Analysis of the middle latency evoked potentials to angular acceleration impulses in man

The middle latency vestibular evoked potential (ML-VsEP) recorded with scalp electrodes in man in response to impulses of angular acceleration is dominated by a forehead positive peak at about 15 ms and a negative peak at about 20 ms; the peak to peak amplitude of this component is about 30 microV. This is followed by slower, smaller amplitude activity. The latency of this initial peak is similar to the latency of the vestibulo-ocular reflex (VOR) in monkeys. The present study was undertaken to elucidate the possible relation between the ML-VsEPs and VOR. This included recordings from forehead-mastoid electrodes (sites used to record VsEP) and other scalp electrodes and the recording of potentials due to eye movement: the electro-oculogram. Direct recording of eye movements was also conducted using an infra-red reflection device in those experiments in which the head was not moved. The recordings were conducted in man during vestibular stimulation eliciting VsEPs, during voluntary eye movements and during caloric and optokinetic stimulation. These experiments indicated that the 15-20 ms component of the ML-VsEP was not due to movements of the eye (corneo-retinal dipole). The large amplitude 15-20 ms component of the ML-VsEP was similar in general magnitude, waveform, polarity, duration and rise time to the highly synchronous pre-saccadic spike (neural and/or myogenic) which precedes nystagmus and voluntary saccades. It therefore probably represents vestibular-initiated electrical activity in motor units of the extra-ocular muscles which then produce anti-compensatory saccades.     

Short latency visual evoked potentials in man

Contrary to auditory and somatosensory evoked potentials, surface recorded visual evoked potentials which arise in subcortical neural elements have rarely been described. Considerable disagreement exists between the reports in the literature on such visual potentials. In this study, flash stimuli were used to evoke the potentials which were recorded from the skin overlying the infra-orbital ridge, outer canthus, middle of the forehead, vertex, mastoid ipsilateral to the stimulated eye and inion, using a non-cephalic reference. The potentials were amplified in a band which was chosen to omit slow retinal and cortical potentials, and to enhance activity which might include compound neural activity. Potentials were recorded from 9 subjects (13 eyes), and for each one the effects of eye position and stimulus intensity were studied. The results indicate that the series of components recorded within the first 100 msec following photic stimulation were volume-conducted activity generated by a subset of the visual system which is activated by luminosity changes. The generators of the first 4 or 5 components seem to be situated within the retina, the subsequent components seem to be generated in the optic nerve or tracts, and the later components may be thalamo-cortical in origin. These potentials may complement pattern evoked potentials in a more accurate definition of sites of lesions along the visual pathway.     

Recording of short latency vestibular evoked potentials to acceleration in rats by means of skin electrodes

Short latency (less than 15 msec) vestibular potentials evoked by short and intense acceleration stimuli were recorded in rats by surface electrodes, using electronic filtering and with averaging techniques. The evoked potential is strongly dependent on the direction of rotation and on the angle of the head, and it disappears after labyrinthectomy or sectioning the 8th nerve. All these facts point to its vestibular origin. Although these results were obtained in rats, the importance and the significance of recording a vestibular evoked potential in man is obvious. It would lead to the possibility of objective verification of a vestibular disorder and localization of the lesion.     

Occasional changes in sound location enhance middle latency evoked responses

Rapid processing of sound location is critical for orienting attention. The present study investigated whether contextually sensitive early neural responses elicited by occasional changes in sound location could be measured. Using an oddball paradigm with stimuli consisting of brief noise bursts whose location was occasionally varied using head-related transfer functions, we found significant enhanced negativities in the event-related potentials elicited by deviant stimuli as early as 25 ms after stimulus onset, in addition to the differences around 125 ms which have previously been reported. Recent research suggests that occasional changes in auditory location information are processed in areas beyond primary auditory cortex. Our data suggest that any such processing is in fact preceded by activation in primary auditory cortex.     

Differential characteristics of the middle latency auditory evoked magnetic responses to interstimulus intervals.

