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PubMed1998

Differential latency testing: a more sensitive test for radial tunnel syndrome.

A modification of the standard electrodiagnostic test was developed in an effort to provide a more sensitive electrodiagnostic evaluation in radial tunnel syndrome. Radial motor nerve latency recordings were obtained in 3 different forearm positions: neutral, passive supination, and passive pronation. The maximal difference in these recordings, the differential latency, in 25 patients with radial tunnel syndrome of greater than 6 months duration (test group) was compared with those in 25 asymptomatic volunteers (control group). Differential latency recordings were obtained in all patients in the test group before and after surgery. Radial nerves that were compressed demonstrated a significantly greater differential latency (0.44+/-0.12 ms) versus controls (0.12+/-0.008 ms). Following radial nerve decompression, differential motor latencies in the test group decreased below control values, demonstrating a resolution of the provoked electrical response with a postoperative differential latency of 0.07+/-0.05 ms. Our results demonstrate the differential motor latency of the radial nerve to be a sensitive electrodiagnostic tool in patients with radial tunnel syndrome. A differential latency of > or =0.30 ms was considered indicative of radial tunnel syndrome.

Adult↗
PubMed1983

Short latency somatosensory evoked potential in children.

The short latency somatosensory evoked potential was studied in 90 normal children of 1 month to 16 years old and 7 adults. Somatosensory stimuli were delivered through a disc electrode placed over the median nerve at the wrist joint. The uniform recording sites used were the central region of the scalp, and the seventh cervical spine or Erb's point. Reference electrodes were placed on the hand contralateral to the median nerve stimulated. Three positive peaks (P1, P2 and P3) and one negative peak (N1) were consistently recorded, a further positive peak (P4) after N1 was not always observed. The latency of each peak per 1 m body length decreased with age until 2 or 5 years of age. The latency of each peak after 2 years of age was positively correlated with the body length and arm length. The value of P1 peak latency per 1 m body length reaches adult values at an earlier rate than the value of P3 peak latency and P2-P3 latency per 1 m body length. This suggests that central lemmiscal pathways mature at a slower rate than peripheral nerve fibers. The wave form pattern of the short latency somatosensory evoked potential changed to the adult pattern at 10 years of age. The peak latency of P4 during deep sleep was slightly prolonged. In recording on infants during sleep, the EEG should be monitored to determine the stage of sleep.

Adolescent↗
PubMed1999

Analysis of volition latency on antisaccadic eye movements.

The antisaccadic paradigm can be applied to test the suppression of reflexive saccades and the activation of volitional saccades simultaneously. The impaired frontal cortex has been shown to have difficulty in suppressing reflexive saccade (prosaccade) to make a successful antisaccade. Degraded antisaccade performance can also be observed in patients with Parkinson's disease (PD). The studies of PD based on the prosaccadic and antisaccadic paradigms have shown controversial findings; the latency between patients and age-matched controls could be either with or without significant difference. Even with this inconsistency, our previous study and recent analysis have supported that the latency of both prosaccade and antisaccade increases significantly for patients with PD. The objective of this study is to investigate whether prolonged antisaccade latency is caused by the affected volitional decision process (volition latency) or simply by the delayed initiation of saccade with direction opposite to the cue, by measuring prosaccade and antisaccade latency from the intermingled paradigms. Eleven mildly affected patients with idiopathic PD and eight age-matched normal subjects were tested in this study. As compared to the age-matched control, the results showed that prosaccade, antisaccadic, and volition latency of the patients was significantly elevated (P<0.01). We conclude that antisaccade performance for the PD patients was degraded for both the volition decision process and the initiation of saccade with direction opposite to the cue. Also, volition latency analysis is a more objective method than prosaccade and antisaccade latency analysis, which can be compared among results obtained from different analysis methodologies.

Aged↗
PubMed2006

Whiplash and concussion: similar acute changes in middle-latency SEPs.

