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At least 253 records · Page 14Linked to original sources
PubMed2003

Latency of the pupil light reflex: sample rate, stimulus intensity, and variation in normal subjects.

PURPOSE: To investigate the clinical usefulness of the latency of the pupil light reflex by optimizing its measurement, characterizing its variability, and determining the sensitivity of pupil latency as a function of stimulus input in normal subjects. METHODS: Computerized binocular infrared pupillography was performed in 14 eyes of seven healthy subjects. Pupils were recorded simultaneously at 60 and 1000 Hz. Each eye was alternatively stimulated eight times for 50 ms every 2.5 seconds, increasing by 0.5 log units over a 2.0-log-unit range. To determine intersubject and intereye variability, 98 eyes of 49 healthy subjects were recorded at 60 Hz over a 3.0-log-unit range (15 degrees radius stimulation, four repetitions at each intensity). RESULTS: Accuracy and resolution of latency were limited by the number of light reflexes used to estimate the average latency and were significantly affected by sampling rate when the number of reflexes recorded was fewer than four. Binocular recording and interpolation of the 60-Hz recording to 300 Hz added resolution to the latency. Biological variability contributed more to interindividual variability than did measurement variability. The range of intereye afferent asymmetry of latency in normal subjects was only between 8.3 and 35 ms-less with brighter stimulus intensity. CONCLUSIONS: An optimal method for determination of the onset of the pupil light reflex was devised that consisted of filtering, interpolation of pupil recordings, and analysis of the first and second derivative of the pupil movement. Most of the variability in latency as a function of intensity in normal subjects was due to interindividual variation and latency was well matched between the two eyes of the subjects.

Adult↗
PubMed1980

The acoustic reflex latency test: clinical application.

Acoustic reflex latency is the time interval between onset of an intense auditory stimulus and onset of middle-ear muscle contraction. The hypothesis was proposed that a retrocochlear lesion involving the afferent (VIIIth nerve) portion of the reflex arc should result in a prolongation of the reflex latency. A clinical procedure, the Acoustic Reflex Latency Test (ARLT), its protocol, methods and equipment were developed in order to test this hypothesis clinically. Absolute latency values and interaural latency differences (ILD) were established on 4 populations which included normals, cochlear lesions due to Ménière's disease, cochlear lesions of variable etiology, and 11 cases of surgically confirmed acoustic tumor. Results reveal a dramatic prolongation of latency in the presence of retrocochlear lesions (all tumors). The test was found to be most effective when 1. both ipsilateral and contralateral measurements were made, 2. stimulus frequencies of 100 Hz and 2000 Hz were employed and 3. both Absolute Latency and ILD were considered. The ARLT, while utilizing an indirect method of measurement, is a valid, cost-effective, and simple clinical procedure, yielding relative latency values and requiring only minor modifications of standard impedance equipment. The ARLT appears to have a higher efficiency rate than BERA, while providing comparable diagnostic information at a considerable saving of time, cost and personnel.

Acoustic Impedance Tests↗
PubMed2006

An antidromic study of the medial antebrachial cutaneous nerve, with a comparison of the differences between medial and lateral antebrachial cutaneous nerve latencies.

