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PubMed2000

Variations in motor evoked potential latencies in the anal sphincter system with sacral magnetic stimulation.

PURPOSE: The anal sphincter system of the skeletal musculature consists of various parts but functions as a single unit. The motor latencies measured at the puborectalis, deep external anal sphincter, superficial external anal sphincter, and subcutaneous external anal sphincter have yet to be clearly elucidated. This study was designed to measure the motor latencies of these sphincters separately and to investigate the electrophysiologic heterogeneity of the anal sphincter system. METHODS: In 20 preoperative patients with colon cancer without either neurologic or anorectal diseases, motor evoked potentials were taken separately bilaterally at levels measuring approximately 5, 3.8, 2.6, and 1.5 cm from the perineal skin using a concentric needle electrode after magnetic stimulation on the sacral region. These latencies were considered to be separately measured at the puborectalis, deep, superficial, and subcutaneous external anal sphincter. RESULTS: The motor latencies (median (95 percent confidence interval)) were 4.33 (4.1-4.93; right) and 4.24 (3.97-5.22; left) ms at the 5 cm level; 5.96 (5.45-7.32; right) and 6.44 (5.49-8.20; left) ms at the 3.8 cm level; 9.28 (7.99-11.21; right) and 8.88 (7.68-10.93; left) ms at the 2.6 cm level; and 11.06 (9.69-14.13; right) and 9.18 (8.09-10.31; left) ms at the 1.5 cm level. Significant differences were seen in the latencies between the 5 cm level and the other levels and between the 3.8 cm level and the other levels. CONCLUSIONS: The motor latencies in the anal sphincter system significantly varied depending on the distance from the skin. The latency may be shortest in the puborectalis and increasingly longer in the deep, superficial, and subcutaneous EAS, in that order.

Aged↗
PubMed2005

Effects of diazepam on the latency of saccades for luminance and binocular disparity defined stimuli.

Saccadic latency is composed of separate sensory and motor processing delays. Therefore, any alteration in the sensory processing should effect the saccadic latency. Because the highest density of benzodiazepine (Bz) binding sites is located in cerebral cortex, sensory processing of stimuli in this cortical area is expected to be substantially effected by administration of Bzs. It is well known that sensory processing of binocular disparity occurs in the cerebral cortical areas and therefore the latency of saccades to stimuli defined by binocular disparity should be substantially affected by Bz intake. In this study, we tested this prediction by comparing the latency of saccadic eye movements for binocular disparity defined stimuli (stereo stimuli) with those for luminance contrast defined stimuli (luminance stimuli), after diazepam or placebo. Eye movements were mainly recorded by use of the magnetic search coil technique, and the study was performed in a randomized, double-blind way. Although diazepam prolonged the latency of saccades for stereo and luminance stimuli, the percentage increases in saccadic latency for the stereo stimuli were significantly larger than those for the luminance stimuli. Saccadic peak velocity, and saccadic amplitude, also significantly decreased after diazepam under conditions of stereo and luminance stimuli. However, there was no significant difference for either saccadic peak velocity or amplitude between the two types of target. The results suggest that the latency of saccades to binocular disparity defined random-dot stimuli could more sensitively reflect the pharmacodynamic effects of Bzs on the cerebral cortex.

Adult↗
PubMed2005

The effect of transcranial magnetic stimulation on the latencies of vertical saccades.

In this study, we investigated the effect of transcranial magnetic stimulation (TMS) over the right posterior parietal cortex (PPC) on the latency of two different types of visually-guided vertical saccades: reflexive saccades triggered by the sudden onset of a target, and saccades towards target locations known in advance. For this reason, we used two oculomotor tasks: a gap and a delay task, respectively. Nine normal subjects performed vertical saccades at +/-7.5 and +/-15 degrees . TMS was applied at 80 and 100 ms after target onset in the gap task, and after fixation offset in the delay task. Without TMS, we confirmed a latency asymmetry in the gap task favouring upward saccades at the lower eccentricity (7.5 degrees ), and a latency symmetry in the delay task. TMS increased the latencies of all saccades in the delay task, when delivered at 100 ms. This effect was mostly pronounced for downward saccades at 7.5 degrees . As a result, saccade latencies showed an asymmetry in this condition, similar to the one observed in the gap task without TMS. The gap task with TMS resulted in a variable latency distribution and no significant overall effect on saccade latency. Our results indicate that the right PPC is involved in the initiation of vertical saccades in the delay task, and that this involvement appears to be enhanced for downward saccades. A conclusion for the involvement of this area in the gap task could not be drawn from this study.

