Neurogenic vestibular evoked potentials using a tone pip auditory stimulus

OBJECTIVES: To obtain neurogenic vestibular evoked potentials (NVESTEPs) with surface scalp recording using a tone pip auditory stimulus. METHODS: Fourteen neurologically normal volunteers (Age range 26-45 years, 10 females and 4 males), and two patients with sensorineural hearing loss and possible multiple sclerosis respectively, were examined. Two channel recordings were obtained, the first channel being P3 referred to Fpz, and the second channel being P4 referred to Fpz. A 1 kHz tone pip stimulus with two cycles was delivered via headphones monoaurally with contralateral masking noise. RESULTS: A consistent negative wave with a mean absolute latency of 4.72 msec was obtained, which we have named N5. 25% of the ears tested had better responses at the ipsilateral parietal electrode. In the patient with bilateral sensorineural hearing loss, NVESTEPs was present, suggesting that the NVESTEP is not a cochlear response. In the patient with possible multiple sclerosis, an abnormal NVESTEP response and a normal BAEP response were found. CONCLUSION: Use of a tone-pip rather than a click auditory stimulus allows a lower click intensity to be used in the production of NVESTEP responses, leads to a shorter testing time, and is therefore more comfortable for the patient. This study adds to our impression that the NVESTEP may be a physiological response that can be used to assess the vestibular system and is different from the BAEP response. Further testing in patients with symptoms of dizziness and with disorders specific for the vestibular nerve is required.     

Parallel auditory vestibular evoked neurogenic and myogenic potential results in a case of peripheral vestibular dysfunction, showing that the former originates from the vestibular system

PURPOSE: Vestibular evoked myogenic potentials (VEMPs) uses high intensity clicks with recording from the tonically active sternocleidomastoid muscle, taking advantage of the close proximity of the saccule to the oval window. Our group has used the same stimulus to record Vestibular Evoked Neurogenic Potentials (VENPs) directly from the brain. VEMPs are now regarded the electrophysiological gold standard in peripheral vestibular system examination. We present a case of peripheral vestibular dysfunction to show that both VEMPs and VENPs provide similar results during recovery. METHODS: A case of Meniere's Disease in recovery is examined. VEMPs were recorded using a 105 dB nHL click stimulus from the ipsilateral sternocleidomastoid muscle. VENPs were recorded using an ipsilateral parietal to Fpz montage and a 1 kHz tone-pip stimulus. Standard BAEPs and threshold latency series (TLS) were performed. RESULTS: VEMP and VENP were unobtainable from the left side at initial presentation in a patient with Meniere's Disease, with normal BAEP and TLS bilaterally. After one month of therapy both the VEMP and VENP normalized. CONCLUSIONS: As VEMPs are known to originate from the vestibular system, the parallel VENP result suggests the same for the latter VENP may prove to be useful and complement VEMP in determining vestibular dysfunction.     

Responses of guinea pig primary vestibular neurons to clicks

Responses of single neurons in the vestibular nerve to high-intensity clicks were studied by extracellular recording in anaesthetised guinea pigs. One hundred and two neurons in the posterior division of the superior branch or in the inferior branch of the vestibular nerve were activated at short latency by intense clicks. The latency of activation was short (median 0.9 ms) and the threshold was high: the click intensity for evoking the response of these cells was around 60 dB above the auditory brainstem response threshold. Animals were tilted and rotated to identify physiologically the sensory region of the labyrinth from which the activated neurons originated. Seventeen neurons responded to static tilt as well as clicks. These results show that vestibular receptors, probably the otoliths, respond to clicks at intensities corresponding to those used in a new clinical test of the vestibulo-collic pathway.     