Electrodiagnostic study of the medial antebrachial cutaneous (MAC) and lateral antebrachial cutaneous (LAC) nerves is not routinely undertaken. Pathology of either nerve or of the brachial plexus may occur from a variety of causes. Iatrogenic injury of these nerves has been rarely reported, but potential exists for nerve damage with a number of medical procedures, implants, or surgeries in the flexor forearm. In any of these situations, nerve conduction studies on the MAC and the LAC can be of benefit. Previous studies have reported normal values and examined side- to-side differences in the LAC, but have not compared the latencies of the MAC to the LAC in the same limb. This study establishes normal nerve conduction study values for the MAC from 207 subjects with no risk factors for neuropathy, using a 10-cm distance and an antidromic technique. It also examines both side-to-side differences in the MAC and same-limb differences between the MAC and LAC. For this study, the upper limit of normal (ULN) was defined as the 97th percentile of observed values. The lower limit of normal (LLN) was defined as the 3rd percentile of observed values. The onset latency, peak latency, onset-to-peak amplitude, peak-to-peak amplitude, rise time, and duration were recorded. For the MAC, the mean onset latency was 1.7 +/- 0.2 ms, with a ULN of 2.0 ms. Mean peak latency was 2.2 +/- 0.2 ms, with a ULN of 2.6 ms. Onset-to-peak amplitude was 13 +/- 7 muV, with a LLN of 4 muV. Peak-to-peak amplitude was 10 +/- 7 muV, with a LLN of 3 muV. Side-to-side differences in MAC onset and peak latencies were 0.0 +/- 0.2 ms, with a ULN of 0.3 ms. Up to a 67% side-to-side decrease in MAC onset-to-peak amplitude was within the normal range. A 78% side- to-side decrease in MAC peak-to-peak amplitude was within the normal range. For the same-limb comparison of the MAC and the LAC, both onset and peak latencies had a mean difference of 0.0 +/- 0.2 ms and a ULN of 0.3 ms, regardless of whether the MAC or the LAC had the longer latency.

Journal Article↗
PubMed1997

Transient evoked otoacoustic emission with unexpectedly short latency.

Two alternative approaches for studying short-latency click-evoked otoacoustic emission (OAE) in normal-hearing subjects were employed. Growth of a click-evoked "ear canal response" with stimulus increase became progressively more non-linear and saturated when the latency of the analyzed segment of response increased. This relation between latency and shape of the response input/output function was observed even after linear component cancellation, indicating that it could be an intrinsic property of OAE. Hence, the existence of an essentially linear short-latency OAE component which is probably eliminated by commonly used artifact cancellation technique is suggested. Taking into account the fact that transient evoked otoacoustic emission (TEOAE) may be completely suppressed by simultaneously presented noise, a "true" artifact cancellation was performed by subtracting the ear canal response in the presence of a masker from the conventional click-evoked OAE recording. An additional TEOAE component with a latency of 2.5-5 ms was found. Its growth with stimulus intensity was indeed more linear than that of later components. However, latency and frequency of this TEOAE component, being specific for each subject, can hardly be explained by both a commonly assumed latency-frequency relationship of TEOAE and a generally used estimation of TEOAE latency as the sum of the forward and backward traveling wave propagation times.

Acoustic Stimulation↗
PubMed1990

Statistical properties of ABR amplitudes and latencies. Implications for computation of reference limits and relation to click phase.

A method for statistical analysis and computation of reference limits for ABR latency and amplitude variables is presented. Condensation and rarefaction ABRs from 47 healthy controls aged 4-58 years were investigated. With respect to gaussianity of distributions, the square root transformation was superior to the logarithmic transformation for amplitudes, while the logarithmic transformation performed better for amplitude ratios. Wave V latency and the I-V interpeak latency were nearly normally distributed, while other latencies and inter-peak latencies displayed varying displacement from a normal distribution. Rarefaction ABR distributions were slightly closer to normality than were condensation ABRs. Amplitude vs. following amplitude and latency vs. amplitude correlation coefficients were larger for R than for C click ABRs; thus R clicks seem to evoke a better synchronized neural volley. Most of the correlation between amplitude and latency could be explained by the influence of age and sex. Hence, age and sex matched reference limits for ABR amplitudes, without correction for latency, seem to be adequate in practical clinical work.

Acoustics↗
PubMed2005

Tail-flick latency and self-mutilation following unilateral deafferentation in rats.

Unilateral deafferentation induced by transection of the C(4)-C(8) dorsal roots of spinal cord, followed by a complex of abnormal self-mutilating behavior, is interpreted as an animal model of chronic nociception. The objective of our study was to test the differences in tail-flick latency between intact control and unilaterally deafferented animals and to assess the changes in their acute nociceptive sensation. The initial hypothesis was that deafferentation-induced painful sensation might cause stress-induced analgesia that should be manifested as prolonged tail-flick latency. The experiment was carried out on 11 male and 10 female adult Wistar rats. The tail-flick latency was repeatedly measured over a period of 10 consecutive weeks both in the preoperative baseline period and following multiple cervical dorsal rhizotomy. Contrary to our hypothesis, unilateral deafferentation was followed by a significant shortening of the tail-flick latency both in males and females. In deafferented animals, compared to the controls, variations of tail-flick latency were reduced. In individual animals after deafferentation, concurrent dynamic changes were observed in self-mutilating behavior, in a loss and regaining of body weight, and in tail-flick latency. Our data suggest that changes in tail-flick latency may be interpreted in terms of central sensitization and that tail-flick latency might be considered as a useful marker of chronic nociception.

