Sensory Delays Research Articles

Effects of diazepam on the latency of saccades for luminance and binocular disparity defined stimuli

Saccadic latency is composed of separate sensory and motor processing delays. Therefore, any alteration in the sensory processing should effect the saccadic latency. Because the highest density of benzodiazepine (Bz) binding sites is located in cerebral cortex, sensory processing of stimuli in this cortical area is expected to be substantially effected by administration of Bzs. It is well known that sensory processing of binocular disparity occurs in the cerebral cortical areas and therefore the latency of saccades to stimuli defined by binocular disparity should be substantially affected by Bz intake. In this study, we tested this prediction by comparing the latency of saccadic eye movements for binocular disparity defined stimuli (stereo stimuli) with those for luminance contrast defined stimuli (luminance stimuli), after diazepam or placebo. Eye movements were mainly recorded by use of the magnetic search coil technique, and the study was performed in a randomized, double-blind way. Although diazepam prolonged the latency of saccades for stereo and luminance stimuli, the percentage increases in saccadic latency for the stereo stimuli were significantly larger than those for the luminance stimuli. Saccadic peak velocity, and saccadic amplitude, also significantly decreased after diazepam under conditions of stereo and luminance stimuli. However, there was no significant difference for either saccadic peak velocity or amplitude between the two types of target. The results suggest that the latency of saccades to binocular disparity defined random-dot stimuli could more sensitively reflect the pharmacodynamic effects of Bzs on the cerebral cortex.

An Optimal Estimator Model of Multi-Sensory Processing in Human Postural Control

We hypothesized that multi-sensory processing at the central nervous system (CNS) in human postural control can be described using an optimal estimator model. The estimates on body dynamics from multi-sensory signals contain sensory noise, transmission delays, and process disturbances. The state estimates approximate actual body movement. Erroneous estimates degrade the performance of feedback control and could cause a loss of balance if distorted severely. To test the hypothesis, we examined the frequency response of a visually-induced postural sway with stimulus frequency ranging from 0.075 to 1Hz and established an optimal estimator model. Two healthy young (33yrs ± 1) subjects stood on a force platform located 1.25m behind a projection screen with their arms crossed over their chests. They were asked to maintain an upright posture against the sinusoidal visual field stimuli. Each sinusoidal visual stimulus was generated by a projector for 200secs in pitch direction with a maximum pitch angle of 20o. Kinematics data was recorded to calculate the frequency response function of the center of mass (COM). There were three components in the modeling procedure: a biomechanical model of body and sensor dynamics, a linear feedback control model to stabilize the biomechanical model, and a state estimator to estimate body dynamic states based on multi-sensory outputs. We modeled the sensor dynamics of the semicircular canal, otolth, vision, and muscle spindles at the ankle and hip joint. We used the Kalman filter and linear quadratic regulator to determine feedback gains. Results showed that the frequency response function of a visually-induced postural sway decreased as stimulus frequency increased, and this low-pass filtering characteristic with an approximate cutoff frequency of 0.2Hz was also simulated by the postural feedback control model with optimal estimator. Low-pass filtering characteristics of the frequency response are mainly due to body and sensor dynamics, which show reduced responses for high frequency stimulus. The Kalman filter represents that the CNS utilizes redundant sensory information in a way that minimizes discrepancies between actual body dynamics and estimated body dynamics based on sensory output and an internal model. The results suggest that the CNS may make use of an internal representation of body dynamics, and can integrate sensory information in an optimal way to best estimate human postural responses.

