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PubMed1984

Intranasal vaccination of pigs against pseudorabies: absence of vaccinal virus latency and failure to prevent latency of virulent virus.

The avirulent Bartha's K strain of pseudorabies virus (PRV) was used to vaccinate 8 pigs at 10 weeks of age by the intransal route (experiment 1). On postvaccination days (PVD) 63 and 91, pigs were treated with corticosteroids. Viral shedding could not be detected. Explant cultures of trigeminal ganglia and tonsils did not produce virus. Four pigs with maternal antibody were vaccinated intranasally with Bartha's (attenuated) K strain of PRV at 10 weeks of age and were challenge exposed with a virulent strain of PRV on PVD 63 (experiment 2). Corticosteroid treatment, starting on postchallenge exposure day 70 (PVD 133) resulted in viral shedding in 1 of 4 pigs. In another pig of these 4, a 2nd corticosteroid treatment was required to trigger reactivation. In both pigs, sufficient reactivated virus was excreted to infect susceptible sentinel pigs. Restriction endonuclease analysis indicated that viruses isolated from the 2 pigs after challenge exposure and corticosteroid treatment were indistinguishable from the virulent virus. Evidence was not obtained for simultaneous excretion of vaccinal and virulent virus. Of 4 pigs without maternal antibody vaccinated twice with 1 of 2 inactivated PRV vaccines, challenge exposed on PVD 84, and treated with corticosteroids on postchallenge exposure day 63 (PVD 147), 1 was latently infected, as evidenced by the shedding of PRV (experiment 3). However, its sentinel pig remained noninfected.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Intranasal↗
PubMed2006

Acceptable differences in sensory and motor latencies between the median and ulnar nerves.

The median and ulnar nerves are often studied during the same electrodiagnostic examination. The sensory and motor latencies of these nerves have been compared to detect a common electrodiagnostic entity: median neuropathy at the wrist. However, this comparison could also be used to diagnose less common ulnar pathology. For this reason, it is important to establish normal values for comparing median and ulnar sensory and motor latencies. Previous research deriving these differences in latency has had some limitations. The purpose of this study was to derive an improved normative database for the acceptable differences in latency between the median and ulnar sensory and motor nerves of the same limb. Median and ulnar sensory and motor latencies were obtained from 219 and 238 asymptomatic risk-factor-free subjects, respectively. An analysis of variance was performed to determine whether physical characteristics, specifically age, race, gender, height, or body mass index (as an indicator of obesity), correlated with differences in latency. Differences in sensory latencies were unaffected by physical characteristics. The upper limit of normal difference between median and ulnar (median longer than ulnar) onset latency was 0.5 ms (97th percentile), whereas the peak latency value was 0.4 ms (97th percentile). The upper limit of normal difference between ulnar-versus-median (ulnar longer than median) onset latency was 0.3 ms (97th percentile), whereas the peak-latency value was 0.5 ms (97th percentile). The mean difference in motor latencies correlated with age, with older subjects having a greater variability. In subjects aged 50 and over, the mean difference in median-versus-ulnar latency was 0.9 ms +/- 0.4 ms. The upper limit of normal difference (median longer than ulnar) was 1.7 ms (97th percentile). The upper limit of normal ulnar motor latency is attained if the ulnar latency comes within 0.3 ms of the median latency. In individuals less than 50 years of age, the mean difference in latency was 0.6 ms +/- 0.4 ms, with the median latency usually being greater than the ulnar. The upper limit of normal difference (median longer than ulnar) was 1.4 ms (97th percentile), whereas the upper limit of ulnar latency relative to median latency was attained if the ulnar latency was equal to median latency.

Journal Article↗
PubMed1983

Antidromic activation of spikes with bimodal and trimodal latencies in the olfactory bulb of rabbits.

