Tinnitus journal neuroscience,hooks for earring making 07,noise in ear bug music - New On 2016

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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. The effect of electrical stimulation on tinnitus gained new interest after House [1] reported that cochlear implants not only improve hearing in deaf patients but relieve their tinnitus.
A 17-year-old male patient had total deafness after an unknown viral infection that occurred 3 years before consultation.
When the external unit is turned off, he has a residual inhibition of tinnitus for 10 minutes. A 23-year-old male patient, with a history of a head injury occurring 10 months before the AllHear cochlear implant was placed, presented with bilateral deafness and a high-frequency disabling tinnitus in the head.
A 64-year-old female patient presented with progressive, bilateral sensorineural hearing loss due to otosclerosis, with a hissing-type bilateral tinnitus of mild intensity. A 41-year-old male patient presented with a progressive sensorineural hearing loss that started 10 years before surgery on the right side and 3 years before it on the left side.
A 52-year-old female patient presented with bilateral, profound hearing loss caused by meningitis that had occurred 18 years ago.
Table 1 displays the data for the six cases just presented: five patients with tinnitus before placement of the cochlear implant, showing the action of electrical stimulation on tinnitus, and one patient in whom tinnitus appeared with electrical stimulation after surgery.
The only case in which the electrical stimulation had no effect on tinnitus is that of the patient who had contracted meningitis 38 years before the surgery (patient 4). Ito and Sakakihara [4] have described two cases in which the tinnitus was aggravated postoperatively. The risk of injury to cochlear structures (due to the insertion of an active electrode inside the scala tympani) is reduced using All Hear implants than it is with multichannel cochlear implant electrodes. How to cite this article Daftary A, Shulman A, Strashun AM, Gottschalk C, Zoghbi SS, Seibyl JP. Tinnitus affects nearly 50 million people in the United States, with a minority demonstrating marked functional impairment.
Tinnitus is defined as a sensory disorder of auditory perception reflecting an aberrant auditory signal produced by interference in the excitatory-inhibitory processes involved in neurotransmission [1]. Although some have speculated regarding the pathophysiological mechanisms associated with severe centraltype tinnitus, little is definitively understood.
123I-iomazenil is a partial inverse agonist of the benzodiazepine receptor (BZR) and has been used in a number of studies evaluating the role of gamma aminobutyric acid (GABA) mechanisms in neuropsychiatry disorders [6-10]. The study was performed in accordance with the protocols approved by the institutional review board at the Yale University School of Medicine. Three venous blood samples were collected at 240, 300, and 360 minutes (means ± SD: 264 ± 25 minutes, 324 ± 2 1 minutes, and 369 ± 1 5 minutes, respectively) after starting the infusion of iomazenil, and blood samples were analyzed as previously described [14].
The primary imaging outcome measures of this study were (1) the homotypic ratio of count density for the a priori selected brain regions, (2) the regional equilibrium distribution volume determined by the ratio of activity in brain region divided by the concentration of parent compound, and (3) statistical parametric analysis of tinnitus patients compared with age-and gendermatched controls.
This study was an intrasubject analysis in which assessment of the asymmetry in distribution of BZR in homotypic brain regions was performed.
The concentration of the free fraction of iomazenil in plasma was calculated at three different time points as described (except in one patient, owing to technical reasons). As regards asymmetry of radiotracer distribution in homotypic brain regions, V3' data from the regions already described were analyzed using a Wilcoxon signed rank test.
Statistical analysis of volume-of-interest activity in homotypic regions showed statistically significant asymmetry in BZR density (expressed as V3' ) in the superior temporal cortical region. Comparison of cases and controls showed a significant decrease in counts in the frontal lobes (p = .000) and an insignificant decrease in the cerebellum. This study evaluated patients with severe intractable tinnitus using a bolus and constant infusion of 123I-iomazenil SPECT brain imaging. In the first part, we analyzed asymmetry in V3' values in each region of interest (volume of interest), findings that would enable us to identify visually detectable difference, which may assist in interpretation of these scans in the future and act as a direct measure of receptor distribution. The results of the voxel-based SPM analysis also suggest changes in BZR distribution in the frontal lobes and, to a lesser extent, in the cerebellum. Conclusions based on these data should be tempered by several issues in the study design; these include a relatively small number of patients studied, potential confound of age on BZR in the healthy control population, and effect of drug treatment on the imaging.
Multiple studies show that short-term administration of benzodiazepines produces mild to no change that reverses rapidly on cessation of therapy [6,27]. Some studies have shown alteration in cerebral metabolism with the presence and absence of symptoms [21]. Finally, imaging measures of alteration in the density of BZR binding may well represent an epiphenomenon associated with tinnitus rather than the primary pathophysiological process. This preliminary study of BZR distribution in a cohort experiencing severe, chronic tinnitus supports temporal, frontal lobe, and cerebellar involvement in the disorder.
This work was generously supported by the Martha Entenmann Tinnitus Research Center, Inc., Brooklyn, NY.
This cross-sectional study was designed to determine the prevalence of carotid artery atherosclerosis in patients with pulsatile tinnitus.
Such conditions as hardening of the arteries (atherosclerosis), benign intracranial hypertension, and heart murmur can be effectively treated with medications, which often, though not always, results in elimination of or dramatic reduction in pulsatile tinnitus. We designed a descriptive cross-sectional study to assess the association between pulsatile tinnitus and atherosclerosis of the carotid artery. Color Doppler ultrasonography was performed on all patients, with patients in the supine position and the head slightly extended and turned away from the site of examination. Patient 1 was a 75-year-old woman who developed leftsided pulsatile tinnitus some 2 months before admission. Patient 2 was a 52-year-old man who presented with left-sided pulsatile tinnitus of 1-month duration. Patient 4 was a 67-year-old man who suffered from pulsatile tinnitus in his right ear from 5 months before admission. Tinnitus is defined as pulsatile when an affected patient describes a rhythmic sound synchronous with the heart beat [2]. A review of 100 cases of pulsatile tinnitus by Sismanis and Smoker [6] revealed that ACAD accounts for 15% of such cases. In our study, atherosclerosis of the carotid artery was the cause of objective pulsatile tinnitus in 4 (11.76%) of 34 patients.
Color Doppler ultrasonography is a noninvasive and cost-effective method to assess suspected extracranial carotid artery atherosclerosis, and carotid artery angiography has largely been replaced with this technique. Atherosclerosis responsible for pulsatile tinnitus is being treated by either endarterectomy for proximal internal carotid artery disease or ligation for distal internal carotid artery lesions [4]. ACAD accounts for pulsatile tinnitus in some 11.76% of patients, and it should be considered in the evaluation of patients, particularly in those with the risk factor of atherosclerosis and in the elderly.
A new trend in tinnitus treatment is the use of veryhigh- frequency maskers, including ultrasound, delivered by bone conduction [1,2].
Human ultrasonic hearing has been independently "discovered," documented, and abandoned more than a dozen times over the last half century [3]. The dynamic aspect of ultrasonic pitch suggests that the ear may not be directly stimulated but rather that an intermediary structure may be involved.
The brain ultrasonic demodulation theory implies that the sound produced by brain resonance will propagate to the ear via fluid channels. The application of ultrasonic noise to the skull by bone conduction should produce cochlear masking in frequencies corresponding specifically to the brain's resonant frequency, raising the question of how brain resonance interacts with conventional hearing. For more than half a century, ultrasound has been reported to be associated with the pitch of air-conducted sound in the range of 8 to 16 kHz and often has been cited to be directly related to the highest frequency audible by a listener [3]. Deatherage [7] first noted an ultrasonic diplacusis; that is, the pitch associated with ultrasound could be International Tinnitus Journal, Vol. If the ultrasonic frequency does not determine the perceived pitch but rather the resonance of the brain, how is the reported pitch discrimination in the ultrasonic range possible [3,S], or is it absent [24-26]?
The effect of airborne ultrasound on hearing has not been thoroughly studied, but young normally hearing adults seem at greater risk for very-high-frequency hearing loss. The correspondence of the results of brain resonance, ultrasonic masking, and ultrasonic pitch-matching data are summarized in Figure 2. Alternatively, just the basal tip of the basilar membrane has been proposed as the site of ultrasonic transduction [7,32].
High- and very-high-frequency stimulation were reported recently to be effective in tinnitus masking [1,2].
If speech is modulated on an ultrasonic carrier, speech monitoring and perception with a high degree of comprehension (approximately 80%) is possible [3,47], even in high ambient noise.
Deatherage swam into a 50-kHz beam and first discovered underwater audible ultrasound 50 years ago [7].
Humans can detect ultrasound up to at least 100 kHz, but perception generally requires direct contact of the source with the body. I gratefully acknowledge the critical but constructive analysis and editorial contributions of Drs.
Nowadays, the neurosensorial disorders, which appreciably diminuate the quality of the life, are in a continuous increase all over the world.
Table 1 presents the main causes responsible for this phenomenon, as well as the extent to which they influence the increase of each type of neurosensorial disorders. In Germany during 1992, we had to deal with about 200,000 cases of whiplash injuries due to traffic accidents.
Basically, the following types of post-traumatic syndromes due to whiplash injuries can be differentiated, as there does not exist one single disease pattern (Table 2).
