Quantitative measurement of airborne particles during endoscopic and microscopic ear surgery in the operating room.

OBJECTIVE: This study aimed to quantitatively investigate airborne particle load in the operating room during endoscopic or microscopic epitympanectomy or mastoidectomy. METHOD: In the transcanal endoscopic ear surgery group, drilling was performed underwater. A particle counter was used to measure the particle load before, during and after drilling during transcanal endoscopic ear surgery or microscopic ear surgery. The device counted the numbers of airborne particles of 0.3, 0.5 or 1.0 µm in diameter. RESULTS: The particle load during drilling was significantly higher in the microscopic ear surgery group (n = 5) than in the transcanal endoscopic ear surgery group (n = 11) for all particle sizes (p < 0.01). In the transcanal endoscopic ear surgery group, no significant differences among the particle load observed before, during and after drilling were seen for any of the particle sizes. CONCLUSION: Bone dissection carries a lower risk of airborne infection if it is performed using the endoscopic underwater drilling technique.

An endoscopic hydro-mastoidectomy technique for cholesteatoma surgery.

OBJECTIVE: Endoscopic hydro-mastoidectomy, in which mastoidectomy is performed underwater, can be employed during transcanal endoscopic ear surgery for cholesteatoma removal. It was hypothesised that endoscopic hydro-mastoidectomy might take less time than endoscopic non-underwater mastoidectomy because the endoscope does not need to be removed for cleaning. METHODS: This study compared the mastoidectomy and total operative durations between the endoscopic hydro-mastoidectomy (n = 25) and endoscopic non-underwater drilling (control, n = 8) groups. Moreover, it compared the size of resected areas of the external auditory canal between the two groups. RESULTS: The mastoidectomy time of the endoscopic hydro-mastoidectomy group was significantly shorter than that of the control group (p < 0.01). The total operative time did not differ significantly between the endoscopic hydro-mastoidectomy and control groups (p = 0.17). The resected area was significantly larger in the endoscopic hydro-mastoidectomy group than in the control group (p < 0.05). CONCLUSION: Endoscopic hydro-mastoidectomy enables more extensive bone resection within a shorter period.

A novel endoscopic hydro-mastoidectomy technique for transcanal endoscopic ear surgery.

BACKGROUND: In order to remove a cholesteatoma in the mastoid under transcanal endoscopic ear surgery, it is necessary to perform transcanal endoscopic mastoidectomy. Bone dust and blood, however, obscure the surgical field. A novel endoscopic hydro-mastoidectomy technique was developed, in which the operator performs the mastoidectomy 'underwater' using a lens cleaning system that provides saline perfusion in the surgical space. METHODS: A curved round coarse diamond bur is attached to an otological drill. A lens cleaning sheath is fitted to the endoscope. The surgeon controls the infusion of saline solution by stepping on a footswitch of the power console. RESULTS: Endoscopic hydro-mastoidectomy washes out bone dust and blood from the surgical field, improving the surgical view during mastoidectomy. Additionally, the operator can easily control the flow of saline perfusion. CONCLUSION: This technique provides a clear surgical view by washing out bone dust and blood from the surgical area. The setup for endoscopic hydro-mastoidectomy technique is easy and the operator needs only to buy sheaths if they already own the power console, as many otological and rhinological surgeons do.

Behavioral assessment and identification of a molecular marker in a salicylate-induced tinnitus in rats.

Tinnitus is a non-observable phantom sensation. As such, it is a difficult condition to investigate and, to date, no effective treatment has been developed. To approach this phantom sensation, we aimed to develop a rat behavioral model of tinnitus using salicylate, an active component of aspirin known to induce tinnitus. We also aimed to establish a molecular marker of tinnitus by assessing the expression of transient receptor potential cation channel superfamily V-1 (TRPV1) in the rat auditory pathway during salicylate-induced tinnitus. Animals were trained to perform "an active avoidance task": animals were conditioned by electrical footshock to move to the other side of the conditioning box when hearing a sound. Animals received a single injection of saline or salicylate (400 mg/kg i.p.) and false positive responses were measured 2 h after injection as the number of movements during a silent period. The number of responses in salicylate-treated animals was highest when the conditioned stimulus was 60 dB sound pressure level (SPL) and 16 kHz. This indicates that animals could feel tinnitus 2 h after salicylate injection, equivalent to that induced by 60 dB SPL and 16 kHz. By means of real-time PCR and western blot analysis, TRPV1 expression was significantly upregulated in spiral ganglion cells 2 h after salicylate injection and this upregulation together with the increase in the number of false positive responses was significantly suppressed by capsazepine (10 mg/kg i.p.), a specific antagonist of TRPV1. This suggests that salicylate could induce tinnitus through activation of TRPV1 in the rat auditory pathway.

