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At least 19 recordsLinked to original sources
PubMed1997

To blink or not to blink: inhibition and facilitation of reflex blinks.

A reflex blink typically inhibits subsequent blinks. In this study, we investigated whether the nature and time course of this inhibition vary when different combinations of blink-evoking stimuli are used. We used the paired stimulus paradigm, in which two blink-evoking stimuli-a conditioning stimulus followed by a test stimulus-are presented with a variety of interstimulus intervals, to examine the interactions between blinks evoked by trigeminal and acoustic stimuli in rats and humans. In addition, we studied the effect of a blink-evoking trigeminal stimulus on subsequent gaze-evoked blinks in humans. The results revealed that long-lasting inhibition occurred when the conditioning and test stimuli were within the same modality. A shorter period of inhibition followed by facilitation occurred when the stimuli were in different modalities. The data demonstrate that a blink-evoking stimulus initiates a lengthy period of inhibition in its own sensory pathway and a shorter period of inhibition in the reticular formation and/or in blink motoneurons. In addition, the results show that the blink-evoking stimulus also initiates a facilitatory process. Thus, the magnitude of a blink reflects a balance between inhibitory and facilitatory processes.

Acoustic Stimulation↗
PubMed1998

The effects of prepulse-blink reflex trial repetition and prepulse change on blink reflex modification at short and long lead intervals.

Prepulse inhibition and facilitation of the blink reflex are said to reflect different responses elicited by the lead stimulus, transient detection and orienting response respectively. Two experiments investigated the effects of trial repetition and lead stimulus change on blink modification. It was hypothesized that these manipulations will affect orienting and thus blink facilitation to a greater extent than they will affect transient detection and thus blink inhibition. In Experiment 1 (N = 64), subjects were trained with a sequence of 12 lead stimulus and 12 blink stimulus alone presentations, and 24 lead stimulus-blink stimulus pairings. Lead interval was 120 ms for 12 of the trials and 2000 ms for the other 12. For half the subjects this sequence was followed by a change in pitch of the lead stimulus. In Experiment 2 (N = 64), subjects were trained with a sequence of 36 blink alone stimuli and 36 lead stimulus-blink stimulus pairings. The lead interval was 120 ms for half the subjects and 2000 ms for the other half. The pitch of the lead stimulus on prestimulus trials 31-33 was changed for half the subjects in each group. In both experiments, the amount of blink inhibition decreased during training whereas the amount of blink facilitation remained unchanged. Lead stimulus change had no effect on blink modification in either experiment although it resulted in enhanced skin conductance responses and greater heart rate deceleration in Experiment 2. The present results are not consistent with the notion that blink facilitation is linked to orienting whereas blink inhibition reflects a transient detection mechanism.

Acoustic Stimulation↗
PubMed1994

The effect of repeated prepulse-blink reflex trials on blink reflex modulation at short lead intervals.

The amplitude of a blink reflex is inhibited if the reflex eliciting stimulus is preceded by a short prestimulus (e.g. < 250 ms). If the prestimulus duration is longer than 1 s, blink reflex amplitude is facilitated. The present study investigated the effect of repeated presentations of prestimulus-blink eliciting stimulus pairings on blink reflex modulation. Subjects in Experiment 1 (N = 59) were presented with a sequence of 12 blocks of 7 trials. Within each block, one trial was a blink stimulus alone, whereas the blink stimulus was preceded by a prestimulus on the other trials. Prestimulus intervals were 30, 60, 120, 240, 500 and 2000 ms. Prestimuli were presented continuously throughout the prepulse interval. The amount of reflex magnitude inhibition at the 60, 120, 240 and 500 ms lead intervals and reflex latency shortening at 30 and 60 ms decreased over blocks. The amount of reflex facilitation at a lead interval of 2000 ms was not reduced. In Experiment 2 (N = 22), two groups of subjects were presented with a sequence of blink stimulus alone presentations and prestimulus-blink stimulus pairings. The prestimulus lasted for 120 ms in one group and for 200 ms in the second. Blink reflex magnitude inhibition declined in both groups over blocks of trials. However, the groups also differed in responding on the blink stimulus alone control trials. Experiment 3 (N = 24) employed the same design as did Experiment 2. No difference in control responding was found. Similar to Experiment 2, blink inhibition decreased over repeated trials in both groups. The present results indicate that prepulse inhibition reflects a process which is affected by repeated presentation of prestimulus-reflex stimulus pairings. However, the conclusion that the reduction of prestimulus effects reflects habituation seems to be premature.

