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PubMed1995

Reduced variance of latencies in pudendal evoked potentials after normalization for body height.

The value of the Somatosensory Evoked Potentials (SEP) in the assessment and detection of neurological disorders could be considerably enhanced if the normative standards of (SEP) characteristic parameters were normalized taking into account all other systematic sources of variance. The present study examines the influence of body height on the peak and interpeak latencies of the pudendal somatosensory evoked potentials. We examined the peak latency (L1) of the evoked potential recorded at the L1 vertebra and the onset latency (ONc) of the cortical evoked potentials, after stimulation of the pudendal nerve, as a function of body height in 40 normal male subjects (age 20-40 years). Significant positive correlation was found between both (ONc) latency and ONc-L1 interpeak latency and body height (H). Assuming that the latter is proportional to the length of the neural pathways, the experimental data were fitted using a theoretical model representing the conduction in the sensory neuraxis as a function of body height. Using the estimated fitting functions, we normalized our data with regard to a typical value of body height. The normalized values of the aforementioned latencies reveal a significantly reduced variance, as compared to the original ones, and consequently their diagnostic importance is significantly increased. Similar procedures applied to the L1 (spinal) latencies and the latencies of the bulbocavernosus reflex (BCR) reveal no correlation with body height and this is discussed on the basis of neuroanatomical considerations.

Adult↗
PubMed1996

Eye position and target amplitude effects on human visual saccadic latencies.

Gaze shifts vary in the extent of eye and head contribution; a large amplitude and/or an eccentric ocular orbital starting position alter the participation of head movement in the shift. The interval between eye onset and head onset determines compensatory counterrolling before and after the shift and the extent of vestibular ocular reflex reduction during the shift. The latency of eye saccades in the head-fixed condition was measured with respect to target amplitude and orbital position in order to establish base-line operations of these two variables as they apply to the head-free condition. Eye movements were measured during single-step saccades in nine young adult humans. The target step, hereafter called a jump, started from three possible fixation lights; e.g., rightward saccades started from the midline (0 degree) or from -20 or -40 degrees left of the midline, with a maximum amplitude of 80 degrees. The latency of saccades starting from the primary position increased with jump amplitude (amplitude-latency relation). When the eye started eccentrically, the latency was decreased (orbital position-latency relation), with the largest jump amplitudes most affected. These changes can be related to active eye-head coordination. Thus, with a leftward maximal orbital eccentricity, compensatory eye rotation would be impossible with a rightward head movement; however, incorporating the orbital position-latency relation, the forward ocular saccade is expedited by 90 ms. Conversely, with a primary starting position, the ocular component of an 80 degrees gaze saccade could be slowed 125 ms by incorporating the amplitude-latency relation, thus facilitating a head contribution to the gaze shift. The orbital position and amplitude-latency relations were prominent in those subjects with habitually large head contributions to the gaze shift and minimal in individuals with typically small head contributions.

Adult↗
PubMed1989

A short-latency transition in saccade dynamics during square-wave tracking and its significance for the differentiation of visually-guided and predictive saccades.

Several recent studies indicate that saccades elicited in the absence of a visual target are slower than visually-guided movements of the same size. In addition, we have shown earlier that the slower saccades observed in two different paradigms had more asymmetrical (skewed) velocity profiles. Recently, it has been reported that predictive saccades are also slower. An interesting question, which arises if predictive and visually-guided saccades do have different velocity profiles, is whether the time when the transition occurs can be determined from their dynamic characteristics (peak velocity and skewness) and whether this transition latency can serve as a plausible criterion for distinguishing predictive and visually-guided saccades. To investigate this problem, visually-guided and predictive saccades were elicited by various experimental paradigms in six normal human subjects. Eye movements were measured using the double-magnetic induction method. We found that scatter plots of normalized peak velocity against latency showed an abrupt, small (10-20%) increase at a surprisingly short latency (about 30-70 ms). Furthermore, skewness of the saccadic velocity profile showed a significant drop at comparable latencies. There was a tight correlation between the peak velocity and skewness transition latencies of each subject. Considering the shape of the latency histograms in this and earlier studies, as well as other data, it appears unlikely that these very short transition latencies demarcate the distinction between predictive and fully visually-guided saccades. Instead, we suggest the possibility that the visual stimulus can speed up saccades at an earlier time than it can initiate and guide them. If this is the case, the very short transition latencies (mean: about 50 ms) probably represent the sum of afferent and efferent pure time delays in the system and do not include the time needed for the computation of saccade metrical properties.

