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PubMed2001

Latencies of the 2f1-f2 distortion product otoacoustic emissions measured using a phase-gradient method in young people, in the elderly and in people exposed to noise.

Distortion product otoacoustic emissions (DPOAE) are generally accepted as a good tool for investigating the micromechanics of the cochlea. The 2f1-f2 DPOAE latencies provide significant data regarding travelling waves. In this study the 2f1-f2 DPOAE latencies were measured using a phase-gradient method, with a swept-f2 procedure, for three groups: Group I comprised 60 healthy young people, aged 17-32 years; Group II comprised elderly patients, aged 56-72 years, with presbyacusis; and Group III consisted of 74 miners, aged 19-35 years, who had been exposed to noise for 2-15 years. Measurements were performed for frequencies between 1.0 and 6.0 kHz. In all groups the latencies were fitted using a non-linear regression model. The aim of the study was to compare the latency and amplitude of 2f1-f2 DPOAE in different inner ear pathologies. The highest DPOAE amplitudes were recorded in Group I and in miners with 2-4 years noise exposure (Group IIIa), and the latencies showed a similar pattern. The lowest DPOAE amplitudes were recorded in the elderly and in miners with 8-15 years noise exposure (Group IIIc), but in contrast the longest latencies were measured in miners and the shortest in the elderly. The latency analysis significantly reinforces opinions on the micromechanics of the cochlea, mostly in terms of the cochlear functioning as a filter and amplifier and with regard to the elasticity of the basilar membrane.

Acoustic Impedance Tests↗
PubMed1987

Long-latency spinal reflex in man after flexor reflex afferent stimulation.

Electromyographic (EMG) flexor muscle responses evoked by electrical stimulation of ipsilateral peripheral nerves were studied in 16 patients with clinically complete spinal cord transection. Stimuli were applied either to a cutaneous nerve (sural) or to a mixed nerve (tibial) and muscle responses were recorded from tibialis anterior, biceps femoris and rectus femoris. EMG recordings after both sural and tibial nerve stimulation showed that distinct early and late ipsilateral flexor muscle responses could be elicited. This distinction was more evident for tibialis anterior. The latency of the early responses averaged approximately 100 ms with sural and 75 ms with tibial nerve stimulation. This corresponds to the latency of the flexion withdrawal reflex previously described in normal man. After sural stimulation, the early reflex appeared in biceps femoris at a threshold intensity not significantly different from that in normal man given the same stimulation parameters. Late responses appeared after a longer latency (130 ms) and at a lower threshold than the early flexor reflex. In all patients a striking feature of the late response was that its latency increased with increasing stimulus intensity, the maximum latency being as long as 450 ms. This increase also occurred with increasing duration of high intensity stimulus trains. Neither the appearance of a late response nor its latency increase could be explained by a peripheral loop due to a preceding muscle contraction (from either motor axon stimulation or motoneuronal discharge corresponding to the early flexion reflex). It was therefore concluded that both were directly elicited by the afferent volley set up by electrical stimulation. The low threshold of the late reflex corresponded to the excitation of relatively rapidly conducting afferents and its central spinal delay was more than 100 ms. The late reflexes were compared with those described by Andén et al. (1964) in the acute spinal cat injected with DOPA and were found to have similar characteristics. The mechanism for the increase in latency of the late response is discussed in relation to the interpretation of Lundberg (1979).

Adolescent↗
PubMed2003

P300 component identification using source analysis techniques: reduced latency variability.

