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PubMed2006

Factors influencing F-wave latency detection of lumbosacral root lesions using a detection theory based model.

OBJECTIVE: To evaluate the F-wave dilution hypothesis; which implies that absolute F-wave latencies obscure the much smaller delay associated with slow intra-lesion conduction, such is caused by nerve root compression in lumbosacral radiculopathy. A corollary objective is to determine how F-wave measurement and pathological factors influence diagnostic accuracy. METHODS: An analytical model is developed based on signal detection theory and a number of simplifying assumptions. Diagnostic accuracy, quantified by the area under the receiver operating characteristic (ROC) curve, is determined for various model realizations derived from the clinical and experimental neurophysiology literature. A preliminary experimental validation of model predictions is also performed. RESULTS: Absolute F-wave latency does not influence the accuracy of focal lesion detection. F-wave latency variance and lesion pathology are the determinant factors. F-wave latencies and distal latencies are estimated to have qualitatively similar detection characteristics, although distal latencies have quantitatively better diagnostic efficacy for comparable focal pathology. Preliminary experimental results support the modeled dependence of diagnostic accuracy on latency variance and lesion severity. CONCLUSIONS: Absolute F-wave latency does not dilute slow conduction within focal lesions, such as in lumbosacral radiculopathy. The dominant measurement factor is F-wave latency variance. SIGNIFICANCE: To maximize the diagnostic utility of F-wave latencies, focus must be placed on reducing latency variance, such as through correction for demographic covariates. This model calls into question the F-wave dilution hypothesis.

Adolescent↗
PubMed1995

Prolongation of conduction time during premature stimulation in the human atrium is primarily caused by local stimulus response latency.

BACKGROUND: Conventional clinical electrophysiological techniques cannot accurately differentiate between local stimulus response latency and propagation time of the atrial response. The purpose of this study was to identify and distinguish local stimulus response latency from impulse propagation time in the human right atrium during programmed electrical stimulation. METHODS: Pacing was performed from two atrial sites (high and low right atrium) in 19 patients, using monophasic action potential recording/pacing combination catheters (interelectrode distance < 2 mm). Local stimulus response latency (interval between stimulus artifact and upstroke of the local monophasic action potential), and propagation time (interval between local and remote monophasic action potential upstroke) were evaluated at a basic cycle length (S1-S1) of 600 ms and as a function of the extrastimulus proximity (interval between extrastimulus and effective refractory period). Data are presented as means +/- SEM. RESULTS: During basic stimulation, local latency was very small (3.8 +/- 1.7 ms). During premature extrastimulation (proximity < 70 ms), local latency increased progressively with decreasing coupling intervals. Prolongation of local latency was most pronounced during stimulation close to the effective refractory period with local stimulus response latency increasing to 18.3 +/- 1.4 ms (380 +/- 7.9%) at 10 ms proximity (P < 0.002) and to 27.9 +/- 3.7 ms (630 +/- 13.2%) at 5 ms proximity, respectively (P < 0.0001). The impulse propagation time between the stimulation site and the remote recording site was on average 54.5 +/- 14.3 ms during basic stimulation, and increased up to 62.1 +/- 13.5 ms (14.0 +/- 8.4%), which was not significant. CONCLUSIONS: The intra-atrial impulse propagation remained essentially unchanged during the entire range of premature stimulation. Local stimulus response latency was negligible and constant during late coupling intervals but increased dramatically when extrastimulation approached the preceding repolarization phase. This has the following clinical impact: first, local stimulus response latency during premature extrastimulation curbs the targeted atrial response interval second, local stimulus response latency, not propagation time, seems responsible for the greater functional than effective refractory period during electrical stimulation; third, local stimulus response latency should be considered in pace mapping for accurate comparison of conduction time before pacing with that during pacing.

Aged↗
PubMed2004

Murine Multiple Sleep Latency Test: phenotyping sleep propensity in mice.