Tinnitus occupy a special place between the complaints of the patients suffering from the Late Whiplash Injury Syndrome (LWIS). Tinnitus is an acoustical phenomenon which is perceived without having an extrinsic source of sound.
Already in 1994, Claussen has reported the results of a study, which compared the data from 206 cases of late whiplash injury syndrome, who were in medical attention only for treatment purposes, with those from 41 neurootological expertise cases after whiplash injury. In the present work we oncentrated our attention upon those cases of LWIS who were labeled and treated by numerous other doctors and representants of insurance companies as so-called "trifle-cases". In the third subsample were included those cases who suffered from the so-called Hypersensitive Ear Syndrome (HES) (Claussen 1985). The audiometrical results then were underpinned through analyses of the acoustical pathway. The subdivision of the main sample from the point of view of the above described criteria is presented in Table 6. Table 7 shows that in all the samples other sensorial disturbances are considerably present.
Table 8 combines the data concerning the hearing disturbances with those concerning the tinnitus.
When analyzing the qualitative characteristics of the ear sensations, the highest incidence of the complaints is found in the sample of patients with maskable tinnitus (Table 9). Two of the 91 patients were notable to make a personal estimation concerning the evolution of their disease.
The results of these complex and sensorial investigations showed that in nearly all the patients tinnitus was not an isolated phenomenon, being mostly associated to other multi sensorial neurootological functional disturbances. As all the cases come to us with a very rich medical, hospital, litigation, and expertise documentation accumulated in the peri od of time following the accident, however, including also pre-accidental patient information, we get comple e information about the evolution of the disease, the inte mediary symptoms and the preexisting medical result and diagnosis.
The problem of tinnitus as a consequence of whiplash injury is intensively discussed in the neurootological literature since 1928. In 1928 tinnitus is ment oned by Barré and Lieou as being the most frequent sym tom in the patients with cervi cospinal injury.
In most of the patients investigated by these authors, tinnitus appears as a result of the so-called "degenerative cervico-spinal injury syndrome". Shulman, who is considered as one of the pioneers and an exceptional specialist in the field of the tinnitus research, shows in his book about the modern diagnosis and therapy of tinnitus, that the severe, disabling tinnitus is usuallly associated with anxiety psychosis.
The observation of Shulman, that in most of the tinnitus cases, there coexists a high tone sensorineural hearing loss, is valid for the patients investigated by us, too.
Fürther on, Shulman shows that about 20% of the patients with severe tinnitus also have vertigo complaints. Based upon the numerous observations from all over the world, concerning the late complications of the whiplash injury, we can affirm that even the simple, non-contact whiplash injury can be the cause of long lasting, cronic polisensorial disturbances.
A retrospective study at the ear, nose, and throat department of the EuromedClinic showed considerable improvements immediately after the end of the treatments for acute and for chronic tinnitus.
The subject of this retrospective study is the results of the treatment of acute and chronic tinnitus with conventional infusion therapy or hyperbaric oxygen (HBO) therapy (or both). One hundred patients with tinnitus (71 male, 29 female) were evaluated in this study, 65 suffering from acute tinnitus and 35 suffering from chronic tinnitus. After analysis of the data, the grade of success was divided into four categories: no tinnitus, reduced, unchanged, and increased. The age distribution in this random sample of patients suffering from tinnitus shows a peak in the group from 41 to 50 years. Only 55 patients could be checked for long-termresults: 42 of the acute tinnitus group and 13 of the chronic tinnitus group (Table 3). An important consideration is that the therapeutic effect of the HBO therapy is proved through clinical and experimental studies [5-7]. The treatment of chronic tinnitus is, in general, less sufficient than treatment of acute tinnitus.
Shulman [4] also described the use of neuroprotective substances for the improvement of inner ear function, even in patients suffering from tinnitus. In our ear, nose, and throat department (one of three study centers in Germany) a caroverin double-blind test has just started. How to cite this article Bittar RSM, Mezzalira R, Furtado PL, Venosa AR, Sampaio ALL, Oliveira CACP. Benign Paroxysmal Positional Vertigo (BPPV) is one of the most prevalent clinical disorders in common Neurotology practice and accounts for approximately 17% of complaints of vertigo1. Given the noteworthy prevalence of BPPV, its health care and societal impacts are tremendous8. Positional vertigo is defined as a spinning sensation produced by changes in head position relative to gravity. Significant improvements in the diagnosis and treatment of patients with BPPV may lead to significant health care quality improvements as well as medical and societal cost savings. The purpose of this paper is to review the available methods for diagnosis and treatment of BPPV intended for clinicians who are likely to diagnose and manage patients with BPPV, and applies to any setting in which BPPV would be identified, monitored, or managed. Of the two variants of BPPV, canalithiasis is the most common, and the posterior semicircular canal is the most affected because of its anatomical position (85-95% of cases of BPPV)8. Recently, Gacek21 proposed a neural theory for BPPV, in which there was degeneration of the saccular ganglion secondary to a latent viral reactivation. Identifying the affected canal includes observation of the position that triggers the dizziness and the resulting type of nystagmus.
When the patient gets in the position that triggers the dizziness, eye movement is observed resulting from the contraction of muscles related to the affected canal (slow component), followed by subsequent rapid correction in the opposite direction (fast component). In the vertical canals, there are excitatory connections to the ipsilateral superior oblique and contralateral inferior rectus to the posterior canal; ipsilateral superior rectus and contralateral inferior oblique to the superior canal, so that the arising movements are always rotational, but the nystagmus is vertical upward in the posterior canal and vertically downward in the superior canal23.
The characterization of the nystagmus, allows the identification of the canal involved as well as the mechanism involved, and it is essential to choose the repositioning procedure. The Dix-Hallpike maneuver is considered the gold standard tool for the diagnosis of BPPV of posterior canal8.
The Dix-Hallpike maneuver is performed by the clinician moving the patient through a set of specified head-positioning maneuvers to elicit the expected characteristic nystagmus of posterior canal BPPV (Figure 1).
The maneuver begins with the patient in the upright seated position with the examiner standing at the patient's side.
After resolution of the subjective vertigo and the nystagmus, if present, the patient may be slowly returned to the upright position. The particles present inside the semicircular canal undergo the effects of gravity and are shifted downward, and after a short latency, the liberating force created on the ampullar crista triggers the vertigo and nystagmus (Figure 2). In the case of the superior semicircular canal, a torsional downbeating nystagmus is exhibited. If the patient has a history compatible with BPPV and the Dix-Hallpike test is negative, the clinician should perform a supine roll test to assess for lateral semicircular canal BPPV8.
Lateral canal BPPV (also called horizontal canal BPPV) is the second most common type of BPPV. In many instances, the presenting symptoms of lateral canal BPPV are indistinguishable from posterior canal BPPV. Due to an adaptation of the central nervous system8,26 or to the reversion of the direction of movement of the debris by the gravitational action26, it is not unusual that nystagmus spontaneously changes the direction without the head turning to the opposite side8,26.
Additional exams are essential to clarify the trigger and associated features of BPPV1,15, 23,35. Imaging is not useful in the routine diagnosis of BPPV because there are no radiological findings characteristic of or diagnostic for BPPV8.
Electronystmography has limited utility in the vertical canal BPPV diagnosis, since the torsional component of nystagmus cannot be registered by conventional techniques. Audiometry is not required for diagnosing BPPV, however it may offer additional information in cases where the clinical diagnosis of vertigo is unclear8. The treatment of BPPV is based on the performance of liberatory maneuvers or canalith repositioning procedures, with the aim of returning the displaced particles to their original location: utricular macula.
A standard protocol, that is described in Table 3, is used in our service, considering the better results for each maneuver indicated for each BPPV variant. Some patients manifest severe symptoms with dizziness, nausea, sweating and vomiting while undergoing diagnostic or therapeutic maneuvers. The Epley maneuver39 is the most frequently performed repositioning maneuver of the vertical canal. According to the clinical practice guideline8, based on the review of the literature, it was not possible to determine the optimal number of cycles for the repositioning maneuvers. The maneuver described by Semont41 is indicated for the treatment of posterior canal cupulolithiasis. Lempert42 described a maneuver (Barbecue Maneuver or Roll Maneuver) which is the most commonly employed maneuver for the treatment of lateral canal BPPV. Forced prolonged position is another treatment maneuver, described by Vannuchi44, for the treatment of lateral canal BPPV. The Brandt-Daroff exercises were developed for home self-administration, as an additional therapy for patients who have been symptomatic, even after Epley or Semont maneuver40.
Many patients complain of imbalance during and between vertigo attacks, as observed by Celebisoy45. The otolithic dysfunction induced by unequal loads of the macular beds has been considered as the underlying mechanism46. The repositioning maneuvers are associated to mild and self-limited adverse effects in about 12 percent of the treated patients8. During the course of repositioning maneuvers of vertical canals, the displaced particles could migrate into the lateral canal, in 6 to 7 % of the cases8. During the repositioning maneuvers, some patients develop severe, persistent vertigo, nausea, vomiting and nystagmus, which has the same features observed in the diagnostic maneuvers. The treatment consists of performance of the reverse maneuver, to aim to eliminate the blockade. By virtue of possible complications during the repositioning procedures, it is not a proper conduct to guide the patient self-treatment at home, without a physician. After repositioning procedures, it is important to keep the patient in sitting position, for 10 minutes, to avoid falls51. Epley39, in his original paper, described the application of a bone conduction vibrator associated to repositioning maneuver, in order to release some adhered particles in the ampullar crista.
