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Comparison of automated and manual F-wave latency measurements.

OBJECTIVE: F-waves are well-established clinical neurophysiological studies. F-wave analysis is now cumbersome limiting the usefulness of F-waves. This study evaluates the accuracy and reliability of an automated analysis method for F-wave latencies. METHODS: F-waves following 20 supramaximal stimuli recorded from the extensor digitorum brevis muscle of 80 limbs (55 subjects) were analyzed. F-wave latencies were determined using a computer program developed by NEUROMetrix (Waltham, MA). These results were compared in a blinded fashion with manual measurements of the same datasets by a clinical neurophysiologist with established expertise in F-waves. The manual measurements were repeated once. RESULTS: The yield rate of automated median F-wave latencies was 100% with a correlation coefficient (CC) of 0.996 when compared with manual assignment results. For individual F-wave latency measurements, comparable values were 90% and 0.977, respectively. The repeated manual measurements revealed a yield rate and CC for median latencies of 100% and 0.998, respectively, with comparable values for individual latency measurements of 95% and 0.992. CONCLUSIONS: These results indicate the feasibility of a reliable computerized automated analysis of F-wave latencies. SIGNIFICANCE: A reliable automated analysis of F-waves should add meaningfully to the value of these responses in clinical neurophysiology.

Adult↗

Vep latency: sex and head size.

OBJECTIVE: To investigate whether differences in visual evoked potential (VEP) latencies in a large sample of healthy subjects are influenced by different head size or sex or both. METHODS: Black-and-white pattern-reversal checkerboard VEPs at a frequency of 2c/deg. were recorded in a group of 54 normal subjects of both sexes (age 30.15+/-9.12 years). P100 latency was measured in all subjects and the data were analyzed in the whole sample and in a selected subgroup of subjects of both sexes with comparable head size. RESULTS: In the study group overall, the P100 latency was slightly shorter in females than males and this small difference reached only weak statistical significance (P<0.04) whereas head size differed significantly between sexes (females<males) (P<0.001). No difference was found in the P100 latency in the subgroup of the two sexes with a comparable range of head size. CONCLUSIONS: These findings suggest that VEP latency is relatively constant in a sample of healthy subjects. The slight sex difference in P100 latencies observed in a normal sample is mainly related to the slightly smaller average head size in females than in males. SIGNIFICANCE: Head size, not sex, should be considered for VEP latency normative studies.

Adult↗

Thoracolaryngeal reflex latencies in Thoroughbred horses with recurrent laryngeal neuropathy.

Electrolaryngeography was used to study the latencies of the thoracolaryngeal adductor reflex in Thoroughbred horses with and without recurrent laryngeal neuropathy (RLN). Latencies were compared in horses with grades 1 and 2 RLN, diagnosed by endoscopy in resting horses. The reliability of the measurements, effect of sedation and correlations of latencies with age of the horse were also studied. There was no effect of sedation on reflex latency periods. The latency of the reflex period measured to a convolved peak of the electromyographic response was significantly different in horses with grades 1 and 2 disease; medians and quartile ranges were 0.067 (0.065-0.073) and 0.072 (0.068-0.074) s, respectively (P<0.05). Significant associations were found between reflex latencies and both horse age and the grade of RLN. Reflex latency measurements are reliable and sensitive, and may assist with the clinical appraisal of Thoroughbred horses with RLN.

Animals↗

Multichannel auditory event-related brain potentials: effects of normal aging on the scalp distribution of N1, P2, N2 and P300 latencies and amplitudes.

Event-related potentials (ERPs) were recorded at 17 leads in an auditory oddball paradigm in 172 normal healthy subjects aged between 20 and 88 years. With advancing age, N1 latency increased parietally (0.12 ms/year), P2 latency increased frontally (0.34 ms/ year) and N2 and P300 latencies increased all over the scalp (0.37 ms/year for N2; 0.92 ms/year for P300). P300 latency/age relationship was curvilinear with accelerated latency increase in elderlies (0.35 ms/year for subjects below 60 years; versus 2.03 ms/year for subjects above 60 years). With advancing age, standard tone ERP amplitudes were enhanced frontally (0.03 microV/year for N1; 0.07 microV/year for P2), N2 amplitudes were attenuated frontally (0.11 microV/year) and P300 amplitudes were attenuated parietally (0.15 microV/year). Multichannel analysis demonstrated that ERP latencies and amplitudes depended on electrode location. Standard tone ERP latencies changed their topographic distribution with age, whereas target tone ERP latencies did not. While N1 amplitude distribution was unaffected by age, P2, N2 and P300 topography changed significantly with age: P2 topography to a more frontal distribution and increased 'global field power'; N2 topography to a more parietal distribution: P300 topography to a more frontal and more equipotential distribution Thus, specific age effects on different ERP components were confirmed.