Adult↗
PubMed1998

The effect of pulse repetition rate, pulse intensity, and bicuculline on the minimum threshold and latency of bat inferior collicular neurons.

This study examines the effect of pulse repetition rate (PRR), pulse intensity, and bicuculline on the minimum threshold (MT) and latency of inferior collicular neurons of the big brown bat, Eptesicus fuscus, under free-field stimulation conditions. It tests the hypothesis that changes in MT and latency of collicular neurons are co-dependent on PRR. The number of impulses in inferior collicular neurons (n = 245) increased either monotonically (25%) or non-monotonically (75%) with pulse intensity. Latencies either decreased to a plateau (72%), fluctuated unpredictably within 3 ms (21%) or changed very little (7%) with increasing pulse intensity. Latencies and MTs of most collicular neurons increased by 1.5-24 ms (mean +/- SD = 4.8 +/- 3.3 ms) and 4-75 dB (mean +/- SD = 22.1 +/- 16.2 dB) with increasing PRR. In most neurons (94%), the latency increase was completely (42%) or partially (52%) eliminated when pulse intensity was compensated for the MT increase with PRR. Complete elimination of latency was achieved by bicuculline application. In a few neurons (6%), the latency increase with PRR was not affected by compensated pulse intensity or bicuculline application.

Animals↗
PubMed1984

Short and long-latency responses in human masseter muscle evoked by chin taps.

Ten healthy subjects received downward, backward and upward chin taps with standardized force and direction. Taps in all three directions elicited short (M1) and long (M2 and M3)-latency excitatory EMG responses in the masseter muscle. M1 (mean latency 8.9 ms, amplitude 150 microV) occurred more frequently and with shorter latency during clenching than during relaxation or opening. Downward taps were more efficient in evoking jaw-jerks (25 per cent) than upward (14 per cent) and backward ones (16 per cent). M2 was a weak biphasic deflection occurring during the silent period (mean latency 42 ms, amplitude 87 microV) and M3 was an EMG burst following the silent period (mean latency 69.3 ms, amplitude 169 microV). No long-latency evoked responses were obtained from the relaxed masseter. Thus, muscle stretch increases M1 response frequency but is not a necessary prerequisite. The hypothesis that vibratory transmission plays an important role was confirmed. Voluntary activation of the stimulated muscle (clenching) increases M1-response frequency and shortens response latency.

Adult↗
PubMed1977

Latency of the steady state visual evoked potential.

A technique has been devised to measure the latency of the steady state evoked potential (EP) to the separate flashes of a flickering light. The steady state method measures the averaged following EP to a flickering light. From the different averaged EP curves resulting from different averaged EP curves resulting from different intervals separating successive flashes, a latency is calculated which can be said to be the latency of a single response to a single flash of light. This latency is shorter for short inter-flash intervals (60-45 msec) than for the long inter-flash intervals (90-105 msec). The average short latency for three subjects was 61 msec and the average long latency 119 msec. These results agree reasonably well with other previous estimates of latency.

Evoked Potentials↗
PubMed1978

Latency of luminance and contrast evoked potentials in multiple sclerosis patients.

Luminance and contrast visual evoked potentials (VEPs), were studied in 18 multiple sclerosis (MS) patients and 11 healthy subjects. Luminance EPs were recorded to stimulation with noise modulated light (0--60 Hz); contrast EPs were obtained to appearance-disappearance or reversal of a checkerboard pattern with various check sizes and repetition periods. Our results indicate that the apparent latency of luminance EPs to noise modulated light can hardly be used for diagnosis of MS, since the range of normal values scatters widely and greatly overlaps the range of latency values in MS patients (detection rate of 3/13). Our data confirm, on the other hand, that the latency of contrast EPs can be used to discriminate between MS patients and healthy subjects (detection rate of 12/18). We recommend for diagnostic purposes to determine the apparent latency from the phase spectrum of the responses to checkerboard reversal at repetition rates between 5 and 20 Hz, since in this frequency range the failure rate was found to be minimal. The specificity of the apparent latency data can be improved if the wave form of the transient reversal EP at a lower repetition rate (around 2 Hz) is also inspected. We suggest that an increased latency can be ascribed to several causes, only one of these being an increased conduction time due to demyelination. Indirectly this confirms that an increased EP latency is not specific for MS.

Adolescent↗
PubMed1992

Actively and passively evoked P3 latency of event-related potentials in Parkinson's disease.