The effectiveness of repositioning and liberatory maneuvers varies from 70% to 100%14,15,23,48. It is important to be careful when performing diagnostic, repositioning and liberatory maneuvers in obese patients, with limited cervical range of motion or with unstable heart failure or carotid stenois8,25,58.
Some authors believe in natural course of BPPV toward spontaneous relief48,59,60,61,62, which is possible in up to 89% of the patients in the first month, with subsequent recurrence in up to 33%, in three years37,38.
Thirty to 50 % of the patients have vestibular system dysfunction associated with initially treated BPPV, which can be demonstrated by caloric testing abnormalities.
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 describe five cases of deaf patients with tinnitus and show that the implant device had a good effect on tinnitus in four.
In several reports, a partial or complete suppression of tinnitus has been described in patients with cochlear implants.
Of a group of 14 patients, 5 had tinnitus before surgery, and 1 presented with tinnitus after surgery only when the device was turned on. The tinnitus disappeared in the ear in which the device was implanted, and a reduction of tinnitus was evident in the right side, presenting residual inhibition for 10 minutes. The best results obtained in this group are related to the two cases of progressive hearing loss (patients 3 and 5). However, her tinnitus was not intense, and the cochlear device has been useful for her hearing. In reporting our results, we presented four cases (80%) in which the electrical device relieved or suppressed the tinnitus. This reduction in risk occurs because residual hearing has been shown to be maintained after the implantation.
Alterations of gamma aminobutyric acid (GABA) neuronal function and benzodiazepine receptor (BZR) function in particular have been implicated in the pathophysiology of severe, chronic tinnitus. The definition of tinnitus is constantly being refined as a result of the integration of information from otolaryngology, psychiatry, neurology, and nuclear medicine.
Current hypotheses implicate excitatory amino acid-induced neuroexcitotoxicity and abnormal epileptiform activity [2-5]; hence, antiseizure drugs have been used in the treatment of tinnitus. Using a method of bolus plus constant infusion to establish equilibrium-binding kinetics in the brain allows the performance of accurate quantitative analyses of the density of BZR binding sites in the cortex. Patients were recruited from the Martha Entenmann Tinnitus Research Center-Health Sciences Center, Brooklyn, State University of New York and Forest Hills, NY.
Of these patients, two had bilateral tinnitus in the ears, two in the head only, and two in both the head and the ears. Sterility was confirmed by lack of growth in fluid thioglycolate at 35? and soybean-casein digest at 25? for 2 weeks.
We chose these intervals on the basis of previous studies indicating that plasma levels of iomazenil reach steady state by these times [15]. All patient and control images were processed as described (see the section, "Image Analysis") and then imported into a commercial image analysis program (MedX, vol.
The results of paired two-tailed comparison of homotypic brain regions with raw counts and V3' levels are described in Table 3. The cerebellum, hippocampus, and thalamic regions did not show any significant asymmetry in receptor density (see Table 3). Cross-sectional appearance of most significant voxels in the two clusters (A, frontal ; E, cerebellar) demonstrating decreased receptor density in subjects with tinnitus. We also compared the SPECT scans of these patients with scans of historically normal control subjects. The first was a study of region (volume) of interest in which we collected data from brain regions that have been implicated in tinnitus [1,19-22] followed by a voxelbased SPM analysis that would not be biased by our previous concerns about specific area involvement in tinnitus. We found that the asymmetries identified in the superior temporal region with V3' data matched with our informal visual estimation of asymmetry. The frontal lobe showed the least asymmetry; for the volume-ofinterest assessment, however, this analysis does not account for the symmetrical relative reduction in frontal lobe receptor concentration. Owing to the low number of healthy control iomazenil SPECT scans, we were unable to age- and gender-match our controls exactly to the cases.
We cannot, however, exclude that these changes may be in part secondary to reduced affinity of BZR to 123I-iomazenil or to changes in receptor distribution from long-term treatment of the condition with benzodiazepines. What is useful to know, however, is that at the time of the study, all these patients were suffering from tinnitus and that their symptoms had been refractory to treatment. This study, however, should prove to be an effective method on which to base future work and improve our understanding of tinnitus, of its pathophysiology, and of monitoring treatment. This study is the first time that quantification of BZR has been performed on patients with severe, chronic, intractable tinnitus, and it should form a framework for some of the larger studies that could bring to bear an improved description of the natural history of the symptoms and improve treatments. Institute for Neurodegenerative Disorders, New Haven, CT; and5National Institutes of Mental Health, Bethesda, MD. All patients who had pulsatile tinnitus and presented to the otolaryngology clinic of Rasoul Akram Hospital, Iran University of Medical Sciences, and to some other private hospitals and clinics were referred to a tertiary referral center.
As few studies have addressed the prevalence of carotid artery atherosclerosis in affected patients, and no study has been carried out in Iranian patients, we decided to determine the prevalence of carotid artery atherosclerosis in patients with pulsatile tinnitus.
From November 1999 to September 2003, 34 patients who had pulsatile tinnitus and attended the otolaryngology clinic at Rasoul Akram Hospital, Iran University of Medical Sciences, and some other private clinics and hospitals were examined. Objective unilateral tinnitus was present in 4 patients, and ipsilateral carotid bruit was heard in all 34. Pulsatile tinnitus is a rare symptom, but correct diagnosis is critical because, in the majority of cases, the underlying etiology is treatable. As the elderly population grows and the risk factors of atherosclerosis (smoking, lack of exercise, and stressful lifestyle) increase, more patients with pulsatile tinnitus due to carotid atherosclerosis will be identified. In another study by Sismanis [7], mild to severe carotid artery stenosis due to ACAD was the cause of pulsatile tinnitus in 24 cases (16%) of 145 patients with pulsatile tinnitus. Tinnitus attributable to stenosis at the common carotid artery bifurcation has been successfully treated by carotid endarterectomy (CEA) [4,14,15].
As pulsatile tinnitus may be the first and sole manifestation of severe carotid artery stenosis, it should prompt immediate color Doppler ultrasonographic study in patients with cardiovascular risk factors.


Department and Research Center of Ear, Nose, Throat, Head, and Neck Surgery, Iran University of Medical Sciences.
Masking and long-term inhibition may involve inducing plastic changes in the brain at the central level. So outlandish is the concept that humans can have the hearing range of specialized mammals, such as bats and toothed whales, that ultrasonic hearing has generally been relegated to the realm of parlor tricks rather than being considered the subject of scientific inquiry. Three lines of evidence suggest that the resonance of the brain is critical for an audible ultrasonic experience.
Using a 7-cm radius as a representation of the human average, the fundamental resonant frequency is calculated to be 13.4 kHz.
Such channels have been proposed by Ranke [13] and confirmed experimentally by Tonndorf [14,15]. Ultrasonic masking has been reported to suppress audio thresholds in the 8- to 12.5-kHz range by 2- 29 dB [22,23].
Masking was less for frequencies higher and lower than the resonance peak, which is characteristic of a resonance phenomena.
Ultrasonic hearing is unique in that even moderate changes in frequency « 10%) are not associated with the dramatic pitch changes as in the conventional audiometric range.
Thus, the brain stimulates each ear equally, but the frequency response of each ear contributes to the perception of pitch.
Each subject matched an air-conducted pure tone (variable frequency) with an ultrasonic tone of 26 or 30 kHz delivered at 5 dB SL. The effects of ultrasound on audio frequency thresholds depicted for the two ultrasonic sources. Note in Figure 1 that a change in the center frequency of the noise, even at a constant intensity (S dB SL), results in a different frequency or place spread of activation. The Occupational Safety and Health Administration (OSHA) has adopted ultrasonic hearing protection working standards [29].
These data clearly support the hypothesis of physical demodulation of ultrasound by brain resonance and the detection of this resonance in the base of the basilar membrane. One-dimensional modeling of the cochlea, incorrectly assuming both scales have equal volumes, results in the prediction that ultrasound activates the first few millimeters (0-7) of the cochlear base. Substantial agreement supports the theory that ultrasound, regardless of its frequency, stimulates an area on the basilar membrane that codes the fundamental resonant frequency on the brain. Summary of the data from modeling, spherical measurement, masking, and pitch match, supporting the theory of ultrasound brain demodulation in the high audio frequencies. Plastic changes in the auditory neural axis in severe tinnitus, particularly in the auditory cortex, may playa role in the continued perception of tinnitus by adding salience to the experience [34,35]. Calibration procedures are based in part on bone-anchored measurements (in the high audio frequencies of 8-20 kHz) [3]. This result opens the possibility of using ultrasonic speech for communication under poor listening conditions and in situations wherein traditional amplification is ineffective.
It seems reasonable to expect that any mammal can detect underwater ultrasound by brain ultrasound demodulation.