OBJECTIVE: The human middle latency auditory evoked magnetic fields were recorded with different interstimulus intervals (ISI) to investigate the differential natures of P30m and the P50m, including whether the P50m source was spatially different or not from the P30m source. METHODS: Twenty right-handed healthy subjects participated in the experiment. Auditory magnetic responses were recorded in the 0.5 s ISI (ISI were between 0.4 and 0.6 s) and the 1.5 s ISI conditions (ISI were between 1 and 2 s). Tone bursts were presented to the right ears 880 times consecutively for each condition. The P30m and the P50m responses were investigated, and the dipole source localization was performed. RESULTS: The P50m latency was significantly prolonged, while the P30m latency did not vary in the shorter ISI. Both P50m and P30m amplitudes were significantly reduced in the shorter ISI. The P50m was located significantly more anteriorly than P30m. CONCLUSIONS: These results suggest the existence of differential characteristic and spatially different magnetic responses in the middle latency range. SIGNIFICANCE: This study has revealed one aspect of the different natures between P30m and P50m, and may provide a key for auditory perceptional processes in humans.     

Short latency vestibular potentials evoked by electrical round window stimulation in the guinea pig

Short-latency potentials evoked by round window electrical stimulation were recorded in guinea pig by means of vertex-pinna skin electrodes using averaging techniques. Constant current shocks of 20 microseconds or 50 microseconds (25-300 microA) were used to evoke both auditory and vestibular brain-stem potentials. Pure auditory potentials, comparable to those evoked by acoustic clicks, were obtained by 20 microseconds electrical stimuli and disappeared during an auditory masking procedure made with a continuous white noise (110 dB SPL). Short latency potentials labeled V1, V2 and V3 were obtained by 50 microseconds electrical stimuli during an auditory masking procedure. This response disappeared after specific vestibular neurectomy, whereas the auditory response evoked by acoustic clicks or by electrical stimulation remained unchanged, suggesting that these latter potentials had a vestibular origin.     

Short latency mechanically evoked somatosensory potentials in humans.

Somatosensory potentials evoked by mechanical stimulation were recorded by surface electrodes over (1) the digital nerves in the index finger, (2) the median nerve at the wrist, (3) the median nerve near the axilla, (4) the brachial plexus, (5) the cervical cord at CII, (6) the scalp overlying the somatosensory cortex. Nerve conduction velocities varied inversely with age and ranged from 43 to 68 m/sec. Mechanically evoked potentials recorded from the electrodes overlying the digital nerves were an artifact of the finger movement. All other electrode configurations recorded potentials comparable to those evoked by electrical stimulation of nerves. These mechanically evoked potentials could prove useful in the assessment of clinical disorders of somatosensory function from receptor to cortex in man.     

Short latency visual evoked potentials in occupational exposure to organic solvents.

OBJECTIVES: Short latency visual evoked potentials (SVEP), in response to high-intensity flashes from light emitting diodes (LED), were used to detect subclinical effects along the visual pathway in four groups of subjects with different levels of exposure to gasoline, all within legally acceptable limits. METHODS: Potentials and exposure levels were obtained from 31 subjects with different occupational exposure levels to gasoline fumes, as well as from 17 non-exposed control subjects. SVEP were recorded from four electrode sites (infra-orbital, Cz, Pz, Oz), in response to flashes presented to each eye in turn from goggle-mounted LEDs. SVEP components were defined after digital filtering, which eliminated the high-frequency oscillatory potentials and accentuated five major components: a periocular P30, attributed to the retina; a fronto-central N50, attributed to the optic nerve; centro-parietal P65 and N85, attributed to the optic tracts and radiation; and an occipital, cortical P105. RESULTS: The latencies of successive SVEP components of the exposed subjects showed a significant latency prolongation compared to controls, beginning with activity attributed to the optic nerve and increasing cumulatively with the later components. Retinal components were not affected by the exposure to organic solvents. Among the exposed groups, differences in latency prolongation corresponded to occupational exposure. CONCLUSION: The low-frequency components of SVEP were reliably measured and proved to be sensitive to subclinical effects of organic solvents on conduction along the visual pathway. These components are likely to be sensitive to other subcortical visual pathway lesions, but their clinical promise needs further verification.     

Acoustically evoked short latency negative responses in hearing loss patients with enlarged vestibular aqueduct

This study aims to assess the diagnostic value of the acoustically evoked short latency negative response (ASNR) during the auditory brainstem response (ABR) test for enlarged vestibular aqueduct (EVA). The ABR test was performed on 175 subjects with severe and profound hearing loss from July 2008 to August 2011. Patients were submitted to high-resolution computed tomography scans for the temporal bone of the inner ear, and were diagnosed with EVA (EVA group; n = 24 cases, 46 ears), no inner ear deformity (no deformity group; n = 136 cases, 272 ears), or other inner ear deformity (other deformities group; n = 15 cases, 29 ears). The prevalence of ASNR was 26/46 ears (56.52 %) in the EVA group, 10/272 ears (3.67 %) in the no deformity group, and 3/29 ears (10.34 %) in the other deformities group. The rate of ASNR in the EVA group was higher than that in other groups (p < 0.05). The rate of ASNR is positively correlated with EVA. Therefore, the recording of ASNRs could be a valuable method for discovering EVA.     

