N-methyl-D-aspartate-sensitive [3H]glutamate binding sites in brain synaptic membranes treated with Triton X-100.

Specific binding activity of radiolabeled L-glutamic acid, a putative central excitatory neutrotransmitter, was drastically increased with increasing concentrations of Triton X-100 used for pretreatment of rat brain synaptic membranes. The binding in these Triton-treated membranes was a protein dependent, inversely temperature-dependent, stereospecific, structure-selective and saturable process with a high affinity for the amino acid. The binding activity was invariably inhibited by agonists and antagonists for the N-methyl-D-aspartic acid (NMDA)-sensitive subclass, but not by agonists for the other subclasses of excitatory amino acid neurotransmitter receptors in the brain. Scatchard analysis revealed that the binding sites consisted of a single component with a Kd of 24.4 +/- 2.5 nM and a Bmax of 0.94 +/- 0.09 pmol/mg protein. Some endogenous tryptophan metabolites such as kynurenic acid and quinolinic acid also inhibited the binding. These results suggest that synaptic membranes may indeed contain the NMDA-sensitive receptors which are disclosed by Triton X-100 treatment.

The morphology of single lateral vestibulospinal tract axons in the lower cervical spinal cord of the cat.

The intraspinal morphology of single lateral vestibulospinal tract (LVST) axons was investigated with the method of intra-axonal staining with horseradish peroxidase (HRP) and three-dimensional reconstruction of the axonal trajectory. Axons penetrated in the ventral funiculus at C5-C8 were identified as LVST axons by their monosynaptic responses to stimulation of the ipsilateral vestibular nerve and by their direct responses to stimulation of the ipsilateral Deiters' nucleus and LVST. Reconstructions were made from 34 well-stained LVST axons. Of these, 23 terminated in the brachial segments (C5-Th1) and the other 11 projected below Th2. These axons were traced over distances of 2.9-16.3 mm rostrocaudally. Within these lengths, one to seven axon collaterals (mean +/- S.D., 3.2 +/- 2.0, N = 19) were given off at right angles from the stem axons of LVST axons terminating in the brachial segments. The mean diameters of stem axons and primary collaterals were 4.5 microns and 1.6 micron, respectively. In the gray matter, collaterals ramified successively, pursued a delta-like path, and terminated mainly in laminae VII and VIII or lamina IX. The rostrocaudal extension of a single collateral was very restricted (mean +/- S.D., 760 +/- 220 microns, N = 16), in contrast to the extensive dorsoventral and mediolateral extent of the terminal arborization. There were usually gaps between adjacent collateral arborizations from the same stem axons, since the intercollateral distances ranged from 400 to 4,300 microns (mean = 1,490 microns). LVST axons terminating in brachial segments were divided into two groups--a medial group and a lateral group--on the basis of their projection sites in the transverse plane of the gray matter. The axons of the medial type had their main projection to laminae VII and VIII of Rexed, while those of the lateral type terminated in lamina IX. The terminal arborizations of the medial type LVST axons were mainly distributed over lamina VIII, where synaptic boutons appeared to make contact with proximal dendrites or somata of medium-sized and large neurons in the ventromedial nucleus and also in the medial portion of lamina VII adjacent to the central canal and dorsal to lamina VIII. Five out of 15 medial type axons had a bilateral projection. One or two collaterals of each of these axons crossed the midline through the anterior commissure and terminated in lamina VII or VIII. It was concluded that the contralateral projection was sparse.(ABSTRACT TRUNCATED AT 400 WORDS)

Morphology of physiologically identified second-order vestibular neurons in cat, with intracellularly injected HRP.

