The balance functions during exposure to intense noise in such patients tend to be more impaired than in those with vestibular dysfunction, vision preference, or a combination of these pattems.
In these patients, disorders were either more central or were presumed to effect peripheral components other than the horizontal semicircular canals (vestibuloocular system).
Consequently, these patients continue to seek medical assistance, and their complaints seem to be psychologically aggravated by frustration accumulated through continual visits, referrals, and failing therapy. On the third (quiet) trial, 20 minutes later, his balance recovered completely (composite score, 80) (see Fig. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. There are significant variations in the average duration of disease, and the onset of symptoms until death, which that tends to occur around the fourth decade of life5-7,10.
Risk of developing drug-induced hearing loss is greater in those with impaired kidney health or inner ear disorders (Ligezinski 2002). We found no significant correlation between sleep disturbance or tinnitus severity and reaction-time testing. Circadian effects were controlled by performing the test at the same time of day (late morning) for all subjects.
That is, the brainstemthalamus is the main relay responsible for the P50 potential so that disorders that involve thalamic structures may exhibit dysregulation of the P50 potential.
Future work in our laboratory will focus on mechanisms involved with this apparent improvement in tinnitus sensation and performance by longitudinally studying individuals who have been treated with rTMS using tinnitus perception, PVT, and functional imagery (PET-CT). The goal of the patient for this consultation was to obtain information about the tinnitus complaint, to obtain tinnitus relief, to identify the medical significance of the tinnitus, to maintain hearing in the left ear in view of right hearing loss associated with congenital atresia in the right external ear, and a concern for the need for long-term prednisone therapy. On nasal assessment, mild right septal deviation and mild right-to-left hypertrophy of the turbinates were seen. UHF electrical-acoustic testing revealed sensorineural hearing loss greater than expected for the age of the patient (Fig. Computed tomography (CT) scan of temporal bones (January 7, 2005) revealed right external canal atresia but no CT abnormality of the right bony labyrinth. A follow-up neurological visit (July 9, 2004) reported the trial of verapamil for 2-3 days to be associated with an increased tinnitus intensity and was stopped by the patient. The neurotological workup and particularly the SPECT of brain identified significant bilateral perfusion asymmetries, greater on the right than on the left (see Fig.
The extensive medical evaluation, to the limits of examina tion, has excluded coagulopathy and autoimmune disease.
Paradoxically, the "dependence" on the steroid for tinnitus relief may have been a sign of a steroid toxicity related to increasing stress before and during the initial course of the tinnitus. Sounds reaching the ear of the animal produced a current in the open canal, also affecting all three semicircular canals simultaneously. In the latter two tests, subjects had only the vestibular system at their disposal (with inputs from other sensory systems canceled or inaccurate). The functional impact of this pattern dwells in the necessity of either a stable support surface or stable visual field to maintain balance.
Indeed, one of our two patients with this disequilibrium pattern mentioned a head injury incurred several years prior to the current investigation (in addition to the NIHL from which he was suffering and for which he was selected). Preferably, this should be carried out by means of CDP with acoustical stimulation for an objective corroboration of their complaint before continuing activity in a noisy environment, thus preventing dangerous loss of balance when exposed to noise. We deem the description of a typical case of TP pedagogically rewarding and suggestive of the problem and therefore appropriate. It is sold on the understanding that the publisher is not engaged in rendering professional services. To evaluate the regularity of the saccadic movements, we used the normal ranges of the following parameters: latency, accuracy, and velocity of movement. The failure to habituate may derive from internal factors, such as readiness to attend or tonic arousal, or may be related to the perceived novelty of the internally generated noise. As far as we can determine, these findings, highlighted by the brain SPECT, have not previously been reported in patients with congenital atresia of the external ear. A dilated right internal auditory canal (IAC) showed no enhancing mass, but the right demonstrated abnormal pinna with calcifications. 4), highlighted by the perfusion asymmetry in regions of interest in brain areas of distribution of the right MCA. The affect component is complex and reflective of the frustration of patients with the complaint of tinnitus and fear of loss of hearing in the left nonatretic ear. Control of the foregoing factors highlighted by control of blood pressure is considered to provide an increased prognosis to maintain hearing and balance and tinnitus relief. Preliminary analyses have led investigators to believe the source of the hum is on or near Zug Island, an industrial area on the Michigan side of the international border, the Wall Street Journal reports.