Adult↗
PubMed2005

Influence of gap and overlap paradigms on saccade latencies and vergence eye movements in seven-year-old children.

The latency of eye movements is influenced by the fixation task; when the fixation stimulus is switched off before the target presentation (gap paradigm) the latency becomes short and express movements occur. In contrast, when the fixation stimulus remains on when the target appears (overlap paradigm), eye movement latency is longer. Several previous studies have shown increased rates of express saccades in children; however the presence of an express type of latency for vergence and combined movements in children has never been explored. The present study examines the effects of the gap and the overlap paradigms on horizontal saccades at far (150 cm) and at close (20 cm) viewing distances, on vergence along the median plane, and on saccades combined with convergence or divergence in 15 normal seven-year-old children. The results show that the gap paradigm produced shorter latency for all eye movements than the overlap paradigm, but the difference was only significant for saccades at close viewing distances, for divergence (pure and combined), and for saccades combined with vergence. The gap paradigm produced significantly higher rates of express latencies for saccades at close viewing distances, for divergence, and for saccades combined with divergence; in contrast, the frequencies of express latencies for saccades at far viewing distances and for convergence (pure or combined) were similar in the gap and the overlap paradigms. Interestingly, the rate of anticipatory latencies (<80 ms) was particularly high for divergence in the gap paradigm. Our collective findings suggest that the initiation of saccades at close viewing distances and of divergence is more reflexive, particularly in the gap paradigm. The finding of frequent anticipatory divergence that occurs at similar rates for seven-year-old children (this study) and for adults (Coubard et al., 2004, Exp Brain Res 154:368-381) indicates that predictive initiation of divergence is dominant.

Aging↗
PubMed2006

Saccadic latency distributions in Parkinson's disease and the effects of L-dopa.

Parkinson's disease (PD) is associated with a loss of central dopaminergic pathways in the brain leading to an abnormality of movement, including saccades. In PD, analysis of saccadic latency distributions, rather than mean latencies, can provide much more information about how the neural decision process that precedes movement is affected by disease or medication. Subject to the constraints of intersubject variation and reproducibility, latency distribution may represent an attractive potential biomarker of PD. Here we report two studies that provide information about these parameters, and demonstrate a novel effect of dopamine on saccadic latency, implying that it influences the neural decision process itself. We performed a detailed cross-sectional study of saccadic latency distributions during a simple step task in 22 medicated patients and 27 age-matched controls. This revealed high intersubject variability and an overlap of PD and control distributions. A second study was undertaken on a different population specifically to investigate the effects of dopamine on saccadic latency distributions in 15 PD patients. L-dopa was found to prolong latency, although the magnitude of the effect varied between subjects. The implications of these observations for the use of saccadic latency distributions as a potential biomarker of PD are discussed, as are the effects of L-dopa on neural decision making, where it is postulated to increase the criterion level of evidence required before the decision to move is made.

Aged↗
PubMed2002

Pudendal nerve "complete" motor latencies at four different levels in the anal sphincter system in young adults.

PURPOSE: Pudendal nerve complete motor latency, or the sum of the conduction time from the root of the sacral nerve to the end of the pudendal nerve and the synaptic delay, varied in length (from shortest to longest) in the puborectalis, the deep external anal sphincter, and the superficial/subcutaneous external anal sphincter, in that order, for middle-aged people. The aim of this study was to elucidate whether such a phenomenon was physiologic or pathologic. METHODS: In 20 young adults (21.9 +/- 1.37 years old, 10 females), pudendal nerve complete motor latencies were measured after magnetic stimulation to the sacral region. Electromyographic recordings were taken at depths of 5, 3.8, 2.6, and 1.5 cm from the perineal skin using a needle electrode and at 3 cm from the anal verge using surface electrodes within the anal canal. The data were compared with the data of the middle-aged cohort (65.4 +/- 7.70 years old) in our previous study. RESULTS: The pudendal nerve complete motor latencies were 3.85 +/- 1.24 ms at 5 cm, 3.97 +/- 1.25 ms at 3.8 cm, 5.41 +/- 2.42 ms at 2.6 cm, 9.98 +/- 4.01 ms at 1.5 cm, and 3.45 +/- 0.52 ms while using surface electrodes. The pudendal nerve complete motor latencies at 5, 3.8, and 2.6 cm were significantly shorter in the young adults than in the middle-aged subjects. The pudendal nerve complete motor latency using surface electrodes was significantly shorter than the pudendal nerve complete motor latency at 2.6 and 1.5 cm (mean +/- standard deviation). CONCLUSIONS: Because pudendal nerve complete motor latency was progressively longer at 5, 3.8, 2.6, and 1.5 cm, in that order, in young adults as well as in middle-aged people, this phenomenon was considered to be physiologic and may be mechanically reasonable and safe in shutting the anal canal and might be useful for milking the residual mucus out of the anal canal to prevent soiling. Aging disturbed the innervation of the upper three levels of the anal sphincter system. Pudendal nerve complete motor latency using intra-anal surface electrodes approximated that at the highest of the anal sphincters.