Event-related potentials (ERPs) generated during the performance of visual discrimination tasks were studied in 31 patients with Parkinson's disease, 9 patients with Alzheimer's disease, and 37 normal control subjects. Actively and passively evoked P3 components (P3b and P3a) were respectively identified as the components of the P3 response to infrequent target stimuli and infrequent non-target stimuli. Both the P3a and P3b latencies were significantly prolonged by normal aging. Nine of the Parkinson's disease patients showed a P3b latency above the 95% confidence limit of the age-adjusted regression line based on the normal controls, while only on patient had a prolonged P3a latency. In 6 patients with demented Parkinson's disease, the P3b latency was significantly longer than in 15 age-equivalent normal subjects, although no significant difference was found in the P3a latency. On the other hand, patients with Alzheimer's disease showed significant prolongation of both the P3a and P3b latencies compared to the normal controls. Furthermore, there was a significant difference in P3a latency between patients with demented Parkinson's disease and those with Alzheimer's disease. These results suggest that the automatic processing stage associated with P3a may be less impaired than the attention-controlled processing reflected by P3b in patients with Parkinson's disease, and also indicate that there may be some differences in the changes of cognitive processing caused by Parkinson's disease and Alzheimer's disease.

Aged↗
PubMed1987

Visual latency of ganglion X- and Y-cells: a comparison with geniculate X- and Y-cells.

Visual response latencies and rise times of X and Y ganglion cells recorded in the optic tract of anaesthetized, paralyzed cats were measured during repeated stimulation with sinusoidal gratings. These measures were compared with visual latencies and rise times of X- and Y-cells in the dorsal lateral geniculate nucleus. Measurements were restricted to individual trials on which the instantaneous discharge rate exceeded a criterion amplitude defined in terms of the statistics of the baseline activity of each cell in order to screen out false alarm responses. The onset and peak latencies of ganglion Y-cells are about 10-15 msec shorter than those of ganglion X-cells at low spatial frequencies (less than 0.25 c/deg) but about 10-20 msec longer at higher spatial frequencies (greater than 0.75 c/deg/). The onset latencies of geniculate X- and Y-cells lag their ganglion counterparts by 10-20 msec. Despite a delay in onsets of geniculate responses, the peak latencies of geniculate and ganglion X-cells are similar, and peak latencies of geniculate Y-cells are even shorter than those of their ganglion inputs. The short latencies of the peak responses of geniculate Y-cells are related to their short response rise times. A functional consequence of the bursty, but fast responses of geniculate Y-cells may be to accelerate the processing of lower spatial frequencies by the retino-geniculate Y-cell pathway.

Action Potentials↗
PubMed1988

Rod-cone dependence of saccadic eye-movement latency in a foveating task.

This study examines the relations between some well known oculomotor functions (saccades) and well known retinal physiology (dark adaptation): it deals with the overall latency versus target luminance functions, with the underlying rod and cone latency-luminance functions, and with the synergistic interaction between these latency functions for mesopic targets. Saccadic latency was measured to small lit targets presented at 10 deg retinal eccentricity in complete darkness. Target luminance and wavelength were varied. Additional measurements were made during dark adaptation or on backgrounds, or at different retinal eccentricities. Luminance matched stimuli and Palmer's (1968) equivalent luminance transformation were also used. Latency is determined by an achromatic luminance mechanism that receives substantial rod inputs above the cone threshold. Latencies for pure rod or pure cone inputs increase rapidly as target luminance decreases. For the rods this latency increase appears to represent the waiting time for the 140 or so photons (lambda = 507 nm) that are required for a saccade. Errors in direction occur at scotopic luminances, or at low photopic luminances when only cones are functioning.

Color↗
PubMed1983

REM latency in neurotic and endogenous depression and the cholinergic REM induction test.

Latency of rapid eye movement (REM) sleep was measured in eight healthy volunteers under baseline conditions and after administration of physostigmine. An infusion of 0.5 mg of physostigmine 5 minutes after sleep onset caused a significant shortening of REM latency in comparison with baseline conditions. In 45 patients with major depression, REM latency during baseline nights was significantly shorter than in control subjects. This shortening of the REM latency was found to be similar in endogenous, neurotic, and unclassified depressed patients. In contrast to findings in the controls, the physostigmine infusion provoked no further significant reduction of REM latency in depressed patients, but awakened the majority of patients. The data concerning spontaneous REM latency and REM latency after physostigmine do not allow a differentiation among the endogenous, neurotic, and unclassified depressed subgroups. The results of the cholinergic REM induction test do not conclusively support the hypothesis of a cholinergic hypersensitivity in depression.

Adult↗
PubMed1991

Latency of motor evoked potentials to focal transcranial stimulation varies as a function of scalp positions stimulated.