A pure-tone stimulus of I,000 Hz at 110 dB was delivered binaurally for 20 seconds during condition 5 and condition 6 of the CDP sensory organization test.
However, the current was predominant and the cristae more easily displaced in the fenestrated canal, accounting for visible movements only in the plane of this canal.
The sensory analysis of the second patient showed mainly vestibular dysfunction and only a borderline visual preference abnormality.
Tinnitus may also be considered to be a varying stimulus due to environmental masking, with some tinnitus representing a complex mix of several sounds. The sequence of six sensory organization conditions was performed three times with two intermissions of 15-20 minutes between the trials. From the different reactions that Tullio observed by stimulating the ears of animals, he proposed that perhaps this was to become a potential diagnostic tool with which one could recognize the seat and nature of lesions in the different parts of the labyrinth.
The latter is described in the literature as accountable to, among other causes, a declining performance caused by fatigue or by exacerbation of the patient's symptoms during repeated trials [29].
We did not find correlation between the overall ENG outcomes and neuropsychological test scores, with one exception; we found the occurrence of abnormal neuropsychological test scores and the ENG outcome indicating central vestibular dysfunction. The new study combines both these ideas into one model that accounts for these microseismic signals. Our study showed that despite a high frequency of vestibular system dysfunction signs and a high incidence of abnormal neuropsychological test scores in tinnitus patients, only one correlation existed between these two results. Auscultation of the left ear side overlying the external auditory meatus and in the postauricular fold discovered a bruit (November 30, 2004). This was followed 20 minutes by a trial carried out in quiet stance in sensory organizations tests (SOTs) I through 4, and with acoustic stimulation in SOT 5 and SOT 6. Ridding, MC and Rothwell, JC (2007) Is there a future for therapeutic use of transcranial magnetic stimulation? Prevalence of leisure noise-induced tinnitus and the attitude towards noise in university students. Salvi, R, Lobarinas, E and Sun, W (2009) Pharmacological treatments for tinnitus: new and old. Changes in the IC, caused by either noise exposure or drug administration, involve fundamental, heterogeneous alterations in the balance of excitation and inhibition. The notorious abundance of tinnitus a€?curesa€™ suggests that there are (at least) as many tinnitus causes, triggers and mechanisms. It will probably always be the case that no one-size-fits-all approach to tinnitus management will succeed, but it is equally likely that a variety of interventions may, in many cases, produce some amelioration of the patienta€™s distress.
Most researchers and practising clinicians report that a combination of sound therapy and counselling facilitates the patienta€™s ability to manage the tinnitus experience. Psychotropic agents produce mixed success from which we infer that, at a minimum, such drugs work well for some patients regardless of whether the influence is upon the tinnitus sound, the patienta€™s psychological health or both. Herbal supplements, vitamins and alternative therapies such as acupuncture, biofeedback and hyperbaric oxygen therapy have produced mixed results that must be weighed against the potential, and substantial, risks associated with their use.
What is the practitioner who answers the call, and decides to work with tinnitus patients, to make of this situation?The second edition of Tinnitus: A multidisciplinary approach promotes tinnitus management strategies built upon the collaborative care for suffering patients and the preparation of clinicians for such practice.
We have a set of authors uniquely qualified to tackle thorny tinnitus problems, and it is clear that their work as clinicians and researchers has crystallised in the group the certainty that our patients more often than not require care that knows no borders.