The morphology of horizontal canal second-order type I neurons was investigated by intracellular staining with horseradish peroxidase (HRP) and three-dimensional reconstruction of the cell bodies and axons. Axons penetrated in and around the abducens nucleus were identified as originating from type I neurons by their characteristic firing pattern to horizontal rotation and by their monosynaptic response to stimulation of the ipsilateral vestibular nerve. A total of 47 type I neurons were stained. The cell bodies were located in the rostral portion of the medial vestibular nucleus (MVN) and were large or medium sized and had rather elongated shapes and rich dendritic arborizations. The neurons were divided into two groups: those which projected to the contralateral side of the brain stem (type Ic neurons) and those which projected to the ipsilateral side of the brainstem (type Ii neurons). All stem axons of type Ic neurons crossed the midline and bifurcated into rostral and caudal branches in the contralateral medial longitudinal fasciculus (MLF). Two or three collaterals arising close to this bifurcation distributed terminals in a relatively wide area in the contralateral abducens nucleus. Some of these collaterals projected further to the contralateral MVN and thus are vestibular commissural axons. Some of the rostral and caudal stem axons had collaterals which projected to the contralateral nucleus prepositus hypoglossi (PH), nucleus raphe pontis, or medullary reticular formation. There were at least six classes of type Ii neurons, most of which distributed to a relatively limited region in the ipsilateral abducens nucleus and they were categorized according to their future projections into the following categories: A) no further collaterals beyond the abducens nucleus; B) collaterals in the abducens nucleus and a branch descending and terminating in ipsilateral PH; C) projected to the abducens nucleus, PH, and an area rostral to the abducens nucleus; D) projected to the abducens nucleus and to ipsilateral reticular formation rostral and caudal to the abducens nucleus; E) collaterals in the abducens nucleus and a thick caudal stem axon entering and descending in ipsilateral MLF; F) a thick caudal stem axon entering and descending in ipsilateral MLF and no collaterals to the abducens nucleus. Some type Ii neurons also had recurrent collaterals which projected back to the ipsilateral MVN; these may inhibit type II neurons during ipsilateral rotation.

Morphology of single medial vestibulospinal tract axons in the upper cervical spinal cord of the cat.

The morphology of single medial vestibulospinal tract (MVST) axons was investigated by iontophoretic injection of horseradish peroxidase into single axons at the upper cervical cord in pentobarbital-anesthetized cats. MVST axons were identified by their monosynaptic responses to stimulation of the vestibular nerve and their direct responses to stimulation of the medial longitudinal fusciculus (MLF). Reconstructions of the axonal trajectory were made from 22 uncrossed and 19 crossed MVST axons at C1-C4. MVST axons ran in the ventral funiculus and gave rise to multiple axon collaterals to the upper cervical gray matter at different segments. These axons could be traced over the distance of 2.5-15.3 mm. Within these lengths, up to 9 axon collaterals were identified per axon (mean +/- s.d., 3.3 +/- 2.0, n = 41). Axon collaterals ramified in the gray matter several times and spread in a delta-like manner in both the transverse and horizontal planes. There were usually gaps free from terminal arborizations between adjacent axon collaterals, since the rostrocaudal extension of individual axon collaterals (mean = 820 microns) was very much limited in contrast to wide intercollateral intervals (mean = 1,510 microns). Axon terminals were distributed mainly in laminae IX, VIII, and VII, and sometimes in laminae VI-IV. Most abundant terminals were observed in lamina IX, including the ventromedial (VM), the spinal accessory (SA) nuclei and the nucleus dorsomedial to the VM nucleus (DM nucleus). A majority of individual axon collaterals provided some terminal branches to at least one of the above three motor nuclei. Axon collaterals projecting to laminae VIII-VI without terminals in the motor nuclei were rarely observed. Individual MVST axons had a preferential terminal distribution in each motor nucleus, but all three motor nuclei were covered by axon terminals of an ensemble of all MVST axons, indicating that all neck muscles innervated by these three motor nuclei are influenced by vestibular inputs through MVST axons. Most collaterals from a single axon produced circumscribed terminal arborizations in one or two common areas in the transverse plane (mainly in lamina IX) that were in line with one another in the longitudinal axis of the cord. This longitudinal arrangement of discontinuous terminal arborizations in lamina IX from a single axon may correspond to a continuous sagittal column of motoneurons for a particular muscle.(ABSTRACT TRUNCATED AT 400 WORDS)

Anatomy of physiologically identified eye-movement-related pause neurons in the cat: pontomedullary region.