Vestibular symptoms and signs are correlated with abnormal neurogenic vestibular evoked potentials in patients with multiple sclerosis

OBJECTIVES: Symptoms of disequilibrium in multiple sclerosis (MS) are common. Neurogenic vestibular evoked potentials (NVsEPs) are saccular responses to tone-pip acoustic stimuli and are recordable from the parietal areas ipsilaterally to the stimulated ear. We wished to determine possible correlations of abnormal findings in NVsEP with clinical neurological findings related to the vestibular system, and demyelination seen on MRI. PATIENTS AND METHODS: NVsEPs were performed by delivering a 1 kHz tone-pip stimulus monoaurally with contralateral masking noise via headphones. Brainstem auditory evoked potentials were performed in the standard manner. RESULTS: Thirty-three patients had either been diagnosed with MS or had possible MS. There is statistical evidence that the presence of symptoms is likely to give an abnormal NVsEP, but no correlation exists between the presence or absence of vestibular symptoms and signs and an abnormal BAEP. No correlation was found between the presence of brainstem lesions on MRI and an abnormal NVsEP. Correlation exists between abnormal NVsEP and the level of disability using Expanded Disability Status Scale scores. CONCLUSION: We have found that with increasing involvement of abnormal NVsEPs, there is a significant correlation with symptoms and signs that can be referred to the vestibular system.     

Brainstem auditory evoked responses that disappear during sleep: a possible manifestation of a neurogenic vestibular evoked response

OBJECTIVE: To present a case of unilateral hearing loss in which a brainstem auditory evoked potential (BAEP) disappeared during sleep on the symptomatic side, and to argue that this may actually be a manifestation of a neurogenic vestibular evoked potential (NVESTEP). MATERIAL AND METHOD: Brainstem auditory evoked potentials were performed in the standard manner. RESULT: A poorly organized response was obtained during wakefulness on the symptomatic side that resembled a BAEP. The BAEP for the right ear was better organized. During sleep, the response for the left ear disappeared. CONCLUSIONS: The poor organization of the response of the left ear compared to the right, and its disappearance during sleep, suggests that the response for the left ear was actually an NVESTEP and not a BAEP. The possibility of recording vestibular responses with auditory stimuli may have important implications for BAEP examinations performed during wakefulness that may lead to false negative results, in neonatal screening for hearing loss that use tone stimuli, and also in brain mapping using magnetic resonance imaging (MRI) and positron emission tomography (PET) relating to the auditory cortex.     

Comparative study of evoked potentials in multiple sclerosis and neuro-Beh?et's syndrome

We studied somatosensory evoked potentials (SEPs) and brainstem auditory evoked potentials (BAEPs) in Japanese patients with multiple sclerosis (MS) and those with neuro-Behcet's disease (NB). Abnormal cortical P37 of posterior tibial nerve SEPs or cervical N13 of median nerve SEPs were more frequently found in the MS patients than in the NB patients. On the other hand, prolongation of the central conduction time of median nerve SEPs or abnormal BAEPs were more common in NB than in MS. The present data showed that lesions were mainly present in the spinal cord in MS and in the brainstem in NB. SEPs and BAEPs were considered of great value for detecting the involvement of the central nervous system in MS and NB and distinguishing between these diseases.     

Action of the efferent vestibular system on primary afferents in the toadfish, Opsanus tau

Spinalized toadfish were held in a lucite chamber and perfused through the mouth with running seawater. Primary vestibular afferents and vestibular efferent axons and somas were studied with glass microelectrodes. Vestibular semicircular canal afferent and efferent axons were visually identified and penetrated with glass microelectrodes. Afferents responded to pulses of injected current with trains of action potentials, whereas efferents responded with only a single spike. This differential response to injected current served to further distinguish these two classes of nerve fibers that share the same canal nerve for part of their course. When current pulses were injected into efferent somadendritic recording sites, cells responded with trains of action potentials similar to those seen in other central nervous system neurons. Semicircular canal afferents were spontaneously active and occupied the same spectrum of regularity as vestibular afferents recorded in other species. Behavioral arousal evoked by lightly touching the fish on the snout or over the eye resembled spontaneous arousal observed in the field and consisted of eye withdrawal, fin erection, and attempted swimming. Efferent vestibular neurons were spontaneously active and increased their frequency of discharge when the fish was behaviorally aroused. Most efferents were briskly activated by behavioral arousal, but the time constant of the decay of their responses was variable ranging from 100 to 600 ms. Not only touch, but multimodal stimuli were capable of increasing the level of spontaneous activity of efferent vestibular neurons. The shortest latency to behavioral activation was 160 ms. Vestibular primary afferents also manifested increase in neuronal activity with behavioral activation. Irregularly discharging afferents were much more responsive than regularly discharging afferents. One rare case of transient inhibition in a regularly discharging afferent is illustrated. Severing the efferent vestibular nerve blocked behavioral activation in vestibular primary afferents. Electrical stimulation of the efferent vestibular nerve produced excitatory postsynaptic potentials (EPSPs) at latencies within the monosynaptic range in vestibular primary afferents. These monosynaptic EPSPs could produce action potentials in primary afferents or could sum with subthreshold depolarizations produced by current passed through the microelectrode to initiate impulses.(ABSTRACT TRUNCATED AT 400 WORDS)     

