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PubMed1987

The effect of frontal eye field and superior colliculus lesions on saccadic latencies in the rhesus monkey.

Rhesus monkeys were trained to make saccadic eye movements to visual targets using detection and discrimination paradigms in which they were required to make a saccade either to a solitary stimulus (detection) or to that same stimulus when it appeared simultaneously with several other stimuli (discrimination). The detection paradigm yielded a bimodal distribution of saccadic latencies with the faster mode peaking around 100 ms (express saccades); the introduction of a pause between the termination of the fixation spot and the onset of the target (gap) increased the frequency of express saccades. The discrimination paradigm, on the other hand, yielded only a unimodal distribution of latencies even when a gap was introduced, and there was no evidence for short-latency "express" saccades. In three monkeys either the frontal eye field or the superior colliculus was ablated unilaterally. Frontal eye field ablation had no discernible long-term effects on the distribution of saccadic latencies in either the detection or discrimination tasks. After unilateral collicular ablation, on the other hand, express saccades obtained in the detection paradigm were eliminated for eye movements contralateral to the lesion, leaving only a unimodal distribution of latencies. This deficit persisted throughout testing, which in one monkey continued for 9 mo. Express saccades were not observed again for saccades contralateral to the lesion, and the mean latency of the contralateral saccades was longer than the mean latency of the second peak for the ipsiversive saccades. The latency distribution of saccades ipsiversive to the collicular lesion was unaffected except for a few days after surgery, during which time an increase in the proportion of express saccades was evident. Saccades obtained with the discrimination paradigm yielded a small but reliable increase in saccadic latencies following collicular lesions, without altering the shape of the distribution. Unilateral muscimol injections into the superior colliculus produced results similar to those obtained immediately after collicular lesions: saccades contralateral to the injection site were strongly inhibited and showed increased saccadic latencies. This was accompanied by a decrease of ipsilateral saccadic latencies and an increase in the number of saccades falling into the express range. The results suggest that the superior colliculus is essential for the generation of short-latency (express) saccades and that the frontal eye fields do not play a significant role in shaping the distribution of saccadic latencies in the paradigms used in this study.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2001

[Study on the latency difference between compound muscle and sensory nerve action potentials].

In motor nerve conduction studies compound muscle action potentials (CMAPs) appear later than sensory nerve action potentials (SNAPs). This time lag originates from the conduction delay at the distal motor axon, neuromuscular transmission time and muscle action potential induction time. To investigate the latency difference between CMAPs and SNAPs we studied 46 healthy individuals, 46 patients with diabetes mellitus and 33 patients with carpal tunnel syndrome, using the lumbrical and interossei recording method. In this method the recording active electrode was placed on the 2nd lumbrical muscle and the reference electrode on the proximal palmar aspect of the index finger. Supramaximal stimulation was given to the median or ulnar nerve trunk at 9-cm proximal to the recording active electrode. The CMAP from the 2nd lumbrical muscle (L) and the SNAP from the digital nerve (N) were recorded after median nerve stimulation, and the CMAP from the 2nd interossei muscles (I) was recorded after ulnar nerve stimulation. The residual latency, which is arbitrary defined as the latency difference (L-N) in this study, was 1.38 +/- 0.15 (mean +/- SD) msec in healthy individuals. About 1 msec of the residual latency is regarded as the time for neuromuscular transmission and the time to evoke muscle activities. Thus, the conduction delay at the distal motor axon was calculated as about 0.4 msec in healthy individuals. The residual latency was relatively constant in 29 diabetic patients without conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) < or = 0.4 msec. Their sensory nerve conduction velocities (calculated from N latency) were always above 40 m/sec. On the other hand in diabetic patients with conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) > 0.4 msec, the residual latency gradually increased as the sensory nerve conduction velocity decreased. Their sensory nerve conduction velocities were mostly less than 40 m/sec. The similar relationship was observed in patients with carpal tunnel syndrome without diabetes mellitus. We consider that the diabetic neuropathy alone doesn't cause the increase of the residual latency. Instead, severe conduction delay across the carpal tunnel decreases the N velocity and increases the residual latency. We can also regard the relationship between the latency difference (L-N) and N velocity as being in inverse proportion. Perhaps the increase of the residual latency was simply caused by the proportional decrease in the conduction velocity at the distal motor axon, not by the special mechanism concerning to the carpal tunnel syndrome. This paper presented the electrophysiological changes seen in the distal segment secondary to the proximal entrapment.