Spikes with bimodal and occasional trimodal latencies were recorded from neurons in the olfactory bulb of rabbits in response to lateral olfactory tract (LOT) stimulation at one site. Among neurons with bimodal spike latencies, two types have to be distinguished. In the case of type I neurons long-latency second-mode spikes were suppressed by short-latency first-mode spikes. Due to this suppression the long-latency second-mode spike could be investigated only, when its threshold was lower than that of the short-latency spike. In the case of type II neurons the long-latency second-mode spike was not suppressed. The collision test was applied to type I bimodal spikes. All short-latency first-mode and long-latency second-mode spikes were suppressed by spontaneous spikes. The suppression time indicated the likelihood of collision in most cases, but one could not entirely exclude the possibility, that short-latency first-mode spikes were suppressed due to refractoriness and long-latency second-mode spikes due to inhibition. To allow a more definite interpretation of collision a multiple collision test was applied, by stimulating axons at several LOT sites. A parallel rise of latency values and suppression time values was measured for 3 and more axonal spikes with different latencies, indicating collision and antidromic activation more definitely. Antidromically activated short-latency first-mode spikes were interpreted to be due to axonal stimulation and antidromically activated long-latency second-mode spikes to be due to axon collateral stimulation. No evidence for any postsynaptic activation of type I short-latency first-mode or long-latency second-mode spikes was gained. An indicator for collision of an antidromic spike with a spontaneous spike is the value collision time minus latency (c-l). The c-l values of axonal spikes ranged from 0.2 to 1.8 ms with a mean of 0.7 ms (n = 25), and c-l values of axon collateral spikes from 0.2 to 2.5 ms, with a mean of 1.1 ms (n = 13). The interpretation of c-l values is discussed. In the multiple collision test the c-l deviations from the lowest c-l value of each neuron ranged for axonal spikes between 0.0 and 0.7 ms (n = 25), with 38% not exceeding 0.1 ms and 81% not exceeding 0.4 ms. Spikes activated via axon collaterals had c-l deviations between 0.0 and 2.0 ms (n = 13). The c-l deviations above 2 ms were remote from other values and considered to be possibly inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1993

GABA shapes a topographic organization of response latency in the mustache bat's inferior colliculus.

Many neurons in the auditory forebrain of the mustache bat act as coincidence detectors for signals separated in time by up to 20 msec. Differences in path lengths cannot adequately explain how the nervous system delays one signal relative to the other to such a large degree. Several researchers have proposed that an inhibitory mechanism might account for long delays, but it has not been known where these delays are created. Previous studies, using a variety of mammals, have reported that the inferior colliculus contains some cells with much longer latencies than those of cells in lower auditory centers, suggesting that the inferior colliculus might be the site where long delays are generated. We characterized the latencies of cells in the 60 kHz contour of the mustache bat inferior colliculus and examined how GABAergic inhibition affected the latencies of those cells. Evaluations of the influence of GABA were made by documenting changes in response latency that occurred when GABAergic inputs were reversibly blocked by iontophoretic application of the GABAA antagonist bicuculline. Prior to bicuculline application, latencies varied over a wide range among the population of cells and we observed a pattern of latency changes with dorsoventral location. The pattern was that the population of neurons in the dorsal regions of the inferior colliculus had a wide range of latencies while the population in more ventral regions had progressively narrower latency ranges. Thus, while some cells at each depth had comparably short latencies, the average latency of the population at a given depth was long in the dorsal inferior colliculus and became progressively shorter ventrally. The same characteristic distribution of latencies and pattern of latency changes with depth were observed for cells that had different aural preferences, different rate-intensity functions, and different discharge patterns, suggesting that latency is an important organizational feature of the inferior colliculus. Bicuculline substantially shortened latency in about half of the cells studied, and it dramatically altered the pattern of latency changes with depth. These results suggest that GABA normally lengthens response latencies and creates a dorsoventral grading of delays in the inferior colliculus. This wide range of latencies could provide the large latency differences necessary for the coincidence detectors in the medial geniculate body tuned to signals separated by up to 20 msec.

Animals↗
PubMedDate not supplied

The a-wave latency in control subjects and patients with retinal diseases.