STUDY OBJECTIVES: Objectives were to (1) establish a measure of sleep propensity for a more comprehensive characterization of sleepiness in murine genetics and interventional studies and (2) to characterize sample sizes necessary for statistical differences in effect. DESIGN: Average multiple sleep latency values were compared in mice, varying strain, circadian time, and forced-wakefulness conditions. SUBJECTS: Adult male mice of inbred strains were studied. INTERVENTIONS: Mice were implanted with electroencephalographic and electromyographic recording electrodes. Twenty-four-hour periods of stable baseline sleep activity (> 600 minutes) were confirmed prior to baseline sleep-latency testing. Average sleep latencies were obtained across 10- and 20-minute nap opportunities within 4 consecutive 30-minute periods. Forced wakefulness protocols were performed prior to additional sleep-latency tests. MEASUREMENTS AND RESULTS: Sleep-latency testing with 20-minute nap opportunities every 30 minutes revealed a shorter sleep latency in the lights-on period (12.4 minutes +/- 0.9 vs 16.5 +/- 1, P < .001), a substantial reduction in sleep latencies in mice subjected to 6-hour forced wakefulness (eg, C57BL/6J baseline: 12.4 +/- 0.9 minutes, and forced wakefulness, 8.5 +/- 0.9 minutes, P < .01), and strain differences in latencies following short-term forced wakefulness (P < .01). Sample sizes for 85% power to detect a 25% reduction in the 20-minute daytime Murine Multiple Sleep Latency Test require fewer than 20 mice per group for commonly used transgenic background strains. CONCLUSIONS: The Murine Multiple Sleep Latency Test is a robust measure of sleep propensity, and the latency varies with homeostatic and circadian influences. The test requires minimal added time to standard murine sleep recordings, yet yields important additive information.

Animals↗
PubMed1998

Azimuth coding in primary auditory cortex of the cat. II. Relative latency and interspike interval representation.

This study was designed to explore a potential representation of sound azimuth in the primary auditory cortex (AI) of the cat by the relative latencies of a population of neurons. An analysis of interspike intervals (ISI) was done to asses azimuth information in the firings of the neurons after the first spike. Thus latencies of simultaneously recorded single-unit (SU) spikes and local field potentials (LFP) in AI of cats were evaluated for sound presented from nine speakers arranged horizontally in the frontal half field in a semicircular array with a radius of 55 cm and the cat's head in the center. SU poststimulus time histograms (PSTH) were made for each speaker location for a 100-ms window after noise-burst onset using 1-ms bins. PSTH peak response latencies for SUs and LFPs decreased monotonically with intensity, and most of the change occurred within 15 dB of the threshold at that particular azimuth. After correction for threshold differences, all latency-intensity functions had roughly the same shape, independent of sound azimuth. Differences with the minimum spike latency observed in an animal at each intensity were calculated for all azimuth-intensity combinations. This relative latency showed a weakly sigmoidal dependence on azimuth that was independent of intensity level >40 dB SPL. SU latency differences also were measured with respect to the latencies of the LFP triggers, simultaneously recorded on the same electrode. This difference was independent of stimulus intensity and showed a nearly linear dependence on sound azimuth. The mean differences across animals for both measures, however, were only significant between contralateral azimuths on one hand and frontal and ipsilateral azimuths on the other hand. Mean unit-LFP latency differences showed a monotonic dependence on azimuth with nearly constant variance and may provide the potential for an unbiased conversion of azimuth into neural firing times. The general trend for the modal ISI was the same as for relative spike latency: the shortest ISIs were found for contralateral azimuths (ISI usually 3 ms) and the longer ones for ipsilateral azimuths (the most frequent ISI was 4 ms, occasionally 5 ms was found). This trend was also independent of intensity level. This suggests that there is little extra information in the timing of extra spikes in addition to that found in the peak PSTH latency.

Acoustic Stimulation↗
PubMed2005

Serotonin shifts first-spike latencies of inferior colliculus neurons.