The centrepiece of this text is its dispensing of practical, evidence-based information from the fields of audiology, otology, psychology, psychiatry and auditory neuroscience. Tinnitus distress may derive from several different factors simultaneously, and the authors remind us to weigh the potential risks and benefits of action and inaction. Throughout, they provide thorough and current reviews of material germane not just to clinical practice but to the educating of individuals who will conduct the practice.The reader will find resources that facilitate the essential task of interacting with patients and determining a tinnitus management plan.
To address the likelihood that all tinnitus patients present unique challenges to the clinician, the authors provide A­guideposts, A­evidence and thoughtful rationales for selecting a course of action tailored to each patienta€™s needs.
For example, some tinnitus programmes focus on modifying a patienta€™s concept of tinnitus and its effects, thereby facilitating a change in the patienta€™s behaviour and approach to the problem (i.e. Others utilise particular protocol-driven therapy, specifying more consistent application of sound levels and A­specific counselling components (i.e. Neuromonics) couple sound or music filtered specifically to account for each patienta€™s hearing sensitivity and loudness tolerance to counselling that varies little across patients. The reviews of these and other management protocols are of great value not only to present practitioners but also to the student or professional who considers working with tinnitus patients.It is admittedly difficult to report clinical success when the approach to patient A­management is idiosyncratic and driven more by the patienta€™s needs than by a cookbook plan of action. Particularly at this time, when clinical success is defined in the context of evidence-based practice, an eclectic approach to management of a potentially disabling condition may provide benefit to patients but may be difficult to sell to peer reviewers and other clinicians.
Yet, when we observe improvements in our patients, it is undeniable, and when we measure a patienta€™s self-assessment of handicap, we may measure statistically significant changes in the patienta€™s tinnitus experience. While it is difficult to define A­precise tinnitus distress or tinnitus relief, clinicians working with tinnitus patients see their share of both.A cliniciana€™s experience with suffering patients provides the impetus to adapt and adjust strategies in order to facilitate the patient managing the condition effectively.
As the authors point out, some of these a€?real timea€™ adjustments may lead to novel methods for use with other patients. However, the cliniciana€™s experience with tinnitus patients likely influences their willingness and ability to adapt clinical approaches with which they are comfortable. It is therefore important to gain, or help others achieve, the experience and confidence required to implement starkly different strategies for different patients. The authors have provided a rich inventory of management strategies that should foster a cliniciana€™s flexibility in order to meet the diverse needs and challenges associated with the tinnitus patient population.Unfortunately, as the professional training of individuals to join the ranks of tinnitus clinicians lags far behind the need for such providers, it is also the case that the need for multidisciplinary patient care goes unrecognised too often. In this second edition, the authors stress the need for professionals across the disciplines of neuroscience, psychology, medicine and audiology to collaborate in the clinic and the lab in order to meet patient needs. Audiologists and otologists have for years recognised that tinnitus is frequently complicated by psychological co-morbidities.
It is imperative for hearing health care professionals to seek out practitioners from related clinical areas to whom patients whose tinnitus is complicated by other factors may be referred. Recognising the signs that would trigger such referrals is the first step to providing comprehensive patient care. The authors provide the means by which tinnitus clinicians can place the patienta€™s needs in a broader context than would be available through the inherently limited view of tinnitus as exclusively an auditory problem. Because the needs of tinnitus patients are difficult to meet in many cases, clinicians must be versed in the literature and practice of related disciplines. Tinnitus distress is multidimensional and this book does not purport to solve the myriad problems that derive from that fact.