Ultrasound sets the brain into forced vibration, and it is the brain oscillation that is detected on the base of the cochlea in normally hearing individuals. Barbara Goldstein and Abraham Shulman at the Martha Entenmann Tinnitus Research Center in the preparation of this manuscript. Occupational Safety and Health Administration Technical Manual, Section III, Chapter 5, subchapter V: Ultrasonics. Reference Equivalent Threshold Force Levels for Audiometric Bone Vibrators (ANSI S3.26, 1981). Some of the most frequent sensorineural disorders are the visual disorders, the hearing loss, the tinnitus and the vertigo. The present work presents a certain neurosensorial disorder related to the head, namely the tinnitus of traumatic etiology. The consequences of the trauma can appear immediatel y after the accident, but most frequently, the traumatic incident is followed by a period of more or less clinical silence and the symptoms become evident only after hours, days or months.
The orthopedic as well as the radiological findings mostly are unsatisfactory with respect to the neurosensorial disturbances. Of a special interest for the present work are the disturbances described as the "cervico-encephalic syndrome." This group also frequently follows a whiplash injury.
In all the cases, the neurootological disorders were late complications of a whiplash injury. As Table 5 shows, these patients had complaints of the LWIS for a long time, and were repeatedly investigated by many different medical specialists prior of coming to us.
The percentage distribution of the most important non-acoustical subjective symptoms in the above described samples of patients is presented in Table 7. The clinical experience showed that in the case of the LWIS, symptoms like otalgia or pressure in the ear may accompany tinnitus. Many patients reported the presence of several complaints and disturbances which we considered as being complications of the tinnitus (Table 11).
The vestibulo-ocular and retino-ocular reactions are investigated by the method of polygraphic electronystagmography and the vestibulo-spinal reaction by cranio-corpo-graphy with simultaneous computer analysis. Because of the medical expertise questioning, a clear differentitation between the disturbances brought about the accident and thos already pre-existing or having other causes must be done for each of the cases. Decher reports in 1966, that 41% of 500 patients with a history of cervico-spinal injury complain of tinnitus.
In many cases the disturbances are also caused by vascular problems in the posterior cranial fossa, due to a narrowing of the vertebral artery in the cervical region. Because of their permanent presence, the ear noises often become intolerable and are seriously disturbing the daily personal life.
We also frequently find this stato-acoustical combination in our tinnitus patients with a cervico-encephalic syndrome, due to a whiplash injury. As it was shown above, tinnitus plays a special role in the complex mosaic of these multisensorial neurootological functional disturbances.
Eighty percent of our patients suffering from acute tinnitus showed an improvement with intravenous medication without hyperbaric oxygen treatment, and 65.7% showed improvement with infusion therapy and hyperbaric oxygen. It includes in the head and the ear all types of noise sensations that are not generated by sound waves coming from outside [1]. Simultaneously, HBO treatment was offered daily (5- 15 times) to 55 patients without inflammatory or cardiac contraindications to this therapy (up to 2.5 AT A up to 3 periods of 30 min breathing of pure oxygen with 2 pauses of 10 min air-breathing). The annoyance of the tinnitus is rated on a subjective scale from 0 (no tinnitus) to 10 (unbearable) by the patients. The data before starting therapy were compared with the data recorded immediately after treatment and again at least 3 months later (long-term-results). The positive treatment effect (improved or stable condition) decreased from 80% (24 cases) to 67% in patients with acute tinnitus (12 patients) and therapy with infusions only and from 65.7% (23 patients) to 46% (11 cases) in patients with combined therapy (infusion and HBO).
The effect of the HBO therapy on tinnitus was investigated in studies with a total of 1,223 patients. This test is being undertaken to prove the possible positive effect of the glutamate antagonist caroverin (cochlea-synaptic effect) [9]. This vestibular syndrome is characterized by transient attacks of vertigo, caused by change in head position, and associated with paroxysmal characteristic nystagmus. It represents the most important peripheral vestibular impairment along the lifespan1,2,3, although the age at onset is commonly between the fifth and seventh decades of life4. It is estimated that it costs approximately US$2000 to arrive at the diagnosis of BPPV, and that 86 percent of patients suffer some interrupted daily activities and lost days at work because of BPPV8.
Benign paroxysmal positional vertigo is defined as a disorder in the inner ear, characterized by repeated episodes of positional vertigo8, with typical paroxysmal nystagmus.
Despite its significant prevalence, and quality of-life and economic impacts, considerable practice variations exist in the management of BPPV across disciplines8. Such improvements may be achievable with the reduction of the inappropriate use of vestibular suppressant medications, decreasing the inappropriate use of unnecessary tests such as radiographic imaging, and by increasing the use of appropriate cost effective therapeutic repositioning maneuvers.
Displaced particles from utricule otoliths float around in the endolymph (canalithiasis)11 or adheren to the cupulae (cupulolithiasis)12 and may change the density relation of the cupulae-endolymph system. The ampulla of the posterior semicircular canal is located in the lower region of the vestibule, both in the supine and standing position. Such reinfection could result in the loss of its antagonistic effect on the posterior semicircular canal. The classic complaint is vertigo in episodes, triggered by changes in the body position or head movements, lasting seconds and ceasing spontaneously. Each of the semicircular canals is directly connected to a pair of extrinsic muscles in the eye, having an excitatory and inhibitory influence, which determines the movement of the eyeball in the same plane as the canal24 (Table 1). This biphasic movement, called nystagmus, is a standard direction that is known as being the same as the fast component. In Table 2, we can observe the main features of involvement of different semicircular canals. Before beginning the maneuver, the clinician should counsel the patient regarding the upcoming movements and warn that they may provoke a sudden onset of intense subjective vertigo, possibly with nausea, which will subside within 60 seconds.
During the return to the upright position, a reversal of the nystagmus may be observed and should be allowed to resolve8. Mechanism of displacement of the debris from the dome of the canal at rest and under the action of gravity (g), indicated by the arrow.
The direction of the torsional component of the positioning nystagmus indicates which ear is the origin of nystagmus. Because this type of BPPV has received considerably less attention in the literature, clinicians may be relatively unaware of its existence and the appropriate diagnostic maneuvers for lateral canal BPPV8. The supine roll test is performed by initially positioning the patient supine with the head in neutral position, followed by quickly rotating the head 90 degrees to one side with the clinician observing the patient's eyes for nystagmus.
In canalithiasis, the movement of the head toward the affected ear promotes the displacement of free particles in the direction of the ampulla, triggering a horizontal nystagmus whose fast component will be toward the tested ear, so geotropic (towards the ground). The mechanisms that initiate geotropic and apogeotropic eye movements can be seen in Figure 3. We can observe the mechanism of displacement of the ampullar crista that is responsible for the origin of geotropic nystagmus in canalithiasis(a), or for apogeotropic nystagmus in cupulolithiasis (b). De la Meilleure et al.26 reported the inversion of the horizontal nystagmus, in electronystagmography, in 75% of patients with BPPV of the lateral canal, always on the affected side. Further radiographic imaging may play a role in diagnosis if the clinical presentation is felt to be atypical, if the diagnostic maneuvers are unusual, or if additional symptoms aside from those attributable to BPPV are present, suggesting an accompanying modifying central nervous system or otological disorders8. On the other hand in horizontal semicircular canal BPPV diagnosis, the nystagmus is present in the positional testing23. These are non-invasive procedures that have been found to be long term effective for BPPV2,14. In these cases, vestibular suppressant medications are recommended as adjuncts not only to relieve the vertigo after maneuver but also to control the clinical symptoms until the procedure can be repeated4. The patient is placed in the upright position with the head turned 45 degrees to left when the left ear is affected.
If the posterior canal is affected, the patient is seated in the upright position; then the patient's head is turned 45 degrees toward the unaffected side, and then is rapidly moved to the side-lying position. Demonstration of Lempert Maneuver sequence - treatment of lateral semicircular canal BPPV (right ear in black). This maneuver involves rolling the patient 360 degrees in a series of steps to effect particle repositioning8.
The strategy consists of maintaining the forced lateral decubitus, with affected ear in the undermost position for 12 hours23,25.
Some authors indicate them one week before the therapeutic maneuver, aiming to improve the patient's tolerability14. This observation lead to the investigation of postural balance in patients with lateral and posterior semicircular canal BPPV. Other possibilities are the persistency of small amounts of residual debris in the canal, paresis of the ampullar receptors or the vestibular re-adaptation after peripheral disorder45. This phenomenon could result from a jamming of the otolithic debris (named jam) when migrating from a wider to narrower segment, such as from the ampulla to the canal or at the bifurcation of the commom crus50.
The use of a cervical collar, positional avoidance, or other restrictions are not necessary52,53,54. However, studies found no benefit in the BPPV treatment, since it does not modify the results of repositioning or liberatory maneuvers2,55,56,57. The successful treatment is based on the identification of the affected semicircular canal, the distinction between cupulolithiasis and canalithiasis, the right choice of the most indicated maneuver2. The spontaneous resolution is faster in the lateral semicircular canal BPPV than in posterior canal because the former spatial and anatomic orientation facilitates the return of the particles to their original place63,64.
Therefore, even if symptoms are typical of BPPV, the diagnostic maneuver has been positive, the repositioning maneuver has been successful, it is important that complete neurotological evaluation is obtained to rule out other vestibular disorders.