Adult↗
PubMed1983

Developmental changes in the human visual system as reflected by the latency of the pattern reversal VEP.

Pattern reversal visually evoked potentials (VEPs) were recorded from 439 infants and young children ranging in age from 1 month to 5 years in response to large and small checks. Qualitative analysis of the VEP wave form showed that the first major positive component, P1, is consistently present at all ages, while the frequency of occurrence of later positive components is more variable. The proportion of infants showing late positive components increases with age; by 1 year, the frequency of occurrence of late components for large checks is more adult-like than for small checks. The latency of P1 was analyzed quantitatively. Results showed that P1 latency decreases rapidly during the first year of life for both large and small checks and that the time course of the latency change differs as a function of check size. VEPs to large checks attain adult-like P1 latency values by about 1 year of age, while the P1 latency of VEPs to small checks has still not reached adult levels by 5 years of age. Data from 12 infants tested longitudinally between 1 and 7 months of age using both checkerboards and square wave gratings show no difference in P1 latency between checkerboards and gratings comprised of large (30-240 min) pattern elements, but for patterns with small (7.5 and 15 min) elements, P1 latency to checks is significantly longer than P1 latency to stripes. These results are explained on the basis of the difference in the fundamental spatial frequency between checks and stripes.

Attention↗
PubMed1983

Exponential electrophysiological aging: P3 latency.

Forty-nine normal volunteer subjects ranging in age from 15 to 80 years were studied in an 'auditory oddball' event-related potential paradigm. In certain respects our results replicate other studies, finding significant correlations between age and both N2 and P3 latency. Slopes of the linear age/ERP latency regression function increased with component number (i.e., N1 less than P2 less than N2 less than P3). Further analysis disclosed that the age/ERP component latency relationship is non-linear. Separate age/ERP component latency linear regression functions were computed for subjects 15-45 and 46-80. None of these functions were significant for subjects under 45. Age/latency slopes were significant in the older group for P2, N2 and P3. The age/P3 latency slope for the subjects under 45 was 0.53 msec/year, versus 3.14 msec/year for the subjects over 45. The data for P3 latency and age are best fitted with a curvilinear first and second degree orthogonal polynomial, which describes a positively accelerating latency increase with age. Clinical implications of the form of the age/P3 latency regression function (curvilinear vs. linear) are discussed.

Adolescent↗
PubMed1983

Frequency specificity of simultaneously recorded early and middle latency auditory evoked potentials.

Early and middle latency auditory evoked potentials were recorded simultaneously with a 2-channel wide-band recording technique. Latency and amplitude distributions of components V, Na and Pa were determined in 20 normal hearing adults for 3 different stimuli (click, plop, 500 Hz tone burst) presented at 70, 30 and 20 dB HL. Normative latency data of the middle latency components are presented. The detectability and amplitude of the Na-Pa complex were considerably larger than those of wave V at 20 and 30 dB HL for the two low frequency stimuli. Ten ears exhibiting high frequency sensorineural hearing loss were examined. In these cases, only click-evoked Na and Pa, but not wave V, were observed down to 20 dB HL. Also, the click latency-intensity function of Na-Pa was found to be similar to the normal low frequency latency functions. The results consistently suggested that the low frequency contributions to wave V cancel in phase because of short duration, whereas the duration of the Na-Pa complex allows for a positive superimposition of all frequency bands. Since these differences in frequency specificity of the EAEP and the MAEP affect latency, care is advised for the interpretation of inter-peak latencies.

Adolescent↗
PubMed1990

Host species and strain differences affect the ability of an HSV-1 ICP0 deletion mutant to establish latency and spontaneously reactivate in vivo.

