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Attentional blink reflex modulation in a continuous performance task is modality specific.

Four experiments investigated the attentional modulation of acoustic blinks during continuous spatial tracking tasks. Experiment 1 found blink magnitude inhibition in a visual tracking task. Experiment 2 replicated this finding and also found blink latency slowing. Experiment 3 varied the difficulty of the task and found larger blink inhibition in the easy condition. Blink latency slowing did not differ and was significant at both difficulty levels. Experiment 4 employed less difficult visual and acoustic tracking tasks at two levels of task load. Blink magnitude inhibition during the visual and facilitation during the acoustic task was significant during high load in both modality groups. Blink latency was slowed in all visual task conditions and shortened in the difficult acoustic task. These results indicate that attentional blink modulation in a continuous spatial tracking task is modality specific.

Acoustic Stimulation↗

Effects of dopamine D1 ligands on eye blinking in monkeys: efficacy, antagonism, and D1/D2 interactions.

Dopamine D1 ligands have been classified and ordered according to efficacy in both in vitro and in vivo studies. In the present experiments, dopamine D1 ligands reported to differ in in vitro efficacy were evaluated for efficacy-related effects on eye blinking in squirrel monkeys. Additional comparisons were made with the effects of D2 receptor agonists and indirect dopamine agonists. The results show that D1 agonists increased eye blinking in an efficacy-related manner, whereas the D1 receptor blocker SCH 39166 [(-)-trans-6,7,7alpha,8,9,13beta-hexahydro-3-chloro-2-hydroxy-N-methyl-5H-benzo[d]naphtho[2,1-b]azepine] only decreased rates of eye blinking. D1 high-efficacy agonists induced rates of eye blinking that were 2- to 3-fold greater than observed with dopamine D2 agonists and indirect agonists. In drug combination experiments, increases in eye blinking induced by the D1 high-efficacy agonist R-(+)-6-Br-APB [R-(+)-6-bromo-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrobromide] were antagonized by both the D1 antagonist SCH 39166 and the lower efficacy agonist SKF 83959 [6-chloro-7,8-dihydroxy-3-methyl-1-(3-methylphenyl)-2,3,4,5-tetrahydro-1H-3-benzazepine hydrobromide], consistent with dopamine D1 receptor mediation of these behavioral effects. The dopamine D2 agonist (+)-PHNO [(+)-N-propyl-hydroxynaphthoxazine], which selectively activates dopamine D2 receptors, also attenuated D1 agonist-induced increase in eye blinking, suggesting that D2 receptor actions may inhibit D1-mediated increases in eye blinking. Overall, eye blink rate appears to be a robust behavioral measure that can be used to measure changes in dopaminergic D1 signaling and as a functional assay of agonist efficacy at dopamine D1 receptors.

Animals↗

Temporal interactions of air-puff-evoked blinks and saccadic eye movements: insights into motor preparation.

Following the initial, sensory response to stimulus presentation, activity in many saccade-related burst neurons along the oculomotor neuraxis is observed as a gradually increasing low-frequency discharge hypothesized to encode both timing and metrics of the impending eye movement. When the activity reaches an activation threshold level, these cells discharge a high-frequency burst, inhibit the pontine omnipause neurons (OPNs) and trigger a high-velocity eye movement known as saccade. We tested whether early cessation of OPN activity, prior to when it ordinarily pauses, acts to effectively lower the threshold and prematurely trigger a movement of modified metrics and/or dynamics. Relying on the observation that OPN discharge ceases during not only saccades but also blinks, air-puffs were delivered to one eye to evoke blinks as monkeys performed standard oculomotor tasks. We observed a linear relationship between blink and saccade onsets when the blink occurred shortly after the cue to initiate the movement but before the average reaction time. Blinks that preceded and overlapped with the cue increased saccade latency. Blinks evoked during the overlap period of the delayed saccade task, when target location is known but a saccade cannot be initiated for correct performance, failed to trigger saccades prematurely. Furthermore, when saccade and blink execution coincided temporally, the peak velocity of the eye movement was attenuated, and its initial velocity was correlated with its latency. Despite the perturbations, saccade accuracy was maintained across all blink times and task types. Collectively, these results support the notion that temporal features of the low-frequency activity encode aspects of a premotor command and imply that inhibition of OPNs alone is not sufficient to trigger saccades.

Animals↗

Blink reflex R2 recovery curves in patients with facial palsy within ten days after onset.