P300 latency variability in normal subjects is a complicating factor in clinical event-related potential studies because it limits diagnostic applicability. The current study was conducted to determine whether identification of P300 (P3A and P3B) components using source analysis techniques can reduce variability in P300 parameters. Data were recorded with a 128-channel EEG system in 18 healthy subjects. The authors used a standard, auditory two-tone oddball paradigm with targets of 2000 Hz and standards of 1000 Hz. Two simple source analysis models with one or two rotating dipoles were applied to grand average data and individual data. Dipole time courses were combined with mapping results to extract P3A and P3B component latencies. Latencies obtained with conventional P300 analysis were compared with source analysis results. The source analysis method identified both P3A and P3B components in a substantially larger percentage of subjects (88% vs. 33%) than the conventional method. The source analysis method yielded a later mean P3B latency (357 msec vs. 323 msec, P < 0,001) with a smaller standard deviation (9 msec vs. 23 msec, P = 0,003) than the conventional P300 method. The relative contribution of the temporally separate P3A and P3B components to the P300 complex amplitude is highly variable. This explains the larger latency standard deviation in conventional P300 analysis. The source analysis method was able to identify P300 components in a large percentage of the cases. The result is a considerable reduction of P300 latency variability in normal subjects. This could have important consequences for clinical event-related potential research, because diagnostic sensitivity and specificity of P300 latency may improve with this method.

Adult↗
PubMed1986

Effects of video display character size, clarity, and color on P-300 latency.

The P-300 is a positive polarity electroencephalographic (EEG) signal occurring about 300 ms after a surprising, novel, or unique stimulus. The amplitude of the P-300 is dependent on the degree of attention and importance the subject has assigned to the stimulus and on its relative novelty. P-300 latency is dependent on the time it takes the subject to mentally process the stimulus and determine if the information it carries is novel. In Experiment I, the latencies of P-300's for 40 and 80 column size video display characters were compared. The effect of dioptric blur (mean add power +2.44 D) on latency was also determined. It was found that 40 column size characters could be interpreted more quickly than 80 column size characters and that blur increased the processing time equally for both character sizes. In Experiment II, P-300 latencies for green and amber display screens were compared. Display screen color did not significantly affect latency, neither did the addition of lens powers ranging from a mean of -1.15 D to a mean of +1.15 D over the subjects' habitual lenses. However, it was found that latencies significantly increased when a mean add of +2.29 D for the green display or a mean add of +2.57 D for the amber display were used. (Chromatic aberration accounted for the difference in lens power for the green vs. amber display.) These results demonstrate that character size and clarity are significant factors in determining the time required to mentally process a stimulus. They also demonstrate that there is no clear advantage to using an amber vs. a green screen when speed of mental processing (as measured by P-300 latency) is used as a criterion.

Adult↗
PubMed1997

P1-latency interroot comparison enhances the validity of scalp-recorded somatosensory-evoked potentials to diagnose nerve root dysfunction in sciatica.

STUDY DESIGN: A prospective validity study was done of scalp-recorded somatosensory-evoked potentials as a diagnostic procedure to show lumbosacral radiculopathy in 100 consecutive patients with unilateral or bilateral sciatica. OBJECTIVE: To determine the validity gained by the use of P1-latency interroot comparison to show P1-latency prolongation. SUMMARY OF THE BACKGROUND DATA: The validity of scalp-recorded somatosensory-evoked potentials in diagnosing lumbosacral radiculopathy has been debated and is uncertain. METHOD: Sensory nerves representing nerve roots L4, L5, and S1 were stimulated bilaterally. Height-corrected P1-latency, two new P1-interroot comparison-based criteria, and absence of P1 were studied. The gold standard was defined as clinically-involved nerve roots with radiologic nerve root compression. The false-positive nerve root compression rate was determined, and the gold standard was corrected accordingly. Clinically relevant cut-off values were defined by multilevel likelihood ratio analysis. RESULTS: The positive and negative likelihood ratios of P1-latency prolongation were 6.79 and 0.53, respectively, for the gold standard, and 10.57 and 0.21, respectively, for the corrected gold standard. The validity was not reduced when scalp-recorded, somatosensory-evoked potentials were blinded to the radiologic results. Absence of P1 was associated to the gold standard and the corrected gold standard. Compared with the combined use of P1-latency interside difference and height-corrected latency, the combination of P1-interroot comparison and height-corrected P1-latency increased the sensitivity by 20% for the gold standard and 32% for the corrected gold standard, and when absent P1 was added, the overall sensitivity was 53% for the gold standard and 81% for the corrected gold standard. The corresponding specificity was 92%, and in asymptomatic nerve roots it was 98%. CONCLUSION: The P1-interroot comparison permits the use of scalp-recorded somatosensory-evoked potentials as a contributory "rule in" procedure in patients with sciatica.