Stapediovestibular dislocation with pneumolabyrinth.

Traumatic luxation of the stapes into the vestibule is a rare entity, and the disease complicated with pneumolabyrinth is extremely rare. We report the case of a 72-year-old woman with pneumolabyrinth associated with a stapediovestibular dislocation. The patient presented with vertigo and nystagmus following penetrating trauma to the middle ear. High resolution computed tomography scans demonstrated air in the vestibule and dislocation of the stapes. Exploratory tympanotomy demonstrated oozing of the perilymph from the oval window and depression of the stapes into the vestibule. Pneumolabyrinth and stapes luxation detected by high resolution computed tomography should be predictive of a perilymphatic fistula.

Vestibular input to brain monoamine neurons--a review.

Yates et al. reported that serotonergic RN neurons are associated with vestibulo-sympathetic responses and may control BP changes during body repositioning (Yates et al., 1992; 1993). Pompeiano et al. demonstrated that LC-NA neurons participate in the postural control and modify the vestibulo-spinal reflex (Pompeiano et al., 1990; 1991a; 2001). Nishiike et al. (1996a) examined the effects of caloric vestibular stimulation on the neuronal activity of LC-NA neurons in rats. The predominant effect of CA with both hot- and cold-water on the electrical activity of LC neurons is inhibitory and persists for several minutes. GABAA receptors located on the postsynaptic membrane of LC neurons are responsible for these inhibitory responses. The VLM may inhibit LC neuronal activity in response to the CA via GABAA receptors (Nishiike et al., 1997). It is suggested that LC-NA inhibition is involved in the development of motion sickness (Nishiike et al., 2001).

Information processing of visually-induced apparent self motion in the cortex of humans: analysis with magnetoencephalography.

The cortical site which processes information on whole-body linear displacement is unknown. In this study, neuromagnetic responses to a visually-induced linear vection were recorded in 5 healthy, right-handed, adult subjects using a 122-channel whole cortex neuromagnetometer. We presented expanding rectangles on the screen which came into view one after another and accelerated in expanding speed at random cycle, giving the subjects the sensation of linear self motion (linear vection) through an illusory tunnel with occasional acceleration. Clear responses of magnetic fields related to the accelerative event were obtained in both hemispheres around the parietal and temporal regions. The dipole sources of the component were estimated in the cortex around the superior temporal sulcus, insula and medial superior temporal area. Some parts of these regions may have been comprised in the vestibular cortex, suggesting that it processes the sensation of linear self motion and plays an important role in space perception.

Noradrenergic pathways involved in the development of vertigo and dizziness--a review.

In this study, vestibular caloric stimulation (CS) inhibited noradrenergic (NA) neurons of the locus coeruleus (LC) in rats. The vestibular input can be modified by the ventrolateral medulla (VLM), which then inhibits the LC neuronal activity via GABAA receptors. Clinically, CS induces vertigo in humans. Thus, LC-NA inhibition may be involved in the development of vertigo. Moreover, it is speculated that Sopite syndrome, one of the major symptom complexes of motion sickness, is also evoked by LC-NA inhibition. The central LC-NA neuronal system may participate in vertigo and motion sickness independent of the histaminergic neuronal system. In contrast, the cholinergic neuronal system may mediate LC-NA inhibition during the vestibulo-atonomic reflex. The LC-NA system projects to most higher centers and affects sensory information processing. Therefore, it is suggested that the suppression of sensory information processing induced by LC-NA inhibition causes drowsiness, one of the major symptoms of vertigo and motion sickness. It is also speculated that LC-NA inhibition participates in the development of sensory mismatch during vertigo and motion sickness.