Analogous Mechanisms Compensate for Neural Delays in the Sensory and the Motor Pathways: Evidence from Motor Flash-Lag

Motor behaviors require animals to coordinate neural activity across different areas within their motor system. In particular, the significant processing delays within the motor system must somehow be compensated for. Internal models of the motor system [1], in particular the forward model [2, 3], have emerged as important potential mechanisms for compensation. For motor responses directed at moving visual objects, there is, additionally, a problem of delays within the sensory pathways carrying crucial position information. The visual phenomenon known as the flash-lag effect has led to a motion-extrapolation model for compensation of sensory delays [4–6]. In the flash-lag effect, observers see a flashed item colocalized with a moving item as lagging behind the moving item. Here, we explore the possibility that the internal forward model and the motion-extrapolation model are analogous mechanisms compensating for neural delays in the motor and the visual system, respectively. In total darkness, observers moved their right hand gripping a rod while a visual flash was presented at various positions in relation to the rod. When the flash was aligned with the rod, observers perceived it in a position lagging behind the instantaneous felt position of the invisible rod. These results suggest that compensation of neural delays for time-varying motor behavior parallels compensation of delays for time-varying visual stimulation.

Sensory processing delays measured with the eye-movement correlogram.

Annals of the New York Academy of SciencesVolume 956, Issue 1 p. 476-478 Sensory Processing Delays Measured with the Eye-Movement Correlogram J. B. MULLIGAN, Corresponding Author J. B. MULLIGAN NASA Ames Research Center, Moffett Field, California 94035, USAAddress for correspondence: Jeffrey B. Mulligan, Ph.D., NASA Ames Research Center, Mail Stop 262-2, Moffett Field, CA 94035-1000. Voice: 650-604-3745; fax: 650-604-0255; [email protected].Search for more papers by this author J. B. MULLIGAN, Corresponding Author J. B. MULLIGAN NASA Ames Research Center, Moffett Field, California 94035, USAAddress for correspondence: Jeffrey B. Mulligan, Ph.D., NASA Ames Research Center, Mail Stop 262-2, Moffett Field, CA 94035-1000. Voice: 650-604-3745; fax: 650-604-0255; [email protected].Search for more papers by this author First published: 24 January 2006 https://doi.org/10.1111/j.1749-6632.2002.tb02859.xCitations: 4Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume956, Issue1NEUROBIOLOGY OF EYE MOVEMENTS: FROM MOLECULES TO BEHAVIORApril 2002Pages 476-478 RelatedInformation

Abnormalities of somatosensory evoked potentials in konzo – an upper motor neuron disorder

Objective: To determine whether the somatosensory pathways are involved or not in konzo.Methods: In 1998, 21 konzo subjects (15 females and 6 males; mean age 21 years) underwent a SEP study with a two-channel-equipment (Medtronic Keypoint, Denmark) whereas in 2000, 15 subjects (7 females and 8 males; mean age 21 years) participated in a study with a 4-channel-equipment.Results: Most subjects (19/21 in 1998 and 12/15 in 2000) showed normal median SEPs. The remainders had no median cortical responses. All 21 subjects in 1998 and 9 out of 15 in 2000 showed abnormalities of tibial SEPs mainly consisting of absence of cortical responses, prolonged cortical latencies, and central sensory delay to the lumbar spine. Most subjects showed normal absolute latencies both at peripheral and spinal levels. The SEP findings did not correlate with the severity, neither the duration of konzo, nor the experience or not of sensory symptoms at the onset of the disease.Conclusion: Our findings are not specific of konzo. However, they suggest involvement of intracranial somatosensory pathways and point to similarities with other motor neuron diseases.

The effects of an NDMA receptor antagonist on delayed visual differentiation in monkeys and rearrangements of neuron spike activity in the visual and prefrontal areas of the cortex.