Pause neurons (PNs) are inhibitory neurons close to the midline at the pontomedullary junction that fire tonically and then cease firing just prior to quick eye movements of visual or vestibular origin. Previous physiological evidence has shown that these neurons have a role of central importance in the generation of rapid eye movements in any direction and all major models of ocular motor control incorporate PNs as major elements. In this study in cats, we injected horseradish peroxidase intracellularly into somata or axons of physiologically identified PNs. After appropriate tissue preparation, cell body and axonal reconstructions were performed, with the aid of a camera lucida-equipped microscope. Fifty-three PNs were stained and reconstructed. These consisted of 17 cell bodies and dendrites and 36 axons. Seven of these included both cell bodies and axons. PN somas lay close to the midline in the nucleus raphe pontis and centralis superior, had extensive dendritic arborizations tending to arise from either pole of the elongated soma, and had axons which typically crossed the midline and bifurcated into long branches which extended rostrally and caudally, inferior to the medial longitudinal fasciculus. There were major terminal arborizations and boutons in areas just rostral and caudal to the abducens nucleus in areas where two types of premotor neurons, excitatory and inhibitory burst neurons, are concentrated. Many axosomatic contacts were noted. Other terminal arborizations and boutons were found close to the midline in a region rostral to abducens nucleus containing other neurons known to burst prior to quick eye movements, and in the nucleus reticularis gigantocellularis. Rostral stem axons could be traced to the level of the trochlear nucleus and inferior to the medial longitudinal fasciculus. The caudal stem axons could be traced parallel to the midline and inferior to the medial longitudinal fasciculus and as far caudally as the hypoglossal nucleus.

Anatomical evidence of the projection of pontine omnipause neurons to midbrain regions controlling vertical eye movements.

Both anatomical and physiological studies have shown that pause neurons (PNs) in the medial pontine reticular formation project to two groups of burst neurons (BNs) involved in the genesis of horizontal saccadic eye movements: The excitatory burst neurons (EBNs), which lie rostral to the abducens nucleus, and the inhibitory burst neurons (IBNs), which lie caudal to the abducens. This study is concerned with the projection from PNs to a group of vertical BNs in the nucleus of the H field of Forel (H FF) in the caudomedial subthalamus. Three anatomical methods were used to demonstrate this connection. First, intra-axonal horseradish peroxidase (HRP) injection into physiologically identified PN axons demonstrated axonal branching and axonal terminations in and around the H FF. Second, micro-injection of the tracer Phaseolus vulgaris leucoagglutinin (PHA-L) into the pontine PN region labelled terminal axons and boutons in the nucleus of the H FF. Third, extracellular pressure injection of HRP into H FF yielded retrogradely labelled pontine PN neurons. These anatomical results confirmed the termination of PNs in areas controlling rapid vertical eye movements as physiologically demonstrated by Nakao et al.: Exp. Brain Res. 70:632-636, '88). This work points to the major role of pontine PNs in the synchronization of BN activity in rapid eye movements in all directions.

Preventive action of quisqualic acid against grayanotoxin-induced suppression of locomotor activity in mice.

Grayanotoxin-III (GTX-III) is a constituent in leaves of Pieris japonica D. Don which exhibits, in vitro, the ability to open voltage-sensitive sodium channels in various excitable tissues. Effects of systemic administration of GTX-III were studied in vivo using Std-ddy mice. Salivation, vomiting and paralysis of the hind paws invariably occurred in mice injected intraperitoneally with 0.1 or 0.25 mg/kg of GTX-III. The writhing response to an intraperitoneal injection of acetic acid was considerably diminished by pretreatment of animals with the toxin. The grayanoid also caused a profound attenuation of the response to caudal compression, while inducing no significant alteration of that to thermal injury. Pretreatment with GTX-III resulted in a significant decrement of the time required for loss of the righting reflex induced by pentobarbital, with a concomitant delay in recovery. Mice injected with the toxin exhibited a significant and restorable suppression of coordination, and a long-lasting suppression of spontaneous locomotor activity in both horizontal and vertical directions. Neither tetrodotoxin (1-5 micrograms/kg, i.p.) nor Ro15-1788 (1-5 mg/kg, i.p.) prevented the GTX-III-induced suppression of locomotion. Atropine (5-10 mg/kg, i.p.) failed to antagonize the GTX-III-induced suppression but protected against salivation induced by the toxin without affecting other symptoms. Intracerebroventricular injection of quisqualic acid (0.5 microgram), one of the agonists for central glutamate receptors, but not that of tetrodotoxin (5 ng) prevented the GTX-III-induced suppression of horizontal movement. These results suggest that GTX-III may elicit its depressant action on horizontal locomotion possibly through interacting with central glutamatergic neurons rather than activating voltage-sensitive sodium channels in the brain. Possible involvement of muscarinic cholinergic neurons in the GTX-III-induced salivation is also suggested.