PURPOSE: To determine the a-wave latency of the electroretinograms (ERGs) recorded from control subjects and patients with retinal diseases. METHODS: The a-wave latency and implicit time (IT) were measured retrospectively from the ERGs of 40 control subjects and 99 patients. The patients included 9 with complete congenital stationary night blindness (cCSNB), 13 with achromatopsia or cone dystrophy, 5 with supernormal and delayed rod ERG syndrome, and 72 with retinitis pigmentosa (RP). To assess whether latency measurements can be obtained reliably by different observers from patients with smaller a-wave amplitudes and noisier baselines, the a-wave latency and IT of the ERG of the right eye of 10 control subjects and 10 patients with RP were measured by three observers. RESULTS: The mean a-wave latency measured for the same 10 control ERGs by three observers differed by less than 1 millisecond while the mean IT differed by 1.7 milliseconds. For 10 ERGs from RP patients, the mean for the a-wave latency measured by the three observers differed by less than 2.0 milliseconds and by 1.1 millisecond for the IT. The coefficient of variation varied from 24.8% to 36.7% for the latency and from 11.5% to 16.0% for the IT. The a-wave latencies elicited by the 0-dB stimulus under scotopic and photopic conditions from the 40 control subjects were not statistically different. The a-wave latency in patients with cCSNB did not differ significantly from that in control subjects. The longer a-wave latency in patients with achromatopsia suggested that the rods have a longer latency than cones. The scotopic and photopic a-wave latencies were significantly longer in RP patients. The longer latency in RP patients was not due to smaller a- or b-wave amplitudes. CONCLUSIONS: The a-wave latency can be measured as reliably as the IT in control subjects but the reliability is not as good for the latency as for the IT in RP patients. The larger coefficients of variation in RP patients were most likely due to the measurements being made from RP patients at different stages of their disease. Our results suggest that the a-wave latency in control subjects is determined by cones under both scotopic and photopic conditions. The longer a-wave latency in RP patients suggests that the rods and cones are altered over a significant area of the retina.

Adolescent↗
PubMed1986

Short and long latency reflexes in human muscles following electrical and mechanical stimulation.

Electromyographic (EMG) recordings were made during slight voluntary contraction or during rest in various human muscles following electrical and mechanical stimulation. The electrical stimuli used in most of these experiments were square wave pulses with the duration of 100 microseconds given at a frequency of 3 Hz on cutaneous and mixed nerves. The mechanical stimuli were constant stretches of the muscle induced by taps of the electromechanical reflex hammer. The aims of the series of studies were to investigate the characteristic features of electrically and mechanically elicited muscular responses, the correspondence between electrically and mechanically elicited responses, the short latency response following muscle afferent stimulation and the modifications of the electrically elicited responses. The electrical stimulation during slight voluntary activity caused short and long latency excitatory phases in averaged and rectified EMG with the onset latencies much shorter than the voluntary reaction time. The responses were considered reflexive. The most constant short and long latency reflexes following electrical stimulation were found in the first dorsal interosseus muscle in the hand and in the extensor digitorum brevis in the foot. The mean onset latency for the short latency reflex was 30.9 +/- 1.7 ms (SD) and for the long latency reflex 50.9 +/- 2.8 ms in the hand muscle. In the foot muscle the mean short latency reflex latency was 54.9 +/- 4.1 ms and the long latency reflex latency was 80.5 +/- 5.5 ms. The onset latencies of the short and long latency reflexes during slight voluntary activity following stretching and following cutaneous nerve stimulation corresponded in the first dorsal interosseus muscle. It was concluded that they are generated at least partly via mutual pathways. The stretches given to the triceps brachii muscle during various head positions, different elbow angles and during the Jendrassik maneuver revealed short latency reflex facititations. The lesser degree of the facilitation was caused by the tonic neck reflex and the Jendrassik maneuver caused the greater degree of the facilitation. The short latency reflex following muscle afferent stimulation (the H-reflex) was elicited in the flexor carpi radialis muscle with a mean latency of 15.4 +/- 0.5 ms. The amplitude of the 50% H-reflex was modified by contracting or by stretching of the muscle. Voluntary contraction increased the 50% H-reflex amplitude about 30% and the passive stretching decreased it to about 80% of the control value. The patients with different central nervous system disorders showed abnormal electrically elicited short and long latency reflexes. The s

Adult↗
PubMed1991

The inverse relationship between nonverbal intelligence and the latency of the Hoffmann reflex from the right and left thenar muscles in right- and left-handed subjects.