Animals↗
PubMed1999

Age and sex differences in latencies of waves I, III and V in auditory brainstem response of normal hearing subjects.

Latencies of auditory brainstem response are known to be affected by age and sex. We have investigated the effects of age and sex on absolute latencies of waves I, III and V, the interpeaks intervals I-V, I-III and III-V for left and right ears in 67 healthy subjects with normal hearing. We evaluated the reproducibility of the response between ears which showed consistent data. Latency-intensity plots for waves I, III and V were compared among men and women by estimating the regression equations, with no significant difference in the slopes. Regression analysis revealed that latencies of waves I and V were increased with age in men from childhood up to fifties, according to a linear function. However, in women latencies were not dependent on age. The intervals I-V, I-III and III-V were independent on age for both men and women. The latencies of waves III and V and the I-III and I-V intervals were significantly shorter in women than in men in both ears. The findings obtained in the present study show that gender have a stronger effect on latencies of waves III and V, shortening the I-III and I-V intervals in women. Moreover, latencies of waves I and V increase with age in men.

Adolescent↗
PubMedDate not supplied

Timing of cortical activation: a latency-resolved event-related functional MR imaging study.

BACKGROUND AND PURPOSE: The time course of cortical activations of different anatomic areas has been demonstrated to reflect, to some degree, the temporal dynamics of the brain network. The purpose of this study was to determine the temporal sequence of the hemodynamic response in the visual, supplemental motor (SMA), and primary motor cortical areas by using a visuomotor reaction time task. METHODS: The reaction times (RTs) of 26 right-handed subjects were recorded in response to a visual cue during an event-related functional MR imaging (fMRI) experiment. Statistical parametric mapping (SPM99) was used, and activation maps were produced for each subject. This was followed by a random-effects group analysis. Using a weighted least-squares approach, we recorded the time at onset of the hemodynamic response of the fMRI activation in four regions of interest: the right occipital (RO) and left occipital (LO) visual cortices, the SMA, and the left sensorimotor area (LM1). Linear regression analysis was done between the RTs and the mean latencies for the four areas. RESULTS: Using the group analysis, the results showed that the first regions to activate were the visual occipital cortices (RO and LO) with mean latency +/- standard error of mean (SEM) of 1.74 +/- 0.05 s and 1.85 +/- 0.08 s, respectively. The visual occipital areas were followed by the SMA of 2.07 +/- 0.16 s and finally the LM1 with a mean latency of 2.1 +/- 0.15 s. There were significant differences in the mean onset of latencies between RO and LO, RO and SMA, and RO and LM1 (P <.05). On performing regression analysis between the RTs and the mean latencies by using the group analysis, there was no significant correlation with any of the four areas. By using an individual subject analysis, the results again showed that the first regions to activate were the visual occipital cortices (RO and LO) with mean latency +/- SEM of 1.75 +/- 0.06 s and 1.84 +/- 0.12 s, respectively, followed by the SMA with a mean latency of 2.19 +/- 0.25 s and finally the LM1 of 2.26 +/- 0.38 s. There was no significant difference between the mean onset latencies. CONCLUSION: The onset of the hemodynamic response started first in the visual cortex (input) followed by the SMA and primary motor cortical area (output). The onset of activation showed no direct correlation with the overall RTs of the subjects, leading one to suggest that the peripheral motor unit may have a greater impact on RT than the central contribution.

Adult↗
PubMedDate not supplied

[Distribution of latencies of visual evoked potentials in a sample of schizophrenic patients].