Action Potentials↗
PubMed1997

Host-cell-determined methylation of specific Epstein-Barr virus promoters regulates the choice between distinct viral latency programs.

Epstein-Barr virus (EBV) is capable of adopting three distinct forms of latency: the type III latency program, in which six EBV-encoded nuclear antigens (EBNAs) are expressed, and the type I and type II latency programs, in which only a single viral nuclear protein, EBNA1, is produced. Several groups have reported heavy CpG methylation of the EBV genome in Burkitt's lymphoma cell lines which maintain type I latency, and loss of viral genome methylation in tumor cell lines has been correlated with a switch to type III latency. Here, evidence that the type III latency program must be inactivated by methylation to allow EBV to enter the type I or type II restricted latency program is provided. The data demonstrates that the EBNA1 gene promoter, Qp, active in types I and II latency, is encompassed by a CpG island which is protected from methylation. CpG methylation inactivates the type III latency program and consequently allows the type I or II latency program to operate by alleviating EBNA1-mediated repression of Qp. Methylation of the type III latency EBNA gene promoter, Cp, appears to be essential to prevent type III latency, since EBNA1 is expressed in all latently infected cells and, as shown here, is the only viral antigen required for activation of Cp. EBV is thus a pathogen which subverts host-cell-determined methylation to regulate distinct genetic programs.

Azacitidine↗
PubMed1992

The origin of short- and long-latency mylohyoid nerve responses elicited by high-intensity electrical stimulation of intradental nerve in cats.

A double reflex response of the mylohyoid nerve to the jaw depressor muscles after electrical stimulation of the intradental nerves was recorded in cats anaesthetized with alpha-chloralose. The threshold value of the long-latency (16-19 ms) response was almost 20 times greater than that of the short-latency (5-8 ms) response. At the threshold intensity of the long-latency response, the short-latency response with shorter latency appeared. After extirpation of the stimulated tooth pulp, the short-latency response with a lower threshold disappeared, whereas the short-latency response with a higher threshold and the long-latency response both persisted and showed no change in threshold or latency. These findings indicate that the low-threshold, short-latency response was due to excitation of pulpal nerve fibres, while the high-threshold, short-latency response and the long-latency response were both due to excitation of extrapulpal afferent fibres as a result of the spread of current outside the tooth.

Animals↗
PubMed1999

The period of latency before a muscle receptor generates an action potential as a response to a muscle stretch.

Six primary (Ia) and seven secondary (II) muscle spindle afferents and eight Golgi tendon organ afferents (Ib) from the tibial anterior muscle of the cat, recorded at the dorsal roots, were subjected to a sinusoidal stretch of the host muscle, the frequency of which increased linearly from 2 to 80 Hz over four different lengths of time. Both the amplitude of the sinusoidal stretch and the prestretch of the muscle were varied. The phase of the action potentials was determined. The phase of the action potential, driven 1:1, increased linearly with frequency. From the gradient of the phase of this action potential the muscle-muscle receptor latency was determined, i.e., the period of latency between the stretch of the muscle and the occurrence of the action potential at the muscle nerve where it enters the muscle. The muscle-muscle receptor latency had values lying between 3 and 8 ms: it was dependent on the experimental parameters and became shorter as the conduction velocity of the afferent fiber increased. In three experiments the muscle latency was determined, i.e., the period of latency before the stretch was transferred from the tendon of the muscle to the proximal third of the muscle belly. The muscle was stretched sinusoidally under the same varying parameters as given above. The length changes occurring in the proximal third of the muscle were measured with a piezo element. The muscle latency was determined from the slope of the phase of the zero points of the sinusoidal piezo length changes; the phase increases linearly with frequency. The muscle latency had values lying between 6 and 15 ms: it was dependent on the experimental parameters. The muscle spindle latency, i.e., the period of latency between the stretch of the polar parts of the intrafusal muscle fibers and the recording of the action potentials from the spindle nerve near the spindle capsule, was determined from 5 Ia fibers and 1 II fiber of isolated muscle spindles. The isolated muscle spindle was stretched under the same varying parameters as given above. The muscle spindle latency was determined from the slope of the phase of the phase-locked action potential. The muscle spindle latency as measured by our method proved to be 0 ms. The latencies of the three elements and their dependence on the experimental parameters are discussed in the light of the transfer properties of the muscle and the muscle receptors.