The relationship between nonverbal reasoning ability and the latency of the Hoffmann (H) reflex was studied in right- and left-handed subjects. The nonverbal reasoning ability was assessed by the Cattell's Culture Fair Intelligence test. Hand preference was assessed by the Edinburgh Handedness Inventory. Hoffmann reflex was recorded from thenar muscles of the right and left thumbs. In left-handers (total sample), IQ was found to be significantly and negatively linearly related to the H-reflex latency from the left side. In strong left-handers, there was a significant negative linear relationship between IQ and the H-reflex latency from right and left sides, but with a higher correlation for the left side. In weak left-handers, IQ did not show any significant relation to the H-reflex latencies from the right and left sides. In right-handers (total sample), there was a significant negative linear correlation between IQ and the H-reflex latency from the right side. In right-handed women without familial sinistrality (FS-), IQ was found to be inversely related to the H-reflex latency from the right and left side, but with a higher correlation for the right side. In right-handed women with FS, IQ did not show any significant relation to the H-reflex latency from the right and left sides. In right-handed men with right eye preference and FS-, IQ was found to be negatively linearly related to the H-reflex latency from the right and left sides equally. In right-handed men with right eye FS+, mixed eye FS-, +, mixed eye-right foot (FS-), mixed eye-mixed foot, and left eye preference there was no significant relationship between IQ and the H-reflex latency from the right and left sides. Only in strong left-handers there was a significant, positive linear correlation between IQ and the right minus left (R-L) difference of latencies. The H-reflex latency from the right and left sides was not significantly correlated with the R-L difference of latencies in left-handers. In right-handed women with right eye preference FS-, and in right-handed men with right eye preferences FS-, The H-reflex latency from the right side was found to be positively linearly correlated with the R-L difference of latencies. In right-handed women FS+, and in right-handed men FS+, and mixed or left eye preference, the H-reflex latency from the left side was found to be negatively linearly related to the R-L difference of latencies.(ABSTRACT TRUNCATED AT 400 WORDS)

Female↗
PubMed1999

Response latency of macaque area MT/V5 neurons and its relationship to stimulus parameters.

A total of 310 MT/V5 single cells were tested in anesthetized, paralyzed macaque monkeys with moving random-dot stimuli. At optimum stimulus parameters, latencies ranged from 35 to 325 ms with a mean of 87+/-45 (SD) ms. By examining the relationship between latency and response levels, stimulus parameters, and stimulus selectivities, we attempted to isolate the contributions of these factors to latency and to identify delays representing intervening synapses (circuitry) and signal processing (flow of information through that circuitry). First, the relationship between stimulus parameters and latency was investigated by varying stimulus speed and direction for individual cells. Resulting changes in latencies were explainable in terms of response levels corresponding to how closely the actual stimulus matched the preferred stimulus of the cell. Second, the relationship between stimulus selectivity and latency across the population of cells was examined using the optimum speed and direction of each neuron. A weak tendency for cells tuned for slow speeds to have longer latencies was explainable by lower response rates among slower-tuned neurons. In contrast, sharper direction tuning was significantly associated with short latencies even after taking response rate into account, (P = 0.002, ANCOVA). Accordingly, even the first 10 ms of the population response fully demonstrates direction tuning. A third study, which examined the relationship between antagonistic surrounds and latency, revealed a significant association between the strength of the surround and the latency that was independent of response levels (P < 0.002, ANCOVA). Neurons having strong surrounds exhibited latencies averaging 20 ms longer than those with little or no surround influence, suggesting that neurons with surrounds represent a later stage in processing with one or more intervening synapses. The laminar distribution of latencies closely followed the average surround antagonism in each layer, increasing with distance from input layer IV but precisely mirroring response levels, which were highest near the input layer and gradually decreased with distance from input layer IV. Layer II proved the exception with unexpectedly shorter latencies (P< 0.02, ANOVA) yet showing only modest response levels. The short latency and lack of strong direction tuning in layer II is consistent with input from the superior colliculus. Finally, experiments with static stimuli showed that latency does not vary with response rate for such stimuli, suggesting a fundamentally different mode of processing than that for a moving stimulus.