AIM: The aim of the study is an analysis of distribution of visual evoked potentials (VEP) latencies in the group of schizophrenic and healthy subjects. METHOD: A study was carried out on a group of 30 patients (8 males and 22 females) with a DSM-III-R diagnosis of schizophrenia (disorganised schizophrenia--5, paranoid schizophrenia--12, residual schizophrenia--6, and undifferentiated schizophrenia--6). During the study 20 patients were given neuroleptics, 10 patients did not receive treatment. A control consisted of 50 healthy persons (25 males and 25 females). A stimulation of a chessboard pattern reversal (0.5 Hz, 30', 50 cd/m2) was applied. Evoked potentials were measured between top of a head (Cz) and occipital leads O1 and O2. RESULTS: Schizophrenic patients have frequently prolonged N2 latency, and shortened P300 latency. Three groups of patients have been distinguished, based on a pattern of latencies: (1) patients with prolonged latencies of all the waves (half of the patients), (2) patients with prolonged N2 latency, and shortened P300 latency (one fourth of the patients), and (3) patients with latencies similar to control (one fourth of the patients).

Adult↗
PubMed1991

[P300 latencies in epileptic children: the differences among various epileptic syndromes].

Auditory event-related potentials (ERPs) were recorded from 129 epileptic children of 5 to 20 years of age. To clarify the developmental changes in each of the epileptic syndromes, P300 latencies of ERPs were examined. ERPs were elicited with the auditory oddball paradigm. P300 detection was occasionally difficult in epileptic children. Mean P300 latency in epileptic children (375 +/- 39.7 msec) was significantly prolonged compared with that in normal control children. (355 +/- 39.1 msec). P300 latencies in the children with symptomatic partial epilepsies were prolonged and were not recognized to be shortened with age. In the idiopathic partial epilepsies of 5 to 12 years of age, P300 latencies showed almost the same values with those in the normal children. However, in the idiopathic partial epilepsies of 13 to 15 years of age, P300 latencies were significantly prolonged compared with those in normal children and there were no difference in P300 latencies with other epileptic syndromes. P300 latencies in idiopathic generalized epilepsies showed intermediate values between that in symptomatic partial epilepsies and idiopathic partial epilepsies. Each epileptic syndrome showed different developments in P300 latencies with age. This results suggests that the development and the disturbance of cognitive functions differ among the epileptic syndromes.

Adolescent↗
PubMed1989

Short- and long-latency median nerve somatosensory evoked potentials in stroke patients.

Short- and long-latency somatosensory evoked potentials (SEPs) were elicited by stimulation of the median nerve in 104 stroke patients, 59 men and 45 women. Their ages ranged from 25 to 90 years, with a mean age of 68 years. All of the patients presented with acute unilateral motosensory or sensory deficits. Based on CT findings, the patients were divided into four groups: thalamic hemorrhage (52 cases), thalamic infarct (21 cases), putaminal hemorrhage or infarct (13 cases) and infarction in the corona radiata or subcortical white matter (18 cases). The criteria for abnormal SEP responses were as follows: (1) absence of N18, (2) prolongation of central conduction time, (3) delay in peak latency of N32, (4) delay in peak latency of N60, and (5) decrease in response amplitude. In patients with thalamic stroke, the abnormality rate of SEPs was 93% (68 out of 73 cases). When the lesions were located primarily in the posterolateral thalamus, all SEP components, particularly the N18 (short-latency) component, were affected. Lesions in other thalamic areas caused changes in the N32 (mid-latency) and the N60 (long-latency) components. In putaminal, corona radiata and subcortical lesions, the abnormality rate of SEPs was 84% (26 out of 31 cases). The N18 component was absent in 3 patients with putaminal hemorrhage. Infarct in the corona radiata and subcortex tended to affect the mid- and long-latency components with relative preservation of the short-latency components.

Adult↗
PubMed1989

[Does a "transcortical" loop of the long-latency muscle reflex exist?].