Vertigo and imbalance caused by a small lesion in the anterior insula

The exact location of the vestibular cortex in humans has not yet been established. Isolated lesions in the insula are exceptional. We describe a patient with recurrent episodes of vertigo and imbalance following a small lesion in the anterior insula. Myogenic and neurogenic vestibular evoked potentials were both performed using auditory stimuli. The former was recorded from the sternocleidomastoid muscle and the latter from the parietal areas on the scalp. Brainstem auditory evoked potentials, threshold latency series, pure tone audiometry and video nystagmography were also performed, as was brain MRI. All evoked potential studies and pure tone audiometry were within normal limits, ruling out peripheral and brainstem causes for the patient's symptoms. Video nystagmography revealed high slow phase velocities bilaterally with caloric stimulation, and saccadic tracking on the smooth pursuit examination. The MRI revealed a small lesion in the right anterior insula. To our knowledge this is the first reported case of vestibular symptoms and signs from a lesion in the anterior insula on MRI. In addition, its effects on the nystagmogram suggest that this area may be part of the pathway that controls smooth pursuit.     

Click-evoked responses in vestibular afferents in rats

Sound activates not only the cochlea but also the vestibular end organs. Research on this phenomenon led to the discovery of the sound-evoked vestibular myogenic potentials recorded from the sternocleidomastoid muscles (cervical VEMP, or cVEMP). Since the cVEMP offers simplicity and the ability to stimulate each labyrinth separately, its values as a test of human vestibular function are widely recognized. Currently, the cVEMP is interpreted as a test of saccule function based on the assumption that clicks primarily activate the saccule. However, sound activation of vestibular end organs other than the saccule has been reported. To provide the neural basis for interpreting clinical VEMP testing, we employed the broadband clicks used in clinical VEMP testing to examine the sound-evoked responses in a large sample of vestibular afferents in Sprague-Dawley rats. Recordings were made from 924 vestibular afferents from 106 rats: 255 from the anterior canal (AC), 202 from the horizontal canal (HC), 177 from the posterior canal (PC), 207 from the superior vestibular nerve otolith (SO), and 83 from the inferior nerve otolith (IO). Sound sensitivity of each afferent was quantified by computing the cumulative probability of evoking a spike (CPE). We found that clicks activated irregular afferents (normalized coefficient of variation of interspike intervals >0.2) from both the otoliths (81%) and the canals (43%). The order of end organ sound sensitivity was SO = IO > AC > HC > PC. Since the sternocleidomastoid motoneurons receive inputs from both the otoliths and the canals, these results provide evidence of a possible contribution from both of them to the click-evoked cVEMP.     

Intracellular study of frog's vestibular neurons in relation to the labyrinth and spinal cord

Summary Field and intracellular potentials were recorded in the vestibular nuclei of the frog following stimulation of the anterior branch of the ipsilateral vestibular nerve and the spinal cord. The field potential induced by stimulation of the vestibular nerve consisted of an early positive-negative wave followed by a slow negativity and that recorded during spinal cord stimulation was composed of an antidromic potential followed by a slow negative wave. These potentials were most prominent in the ventral region of the stato-acoustic complex. Mono- and polysynaptic EPSPs were recorded from vestibular neurons following vestibular nerve stimulation. Short latency depolarizations of small amplitude preceded the monosynaptic EPSPs in some neurons. Spike-like partial responses were commonly superimposed on the EPSPs. These all-or-none depolarizations probably originated in the dendrites. In a group of vestibular neurons stimulation of the vestibular nerve evoked full action potentials with latencies ranging from 0.2 to 1.1 msec. They are presumably caused by antidromic activation of neurons which send their axons to the labyrinth. The presence of efferent neurons in the vestibular nuclei was confirmed by their successful staining with Procion Yellow following axonal electrophoresis.After stimulation of the spinal cord, antidromic spike potentials and EPSPs were recorded in vestibular neurons. In addition, short-latency depolarizing potentials (EDPs) were evoked by spinal stimulation, with latencies similar to those of antidromic potentials. The EDPs are suggested to be induced by electrotonic transmission from the neighboring cell and likely to be active spike potentials produced at some distance away from the soma.     