Adolescent↗
PubMed2003

Reference values for peroneal nerve motor conduction to the tibialis anterior and for peroneal vs. tibial latencies.

OBJECTIVE: To generate a large normative database for the peroneal study to the tibialis anterior and to analyze differences between the peroneal latency to the extensor digitorum brevis and the tibial latency to the abductor hallucis. DESIGN: A total of 244 asymptomatic subjects without risk factors for neuropathy were tested for latency, amplitude, area, duration, and nerve conduction velocity to the tibialis anterior. For the peroneal/tibial analysis, 221 subjects were included. Temperature control was used, and demographic characteristics were recorded. RESULTS: Latency to the tibialis anterior increased and nerve conduction velocity decreased with increasing height. Amplitudes, area, and nerve conduction velocity were lower in older persons. The upper limits of normal (97th percentile) were 4.9 msec (latency) and 15.0 msec (duration). The lower limits of normal (3rd percentile) were 1.7 mV (amplitude), 6.8 microV/sec (area), and 43 m/sec (nerve conduction velocity). The upper limits of normal side-to-side difference was 1.2 msec (latency), 6.3 msec (duration), 50% (amplitude), 47% (area), and 20% (nerve conduction velocity). The upper limits of normal drop from below- to above-fibular-head stimulation was 36% (amplitude) and 43% (area). For the peroneal/tibial comparison, the upper limits of normal latency increase of peroneal over tibial was 1.8 msec and tibial over peroneal was 1.5 msec. CONCLUSION: A large normative database was collected. Upper and lower limits of normal were calculated, and side-to-side differences were analyzed. For the peroneal/tibial comparison, an upper limits of normal difference was described.

Adult↗
PubMed1996

Long latency ankle responses to dynamic perturbation in older fallers and non-fallers.

OBJECTIVE: The purpose of this study was to examine the effects of falling history and aging on the latency and magnitude of long latency responses in the lateral gastrocnemius (LG) and tibialis anterior (TA) muscles of older adults. DESIGN: Single observation study. SETTING: Emory University School of Medicine, Center for Rehabilitation Medicine, serving the greater Atlanta, Georgia, area. PARTICIPANTS: There were 62 community-dwelling adults aged 60 or older, 32 with a history of two or more unexplained falls in the past year and 30 with no history of falls in the past year. MEASUREMENTS: The electromyographic activity of the gastrocnemius and tibialis anterior muscles was recorded bilaterally during repeated 10 degree dorsiflexion perturbations to standing subjects at the acceleration of gravity and a velocity of approximately 100 deg/sec. The latency and magnitude of the long latency EMG responses (LLR) of both muscles were determined and compared between individuals by falls history and by decades of age. MAIN RESULTS: No significant differences between falls status groups existed for mean LLR latencies or magnitudes of either LG or TA. Attenuation of the LLR throughout the trials was significantly different between groups. Non-fallers demonstrated attenuation of the LG magnitude over the first five stretches. Fallers showed maladaptation of the LG response, with the latency becoming shorter over 25 trials. More than half of the subjects in both groups had one or more instances of temporal reversal of the response latencies, with the TA response occurring earlier than the LG response during the first five stretches. No differences existed in the LLR between age decades within faller or non-faller groups. A timed measure of mobility (Up & Go) showed a significant difference between falls status, but not between age decades in either group. CONCLUSIONS: Lack of differences between falls status and age decade groups over all trials suggests that LLRs remain intact between older fallers and non-fallers and between older age groups. The mechanism of perturbation is a distinguishing feature of this study and probably contributes to our findings. The appearance of an atypical response strategy in both groups, where the TA response often occurs before the LG response, has raised the question of whether there is always a stereotypical pattern of LLRs during postural perturbations outside the experimental setting.

Accidental Falls↗
PubMed1983

Latency of pancreatic fluid secretory response to intestinal stimulants in the dog.