EMG responses were produced by electric stimulation of the dermal branches of the nn. digilates of the index finger of the right hand and recorded from the m. interosseus dorsalis I. during its slight isometric contraction. The mean initial latency of a long-latency muscular reflex was 50.68 ms in men and 49.13 in women. The author mentions some arguments indicating the probable existence of a transcortical loop: The latency of long-latency reflexes increases gradually from proximal to distal muscles. The short-latency component of the somatosensory evoked potential N20 appears mid-time between the time of the stimulus and the onset of the long-latency reflex and thus the time interval in the long-latency reflex is sufficient for a transcortical loop. The author found a facilitation of the muscular reflex response as well as of the preparatory cortical potential during the preparatory period of voluntary flexion of the fingers during concurrent electric stimulation of the peripheral nerve. The late reflex component increases considerably and is better synchronized during the movement of the thumb instead of isometric contraction, because during kinetic innervation afferent impulses reach the precentral cortex at a higher facilitated level. These results document well the modifiable, plastic behaviour of transcortical reflexes. The method of long-latency reflexes can be used in electrophysiological diagnosis of disorders of the CNS and it is promising also in therapeutic stimulation rehabilitation and in locomotor reeducation.

Adult↗
PubMed1995

[Effects of anesthetic drugs and temperature on brain stem and mid-latency evoked potentials].

We evaluated the effects of anesthetic drugs and temperature on brain stem and mid-latency evoked potentials (BAEP and MLAEP) in 20-patients who were scheduled for elective cardiac operation using cardiopulmonary bypass with moderate hypothermia. At esophageal temperature of 36 degrees C, the latency of MLAEP was slightly prolonged by the increase of fentanyl dose, which suggested that the latency prolongation of MLAEP could not block the oscillation of auditory stimulation. At esophageal temperature of 27 degrees C, the latency of MLAEP nearly disappeared, and the latency of MLAEP gradually returned with the recovery of the esophageal temperature. The latency of BAEP was markedly prolonged at 27 degrees C and returned to the normal latency at 36 degrees C. The latency of MLAEP retained by high dose fentanyl suggests that patients may be aware during cardiopulmonary bypass at normothermia, and BAEP may be one of the useful brain function monitors during cardiopulmonary bypass.

Adolescent↗
PubMed1998

Postperceptual effects and P300 latency.

P300 latency is commonly thought to provide a chronometric index of the duration of perceptual processing. Because the evidence in favor of this assumption is controversial, we examined whether P300 latency is influenced by perceptual processes, response selection, and by motoric processes in two experiments using a two-choice spatial stimulus-response compatibility (SRC) task. Both experiments revealed additive effects of perceptual difficulty with spatial SRC in reaction time and P300 latency. In addition, Experiment 2 showed that P300 latency measured in average waveforms is insensitive to motoric processes. The influence of spatial SRC on P300 latency disagrees with the view that P300 latency is sensitive only to stimulus evaluation processes. However, P300 latency may be used to discriminate between influences on premotoric and motoric processing stages. A response conflict account for the SRC effect on P300 latency is suggested.

Acoustic Stimulation↗
PubMedDate not supplied

Varicella-zoster virus latency in human ganglia.

Varicella-zoster virus (VZV) is a human herpesvirus which causes varicella (chickenpox) as a primary infection, and, following a variable period during which it remains in latent form in trigeminal and dorsal root ganglia, reactivates in later life to cause herpes zoster (shingles). VZV is a significant cause of neurological disease including post-herpetic neuralgia which may be persistent and highly resistant to treatment, and small and large vessel encephalitis. VZV infections are more frequent with advancing age and in immunocompromised individuals. An understanding of the mechanisms of latency is crucial in developing effective therapies for VZV infections of the nervous system. Such studies have been hampered by the difficulties in working with the virus and also the lack of a good animal model of VZV latency. It is known that the ganglionic VZV burden during latency is low. Two of the key questions that have been addressed are the cellular site of latent VZV and the identity of the viral genes which are transcribed during latency. There is now a consensus that latent VZV resides predominantly in ganglionic neurons with less frequent infection of non-neuronal satellite cells. There is considerable evidence to show that at least five viral genes are transcribed during latency. Unlike herpes simplex virus-1 latency, viral protein expression has been demonstrated during VZV latency. A precise knowledge of which viral genes are expressed is crucial in devising novel antiviral therapy using expressed genes as therapeutic targets. Whether gene expression at both the transcriptional and translational levels is more extensive than currently reported will require much more work and probably new molecular technology.

Chickenpox↗
PubMed2005

Functional analysis of bovine herpesvirus 1 (BHV-1) genes expressed during latency.