The effects of perfusion of field 17 with the glutamate receptor antagonist 2-amino-5-phosphonovaleric acid (APV) on the characteristics of visual recognition and short-term memory were studied, along with the effects of APV on the responses of neurons in the visual and prefrontal areas of the cortex in rhesus macaques. In the test for delayed visual differentiation of stimuli of different colors, behavioral data were recorded simultaneously with multichannel recordings of the spike activity of single cells in cortical field 17 (directly within the microdialysis zone) and field 8. Multifactor dispersion analysis (ANOVA) showed that APV significantly worsened the behavioral characteristics in monkeys, with significant reductions in the duration of short-term storage of information (by factors of 2-4) and significant increases in the motor response times. These changes in cognitive characteristics induced by APV were accompanied by changes in the spike activity of neurons in the visual and prefrontal areas of the cortex during the sensory analysis and delay stages; changes in spike activity consisted of significant desynchronization. These results show that cognitive dysfunctions consisting of worsening of short-term remembering of information and increases in the duration of motor responses during exposure to APV may be caused by desynchronization of neuron activity in various areas of the cortex, these being involved in neuron ensembles responsible for the mechanisms of short-term memory, in which glutamatergic structures play an important role.

Assessment of muscle flap sensibility by evoked potentials in the rat.

This study investigated whether the sensory-to-motor reinervation of the muscle flap provides a better sensory recovery of an overlying skin graft. Fifty-four animals were studied in three groups of 18 rats each: group I (control): 1 cm of the gastrocnemius muscle motor nerve was excised and no repair was performed; group II (motor-to-motor repair): the motor nerve of the gastrocnemius flap was transected and repaired; group III (sensory-to-motor repair): the motor nerve of the gastrocnemius muscle and sural nerve were transected and their distal and proximal ends, respectively, were repaired. At follow-up periods of 6, 12, and 24 weeks, evaluation of hair growth, muscle atrophy, and sensory evoked potentials was performed. Somatosensory evoked potentials (SSEP) at 6 weeks in the sensory-to-motor repair (group III) revealed a significant (P < 0. 05) increase (104.4% +/- 22.9) in the relative response of peak-to-peak potentials when compared with group I (46.6% +/- 19) and group II (51.8% +/- 14.0). Muscle flap stimulation was most prominent at 6 weeks in sensory-to-motor reinvervated flaps (group III 133.1% +/- 25.4; group I 84.9% +/- 20.2). In this study, sensory-to-motor nerve repair significantly improved the sensibility of skin flaps at 6 weeks. Denervated flaps presented with 3 months of sensory recovery delay.

Prior Collateral Sprouting of Sensory Axons Delays Recovery of Pain Sensitivity after Subsequent Nerve Crush

Regeneration of motor axons is enhanced if they have sprouted prior to nerve injury. We examined whether sensory axon regeneration and recovery of pain response was affected by previous collateral sprouting. In the experimental group of rats, the right saphenous, tibial, and sural nerves were transected and ligated. The peroneal nerve was left to sprout into the adjacent denervated skin. Two months later, the axons of the peroneal nerve were crushed in the sciatic nerve. In the control group, the right sciatic nerve was crushed at the same time that the saphenous, tibial, and sural nerves were transected. Recovery of pain response in the foot was determined by the skin pinch test. Sensory axon elongation rate was measured by the nerve pinch test. The number of myelinated axons was determined in nerve cross sections stained by Azur blue. Recovery of pain sensitivity in the animals of the experimental group was delayed for 2–3 weeks in comparison to the control group. Moreover, the spatial pattern of pain response in the experimental group was irregular, displaying residual regions of insensitive skin which were not present in controls. The elongation rate of regenerating sensory axons in the experimental group was not decreased, and the number of myelinated axons in the peroneal nerves was even about 10% higher than in the control group. Therefore, we assume that the terminal arborization of the neurilemmal tubes pertaining to the former axon sprouts delayed regrowth of sensory axon terminals in the skin.

Infants with bronchopulmonary dysplasia: A developmental perspective

Infants with bronchopulmonary dysplasia (BPD) are medically fragile and developmentally at risk for neuromotor and sensory delays. long-term neurodevelopmental outcomes can be positively impacted by an organized and purposeful program of developmental follow-up and early intervention. Nurses play an integral role in provision and coordination of the multifaceted health care required by these medically fragile infants.