Many studies of neuromodulators have focused on changes in the magnitudes of neural responses, but fewer studies have examined neuromodulator effects on response latency. Across sensory systems, response latency is important for encoding not only the temporal structure but also the identity of stimuli. In the auditory system, latency is a fundamental response property that varies with many features of sound, including intensity, frequency, and duration. To determine the extent of neuromodulatory regulation of latency within the inferior colliculus (IC), a midbrain auditory nexus, the effects of iontophoretically applied serotonin on first-spike latencies were characterized in the IC of the Mexican free-tailed bat. Serotonin significantly altered the first-spike latencies in response to tones in 24% of IC neurons, usually increasing, but sometimes decreasing, latency. Serotonin-evoked changes in latency and spike count were not always correlated but sometimes occurred independently within individual neurons. Furthermore, in some neurons, the size of serotonin-evoked latency shifts depended on the frequency or intensity of the stimulus, as reported previously for serotonin-evoked changes in spike count. These results support the general conclusion that changes in latency are an important part of the neuromodulatory repertoire of serotonin within the auditory system and show that serotonin can change latency either in conjunction with broad changes in other aspects of neuronal excitability or in highly specific ways.

Acoustic Stimulation↗
PubMed1999

Association between the Epworth sleepiness scale and the multiple sleep latency test in a clinical population.

BACKGROUND: Excessive daytime sleepiness can be evaluated with both subjective and objective tests. OBJECTIVE: To examine the association between Epworth Sleepiness Scale scores and sleep latency on the multiple sleep latency test. DESIGN: Case series. SETTING: Referral sleep disorders center. PATIENTS: 102 consecutive patients evaluated for excessive daytime sleepiness. MEASUREMENTS: Epworth Sleepiness Scale scores and mean sleep latency on the multiple sleep latency test. RESULTS: No significant association was seen between Epworth scores and mean sleep latency (Pearson correlation, -0.17 [95% CI, -0.35 to 0.03]; P = 0.09) (analysis of variance, P = 0.13). The mean Epworth score did not differ in three groups of patients who were defined by mean sleep latency as having normal sleep latency (>10 minutes), moderate sleep latency (5 to 10 minutes), or severe sleep latency (<5 minutes) (analysis of variance, P = 0.13). CONCLUSIONS: No statistically or clinically significant association was seen between Epworth scores and mean sleep latency. The subjective Epworth Sleepiness Scale and the objective multiple sleep latency test may evaluate different, complementary aspects of sleepiness.

Humans↗
PubMed1999

Twin vs. singleton pregnancy. Clinical characteristics and latency periods in preterm premature rupture of membranes.

OBJECTIVE: To compare the clinical characteristics and latency periods (latencies) of preterm premature rupture of the membranes (PPROM) in twin vs. singleton pregnancy. STUDY DESIGN: Between January 1986 and December 1996, data on all women with singleton and twin gestations complicated by PPROM were reviewed. Perinatal morbidity, mortality and latencies between singleton and twin pregnancies were compared. A further division according to PPROM at < 30 and > or = 30 weeks' gestation was made in both groups. Their latencies were compared. RESULTS: A total of 131 singleton and 48 twin pregnancies with PPROM between 20 and 36 weeks' gestation were included in this series. Regardless of the gestational age at PPROM, the mean latencies of singleton and twin pregnancies were statistically similar (4.4 +/- 3.3 vs. 3.4 +/- 2.9 days, nonsignificant). When PPROM occurred at > or = 30 weeks, the latency of twin pregnancies was shorter than that of singleton pregnancies (2.5 +/- 1.9 vs. 3.7 +/- 2.6 days, P < .05). In both groups, the latencies of PPROM at < 30 weeks were longer than that at > or = 30 weeks (singleton, 5.6 +/- 4.0 vs. 3.7 +/- 2.6 days, P < .005; twin, 4.8 +/- 3.5 vs. 2.5 +/- 1.9 days, P < .05). We also observed a higher percentage of deliveries within the initial 48 hours in twin pregnancies: 50% of women delivered within 48 hours after PPROM and 91.7% within 7 days. In contrast, 26.7% and 85.5% of singleton pregnancies with PPROM were delivered within 48 hours and 7 days, respectively. Perinatal and neonatal outcomes in both groups were similar. CONCLUSION: This investigation provides the basis for patient counseling and management in twin pregnancies with PPROM. In general, singleton and twin pregnancies with PPROM had similar latencies. Latency in PPROM at < 30 was longer than that of PPROM at > or = 30 weeks' gestation in both singleton and twin pregnancies. When PPROM occurred at < 30 weeks' gestation, both groups appeared to have similar latencies. In pregnancies with PPROM at > or = 30 weeks' gestation, latency in twins was shorter than in singleton pregnancies. In twin pregnancies with PPROM after 30 weeks' gestation, prompt steroid administration for fetal lung maturity should be considered.