Neural mechanisms of motion sickness.

Three kinds of neurotransmitters: histamine, acetylcholine and noradrenaline, play important roles in the neural processes of motion sickness, because antihistamines, scopolamine and amphetamine are effective in preventing motion sickness. Histamine H1-receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. On provocative motion stimuli, a neural mismatch signal activates the histaminergic neuron system in the hypothalamus, and the histaminergic descending impulse stimulates H1-receptors in the emetic center of the brainstem. The histaminergic input to the emetic center through H1-receptors is independent of dopamine D2-receptors in the chemoreceptor trigger zone in the area postrema and serotonin 5HT3-receptors in the visceral afferent, which are also involved in the emetic reflex. Antihistamines block emetic H1-receptors to prevent motion sickness. Scopolamine prevents motion sickness by modifying the neural store to reduce the neural mismatch signal and by facilitating the adaptation/habituation processes. The noradrenergic neuron system in the locus coeruleus is suppressed by the neural mismatch signal. Amphetamine antagonizes mismatch-induced suppression of noradrenergic neural transmission, resulting in preventing motion sickness.

Effect of AF64A, a cholinergic neurotoxin, on footshock stimulation-induced locus coeruleus excitation in rats.

We studied the effect of ethylcholine mustard aziridinium ion (AF64A), a cholinergic neurotoxin, on the footshock stimulation (FS)-induced excitation of the locus coeruleus (LC) neurons in rats. The FS-evoked LC excitation was significantly reduced in AF64A-treated rats, in comparison with normal rats. In particular, the early component of LC excitation was less pronounced. The number of choline acetyltransferase immunoreactive neurons in the septal complex was significantly lower than those in normal rats, except for in the ventral subgroup. These findings suggest that the cholinergic neuron system is involved in the early component of LC excitation in rats.

[Effects of steroid therapy on long-term canal prognosis and activity in the daily life of vestibular neuronitis patients].

We studied 28 patients with vestibular neuronitis treated at our hospital between 1997 and 1999. To determine the effects of steroid therapy on long-term canal prognosis and daily activity, we examined caloric tests and gave questionnaires to 12 steroid-treated and 16 nonsteroid-treated patients 2 years after onset. We found that canal improvement was 50% in the nonsteroid-treated group and 75% in the steroid-treated one. In cases with severe canal paresis (CP > or = 60%), canal improvement was 33% in the nonsteroid-treated group and 67% in the steroid-treated one. Steroid therapy at the acute stage of this disease significantly reduced the duration of spontaneous nystagmus and handicap in daily life due to dizziness induced by head and body movement, decreasing mood disturbance.

Cholinergic influence on vestibular stimulation-induced locus coeruleus inhibition in rats.

In our previous study, caloric stimulation (CS) of the vestibular apparatus inhibited noradrenergic neuronal activity in the locus coeruleus (LC) in urethane-anaesthetized rats. Therefore, the inhibition of LC noradrenergic neurons is involved in vestibulo-autonomic responses. Since motion sickness can be cured by scopolamine, cholinergic neuron system may also be involved in vestibulo-autonomic responses. The present study examined the effects of intracerebroventricular injection of ethylcholine mustard aziridinium ion (AF64A), a presynaptic cholinergic neurotoxin, on CS-induced LC inhibition. In AF64A-treated rats, the CS-induced LC inhibition was less pronounced than in normal rats. In a subsequent series of experiments, the intravenous injection of scopolamine blocked the CS-induced LC inhibition. These findings suggest that central cholinergic neurons are associated with noradrenergic neuronal inhibition during the vestibulo-autonomic reflex.

[Seven cases of tuberculous otitis media].