Analysis of Variance↗
PubMed1999

Effects of adenosine on local stimulus-response latency and induction of atrial fibrillation by premature stimuli.

Premature atrial stimuli delivered during the relative refractory or "vulnerable" period exhibit increased local stimulus-response latency and may occasionally induce atrial arrhythmias. The use of adenosine to treat supraventricular tachycardias may also provoke atrial arrhythmias. In this study we investigated the effects of adenosine on the latency of premature complexes in relation to repolarization and induction of atrial arrhythmias in 14 patients without structural heart disease. A monophasic action potential catheter was used for recording in the right atrium and introducing premature stimuli (S2) at twice diastolic threshold after eight paced (S1) complexes. At short coupling intervals, S2 latency increased relative to S1 latency. S2 was delivered repeatedly at a fixed coupling interval (producing maximal local response latency) and adenosine (6 mg) was given intravenously. Adenosine decreased S2 latency significantly (23+/-5 to 11+/-3 ms, P<0.01), to values similar to S, latency. However, despite the decrease in S2 latency, the combination of adenosine and S2 more often resulted in transient atrial arrhythmias (11 of 14 patients vs 2 of 14 patients without adenosine, P<0.05). Adenosine had no effect on S, latency (9+/-2 vs. 9+/-2 ms) but decreased monophasic action potential duration from 202+/-37 to 158+/-38 ms (P<0.01). Adenosine was also given to 10 patients with S2 introduced at a coupling interval 40-50 ms less than the baseline effective refractory period. This resulted in a decrease in atrial refractoriness and capture of S2 in all cases. Latency for S2 was significantly greater than Si latency (21+/-12 vs. 9+/-2 ms, P<0.01) and transient atrial arrhythmias were induced in 9 of 10 patients. We conclude that for a given S2 coupling interval, adenosine decreases local stimulus-response latency but increases atrial vulnerability to transient atrial arrhythmias. Decreased latency may be related to a shift in the zone of relative refractoriness associated with an adenosine-mediated decrease in monophasic action potential duration. Induction of atrial arrhythmias in the presence of adenosine occurs independently of increased latency and is therefore not dependent on S2 falling within the relative refractory period at the site of stimulation.

Action Potentials↗
PubMed1983

Median nerve residual latency: normal value and use in diagnosis of carpal tunnel syndrome.

If normal variability in nerve conduction velocity (NCV) were eliminated from distal latency measurements, standard deviations of distal latencies should be reduced and normal ranges narrowed. This should be especially useful in diagnosing carpal tunnel syndrome. In this study, the median motor distal latencies, the sensory distal peak latencies, motor NCVs and motor residual latencies were determined in 100 normal subjects. Residual latency was calculated by dividing the distance between the cathode and active electrode by the motor NCV and subtracting the quotient from the motor distal latency. Results showed that the standard deviation and normal range of the residual latency were smaller than those of the motor distal latency or sensory distal latency. Data were also compared by age decade. Residual latencies hold constant into the 9th decade, while motor distal and sensory distal latencies increase with age. Three patients with recent onset of carpal tunnel syndrome are described who had prolonged residual latencies as their only abnormalities. Residual latency determination is particularly attractive because it does not require additional stimulation of the median nerve and the additional discomfort associated with it.

Adult↗
PubMed1995

Latency variability of responses to visual stimuli in cells of the cat's lateral geniculate nucleus.