Adult↗
PubMed1996

[Median nerve somatosensory evoked potentials--studies on latency variability as a function of subject height and age].

Somatosensory evoked potentials (SEP) to median nerve stimulation were studied in a group of 61 healthy volunteers (36 men, 25 women) between 15 and 79 years of age. The absolute peak latencies of peripheral N9, Erb, cervical N11 and N13, cortical N20, N32 and N60 were analyzed as a function of height and age. Three interpeak latencies, Erb-N13, Erb-N20 and N13-N20, were equally studied. There was no gender difference in the latencies and interpeak latencies of SEP in multiple correlation analysis involving height and age. Multiple regression analysis showed that except for N60 peak latency, the subject's height and age provided better prediction of other SEP latencies, and Erb-N13 and Erb-N20 interpeak latencies than simple and polynomial [correction of polynominal] linear regression. Multiple regression analysis was found to provide better optimal clinical upper limits for individual SEP latencies and interpeak latencies, and may increase the diagnostic sensitivity. The t-value of the multiple regression coefficient for standardized height and standardized age showed that the effects of age on N32 and N60 peak latencies, and on Erb-N13 and Erb-N20 interpeak latencies were a more important factor than those of height. A negative correlation was found between height and age in our subjects. Although this may be a characteristic of modern Japanese, it suggests the necessity of renewing regression models at intervals of 5 or 10 years.

Adolescent↗
PubMed1998

Herpes simplex virus latency after direct ganglion virus inoculation.

Herpes simplex virus (HSV) latent infection of ganglion neurons follows axoplasmic transport of HSV, probably in the form of nucleocapsid from peripheral sites of infection (e.g. footpad). This raises the possibility that latency is dependent on this particular means of presenting HSV to ganglion neurons. To investigate this, we directly infected ganglia of mice with HSV and evaluated latency. Initially, ganglia were surgically exposed in intact mice, infected with HSV and after 4 weeks evaluated for HSV latency-associated transcript (LAT) expression. LAT expression suggested latency. To more fully evaluate latency after direct ganglion inoculation, a transplant model was developed. In this model, ganglia were removed from mice, inoculated with HSV, transplanted into syngeneic recipients and evaluated for latency after several weeks. Latency was evident in transplanted ganglia by (1) the presence of LAT in neurons; (2) the lack of HSV ICP4 RNA or viral antigen, and (3) the isolation of HSV from explants of transplants but not from direct homogenates. The transplant model was then used to evaluate the effect of inhibition of HSV replication on latency. Antivirals which inhibited HSV replication markedly decreased the number of LAT-positive neurons in transplants, suggesting a role for HSV replication mechanisms and latency. It is thought that direct ganglion inoculation and ganglion transplant methods will permit unique investigations of mechanisms of latency.

2-Aminopurine↗
PubMed1978

Changes in latency and duration of neural responding following developmental auditory deprivation.

The initial latency of spikes evoked by click stimulation and the duration over which spiking occurred were observed in the inferior colliculi of rats. One ear of these animals had been deprived of early auditory stimulation by ligation of the external meatus. Clicks presented to the normally experienced ears evoked spikes in the opposite colliculus with latencies that depended on the characteristic frequency of the unit. Low-frequency (less than 5 kHz) units had latencies from 6-10 msec. Latencies declined to 3-4 msec for high frequency (greater than 20 kHz) units. After an ear had been deprived of sound from 10 days after birth, response latencies of units in the opposite colliculus with characteristic frequencies below about 10 kHz were comparable to controls, but most units above 10 kHz had latencies 2-3 times control latencies. Spike activity evoked in these units did not continue as long as that for most comparable control units. Ears sound deprived for an equal period from 60 days after birth also had changes in latencies and response durations, but these were much less than in the developmentally deprived. Latencies of gross potentials at the auditory nerve were not affected by early deprivation, indicating a central origin for the latency changes.

Acoustic Stimulation↗
PubMed1981

The latency of auditory nerve-brainstem responses in sensorineural hearing loss.