Short latency somatosensory evoked potential in children

The short latency somatosensory evoked potential was studied in 90 normal children of 1 month to 16 years old and 7 adults. Somatosensory stimuli were delivered through a disc electrode placed over the median nerve at the wrist joint. The uniform recording sites used were the central region of the scalp, and the seventh cervical spine or Erb's point. Reference electrodes were placed on the hand contralateral to the median nerve stimulated. Three positive peaks (P1, P2 and P3) and one negative peak (N1) were consistently recorded, a further positive peak (P4) after N1 was not always observed. The latency of each peak per 1 m body length decreased with age until 2 or 5 years of age. The latency of each peak after 2 years of age was positively correlated with the body length and arm length. The value of P1 peak latency per 1 m body length reaches adult values at an earlier rate than the value of P3 peak latency and P2-P3 latency per 1 m body length. This suggests that central lemmiscal pathways mature at a slower rate than peripheral nerve fibers. The wave form pattern of the short latency somatosensory evoked potential changed to the adult pattern at 10 years of age. The peak latency of P4 during deep sleep was slightly prolonged. In recording on infants during sleep, the EEG should be monitored to determine the stage of sleep.     

Short latency somatosensory evoked potentials from radial, median and ulnar nerve stimulation in man

Short latency somatosensory evoked potentials (SEPs) were elicited by stimulation at the wrist of median, radial, and ulnar nerves, singly or in combination, using normal subjects. Amplitude of P10 was strikingly lower with radial stimulation than with median stimulation, while ulnar-derived P10 was intermediate in amplitude. This difference probably reflects the antidromic firing of motor fibers contained in median nerves as compared with the superficial branch of radial nerve, which is entirely sensory. Beyond P10, there appear to be no significant differences between median, radial and ulnar-derived SEPs. With simultaneous stimulation of several nerves within one arm, larger potentials were sometimes achieved but with poorer definition of P12 and P14. The clinical utility of radial, ulnar, and median stimulation for localizing peripheral lesions derives from the distinct anatomical pathways of the stimulated fibers through the brachial plexus and from the separable motor and sensory components of P10. SEP is less invasive than EMG; this fact, plus its freedom from sampling error, make it potentially more suitable than conventional EMG for sequentially following a patient's clinical course.     

Short latency somatosensory evoked potentials in infants

Short latency somatosensory evoked potentials (SEPs) to unilateral median nerve electrical stimulation were recorded from normal infants at birth and at 2, 4, 6, 8, 10 and 12 months of age. Three channels were recorded: Erb's point-Fz; C II (over 2nd cervical vertebra)-Fz; contralateral C' (2 cm posterior to C3 or C4)-Fz. Sweep time = 50 msec. At birth, the C II potential was seen in all infants; the Erb's point and C' potentials were seen in two-thirds. All older infants had well developed potentials at all sites. The mean latency of the Erb's point potential was stable over time. The latency of the C II potential decreased with maturation. At C', 4 components were seen, the latencies of which decreased with maturation: N1, P1, N2 and P2. The duration of N1 and P1 decreased with maturation. Standard deviations were relatively small for latencies and large for amplitudes. SEPs were adversely affected by using the 60 c/sec filter. Increasing the low frequency filter from 1 to 30 c/sec changed SEP, particularly in younger infants. Abnormal SEPs were seen in prematures surviving periventricular hemorrhage.     

Coronal topography of the middle latency auditory evoked potentials (MLAEPs) in man

Scalp recorded middle latency auditory evoked potentials (MLAEPs) were obtained from 7 human subjects to monaural click stimulation from a coronal chain of 7 electrodes extending from a point anterior to Cz to the mastoid prominence. All electrode outputs were referred to the tip of the nose. Polarity reversals of Pa occurred between the fourth and fifty coronal electrodes, while reversals of Na for Nb were inconstant. Voltage gradients for Pa along the coronal chain are maximal at the level of polarity reversal. Polarity reversals of components of the brain stem auditory evoked potential (e.g., wave 5) occurred just below the level of MLAEP inversion.     