HSV-1 latency and reactivation were studied in vivo by spontaneous and iontophoresis-induced ocular viral shedding in New Zealand rabbits, Balb/c and A/J mice latently infected with wild-type KOS, and dl x 3.1, a progeny ICP0 deletion mutant. The presence of trigeminal ganglionic latency was demonstrated by the in vitro methods of cocultivation and in situ hybridization. Although the efficiency of ganglionic latency was significantly less (P less than .0001) for dl x 3.1 than for KOS in both mice and rabbits, only dl x 3.1 shed spontaneously in the NZ rabbit. Iontophoresis of adrenergic agents failed to induce reactivation and ocular viral shedding of KOS or dl x 3.1 in mice or rabbits. The establishment of latency and reactivation of KOS and dl x 3.1 was dependent on the host animal. We conclude that host factors as exemplified by host species and host strain differences significantly affected the ability of KOS and dl x 3.1 to establish latency, to reactivate, and to shed spontaneously. ICP0 expression was not required for the establishment or maintenance of latency, nor was it required for the reactivation of latent HSV-1. Furthermore, the biological activity of KOS and dl x 3.1 during latency in vivo did not correlate with latency studies based on in vitro methods.

Animals↗
PubMed1990

Latency to initiate locomotion elicited by stimulation of the diencephalon positively correlates in awake and anesthetized rats.

Locomotor stepping can be elicited by brain stimulation at various diencephalic sites under moderate levels of Nembutal. This study determined if locomotor initiation measured under anesthesia provides a valid measure of the intersite factors which determine initiation in the awake condition. We compared the latencies to initiate locomotor stepping elicited by electrical stimulation (50 microA, 0.5-msec pulses, 10 to 160 Hz) by rats tested while awake and unrestrained in a rotary runway or anesthetized and held in a stereotaxic apparatus. In the latter tests, initial anesthesia was provided by Nembutal (25 mg/kg) and 2% halothane and maintenance anesthesia was provided by 7 mg/kg as needed and local injections of lidocaine. For 30 sites in 16 rats, average locomotor initiation latency in the awake condition and the shortest latencies in the anesthetized condition were positively correlated (r = .78). Locomotion at sites with long latencies in the awake condition was frequently blocked in the anesthetized condition, but sites with short latencies were rarely blocked. The results indicate that the shortest locomotor latencies in the anesthetized condition approximate the latencies measured in the awake condition. It is concluded that the anesthetized condition can provide valid initiation measures, but sites with long latencies in the awake condition are prone to depression under anesthesia.

Anesthesia↗
PubMed1984

Intracranial recording of short latency somatosensory evoked potentials in man: identification of origin of each component.

In normal subjects the short latency SEPs generally consisted of 3 positive waves (P9, P11, P14) and a succeeding negative wave (N20). To determine the origins of these waves we have made intracranial records from 17 patients, which suggest the following results. P9 originates in stimulated median nerve peripheral to the dorsal roots such as brachial plexus, P11 in the dorsal column of the cervical cord, P14 in the cuneate nucleus and medial lemniscal pathway, and N20 in the cerebral cortex. On the basis of intracranial and intraspinal records, the onset of P11 indicates the arrival of the afferent volley at the cord entry and the peak latency of P11 its arrival time at the C1-2 level dorsal column. The onset latency of P14 indicates the onset of postsynaptic events in cuneate nucleus neurons and the peak latency of P14 arrival at the midbrain. From the ventral surface of the brain-stem 3 positive waves (P'9, P'11, P'14) like the initial positive components of the scalp short latency SEPs (P9, P11, P14) were recorded. The amplitude of P'14 was large compared to that of P14. The peak latencies of P'14 recorded at the medulla and the pons were shorter than that of P14 by 0.7-0.8 msec and 0.2-0.5 msec, respectively. The peak latency of P'14 at the midbrain was almost the same as that of P14. By measuring the distance between the recording electrodes in the brain-stem and the peak latency difference of P'14, the fastest lemniscal conduction velocity was estimated as 56 m/sec.

Adult↗
PubMed1987

Generators of middle- and long-latency auditory evoked potentials: implications from studies of patients with bitemporal lesions.