Response of guinea pig vestibular nucleus neurons to clicks

Responses of single neurons in the vestibular nuclei to clicks were studied by extracellular recording in anaesthetised guinea pigs. Eighty-four neurons in the ipsilateral vestibular nuclei were activated with an average latency of 1.75±0.30 ms, which is about 0.9 ms longer than the mean latency of activation of click-sensitive vestibular afferents to intense clicks. The threshold of clicks for evoking the response of these neurons was around 70 dB above the auditory brainstem response threshold. Earlier studies have indicated that click-sensitive vestibular afferents are tilt-sensitive and likely to originate from saccular receptors, and in the present study nine of the click-sensitive vestibular nucleus neurons were tilt-sensitive, suggesting that these central neurons receive monosynaptic input from the corresponding saccular afferents. Recording sites were marked by means of iontophoretic injection of FCF green dye; they were located in the lateral portion of the descending vestibular nucleus and the caudal and ventral regions of the lateral vestibular nucleus.     

Abnormal brainstem evoked potentials in diabetes mellitus. Evoked potential testings and magnetic resonance imaging

Brainstem auditory evoked potentials (BAEPs) and median nerve somatosensory evoked potentials (MN-SEPs) were measured in 53 diabetic patients. Magnetic resonance imaging (MRI) was performed 12 patients with abnormal BAEPs and/or MN-SEPs in order to confirm the existence of lesions in the central nervous system. Twenty-six percent of the diabetic patients had abnormal BAEPs and three had a prolongation of the central conduction time in the MN-SEPs. MRI findings of ten of the 12 patients with abnormal BAEPs or MN-SEPs showed multiple small lesions in the pons, thalamus, and centrum semiovale etc. Two of them showed small lesion in the pontine basis which could induce prolonged interpeak latencies of BAEPs. Our MRI study might suggest that abnormal brainstem evoked potentials in diabetic patients were induced by diabetic macroangiopathy or microangiopathy.     

Expansion of afferent vestibular signals after the section of one of the vestibular nerve branches

The anterior branch of N. VIII was sectioned in adult frogs. Two months later the brain was isolated to record in vitro responses in the vestibular nuclei and from the abducens nerves following electric stimulation of the anterior branch of N. VIII or of the posterior canal nerve. Extra- and intracellularly recorded responses from the intact and operated side were compared with responses from controls. Major changes were detected on the operated side: the amplitudes of posterior canal nerve evoked field potentials were enlarged, the number of vestibular neurons with a monosynaptic input from the posterior canal nerve had increased, and posterior canal nerve stimulation recruited stronger abducens nerve responses on the intact side than vice versa. Changes in the convergence pattern of vestibular nerve afferent inputs on the operated side strongly suggest the expansion of posterior canal-related afferent inputs onto part of those vestibular neurons that were deprived of their afferent vestibular input. As a mechanism we suggest reactive synaptogenesis between intact posterior canal afferent fibers and vestibularly deprived second-order vestibular neurons.     