The use of auditory nerve-brainstem responses in differential diagnosis of hearing loss is based on several properties of these responses including response latency. The auditory nerve response latency has been shown to be prolonged in conductive hearing loss. The latency of the brainstem responses is also often prolonged in retrocochlear hearing loss. However, the effect of sensorineural hearing losses on auditory nerve response latency is not clear. Several authors report that response latency is prolonged in sensorineural loss, whereas others claim that it is unchanged. To study this, auditory nerve-brainstem responses to 75 dB HL clicks were recorded in normal-hearing subjects and in those with various degrees of high-frequency sensorineural hearing loss. In the more extreme hearing losses, the auditory nerve response could not be seen in the response trace, so the latency of the earlobe positive wave from the region of the inferior colliculus was considered as mirroring auditory nerve response latency, since the time interval between these two waves has been shown to be constant. The average latency of the more severe hearing loss group (more than 40 dB hearing loss at 4kHz) was found to be only 0.35 ms longer than that of the normal-hearing group. This value is smaller than that seen in most conductive and retrocochlear hearing losses. This result warrants continued use of prolonged auditory nerve response latency (greater than 0.35 ms) as an indicator of conductive hearing loss. Possible explanations for smaller latency prolongation than expected of the auditory nerve response in sensorineural hearing loss are discussed based on the properties of single auditory nerve fibers.

Audiometry↗
PubMedDate not supplied

Delayed P300 latency correlates with abnormal Test of Variables of Attention (TOVA) in adults and predicts early cognitive decline in a clinical setting.

Delayed P300 latency identifies dementia better than the Mini-Mental Status Exam and, in some cases, the Wechsler Memory Scale (WMS-III). The purpose of this study was to determine whether the outcome of an objective Test of Variables of Attention (TOVA) correlates with the findings of an electrophysiologic test-P300 latency-in patients 40 y of age or older. Adult attention deficit disorder may be an important premorbid marker of memory dysfunction or dementia. In males, the means for P300 latency and age-adjusted P300 latency were significantly greater for patients classified as SD-BL (significantly deviant or borderline: TOVA<-1.0) than for those categorized as normal (TOVA(3)0) for attention failure (ie, omissions [P<.010] and commissions [P<.005]) but not for response time or for variability. Males with >2 SD-BL quarters had significantly delayed P300 latency and age-adjusted P300 latency compared with males who had 0 SD-BL quarters (P<.020) and 1 SD-BL quarter (P<.005). In females, the means for P300 latency and age-adjusted P300 latency were significantly delayed for those grouped as SD-BL than for those labeled normal for response time (P<.001) and variability (P<.010), but not for omissions or for commissions. Females with >2 SD-BL quarters had significantly delayed P300 latency and age-adjusted P300 latency compared with females who had 0 SD-BL quarters (P<.005) and 1 SD-BL quarter (P<.010). Results suggest that TOVA abnormalities may be an indicator of delayed P300 and attention disorder. Recent research correlates TOVA abnormalities with impaired WMS scores of early dementia. Coupling of TOVA assessment findings with results of P300, Mini-Mental Status Exam, and WMS-III may allow for enhanced accuracy in the diagnosis and evaluation of the complex pathway of failing attention, memory, and cognition that leads to dementia.

Adult↗
PubMed2002

Inhibition has little effect on response latencies in the inferior colliculus.

The inferior colliculi of all mammals are characterized by a wide range of first-spike response latencies that can greatly exceed the minimum time required for the transmission of input through the lower brainstem. The mechanisms that account for long response latencies of up to 50 ms are unclear, but one hypothesis is that an early inhibition plays a role in shaping latency. To test this hypothesis, response latencies were measured in the inferior colliculi of the pallid and mustached bats before and during the blockade of GABAa and glycine receptors. The effect of blocking inhibition on response latency was compared under stimulus conditions that produced the shortest latency in the predrug condition. Multibarrel "piggyback" electrodes were used to iontophoretically apply bicuculline and strychnine sequentially while recording from single neurons. Predrug latencies ranged from 9 to 26 ms in the pallid bat and from 4 to 17 ms in the mustached bat. Despite large increases in response magnitude and response duration following disinhibition, the blockade of inhibitory receptors had modest effects on response latency. In the pallid bat, blocking GABA receptors produced latency changes that ranged from -3.8 to +0.2 ms, while blocking glycine receptors produced changes from -0.1 to +1.7 ms. Similarly, in the mustached bat, blocking GABA receptors caused changes ranging from -10.3 to +1.4 ms; blocking glycine receptors in the mustached bat caused changes from -3.6 to +1.0 ms. The large change of -10.3 ms was an exception. In both species, the majority of neurons showed changes of <1 ms. We conclude that a fast, early inhibitory input does not appear to play a significant role in shaping the wide range of response latencies present in the inferior colliculi of mustached and pallid bats.