Acoustic Stimulation↗

Saccadic latency effects of progressively deleting stimulus offsets and onsets.

We designed two extensions of Saslow's well-known gap and overlap conditions that require increased voluntary effort because of the progressive elimination of target onsets and fixation point offsets, and obtained repeatable data obeying simple numerical relations. For each of the five stimulus lighting conditions, saccadic latency was measured as a function of the retinal eccentricity or displacement of the target. Latencies were fitted by a serial processing model in which the visually guided minimum tracking latency VGL(min) is supplemented by two types of delay, dubbed 'unlock' and 'target', that can be either short or long ('direct' or 'indirect'), depending on the conditions. There are two findings: (1) The model has utility. The rank order of saccadic latencies for the five stimulus lighting conditions was constant across all subjects, sessions and eccentricities in the range 7.5'-6 degrees left or right. For pooled data, and the saccadic latency plateau (1-6 degrees), the model was also within +/-3 ms of the mean latencies. (2) Latencies of tiny saccades to intrafoveolar stimulation (7.5-45') were invariably long in all five stimulus conditions. One factor here must be the experimentally measured local prolongation of VGL(min).

Fixation, Ocular↗

Spatial attention and latencies of saccadic eye movements.

Recent theories of visual attention, such as the oculomotor readiness theory of Klein (1980) (Does oculomotor readiness mediate cognitive control of the visual attention. In: R. Nickerson, Attention and performance, Hillsdale: Erlbaum), the premotor theory of Rizzolati (1983) (Mechanisms of selective attention in mammals. In: J.P. Ewart, R.R. Capranica, D.J. Ingle, Advances in vertebrate Neuroethology (pp. 261-297). New York: Plenum) and the sequential attention theory of Henderson (1992) (Visual attention and eye movement control during reading and scene perception. In K. Rayner, Eye movements and visual cognition (260-283). New York: Springer-Verlag), propose a link between shifts in spatial attention and the generation of saccadic eye movements. In this paper we show that a winner-take-all model of spatial attention, combined with a simple model for the link between attention and eye movements, can account for the variation in saccadic latency observed in many oculomotor phenomena. These phenomena include the gap effect (Saslow M.G. (1967). Effects of components of displacement-step stimuli upon latency for saccadic eye movement. Journal of the Optical Society of America, 57, 1024-1029), the effect of target jumps on saccadic latency (Becker W. & Jurgens R. (1979). An analysis of the saccadic system by means of double step stimuli. Vision Research, 19, 967-983), the increase of saccadic latency as target eccentricity drops (Kalesnykas R.P. & Hallett P.E. (1994). Retinal eccentricity and the latency of eye saccades. Vision Research, 34, 517-531), and the modulation of saccadic accuracy using target predictability and saccadic latency (Coëffé C. & O'Regan J.K. (1987). Reducing the influence of non-target stimuli on saccade accuracy: predictability and latency effects. Vision Research, 27 (2), 227-240).

Attention↗

Auditory event related potentials in major depression: prolonged P300 latency and increased P200 amplitude.

BACKGROUND: Some studies have shown disturbances in auditory event related potentials (AERPs) in patients with major depression. METHODS: In this exploratory study, the late AERP components, N100 (latency), P200 (amplitude and latency) and P300 (amplitude and latency) were recorded in 68 subjects, i.e. 39 major depressed subjects, with (n=4) or without (n=35) cognitive deterioration, 18 patients with Alzheimer's dementia (SDAT) and 11 normal volunteers. Twenty-five major depressed patients had repeated measurements of AERPs both before and after treatment with antidepressants. RESULTS: Major depressed subjects without cognitive deterioration had significantly higher P300 latency and P200 amplitude than normal volunteers. SDAT patients and major depressed patients with cognitive impairment had a significantly higher P300 latency than depressed patients without cognitive impairment. In the latter, no significant alterations in any of the AERP components upon subchronic treatment with antidepressants were recorded. Nonresponders to antidepressant therapy had significantly higher pretreatment P300 latency and P200 amplitude than responders to treatment (P=0.006) and normal volunteers (P=0.0004). CONCLUSIONS: The findings may suggest that delayed P300 latency as well as increased P200 amplitude accompany major depression and may predict a nonresponse to subsequent antidepressive therapy.

Aged↗

Factors shaping the response latencies of neurons in the cat's auditory cortex.