FULL TEXT Abstract: Tinnitus, the most common auditory disorder, affects about 40 million people in the United States alone, and its incidence is rising due to an. This is not restricted to the traditional themes of cochlear hair cells, and of sound-based and counselling-based therapies, but also involves robust pharmaceutical research, and also the design, implementation and evaluation of novel approaches to treatment.Additionally there are indications that a multidisciplinary ethos is permeating the tinnitus world, with voices from neuroscience, pharmacology, psychology and audiology interweaving as we investigate this fascinating and sometimes debilitating symptom. However, the effectiveness of drugs that modulate serotonin is largely untested in tinnitus patients. New findings abound, and there are new treatments to describe and novel perspectives through which to consider tinnitus. While the magic pill continues to elude us, there are indications that progress is being made in effective intervention and that many more patients are accessing clinical services.The distinctive perspective of this book is that each of the four authors is a practising clinician while also involved in research. The emphasis for each of us is different, but being able to inhabit both worlds gives, we hope, insight into the translational nature of tinnitus work: that is, that the clinic must influence the research agenda and that research should underpin and inform clinical practice. Seeing tinnitus patients in the clinic on a regular basis also gives an authenticity to what one believes about tinnitus and how it can best be treated. Some of the insights in this book have been hard won.Our Editors at Wiley-Blackwell are to be thanked, not least for the patience they have shown to four authors who have been weighed down at times with administrative and clinical responsibilities. Our colleagues too have been patient and supportive, but most of all our families and friends have been mainstays of support. That so many people can have some experience of these symptoms and not be distressed, while others are troubled to the point that they are no longer able to perform their normal daily activities remains paradoxical.
Furthermore, researchers have reported that when tinnitus is matched in intensity in this troubled group of people, it has been indicated to match to sound of low intensity (though the complexities of such experiments will be discussed below). Despite this apparent low intensity the intrusiveness of the symptom in patients with severe tinnitus is remarkable. Given these paradoxes, it is unsurprising that no single approach to tinnitus and hyperacusis has been shown to be overwhelmingly stronger than any other in terms of understanding and managing these symptoms.The aim of this book is to present a multidisciplinary approach to tinnitus and hyperacusis, incorporating insights from Audiology, Otology, Psychology, Psychiatry and Auditory Neuroscience.
It is hoped that this will inspire a collaborative approach to tinnitus and hyperacusis management that will benefit patients and clinicians alike. There is already good evidence that such collaborative and multidisciplinary initiatives in other fields, such as chronic pain, have increased the efficacy of treatments.DefinitionsThe word tinnitus derives from the Latin verb a€?tinnirea€™ meaning a€?to ringa€™, and in common English usage is defined as a€?a ringing in the earsa€™ (Concise Oxford English Dictionary, Allen, 1990).
The first recorded use of the word occurred in 1693 in Blancharda€™s Physiciana€™s Dictionary, second edition as follows (Stephens, 2000):Tinnitus Aurium, a certain buzzing or tingling in the Ears proceeding from obstruction, or something that irritates the Ear, whereby the Air that is shut up is continually moved by the beating of the Arteries, and the Drume of the Ear is lightly verberated, whences arises a Buzzing and a Noife (p. 201).At the time that this Dictionary was compiled there were many conditions that were thought to be due to trapped air, and procedures were developed to address that.
It is interesting that the Blanchard definition fits well with the experience of pulsatile tinnitus, where an individual becomes aware of the sound of arterial or venous blood flow (see Chapter 5).Some other languages have a variety of words to describe the phenomenon of tinnitus (Stephens, 2000), notably French, where five words are in regular use, each describing a particular timbre or quality of sound. In Swedish the word for tinnitus used to be A–ronsus, which in direct translation stands for ear breeze.
Few patients would agree that their tinnitus sounds like a breeze and this word does not catch the emotional impact experienced by some. MA?ller (2011b) distinguishes between objective tinnitus (which can be heard, measured or recorded by an external observer) and subjective tinnitus, which can be heard by the person alone.
MA?ller defines subjective tinnitus as follows:Subjective tinnitus is a broad group of sensations that are caused by abnormal neural activity in the nervous system that is not elicited by sound activation of sensory cells in the cochlea (MA?ller, 2011b, p.