Comparison of the branching patterns of lateral and medial vestibulospinal tract axons in the cervical spinal cord.

The morphology of single physiologically-identified lateral and medial vestibulospinal tract (LVST and MVST) axons was analysed, using intracellular staining with horseradish peroxidase (HRP) and three-dimensional reconstruction of axonal trajectories in the cat. Axons were penetrated in the cervical cord at C1-C8 with a microelectrode filled with 7% HRP. These axons were identified as vestibulospinal axons by their monosynaptic responses to stimulation of the vestibular nerve and further classified as either LVST or MVST axons by their responses to stimulation of the LVST and MVST. The stained axons could be traced over distances of 3-16 mm rostrocaudally. Within these lengths, both LVST and MVST axons were found to have multiple axon collaterals at different segments in the cervical cord. Up to seven collaterals were given off from the stems of MVST axons and LVST axons. The LVST axons included both neurones terminating at the cervical cord and those projecting further caudally to the thoracic or lumbar cord. Each collateral of these LVST axons, after entering into the gray matter, ramified successively in a delta-like fashion and terminated mainly in lamina VIII and in the medial part of lamina VII. Many boutons of both terminal and en passant types seemed to make contact with the cell bodies and proximal dendrites of neurones in the ventromedial nucleus (VM). Each collateral had a narrow rostrocaudal extension (0.2-1.6 mm, average 0.8 mm) in the gray matter in contrast to a much wider intercollateral interval (average 1.5 mm), so that there were gaps free from terminal boutons between adjacent collateral arborizations. The morphology of axon collaterals of MVST axons was very similar to that of LVST axons. The rostrocaudal extent of single axon collaterals was very restricted (0.3-2.1 mm) in contrast to the wide spread in a mediolateral or a dorsoventral direction. MVST axons had intensive projections to the upper cervical cord with multiple axon collaterals. One to seven collaterals of single MVST axons were found at C1-C3. Terminals of MVST axons were distributed in laminae VII, VIII and IX, including the VM, the nucleus spinalis n. accessorii (SA), and the commissural nucleus. Many terminals seemed to make contact with retrogradely-labelled motoneurones of neck muscles. Both axosomatic and axodendritic contacts were observed on motoneurones in various sizes. Some collaterals gave rise to terminal arborizations in both the VM and the SA. These results suggest that single LVST and MVST axons may control excitability of multiple dorsal axial muscles concurrently with their multiple axon collaterals at multisegmental levels.

Effects of ifenprodil on the N-methyl-D-aspartate receptor ionophore complex in rat brain.