Action Potentials↗
PubMedDate not supplied

Reliability and significance of measurements of a-wave latency in rats.

PURPOSE: To determine whether measurements of the a-wave latency of the electroretinogram (ERG) can be made as reliably as that of the implicit time (IT) in rats. In addition, to determine the relationship between the potential level selected for the latency and the baseline potential level. METHODS: ERGs, elicited by different stimulus intensities, were recorded from Long-Evans rats. The a-wave latency was determined by measuring the time between the stimulus onset and the beginning of the negative-going a-wave, and the IT was measured as the time between the stimulus onset and the peak of the a-wave. To test the reliability of the measurements of the latency, the a-wave latency and the IT were measured by three independent observers for the same 15 ERGs. RESULTS: The mean a-wave latency was approximately 14 milliseconds, and the mean a-wave implicit time was approximately 36 milliseconds. The mean of the a-wave latency and the IT, as measured by the three observers, were within 1 millisecond of each other. The coefficient of variation was as good for the latency as for the IT of the a-wave. The potential level selected for the latency was lower than the mean baseline potential level by 1 to 2 standard deviations. CONCLUSIONS: Selection of the a-wave latencies can be made as reliably as that for the IT. Because the a-wave latency is not affected by the activity of the second order neurons, the latency is a better measure than the IT of the time course of the a-wave.

Animals↗
PubMed1998

Normative Wave V latency-intensity functions using the EARTONE 3A insert earphone and the Radioear B-71 bone vibrator.

Early auditory evoked response (ABR) audiometry is useful for estimating auditory sensitivity in infants and other difficult-to-test populations. Several investigations advocate using bone-conducted stimuli, in addition to air-conducted stimuli, for screening infants with hearing loss or for ascertaining the presence and magnitude of a conductive hearing loss. The present study was designed to gather normative Wave V latency-intensity data with an insert earphone (EARTONE 3A) and a bone vibrator (Radioear B-71). Forty normal-hearing subjects were tested with air-conducted and bone-conducted clicks at intensities of 55, 40, 30, 20, and 10 dB SL. The stimulus waveforms showed a click onset delay of 0.1 ms for the 3A insert earphone. It is important to note that our ABR latencies were not adjusted to account for these differences. The results revealed that both the air-conduction and bone-conduction functions exhibited Wave V latencies of 7.0 ms at 55 dB SL. Although both functions exhibited increased latencies as intensity decreased to 10 dB SL, the air-conducted clicks yielded somewhat longer latencies than the bone-conducted clicks. To allow direct comparison of the air-conduction and bone-conduction latency-intensity function, the bone-conduction function must be corrected by approximately +0.3 ms at 40 dB, +0.4 ms at 30 dB, +0.5 ms at 20 dB, and +0.8 ms 10 dB nHL. No correction is needed at 55 dB. The present study suggests that it may not be appropriate to apply a single correction value (e.g., 0.5 ms) to the entire latency-intensity function. If clinicians elect to use published latency-intensity data, they must employ procedure similar to those that were used to collect the normative data. Otherwise, individual clinics should generate normative latency-intensity data using well-defined procedures. An alternative to generating latency-intensity functions is to compare ABR air-conduction and bone-conduction thresholds. This procedure is advantageous because threshold responses are not as sensitive as latency measures to slight changes in instrumentation and procedures. The normative air-conduction and/or bone-conduction values presented in this investigation are offered as a baseline for either latency-intensity or threshold comparisons.