Tuberculous otitis media (TOM) is a variable and puzzling infectious disease that is sometimes confused with other chronic middle ear diseases. A series of 7 cases (9 ears) of TOM recently treated at Osaka Prefectural Habikino Hospital is reviewed to assess the recent features of the disease. In most cases, the pathogenetic mechanism was probably aspiration of tubercle bacilli through the eustachian tube. In most cases, abundant granulations were observed in the middle and external ears, but multiple perforations of the tympanic membrane were not seen. The manifestations were variable, such as otorrhea from the perforation and otitis media with effusion. In their early stage, most cases of TOMs due to transmission via the eustachian tube are tend to resemble otitis media with effusion. Smear tests, culture, PCR, and histopathological examinations, each of which has advantages and disadvantages, must be repeated to achieve a definitive diagnosis. Tuberculin tests can be unreliable, but a chest x-ray is indispensable whenever TOM is suspected. Antitubercular chemotherapy and 2% kanamycin earwash yielded good results. Since the classical criteria for the diagnosis of TOM are no longer valid, we propose a new criterion for diagnosis in the early stage of the disease.

Corticofugal connections between the cerebral cortex and the vestibular nuclei in the rat.

The distribution of cortical efferent connections to the vestibular nuclei was quantitatively analyzed by means of retrograde axonal transport of horseradish peroxidase, wheat germ agglutinin-horseradish peroxidase, and Fast Blue in rats. The tracer substances were injected into the spinal vestibular nucleus (SpVe), the caudal part of the medial vestibular nucleus (MVe), and nucleus X of Brown Norwegian rats. Projections to the vestibular nuclei were revealed bilaterally, but predominantly contralaterally from five cortical areas: (1) the parietotemporal region (PT) which occupied the caudal two-thirds of the secondary somatosensory area and spread over the caudal part of the primary somatosensory area and the visceral cortex; (2) the anterior forelimb (AF) overlapping the anterior part of the forelimb area and the transitional zone; (3) the anterior hindlimb (AH) overlapping the anterior part of the hindlimb area and the transitional zone; (4) the lateral forelimb (LF) centered in the intercalated zone lateral to the forelimb area; and (5) the ventrotemporal region (VT) located at the ventral part of the temporal cortex. In addition to these cortical fields, the frontal cortex was found to project directly to the vestibular nuclei. These corticofugal projections were verified in experiments in which biocytin was injected into the rat PT. Anterogradely labelled fibers were traced predominantly contralaterally to the SpVe, caudal part of the MVe, and nucleus X. It is suggested that the rat corticofugal projections to the caudal vestibular nuclei modify vestibular reflexes to assist in coordinating eye, head and body movements during locomotion.

Co-localization of glutamate, choline acetyltransferase and glycine in the mammalian vestibular ganglion and periphery.

Glutamate (Glu) is considered to be the main transmitter at the central synapses of primary vestibular afferents (PVA) and glycine (Gly) is assumed to play a modulatory role. In the vestibular periphery a transmitter role for acetylcholine (ACh) has been attributed chiefly to vestibular efferents (VE), however only a subset of VE neurons displays immunoreactivity (ir) for choline acetyltransferase (ChAT) and acetylcholine esterase (AChE). Controversial results exist on the presence of these two enzymes in PVA. In this study the presence of Glu, ChAT, Gly and their co-localization in the vestibular ganglia (VG) and end organs of mouse, rat, guinea pig and squirrel monkey were investigated. In the VG all bipolar neurons display strong Glu-ir and the majority of cells show a graded ChAT-ir and Gly-ir in all species examined. ChAT and Gly are present in highly overlapping neuronal populations and with a similar gradation. In the end organs ChAT and Gly are again co-localized in the same sets of fibers and endings. In conclusion, in the vestibular ganglion and end organs ChAT appears also to be present in primary afferents rather than being restricted to efferent processes. ChAT in primary afferents might indicate a modulatory or co-transmitter function of acetylcholine.

Histaminergic influence on vestibular stimulation-induced locus coeruleus inhibition in rats.

In previous reports we have shown that caloric stimulation (CS) of the vestibular apparatus inhibits locus coeruleus (LC)-noradrenergic neuronal activity in urethane-anaesthetized rats. The present study examined the effect of neural histamine depletion by alpha-fluoromethylhistidine (alpha-FMH) on CS-induced LC inhibition. In alpha-FMH treated rats, LC neuronal inhibition caused by CS was still observed. This finding indicates that the central histaminergic neuron system does not participate in the CS-induced LC-noradrenergic inhibition. It is suggested that the noradrenergic neuron system is involved in the development of vestibulo-autonomic response, independent of the histaminergic neuron system.