Les potentiels évoqués somesthésiques et les potentiels évoqués moteurs étagés dans l'étude de la conduction nerveuse périphérique proximale: A propos de 7 observations

The study of proximal motor and sensory nerve conduction in the thoracic outlet syndrome is still difficult and laborious in 1994. However, these conductions can be measured at different levels by means of somaesthetic evoked potentials and motor evoked potentials, when one takes the time to perform them. The study in normal subjects demonstrates that the proximal sensory and motor conduction delays are approximately 3.2 ms and are therefore comparable to that of the median nerve at the wrist. The study of 7 cases related to various diseases shows that these techniques, performed after electromyogram of both upper limbs, an essential prerequisite to their interpretation, are able to clearly demonstrate abnormalities of proximal conduction in patients suffering from of a scalene syndrome, a cervical epiduritis, radiation plexopathy, hereditary sensible to pressure neuropathy, motor neuropathy with persistent multifocal conduction blocks, or, on the contrary, may confirm the normality of conduction, for example in anterior horn disease.

Proprioceptive coordination of movement sequences: role of velocity and position information

1. Recent studies have shown that the CNS uses proprioceptive information to coordinate multijoint movement sequences; proprioceptive input related to the kinematics of one joint rotation in a movement sequence can be used to trigger a subsequent joint rotation. In this paper we adopt a broad definition of "proprioception," which includes all somatosensory information related to joint posture and kinematics. This paper addresses how the CNS uses proprioceptive information related to the velocity and position of joints to coordinate multijoint movement sequences. 2. Normal human subjects sat at an experimental apparatus and performed a movement sequence with the right arm without visual feedback. The apparatus passively rotated the right elbow horizontally in the extension direction with either a constant velocity trajectory or an unpredictable velocity trajectory. The subjects' task was to open briskly the right hand when the elbow passed through a prescribed target position, similar to backhand throwing in the horizontal plane. The randomization of elbow velocities and the absence of visual information was used to discourage subjects from using any information other than proprioceptive input to perform the task. 3. Our results indicate that the CNS is able to extract the necessary kinematic information from proprioceptive input to trigger the hand opening at the correct elbow position. We estimated the minimal sensory conduction and processing delay to be 150 ms, and on the basis of this estimate, we predicted the expected performance with different degrees of reduced proprioceptive information. These predictions were compared with the subjects' actual performances, revealing that the CNS was using proprioceptive input related to joint velocity in this motor task. To determine whether position information was also being used, we examined the subjects' performances with unpredictable velocity trajectories. The results from experiments with unpredictable velocity trajectories indicate that the CNS extracts proprioceptive information related to both the velocity and the angular position of the joint to trigger the hand movement in this movement sequence. 4. To determine the generality of proprioceptive triggering in movement sequences, we estimated the minimal movement duration with which proprioceptive information can be used as well as the amount of learning required to use proprioceptive input to perform the task. The temporal limits for proprioceptive processing in this movement task were established by determining the minimal movement time during which the task could be performed.(ABSTRACT TRUNCATED AT 400 WORDS)

Tibial nerve somatosensory evoked potentials at various stages of peripheral neuropathy in insulin dependent diabetic patients.