OBJECTIVE: Middle-latency somatosensory evoked potentials (SEPs) following median nerve stimulation can provide a sensitive measure of cortical function. We sought to determine whether the mechanical forces of whiplash injury or concussion alter normal processing of middle-latency SEPs. METHODS: In a cross-sectional pilot study 20 subjects with whiplash were investigated (50% between 0.5-2 months and 50% between 6-41 months post injury) and compared to 83 healthy subjects using a standard middle-latency SEP procedure. In a subsequent prospective study subjects with either acute whiplash (n=13) or Grade 3 concussion (n=16) were investigated within 48 hours and again three months post injury. RESULTS: In the pilot study the middle-latency SEP component N60 was significantly increased in the ten subjects investigated within two months after whiplash. In contrast, the ten subjects examined more than six months after injury showed normal latencies. In the prospective study N60 latencies were increased after whiplash and concussion when tested within 48 hours of injury. At three months, latencies were improved though still significantly different from controls post whiplash and concussion. CONCLUSIONS: Both whiplash injury and concussion alter processing of the middle-latency SEP component N60 in the acute post traumatic period. The acute changes appear to normalize between three-six months post injury. The SEP similarities suggest that the overlapping clinical symptomatology post whiplash and concussion may reflect a similar underlying mechanism of rotational mild traumatic brain injury.

Adolescent↗
PubMed1978

The temperature-dependence of the loss of latency of lysosomal enzymes.

1. When Triton-filled lysosomes from rat liver are incubated for up to 50min at 37 degrees C, pH7.4, in 0.25m-sucrose, no loss of latency of N-acetyl-beta-glucosaminidase or p-nitrophenyl phosphatase occurs unless the incubated lysosomes are cooled to approx. 15 degrees C. 2. It is suggested that a phase change takes place in the incubated lysosomal membranes on cooling; it starts at approx. 15 degrees C and probably is not complete at 0 degrees C. 3. Incubation of the lysosomes causes an increased potential for loss of latency of the lysosomal enzymes. This potential is not fully expressed at elevated temperature (e.g. 37 degrees C), but is expressed on cooling. 4. The increase at elevated temperature in potential for loss of latency exhibits biphasic kinetics, with an initial rapid phase followed by a slower phase, which is linear with respect to time. The extra loss of latency resulting from the rapid phase in proportional to the temperature of the incubation. 5. Arrhenius plots of the increase is potential for loss of latency during the slow phase for N-acetyl-beta-glucosaminidase and p-nitrophenyl phosphatase exhibit marked deviations from linearity beginning at approx. 15 degrees C. This suggests that the increase in potential for loss of latency is affected by a phase change that occurs around this temperature. 6. Activation energies for the increase in potential for loss of latency at and above 22 degrees C are 53.1+/-5.4kJ/mol (12.7+/-1.3kcal/mol) for N-acetyl-beta-glucosaminidase and 45.2+/-7.5kJ/mol (10.8+/-1.8kcal/mol) for p-nitrophenyl phosphatase. It is postulated that these energies reflect enzymic action, the products of which cause loss of latency to occur on cooling.

4-Nitrophenylphosphatase↗
PubMed2002

Hippocampal serotonin responses in short and long attack latency mice.

Short and long attack latency mice, which are selected based on their offensive behaviour in a resident-intruder model, differ in their neuroendocrine regulation as well as in aspects of their brain serotonin system. Previous studies showed that the binding capacity and expression of serotonin-1A receptors in the hippocampal CA1 field of long attack latency mice are significantly lower than that found in short attack latency mice. We tested whether the functional responses of CA1 hippocampal cells to serotonin are also reduced in long attack latency mice. To this end, serotonin-induced changes in the membrane potential and input resistance were recorded in vitro with microelectrodes in CA1 pyramidal neurones of long and short attack latency mice. The data show that in long attack latency mice, along with a reduction of the serotonin-1A receptor mRNA expression, the serotonin-induced membrane hyperpolarization and decrease in resistance are attenuated. Basal membrane properties of CA1 neurones in the two.mice lines were comparable. Plasma corticosterone levels in response to a novelty stress were elevated in long compared to short attack latency mice and inversely related to the serotonin-induced responses. We tentatively conclude that long attack latency mice show attenuated functional responses to serotonin in the hippocampus, possibly linked to a chronic perturbation of hormonal levels.

Aggression↗
PubMed2003

Effects of latency period in a rabbit mandibular distraction osteogenesis.

Recently, distraction osteogenesis has been widely used in the craniomaxillofacial skeleton. There are varying views, however, about the need for a latency period for mandibular distraction, which has been reported from 0 to 14 days. We used a rabbit model to determine the ideal latency period for mandibular distraction osteogenesis. We performed a subperiosteal corticotomy of the bilateral mandible and then applied an external device. We used 0-, 2-, 5-, and 10-day latency periods. Distraction was done at a rate of 0.5 mm per day (0.25 mm every 12 h) to elongate by 5 mm after each latency period. Hematoxylin-eosin stain was used for histologic observation, and bone labelling was observed with a fluorescence microscope. In the 0-day latency, the lengthened region was filled with fibrous tissue. Cartilage formed like isles along the lengthened edge. In the 10-day latency, the lengthened region was almost completely filled with woven bone. In the 2- and 5-day latency, there were mineralization zones at the periphery of this fibrous interzone. The primary osteon remodelling zones were located at both ends of the zones of mineralization zones. In the 5-day latency, new bone formation was observed around the periosteum.