We recorded motor evoked potentials (MEP) to transcranial magnetic stimulation from abductor pollicis brevis (APB), flexor carpi radialis (FCR), biceps brachii and deltoid muscles at rest and during slight voluntary activation. An 8-shaped coil connected to a Cadwell MES-10 magnetic stimulator was positioned over different scalp positions 1 cm apart. At least 24 stimuli were delivered at each location. Latencies of MEPs were compared with those obtained by electrical and magnetic stimulation during muscle activation. Progressively longer MEP latencies were obtained in 5 groups depending on the type and position of stimulation. The shortest latencies were obtained with (1) electrical stimulation during muscle contraction and (2) non-focal magnetic stimulation during muscle contraction; magnetic stimulation at rest produced longer latencies with stimulation of (3) an optimal position, (4) a suboptimal position, and (5) a non-optimal position. Mean latency differences between successive groups were 1.9, 2.0, 1.6, and 2.6 msec for APB. Similar latency differences were found for the other arm muscles. The results are compatible with the hypothesis that the different latencies evoked by stimulation at different scalp locations are determined by the summation at spinal motoneurons of excitatory postsynaptic potentials generated by successive numbers of I waves.

Action Potentials↗
PubMed1994

P3 latency jitter assessed using 2 techniques. I. Simulated data and surface recordings in normal subjects.

Latency variability measurement using cross-correlational techniques has the drawback of alignment to background noise not related to ERP activity. We compared latency jitter estimation in simulated and real P3 recordings using Woody's algorithm and a non-cross-correlational technique, the maximum likelihood technique (MLT). Simulated ERPs (with introduced latency jitter) were generated using either a 1/2 cycle 2 Hz sine wave or an averaged P3 ERP with 1 of 3 added noise types in 5 signal to noise ratios (SNRs): (i) white noise; (ii) a 10 Hz sine wave; (iii) a 7.5 Hz sine wave. Jitter measurement accuracy was assessed using mean square error (MSE) for 1 iteration of the Woody method and each of 4 iterations of the MLT. Lowest MSEs occurred for higher SNRs and 1 iteration of the MLT. The MLT and Woody method were applied to P3 ERPs of 13 subjects with SNRs greater than 0.4 P3 latency jitter was significantly lower for the MLT. Latency jitter (both methods) did not differ between homologous electrodes and was highest in posterior electrodes. In the latency corrected ERP data of subjects with persistent alpha activity periodic components occurred in the Woody corrected average (not seen in the conventional or the MLT corrected averages). Our data indicate that the MLT is the more accurate method for determining latency jitter.

Adult↗
PubMedDate not supplied

Improvement of metabolic control does not normalize auditory brainstem latencies in subjects with insulin-dependent diabetes mellitus.

INTRODUCTION: In our previous study (Am J Otolaryngol 14:413-418, 1993), we reported that prolonged auditory brainstem response latencies are associated with microvascular complications and the duration of diabetes in patients with insulin-dependent diabetes mellitus (IDDM). To investigate whether short-term improvement in metabolic control also affects ABR-responses, we compared ABR-latencies in subjects with IDDM before and after intensified insulin and diet therapy. MATERIALS AND METHODS: Auditory brainstem latencies were measured in 13 subjects with IDDM (mean age: 25 years) before and after intensified insulin and diet therapy. The acoustic stimulus was a half sine wave with a duration of 0.250 millisecond and a frequency of 2,000 Hz. The stimulus was presented monaurally with fixed polarity through shielded headphones TDH-39 at repetition rate of 10 Hz and at 90 dB hearing level. All subjects had normal hearing ability. Glycated hemoglobin A1C (GHbA1C), blood glucose immediately before ABR-measurements, and mean blood glucose during 24 hours before auditory studies were measured before and after intensified therapy. RESULTS: During intensified insulin therapy, GHbA1C improved significantly (P < .05) in study subjects. However, no changes were observed in ABR-latencies. We also studied those 10 patients whose blood glucose improved during intensified insulin therapy. Although blood glucose was significantly lower (P < .01) after intensified insulin therapy compared with that at baseline, no changes were observed between ABR-latencies at baseline and follow-up. CONCLUSION: ABR-latencies were not affected by improvement in metabolic control in patients with IDDM. Our finding suggests that delayed ABR-latencies found in patients with IDDM are not caused by poor metabolic control of diabetes but rather by other mechanisms, for example, microvascular complications.

Adult↗
PubMed1995

The pontomesencephalic tegmentum delays the peak latency of the visual evoked potential in rats.