The effect of atropine and truncal vagotomy on the latency of the secretory response of the exocrine pancreas to rapid intraduodenal injection of L-tryptophan, sodium oleate and HCl or to rapid intraportal injection of secretin or CCK octapeptide has been determined in conscious dogs with pancreatic fistulae. The intraduodenal stimulants were injected either alone or in the presence of an intravenous infusion of secretin, CCK octapeptide or a combination of both hormones. The mean latency of response to tryptophan alone (62 +/- 2 s), oleate alone (64 +/- 5 s) and HCl alone (91 +/- 3 s) was significantly longer (P less than 0.05) than the latency to intraportal secretin (28 +/- 5 s) or CCK octapeptide (45 +/- 4 s). Infusion of secretin alone or with CCK octapeptide significantly shortened the latency of response to tryptophan (38 +/- 3 s) and oleate (41 +/- 5 s), but had no effect on the latency to intraduodenal HCl (96 +/- 4 s). Atropine and truncal vagotomy both increased the latency to intraduodenal tryptophan and oleate threefold but did not affect the latency to intraduodenal HCl or intraportal secretin or CCK octapeptide. These data support the hypothesis that the stimulus to pancreatic fluid secretion evoked by intraduodenal HCl is humoral rather than neural, while the responses to intraduodenal tryptophan and oleate are mediated, at least in part, via an enteropancreatic, vago-vagal, cholinergic reflex.

Animals↗
PubMed1984

Corticomotoneuronal cells contribute to long-latency stretch reflexes in the rhesus monkey.

To test the hypothesis that a transcortical reflex contributes to the stretch-evoked long-latency electromyographic (e.m.g.) response we documented the responses of identified corticomotoneuronal (c.m.) cells and their target muscles to perturbations of active wrist movements. Macaque monkeys performed ramp-and-hold wrist movements against elastic loads, alternating between flexion and extension zones; brief (25 ms) torque pulses were intermittently applied during the hold period. C.m. cells were identified by a clear post-spike facilitation in spike-triggered averages of forelimb muscle e.m.g. activity. Activity of c.m. cells and twelve wrist and digit flexor and extensor muscles was recorded during: (a) active ramp-and-hold wrist movements, (b) passive ramp-and-hold wrist movements, and (c) torque perturbations applied during the hold phase of active flexion and extension which either lengthened or shortened the c.m. cell's target muscles. Muscle-lengthening perturbations evoked a reproducible pattern of average e.m.g. activity in the stretched muscles, consisting of two peaks: the first response (M1) had an onset latency of 11.2 +/- 2.1 ms (mean +/- S.D.), and the second (M2) began at 27.9 +/- 5.1 ms. Torque perturbations which shortened the active muscles also evoked a characteristic e.m.g. response consisting of an initial cessation of activity at 13.5 +/- 3.4 ms followed by a peak beginning at 33.9 +/- 3.0 ms. The responses of twenty-one c.m. cells which facilitated wrist muscles were documented with torque pulse perturbations applied during active muscle contraction. Twenty of twenty-one c.m. cells responded at short latency (23.4 +/- 8.8 ms) to torque perturbations which stretched their target muscles. For each c.m. cell-target muscle pair, transcortical loop time was calculated as the sum of the onset latency of the c.m. cell's response to lengthening perturbations (afferent time) and the onset latency of post-spike facilitation (efferent time). The mean transcortical loop time was 30.4 +/- 10.2 ms, comparable to the mean onset latency of the M2 peak (27.9 +/- 5.1). The duration of a c.m. cell's response to torque perturbations provides a further measure of the extent of its potential contribution to the M2 muscle response. In all cases but two, the c.m. cell response, delayed by the latency of the post-spike facilitation, overlapped the M2 e.m.g. peak.

Action Potentials↗
PubMed1992

Evidence that a long latency stretch reflex in humans is transcortical.