[Clinical features in patients with delayed endolymphatic hydrops].

We report clinical features in patients with delayed endolymphatic hydrops (DEH) with juvenile unilateral deafness. Among 23 patients with DEH, 15 cases were diagnosed as ipsilateral DEH and 8 cases as contralateral DEH. The distribution of onset age showed two peaks at ages of < 30 years and > 40 years. In 80% of the ipsilateral DEH cases, the onset of episodic vertigo was at younger ages. On the other hand, in 75% of the contralateral DEH cases, the onset of fluctuation hearing loss of the contralateral ear was at older ages. Ispilateral DEH and Meniere's disease may show different pathophysiologies. The incidence of dominant negative summating potential in the better-hearing ear was 20% in the ispilateral DEH cases and 60% in the contralateral DEH cases. It is suggested that endolymphatic hydrops is in the better-hearing ear of contralateral DEH.

Antidromic burst activity of locus coeruleus neurons during cortical spreading depression.

The electrical activity of locus coeruleus neurons was investigated during cortical spreading depression in urethane-anaesthetized rats. Cortical spreading depression was induced by a direct application of 1-3 M KCl solution to the surface of the cerebral cortex. The occurrence of cortical spreading depression was assessed by recording negative d.c. shifts and in some experiments by monitoring the extracellular potassium concentrations. The mean spontaneous firing rate of locus coeruleus neurons was significantly reduced during cortical spreading depression. Approximately 60% of locus coeruleus neurons recorded during cortical spreading depression revealed anomalous burst activity consisting of multiple initial segment spikes as well as full initial segment-somatodendritic spikes with a marked initial segment-somatodendritic break. Each spike of the cortical spreading depression-related burst activity occurred at intervals ranging from 15.0 ms to 90.1 ms (34.9 +/- 0.5 ms). The burst activity appeared unpredictably at variable intervals in a phasic or tonic manner during cortical spreading depression. The cortical spreading depression-related burst activity of locus coeruleus neurons mimicked antidromic spikes induced by train stimulation of the cerebral cortex at short interspike intervals during iontophoretic application of GABA to locus coeruleus neurons, whereas it was totally different from synaptically-activated burst activity induced by tail pinch. The full spikes and initial segment spikes in the cortical spreading depression-related burst activity failed to collide with cortically elicited antidromic spikes, even when they appeared within the collision interval. The proportion of initial segment spikes in the cortical spreading depression-related burst activity was reduced following an increase in membrane excitability by iontophoretic application of glutamate, and increased during a decreased membrane excitability by GABA application. The antidromic burst activity of locus coeruleus neurons also appeared for a short time during cortical spreading depression prior to the occurrence of seizure waves induced by GABA antagonists, while the burst activity could not be observed during seizure activity. These results indicate that the cortical spreading depression-related burst activity was of antidromic origin and that the marked initial segment-somatodendritic break in spontaneous spikes of locus coeruleus neurons during cortical spreading depression was due to reduced excitability of the somatodendritic membrane. The cortical spreading depression-related burst activity may cause release of a large amount of noradrenaline in vast regions of locus coeruleus terminal fields through the numerous axon collaterals, thereby playing a role in functional changes of brain neurons related to cortical spreading depression.

[Clinical features and utricular dysfunction in patients with benign paroxysmal positional vertigo].

We report the clinical features in patients with benign paroxysmal positional vertigo (BPPV), who met the following criteria; (1) a history of brief episodes of positional vertigo, and (2) a characteristic torsional paroxysmal positional nystagmus that was observed visually. The mean age of onset was 55 years. There was no sex predominance. In most patients, positional vertigo disappeared within 2 months. We then used the eccentric rotatory test to examine the patients otolithic function. In the eccentric rotatory test, a patient is rotated around an axis located behind his head (eccentric rotation, ECR). We have demonstrated that the enhancement of vestibulo-ocular reflex (VOR) gain in ECR can be used as an index of the utricular function. Enhancement of VOR gain was observed in ECR to the lower ear in positional vertigo, but not to the uppermost ear. The findings suggest an imbalance in utricular function in patients with BPPV. Otoconia dislodged from the deranged utricle may be a source of canalolithiasis/cupulolithiasis.