Acoustic Impedance Tests↗
PubMed1989

Latencies of membrane currents evoked in Xenopus oocytes by receptor activation, inositol trisphosphate and calcium.

1. Application of serum to Xenopus oocytes elicits an oscillatory chloride membrane current, which begins after a latency of several seconds or minutes, and is mediated through a phosphoinositide-calcium signalling pathway. We studied the characteristics and origin of this latency in voltage-clamped oocytes. 2. Bath application of low doses of serum evoked responses beginning after latencies of 1 min or more. The latency decreased with increasing dose and reached a minimal value of several seconds that did not decrease with further increases in serum concentration. Experiments to study this minimal latency were done by applying brief 'puffs' of serum and other agonists at high concentrations from a local extracellular pipette. 3. The mean latency of the response evoked by local serum application was about 7 s (at 22-24 degrees C), but individual responses showed a wide variation, from 2 s to over 20 s. Diffusion of serum from the pipette tip to the membrane did not contribute appreciably to this delay, since short (less than 100 ms) delays were obtained when KCl was applied in the same way. 4. Currents evoked by acetylcholine and serotonin, in oocytes induced to acquire muscarinic and serotonergic receptors following injection of brain messenger RNA, began following latencies similar to that of the serum response. 5. The response latency was shorter when serum was applied to the vegetal rather than the animal hemisphere of the oocyte, even though smaller currents were obtained. 6. The latency showed a slight dependence upon membrane potential, becoming shorter with depolarization. 7. Cooling to temperatures below about 22 degrees C produced a striking lengthening of the delay, corresponding to a Q10 of about 5. In contrast, above 22 degrees C the temperature dependence was slight, with a Q10 of about 1.25. 8. Intracellular injections of calcium and inositol 1,4,5-trisphosphate (IP3) evoked chloride currents with short (a few tens of milliseconds) latency. Short (100 ms) latency responses were also evoked when intracellularly loaded caged IP3 was photolysed by strong illumination, but weak illumination gave responses with latencies of over 1 min. 9. Measurements of intracellular free calcium, made with Fura-2 and Indo-1, showed an increase following serum application beginning coincident with the onset of the membrane current response.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1975

Latency of unit responses in cochlear nucleus determined in two different ways.

The latency revealed by poststimulus time histograms of the responses of single units in the cochlear nucleus to tone bursts was compared with the latency of the change in discharge frequency in response to small increments in the amplitude of the stimulus. The latter was derived on the basis of statistical signal analysis of the discharge pattern in response to tones amplitude modulated with pseudorandom noise. The "step response" of the system was computed by time integration of the cross covariance between modulation and spike density. The following observations can be made: 1. The latency of the responses to tone bursts always decreased with increasing sound intensity, whereas the latency of the step response was almost constant for intensities from immediately above threshold to the highest intensity used (60-70 dB above threshold). 2. In most units the latency revealed by the PST histogram of the responses to tone bursts approached the value of latency of the step response asymptotically. 3. In some units with longer latency, the latency of the response to tone bursts was many times greater than the latency of the step response, even at high sound intensities. 4. A histogram of latency values of the step response of the units studied showed narrow peaks at 2.8 and 4.7 ms. 5. On the basis of the present results it is concluded that the latency values of the step response represent the true sum of synaptic and axon dendritical propagation delay, whereas the latency of the responses to tone bursts also includes the temporal summation at the synaptic level.

Animals↗
PubMed1990

Visual tracking in monkeys: evidence for short-latency suppression of the vestibuloocular reflex.