The effects of a cerebral anti-ischemic drug ifenprodil on the receptor ionophore complex of an N-methyl-D-aspartate (NMDA)-sensitive subclass of central excitatory amino acid receptors were examined using [3H](+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10- imine (MK-801) binding in rat brain synaptic membrane preparations as a biochemical measure. The binding in membrane preparations not extensively washed was markedly inhibited not only by competitive NMDA antagonists such as (+/-)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic, D-2-amino-5-phosphonovaleric and D-2-amino-7-phosphonoheptanoic acids, but also by competitive antagonists at the strychnine-insensitive glycine (Gly) site including 7-chlorokynurenic acid and 6,7-dichloroquinoxaline-2,3-dione. Among several proposed ligands for alpha-adrenergic receptors tested, ifenprodil most potently inhibited the binding in these membrane preparations due to a decrease in the density of the binding sites without significantly affecting the affinity. Ifenprodil also inhibited the binding of [3H]N-[1-(2-thienyl)cyclohexyl]piperidine as well as of [3H]MK-801 to open NMDA channels in a concentration-dependent manner at concentrations above 10 nM in membrane preparations extensively washed but not treated by a detergent, with a Hill coefficient of less than unity. Further treatment of extensively washed membrane preparations with a low concentration of Triton X-100 resulted in an almost complete abolition of [3H]MK-801 binding, and the binding was restored to the level found in membrane preparations not extensively washed following the addition of both L-glutamic acid (Glu) and Gly. Ifenprodil was effective in inhibiting [3H]MK-801 binding via reducing both initial association and dissociation rates in Triton-treated membrane preparations, irrespective of the presence of Glu and Gly added. The binding in Triton-treated membrane preparations was additionally potentiated by the polyamine spermidine in a concentration-dependent manner at concentrations above 10 microM in the presence of both Glu and Gly at maximally effective concentrations. Ifenprodil invariably diminished the abilities of these three stimulants to potentiate [3H]MK-801 binding at concentrations over 1 microM in a manner that the maximal responses each were reduced. These results suggest that ifenprodil does not interfere with the NMDA receptor complex as a specific isosteric antagonist at the polyamine domain in contrast to the prevailing view.

High concentrations of calmodulin antagonists inhibit accumulation and binding activities of [(3)H]glutamate in rat brain.

Sodium- and energy-dependent accumulation of [(3)H]l-glutamic acid (Glu) into rat cerebral cortical slices was inhibited by relatively high concentrations (40-100 ?M) of calmodulin antagonists, such as N-(6-aminohexyl)-1-naphthalenesulfonamide and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, in concentration-dependent and noncompetitive manners. The latter antagonist not only diminished the basal binding activity of [(3)H]Glu in synaptic membranes of the rat brain, but also eliminated the activities found in the presence of Cl(?) and Cl(?)/Ca(2+) ions. However, N- methyl- d -aspartate-sensitive [(3)H]Glu binding was not affected by these antagonists. These results suggest the possible involvement of the calmodulin system in glutamatergic neurotransmission in the brain.

Possible interaction of [(3)H]glutamate binding sites with anion channels in rat neural tissues.

The effect of various ions on [(3)H]l-glutamic acid (Glu) binding was examined using crude synaptic membrane preparations from the rat brain. In vitro addition of sodium acetate (1-100 mM) exhibited a significant enhancement of the binding in a concentration dependent manner. Ammonium chloride (20 mM) prevented the potentiation by sodium acetate at 2 degrees C, whereas sodium acetate exerted an inhibitory action on the ammonium chloride-induced augmentation of the binding at 30 degrees C. Ammonium chloride (1-100 mM) itself elicited a temperature dependent stimulation of the binding, which was invariably attenuated by an antagonist for the anion channels such as picrotoxinin (10(?3) M) as well as by inhibitors of anion transport including ethacrynic acid (10(?3) M) and 4,4?-diisothiocyanatostilbene-2,2?-disulfonic acid (10(?4)?10(?3) M), respectively. The later two inhibitors also caused a significant additional raise of the sodium acetate-induced enhancement of the binding. A significant augmentation of the binding resulted from the addition (20 mM) of various anions known to penetrate the anion channels such as bromide, iodide, nitrate, bicarbonate and thiocyanate in a permeability related manner, while that of non-permeable anions including fluoride, sulfate, acetate, formate, phosphate, oxalate, lactate, succinate and tartarate had no such a profound effect on the binding. Addition of d-aspartic acid resulted in the complete abolition of the Na(+)-dependent binding while sparing the Cl(?)-dependent binding. Scatchard analysis revealed that Cl(?) ions induced a two-fold increase in the number of the binding sites without affecting their affinity, whereas Na(+) ions reduced the affinity with a concomitant increase of the number of the binding sites. Addition of quisqualic acid (10(?5)?10(?3) M) inhibited the Cl(?)-dependent binding of [(3)H]Glu to a significantly greater extent than the inhibition on Na(+)-dependent binding. N- Methyl- d -aspartic acid and kainic acid exerted no preventive action on the basal, Cl(?)-dependent and Na(+)-dependent binding. respectively. The highest basal binding activity was found in the retina among various central structures examined. A significant basal binding activity of [(3)H]Glu was also detected in the pituitary and adrenal but not in the kidney. Chloride ions exhibited a significant facilitation of [(3)H]Glu binding to central regions without altering that to peripheral tissues such as pituitary and adrenal. In contrast, Na(+) ions induced significant attenuation of the binding to the pituitary, adrenal and retina despite the occurrence of augmentation of the binding to other central structures. These results suggest the Glu binding sites may be linked to the anion channels in the rat central nervous system and that this linkage may be absent from the pituitary, adrenal and retina.