Animals↗
PubMed1980

Dispersion of latencies in photoreceptors of Limulus and the adapting-bump model.

To light stimuli of very low intensity, Limulus photoreceptors give a voltage response with a fluctuating delay. This phenomenon has been called "latency dispersion." If the generator potential is the superposition of discrete voltage events ("bumps"), and if the effect of light upon bump size is negligible, then the latency dispersion and the bump shape completely characterize the frequency response to sinusoidal flicker. For very low light intensities, the latency dispersion of the bumps, the bump shape, and the frequency response are measured. It is found that for data obtained at 20 degrees C, the frequency response can be accounted for completely by the latency dispersion and by the bump shape derived from steady-state noise characteristics. At 10 degrees C, the time scale of the response of the photoreceptor is lengthened. The dispersion of latencies and the bump shape are found not to have the same temperature dependence. However, just as those measured at 20 degrees C, the bump shape and the dispersion of latencies measured at 10 degrees C can predict the frequency response measured under the same conditions. These results strongly suggest that the major mechanisms involved in the generator potential are the latency process and the bump process. At high light intensities, the time scale of the generator potential shortens. The decrease in time scale of the generator potential can be attributed to the decreases in time scales of the bumps and of the latency dispersion process.

Animals↗
PubMed2003

The clinical predictors of sleepiness correlated with the multiple sleep latency test in an Asian Singapore population.

STUDY OBJECTIVES: To explore the clinical predictors of sleepiness as objectively determined by the Multiple Sleep Latency Test with the Epworth Sleepiness Scale, age, body mass index, and overnight polysomnographic parameters at a tertiary referral center Sleep Disorders Unit. DESIGN: Retrospective, consecutive case series review. SETTING: A multidisciplinary sleep disorders unit in Singapore General Hospital, a tertiary-care university-affiliated hospital. PATIENTS: 72 consecutive patients evaluated for sleep disorders with overnight polysomnograms and Multiple Sleep Latency Tests between March 2002 and September 2002. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Mean sleep latency on the Multiple Sleep Latency Test was 9.0 +/- 4.4 minutes, and mean Epworth Sleepiness Scale score was 10.8 +/- 5.8. On univariate analysis, mean sleep latency on the Multiple Sleep Latency Test showed a significant negative correlation with the Epworth Sleepiness Scale score, apnea-hypopnea index, body mass index, arousal index, and time spent below 90% oxygen saturation during overnight polysomnography. After performing multiple linear regression, only Epworth Sleepiness Scale score and apnea-hypopnea index remained significantly correlated (P = .039 and P = .008, respectively). An Epworth Sleepiness Scale score of 8 or above predicted a mean sleep latency on the Multiple Sleep Latency Test of less than 10 minutes with a sensitivity of 73.9% and specificity of 50.0%. CONCLUSIONS: The Epworth Sleepiness Scale and apnea-hypopnea index are useful predictors of sleepiness in our Asian Singapore population.

Adult↗
PubMed2006

The influence of age and sex on sleep latency in the MSLT-30--a normative study.

STUDY OBJECTIVES: The Multiple Sleep Latency Test-30 (MSLT-30) is a variation of the Multiple Sleep Latency Test with a fixed duration of 30 minutes for each of 5 test sessions. It requires less effort for reliable recording and is not susceptible to on-line scoring errors. The aim of the study was to provide normative data for the clinical use of the MSLT-30 and to evaluate the influence of age, sex, and other sociodemographic variables. DESIGN: An MSLT-30, along with measures of mood, objective, and subjective sleepiness was performed in a sample of healthy subjects in a balanced quota design. SETTING: Sleep laboratory in a sleep disorders center. PARTICIPANTS: One hundred subjects with no complaint of sleep disturbance or daytime sleepiness, 10 men and 10 women each from 5 age decades from 20 to 69 years. INTERVENTIONS: None. RESULTS: Mean latency to sleep stage 1 or any other sleep stage was 13.9 +/- 6.9 minutes. The SL-30 showed a clear quadratic association with age, with the shortest latencies in the middle age groups. No correlation was found between the mean latency to sleep stage 1 or any other sleep stage and sociodemographic variables or other measures of daytime sleepiness (Epworth Sleepiness Scale, vigilance test), mood scales, sleep quality (Pittsburgh Sleep Quality Index), and amount of prior sleep. CONCLUSIONS: Sleep latencies in normal subjects are age dependent in a quadratic fashion, with a minimum in middle-aged subjects. This reconciles the findings of a long mean sleep latency in the MSLT of adolescents and of an increase on the mean sleep latency with age in adults.