1. The hypothesis that the long latency reflex response to muscle stretch in humans uses a transcortical pathway was tested by looking for convergence onto cortical neurones in eleven normal subjects. 2. Postsynaptic events in single flexor pollicis longus (FPL) motoneurones were derived from changes in the firing probability of individual FPL motor units. 3. Extension of the terminal phalynx of the thumb resulted in both short latency and long latency facilitations of individual FPL motoneurones. These were not reproduced by electrical stimulation of afferents in the terminal phalynx. Magnetic stimulation over the contralateral motor cortex produced strong, short latency facilitation of FPL motoneurones. 4. When the facilitation produced by stimulation over the cortex was superimposed on the long latency facilitation produced by extension of the thumb, the facilitation produced by both stimuli was greater than the sum of the individual facilitations produced by either stimulus given alone. This was not the case when the superimposition occurred on the short latency response to stretch. 5. We conclude that afferent systems excited by the stretch of FPL converge onto cortical neurones which are known to facilitate motoneurones. Thus the cortex is likely to contribute to the long latency stretch reflex in humans.

Adult↗
PubMed2004

Age reduces response latency of mouse inferior colliculus neurons to AM sounds.

Age and stimulus rise time (RT) effects on response latency were investigated for inferior colliculus (IC) neurons in young-adult and old CBA mice. Single-unit responses were recorded to unmodulated and sinusoidal amplitude modulated (SAM) broadband noise carriers, presented at 35 to 80 dB SPL. Data from 63 young-adult and 76 old phasic units were analyzed to identify the time interval between stimulus onset and driven-response onset (latency). When controlling for stimulus sound level and AM frequency, significant age-related changes in latency were identified. Absolute latency decreased with age at all stimulus AM frequencies, significantly so for equivalent rise times (RT) < or = 12.5 ms. The linear correlation of latency with AM stimulus RT was significant for both young-adult and old units, and increased significantly with age. It is likely that both the decrease in absolute latency and the increase in latency/RT correlation with age are consistent with a reduction of inhibitory drive with age in the IC. These latency changes will result in age-related timing variations in brainstem responses to stimulus onsets, and therefore affect the encoding of complex sounds.

Aging↗
PubMed1979

Narrow-band AP latencies in normal and recruiting human ears.

Derived narrow-band action potential latencies increase monotonically with decreasing central frequency, and can be interpreted as reflecting the traveling wave delay in the cochlea. It was found that, for recruiting human ears with average flat hearing losses around 40 dB, this accumulating latency increase was smaller than for normal ears. A comparison of 15 normal ears and 37 recruiting ears showed, however, that in only half of the recruiting ears this difference was significant. These recruiting ears were therefore divided in two groups based on the waveform of the narrow-band action potential AP, which correlated well with the subdivision according to latency. The findings have been explained on the basis that latency of the narrow-band APs is not determined solely by the mechanical traveling-wave delay, but also by the response time of the (second?) cochlear filter. When this filter broadens, one expects a decrease in its impulse response time. Since this impulse response time. Since this impulse response depends on the sum of the high- and low-frequency slope values of the cochlear filter, one expects only a latency decrease when the steep high-frequency slope also becomes more shallow. A support for the influence of the response times of the cochlear filter is found in the narrow-band AP latencies for restricted cochlear losses (e.g., in a 4-kHz noise dip). It appears that the latency in that area actually is shorter than for the higher central frequencies, a fact which cannot be explained solely on the basis of a traveling wave phenomenon.

Acoustic Stimulation↗
PubMed1996

Latency and multiple sources of distortion product otoacoustic emissions.

A novel analysis approach has been developed to examine the latency of distortion product otoacoustic emissions (DPOAEs). DPOAEs were measured in ten normal-hearing adults in a paradigm in which f2 was held constant and f1 was varied. This paradigm was used with a wide range of primary levels. Latency was estimated in two ways. In the first, a phase-slope delay measurement was used which showed a significant response latency increase as stimulus intensity was decreased. In the second approach, an inverse-FFT procedure was used to provide a temporal analysis of the data. Results of this analysis reveal a complex latency structure with multiple peaks in the envelope of the time waveform. The latencies of individual peaks remain constant across level, however, short latency peaks have the greatest amplitudes at higher levels, and longer latency peaks are largest at low levels. These results would be consistent with the idea that there are multiple intracochlear sources for distortion product generation; however, a simple model, in which generation is assigned to the f2 and the 2f1-f2 place, does not adequately explain the number of envelope peaks that were present in many ears.