Acepromazine↗
PubMed2002

Pudendal nerve terminal motor latency testing: assessing the educational learning curve: can we teach our own?

PURPOSE: Pudendal nerve terminal motor latency testing is useful as a diagnostic tool in fecal incontinence. It has also been used as a predictive factor in sphincteroplasty repairs. The technique is seldom taught and mastered in colorectal training programs. The purpose of this study was to assess a learning curve for teaching this procedure. METHODS: The student was a formally trained colorectal surgeon with no pudendal nerve terminal motor latency experience; the instructor has performed more than 3,000 pudendal nerve terminal motor latency studies. Fifty consecutive patients had manometry and pudendal nerve terminal motor latency testing. Both the student and instructor performed pudendal nerve terminal motor latency in a sequential fashion. Variables collected included pudendal nerve terminal motor latency, completion of test, time to complete test, and accuracy of the test. Variables were analyzed with paired t-test and chi-squared analysis. RESULTS: The study group included 41 female and 9 male patients. The average age of the patients was 53 years. Bowel complaints included constipation in 16 and incontinence in 34 patients. Data were analyzed in their entirety and at ten-patient intervals. The student tended to record longer latencies (P < 0.001). This led to false-positive rates of 23 and 21 percent, respectively, for left and right pudendal nerve terminal motor latency. On average, the time to complete the procedure was three times longer for the student than for the instructor (P < 0.001). At ten-patient intervals, the pudendal nerve terminal motor latency difference between the two groups disappeared at the 41-to-50-patient mark. CONCLUSION: Given the proper learning environment, pudendal nerve terminal motor latency testing can be mastered in a relatively short period. On the basis of this study, our estimation is 40 patients are required for a student to master this technique. The novice examiner can expect false-positive results early in the learning curve, and these should be validated accordingly.

Constipation↗
PubMed1989

P300 latency variability in normal elderly: effects of paradigm and measurement technique.

The discrepancy in the literature concerning the sensitivity of delayed P300 latency in dementia revolves around the variability of P300 latency in normal elderly. Previous studies, which have produced conflicting results, have utilized different P300 paradigms and different methods for measuring P300 latency. We demonstrate that the reported differences in the variability of P300 latency in normal elderly are likely to have resulted from these differences in paradigm and measurement method. We gathered auditory P300 data from a sample of 50 normal elderly using both a 3-tone RT paradigm and a 2-tone oddball paradigm and measured P300 latency using both peak-picking on the average EP and a single-trial template-fitting procedure. P300 latency variability was increased for the 3-tone paradigm compared to the auditory oddball paradigm, and for the template-fitting method. compared to peak-picking. The increased P300 latency variability when the template-fitting method was employed resulted, in part, from the template-fitting procedure focussing on random noise when the signal-to-noise ratio was low. Increased variability of P300 latency in the 3-tone paradigm resulted from 13 subjects who had a very long-latency positive component (often in addition to an earlier, smaller component) in this paradigm that met the scoring criteria for P300, but that was not seen in the oddball paradigm. We speculate that for the 3-tone task, some subjects may adopt a strategy involving 2 stages of stimulus processing, which results in the generation of 2 positive components, obscuring group differences in P300 latency. These results raise questions concerning the use, in clinical studies designed to yield diagnostic measures, of complicated paradigms in which subjects might adopt varying processing strategies.

Aged↗
PubMedDate not supplied

Latency variability of the components of auditory event-related potentials to infrequent stimuli in aging, Alzheimer-type dementia, and depression.