To determine whether central nervous conduction deficits are related to the degree of peripheral neuropathy somatosensory evoked potentials (SEP) were measured after tibial nerve stimulation in 51 healthy subjects aged 39.3 (SE 2.0, (range 21-71) years and 100 insulin dependent diabetic patients aged 37.3 (1.5, 18-73) years. Five criteria were used for staging of peripheral neuropathy: nerve conduction; thermal discrimination threshold; vibration perception threshold; tendon reflexes; and neuropathic symptoms. Thirty seven patients had fewer than two abnormalities among the first four criteria and no symptoms (stage 0 = no neuropathy), 37 had 2 or more abnormalities but no symptoms (stage 1 = subclinical neuropathy); 26 had 2 or more abnormalities in conjunction with symptoms (stage 2 = symptomatic neuropathy). Multiple regression analysis was used to define the age and height dependent limits of normal of SEP at the 97.5th and 2.5th centiles. In five patients with stage 1, seven patients with stage 2, but no patient with stage 0 the individual SEP components were unrecordable. The relative frequencies of abnormally prolonged or non-evokable popliteal N8 latency as well as cortical N33 latency and N33/P40 amplitude increased significantly from stage 0 (3-30%) to stage 1 (22-62%) and stage 2 (46-84%) (p < 0.05 for each component and stage). The numbers and percentages of abnormal recordable spinal N22-30 and supraspinal N30-33 interpeak latencies were two (6.3%) and four (11.8%) in patients with stage 0, but these rates did not increase in subjects with stage 1 or 2. The components of SEP were significantly associated with the indices of peripheral and autonomic function tests. There were no major relations between the latencies of SEP and duration of diabetes or prevailing glycaemic control. These findings suggest that the degree of dysfunction along the somatosensory afferent pathways in insulin dependent diabetic patients depends on the stage of peripheral neuropathy; is not related to the degree of glycaemic control or duration of diabetes; and can be characterized mainly by an alteration of the cortical sensory complex and peripheral transmission delay, while spinal and supraspinal conduction deficits are detected infrequently.

Perception of timing of movement-onset in a simple reaction time task

Subjects judged verbally on temporal order between pressing a switch and a marking sound (MS) in a simple reaction time paradigm. They were uncertain when sound preceded movement by less than about 60 ms or followed it by less than 130 ms (transient zone--TZ). The point of subjective equality (defined by 0.5 probability of correct judgements of temporal order of sound and switching onsets) and the median of TZ were shifted about 60 and 35 ms prior movement onset, respectively. Estimating mutual timing of movement preparation and execution and sensory delays, these shifts correspond to the simultaneity of onsets of MS and proprioceptive feedback in the brain. Thus the results suggest about proprioceptive origin of perception of active movement onset.

Investigation of mode of action of biofeedback in treatment of fecal incontinence

A study was carried out in 25 incontinent patients to evaluate some of the factors thought to be responsible for the success of retraining for fecal incontinence. Subjects were initially allocated to one of two groups; one group was trained to perceive small rectal volumes (active retraining), the other group carried out the same maneuvers but were not given any information or instruction. Active sensory retraining reduced the sensory threshold from 32 +/- 8 to 7 +/- 2 ml (P less than 0.001), corrected any sensory delay that was present (P less than 0.004), and reduced the frequency of incontinence from 5 +/- 1 to 1 +/- 1 episodes per week (P less than 0.01). Sham retraining caused a modest reduction in the sensory threshold (from 29 +/- 9 to 20 +/- 8; P less than 0.05) but did not significantly reduce the frequency of incontinence. Subsequent strength and coordination training did not significantly improve continence, although at the end of the study, 50% of patients had no incontinent episodes at all and 76% of patients had reduced the frequency of incontinence episodes by more than 75%. This improvement in continence was not associated with any change in sphincter pressures or in the continence to rectally infused saline but was associated with significant improvements in rectal sensation. The functional improvement was sustained over a period of two years in 16 of the 22 patients available for follow-up. In conclusion, the results support the use of retraining in the management of fecal incontinence and suggest that retraining may work by enhancing rectal sensitivity and instilling confidence.

Delayed Rectal Sensation With Fecal Incontinence: Successful Treatment Using Anorectal Manometry

Retraining of the external sphincter response to rectal distention and improving the sensory threshold to balloon distention is documented as effective treatment for fecal incontinence in selected patients. Using anorectal manometric techniques, delayed conscious rectal sensation was demonstrated in 28% of 46 consecutive patients referred for fecal incontinence. In patients with delayed recognition of balloon distention, conscious rectal sensation seemed to correlate with a consistent level of internal sphincter relaxation rather than the primary stimulus of balloon distention of the rectum. Anorectal retraining techniques resulted in correction of sensory delay of 2-22 s, elimination of fecal incontinence, and improved sensory threshold in 10 of 13 patients. This previously unreported sensory abnormality represents a treatable manometric abnormality identified by anorectal motility in patients with fecal incontinence.