For the therapeutic maneuvers, correct diagnosis of the BPPV variant and affected semicircular canal is necessary.
Central etiologies must be investigated when atypical nystagmus is found and therapeutic maneuvers are unsucessfully. Bhattacharayya N, Baugh RF, Orvidas L, Barrs D, Bronston LJ, Cass S, Chalian AA, Desmond AL, Earll JM, Fife TD, Fuller DC, Judge JO, Mann NR, Rosenfeld RM, Schuring LT, Steiner RWP, Whitney SL, Haidari J.
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. Some of them present a residual inhibition [2,3], and others relate an effect on the contralateral ear [4]. The purpose of this study is to evaluate the action of the All Hear cochlear implant on tinnitus in six patients. With the implanted device, she complained of shock, pain, and tinnitus as soon as the electrical device was turned on. In patient 2, whose hearing loss was caused by head injury, the result may be considered good, as the tinnitus was as troublesome as the deafness.
In addition, owing to a small posterior tympanotomy area, guiding the drill to the scala tympani was difficult, and possibly we drilled the modiolus and exposed the neurons in the spiral ganglion.
There-fore, the All Hear cochlear implant is useful in restoring hearing in deaf patients, and it has shown additional beneficial effects on tinnitus in the majority of them. Tinnitus suppression by electrical stimulation of the cochlear wall and by cochlear implantation. The purpose of our study was to evaluate the distribution of BZR in the brain using 123I-iomazenil single-photon emission computed tomography (SPECT) imaging in patients with severe, intractable central tinnitus. Tinnitus has been attributed to peripheral abnormality in the function of the vestibulocochlear apparatus, to cranial nerve dysfunction, or to central nervous system causes. The therapeutic effect of benzodiazepines in treating tinnitus was studied initially by Melding et al.
An intrasubject study comparing nC-iomazenil positron emission tomography (PET) and 123I-iomazenil single-photon emission tomography (SPECT) in healthy subjects demonstrated excellent comparability of these tracers for in vivo assessment of BZR binding [11].
SPECT images were coregistered to the respective magnetic resonance images using Statistical Parametric Mapping (SPM96) [18].
The variability of V3' data in each volume of interest, when compared to the opposite side, was calculated using the Wilcoxon signed rank test. To the best of our knowledge, this is the first time BZR imaging studies have been performed on patients with severe, chronic central tinnitus. This brought up an interesting question: Were age- and gender-matching of controls actually necessary in iomazenil studies?
Neuroprotective drug therapy: A medical and pharmacological treatment for tinnitus control. Changes of benzodiazepine receptors during chronic benzodiazepine administration in humans. Alterations of benzodiazepine receptors in type II alcoholic subjects measured with SPECT and [123I] Iomazenil. Decreased benzodiazepine receptor binding in prefrontal cortex in combat-related posttraumatic stress disorder. Quantitation of benzodiazepine receptor binding with PET [11C] Iomazenil and SPECT [123I] Iomazenil: Preliminary results of a direct comparison in healthy human subjects.
Formation of 1-[123I] Iodobutane in labeling [123I] Iomazenil by iododestannylation: Implications for the reaction mechanism. Pharmacokinetics of the SPECT benzodiazepine receptor radioligand [123I] Iomazenil in human and non-human primates.
SPECT measurement of benzodiazepine receptors in human brain with iodine-123-iomazenil: Kinetic and equilibrium paradigms. Evaluation of ultrafiltration for the free-fraction determination of single photon emission computed tomography (SPECT) radiotracers: beta-CIT, IBF, and iomazenil. Focal metabolic activation in the predominant left auditory cortex in patients suffering from tinnitus a PET study with [18F] deoxyglucose.
No age-related changes in human benzodiazepine receptor binding measured by PET with [11C] Ro 15-4513. From November 1999 to September 2003,34 patients with pulsatile tinnitus underwent a clinical evaluation.
When the tinnitus is rhythmic and synchronous with the heartbeat, it is called pulsatile tinnitus [2].
All underwent a clinical evaluation consisting of a thorough medical history, otoscopic examination, and auscultation of the head, neck, and chest. Color Doppler ultrasonography showed a 70% decrease in diameter of the distal portion of his common carotid artery due to an atherosclerotic plaque. Color Doppler ultrasonography revealed an atherosclerotic plaque in the proximal part of his right internal carotid artery, which caused 50% decrease in diameter. He had a history of transient ischemic attack 3 months previously and amaurosis fugax 1 month previously. Thus, carotid artery atherosclerosis should be highly suspected in patients who are older than 50 years and have risk factors of atherosclerosis. Color Doppler ultrasonography can also facilitate measurement of the degree of stenosis [12].
Results of different trials demonstrated that CEA is more beneficial than medical therapy in symptomatic patients with greater than 70% carotid stenosis.
Incidence of Doppler ultrasound-detectable stenoses of cervical arteries in patients with cochlear-vestibular symptoms. The application of high audio frequencies (10-20 kHz), which stimulate the base of the cochlea through bone conduction, is a conventional auditory technique.
More recently, the primary auditory cortex has been implicated, using magnetoencephalography, in processing ultrasound tonotopically, consistent with veryhigh- frequency hearing [5]. Support for a brain ultrasound demodulation theory stems from spherical models of brain and psychoacoustic metrics of masking audio frequencies by ultrasonic noise and by matching the pitch of audible ultrasound with conventional air conduction sound.
Direct vibration of the brain, but not skull, is sufficient to record auditory evoked potentials [16-18], thus verifying the brain-ear mechanism.
This experiment was repeated using seven normal hearing listeners with no history of otological disease.
Note also that the masker with noise centered at 39 kHz was less effective, as it is almost two octaves above the fundamental brain frequency (see Table 2). Further, pitch generally asymptotes approximately at the air-conduction match of some 16 kHz, rendering judgments difficult [3,24,25]. The change in the area activated and the subsequent neural coding likely contributed to crude detection of pitch change. Ultrasonic cleaners and related technology (ultrasonic welders, etc.) are an industrial source of high audio and ultrasound of sufficient energy to induce hearing loss. Although some overlap is seen with the brain ultrasound demodulation place of transduction in the cochlea, the mechanism is assumed to be direct stimulation via bone conduction. The psychoacoustical findings, despite the methodological differences, are also consistent with the brain ultrasound demodulation theory. Plastic changes reflecting neural reorganization secondary to peripheral hearing loss have also been well documented [36].
Presumably, the increased ultrasonic energy increases the displacement spread on the basilar membrane toward the apex, thus accounting for the observation that the ultrasonic pitch is related to the highest frequency detectable by air conduction. Echolocation is also possible by direct listening to the reflected ultrasonic echoes in the high audio range, after brain ultrasonic demodulation, which, owing to its frequency separation, will not interfere with speech communication. With hearing loss, greater ultrasonic energy is needed to spread the displacement on the basilar membrane toward the region of intact hair cells.
Theoretical analysis of acoustic signal generation in materials irradiated with microwave energy. Auditory perception of radio frequency electromagnetic fields J Acoust Soc Am 71 : 1321- 1334, 1982.
Oscillations of the internal ear basilar membrane in the sonic and ultrasonic range from the data of mathematical analysis of the hydrodynamic model of the cochlea. The functional anatomy of tinnitus: Evidence for limbic system links and neural plasticity.
Plastic changes in the auditory cortex induced by intensive frequency discrimination training.
Vestibular hypersensitivity to sound (Tullio phenomenon): Structural and functional assessment. The otolithic organ as a receptor of vestibular hearing revealed by vestibularevoked myogenic potentials in patients with inner ear anomalies. Thresholds of Hearing by Air Conduction and by Bone Conduction Under Different Masking Conditions. The incidence and variety of the head and neck injuries due to traffic accidents have extremely increased in recent years. Statistically, about 80% of the cases with whiplash injuries due to traffic accidents recover within a few months. Therefore many of these patients are under suspicion of malingering, or their disturbances are considered as being of a psychic type. They develop as the result of the years long lasting cronification degenerative processes of the lesions induced by the trauma incident.
Likewise, in none of these cases a cerebral commotion or a cerebral concussion could be established after the accident. Therefore, the audiological investigations by the tinnitus masking method mostly cannot determine the presence of the tinnitus' at the moment of the examination. Their presence can be due to traumatical changes induced during the accident in the maxillary sinuses, as well as in the temporomandibular joints. Thereby taken into consideration only hearing losses of perception type, assessed by the bone conduction testing.
The vestibulo-vegetative reactions are permanently monitored by a simultaneous EKG-registration. In our study, the multisensorial neurootological disturbances were caused in nearly all the patients, by the whiplash injury (Table 16).
The degree of the psychical impairment is directly depending on the intensity of the tinnitus. By means of the modern functional neurootological network analysis we can contribute much to clarify and to verify the disabling complaints which appear in the late whiplash injury syndrome.