Acoustic Stimulation↗
PubMed1988

Expression of herpes simplex virus type 1 (HSV-1) latency-associated transcripts and transcripts affected by the deletion in avirulent mutant HFEM: evidence for a new class of HSV-1 genes.

During latent herpes simplex virus type 1 (HSV-1) infection in the trigeminal ganglia of mice, three virus-specific transcripts, 2.0, 1.5, and 1.45 kilobases (kb), are detectable by Northern (RNA) blot analysis, but only the 2.0-kb transcript can be detected in HSV-1-infected tissue culture cells (J.G. Spivack and N. W. Fraser, J. Virol. 61:3842-3847, 1987). Since these latency-associated genes map to a diploid region of the genome, transcription from the deletion mutant HFEM, which contains only one complete copy of these genes, was investigated to determine the effect of gene dosage. The 4.1-kb HFEM deletion is located between the alpha genes ICP0 and ICP27. ICP0 mRNA and the 2.0-kb latency-associated transcript were present at normal levels during HFEM infection, but ICP27 mRNA and 0.9- and 1.1-kb transcripts that map near the deletion were not readily detectable. The levels of expression of one or more of these genes might be an important determinant of HSV-1 virulence in animal hosts. ICP27 mRNA accumulated when protein synthesis was inhibited before HFEM infection, implying that the deletion may affect ICP27 regulatory rather than coding elements. Expression of the 2.0-kb latency-associated transcript was characterized in infected CV-1 cells with metabolic inhibitors and strand-specific probes. On the basis of metabolic inhibitor studies, the gene encoding the 2.0-kb latency-associated transcript is not an alpha gene. During HSV-1 replication in infected tissue culture cells, the beta and gamma genes require the prior expression of alpha gene products. However, the latency-associated RNAs are expressed in the absence of detectable levels of alpha transcripts in latently infected mice. Thus, this latency-associated gene family appear to be regulated quite differently than alpha, beta, or gamma genes. For these reasons, and because the latency-associated genes may perform latent rather than replicative functions, we propose that they should be considered members of a new HSV-1 gene class, the lambda genes.

Cell Line↗
PubMed1983

The behaviour of the long-latency stretch reflex in patients with Parkinson's disease.

The size of the long-latency stretch reflex was measured in a proximal (triceps) and distal (flexor pollicis longus) muscle in 47 patients with Parkinson's disease, and was compared with that seen in a group of 12 age-matched normal control subjects. The patients were classified clinically into four groups according to the degree of rigidity at the elbow or tremor. Stretch reflexes were evaluated while the subject was exerting a small force against a constant preload supplied by a torque motor, and the size of the reflex response was measured as fractional increase over basal levels of activity. When stretches were given at random intervals by increasing the force exerted by the motor by a factor of 2 or 3, there was a clear trend for the more severely affected patients to have larger long latency responses in the triceps muscle, although there was no change in the size of the short-latency, spinal component of the response. In contrast, there was no change in the size of the long-latency response of the flexor pollicis longus in any group of patients with Parkinson's disease. Despite any differences in reflex size, the inherent muscle stiffness of both muscles appeared to be normal in all groups of patients with Parkinson's disease, since the displacement trajectory of the limb following the force increase was the same as control values in the short (25 ms) period before reflex compensation could intervene. In 20 of the patients and in seven of the control subjects, servo-controlled, ramp positional disturbances were given to the thumb. Up to a velocity of 300°/s, the size of the long-latency stretch reflex was proportional to the log velocity of stretch. This technique revealed, in both moderately and severely rigid patients, increases in the reflex sensitivity of the flexor pollicis longus, which had not been clear using step torque stretches alone. However, whether using ramp or step displacements, long latency stretch reflex gain was not closely related to rigidity; reflex size was within the normal range in many patients with severe rigidity. Enhanced long latency stretch reflexes thus contribute to, but may not be solely responsible for, rigidity in Parkinson's disease.