Vestibular short latency responses to pulsed linear acceleration in unanesthetized animals.

Linear acceleration transients were used to elicit vestibular compound action potentials in non-invasively prepared, unanesthetized animals for the first time (chicks, Gallus domesticus, n = 33). Responses were composed of a series of up to 8 dominant peaks occurring within 8 msec of the stimulus. Response amplitudes for 1.0 g stimulus ranged from 1 to 10 microV. A late, slow, triphasic, anesthesia-labile component was identified as a dominant response feature in unanesthetized animals. Amplitudes increased and latencies decreased as stimulus intensity was increased (MANOVA P less than 0.05). Linear regression slope ranges were: amplitudes = 1.0-5.0 microV/g; latencies = -300 to -1100 microseconds/g. Thresholds for single polarity stimuli (0.035 +/- 0.022 g, n = 11) were significantly lower than those of alternating polarity (0.074 +/- 0.028 g, n = 18, P less than 0.001). Bilateral labyrinthectomy eliminated responses whereas bilateral extirpation of cochleae did not significantly change response thresholds. Intense acoustic masking (100/104 dB SL) produced no effect in 2 animals, but did produce small to moderate effects on response amplitudes in 7 others. Changes were attributed to effects on vestibular end organs. Results of unilateral labyrinth blockade (tetrodotoxin) suggest that P1 and N1 preferentially reflect ipsilateral eighth nerve compound action potentials whereas components beyond approximately 2 msec reflect activity from vestibular neurons that depend on both labyrinths. The results demonstrate that short latency vestibular compound action potentials can be measured in unanesthetized, non-invasively prepared animals.     

Short latency somatosensory evoked responses to median nerve stimulation in healthy humans: electric and magnetic recordings

Somatosensory Evoked Potentials (SEPs) and Somatosensory Evoked magnetic Fields (SEFs) to median nerve stimulation at wrist were recorded in 5 healthy subjects and the components between 15 and 30 ms after the stimulus were evaluated on the hemiscalp contralateral to the stimulated wrist. SEPs were measured by means of a 32-channel recorder and compared with SEFs obtained via multiple measurements with a 4-channel sensor. Equivalent dipole localization was carried out for the magnetic components peaking at about 15, 20 and 24 ms. The scalp distribution of SEPs, illustrated by bit mapped color images, were qualitatively explained by three separate sources. The first is described as a tangentially oriented dipole placed behind the Central Sulcus and responsible for the parietal N20-"late P25" waves and for the frontal P20-N30 ones. The second is represented by a radieal dipole placed just in front of the Central Sulcus and pointing towards the motor strip, responsible for the rolandic P22 component. The third is just behind the Central Sulcus and is radieally oriented towards the surface of the postcentral sensory area for the "early P25" parietal wave. The SEFs distributions, illustrated by color isofield contour maps, were quantitatively explained by a unique tangential dipole localized, with good resolution, well behind the Sulcus for the 15 ms waves and slightly frontal to this site for the waves peaking at around 20 and 24 ms. The equivalent dipole has been localized at a depth of about 5 cm (15 ms component), 2 cm (20 ms components) and 4 cm (24 ms component), across the studied subjects. It is stressed that the dipole responsible for the magnetic pattern is likely to be the same tangential dipole responsible for a part of the electric pattern. Due to their radieal orientation, the other two dipoles, proposed for the SEPs maps, would be mostly undetectable by a magnetic investigation.     

Short latency somatosensory evoked potentials in Charcot-Marie-Tooth Disease

9 patients with Charcot-Marie-Tooth Disease (CMTD) of intermediate type (PMA type II, 10), all from the same family, presented with a significant increase of the interpeak N9-N13 latency. This increase is already present in the pre-symptomatic phase of the disease and there is no significant difference between the various patients of different ages and clinical severity, indicating that the lesions appears very early and tends to establish itself equally early. Similar behaviour is also seen in the distal conduction velocity along the sensitive fibres, while the more proximal areas seem to be relatively spared. The authors interpret these data as an expression of a distal central peripheral sensory neuropathy. In contrast, the lesion of the peripheral motor fibres, particularly in the legs, has a different and more severe pattern of evolution. Alterations in central conduction time (N13-N20) were not seen in any of the 9 patients studied.