Adolescent↗
PubMed1995

[Study on human eye movements induced by blinks--report 1. Three kinds of blinking].

The eye movement associated with blinking was studied with a magnetic search coil method. Lid movements and eye movements associated with spontaneous blinks, voluntary blinks, and reflex blinks induced by puffs of air or flashes of light were analysed. Eye movements associated with spontaneous blinks and voluntary blinks had initial downward and adducted movements followed by upward and abducted movements of the eyeball. Reflex blinks initially showed the same downward and adducted movements, but upward and abducted movements were not constantly obtained in given subjects. The velocity-amplitude ratio was equal among the three kinds of blinks in both horizontal and vertical movements. The velocity-amplitude ratio of the eye movements associated with blinks and visually-guided saccadic eye movements was compared. The horizontal and vertical eye movements associated with blinks were slower than those of saccadic eye movements in the same subject. Therefore, the eye movements associated with the blinks may have a different neural mechanism in the brain from that of the saccadic eye movement system.

Adult↗
PubMed1979

Ontogeny of spontaneous blinking and of habituation of the blink reflex.

Habituation of the blink reflex to glabellar percussion was examined in 164 infants and children from ages 2 days to 18 years and in 18 adults aged 18 to 50 years. Spontaneous blink rates were measured in 269 children and 179 adults. The mean number of glabellar taps required for habituation of the blink reflex increased from 2.7 (SD 1.2) at 0 to 2 months of age to a peak of 13.3 (SD 5.6) at age 3 to 4, remained at more than 10 until age 6, after which a rapid decline occurred, reaching the adult level of 2 to 5 blinks to habituation at age 12 years. The mean rate of spontaneous blinking was less than 2 per minute in early infancy and increased steadily during childhood up to age 14 or 15. The inverse relationship of spontaneous blink rate and number of blink reflexes to habituation in early childhood and in disorders of dopamine transmission suggests that spontaneous blink rate and habituation of the blink reflex reflect maturation and integrity of dopaminergic circuits in the brain.

Adolescent↗
PubMed2006

Further analysis of the human spontaneous eye blink rate by a cluster analysis-based approach to categorize individuals with 'normal' versus 'frequent' eye blink activity.

PURPOSE: To further analyze the possible causes of variability in spontaneous eye blink activity in apparently healthy humans. METHODS: One hundred men, aged between 23 and 57 years and with no significant eye disease, were questioned on the number of ocular symptoms they experienced (one, two, three, and so forth). Five-minute video recordings were made of the eyes in primary gaze and in silence between 11:00 and 17:00 hours. The spontaneous eye blink rate (SEBR) and palpebral aperture features were assessed from the video recordings. The central corneal threshold touch sensitivity was then assessed with a Cochet-Bonnet aesthesiometer. RESULTS: The average SEBR was 13.8 +/- 9.7 blinks per minute (range, 2.8-48 blinks per minute), but the distribution was heterogeneous and skewed to higher values. The SEBR was not obviously dependent on the time of day that the recordings were made, on the number of mild symptoms that the subjects reported, or on the central corneal sensitivity (P> or =0.6). Analysis of SEBR in relation to age showed a possible weak association (P=0.082, r = 0.175), but SEBR showed absolutely no correlation with palpebral aperture height (P=0.546). A hierarchic cluster analysis clearly resolved the distribution of SEBR values into two distinct groups (P<0.001, F ratio = 222). CONCLUSIONS: Spontaneous eye blink activity can be rather different between healthy individuals, even under a single experimental condition. These differences do not appear to be caused by the time of day, mild symptoms, corneal sensitivity, age, or palpebral aperture features. In line with previous metaanalyses, it is therefore proposed that individuals could be grouped as to whether they have "normal" eye blink activity or be classified as having "frequent" eye blink activity. The latter group would include those who had an SEBR greater than 20 blinks per minute when assessed in primary eye gaze and in silence.

Adult↗
PubMed1995

[A characteristic blink response observed in a patient with Lance-Adams syndrome--somatosensory-evoked blink response].