Adult↗
PubMed1989

Statistical dependence among the wave latencies of the auditory brain stem response.

If the interpeak intervals in the auditory brain stem response (ABR) are assumed to be statistically independent variables that represent the neural transmission time between loci, then the absolute latency of an ABR wave is the sum of the transmission times between successive loci. Consequently, the correlations between the absolute latencies of the ABR waves would be part-whole correlations whose expected values are appreciably different from r = 0. We derived the expected values of the correlations between the latencies of the ABR waves on the assumption that their latencies are the sum of independent elements (transmission times) and found them to be 0.707, 0.577, and 0.816 for I.III, I.V, and III.V, respectively. In addition, the expected values of the correlations between the latencies of the ABR waves assuming that the absolute wave latencies themselves are independent variables (e.g., rI.III = 0) were derived. Several of the correlations among interpeak and between the interpeak and absolute latencies were demonstrated to be appreciably different from r = 0. It would appear that it is more reasonable to assume that the elements (transmission times) rather than the component latencies are the variables of choice for statistical analysis of ABR data.

Brain Stem↗
PubMed1991

Auditory brainstem and middle latency evoked responses in the clinical evaluation of diabetes.

The measurement of auditory brainstem evoked responses and middle latency evoked responses may improve the evaluation of diabetic neuropathy. Twenty diabetic patients were studied (12 males, 8 females), aged 21 to 63 years with normal hearing, together with 20 age- and sex-matched normal subjects (10 males, 10 females). Auditory brainstem evoked responses were induced by rarefaction clicks of 0.1 ms at a repetition rate of 21.1 CPS and an intensity of 75 dB hearing level. Middle latency evoked responses were induced with clicks of 0.1 ms, a repetition rate of 7.7 CPS and an intensity of 75 dB hearing level. Diagnostic criteria were: a I-V interval latency shift greater than 2SD of the control group for the auditory brainstem evoked response test or the interval difference of wave V greater than 0.2 ms. Middle latency evoked response was diagnostic if the latency of the Pa component was greater than 2SD of normals. Twenty-five per cent of subjects had retrocochlear impairment (absence of I wave) even in the absence of symptoms. The combined technique of auditory brainstem evoked response and middle latency evoked response improved the detection rate of central nervous system dysfunction. Auditory brainstem response is important for detecting desynchronization of the auditory response, whereas middle latency evoked response detects abnormalities in the more rostral regions of the central nervous system. In conclusion, there is a role for auditory brainstem evoked response and middle latency evoked response in the global assessment of diabetic neuropathy.

Brain Stem↗
PubMed1991

Evidence for a contribution of the motor cortex to the long-latency stretch reflex of the human thumb.

1. In normal subjects, transcranial magnetic stimulation of the hand region of the motor cortex evokes motor responses only in contralateral hand muscles at a latency of about 19-24 ms. In contrast, stimulation of the motor cortex of three mirror movement subjects evoked, nearly simultaneously, motor responses in hand muscles on both sides of the body at latencies similar to those of normal subjects. In these subjects no other neuroanatomical pathways appear to be abnormally directed across the mid-line. Thus, their mirror movements are probably due to a projection of the corticospinal tract to homologous motoneurone pools on each side of the body. 2. We reasoned that if the motor cortex contributes to the generation of long-latency stretch reflex responses then in these mirror movement subjects stretching a muscle on one side of the body should produce long-latency reflex responses in the ipsilateral and the homologous contralateral muscle. 3. To test this idea experiments were done on normal human subjects and on the subjects with mirror movements. The electromyographic (EMG) activity of the flexor pollicis longus muscle (FPL) on each side of the body was recorded. Stretch of the distal phalanx of the thumb of one hand produced a series of distinct reflex EMG responses in the ipsilateral FPL. The earliest response, when present, began at 25 ms (S.D. = 3.5 ms) and was followed by responses at 40 (S.D. = 3.9 ms) and 56 ms (S.D. = 4.3 ms). There was no difference, either in timing or intensity, between the ipsilateral FPL EMG responses of normal subjects and those of the mirror movement subjects. 4. No response of any kind was observed in the contralateral (unstretched) FPL of normal subjects. In contrast, we observed in all three mirror movement subjects EMG responses in the contralateral (unstretched) FPL beginning at 45-50 ms. The latency of this response is considerably shorter than the fastest voluntary kinaesthetic reaction time, which was on average 130 ms (S.D. = 11 ms). The contralateral long-latency EMG response observed in the mirror movement subjects was on average 30% (range 5-60%) of that on the ipsilateral side. No short-latency response (25 ms) was ever observed in the contralateral FPL of these subjects. 5. These observations are quite consistent with the idea that the long-latency stretch reflex responses of hand and finger muscles are produced, at least in part, by the motor cortex.