1. Monkeys normally use a combination of smooth head and eye movements to keep the eyes pointed at a slowly moving object. The visual inputs from target motion evoke smooth pursuit eye movements, whereas the vestibular inputs from head motion evoke a vestibuloocular reflex (VOR). Our study asks how the eye movements of pursuit and the VOR interact. Is there a linear addition of independent commands for pursuit and the VOR? Or does the interaction of visual and vestibular stimuli cause momentary, "parametric" modulation of transmission through VOR pathways? 2. We probed for the state of the VOR and pursuit by presenting transient perturbations of target and/or head motion under different steady-state tracking conditions. Tracking conditions included fixation at straight-ahead gaze, in which both the head and the target were stationary; "times-zero (X0) tracking," in which the target and head moved in the same direction at the same speed; and "times-two (X2) tracking," in which the target and head moved in opposite directions at the same speed. 3. Comparison of the eye velocities evoked by changes in the direction of X0 versus X2 tracking revealed two components of the tracking response. The earliest component, which we attribute to the VOR, had a latency of 14 ms and a trajectory that did not depend on initial tracking conditions. The later component had a latency of 70 ms or less and a trajectory that did depend on tracking conditions. 4. To probe the latency of pursuit eye movements, we imposed perturbations of target velocity imposed during X0 and X2 tracking. The resulting changes in eye velocity had latencies of at least 100 ms. We conclude that the effects of initial tracking conditions on eye velocity at latencies of less than 70 ms cannot be caused by visual feedback through the smooth-pursuit system. Instead, there must be another mechanism for short-latency control over the VOR; we call this component of the response "short-latency tracking." 5. Perturbations of head velocity or head and target velocity during X0 and X2 tracking showed that short-latency tracking depended only on the tracking conditions at the time the perturbation was imposed. The VOR appeared to be suppressed when the initial conditions were X0 tracking. 6. The magnitude of short-latency tracking depended on the speed of initial head and target movement. During X0 tracking at 15 deg/s, short-latency tracking was modest. When the initial speed of head and target motion was 60 deg/s, the amplitude of short-latency tracking was quite large and its latency became as short as 36 ms.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

A-type and T-type currents interact to produce a novel spike latency-voltage relationship in cerebellar stellate cells.

The modification of first-spike latencies by low-threshold and inactivating K+ currents (IA) have important implications in neuronal coding and synaptic integration. To date, cells in which first-spike latency characteristics have been analyzed have shown that increased hyperpolarization results in longer first-spike latencies, producing a monotonic relationship between first-spike latency and membrane voltage. Previous work has established that cerebellar stellate cells express members of the Kv4 potassium channel subfamily, which underlie IA in many central neurons. Spike timing in stellate cells could be particularly important to cerebellar output, because the discharge of even single spikes can significantly delay spike discharge in postsynaptic Purkinje cells. In the present work, we studied the first-spike latency characteristics of stellate cells. We show that first-spike latency is nonmonotonic, such that intermediate levels of prehyperpolarization produce the longest spike latencies, whereas greater hyperpolarization or depolarization reduces spike latency. Moreover, the range of first-spike latency values can be substantial in spanning 20-128 ms with preceding membrane shifts of <10 mV. Using patch clamp and modeling, we illustrate that spike latency characteristics are the product of an interplay between IA and low-threshold calcium current (IT) that requires a steady-state difference in the inactivation parameters of the currents. Furthermore, we show that the unique first-spike latency characteristics of stellate cells have important implications for the integration of coincident IPSPs and EPSPs, such that inhibition can shift first-spike latency to differentially modulate the probability of firing.

Action Potentials↗
PubMed2003

Herpes simplex virus type 1 and bovine herpesvirus 1 latency.