Profiles of [3H]N-[1-(2-thienyl)cyclohexyl]piperidine binding in brain synaptic membranes treated with Triton X-100.

Binding of [3H]N-[1-(2-thienyl)cyclohexyl]piperidine (TCP) was examined using rat brain synaptic membranes treated with a low concentration of Triton X-100. This compound is assumed to be a non-competitive antagonist for the N-methyl-D-aspartate(NMDA)-sensitive subclass of central excitatory amino acid receptors. Binding was quite low but detectable in Triton-treated membranes irrespective of the incubation temperature, and the temperature-dependent portion of the binding was greatly reduced in these Triton-treated membranes. However, binding was drastically potentiated by the inclusion of L-glutamate and its analogous amino acids in a concentration-dependent manner at a concentration range of 10 nM to 0.1 mM. Agonists for the NMDA-sensitive subclass also potentiated binding, with agonists for the other subclasses being ineffective. Glycine at a concentration above 10 nM was not only effective as a stimulant of potentiated binding by glutamate, but was also active in enhancing binding in the absence of added glutamate. Glycine increased both the association and dissociation rates without significantly affecting the dissociation constant. Pharmacological profiles of binding in Triton-treated membranes were not significantly different from those in untreated membranes, except for that of haloperidol. Haloperidol is proposed to be highly selective for brain sigma-receptors on the basis of a potent inhibition of sigma-receptor binding. The inhibitory potency of this sigma-ligand was markedly attenuated in the presence of both glutamate and glycine in Triton-treated membranes, as compared with that in untreated membranes. These results suggest that [3H]TCP binding in Triton-treated membranes is a useful biochemical tool to evaluate predominantly the activated state of ion channels associated with the NMDA-sensitive receptors in terms of freedom from the confounding effects of endogenous amino acids.

Tetrodotoxin-insensitive central depression by grayanotoxin-III in mice.

The effect of systemic administration of grayanotoxin (GTX)-III, a constituent in leaves of Pieris japonica D. Don with an ability to activate the voltage-sensitive sodium channels in excitable tissues, on general behaviors of animals was studied using Std-ddy mice. Intraperitoneal administration of the toxin (0.1-0.25 mg/kg b. wt.) resulted in a dose-dependent manner in a significant and reversible muscle relaxation, and a profound and long lasting (greater than or equal to 60 min) depression of locomotor activity. Pretreatment with GTX-III caused a profound potentiation of the duration of loss of righting reflex by pentobarbital with a concomitant delay of the onset of convulsive seizures by various convulsants such as strychnine, picrotoxin and pentetrazol. Neither tetrodotoxin (1-5 micrograms/kg, i.p.) nor Ro15-1788 (1-5 mg/kg, i.p.) prevented the GTX-III-induced suppression of locomotor activity. These results suggest that GTX-III may elicit a central depressant action in mice through a molecular mechanism other than activation of the voltage-sensitive sodium channels in the brain.

Progressive sensorineural hearing impairment in professional fishery divers.