This article addresses two issues. Firstly, the hypothesis that response latency might be a neural code for tone frequency was examined in single-neuron data from the primary auditory cortex of anesthetized cats. Minimal response latencies for characteristic frequency (CF) tones were independent of neural CF. Mean response latencies for a constant amplitude CF tone were also independent of CF. These data, and the fact that cortical neurons do not have an obvious independent referent for stimulus onset time, do not support the view that latency is a code for frequency. Secondly, to investigate a simple threshold model of spike initiation time, we describe the prolongations of response latency with increases in stimulus rise time and their dependence on the peak amplitude of the stimulus. These data show that in cortical neurons, it is not the peak stimulus intensity which determines first-spike latency, and second, that the response latencies are systematically not those expected on the basis of simple threshold model.

Acoustic Stimulation↗

Normal values of patellar and ankle tendon reflex latencies.

The clinical value of latency measurement of tendon reflexes in neurological patients has been reported by several authors. However, normal values are not readily comparable. In the present study, latencies and amplitudes of patellar (PTR) and ankle tendon reflexes (ATR) were measured at rest and after facilitation in 102 normal controls. A manually operated reflex hammer, tipped with electrically conductive rubber, ensured an immediate start of the sweep of the oscilloscope. Latencies showed a significant correlation with height (r = 0.70 for PTR and r = 0.72 for ATR, P < 0.0001) and to a lesser degree with age (r = 0.16 and r = 0.30, P < 0.0001). While amplitudes were highly variable, rendering them less useful for diagnostic purposes, latencies showed minimal intra-individual variability (CV 1.5 and 0.8%, respectively). Correlation of ATR-latency with the H-reflex latency of the soleus muscle was very high (r = 0.97, P < 0.0001). Comparison with three other hammer types yielded corresponding results with a hammer supplied with a piezo-electric element; however, significantly shorter latencies were found with a hammer with a microswitch, and with another hammer with a spring-contact, due to a delay from the tap on the tendon until the start of the sweep of the monitor.

Adult↗

[Characteristics of middle-latency auditory evoked potentials in awake and anesthetized patients].

Late auditory evoked potentials (50-500 msec latency) can be evoked by tonal stimuli but their instability prevents their use in many clinical situations. In contrast, the early responses (up to 10 msec) are stable, regardless of sleep or sedation, but they can only be evoked by transient, non-tonal stimuli. Therefore neither type may be used for an evaluation of frequency thresholds. The middle latency responses represent a compromise: first, they can be evoked by tonal stimuli of the tone-pip type and, second, they are relatively stable. For these reasons the authors have carried out a general study on the middle latency responses in subjects with normal hearing, in patients with impaired hearing and in patients under a variety of surgical anesthesia. The middle latency response evoked by clicks and tone-pips (4 sines of 500, 1000, 2000 and 4000 Hz) have a series of characteristic waves named, according to their latency, A(V), B(No), C(Po), D(Na), E(Pa). The threshold of visual detection for these potentials is situated near that of the psycho-acoustic threshold (0-20 dB). The authors point out the clinical utilization of the middle latency response especially in cases in which one desires an objective evaluation of the auditory threshold in the lower frequency range. It is important to know that the middle latency response remains present using some types of anesthesia (Ketalar, ataralgesy), disappears partially with neuroleptanesthesia and completely with inhalation anesthesia (fluothane, halothane).

Adult↗

Latencies of REM sleep and awakening in major depression: possible indicators of cholinergic activity.

REM latency and awakening latency were analyzed in a sample of 26 major depressive inpatients and 8 male controls recorded for two consecutive nights. A significant inverse relationship appeared between REM latency and awakening latency in depressed patients. The relationship was more marked in male than in female patients. No significant correlation between REM latency and awakening latency was observed in male healthy volunteers. The hypothetical cholinergic supersensitivity in major depression is proposed to explain the present relationship. These results suggest that awakening latency might also be taken into account in the evaluation of sleep disturbances in depressive illness.

Acetylcholine↗

Increased rate of P300 latency prolongation with age in drug-naive and first episode schizophrenia.

OBJECTIVE: Previous studies have found an increased rate of P300 latency prolongation with age in medicated chronic patients with schizophrenia, suggesting a pathological neurodegenerative process. In this study, we investigated whether this abnormality was identified in drug-naive and first episode patients with schizophrenia. METHODS: P300 from auditory stimuli was recorded from 20 drug naive and first episode male patients with schizophrenia and compared with 23 age and handedness matched healthy male controls. The relationship of P300 latency and P300 amplitude to age in each group was evaluated using polynomial regression analyses. RESULTS: Reduction of P300 amplitude was significant in drug-naive and first episode schizophrenia patients. P300 amplitude negatively correlated with age in schizophrenia patients but not in controls. Although the prolongation of P300 latency with age was observed in both groups, the regression slope for P300 latency with age was significantly steeper in patients with schizophrenia than in normal controls. Significant overall curvilinear correlations with age were also found for P300 latency and amplitude in patients with schizophrenia, and for P300 latency in normal controls. CONCLUSIONS: The greater increase in P300 latency and reduction in P300 amplitude with age may be a primary neuropathological effect of schizophrenia. SIGNIFICANCE: This study suggests that neurodegenerative processes are involved in the etiology of schizophrenia.