9).This definition has some insights, as it implies that tinnitus can be varied, both within and between individuals. One might question whether anomalous might be a better word than abnormal, and this will be unpacked when we consider the neuroscience of tinnitus.Definitions of hyperacusis have tended to illustrate the perspective of the author. For instance, Vernon (1987a) proposed an open definition asa€¦ unusual tolerance to ordinary environmental sounds.For Vernon the emphasis may have been upon the unusual, as he could only recall four such cases, having seen over 4000 persons with tinnitus. In an initial differentiation between these two the second experience was entitled phonophobia, a term that is commonly used in neurology (Woodhouse and Drummond, 1993), in particular in association with migraine attacks. However, the inference that this phenomenon was essentially phobic in nature can be unhelpful to some patients.
Definitions of hyperacusis are further explored in Chapter 10.Historical aspectsThe experience of the perception of sound generated internally has been mentioned in many historical medical texts. These original sources have been reviewed by Stephens (1987, 2000) and Feldmann (1997), and while these authors have many detailed issues upon which they are at variance, they are in broad agreement on the interest expressed in tinnitus by medical authors from historical times.
A series of ancient Babylonian medical texts, inscribed upon clay tablets, were housed in the library of King Assurbanipal (668a€“626 BC) in Ninevah.
These were translated by Thompson (1931) and were found to include 22 references to tinnitus, described variously as the ears a€?singinga€™, a€?speakinga€™ or a€?whisperinga€™.
Treatments are described, including whispered incantations, the instillation of various substances into the external auditory meatus and the application of charms (such as the tooth of a female ibex): specific treatments were advised for each experience of tinnitus as described above (Feldmann, 1997). Other authors writing in Graeco-Roman times mentioning tinnitus include Celsus (25 BCa€“50 AD) who described treatments with diet and abstinence from wine and Pliny the Elder (23a€“79 AD) who advocated the use of wild cumin and almond oil in cases of tinnitus (Stephens, 2000). The use of sedative medication to treat persons suffering with tinnitus, still in common use in the United States of America and Western Europe, was first described by Galen (129a€“199 AD), who considered the benefits of opium and mandrake.Dan (2005) considers a report that the Roman Emperor Titus (39a€“81 AD) experienced tinnitus. This is found in the Babylonian Talmud, and the tinnitus was considered to be punishment for the destruction of the Second Temple in Jerusalem (70 AD), though the report that at post mortem Titus was found to have a large intracranial tumour offers another perspective on this.
Titus is said to have enjoyed some short-lived relief from sound therapy:A gnat entered his nostril and pecked at his brain for seven years. For thirty days this worked fine but then the gnat became accustomed and resumed pecking (quoted in Dan, 2005).There are mentions of tinnitus in texts within the Islamic medical tradition from the period following the decline of medicine in Rome (Stephens, 1987, 2000, and Feldmann, 1997). These include the first mention of the coincident complaint of tinnitus and hyperacusis (described as an a€?increased sensibilitya€™) by Paul of Aegina (625a€“690 AD) (Stephens, 2000, after Adams, 1844).Advances in the understanding and treatment of tinnitus were not to be seen until the seventeenth century, with the publication of the first text entirely dedicated to the ear and hearing. The insights into tinnitus represented a move away from the concept that tinnitus may arise from trapped air in the ear, this having persisted since Roman times, towards a model of tinnitus arising from diseases of the ear and disorders of the brain. The implication of the influence of the brain over the ear is prophetic of later concepts of the function of the efferent auditory system in humans. This comprehensive text was based upon 20 years of experience in working with the deaf, and contained numerous case studies, including that of Jean-Jacques Rousseau (1712a€“1778), the eminent philsosopher who became afflicted by tinnitus in later life (Feldmann, 1997). Itard made the distinction between tinnitus experiences arising from sound, thus a€?objective tinnitusa€™ such as that caused by somatosounds, and that arising without any acoustic basis, a€?false tinnitusa€™ (now described as a€?subjectivea€™ tinnitus). In addition to such medical insights Itard described the effect of tinnitus upon an individual: a€?an extremely irksome discomfort which leads to a profound sadness in affected individualsa€™ (translation by Stephens, 2000, p. The treatment of tinnitus was, as with previous authors, based upon treatment of the underlying otological condition, though when such treatment failed, however, Itard advocated attention to the behavioural manifestation of tinnitus and in particular to sleep disturbance, when the use of external environmental sounds (such as a watermill for low-pitched tinnitus or an open fire burning damp wood for high-pitched tinnitus) to mask the tinnitus was suggested.In the late nineteenth century the medical specialty of Otology underwent a renewal of interest and effort, and several individuals have been identified as leaders in this field. Joseph Toynbee (1815a€“1866) and William Wilde (1815a€“1876) (the father of Oscar Wilde) were pre-eminent in this regard and wrote extensively on ear disease, including consideration of tinnitus arising from such conditions.