In previous experiments it was found that physostigmine application in unrestrained rats delayed the peak latency of the visual evoked potential (VEP). The present study was carried out to find the putative site that cholinergically mediates the latency delay of rat's VEP. After unilateral ibotenic acid lesions of the nucleus basalis magnocellularis (NBM) and the pedunculopontine tegmental nucleus (PPTg), respectively, the VEPs of freely moving rats were recorded in different behavioural states. While NBM lesion did not alter the behavioural modulation of the VEP latency, the PPTg lesion produced shorter VEP latencies in the occipital cortex of the lesioned hemisphere in high and moderate arousal states. The peak latency shortening was significant for exploratory sniffing. Physostigmine but not nicotine application abolished the shorter VEP latency. The results indicate a muscarinic mechanism within the pontomesencephalic tegmentum that ipsilaterally delayed the VEP latency in high and moderate but not in low arousal states.

Adrenergic Agonists↗
PubMed1983

Middle and long latency auditory evoked potentials in cat. I. Component definition and dependence on behavioral factors.

Middle (10-50 ms) and long (50-600 ms) latency auditory evoked potentials (AEPs) were investigated in artificially respired, muscle-paralyzed cats. Similarity to human potentials of comparable latencies was examined in two ways: (1) the similarity of waveform features such as peak amplitude, polarity and latency, and (2) the effects of task-related variables on these various waveform features. Four behavioral variations of a classical pupillary conditioning paradigm were used to vary attention and arousal. Twelve peaks and troughs were identified in the AEP: P10, N13, P17, N22, P31, N41, P55, N70, N100, N140, P260 and N520. Principal components analysis (PCA) defined 7 AEP components, some of which spanned several peaks. Analysis both of peak latencies and amplitudes, and of principal component scores, revealed differential effects of the behavioral manipulations on these components: those with latencies longer than 50 ms were strongly influenced by behavioral variations, while earlier components were relatively immune to these effects. On the basis of these findings, several relationships between cat and human AEP components were suggested. Specifically, peaks P10-P41 in the cat were thought related to human middle latency components, cat P55 to human P50, cat N140 to human N300, and cat P260 to human P300. Cat N520 was comparable to several long latency components in humans. No obvious correspondences between cat AEP components and human N90 and P170 were identified.

Acoustic Stimulation↗
PubMed1992

Comparisons of the development of auditory brainstem response latencies between cats and humans.

Developmental changes in the peak latencies of auditory brainstem responses (ABR) recorded from humans and kittens were compared to test the hypothesis that developmental time courses among mammals are the same when appropriately normalized. Response latencies were computed as the difference from adult latency and conceptional ages were represented as percentages relative to the age that ABR wave latencies achieved a criterion value within 0.2 ms of asymptotic latency (i.e., adulthood). An underlying assumption of this exercise is that far-field response latency is an appropriate index of overall 'auditory development'. Results of this analysis suggest that developmental changes in latency of responses arising within the auditory periphery are similar between humans and cats, when appropriately normalized, and that more central changes show less correspondence. Consequently, absolute time course differences for specific developmental parameters must be considered and caution should be exercised when extrapolating results acquired from one species to the other.

Acoustic Stimulation↗
PubMed1994

Temporary latency shifts in auditory evoked potentials by injection of lidocaine in the rat.

Temporary latency shifts in auditory evoked potentials by intravenous injection of lidocaine were investigated in albino rats. Auditory brainstem responses (ABR) were recorded with 4000Hz short tone bursts. There was no significant difference of latencies in wave Pl of the ABR between drug-administered group (6 mg/kg body weight of lidocaine) and control group (0.6 ml/kg of 0.9% saline). As for waves P2. P3 and P4 of ABR, the latencies of the waves were significantly prolonged after the lidocaine injection (p < 0.05. U-test). The prolongation of latency of wave P4 was the most prominent in the fast waves and dependent on the dose of lidocaine. The latencies of the slow positive wave of the evoked potentials on the inferior colliculus (wave S) with clicks and the slow positive wave (wave P) and the negative wave following ABR (wave NA) with 4000Hz short tone bursts were also studied. The latencies of waves S. P and NA showed significant temporal prolongation (p < 0.05, U-test) after lidocaine injection. The present study revealed that a relatively small dose of lidocaine can cause temporary prolongation of latencies of auditory evoked potentials not only in the fast components but also in the slow components including wave NA which is a large slow negative wave following the ABR. The effects are considered to be caused by the action of lidocaine which reduces the excitabilities on the auditory nervous system.

Acoustic Stimulation↗