The purpose of this study was to investigate the acute changes in blink reflex responses in patients with facial palsy. We used the blink reflex R2 recovery curves as an index of the excitability of the blink reflex neural circuit and evaluated the excitability of the blink reflex within 10 days after onset. Twelve patients with peripheral facial palsy were selected on condition that the degree of facial palsy was so mild that R2 responses of the blink reflex were measurable on the affected side, and they were compared with 12 healthy volunteers. Conditioning and test electrical stimuli were delivered on the affected side of the supraorbital nerve. Ipsilateral R2 response (iR2) of the blink reflex in patients was significantly enhanced at interstimulus intervals (ISIs) between conditioning and test stimuli from 100 to 1,000 ms, in comparison with the control subjects. These findings suggested hyperexcitability of the blink reflex neural circuit in patients with facial palsy. In addition to iR2, contralateral R2 response (cR2) in the patients was also significantly increased at ISIs of 100-1,000 ms to the same extent as the enhancement of iR2. All these findings suggested that the hyperexcitable changes developed in a common pathway of iR2 and cR2, but not in the ipsilateral facial motor neurons. It is suggested that the hyperexcitability of the neural circuit of the blink reflex during an acute period of facial palsy is an adaptive response to compensate for impaired facial motor function.

Adult↗

Asymmetry of blinking.

PURPOSE: Too investigate asymmetry in eyelid movements with blinking, the stability of the asymmetry, and its modifiability in normal humans. METHODS: Differences in the start time and amplitude between the two eyelids were assessed for voluntary blinks and reflex blinks evoked by supraorbital trigeminal nerve stimulation. These variables were also measured before and up to 18 months after 2 hours of unilateral upper lid restraint. RESULTS: With voluntary blinks, one eyelid consistently began to close earlier and made a larger eyelid movement than the other eyelid. Stimulation of the supraorbital branch of the trigeminal nerve evoked relatively larger amplitude blinks in one eyelid that correlated with the asymmetries of voluntary blinks. There was a continuum of eyelid asymmetry across all subjects that was stable and independent of other biological asymmetries, such as handedness. Briefly reducing eyelid mobility created a long-lasting change in eyelid asymmetry with blinking. CONCLUSIONS: Eyelid asymmetry results from differences in the excitability of motoneurons in the left and right facial motor nuclei and does not appear to involve asymmetries in cortical inputs to the brain stem. Because adaptive processes modify the motoneuron excitability that creates eyelid asymmetry, these processes may underlie changes in blinking associated with facial palsy and may play a role in the development of disorders that affect one side of the face, such as hemifacial spasm.

Adult↗

Blink recovery in patients with Bell's palsy: a neurophysiological and behavioral longitudinal study.

PURPOSE: To examine the recovery process of blinking in a longitudinal study of nine patients severely affected by Bell's palsy. METHODS: Kinematics of bilateral eyelid and eye movements and concomitant orbicularis oculi activity during voluntary blinking and air-puff- and acoustic-click-induced reflex blinking were determined by using the magnetic search coil technique and electromyographic recording of the orbicularis oculi muscle (OO-EMG). RESULTS: In the first 3 months of absence of OO-EMG activity, reduced eyelid and eye movement of the palsied eyelid were observed during all types of blinking. First OO-EMG activity was determined 3 months after onset of the affliction. After 1 year, OO-EMG activity was normalized and showed values similar to those on the nonpalsied side. Clinically, eyelid movements were normal after 1 year, although corresponding maximum amplitudes and corresponding velocities were two times smaller, expressed in reduced eyelid motility. Directions of eye movement during reflex blinking were normal after 1 year, although maximum amplitudes were smaller on the palsied side. Eye movements during voluntary blinking remained impaired. A simultaneous horizontal upward shift of both eyes in the same direction was recorded throughout the study. CONCLUSIONS: Although OO-EMG activity on the palsied side was normalized 1 year after onset of the affliction, the accompanying eyelid movements and their maximum amplitudes and velocities remained smaller throughout the study. The consistent impairment of eye movements in voluntary blinking during the study and reduced motility of eyelid movements indicates that higher brain structures, which modify eyelid and eye movement control during blinking, may be altered by the affliction.

Adult↗

Blink reflex recovery in facial weakness: an electrophysiologic study of adaptive changes.