Toynbee experienced distressing tinnitus himself and died during an experiment in which he attempted to determine a€?the effect of inhalation of chloroform upon tinnitus, when pressed into the tympanuma€™ (Feldmann, 1997, p. MacNaughton Jones (1981) has been credited (Stephens, 2000) with A­producingthe first book in English on tinnitus alone, which contained a classification of tinnitus based upon the site of origin and a review of contemporary treatments.The ability to use electronic instruments to measure hearing thresholds accurately by audiometry, and the consequent ability to determine hearing status in patients with a complaint of tinnitus, was developed in the early twentieth century, and became widespread in Western Europe and the United States of America from the 1940s (Weir, 1990).
At this time Fowler (1941) considered the characteristics of tinnitus and is credited with the first comprehensive attempts to determine the matching and masking characteristics of tinnitus (Stephens, 2000).
Among the insights gleaned by Fowler were that subjectively loud tinnitus is often matched to a low-level stimulus, that tinnitus may be masked by a broad-band noise and that it is not possible to generate beats between tinnitus and externally generated tones (Fowler, 1941). In subsequent writings Fowler collaborated with his son, also an Otologist, and formulated a protocol for the examination of tinnitus patients considering the qualities of the sound, the distress associated, as well as the otological health of the patient (Fowler and Fowler, 1955).In the late twentieth century there was little scientific or clinical interest in tinnitus and the field was kept alive by a small number of dedicated individuals. The work of Jack Vernon has already been cited: Vernon was a Professor of Audiology working for most of his career in Oregon, USA, and developed the first practical wearable masking devices for tinnitus.
In the United Kingdom, Ross Coles was a prolific tinnitus researcher, clinician and teacher, and his influence and mentorship is still felt to this day. Coles worked as a Consultant Physician and academic at both Southampton and Nottingham Universities, and was the founder of the long-running European Tinnitus Course. Also from a medical background, though working as a surgeon rather than a physician, Jonathan Hazell specialised in tinnitus, and in his collaborations with Pawel Jastreboff (a neuroscientist) developed an influential model of tinnitus and a concomitant treatment protocol (Tinnitus Retraining Therapy). From an Audiology perspective, Richard Tyler, working at the University of Iowa, has written, researched and taught extensively on how tinnitus can be managed and has been extremely influential. In the early 1980s Richard Hallam, a psychologist working in London, proposed that the natural history of tinnitus is characterised by the process of habituation and pointed out the influence of psychological factors on this process. His work has had a major influence on the clinical management of tinnitus, particularly by psychologists.Thus there has been evidence of input to tinnitus research from otology, audiology, and to some extent neuroscience.
What has been missing until recently, however, has been substantial input from pharmacology, from psychiatry and from auditory neuroscience. There are indications that this is now underway and that the field is becoming characterised by collaboration and teamwork rather than a small number of experts.Given the existence of tinnitus throughout history and the wide prevalence of tinnitus experience (see Chapter 11 for details), one should expect mentions in art and literaA­ture.
A comprehensive survey of such mentions will have to await another day, but some can be considered here as examples.