We recorded middle- and long-latency auditory evoked potentials (AEPs) in 5 patients (ages 39-72 years) with bilateral lesions of the superior temporal plane. Reconstructions of CT sections revealed that primary auditory cortex had been damaged bilaterally in four of the patients, while in the fifth an extensive left hemisphere lesion included primary auditory cortex while a right hemisphere lesion had damaged anterior auditory association areas but spared primary auditory cortex. Normal middle-latency AEPs (MAEPs) were recorded at the vertex electrode in all of the patients. In 3 of the 5 patients, MAEPs also showed normal coronal scalp distributions and were comparable in amplitude following stimulation of either ear. Two patients showed abnormalities. In one case, Na (latency 17 msec)-Pa (latency 30 msec) amplitudes were reduced over both hemispheres following stimulation of the ear contralateral to the more extensive lesion. In another, with both subcortical and cortical involvement, the Pa was abolished over the hemisphere with the more extensive lesion. Long-latency AEPs were normal in 2 patients whose lesions were largely confined to the superior temporal plane. In 2 patients with lesions extending into the inferior parietal lobe, N1s were abolished bilaterally. In the fifth patient, the N1 showed a slight reduction over the hemisphere with the more extensive lesion. Middle- and long-latency AEPs were differentially affected by some lesions. For example, patients with absent N1s could produce normal Pas. A review of these results and those of previous studies of bitemporal patients suggests that abnormalities in middle- and long-latency AEPs do not necessarily reflect damage to primary auditory cortex per se, but rather the degree of damage to adjacent areas. Abnormalities in MAEPs are associated with subcortical lesions, or cortical lesions extensive enough to denervate thalamic projection nuclei. Abnormalities in the long-latency N1 reflect lesion extension into the multi-modal areas of the inferior parietal lobule. This area appears to exert a critical modulatory influence over N1 generators outside of the superior temporal plane.

Adult↗
PubMed1981

P3 latency in threshold signal detection.

The EOG, EEG(Cz, Pz) and response latencies were obtained from ten subjects in an auditory threshold detection task with a signal probability of 0.5. In order to minimize any interaction of signal condition (signal-presence vs. signal-absence) and uncertainty about the moment of signal occurrence (temporal equivocation), the observation period was marked with a cue light. The single-trial latencies of the P3 component associated with correct signal-present and signal-absent decisions were assessed on the basis of the cross-covariance functions of the EEG epochs and a template of the P3. Trials with values of covariance smaller than a criterion value were discarded. The mean and dispersion of the P3 latency proved larger for signal-absent than for signal-present trials, while the mean values of covariance were smaller for signal-absent than for signal-present trials. In addition, the mean and dispersion of the P3 proved smaller for high confidence than for medium confidence signal-present trials. Nearly all these effects also proved significant for the response latency. The single-trial P3 latencies were positively correlated with the response latencies of the same trials. The observed latency variations of the P3 were interpreted in terms of changes in the detectability of the stimulus events. It was concluded that the signal condition had a significant effect upon the latency of the P3 associated with signal-present and signal-absent decisions over and above that due to temporal equivocation.

Adult↗
PubMed2004

Contextual influence of TMS on the latency of saccades and vergence.

This study examines the effects of TMS of the right PPC on the latency of saccades and vergence alone or combined and the role of experimental design. Two designs were used: pure blocks with exclusively no-TMS or TMS trials; mixed blocks in which no-TMS and TMS trials were interleaved; a control study with TMS of the primary motor cortex (pure blocks) was also conducted and showed no effects on latencies. In contrast, in the experiment with TMS of the PPC latencies for TMS trials increased relative to no-TMS trials for almost all eye movements (isolated saccades, convergence, divergence, and for saccade and divergence components of combined eye movements). However, such increase was significant for pure blocks only. In mixed blocks no difference between TMS and no-TMS was found mainly because the latency of no-TMS trials increased relative to corresponding latencies in pure blocks. A second study centered on isolated convergence and divergence confirmed the interaction between block-design and TMS effects, and showed significant TMS/no-TMS differences only for the pure design and for a design in which the rate of TMS trials was high (75%). Again, the absence of difference was due to increase of latency for no-TMS trials in mixed blocks with low rates of TMS trials (50% or 25%), but also to decreased effects for the TMS trials themselves. We conclude that latency of all eye movements, saccades and vergence is highly influenced by the context. Such a contextual factor is the number of TMS versus no-TMS trials within a block; low numbers of TMS trials (50% or less) increases baseline latencies. The design of mixed blocks with 50% or less of TMS trials should not be recommended as it underestimates the direct effects of TMS on cortical processing. In fact, the majority of TMS studies on eye movements do use paradigms with high rates of TMS trials (75% or more). Our study confirms the validity of such paradigms.