Electromyography↗
PubMed2006

Herpes simplex virus type 1 latently infected neurons differentially express latency-associated and ICP0 transcripts.

During the latent phase of herpes simplex virus type 1 (HSV-1) infection, the latency-associated transcripts (LATs) are the most abundant viral transcripts present in neurons, but some immediate-early viral transcripts, such as those encoding ICP0, have also been reported to be transcribed in latently infected mouse trigeminal ganglia (TG). A murine oro-ocular model of herpetic infection was used to study ICP0 gene expression in the major anatomical sites of HSV-1 latency, including the TG, superior cervical ganglion, spinal cord, and hypothalamus. An HSV-1 recombinant strain, SC16 110LacZ, revealed ICP0 promoter activity in several neurons in latently infected ganglia, and following infection with wild-type HSV-1 strain SC16, in situ hybridization analyses identified ICP0 transcripts in the nuclei of neurons at times consistent with the establishment of latency. Reverse transcription (RT)-PCR assays performed on RNA extracted from latently infected tissues indicated that ICP0 transcripts were detected in all anatomical sites of viral latency. Furthermore, quantitative real-time RT-PCR showed that neurons differentially expressed the LATs and ICP0 transcripts, with splicing of ICP0 transcripts being dependent on the anatomical location of latency. Finally, TG neurons were characterized by high-level expression of LATs and detection of abundant unspliced ICP0 transcripts, a pattern markedly different from those of other anatomical sites of HSV-1 latency. These results suggest that LATs might be involved in the maintenance of HSV-1 latency through the posttranscriptional regulation of ICP0 in order to inhibit expression of this potent activator of gene expression during latency.

Animals↗
PubMed1976

Normal median nerve proximal latency in carpal tunnel syndrome: a clue to coexisting Martin-Gruber anastomosis.

Five of 65 patients referred for electrodiagnosis because of clinical evidence of carpal tunnel syndrome were found to have near normal latency on proximal stimulation of the median nerve, although the distal motor latency was prolonged. In one patient, the proximal latency was actually shorter than the distal latency. The failure of the proximal latency to be prolonged in proportion to the distal latency results in a spuriously high apparent conduction velocity in the forearm segment of the nerve. This value may even exceed the conduction velocity of the corresponding nerve segment in the unaffected arm. Stimulation studies on the ulnar nerve reveal that this disparity is the result of some of the median nerve fibres destined for the thenar muscles taking an aberrant course through the ulnar nerve and thus escaping compression at the wrist. A median-ulnar communication in the forearm, the 'Martin-Gruber' anastomosis, may occur in up to 15% of the population. The presence of the Martin-Gruber anastomosis in patients with carpal tunnel syndrome results in a partial or total sparing of thenar muscles from denervation and the paradoxical recording of normal proximal latencies in the median nerve when the distal latency is prolonged.

Adult↗
PubMed1997

Latency of muscle chemoreflex to vascular occlusion of active muscle during dynamic exercise.