The Czech composer Smetana (1824a€“1884) suffered progressive, and eventually profound, hearing loss and associated tinnitus. He wrote his tinnitus into his string quartet a€?From my lifea€™ (1876) as a prolonged sustained high violin note towards the end. Thomas Hardy (1840a€“1928) has a character named William Worm, in his novel the A Pair of Blue Eyes (1873), speak of tinnitus:Ia€™ve got such a noise in my head that therea€™s no living night nor day.
God Aa€™mighty will find it out sooner or later, I hope, and relieve me (Chapter 4).More recently, Woody Allen has the male lead, played by himself, in the film Hannah and Her Sisters (1986) experience unilateral tinnitus and hearing loss, and is investigated for an acoustic neuroma. The first is that any consideration of tinnitus and formulation of possible treatment should consider the otological status of the patient and thus involve the treatment of ear disease where indicated. The second is that this otological focus does not obviate the clinician of the responsibility to consider the distress caused by the tinnitus experience and, where significant behavioral manifestation of this is present, to treat that distress. The third is that the understanding and treatment of tinnitus is a changing and developing science.SummaryFrom the above it is evident that concern with tinnitus is not new, and in fact is demonstrated throughout written human history. Many scientists, clinicians and artists have considered tinnitus and the involvement of systems of reaction, arousal and emotion.
The indications are that a holistic view of tinnitus must consider the involvement of such systems.Chapter 2Prevalence and natural historyKnowledge of the epidemiology of tinnitus is fundamental to tinnitus cliniciansa€™ and researchersa€™ understanding of the subject.
Studies tell us that tinnitus is one of the most common physical symptoms experienced by humans, which inevitably leads to the question of why it is so common.
One of the greatest challenges facing the tinnitus community is to understand why, if it is so common, do only some people suffer as a consequence of tinnitus? This question will be dealt with in other chapters, but knowledge of the epidemiology of tinnitus provides a backdrop against which to understand this fundamental issue. In the famous experiment by Heller and Bergman (1953), subjects were asked to enter a soundproof booth and to report all the sounds they could hear; 94% reported some form of tinnitus-like perception, using terms like buzz, hum and ring. Unfortunately, the conditions in which the Heller and Bergman (1953) study was conducted were not well controlled.
It has been even suggested (Graham and Newby, 1962) that they did not assess subjectsa€™ hearing audiometrically; the idea that the subjects had normal hearing is therefore only an assumption. Attempts to replicate the study have not revealed the same proportion of subjects reporting tinnitus-like experiences.
A replication by Graham and Newby (1962) found that only 40% of their normal hearing subjects reported tinnitus.
Levine (2001) found that 55% of his normal hearing subjects had ongoing tinnitus when they were placed in a low-noise room. On the face of it, working out how many people have tinnitus experiences at any given moment in time might seem straightforward, but it is, in fact, a difficult thing to do. There are considerable variations in the way that people experience tinnitus and in the way that they talk about it. Formal definitions of tinnitus can be complex and not easily understood by the general population. Prevalence studies have tended to rely on simplified definitions that can be open to interpretation and different studies have used slightly different definitions. Participants were interviewed in their homes and asked a€?Have you at one time or another noticed noises in your ears or head?a€™ The prevalence of tinnitus showed a tendency to increase with age as follows 21% (18a€“24 years), 27% (25a€“34 years), 24% (35a€“44 years), 27% (45a€“54 years), 39% (55a€“64 years) and 37% (65a€“74 years).
This was carried out by the Medical Research Councila€™s Institute of Hearing Research and reported by Davis and El Rafaie (2000).
In this study questions about tinnitus were incorporated into the National Study of Hearing, a longitudinal study that sampled a very large number of the population (n = 48 313) in four major cities (Cardiff, Glasgow, Nottingham and Southampton).