We constructed average histograms from responses evoked by flashing stimuli and noted previously described variations in the shape of the response profile, particularly with respect to sharpness of the peak. To express this variable, we measured the half-rise latency, which is the latency from stimulus onset required to reach half the maximum response. A short half-rise latency, which is characteristic of nonlagged cells, is associated with a brisk response and sharp peak; a long half-rise latency, characteristic of lagged cells, is associated with a sluggish response and broad peak. Nonlagged cells were readily seen; we attempted to identify cells with long latencies as lagged, but we were unable to do so unambiguously due to failure to observe lagged properties other than latency. We thus refer to these latter cells as having "lagged-like" responses to indicate that we are not certain whether these are indeed lagged cells. In addition to the histograms, we analyzed the individual response trials that were summed to create each histogram, and we used spike density analysis to estimate the initial response latency to the flashing spot for each trial. We found that lagged-like responses were associated with more variability in initial response latency than were nonlagged responses. We then employed an alignment procedure to eliminate latency variation from individual trials; that is, responses during individual trials were shifted in time as needed so that each had a latency equal to the average latency of all trials. We used these "aligned" trials to create a second, "aligned" response histogram for each cell. The alignment procedure had little effect on nonlagged responses, because these were already well aligned due to consistent response latencies amongst trials. For lagged-like responses, however, the alignment made a dramatic difference. The aligned histograms looked very much like those for nonlagged responses: the responses appeared brisk, with a sharply rising peak that was fairly high in amplitude. We thus conclude that the slow build up to a relatively low peak of firing of the lagged-like response histogram is not an accurate reflection of responses on single trials. Instead, the sluggishness of lagged-like responses inferred from average response histograms results from temporal smearing due to latency variability amongst trials. We thus conclude that there is relatively little difference in briskness between nonlagged and lagged-like responses to single stimuli.

Animals↗
PubMed2003

Gap effects on saccade and vergence latency.

To explore visual space, we make saccades, vergence, and, most frequently, combined saccade-vergence eye movements. The initiation of saccades is well studied, while that of vergence is less explored. Saccade latency is influenced by the fixation task: when the target appears simultaneously with the offset of the fixation point, latencies tend to be regular, whereas the introduction of a gap period before target onset causes the emergence of express latencies (80- to 120-ms). This study examines in ten normal adults whether the gap paradigm has a similar effect on the latency of vergence and combined eye movements. The second goal is to identify contextual factors that favor the emergence of short latencies, by comparing a condition in which gap and simultaneous trials were performed in separate blocks (pure blocks) with a condition in which the two types of trials were interleaved randomly (mixed blocks). The results are: (1) the gap paradigm reduced similarly (by approximately -30 ms) the mean latency of saccades, convergence, divergence, and both the saccadic and vergence components of combined eye movements; (2) the gap paradigm was responsible for the emergence of 80- to 120-ms latencies for saccades and divergence (pure or combined), but rarely for convergence; (3) inspection of the latency distributions showed that such short latencies formed a clearly distinct population, different from anticipatory responses or regular latencies, for saccades (pure or combined) but not for pure vergence; importantly, distinct express latencies were found also for the convergence and divergence components of combined eye movements; (4) no difference was found for the group of subjects between pure and mixed blocks, but the latter yielded shorter latencies for some subjects, suggesting an idiosyncratic phenomenon. We suggest that distinct express latencies are specific to saccades and could correspond to a specific mode of saccade initiation. Interestingly, the express mode of triggering can be transferred to the vergence component in the ecological condition in which saccade is combined with vergence.

Adolescent↗
PubMed1996

Nocturnal sleep latencies among alert, alert-deprived and sleepy subjects.