Adult↗
PubMed2004

Differential morphine effects on short- and long-latency laser-evoked cortical responses in the rat.

Evoked potential and ensemble neuronal activities were used to study the responses of the primary sensorimotor cortex (SmI) to noxious CO(2) laser irradiation of the middle part of the tail in conscious behaving rats. The hypothesis that systemic morphine treatment preferentially attenuates the longer-latency laser-evoked cortical responses was also tested. Laser-evoked potentials (LEPs) and multiple single-unit (SU) activities were, respectively, recorded from chronically implanted stainless-steel screws and microwire electrodes. When examined individually, many SmI neurons showed either short-latency (<100 ms) or long-latency (300-500 ms) responses to laser irradiation. These neurons are widely dispersed in the tail region and hind limb region of the SmI, and also in the forelimb and head regions of the primary motor cortex (MI). Quantitatively, a higher percentage of neurons in the SmI tail region responded with shorter latencies compared to those in the SmI hind limb region or in the MI. When responses of many simultaneously recorded SU were examined together, short-latency and long-latency SmI ensemble activities matched the LEP1 and LEP2, respectively. Systemic morphine significantly attenuated the long-latency but not the short-latency component in both LEPs as well as ensemble neuronal activity in the tail region of the SmI. These effects were blocked by naloxone pretreatment.

Action Potentials↗
PubMed2004

Altered sleep latency and arousal regulation in mice lacking norepinephrine.

Latency to sleep and the amount of sensory stimulation required to awaken an animal are measures of arousal threshold, which are ultimately modulated by an arousal regulation system involving many brain areas. Among these brain areas and network connections are wake-promoting nuclei of the brainstem and their corresponding neurotransmitters, including norepinephrine (NE). In this study, we used mice that are unable to produce NE to study its role in regulating sleep latency after a variety of interventions, and to study arousal from sleep after sleep deprivation (SD). Sleep latency was measured after gentle awakening or after injections of saline, caffeine or modafinil. Sleep latency was also measured before and after partial restoration of NE pharmacologically. Arousal threshold was measured by recording the number of decibels of white noise required to wake each mouse from NREM sleep after 0, 3 and 3 + 3 h SD (3 h SD followed by < 2 min sleep, followed by an additional 3 h SD). Results showed that when mice were awakened without being touched, there were no differences in sleep latency between the genotypes. However, after an injection of saline, the control mice increased their sleep latency, whereas the NE-deficient mice did not. There were no group differences in sleep latency after treatment with either stimulant. The sleep latency difference between the genotypes was ameliorated by partial restoration of NE. The arousal threshold experiments revealed that significantly more noise was required to wake the NE-deficient mice after 3 and 3 + 3 h of SD. These findings show that mice lacking NE fall asleep more rapidly only after a mild stressor, such as an intraperitoneal injection. NE-deficient mice are also more difficult to wake up using audio stimulation after SD. The results presented here suggest that NE promotes wakefulness during transitions between sleep and wake under conditions involving mild stress and SD, but not under baseline circumstances.

Amphetamine↗
PubMed2006

Effects of uncertainty and target displacement on the latency of express saccades in man.

Saccadic eye movements generated in response to a gap paradigm in which the fixation light spot was extinguished 200 ms prior to presentation of the target light spot showed appreciably shorter latencies than for the overlap paradigm in which the target light spot was presented 200 ms prior to extinction of the fixation light spot. When there was unpredictability in the direction of target presentation, i.e., to the left or right of the fixation light spot, the gap paradigm evoked mainly fast regular saccades of peak latency of 155 ms with relatively few express saccades which were defined as having latencies of less than 120 ms. By contrast, when the target always appeared to the right, a substantial population of express saccades with peak latency 95 ms was now generated. There was also a change in the relationship between saccadic latency and target angular displacement which covered the range 5-35 degrees . With the overlap paradigm and unpredictability of target direction, the latencies of the slow regular saccades increased markedly with target angular displacement. This was not the case with the same target direction when the latency of slow regular, fast regular, and express saccades remained constant with increasing target angular displacement. This indicates for targets appearing in the same hemifield that the ocular motor system operates with shortest latency irrespective of target angular displacement.

Adult↗