The first part of the study involved a postal survey of 48 313 randomly selected people, with a response rate of over 80%. The questions used were a€?Nowadays do you get noises in your head or your ears?a€™ and a€?Do these noises last longer than five minutes?a€™ In this way these researchers used the concept of prolonged spontaneous tinnitus (PST). Tinnitus was defined by the question, a€?During the past 12 months have you had noises in your head or ears (such as ringing, buzzing or whistling) that lasted longer than five minutes?a€™ One additional common restriction was that only tinnitus reported to occur most or all of the time was defined as persistent tinnitus (cf.
For men, the age-standardised prevalence of persistent tinnitus was 16.1% in those who reported severe hearing difficulties, whereas for those men with slight or no hearing problems the prevalence was only 5%. They received a response rate of 64.2%, with 20% answering a€?yesa€™ to a question about experiencing noises in their heads or ears lasting more than 5 minutes.
They asked 3600 people a€?Do you suffer from tinnitus?a€™ They also asked people how often they experienced ear noises and asked questions about localization and severity. Scott and Lindberg (2000) approached a random sample of 2500 Swedish citizens from a population register (in which all citizens are registered). Responses were obtained from 1538 subjects (62%) and among these 15.8% responded a€?yesa€™ to the question, a€?Have you heard buzzing, roaring or tones, or other sounds which seem to come from inside the ears or the head and that have persisted for five minutes or longer (so-called tinnitus)?a€™ In addition, tinnitus was graded by use of the Klockhoff and Lindblom (1967) severity definition of mild, moderate or severe tinnitus, where it is masked by environmental sound, not masked but not affecting sleep or not masked and affecting sleep, respectively . As results were analysed separately for help-seeking and non-help-seeking people with tinnitus (with additional participants recruited from a clinic), no exact estimate of severe tinnitus in the general population can be derived. As only a minor proportion of subjects in the population survey had sought help (n = 7), however, the figures for the population-derived non-help-seeking group provide an estimate of the proportion of severe (grades IIa€“III) tinnitus. Slightly below 50% had tinnitus of grades IIa€“III, with only a few (12.2% of the tinnitus sample) having tinnitus of grade III. Hence, a conservative estimate is that about one person in ten has severe tinnitus in the general population.In another study, Johansson and Arlinger (2003) studied 590 randomly selected subjects from the province of A–stergA¶tland.
As many as 31%, however, had noticed tinnitus at some point in time and 19.5% had temporary tinnitus lasting not longer than five minutes. It is uncertain if this was a random sample (average cross-section) and severity of tinnitus was not clearly outlined. This study was published as a conference proceedings report and therefore the results were not described in much detail.
The authors derived that 13% of the German population has, or once had, noise in the ears lasting longer than five minutes.
They also provided an estimate of those having tinnitus at the time of the investigation, which was 3.9% of the population. They also estimated that approximately 50% of those with ongoing tinnitus considered the effect of their tinnitus as moderately serious or unbearable.
The authors reported that the prevalence increased with age up to 79 years and that manual work, dyslipidosis, hypertension, liver diseases, cervical arthrosis and alcohol consumption were statistically significant risk factors. She reported data from a national health examination survey dating back to 1960a€“1962 with a total of 6672 subjects.
Respondents were asked, a€?At any time over the past few years, have you ever noticed ringing (tinnitus) in your ears or have you been bothered by other funny noises?a€™ Given this very broad definition, it is not surprising that as many as 32.4% of adults aged 18a€“79 years said that they did. Interestingly, a linear association was found between age and presence of both mild and severe tinnitus. In common with many other studies, a strong association was found between severity of tinnitus and hearing impairment.Almost a decade later Brown (1990) explored the prevalence of tinnitus in older adults using data from the 1982a€“1987 USA Health Interview Survey together with the supplement on ageing to the 1984 Health Interview Surveys and the first Health and Nutrition Examination Survey 1971a€“1975.
Participants were asked: a€?At any time over the past few years have you ever noticed ringing a€¦a€™, so providing information about prevalence over a period of time.

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