Responses of neurons of lizard's,lacerta viridis,vestibular nuclei to electrical stimulation of the ipsi- and contralateral VIIIth nerves

Summary Field and intracellular potentials were recorded in the vestibular nuclei of the lizard following stimulation of the ipsi-and contralateral vestibular nerves. The field potentials induced by ipsilateral VIIIth nerve stimulation consisted of an early negative or positive-negative wave (presynaptic component) followed by a slow negativity (transsynaptic component). The spatial distribution of the field potential complex closely paralleled the extension of the vestibular nuclei. Mono- and polysynaptic EPSPs were recorded from vestibular neurons after ipsilateral VIIIth nerve stimulation. In some neurons early depolarizations preceded the EPSPs. These potentials may be elicited by electrical transmission. Often spikelike partial responses were superimposed on the EPSPs. It is assumed that these potentials represent dendritic spikes.Contralateral VIIIth nerve stimulation generated disynaptic and polysynaptic IPSPs in some neurons and EPSPs in others. The possible role of commissural inhibition in phylogeny is discussed.In a group of vestibular neurons stimulation of the ipsilateral VIIIth nerve evoked full action potentials with latencies ranging from 0.25–1.1 msec. These potentials are caused by antidromic activation of neurons which send their axons to the labyrinth.     

The lateral vestibular nucleus of the toadfish Opsanus tau: Ultrastructural and electrophysiological observations with special reference to electrotonic transmission

The lateral vestibular nucleus of the toadfish Opsanus tau was localized by means of axonal iontophoresis of Procion Yellow. The ultrastructure of the lateral vestibular nucleus neurons was then correlated with their electrophysiological properties. The lateral vestibular nucleus consists of neurons of various sizes which are distributed in small clusters over a heavily myelinated neuropil. The perikarya and main dendrites of the large and the small neurons are surrounded by a synaptic bed, which is separated from the neighboring neuropil by a layer of thin astrocytic processes. The synaptic bed contains three main classes of axon terminals, club endings, large and small terminals, the first being quite infrequent. All the large terminals as well as the occasionally observed club endings contain a pure population of rounded synaptic vesicles. In some of the small axon terminals there are also rounded vesicles; however, the majority contain flattened vesicles or a pleomorphic population. These data indicate that the small terminals originate from different afferent sources. The synaptic interfaces of the large boutons and of the club endings bear three types of junctional complexes: attachment plates, gap junctions and active zones. Those showing both gap junctions and active zones were designated as morphologically ‘mixed synapses’. Gap junctions, although in large number, have only been observed at the synaptic interfaces between terminals with rounded vesicles and the perikarya or the dendrite of the lateral vestibular nucleus neurons. Therefore electrotonic coupling would only be possible by way of presynaptic fibers. Some axons observed in the neuropil were found to establish gap junctional complexes with two different dendritec profiles and this observation is in favour of electrotonic coupling by way of presynaptic terminals.Field and intracellular potentials were recorded in the lateral vestibular nucleus. The field potential evoked by stimulation of the vestibular nerve consisted of an early positive-negative wave followed by a slow negativity, and that evoked by spinal cord stimulation was composed of an antidromic potential followed by a slow negative wave. Vestibulo-spinal neurons were identified by their antidromic spikes. In these cells, stimulation of the ipsilateral vestibular nerve evoked an excitatory postsynaptic potential with two components. The short delay of the first component of this excitatory postsynaptic potential and its ability to follow paired stimulation at close intervals without reduction of the second response suggest that it is transmitted electrotonically from primary vestibular afferent fibers. By contrast the latency of the second peak of the vestibular evoked excitatory postsynaptic potential and its sensitivity to high stimulus frequencies are compatible with monosynaptic chemically mediated transmission from primary vestibular afferents. Spinal stimulation evoked graded antidromic depolarizations in vestibulo-spinal neurons. The latency of these potentials was too short to allow for chemical transmission through afferents or recurrent collaterals and suggests electrotonic spread of antidromic activity from neighboring neurons. An important finding is that the graded antidromic depolarizations can initiate spikes; thus coupling between neurons in the lateral vestibular nucleus is sufficiently close that a cell can be excited by activity spread from neighboring cells. Similar graded depolarizations were recorded in identified primary vestibular afferents; their latencies and time course indicate that they were brought about by electrotonic spread of postsynaptic potentials and spikes to the impaled presynaptic fibers; this confirms the morphological evidence that coupling between lateral vestibular nucleus neurons occurs, at least in part, by way of presynaptic vestibular axons. As the spinal stimulus strength was increased, these graded depolarizations became large enough to initiate spikes which presumably propagate to the vestibular receptors. Thus antidromic invasion of the presynaptic terminals may provide negative feedback by preventing their re-excitation at short intervals after a synchronous discharge of an adequate number of postsynaptic cells. Excitatory inputs to the neurons of the lateral vestibular nucleus were identified from the spinal cord and from the contralateral vestibular nerve. Long latency excitatory postsynaptic potentials large enough to excite the cells were recorded following spinal stimulation; the threshold intensity for evoking them was consistently higher than that adequate to generate the graded antidromic depolarizations. Field potentials recorded after stimulation of the contra lateral vestibular nerve consisted of an initial positive negative wave followed by a slow negative wave. the stimulus intensity for evoking these potentials was the same or slightly above the threshold for those evoked in the lateral vestibular nucleus on the stimulated side. Also lateral vestibular nucleus neurons exhibited excitatory postsynaptic potentials large enough to excite the cells following stimulation of the contralateral vestibular nerve. but no inhibitory postsynaptic potentials were detected. This lack of commissural inhibition indicates a qualitative difference between the central organization of these cells in the toadfish and in mammals.The presence of neurons in the lateral vestibular nucleus which send their axons to the labyrinth was confirmed by their heavy staining with Procion Yellow following axonal iontophoresis. In a number of vestibular neurons. abruptly rising spikes were evoked at short latencies after adequate stimulation of the ipsilateral vestibular nerve. Graded stimuli applied to the vestibular nerve evoked graded short latency depolarizations as well as long latency excitatory postsynaptic potentials in these presumed efferent neurons to the labyrinth; the former could indicate electrotonic coupling of the efferent cells or electrotonic transmission from primary afferents, resulting in a short latency feedback loop.From these studies, the synaptic organization of the lateral vestibular nucleus neurons is compared with that of the Mauthner cells of teleosts, and the possibility of a dual mode of transmission, electrical and chemical, by primary vestibular afferents is discussed.     