Bovine herpes virus 1 (BHV-1) establishes latency in sensory neurons of trigeminal ganglia (TG), and germinal centers of pharyngeal tonsil. Periodically BHV-1 reactivates from latency, virus is shed, and consequently virus transmission occurs. Two transcripts, the latency related (LR) RNA and ORF-E, are abundantly expressed in TG of latently infected cattle. A LR mutant strain of BHV-1 was constructed that contains stop codons near the beginning of the LR-RNA. The LR mutant virus does not express two proteins encoded by the LR gene, or reactivate from latency suggesting that LR protein expression regulates the latency-reactivation cycle. Higher levels of apoptosis occur in TG of calves infected with the LR mutant versus wild type BHV-1 indicating that the anti-apoptotic properties of the LR gene regulate the latency-reactivation cycle. The LR gene also inhibits bICP0 expression and mammalian cell growth, but these functions do not require LR protein expression. In contrast, the ability of the LR gene to inhibit apoptosis appears to require LR protein expression. A small open reading frame (ORF-E) that is located within the LR promoter is expressed in the nucleus of neuroblastoma cells. We predict that the LR gene and ORF-E regulate the BHV-1 latency-reactivation cycle.

Animals↗
PubMed2002

Gamma-herpesvirus latency is preferentially maintained in splenic germinal center and memory B cells.

The gamma-herpesviruses are oncogenic B cell lymphotrophic viruses that establish life-long latency in the host. Murine gamma-herpesvirus 68 (MHV-68) infection of mice represents a unique system for analyzing gamma-herpesvirus latency in splenic B cells at different stages of infection. After intranasal infection with MHV-68 we analyzed the establishment of latency 14 days after infection, and the maintenance of latency 3 months after infection in different purified subpopulations of B cells in the spleen. The data show that MHV-68 latency is mainly established in germinal center B cells and that long-term latency is preferentially maintained in two different subsets of isotype-switched B cells, germinal center and memory B cells. Cell cycle analysis indicates that MHV-68 is located in both cycling and resting isotype-switched B cells. Analysis of viral gene expression showed that both lytic and latent viral transcripts were differentially expressed in germinal center and memory B cells during long-term latency. Together, these observations suggested that gamma-herpesviruses exploit the B cell life cycle in the spleen.

Animals↗
PubMed2006

Herpes simplex virus type 2 (HSV-2) establishes latent infection in a different population of ganglionic neurons than HSV-1: role of latency-associated transcripts.

Herpes simplex virus type 1 (HSV-1) and HSV-2 cause very similar acute infections but differ in their abilities to reactivate from trigeminal and dorsal root ganglia. To investigate differences in patterns of viral infection, we colabeled murine sensory ganglia for evidence of HSV infection and for the sensory neuron marker A5 or KH10. During acute infection, 7 to 10% of HSV-1 or HSV-2 antigen-positive neurons were A5 positive and 13 to 16% were KH10 positive, suggesting that both viruses reach each type of neuron in a manner proportional to their representation in uninfected ganglia. In murine trigeminal ganglia harvested during HSV latency, 25% of HSV-1 latency-associated transcript (LAT)- and 4% of HSV-2 LAT-expressing neurons were A5 positive, while 12% of HSV-1 LAT- and 42% of HSV-2 LAT-expressing neurons were KH10 positive. A similar difference was observed in murine dorsal root ganglia. These differences could not be attributed to differences in LAT expression levels in A5- versus KH10-positive neurons. Thus, HSV-1 demonstrated a preference for the establishment of latency in A5-positive neurons, while HSV-2 demonstrated a preference for the establishment of latency in KH10-positive neurons. A chimeric HSV-2 mutant that expresses the HSV-1 LAT exhibited an HSV-1 phenotype, preferentially establishing latency in A5-positive neurons. These data imply that the HSV-1 and HSV-2 LAT regions influence the ability of virus to establish latency in different neuronal subtypes. That the same chimeric virus has a characteristic HSV-1 reactivation phenotype further suggests that LAT-influenced establishment of latency in specific neuronal subtypes could be an important part of the mechanism by which LAT influences viral reactivation phenotypes.

Animals↗