Primary infection by herpes simplex virus type 1 (HSV-1) can cause clinical symptoms in the peripheral and central nervous system, upper respiratory tract, and gastrointestinal tract. Recurrent ocular shedding leads to corneal scarring that can progress to vision loss. Consequently, HSV-1 is the leading cause of corneal blindness due to an infectious agent. Bovine herpesvirus 1 (BHV-1) has similar biological properties to HSV-1 and is a significant health concern to the cattle industry. Latency of BHV-1 and HSV-1 is established in sensory neurons of trigeminal ganglia, but latency can be interrupted periodically, leading to reactivation from latency and spread of infectious virus. The ability of HSV-1 and BHV-1 to reactivate from latency leads to virus transmission and can lead to recurrent disease in individuals latently infected with HSV-1. During latency, the only abundant HSV-1 RNA expressed is the latency-associated transcript (LAT). In latently infected cattle, the latency-related (LR) RNA is the only abundant transcript that is expressed. LAT and LR RNA are antisense to ICP0 or bICP0, viral genes that are crucial for productive infection, suggesting that LAT and LR RNA interfere with productive infection by inhibiting ICP0 or bICP0 expression. Numerous studies have concluded that LAT expression is important for the latency-reactivation cycle in animal models. The LR gene has recently been demonstrated to be required for the latency-reactivation cycle in cattle. Several recent studies have demonstrated that LAT and the LR gene inhibit apoptosis (programmed cell death) in trigeminal ganglia of infected animals and transiently transfected cells. The antiapoptotic properties of LAT map to the same sequences that are necessary for promoting reactivation from latency. This review summarizes our current knowledge of factors regulating the latency-reactivation cycle of HSV-1 and BHV-1.

Animals↗
PubMed2005

Using automated morphometry to detect associations between ERP latency and structural brain MRI in normal adults.

Despite the clinical significance of event-related potential (ERP) latency abnormalities, little attention has focused on the anatomic substrate of latency variability. Volume conduction models do not identify the anatomy responsible for delayed neural transmission between neural sources. To explore the anatomic substrate of ERP latency variability in normal adults using automated measures derived from magnetic resonance imaging (MRI), ERPs were recorded in the visual three-stimulus oddball task in 59 healthy participants. Latencies of the P3a and P3b components were measured at the vertex. Measures of local anatomic size in the brain were estimated from structural MRI, using tissue segmentation and deformation morphometry. A general linear model was fitted relating latency to measures of local anatomic size, covarying for intracranial vault volume. Longer P3b latencies were related to contractions in thalamus extending superiorly into the corpus callosum, white matter (WM) anterior to the central sulcus on the left and right, left temporal WM, the right anterior limb of the internal capsule extending into the lenticular nucleus, and larger cerebrospinal fluid volumes. There was no evidence for a relationship between gray matter (GM) volumes and P3b latency. Longer P3a latencies were related to contractions in left temporal WM, and left parietal GM and WM near the interhemispheric fissure. P3b latency variability is related chiefly to WM, thalamus, and lenticular nucleus, whereas P3a latency variability is not related as strongly to anatomy. These results imply that the WM connectivity between generators influences P3b latency more than the generators themselves do.

Adult↗
PubMed1976

Quantitative studies of intracellular postsynaptic potentials in the lateral geniculate nucleus of the cat with respect to optic tract stimulus response latencies.