However, at 3 months and then later (long-term results), the figures decreased to 67% and 46%, respectively. Loudness and character of the tinnitus in comparison to sinusoidal tones, narrow-band noise, and broad-band noise also were monitored every second day. In this case, according to a study of Almeling, [8] positive results were achieved also with patients who had experienced their tinnitus for even longer than 6 months. For tinnitus that exists for more than half a year, Biesinger [2] recommended a drug therapy that can interfere with the transmission of the auditory signal in the inner ear and brain. Der Einfluss der hyperbaren Sauerstofftherapie auf den Tinnitus und den Horverlust bei akuten und chronischen Innenohrschaden. The symptoms result from movement of the free floating otoconia particles in the endolymph or their attachment to the cupulae of the semicircular canal. These variations relate to both diagnostic strategies for BPPV and rates of utilization of various treatment options available for BPPV within and across the various medical specialties and disciplines involved in its management.
In this context, BPPV should be mentioned not only because of the high prevalence, but also because of the relative simplicity of the diagnosis and cost effectiveness of the treatment9. The semicircular canals change their gravitational orientation plane while the patients move their head. The fragments in suspension inside the labirinth tend to be deposited in this region, by the action of gravity1,13,14,15.
Typically, the vertigo arises in the lateral position of one or both sides, in hyperextension of the head, when standing up or lying down.
Because the patient is going to be placed in the supine position relatively quickly with the head position slightly below the body, the patient should be oriented so that, in the supine position, the head can "hang" with support off the posterior edge of the examination table by about 20 degrees. The examiner rotates the patient's head 45 degrees to the left and, with manual support, maintains the 45-degree head turn to the left during the next part of the maneuver8. The Dix-Hallpike maneuver should then be repeated for the right side, with the right ear arriving at the dependent position. If the upper pole of the eye beats away from the ground toward the uppermost ear, then it originates from the anterior canal of the uppermost ear. Patients with a history compatible with BPPV (ie, repeated episodes of vertigo produced by changes in head position relative to gravity) who do not meet diagnostic criteria for posterior canal BPPV should be investigated for lateral canal BPPV. After the nystagmus subsides (or if no nystagmus is elicited), the head is then returned to the straight face-up supine position. When the head is rotated to the healthy side, the particles displace and lead to a current moving in the opposite direction from the ampulla (also generating geotropic nystagmus), and the stimulation is less intense than that observed on the affected side. Lee and colleagues27 described the spontaneous reversal of nystagmus bilaterally, and the primary phase of nystagmus was shorter and with greater velocity of the slow-phase. Other possible causes are ovarian hormonal dysfunction, hyperlipidemia, hypoglycemia or hyperglycemia, hyperinsulinemia, migraine, cervical trauma, otological surgery, sedentary and prolonged bed rest2,15,32,33,34. Successful treatment depends mainly on the choice of the most appropriate maneuver for the case. The patient is rapidly laid back in a supine head-hanging position, which is maintained for a period of 1 to 2 minutes. The patient is in supine position; the patient's head is turned 90 degrees slowly toward the unaffected side.
The Brandt-Daroff exercises (Figure 8) are positioning exercises that, theoretically, promote habituation4. The treatment of each affected semicircular canal will be performed, in protocols according to the observed ocular movements and the correct identification of each affected semicircular canal. Patients with posterior BPPV had impaired static balance ability when visual and proprioceptive inputs were inadequate as described by Celebisoy45, Di Girolamo46. The conversion to lateral canal BPPV (so called canal switch) and Canalith Jam are unusual conditions, however when present must be promptly diagnosed and treated47. In the Epley Maneuver, it happens when the head of the patient is turned to facedown position (Figure 5 - position c and d). If the patient develops important symptoms, vestibular suppressant medications may be considered to help in a later repositioning. Therefore, it is possible to propose to the patient to wait the spontaneous resolution, in cases where the maneuver can't be indicated.


Benign paroxysmal positional vertigo: 10 year experience in treating 592 patients with canalith repositioning procedure. Neuro-otological features of benign paroxysmal vertigo and benign paroxysmal positioning vertigo in children: a follow-up study. Free-floating endolymph particles: a new operative finding during posterior semicircular canal occlusion. Effectiveness of treatment techniques in 923 cases of benign paroxysmal positional vertigo.
Benign paroxysmal positional vertigo due to a simultaneous involvement of both horizontal and posterior semicircular canals. Monitoring of caloric response and outcome in patients with benign paroxysmal positional vertigo.
Diagnostic, pathophysiologic, and therapeutic aspects of benign paroxysmal positional vertigo. Reversal of initial positioning nystagmus in benign paroxysmal positional vertigo involving the horizontal canal. Eletronytagmographic (ENG) findings in paroxysmal positional vertigo (PPV) as a sign of vestibular dysfunction. Canalith repositioning for benign paroxysmal positional vertigo: a randomized controlled trial. The canalith repositioning procedure for treatment of benign paroxysmal positional vertigo. A positional maneuver for treatment of horizontal-canal benign paroxysmal positional vertigo.
Balance in posterior and horizontal canal type benign paroxysmal positional vertigo before and after repositioning maneuvers.
Treatment efficacy of benign paroxysmal positional vertigo (BVVP) with canalith repositioning maneuver and Semont liberatory maneuver in 376 patients. Treatment of benign paroxysmal ositional vertigo: necessity of postmaneuver patient restrictions. Vibration with the canalith repositioning maneuver: a prospective randomized study to determine efficacy.
The canalith repositioning procedure with and without mastoid oscillation for the treatment of benign paroxysmal positional vertigo. Natural course of the remission of vertigo in patients with benign paroxysmal positional vertigo. Natural history of benign paroxysmal positional vertigo and efficacy of Epley and Lempert maneuvers.
Treatment of anterior canal benign paroxysmal positional vertigo by a prolonged forced position procedure. Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review.
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 authors conclude that AllHear cochlear implants have a good effect on tinnitus in the majority of patients. Its active electrode is inserted only 5 mm through the round window into the scala tympani, therefore reducing the risk of damage to the inner ear structures, as compared with other active electrodes that are inserted approximately 20 mm. That patient felt relieved because the tinnitus was not as intense as it was before the cochlear implantation.
The unusual fact is that tinnitus appears only with electrical stimulation, associated with a sensation of pain and electrical shock, disappearing 1 minute after the device is turned off.
Six patients with severe intractable tinnitus received a bolus and constant infusion of 123I-iomazenil intravenously over 7 hours with SPECT and magnetic resonance imaging of the brain. According to the American Tinnitus Association, approximately 50 million people are affected with tinnitus in the United States. The purpose of our study was to apply these techniques to evaluate cortical BZR using 123I-iomazenil SPECT imaging in patients with severe, central-type tinnitus as compared with healthy age-matched controls. Patients were excluded from the study for (1) pregnancy, (2) neurological or axis I psychiatric illness, (3) significant medical disease, (4) intake of medications known to affect GABA or BZR in 2 weeks before radiopharmaceutical administration, and (5) alcohol or psychotropic drug use within 2 weeks before the SPECT study.
All patients received potassium iodide (0.6 g SSKI solution) in the 24-hour period before the scan. An operational method for a standardized region-ofinterest strategy was developed by consensus of two experienced research nuclear medicine physicians, and regions of interest were placed. The V3' value for the radiotracer in each region of interest was calculated using the free fraction of the parent.
The findings of this study do not correlate with the current understanding of tinnitus, which indicates a possible seat of pathology in the temporal lobes [1,19,23,24]. In 16 healthy volunteers aged 21-78 years and studied with 11C-RO-4513 PET, no significant change with age was seen in 10 brain regions studied [26].
A small percentage (8-10%) of people, however, experience tinnitus that they describe as rhythmic, beating, pounding, throbbing, or "swooshing" in nature [3]. In addition to a medical examination, patients underwent a complete audiologic examination. We evaluated instances of atherosclerotic plaque in the carotid artery as to their location, extent, thickness, and degree of stenosis. All four patients with diagnosed ACAD underwent brain computed tomography, and the findings were normal. Color Doppler ultrasonography revealed an atherosclerotic plaque in the distal portion of her left common carotid artery, with the resultant 40% decrease in diameter. Color Doppler ultrasonography revealed an atherosclerotic plaque in the proximal part of his right internal carotid artery, with the resultant 75% decrease in diameter. According to several studies, the frequency of tinnitus increases in the elderly, so carotid artery atherosclerosis may be one of its possible causes [1]. It is also important for identifying patients who would benefit from surgical interventions.
Recent data have also demonstrated a 19% decrease in the incidence of ipsilateral stroke in symptomatic patients who had stenosis greater than 70% and underwent CEA [12,16]. The peripheral site of action of low-frequency ultrasound is more problematic but, in this study, we argue that the ultrasonic transduction is also parsimonious with conventional auditory theory, with the exception of its demodulation.