We report a patient with Lance-Adams syndrome, in whom a characteristic blinking response was observed. In this patient, the reflex blinking was elicited by electrical stimulations applied not only to the supraorbital nerve but also to peripheral nerves of both upper and lower extremities. The EMG discharges responsible for the blinking response were found to consist of some components. The pathophysiological mechanism underlying the characteristic blinking response was discussed. It is speculated that increased excitabilities of the brainstem reticular formation may play a role in generating this type of blinking response, namely the somatosensory-evoked blink response.

Adult↗
PubMed2005

[Blinking activity during visual display terminal work. 2: reduced blinking and therapeutic approaches].

New findings based on a noninvasive, automated long-term measurement method revealed interindividual differences in lid movement behavior, existence of blinking patterns, and the dominance of cognitive influence in the regulation of blinking frequency during increased concentration and especially visual attention. The development of an individual blinking animation promises long-lasting increase and harmonization of lid movements during visual display work. Maintenance of the integrity of the ocular surface by preventing surface evaporation and providing sufficient precorneal environment eradicates important pathogenic factors of ocular discomfort. An animation program for stimulation of blinking has been developed. First results showed that an increase in blinking rate initiated by the computer itself is feasible in principle during work at a visual display terminal. Further improvement of this new approach is promising.

Blinking↗
PubMed1990

Electrically and mechanically elicited blink reflexes in infants and children--maturation and recovery curves of blink reflex.

We studied the electrically and mechanically elicited blink reflexes in 2 groups of subjects, i.e., 237 newborn infants, 25-41 weeks of conceptional age, and 74 children, 1 month-12 years of age. In infants after 25 weeks of conceptional age we could usually induce the early response (R1) and ipsilateral late response (R2), while the contralateral late response (R2') of the electrical blink reflex became apparent after 33 weeks of conceptional age and the frequency of the appearance of R2' reached more than 60% after 38 weeks of conceptional age. After 7 months of age, R2' was usually observed. The R1 latency in full-term newborns was close to adult values, while the R2 and R2' latencies reached adult values at 7-12 years. After 1 year of age the latency of the R2 mechanical blink reflex had a tendency to be shorter than that of the electrical blink reflex. Under 35 weeks of conceptional age, the recovery curves of the blink reflex were considerably different from those of full-term infants, and premature infants showed little or no evidence of inhibition. These results indicate the absence of inhibitory interneurones in premature infants.

Blinking↗
PubMed1995

Electrically induced blink reflex and clinical blinking ability in patients with amyotrophic lateral sclerosis.

A study of the electrically induced blink reflex was performed on 17 patients with amyotrophic lateral sclerosis (ALS), graded according to the voluntary and reflexive blinking ability. In the early stage, delay of bilateral R2 latencies, decrease of bilateral R2 amplitudes and disappearance of the contralateral R2 component occurred. Then, the ipsilateral R2 component vanished when the voluntary blinking was incomplete. In cases with the remaining R2 component, the recovery curves of R2 amplitude revealed the weakened influence of the central nervous system to the interneurons that constructed the R2 component. In highly impaired patients who had lost the reflexive blinking ability, the R1 component had disappeared. Electrically induced blink reflex is useful in assessing the degree of disability in the upper facial muscles.

Adult↗
PubMed1985

Blink reflex in patients with hemispheric cerebrovascular accident (CVA). Blink reflex in CVA.

A blink reflex consists of an early unilateral component, R1, and a late bilateral component, R2. During an acute phase of hemispheric cerebrovascular accident, R1 and R2 were abnormal in 30 and 50 of 66 patients, respectively. Paired stimuli usually corrected R1 but not R2, which was profoundly suppressed. The discrepancy between polysynaptic R2 and oligosynaptic R1 indicates a greater disfacilitation at the level of interneurons than at the motoneuron, which serves as the final common path. Abnormality of R2 occurred bilaterally with stimulation on the affected side of face and contralaterally after stimulation on the normal side in 31 patients. This finding suggests a diffuse loss of internuncial excitability, contralateral to the hemispheric lesion. Changes of R2 implicated the brainstem pathways forming the afferent and efferent arc of the reflex in 7 and 8 patients, respectively. The remaining 4 comatose patients had no R2 irrespective of stimulus sites. Clinical localization of the hemispheric lesion showed no consistent correlation with the type of blink reflex abnormalities. The CT scans revealed widely scattered changes in 29 patients with abnormal blink reflex but with a tendency to overlap in the inferior Rolandic area. This contrasted with conspicuous sparing of the inferior post-central region in 10 patients with normal blink reflex. These findings suggest the presence of crossed facilitation to this reflex from wide areas of the cortex but most prominently from the sensory representation of the face.