Effects of intensity of repetitive acoustic stimuli on neural adaptation in the ventral cochlear nucleus of the rat

To study neural adaptation as a function of stimulus intensity, auditory near-field evoked potentials were recorded from the ventral cochlear nucleus in awake Long Evans rats. Responses to 250-ms trains of repetitive clicks (pulse rates ranging from 100 to 1000 pulses per second) were collected at stimulus intensities of 5, 10, 30, 50 and 70 dB SPL. The amplitude of the first negative (N₁) component of the average evoked potentials to individual pulses in the train was measured by using a subtraction method. The N₁ responses were normalized with respect to the highest cochlear nucleus potential observed in the train, and then plotted as a function of click position in the train. As expected, the general trend of the curves was an exponential decay reaching a plateau more or less rapidly as a function of both intensity and rate of stimulation. Fitting these curves with exponential decay equations revealed that the rapid time constant decreased for increasing stimulus intensities whereas the short-term time constant is relatively independent of intensity. The amount of adaptation (expressed as the ratio of the plateau to the first peak amplitude) was substantially less prominent at low intensities (5–10 dB SPL) and low rates (100–200 pulses per second) than at higher intensities and high rates. These results indicate that adaptation patterns obtained in the ventral cochlear nucleus by using near-field evoked potentials exhibit properties comparable to those already present at the level of the auditory nerve.     

Convergence pattern of uncrossed excitatory and inhibitory semicircular canal-specific inputs onto second-order vestibular neurons of frogs