The same authors confirmed ultrasonic hearing and ultrasonic speech perception in approximately one-half their deaf subjects. Taken together, these findings suggest the absence of a specific place of ultrasonic frequency mapping on the cochlea but a dynamic mechanism that is a function of remaining hearing or hair cells and intensity of the ultrasonic stimulation. Audiometric thresholds were obtained in the conventional audiometric frequencies and extended through the high audio frequencies (10 - 20 kHz) using a Virtual 310 audiometer (Virtual Corporation, Portland, OR). Recall that 26- and 30-kHz center noise maskers were both at an equal SL (5 dB); therefore, the relative energy is not a principle factor but only its relationship to the fundamental frequency of the brain being forced into vibration. Note that the 26-kHz noise resulted in an increase in frequencies as well as masker threshold shift as compared with 39 kHz. Further, the multiple coupled resonances of the brain and skull can yield subtle intensity cues [27,28] but, in any event, changes of perhaps 10% of the frequency are required in the ultrasonic range to be detected as a pitch shift [3]. The model also predicts multi peaked or "slurred" waves higher than 20 kHz, rather than a conventional single traveling wave peak [33]. Characteristically, neurons sensitive to a damaged cochlear region will reprogram their best frequencies either higher or lower, resulting in greater neural representation of frequencies on the "edge" of the damaged peripheral region. In the case of severe deafness, with ultrasonic thresholds approximately at 30 dB above normal, insufficient surviving hair cells exist in the apex to detect the basilar membrane motion. In fact, what humans experience as ultrasonic perception may have been a necessary precursor in the evolution of echolocation specialization in marine mammal ears and brains. Ultrasonic pitch is not related to the stimulating frequency but rather to the remaining high audio frequency ability of the listener. Paper presented at the Twenty-First Annual Meeting of the Association for Research in Otolaryngology, St. By using seat belts, shoulder harnesses and head rests the amount of direct wounds and fractures are reduced in modern motor vehicles. Problems of evidence also arise in compensation claims calling for an additional neurootological medical expertise. By means of the modern functional neurootological network analysis we can nowadays contribute much to clarify and to verify the disabling complaints of the late whiplash injury syndrome. These cases were classified and treated as "trifle-and minor-traumas" by all the doctors and experts who have seen them prior to him.
This is very important on one side for the medical expertise and on the other hand for the correct diagnostic and therapeutical evaluation of these patients. In the chronic tinnitus group, the therapeutic effect dropped from 66.7% to 34% (with only intravenous medication) and from 60% to 28% (with combined therapy).
Side preference of tinnitus was not observed (28 right ear, 30 left ear, and 42 both ears). He preferred lidocaine (as a drug for stability of the nerve cell membrane and for blocking the transmission of stimuli), a calcium antagonist, glutamate, or glutamate antagonists [2]. The diagnosis is essentially clinical and should be confirmed by performing diagnostic maneuvers. Delays in the diagnosis and treatment of BPPV have both cost and quality-of-life implications for both patients and their caregivers8. The debris dislocates and promotes anomalous activation of the ampullar crista and may interfere with the neuronal output index that normally would be expected for that head and canal position. The lateral semicircular canal may be involved in 5 to 15% of patients8 and the anterior canal is rarely involved8; but there is still the possibility of simultaneous involvement of two canals18,19,20.
The examiner should ensure that he can support the patient's head and guide the patient through the maneuver safely and securely, without the examiner losing support or balance himself8. Next, the examiner fairly quickly moves the patient (who is instructed to keep the eyes open) from the seated to the supine left-ear down position and then extends the patient's neck slightly (approximately 20 degrees below the horizontal plane) so that the patient's chin is pointed slightly upward, with the head hanging off the edge of the examining table and supported by the examiner.
Again, the examiner should inquire about subjective vertigo and identify objective nystagmus, when present. After any additional elicited nystagmus has subsided, the head is then quickly turned 90 degrees to the opposite side, and the eyes are once again observed for nystagmus. Thus, the resulting eye movement is always stronger when the affected ear is placed downward23.
The arrows indicate the direction of displacement of the cupulae by gravity with the lateralization movement of the head. It has been proposed by Korres22 that the unilateral vestibular hypofunction is more common in cases secondary to head trauma or viral infection. Next, the head is turned 90 degrees, to the right (usually necessitating the patient's body to move from supine position to the lateral decubitus position).
The jam generates a constant counter-attraction force in the cupulae, as result from negative pressure. Possible explanations include some comorbidities and patient limitations during the maneuvers (for example: limited cervical range of motion or vascular failure)14.
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.
After magnetic resonance imaging coregistration, standardized regions of interest were placed over the cerebellar, frontal (control), superior temporal, hippocampal, and thalamic regions bilaterally on (SPECT) images.
Twelve control subjects were selected from a database of healthy controls with no lifetime psychiatric diagnosis and no clinically significant medical or neurological history, including tinnitus, on the basis of physical examination and laboratory studies. The mean bolus-to-infusion ratios were comparable to those from our previous studies, where they were shown to be optimal in achieving steady state of parent compound and unchanging time-activity curves in cortex [15]. The a priori hypothesis in this preliminary investigation was that chronic tinnitus would show abnormalities in the cerebellum, hippocampus, temporal lobes, and thalamic nuclei [19]. At an earlier stage of this project, we noted a trend showing decreased receptor density in the right cerebellum [25]; however, since then, we have reanalyzed data with closer age matching and also using newer image-processing techniques. Also, correlation between 123I-iomazenil SPECT and 11C-iomazenil PET studies has been good [11]; however, in both these studies, only a bolus injection of the tracer was performed, which does not necessarily produce equilibrium binding offered by the bolus and constant infusion method used in our study.
Atherosclerotic carotid artery disease (ACAD) was found to be a cause of pulsatile tinnitus in four patients (11.76%). Pulsatile tinnitus is a rare symptom and is believed to be a consequence of sound transmission created by turbulent blood flow through the petrous bone to the inner ear [2,4]. In three (8.82%) of our patients (patients 2, 3, and 4), pulsatile tinnitus was the first manifestation of ACAD [9]. In two (8.33%) of our patients (patients 2 and 4), CEA would be the most beneficial management approach and decreases the risk of stroke. Maass, never credited again for his original discovery, made all the essential observations in regard to ultrasonic hearing phenomenology. Ultrasound would then be unique as a form of auditory stimulation that any listener with any degree of hearing loss could detect given sufficient ultrasonic energy. Modeling the brain with such a boundary condition, the F is reported to be approximately 70% higher [8].
Monitoring neural vascular function with Doppler ultrasonic imaging provides unexpected support for the brain ultrasound demodulation theory.
Thresholds were repeated in the presence of ultrasonic masking noise, with peak energy centered at either 26 or 39 kHz. Note that the masker centered at 1 octave above the brain fundamental (26 kHz) produces more masking and a wider range of masking than does the masker approximately 2 octaves above (39 kHz). Note the close correspondence of the maximal hearing loss and frequencies within the brain's resonance. This model would not predict a peak frequency for masking or pitch matching in the range observed as does the brain ultrasound demodulation theory. In the only tinnitus-imaging study of neural reprogramming [34], the tinnitus frequency area expanded (more than twice the size) with some hint of lower-frequency expansion below the tinnitus frequency, as expected subsequent to hearing loss. Placing a transducer on the water surface and measuring the pressure output in a small tank can be complicated, even when brain and water impedances are similar [24]. In the case of complete deafness, the increased ultrasonic energy likely displaces the otolith organs, resulting in saccular stimulation. However, the energy impact upon a person, sitting in a car involved in a traffic accident of the surprise-rear-end-collision type, is absorbed in the head and neck through an abrupt hyperextension and hyperflexion movement, which also is called the whiplash injury mechanism.
Once more it reflects the uncertainty of the doctors as it concerns the neurosensorial disturbances, and appeared as late complications of the whiplash injury. For this Dutch team, the neurootological investigations are of an exceptional importance for a correct judgement of the patients with whiplash injury, as namely they can reveal the long lasting degenerative and cronification processes following the trauma. Therefore, what appears to be essential is not only to examine people who suffer from tinnitus but to offer them treatment.
In 23 patients, tinnitus was accompanied by a sudden hearing loss, in 12 by sensorineural hearing loss, in 9 by ventilation disturbance of the eustachian tube because of a chronic sinusitis, and in 1 by a vestibular neuritis. The results of our indoor patients with acute tinnitus were at first excellent (80% success rate). Treatment is based on the identification of the affected semicircular canal and performance of liberatory maneuvers or repositioning of free floating particles of otoliths. Some other symptoms could be associated and often persist after the interruption of the episode, such as nausea, imbalance, or postural instability1,15.
The examiner observes the patient's eyes for the latency, duration, and direction of the nystagmus.
Two potential nystagmus findings may occur with this maneuver, reflecting two types of lateral canal8.
In cupulolithiasis, the fragments are adhered to the cupulae of the affected semicircular canal, which make them heavier than the endolymph. Some authors prefer to wait for the natural course towards a spontaneous relief, considering BPPV a self-limited condition. The patient is rapidly moved to the opposite side-lying position without pausing in the sitting position and without changing the head position relative to the shoulder. Then, the head is turned to the facedown position and the body is moved to the ventral decubitus. The jam pressure induces cupulae displacement and consequent depolarization (vertical canals) or hyperpolarization (lateral canals). 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]. Venous blood samples were drawn at specified intervals to determine equilibrium distribution volumes (V3') for each of the regions. This procedure was repeated for each patient, and correction to the time of injection was performed.