Adolescent↗

Repeated nocturnal sleep latencies in narcoleptic, sleepy and alert subjects.

OBJECTIVES: The purpose of this study was to assess nocturnal sleep latencies among narcoleptics. METHODS: Thirteen narcoleptics and matched sleepy and alert controls participated in this study. Subjects were awakened three times on each of two experimental nights. The latencies to sleep and rapid eye movement sleep were evaluated at the beginning of the night and following each experimental awakening. RESULTS: The alert group (AG) had a significantly longer mean nocturnal sleep latency than the narcoleptic (NG) and sleepy groups (SG). The sleep latencies at 23:00 and 01:10 h were significantly longer than the latencies at 03:10 and 05:10 h. The interaction between group and time of night demonstrated longer latencies at 23:00 and 03:10 h for the AG when compared to the SG and the NG. At 01:10 and 05:10 h all groups had comparable latencies. The number of subjects in the NG who had multiple sleep onset REM periods (SOREMPs) was significantly higher than in either the AG or the SG. CONCLUSIONS: Narcoleptics were found to have a heightened propensity to fall asleep and increased number of SOREMPs during nocturnal sleep opportunities. These characteristics are consistent with the daytime polysomnographic findings known in this patient population.

Adult↗

The effect of remifentanil on the middle latency auditory evoked response and haemodynamic measurements with and without the stimulus of orotracheal intubation.

BACKGROUND AND OBJECTIVE: Changes in the middle latency auditory evoked response following the administration of opioids have been shown. However, it remains unclear as to whether these changes are due to a direct depressant effect of opioids on the middle latency auditory evoked response itself, or an indirect effect on account of their action in attenuating central nervous system arousal associated with noxious stimuli. By comparing changes in the middle latency auditory evoked response in intubated and non-intubated patients, receiving saline or remifentanil in different doses, this study attempts to answer this question. METHODS: Fifty-four patients were anaesthetized with isoflurane and nitrous oxide (0.9 MAC) and randomized to 1-6 groups. Groups 1-3 received a bolus injection of either saline 0.9%, low-dose remifentanil (1 microg kg(-1)) or high-dose remifentanil (3 microg kg(-1)) prior to intubation of the trachea. Groups 4-6 were not intubated following the bolus injection. RESULTS: Pa and Nb amplitudes of the middle latency auditory evoked response increased by 82% and 79% with intubation in the saline group (P < 0.005) and these changes were not seen in the patients given remifentanil. There was a significant linear trend for the reduction in Pa and Nb amplitude with increasing remifentanil dose (P < 0.05). In the absence of endotracheal intubation remifentanil had no effect on either the amplitudes or latencies of the waves Pa and Nb and there was no effect of dose. For the haemodynamic measurements remifentanil attenuated the pressor response to intubation (P < 0.001) and had a significant dose-related effect (P < 0.001) in the absence of intubation. CONCLUSIONS: We demonstrated an effect of remifentanil on both the middle latency auditory evoked response and haemodynamic changes to endotracheal intubation. For the non-intubated patients there was only an effect of remifentanil on the haemodynamic measurements. This suggests that remifentanil has an effect on the middle latency auditory evoked response in attenuating the arousal associated with intubation of the trachea but has no effect in the absence of a stimulus.

Adult↗

Mechanisms of differences in gating effects on short-and long-latency somatosensory evoked potentials relating to movement.

We investigated the mechanisms underlying the differences in gating effects on short- and long-latency somatosensory evoked potentials (SEPs) relating to movement. SEPs were recorded in normal subjects for 6 different tasks in Experiment 1: Control, Movement, Distraction, Attention, Movement during Distraction and Movement during Attention, and for 4 different tasks in Experiment 2: Control, Passive Movement, Contralateral Movement and Movement Imagery. The amplitudes of short-latency SEPs were significantly reduced by active and passive movement of the stimulated hand, but long-latency SEPs (N140-P200) were significantly enhanced by active movement of the stimulated hand. Attention, Distraction, Contralateral Movement and Movement Imagery did not affect the amplitudes of SEPs. The degree of enhancement of long-latency SEPs by active Movement was greater than that by active movement with Attention or Distraction. Gating effects on long-latency SEPs were different from those on short-latency SEPs. Since this effect was not related to Attention/Distraction, Passive Movement, Movement Imagery or Movement of another site, it is probably due to specific centrifugal effects, which are different from more direct gating effects on short-latency components. This study showed the difference in gating effects on somatosensory perception depending on time periods following stimulation, which may indicate an interaction between motor and somatosensory cortex.