When oxygen delivery to active muscle is too low for the ongoing rate of metabolism, metabolites accumulate and activate a muscle chemoreflex that raises arterial pressure. During static muscular contractions, the latency of the onset of increments in sympathetic activity attributed to the muscle chemoreflex is long (1-2 min). This long latency might be caused by slow accumulation of metabolites attributable to low rates of metabolism. Because shortening contractions at a given force per unit time have a much higher energy cost than do static contractions, the muscle chemoreflex should have a much shorter latency during dynamic exercise than during static contractions, and the latency should shorten further with rising exercise intensity. To test these ideas, the latency to the onset of the rise in arterial pressure induced by the muscle chemoreflex following vascular occlusion of active muscle was measured in four dogs exercising on a treadmill. During steady-state exercise of mild to moderate intensity, pressor responses to muscle ischemia were elicited by rapid, complete occlusion of the terminal aorta; this procedure mimics the blockage of muscle blood flow that occurs normally during static contractions. There was a statistically significant effect of exercise intensity on latency (P < 0.001). The latency was 23.5 +/- 4.5, 16.4 +/- 5.6, and 10.1 +/- 2.3 s (means +/- SE) at 3.2 km/h 0% grade, 6.5 km/h 0% grade, and 6.5 km/h 10% grade, respectively. Also, the rate of rise of arterial pressure during chemoreflex activation increased progressively with rising exercise intensity from 0.8 +/- 0.2 mmHg/s during exercise at 3.2 km/h 0% grade to 2.0 +/- 0.5 mmHg/s during exercise at 6.5 km/h 10% grade. Thus the latency of the muscle chemoreflex in response to vascular occlusion during mild dynamic exercise is shorter than has been reported during static contractions of moderate intensity.

Animals↗
PubMed1992

Visual response latencies in striate cortex of the macaque monkey.

1. Many lines of evidence suggest that signals relayed by the magnocellular and parvocellular subdivisions of the primate lateral geniculate nucleus (LGN) maintain their segregation in cortical processing. We have examined two response properties of units in the striate cortex of macaque monkeys, latency and transience, with the goal of assessing whether they might be used to infer specific geniculate contributions. Recordings were made from 298 isolated units and 1,129 multiunit sites in the striate cortex in four monkeys. Excitotoxin lesions that selectively affected one or the other LGN subdivision were made in three animals to demonstrate directly the magnocellular and parvocellular contributions. An additional 435 single units and 551 multiunit sites were recorded after the ablations. 2. Most units in striate cortex had visual response latencies in the range of 30-50 ms under the stimulus conditions used. The earliest neuronal responses in striate cortex differed appreciably between individuals. The shortest latency recorded in the four animals ranged from 20 to 31 ms. Comparable values were obtained from both single unit and multiunit sites. After lesions were made in the magnocellular subdivision of the LGN in two animals, the shortest response latencies were 7 and 10 ms later than before the ablations. A larger lesion in the parvocellular subdivision of another animal produced no such shift. Thus it appears that the first 7-10 ms of cortical activation can be attributed to activation relayed by the magnocellular layers of the LGN. 3. The units with the shortest latencies were all found in layers 4C or 6 and their responses were among the most transient in striate cortex. Furthermore, their responses all showed a pronounced periodicity at a frequency of 50-100 Hz. This periodicity was stimulus locked, and the responses of all short-latency units oscillated in phase. 4. An index of response transience was computed for the units recorded in striate cortex. The distribution of this index was unimodal and gave no suggestion of distinct contributions from the geniculate subdivisions. Magnocellular and the parvocellular lesions affected the overall transience of responses in striate cortex. The changes, however, were very small; extremely transient responses and extremely sustained responses survived both types of lesions. 5. A characteristic profile was observed in the response latencies in superficial layers. Latencies appeared to increase monotonically from layer 4 toward the surface of cortex, with the most superficial neurons not becoming active until 15 ms after responses were observed in layer 4C.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

Short-latency primate vestibuloocular responses during translation.

Short-lasting, transient head displacements and near target fixation were used to measure the latency and early response gain of vestibularly evoked eye movements during lateral and fore-aft translations in rhesus monkeys. The latency of the horizontal eye movements elicited during lateral motion was 11.9 +/- 5.4 ms. Viewing distance-dependent behavior was seen as early as the beginning of the response profile. For fore-aft motion, latencies were different for forward and backward displacements. Latency averaged 7.1 +/- 9.3 ms during forward motion (same for both eyes) and 12.5 +/- 6.3 ms for the adducting eye (e.g., left eye during right fixation) during backward motion. Latencies during backward motion were significantly longer for the abducting eye (18.9 +/- 9.8 ms). Initial acceleration gains of the two eyes were generally larger than unity but asymmetric. Specifically, gains were consistently larger for abducting than adducting eye movements. The large initial acceleration gains tended to compensate for the response latencies such that the early eye movement response approached, albeit consistently incompletely, that required for maintaining visual acuity during the movement. These short-latency vestibuloocular responses could complement the visually generated optic flow responses that have been shown to exhibit much longer latencies.

Acceleration↗