Imaging was started on average within 345 ± 19 minutes and 363 ± 3 8 minutes after bolus radiotracer administration, respectively, for cases and controls. The study group (n = 6) was compared to the control group (n = 12) using a two-sample t-test for areas of relative increase or decrease in radiotracer accumulation. At times, however, these pulsations occur in or around the middle ear or inner ear or near the hearing nerve and become audible to us. In addition, tympanometry and tinnitus evaluation were performed in an attempt to record objective evidence of the pulsatile tinnitus from patients' ear canal. In patients 2 and 4, pulsatile tinnitus occurred as the first symptom when the degree of stenosis increased to more than 70%. In contrast, this suggests an apical cochlear site or other noncochlear acoustic site that is activated in the presence of severe deafness. Ultrasound refinement could lead to new types of audio amplification, auditory orientation (echolocation), and tinnitus treatment, if the mechanism can be clearly elucidated. When the imaging beam was focused at the center of the brain, patients reported hearing a high audio sound, much like tinnitus. Thus, ultrasound will map in the high audio frequencies, because the brain is the demodulator regardless of the stimulating ultrasonic frequency. Note the close correspondence of the masking curves for 26- and 39-kHz-centered ultrasonic noise and the noise-induced hearing loss (NIHL) composite audiograms reported for industrial worker exposed to intense ultrasound [30]. The concept of brain ultrasonic demodulation as applied to industrial exposure is unique and begs for further exploration.
This pattern was striking in only four of the subjects, and the mean high-frequency hearing loss for all subjects was just outside the normal range.
Indirect high audio frequency stimulation (ultrasound) or direct highfrequency stimulation can be an effective masker in tinnitus and can contribute to long-term tinnitus relief through neural repogramming. These abrupt movements of the head and neck may have several morpho-functional consequences upon the cervical region, as well as upon the nervous and sensorial structures of the head. The characteristics of the ear noises were specifically investigated through the tinnitus masking method.
Their studies and conclusions are based upon the numerous pathological electronystagmographical findings, and also the corresponding pathological audiological results. In eight patients, the tinnitus was caused by an acute otitis media, in three by an acoustic trauma, in two by a chronic otitis media, and in one by a labyrinthine contusion (Table 1).
The positive effect was shown for 77% of patients immediately after the application and for 68% of patients even 6 months after the application [10]. Besides the clinical history, the diagnosis of BPPV takes into account the type, direction and duration of nystagmus provoked by maneuvers that provide clues for identifying the affected canal and the pathophysiological mechanism involved (whether canalithiasis or cupulolithiasis). Again, the provoked nystagmus in posterior canal BPPV is classically described as a mixed torsional and vertical movement with the upper pole of the eye beating toward the dependent ear. When the head is rotated to one side, the action of gravity on the ampullar crista moves the debris into the opposite direction and it is possible to observe the nystagmus that is in the opposite direction from the tested ear (apogeotropic type)24,25. Gradually the patient resumes the upright sitting position8.If the superior semicircular canal is affected, the movement is performed in the direction opposite to the procedure for posterior semicircular canal4,15,23,40.
Later the patient's head is turned 90 degrees, and the body is placed on lateral decubitus.
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).
Variation in V3' values in homotypic regions were calculated using a Wilcoxon signed rank test. The extent threshold (k), below which clusters were rejected, was 125 voxels, which corresponds to the approximate resolution of SPECT imaging in tissue, which is 1 mm3. The perception of the rhythmic flow of blood through the head or neck region is also termed pulsatile tinnitus. That study found that patients with tinnitus had a greater risk of atherosclerotic stenosis of extracranial arteries (18%) than did asymptomatic people (1%). Thus, early and accurate diagnosis of atherosclerosis is imperative and will prevent stroke and other central nervous system complications.
Some deaf patients could hear ultrasound, albeit at levels higher than those in normal listeners, and frequency discrimination was possible, although far poorer than in the audio range. The implication is that different sites on the inner ear's basilar membrane are activated, depending only on the proportion of hair cells present.
For all practicality, the exact resonant frequency of a brain with a 7-cm radius is probably a number between the free and boundary states. The higher the ultrasonic frequency is in regard to the brain resonance, the more energy is required to set the brain into forced resonance, accounting for the wider spread of masking for 26 versus 39 kHz (Fig. In addition, the presence of both high audio frequencies and ultrasound in the workplace can increase the ear damage risk, as a place-coding overlap exists on the basilar membrane (see details later). Assuming that maximal displacement of the basilar membrane is at the place corresponding to the brain's fundamental frequency (1.5 mm from the base for 26 kHz), bulk innerear fluid displacement, permitted by compliant oval and round windows at very high intensities (100 SL+), could conceivably create fluid flow in the saccule, not unlike the Tullio effect [39]. The state of the acoustical pathways was investigated by means of the acoustically evoked brain stem potentials as well as the acoustically evoked late (cortical) potentials.
In one patient with a unilateral tinnitus, a diagnosis of acoustic neuroma could be made, and this patient was excluded from this study.
The positive atmosphere from a private clinic might be the reason for the good early results in comparison with the later results (obtained from patient questionnaire). Then the patient is asked to rest the chin on the shoulder and sit up slowly, completing the maneuver8 (Figure 4). Figure 6 demonstrates the Semont Maneuver for treatment of right-sided posterior semicircular canal cupulolithiasis.
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.
Twelve normal control subjects were compared to the study subjects using statistical parametric mapping. Control subject images were acquired by three serial 18-minute scans that were summed before being used in image analysis.
It may be subjective (perceived by the patient only) or objective (perceived by both the patient and the examining physician) [5].
Applying a microwave burst to a 7-cm radius sphere containing fluid with properties similar to those of brain results in a measured peak frequency of 11.4 kHz. Setting the brain into resonance resulted in a clear, high-pitch, audible sensation consistent with brain resonance in the 11- and 16-kHz range. The very short cilia of saccular hair cells, not mass-loaded by gel or otoconia [40] in the striola region, are likely fluid velocity-sensitive. No significant difference was observed between the positive effect of intravenous medication only and combined treatment (intravenous medication and HBO). The head must stay in that position for some moments, before it returns to the normal position1,4,23,40. Each step is maintained for 15 seconds - for slow migration of the particles, in response to gravity. Tinnitus may also be considered to be a varying stimulus due to environmental masking, with some tinnitus representing a complex mix of several sounds. Comparison of homotypic brain regions showed statistically significant asymmetry in the V3' data in the superior temporal cortex (p = .03 for both).
In three patients, pulsatile tinnitus was the first manifestation of ACAD; in two of these, this symptom occurred when the stenosis affected more than 70% of the artery's diameter. Pulsatile tinnitus usually occurs in one ear only, and it is an important variant among tinnitus patients. Microwave absorption causes a rapid heating that launches a pressure wave within the sphere.
The use of imaging ultrasound has had mixed success [20,21], but the critical feature in failure might be not focusing the beam at the brain's center to maximize brain ultrasonic demodulation. High-frequency stimulation (high audio and ultrasound) have been shown to mask tinnitus and produce varying degrees of residual inhibition [1,2].
To complete the maneuver, the patient is brought into the upright sitting position with head bowed down at 30 degrees23,43,44. ACAD should be considered in evaluation of all patients with pulsatile tinnitus and associated cardiovascular risk factors. If the head is exposed to such microwave stimulation, the fundamental brain frequency is proportional to the brain size.
Because ultrasound produces high audio stimulation by virtue of brain resonance, the direct use of high audio stimulation is more economical in power requirements and still stimulates the brain at resonance. 9, No.2, 2003 Stimulating the saccule, an organ having input into the auditory pathways in mammals [37,41,42], may explain ultrasonic detection in the deaf. All tinnitus patients underwent MRI and coregistration with SPECT scans (as described later) for directing region-of-interest placement. As pulsatile tinnitus may be the sole manifestation of severe carotid artery stenosis, immediate color Doppler ultrasonographic study is recommended in those patients with risk factors and in the elderly. One of the reported etiologies of pulsatile tinnitus is atherosclerotic disease of the carotid arteries. A human infant would have a resonant frequency between 16 and 22 kHz assuming a 5-cm radius. Anecdotally, a graduate engineering subject who had no measurable hearing and who was an unsuccessful cochlear implant user described the perception of 26 kHz and an alternating knocking in her head.
Current understanding suggests GABA receptors and the temporal lobe system as the final common pathway. Diagnosis of atherosclerosis in affected patients is critical to prevent the more serious central nervous system complications and to guide treatment.
The cilia of hair cells have opposite orientation on either side of the saccular striola, which could neurally code the alternating phase of a sine wave as an alternating knocking. This pilot study suggests possible alterations on 123I-iomazenil SPECT imaging and the need for larger studies. A hydrophone implanted in the brain of a cat recorded peak pressure at 39 kHz as a result of microwave pulses [11]. Other subjects reported unsteadiness when rising from a seated position after ultrasonic listening, which also was suggestive of saccular stimulation.
Clearly, more work must be conducted to elucidate the source of nonauditory coding of ultrasound in humans, but complete loss of hearing and balance seems to preclude its detection. As deduced from the foregoing data, the human brain resonant frequency is likely between 11 and 16 kHz, with the exact value being determined by individual skull geometry. No published reports have cited the use of ultrasound in treating tinnitus in severely deaf individuals in spite of a high incidence of tinnitus in this population [43].



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