Second-order vestibular neurons of frogs receive converging monosynaptic excitatory and disynaptic excitatory and inhibitory inputs following electrical pulse stimulation of an individual semicircular canal nerve on the ipsilateral side. Here we revealed, in the in vitro frog brain, disynaptic inhibitory postsynaptic potentials (IPSPs) by bath application of antagonists specific for glycine or gamma-aminobutyric acid-A (GABA(A)) receptors. Differences in the response parameters between disynaptic IPSPs and excitatory postsynaptic potentials (EPSPs) suggested that disynaptic IPSPs originated from a more homogeneous subpopulation of thicker vestibular nerve afferent fibers than mono- or disynaptic EPSPs. To investigate a possible size-related organization of these canal-specific, parallel pathways, we combined long-lasting anodal currents of variable intensities with strong cathodal test pulses, to block pulse-evoked responses reversibly in a graded manner according to the size-related sensitivity of vestibular nerve afferent fibers. The anodal current intensity required to block a particular response component was about 15 times lower than the strength of the cathodal test pulse that activated this response component. These large threshold differences were exploited for a selective anodal suppression of the responses from thick vestibular nerve afferent fibers. In fact, response components known to originate exclusively from thick-caliber afferent fibers such as the electrically transmitted monosynaptic EPSP component exhibited the lowest thresholds for cathodal test pulses and were the first to disappear in the presence of small anodal polarization steps. Thresholds for the activation/inactivation of responses and current intensities required for response saturation/blockade were used to assess the fiber spectrum that evoked the different response components. Mono- and disynaptic EPSPs appeared to originate from a broad spectrum of thick and thin vestibular nerve afferent fibers. The spectrum of afferent fibers that activated disynaptic IPSPs on the other hand was more homogeneous and consisted of thick and intermediate fibers. Such a canal-specific and fiber type-related organization of converging inputs of second-order vestibular neurons via feedforward projections was shown for the first time by this study in frogs, but might also prevail in mammals. Similar differences in these feedforward pathways have been proposed earlier in a vestibular side-loop model. Our results are consistent with the basic assumptions of this model and relate to the processing and tuning of dynamic vestibular signals.     

Neurogenic vestibular evoked potentials in the diagnosis of multiple sclerosis

OBJECTIVES: To determine the value of neurogenic vesibular evoked potential (NVESTEP) studies in comparison with other paraclinical tests in demonstrating dissemination in time and space in Multiple Sclerosis (MS) and in identifying clinically silent lesions. METHOD: All patients in whom MS was suspected but the diagnosis of MS was not possible based on the McDonald criteria were included in this study. We studied 14 patients and performed visual, brainstem auditory, somatosensory and neurogenic vestibular evoked potentials in all patients, together with MRI and CSF analysis of oligoclonal bands (OB). RESULTS: Two out of the thirteen patients could be movedfrom the category of "possible MS" to "MS" using the McDonald criteria based on an abnormal NVESTEP result. CONCLUSION: Neurogenic vestibular evoked potentials are potentially useful in identifying clinically silent lesions in patients with possible MS.     

Functional characteristics of the input-output correlation in the vestibular nuclear complex of the frog

Experiments on perfused frog brains were used to record focal and intracellular potentials of neurons in the vestibular nuclear complex produced in response to stimulation of the anterior branch of the ispilateral vestibular nerve and the spinal cord. Stimulation of the vestibular nerve evoked mono- and polysynaptic EPSP with orthodromic action potentials. These were accompanied by recordings of antidromic activation (with a mean latent period of 0.75 sec) of neurons which send their axons into the labyrinth. Antidromic action potentials from vestibular neurons arose with latent periods of the order of 1.43 msec in response to stimulation of the cervical thicknening and 2.19 msec in response to stimulation of the lumbar thickening of the spinal cord. Bursts from the spinal cord often evoked EPSP with orthodromic action potentials in vestibular neurons. The characteristics of the functional correlation between the vestibular input and the vestibulospinal system are discussed. Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 84, No. 10, pp. 1085–1092, October, 1998.     

Directing Attention Toward Stimuli Affects the P300 But Not the Orienting Response

Whether attending to stimuli affects the orienting response and its habituation is not yet clear. EEG alpha suppression responses, electrodermal responses, and EEG evoked potential responses of two groups of subjects were compared. The Attend group was given instructions to pay attention to and count the 59 moderate intensity clicks (interstimulus interval = 15 sec). The Ignore group was instructed to “try not to let the clicks disturb your relaxed state.” Separate ANOVAs with repeated measures were used to evaluate all measures, and all showed significant effects for click repetition (habituation). Alpha suppression and change in log conductance showed no differences related to group. The P300 component of the average evoked potentials was significantly larger for the Attend group. We concluded that attending to, versus ignoring, stimuli does not have an appreciable effect on these two traditional measures of the orienting response, but it does affect the evoked potentials. The relationship between attention and “significance” is discussed.