LGN cells were intracellularly recorded with glass micropipettes. Electrical stimuli of different amplitude and frequency were applied to the optic tract close to the optic chiasm. The cells were classified according to stimulus response latencies of action potentials as belonging to class I (1.0-16 msec) Or class II (1.7-3.0 MSEC). Class I EPSPs had shorter latencies (1.0-1.5 msec), durations (4-12 msec), rise times to peak (0.5-1.4 msec), and decay times (3.0-8.5 msec); the synaptic transmission time was on the average 0.41 msec. Class II EPSPs (1.6-2.6 msec latency) had longer durations (10-30 msec), rise times (1.6-3.7 msec), and decay times (9.0-25 msec); the synaptic transmission time was on the average 0.67 msec. With repetitive stimulation the EPSPs of latency class I revealed almost no stimulus frequency dependence between 1 and 120 HZ, while class 22 EPSPs decrease in amplitude between 30 and 70% with increasing frequency. Comparable temporal summation of excitation occurred in cells of both latency classes. Negative serial correlation coefficients of first order were found for consecutive EPSP amplitudes of all cells recorded for sufficient periods of time. The IPSPs were subdivided into two groups according to their optic tract response latency. Group 1 IPSPs had shorter latencies (2.0-2.6 msec), durations (15-50 msec), and times from the onset to maximal hyperpolarization (2.4-4.2 msec) than group 2 IPSPs (3.0-4.8 msec latency, 40-100 msec duration, 2.7-7.5 msec time from onset to extremum). The group 2 IPSPs decreased in amplitude by about 90% when the stimulus frequency was increased form 1 to 50 HZ, while the group 1 IPSPs displayed a comparable decrease in the frequency range between 50 and 120 HZ. Effective temporal summation was found in group 2 IPSPs in the frequency range below 70 HZ, and in group 1 IPSPs at stimulus frequencies between 70 and 120 HZ. The EPSP peak latencies and the latencies to the minimum of IPSPs proved to be invariant with respect to PSP amplitude and stimulus fre quency in individual cells. The latencies to the extrema of EPSPs and IPSPs as well as the amplitude values were symmetrically distributed.

Animals↗
PubMed2001

The relationship of pudendal nerve terminal motor latency to squeeze pressure in patients with idiopathic fecal incontinence.

PURPOSE: With the advent of transanal ultrasonography it has been possible to identify those incontinent patients without sphincter defects. The majority of these patients are now thought to have neurogenic fecal incontinence secondary to pudendal neuropathy. They have been found to have reduced anal sphincter pressures and increased pudendal nerve terminal motor latencies. The aim of this study was to determine whether in those incontinent patients who do not have a sphincter defect, prolonged pudendal nerve terminal motor latency correlates with anal manometry, in particular maximum squeeze pressure. METHODS: Sixty-six incontinent patients were studied with transanal ultrasonography, anorectal manometry, and pudendal nerve terminal motor latency. Twenty-seven continent controls had anorectal manometry and pudendal nerve terminal motor latency measured. RESULTS: Maximum resting pressure and maximum squeeze pressure were significantly lower in the group of incontinent patients with bilateral prolonged pudendal nerve terminal motor latency (median maximum resting pressure = 26.5 mmHg; median maximum squeeze pressure = 60 mmHg) when compared with incontinent patients with normal bilateral pudendal nerve terminal motor latencies (median maximum resting pressure = 46 mmHg; median maximum squeeze pressure = 79 mmHg; maximum resting pressure P = 0.004; and maximum squeeze pressure P = 0.04). In incontinent patients with no sphincter defects no correlation between pudendal nerve terminal motor latency and maximum squeeze pressure was found (r = -0.109, P = 0.48) and maximum squeeze pressure did not correlate with bilateral or unilateral prolonged pudendal nerve terminal motor latency (r = -0.148, P = 0.56 and r = 0.355, P = 0.19 respectively). CONCLUSIONS: In patients with idiopathic fecal incontinence damage to the pelvic floor is more complex than damage to the pudendal nerve alone. Although increased pudendal nerve terminal motor latency may indicate that neuropathy is present, in patients with neuropathic fecal incontinence, pudendal nerve terminal motor latency does not correlate with maximum squeeze pressure. Normal pudendal nerve terminal motor latency does not exclude weakness of the pelvic floor.

Adult↗
PubMed1983

REM latency: development in the first year of life.