Electromyography↗
PubMed2004

Latency of pupillary reflex dilation during general anesthesia.

Areas of insensibility produced by neuraxial anesthesia or peripheral nerve blocks can be detected during general anesthesia by failure of noxious stimulation to trigger pupillary reflex dilation. We examined the latency of pupillary reflex dilation and the effect of fentanyl on the latency of reflex dilation during anesthesia in nine volunteers. We hypothesized that the reflex was generated by slowly conducting C nociceptive fibers and would be significantly delayed if a distal dermatome (L(4)) was stimulated compared with a proximal dermatome (C(5)). We also hypothesized that fentanyl would prolong the latency and alter the shape of the reflex. After induction of general anesthesia, pupillary reflex dilation was measured with an infrared pupillometer every 5 min after stimulations of the L(4) and C(5) dermatomes. Fentanyl (3 microg/kg) was then given intravenously. Pupillary reflex dilation latencies were calculated by examining each individual measurement. After 3 h, naloxone (400 microg) was given intravenously; anesthesia was then discontinued. Pupillary reflex dilation had a long latency and consisted of distinct early and late phases. No differences were found between latencies of reflex dilation after simulation of L(4) and C(5) dermatomes either before or after fentanyl administration. Fentanyl at high concentrations essentially eliminated pupillary reflex dilation; but over the 180-min observation period, first early and then late dilation returned. Fentanyl produced a small increase in the latency of the initial early dilation. We conclude that pupillary reflex dilation during anesthesia is not initiated by slowly conducting C fibers and that fentanyl depresses the reflex in a stereotypical manner.

Adult↗
PubMed1988

Regularity and latency of units in ventral cochlear nucleus: implications for unit classification and generation of response properties.

1. The responses of neurons in the ventral cochlear nucleus (VCN) of decerebrate cats are described with regard to their regularity of discharge and latency. Regularity is measured by estimating the mean and standard deviation of interspike intervals as a function of time during responses to short tone bursts (25 ms). This method extends the usual interspike-interval analysis based on interval histograms by allowing the study of temporal changes in regularity during transient responses. The coefficient of variation (CV), equal to the ratio of standard deviation to mean interspike interval, is used as a measure of irregularity. Latency is measured as the mean and standard deviation of the latency of the first spike in response to short tone bursts, with 1.6-ms rise times. 2. The regularity and latency properties of the usual PST histogram response types are shown. Five major PST response type classes are used: chopper, primary-like, onset, onset-C, and unusual. The presence of a prepotential in a unit's action potentials is also noted; a prepotential implies that the unit is recorded from a bushy cell. 3. Units with chopper PST histograms give the most regular discharge. Three varieties of choppers are found. Chop-S units (regular choppers) have CVs less than 0.35 that are approximately constant during the response; chop-S units show no adaptation of instantaneous rate, as measured by the inverse of the mean interspike interval. Chop-T units have CVs greater than 0.35, show an increase in irregularity during the response and show substantial rate adaptation. Chop-U units have CVs greater than 0.35, show a decrease in irregularity during the response, and show a variety of rate adaptation behaviors, including negative adaptation (an increase in rate during a short-tone response). Irregular choppers (chop-T and chop-U units) rarely have CVs greater than 0.5. Choppers have the longest latencies of VCN units; all three groups have mean latencies at least 1 ms longer than the shortest auditory nerve (AN) fiber mean latencies. 4. Chopper units are recorded from stellate cells in VCN (35, 42). Our results for chopper units suggest a model for stellate cells in which a regularly firing action potential generator is driven by the summation of the AN inputs to the cell, where the summation is low-pass filtered by the membrane capacitance of the cell.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMed1989

Human cortical potentials evoked by stimulation of the median nerve. I. Cytoarchitectonic areas generating short-latency activity.

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain↗