Auditory event-related potentials (ERPs) were investigated in 15 demented (12 presumed Alzheimer's, 3 cerebrovascular), 8 depressed, and 15 normal older, and 12 normal young, subjects. Both latencies from conventional averages and latency variability measures from single trials were derived for the N100, P200, N200, and P300 components of the ERP recorded from Fz, Cz and Pz scalp placements in a task requiring detection of an infrequent target tone among a series of frequent non-target tones. The P300 component most consistently separated the groups. Demented subjects had longer P300 latencies and greater P300 latency variability than both control groups and the depressed group. Age differences were observed for P300 latency, but not for P300 latency variability. Amplitudes were not significantly different among the groups. Reaction times (RTs) to the targets were longest for the demented subjects and shortest for the young controls, with the depressed and normal older control groups falling in between. Correlations between RT and P300 latency from single trials did not differentiate the groups. Using regression analysis to evaluate the deviation of P300 latency and latency variability for the patients from the predicted values for normal controls, no misclassifications of depressed patients occurred, but only 27% of the demented individuals were correctly classified using P300 variability, and 13% using P300 latency. These findings indicate that ERP measures using the 'oddball' target detection paradigm were useful in describing group differences, but were not sufficiently sensitive to be used in differentiating demented persons on an individual basis for clinical diagnosis.

Adult↗
PubMedDate not supplied

Auditory brainstem latencies in type I (insulin-dependent) diabetic patients.

INTRODUCTION: This study was undertaken to compare auditory brainstem response latencies in insulin-dependent diabetics, and to compare these findings with metabolic control, microangiopathy, neuropathy, and the duration of diabetes. METHODS: Auditory brainstem latencies were studied in 53 type I diabetic patients and 42 randomly selected nondiabetic control subjects, aged between 20 and 40 years. Three different stimulus repetition rates (10, 30, and 50 Hz) were used. All subjects had normal hearing ability. RESULTS: Wave V latencies were longer in diabetic patients when compared with those of control subjects at all repetition rates. At repetition rates of 10 and 50 Hz, diabetic patients had a prolonged I-V interwave latency, and at a repetition rate of 50 Hz, diabetics had a longer III-V interwave latency than control subjects. These findings indicate a central disturbance in the auditory pathway. Microvascular complications (retinopathy, nephropathy) and the duration of diabetes were associated with the prolongation of auditory brainstem latencies. In contrast, poor metabolic control (high fasting blood glucose and glycated hemoglobin A1c) at the time of the present study was only marginally associated with prolonged auditory brainstem latencies. The changes in auditory brainstem latencies associated with diabetic neuropathy (measured with five cardiac autonomic nervous function tests) appeared simultaneously with microvascular complications and in patients with diabetes of long duration, and thus a causative role of diabetic neuropathy in the pathogenesis of prolonged auditory brainstem latencies remains unsolved. CONCLUSION: Delayed auditory brainstem latencies in type I diabetic patients are probably caused by the long duration of diabetes and the microvascular complications associated with it.

Adult↗
PubMedDate not supplied

Evidence that a-wave latency of the electroretinogram is determined solely by photoreceptors.

PURPOSE: To identify the retinal cells that determine the a-wave latency of rats. METHODS: Electroretinograms (ERGs) were recorded from the rod-dominated (0.85% cones) retinas of Long-Evans rats following an intravitreal injection of 1 microL of 40 mM 2-amino-4-phosphonobutyric acid to block the activity of the ON pathway of the second order retinal neurons. ERGs were also recorded following an intraperitoneal injection of sodium iodate to destroy the retinal pigment epithelial (RPE) cells. Damage to a large area of the retina was produced by constant light exposure, and focal damage to the retina was induced by argon laser photocoagulation. The effects of age and anesthesia level on the a-wave latency were also determined. RESULTS: Blocking the activity of the ON pathway of the second order retinal neurons did not alter the a-wave latency, and destroying the RPE cells also did not alter the a-wave latency. Damage to a large area of the retina resulted in prolonging the latency but focal retinal damage did not alter the a-wave latency. The a-wave latency was longer in young rat pups but was adult-like by 18 days. The level of anesthesia had no effect on the latency except at very deep stages. CONCLUSIONS: The a-wave latency is determined solely by the activity of the photoreceptors. A prolonged latency would indicate that the photoreceptors are damaged over a large area of the retina.

Aminobutyrates↗