The development of REM latency in the first year of life was investigated in two groups of 10 infants each. While 10 infants were normal, the other 10 underwent continuous feeding for various gastrointestinal diseases. Each infant was continuously recorded polygraphically for 24 h. While younger infants (less than or equal to 3 months) manifested predominantly shorter REM latencies (less than or equal to 8 min), older infants (4-13 months) produced a mixed distribution of short and long REM latencies. The total distribution of the REM latencies appears to be bimodal with latencies either shorter than 8 min or longer than 16 min. It is only in the group of older infants that the temporal distribution of REM latencies constitutes a diurnal rhythm, with the longest latencies in the interval between 12:00 and 16:00 and the shortest between 4:00 and 8:00. In the group of older infants, REM latency also depends on the duration of prior wakefulness. Long REM latencies are significantly more often preceded by long episodes of wakefulness than are short REM latencies. The different feeding conditions had only a minor effect on REM latency.

Humans↗
PubMed1986

Visual response latency of X- and Y-cells in the dorsal lateral geniculate nucleus of the cat.

Visual response latencies and rise times of X- and Y-cells in the dorsal lateral geniculate nucleus (dLGN) of anaesthetized, paralyzed cats were measured during repeated stimulation with sinusoidal grating patterns. Measurements were restricted to individual stimulus trials on which the instantaneous discharge rate exceeded a criterion amplitude defined in terms of the baseline activity of each cell. The latencies of response onsets and response peaks were systematically related to the spatial frequency and contrast of the grating stimuli. Response latencies of Y-cells were shortest for gratings of low spatial frequency (0.17 c/deg) and increased monotonically with increases in spatial frequency. Response latencies of X-cells were shortest for gratings of intermediate spatial frequency (0.75 c/deg) and longer for lower and higher spatial frequencies. Latencies decreased monotonically with increases in stimulus contrast from 5 to 40% for both X- and Y-cells. In general, short-latency responses were less variable than long-latency responses. This was true for absolute as well as relative measures of variability. The mean onset and peak latencies of Y-cell responses were 10-15 msec shorter than the corresponding latencies of X-cell responses to stimuli of optimal spatial frequency and contrast. The rise times (latency of response peak minus latency of response onset) of Y-cell responses were consistently shorter than those of X-cells in spite of the higher peak responses of Y-cells. The results of this study are consistent with the idea that low spatial frequency information is passed through the lateral geniculate nucleus more quickly than is high spatial frequency information. These data provide support for models of visual processing wherein a coarse, global analysis of the visual scene by Y-cells precedes a finer, local analysis by X-cells.

Action Potentials↗
PubMed1994

The relationship between auditory brainstem response latencies and behavioral thresholds in normal hearing infants and adults.

The relationship between behavioral thresholds and auditory brainstem response (ABR) latencies for 4 and 8 kHz tone pips were examined in normal-hearing 3-month-olds, 6-month-olds and adults. The latencies of waves I and V and the I-V interval of the ABR were analyzed. A linear latency-intensity function was also fit to each subject's latencies for each wave at several levels. The y-intercept of the latency-intensity function was used as a summary measure of latency to examine behavior-ABR correlations. The pattern of age-related change in behavioral threshold was not closely matched by age-related latency reduction for Wave I, Wave V or the I-V interval. However, 3-month-olds with higher behavioral thresholds had longer Wave V latencies and longer I-V intervals than 3-month-olds with lower behavioral thresholds. There was no significant difference in latency between 6-month-olds or adults with higher thresholds and 6-month-olds or adults with lower thresholds. There was also a significant correlation between the Wave V-Wave I latency-intensity intercept difference and behavioral threshold at both 4 and 8 kHz among 3-month-olds. The correlation was not significant among 6-month-olds or adults. These findings suggest that one of the factors responsible for immature behavioral thresholds at 3 months is related to transmission through the auditory brainstem. Because variability in hearing threshold among normal-hearing adults is low, it is not surprising that behavioral threshold is unrelated to ABR latency in this group. However, the lack of such a relationship among 6-month-olds implies that structures central to the auditory brainstem, either sensory or nonsensory, or both, must be responsible for immature behavioral thresholds after 6 months of age.

Acoustic Stimulation↗