Laws of the simple visual reaction time.

Fourteen studies from the literature on the reaction time (RT) to a flash of light provided sufficient methodological detail and data to allow for a quantitative analysis of the effects of the following selected variables: luminance, duration, size of stimulus, response to onset versus termination of the signal, and monocular versus binocular viewing. Mathematical relationships were developed which can be used to predict binocular rts over a wide range of luminance, signal duration, and signal size. It was also shown that the product of rt and luminance may be used to represent a response criterion in the sense implied by the theory of signal detection as developed in recent latency models. The results were interpreted as suggesting two general energy processing activities--criterion development and an impulse countdown--going on in parallel which are in series with a sensory delay.

Effect of sensory modality and delay on form recognition.

Effect of sensory modality and delay on form recognition.

Perception speed and behavior: a theoretical note.

In feedback control systems, delay of the feedback information can produce oscillations or other distortions of system output. Previously unrelated work by others, when viewed as aspects of a single functional process, point co the potential effect of temporal factors in sensory processes on aspects of behavior. The three areas of research to be related are as follows: 1. Human behavior is disrupted if conditions external to S produce a delay in sensory feedback. The experimental techniques involved electromechanical delay of visual, auditory or tactile feedback (Chase, Sumon, & Rapin, 1961). The disrupted behaviors grossly simulate stuttering or neuropachological disability. 2. Physiological mechanisms, related to the functioning of the reticular activating system, can vary the latency of afferent transmission. Thus, a mechanism for variable internal sensory delay exists (Magoun, 1958). 3. Psychophysical measurement shows that perception speeds can differ in differenc sensory modalities. These differences reflect stable individual difference and also vary with direction of attention (Angel1 & Pierce, 1892; Stone, 1926). The present authors hypothesize that physiological changes in latency of either afferent transmission or perceptual registration may produce changes in behavior similar to thac induced by externally delayed feedback. Psychophysical measures of relative perception speed reflect the changes in lacency and, thus, these measures of perception speed might be profitably employed in attempts to explain some of the normal individual differences in motor skills and aspects of parkinsonian disability. Normal behavior.-The speed of perception normally differs in differenc sensory modalities. These intermodal differences in perception speed vary among individuals. For individuals showing unusually long perceptual delays in given modalities, one would expect to find corresponding relative slowness or inefficiency of those behaviors which depend on the specific modalities for feedback control. For example, Ss with below average speed in auditory and kinesthetic perception should show slowness in speech; Ss slow in visual and kinesthetic perception should be poor in visual-motor coordination tasks, and Ss slow only in kinesthesis should be slow specifically in making simple arm movements. These deductions, never tested, follow directly from the facts concerning externally delayed feedback and from the data concerning normal individual differences in perception speed.

TABES DORSALIS

We have previously described the significance of the sensory dissociation and delay in pain perception which are associated with the peripheral neuropathy of chronic alcoholism, 1 and of a similar picture produced by temporarily interrupting the blood supply to an extremity. 2 It was observed that modalities which are eventually to be carried in the posterior columns and which are of more recent development in the phylogenetic scale are more likely to be impaired earlier and more severely. Light touch, vibration and position senses suffer most, while pain sense is fairly well preserved or, more commonly, preserved in a dysesthetic hyperpathic fashion. This picture is the result of the blocking of impulses which normally traverse the larger, myelinated nerve fibers, with preservation of the continuity of those impulses which are transmitted by the slower, unmyelinated fibers. A similar sensory dissociation, delay in pain perception and dysesthesia are also noted in