There have been many reports of a high rate of hearing impairment in divers. A prospective study was performed to determine whether sensorineural hearing acuity in the same divers deteriorated faster than in a normal population as they continued diving. After an observation period of approximately 5 years, audiometric examination was performed on a group of professional fishery divers who had normal hearing or sensorineural hearing loss at the time of initial study. Thirty-three ears of 18 divers were included in statistical analyses. The average hearing deterioration in the divers in 5 years, after elimination of the aging effect, was 6.6 dB (SD 4.5) and was statistically significant. We concluded that the hearing acuity of our subjects deteriorated faster than that of normal Japanese.

Schwannoma of the posterior pharyngeal wall: a case report.

Schwannoma arising in the posterior pharyngeal wall is rare. We report on a 60-year-old man who complained of discomfort in his pharynx, from whom a tumour was excised via an intraoral approach. No recurrence was seen after an 11-year follow-up. The nerve origin of the tumour is most likely to be the peripharyngeal plexus. This is the third such case reported.

[Exostosis of the external auditory canal and sensorineural hearing loss in professional divers].

Audiometric survey and endoscopic study of the external auditory canal were performed on a group of 31 professional divers, all of whom had experienced frequent exposure to dysbaric conditions. The results are as follows. 1) Over 40% had exostosis of the external auditory canal. There was no relationship between the incidence of the exostosis and the length of their occupational career as a diver. Many of the divers had hearing loss whether they had exostosis or not. 2) Over 70% had sensorineural hearing loss, taking into account hearing loss due to aging. Most had no experience of inner ear barotrauma on descent, causing sudden a shift in hearing threshold. Deafness was related to the length of their occupational career as a diver. In conclusion, we speculate that repetitive small changes in barometric pressure on the outer ear influences the pressure on the middle ear and further on that of the perilymph, finally damaging the inner ear auditory system.

[Clinical study in vertiginuous patients suspected of having neurovascular compression syndrome of the eighth cranial nerve].

Neurovascular compression syndrome of the 5th and 7th cranial nerves has been recognized as the cause of trigeminal neuralgia and hemifacial spasm. On the other hand, it is still difficult to diagnose vertigo as neurovascular compression syndrome of the 8th cranial nerve. To detect some specific finding in this syndrome of the 8th cranial nerve, 5 patients with vertigo with hemifacial spasm were examined for the clinical course and neuro-otological features. In all patients MRI and/or angiography suggested vascular compression against the 8th cranial nerve. The clinical courses of these patients revealed various symptoms resembling benign paroxysmal positional vertigo, vestibular neuronitis and Meniere's disease. Audiograms showed two normal hearing patterns, bilateral high frequency hearing loss probably due to aging in one case, bilateral C5-dip in one and fluctuating unilateral hearing loss like Meniere's disease in one. The prolongation of IPL I-III on auditory brainstem response proposed as a criterion by Møller was detected in one case. No response in the caloric test was found in two cases. These abnormalities in the auditory brainstem response and caloric test appeared to be useful for diagnosis but were uncommon findings in all cases. Electronystagmographic examinations including the eye tracking test, optokinetic nystagmus and optokinetic pattern were all normal. We could not find any specific clinical findings valuable for diagnosis of neurovascular compression syndrome of the 8th cranial nerve. It is proposed that the indication of microvascular decompression should be decided carefully.

[A case of rhinosporidiosis].

Rhinosporidiosis is due to fungal infection by Rhinosporidium seeberi, which affects predominantly the mucous membrane of the nose and nasopharynx. This disease is characterized by the formation of papillomatous and polypoid lesions and is known to be endemic in India and Sri Lanka. The first case of rhinosporidiosis in Japan is reported in this paper. A 25-year-old male Indian, born in India, living in Japan for a year, visited the outpatient clinic complaining of nasal obstruction and swallowing pain. A friable, irregular, reddish polypoid mass was found in the right nasal cavity. Endoscopy as well as plain X-ray and CT examination showed that the mass originated from the right inferior turbinate and extended into the choana without any sign of bone destruction. The mass removed under general anesthesia showed the typical feature of rhinosporidiosis, that is, papillomatous hyperplasia of the mucosa with sporangia full of spores in different stages of development. One year after treatment, no relapse has been seen in this case.