Twenty-seven healthy, asymptomatic subjects participated in a study to determine repeated nocturnal sleep latencies as a function of level of daytime sleepiness. Subjects were screened polysomnographically and were determined to be free of any sleep pathology. Nine subjects had a screening multiple sleep latency test (MSLT) of < or = 5 min and 18 had a MSLT of > or = 10 min. Subjects were assigned to 3 groups, sleepy (MSLT < or = 5 min), alert, and alert sleep-deprived groups (MSLT > or = 10 min). Repeated nocturnal latencies to sleep were determined at 2300, 0110, 0310 and 0510 h on 2 nights with at least 5 days between nights. The results showed a main effect of group on the repeated nocturnal sleep latencies. Post-hoc tests demonstrated longer repeated nocturnal latencies among alert subjects compared to the sleepy and alert sleep-deprived subjects. The latter two groups had comparable sleep latencies. A significant main effect of time of night was also shown. The 0510 h latency was significantly shorter than the latencies at 2300 and 0110 h. The 0310 h latency was significantly shorter than the 0110 h latency and comparable to the 2300 and 0510 h latency. Significant correlations were found between daytime MSLT, repeated nocturnal sleep latencies, and nocturnal sleep time. These results show systematic differences in repeated nocturnal sleep latencies among sleep and alert subjects and extend the already described characteristics of these subjects by comparing them to a group of alert sleep-deprived subjects.

Adult↗
PubMed2001

Group II muscle afferents probably contribute to the medium latency soleus stretch reflex during walking in humans.

1. The objective of this study was to determine which afferents contribute to the medium latency response of the soleus stretch reflex resulting from an unexpected perturbation during human walking. 2. Fourteen healthy subjects walked on a treadmill at approximately 3.5 km h(-1) with the left ankle attached to a portable stretching device. The soleus stretch reflex was elicited by applying small amplitude (approximately 8 deg) dorsiflexion perturbations 200 ms after heel contact. 3. Short and medium latency responses were observed with latencies of 55 +/- 5 and 78 +/- 6 ms, respectively. The short latency response was velocity sensitive (P < 0.001), while the medium latency response was not (P = 0.725). 4. Nerve cooling increased the delay of the medium latency component to a greater extent than that of the short latency component (P < 0.005). 5. Ischaemia strongly decreased the short latency component (P = 0.004), whereas the medium latency component was unchanged (P = 0.437). 6. Two hours after the ingestion of tizanidine, an alpha(2)-adrenergic receptor agonist known to selectively depress the transmission in the group II afferent pathway, the medium latency reflex was strongly depressed (P = 0.007), whereas the short latency component was unchanged (P = 0.653). 7. An ankle block with lidocaine hydrochloride was performed to suppress the cutaneous afferents of the foot and ankle. Neither the short (P = 0.453) nor medium (P = 0.310) latency reflexes were changed. 8. Our results support the hypothesis that, during walking the medium latency component of the stretch reflex resulting from an unexpected perturbation is contributed to by group II muscle afferents.

Adrenergic alpha-Agonists↗
PubMed1988

Long-latency stretch reflexes as co-ordinated functional responses in man.

1. Reflex activity in human arm muscles has been measured in response to torque perturbations around the elbow joint in the flexion-extension direction and/or the supination-pronation direction. Intramuscular fine-wire electrodes were used to record electromyographic (EMG) activity in the muscles. A pre-load was applied in the same direction as or in a different direction to the perturbation. The subjects were instructed to 'hold on', which means that they had to actively resist the perturbation without unduly co-activating their muscles. 2. The EMG activity showed segmented reflex responses with short-latency (25-50 ms) and long-latency (50-75 ms) components, followed by other bursts of activity which probably originated from the subject's voluntary or triggered reactions. 3. Motor units in m. triceps gave short-latency and long-latency responses to imposed elbow extension but only long-latency responses were seen to imposed pronation, which does not stretch m. triceps. Motor units in m. brachialis gave short-latency and long-latency excitatory (inhibitory) responses to imposed extension (flexion) torques. However, only long-latency inhibitory responses were observed to imposed pronation torques. Motor units in m. biceps gave short-latency and long-latency excitatory responses to imposed pronation torques. 4. These results show that the long-latency reflex cannot be the result of a simple feed-back mechanism that controls muscle length only. We argue that the long-latency reflex activity reflects the co-ordinated activation of muscles which is necessary for an adequate response. This hypothesis is supported by the fact that the distribution of long-latency reflex activity over muscles was found to be similar to the distribution of activation found during a voluntary exerted torque in the direction opposite to the applied perturbation.

Action Potentials↗