Acute Disease↗
PubMed2004

Blink and shrink: the effect of the attentional blink on spatial processing.

The detection or discrimination of the second of 2 targets in a rapid serial visual presentation (RSVP) task is often temporarily impaired-a phenomenon termed the attentional blink. This study demonstrated that the attentional blink also affects localization performance. Spatial cues pointed out the possible target positions in a subsequent visual search display. When cues were presented inside an attentional blink (as induced by an RSVP task), the observers' capacity to use them was reduced. This effect was not due to attention being highly focused, to general task switching costs, or to complete unawareness of the cues. Instead, the blink induced a systematic localization bias toward the fovea, reflecting what appears to be spatial compression.

Adolescent↗
PubMed2004

Blink rate does matter: a study of blink rate, sustained attention, and neurological signs in schizophrenia.

This study aimed to explore the relationships among cognitive functions, neurological soft signs, and clinical symptoms in a group of patients with chronic schizophrenia. A total of 90 patients were recruited. Blink rate was recorded when patients were in a resting and relaxed condition. Significant correlations were found only between blink rate and general psychopathology (p < .01) and disinhibition soft signs (p < .05). When the group was further divided into two subgroups by taking the lower and upper quartiles of their blink rate, patients at the upper quartiles exhibited significantly more disinhibition signs than those at the lower quartiles. There was also a trend for those patients at the upper quartiles to commit more error in a sustained attention task. These findings suggest that blink rate is associated with disinhibition signs in the present sample.

Adult↗
PubMed1981

Light-stimulus-evoked blink reflex: methods, normal values, relation to other blink reflexes, and observations in multiple sclerosis.

The blink reflex may be evoked by auditory click or light stimulation, the latter being constantly present in all healthy subjects. The latency and amplitude of the light-stimulus-evoked blink response (L-BR) is influenced by the light intensity, distance between the light stimulus and the eye, attention, and background facilitation. The L-BR was abnormal in 75% of definite and 61% of probable multiple sclerosis (MS) patients. When abnormal, the L-BR was more commonly absent than delayed. Optic nerve lesions could be identified by the pattern of abnormalities in the L-BR in some patients. The L-BR has proved to be a sensitive detector of abnormalities in the visual connections and, in combination with the Vth nerve stimulation-evoked blink response, a valuable detector of brainstem lesions.

Adult↗
PubMed2002

Made you blink! Contingent attentional capture produces a spatial blink.

Previous studies have shown that the capture of attention by an irrelevant stimulus can be eliminated by fore knowledge of the spatial location of the relevant target stimulus. To explore whether spatial certainty is sufficient to eliminate capture, four experiments are reported in which the spatial location of the target is certain but the temporal position is uncertain. Subjects viewed a central rapid serial visual presentation stream in which a target letter was defined by a particular color (e.g., red). On critical trials, irrelevant color singletons appeared in the periphery. In Experiments 1 and 2, peripheral singletons produced a decrement in central target identification that was contingent on the match between the singleton color and the target color. Experiments 3 and 4 provided evidence that this decrement reflected a shift of spatial attention to the location of the distractor. The results suggest that spatial certainty is not sufficient to eliminate attentional capture and that attentional capture can result in a spatial "blink" that is conditional on top-down attentional control settings.

Attention↗
PubMed2005

How the brain blinks: towards a neurocognitive model of the attentional blink.

When people monitor a visual stream of rapidly presented stimuli for two targets (T1 and T2), they often miss T2 if it falls into a time window of about half a second after T1 onset-the attentional blink (AB). We provide an overview of recent neuroscientific studies devoted to analyze the neural processes underlying the AB and their temporal dynamics. The available evidence points to an attentional network involving temporal, right-parietal and frontal cortex, and suggests that the components of this neural network interact by means of synchronization and stimulus-induced desynchronization in the beta frequency range. We set up a neurocognitive scenario describing how the AB might emerge and why it depends on the presence of masks and the other event(s) the targets are embedded in. The scenario supports the idea that the AB arises from "biased competition", with the top-down bias being generated by parietal-frontal interactions and the competition taking place between stimulus codes in temporal cortex.

Attention↗