Adult↗

Mechanisms of loss of latency of lysosomal enzymes. Effects of incubation on the properties of lysosomal membranes.

1. The effects of sucrose and KCl on the loss of latency of lysosomal enzymes caused by incubation at 37 degrees C, pH 7.4, were examined by using Triton-filled lysosomes from rat liver and two fractions from livers of rats not injected with Triton. 2. After incubation, the percentage free activity of lysosomal enzymes was measured before and after cooling to 0 degrees C in order to determine the amount of latency lost at 37 degrees C without cooling and the additional amount lost on cooling the incubated lysosomes to 0 degrees C. 3. The latency that is lost without cooling is first decreased and then increased by increasing the osmotic strength of the incubation medium with KCl, or with sucrose in the presence of KCl. However, if the osmotic strength is increased with sucrose alone, loss of latency is decreased up to 0.25M-sucrose, but is increased only slightly at higher sucrose concentrations. Apparently the lysosome is permeated by hyperosmolar KCl but not by sucrose during incubation. 4. If the osmotic strength of the assay medium is increased with KCl, the loss of latency caused by incubation for 60 min in hyperosmolar KCl is repressed. Thus it appears that a KCl-permeated lysosome can be obtained which is relatively stable until exposure to lower osmolarities. 5. The loss of latency caused by cooling incubated lysosomes to 0 degrees C is largely eliminated if the osmotic strength of the medium in which the lysosomes are cooled is raised sufficiently with either sucrose or KCl. 6. Osmotic-fragility curves were obtained after incubation for 1 and 60 min at iso-osmoticity (0.2M-KCl or 0.25 M-sucrose). Although little loss of latency occurs at iso-osmoticity, lysosomes incubated for 60 min display greatly increased fragility on exposure to hypo-osmolar KCl, hypo-osmolar sucrose or hyperosmolar KCl. 7. It is suggested that permeability to KCl at 37 degrees C and the increase in fragility on exposure to hypo-osmolar conditions are both consequences of injury, probably from enzymic action, sustained by the lysosomal membrane during incubation at 37 degrees C.

Animals↗

Detection latency of added loads to breathing.

1. Detection latency of a range of added elastic (0.95-4.50 kPa/l) and resistive (0.73-3.29 kPa l-1 s) loads to breathing were measured in five normal subjects. Detection latency was defined as the time from the onset of the breath to detection of the load. 2. Detection latency followed a curvilinear relationship when plotted as a function of the magnitude of the added loads. A similar relationship was found with both elastic and resistive loads although detection latencies to added elastances were longer than for added resistances. 3. When the added load was expressed in terms of comparable magnitude (peak inspiratory pressure) detection latencies for added elastances were found to be consistently longer than for added resistive loads. 4. These studies show that the detection latency to added inspiratory loads follows a reciprocal relationship, that detection latencies for elastic and resistive loads are clearly different and suggest that these loads are detected during the respiratory cycle at a time when the mechanical information regarding muscular pressure is greatest.

Adult↗

The effect of arousals during sleep onset on estimates of sleep onset latency.

It is well established that insomniacs overestimate sleep-onset latency. Furthermore, there is evidence that brief arousals from sleep may occur more frequently in insomnia. This study examined the hypothesis that brief arousals from sleep influence the perception of sleep-onset latency. An average of four sleep onsets was obtained from each of 20 normal subjects on each of two nonconsecutive, counterbalanced, experimental nights. The experimental nights consisted of a control night (control condition) and a condition in which a moderate respiratory load was applied to increase the frequency of microarousals during sleep onset (mask condition). Subjective estimation of sleep-onset latency and indices of sleep quality were assessed by self-report inventory. Objective measures of sleep-onset latency and microarousals were assessed using polysomnography. Results showed that sleep-onset latency estimates were longer in the mask condition than in the control condition, an effect not reflected in objective sleep-stage scoring of sleep-onset latency. Furthermore, an increase in the frequency of brief arousals from sleep was detected in the mask condition, and this is a possible source for the sleep-onset latency increase perceived by the subjects. Findings are consistent with the concept of a physiological basis for sleep misperception in insomnia.

Adult↗