OBJECTIVE: To study the electrophysiologic effects of unilateral facial weakness on the excitability of the neuronal circuitry underlying blink reflex, and to localize the site of changes in blink reflex excitability that occur after facial weakness. BACKGROUND: Eyelid kinematic studies suggest that adaptive modification of the blink reflex occurs after facial weakness. Such adaptations generally optimize eye closure. A report of blepharospasm following Bell's palsy suggests that dysfunctional adaptive changes can also occur. METHODS: Blink reflex recovery was evaluated with paired stimulation of the supraorbital nerve at different interstimulus intervals. Comparisons were made between normal control subjects and patients with Bell's palsy who either recovered facial strength or who had persistent weakness. RESULTS: Blink reflex recovery was enhanced in patients with residual weakness but not in patients who recovered facial strength. Facial muscles on weak and unaffected sides showed enhancement. In patients with residual weakness, earlier blink reflex recovery occurred when stimulating the supraorbital nerve on the weak side. Sensory thresholds were symmetric. CONCLUSION: Enhancement of blink reflex recovery is dependent on ongoing facial weakness. Faster recovery when stimulating the supraorbital nerve on the paretic side suggests that sensitization may be lateralized, and suggests a role for abnormal afferent input in maintaining sensitization. Interneurons in the blink reflex pathway are the best candidates for the locus of this plasticity.

Adaptation, Physiological↗

Blink activity and task difficulty.

This study investigated the relationship between task difficulty and blink activity, which includes blink rate, blink amplitude, and blink duration. Two kinds of tasks established two levels of difficulty. In Exp. 1, a mental arithmetic task was used to examine the relationship. Analysis showed that blink rate for a difficult task was significantly higher than that for an easier one. In Exp. 2, a letter-search task (hiragana Japanese alphabet) was used while the other conditions were the same as those in Exp. 1; however, the results of this experiment were not influenced by the difficulty of the task. As results indicate that blink rate is related to not only difficulty but also the nature of the task, the nature of the task is probably dependent on a mechanism in information processing. The results for blink amplitude and blink duration showed no systematic change during either experiment.

Adult↗

The significance of eye blink rate in parkinsonism: a hypothesis.

Alterations in blink rate have been reported in several neuropsychiatric disorders presumed to result from abnormal central dopaminergic functions. Increased blink rate in schizophrenia, Tardive dyskinesia, Tourette's syndrome and Meige's disease are associated with enhanced dopaminergic functions. Parkinson's disease is associated with reduced dopaminergic functions and decreased blink rate. Thus, blink rate may reflect striatal and mesolimbic dopaminergic activity. Since acute light exposure suppresses melatonin production and darkness stimulates melatonin secretion, blinking may serve to regulate light-dark exposure to the pineal gland and thus to 'fine tune' melatonin production. As there is evidence to suggest that melatonin inhibits the release of dopamine in the striatum and limbic system, increased blink rate may serve to reduce light exposure, increase melatonin secretion and attenuate dopaminergic functions. Conversely, decreased blinking (as is observed in patients with Parkinson's disease) could reflect a compensatory mechanism to increase light exposure, reduce melatonin production and ultimately increase dopamine functions. This model is novel in that for the first time it suggests a functional link among blink rate, melatonin secretion and striatal dopaminergic functions in movement disorders.

Blinking↗

Lacrimal drainage capacity, age and blink rate.

PURPOSE: The aim of this study was to investigate the influence of blink rate on lacrimal drainage capacity in different age groups. METHODS: The drop test for lacrimal drainage capacity was recently described by us. In the drop test, drops of 10 &mgr;l, 15 &mgr;l or 20 &mgr;l of lukewarm saline are repeatedly instilled in the tear film during three minutes. Excessive saline solution is then removed and the volume drained by the lacrimal passages is calculated. The drop test was performed in 40 individuals of two age groups, 10-30 years and 60-80 years. The drop test results were recorded when the subjects tried to blink at frequencies of 90 and 180 blinks/three minutes. RESULTS: The drop test results were significantly higher in the young than in the old subjects. At the lower blink rate, the lacrimal drainage capacity was 363 &mgr;l/3 min. in the young and 155 &mgr;l/3 min. in the old subjects. At the higher blink rate, the lacrimal drainage capacity was 520 and 200 &mgr;l/3 min., respectively. The increases in lacrimal drainage capacity with increasing blink rate were significant in both age groups. CONCLUSION: The lacrimal drainage capacity increased with increasing blink rate in both younger and older subjects. The lacrimal drainage capacity was significantly lower in the old age group at each blink frequency, indicating that other factors than blink rate are responsible for the lower lacrimal drainage capacity in older age.

Journal Article↗

Long-term trends in human eye blink rate.

Long-term recordings of normal human eye blink behavior (up to 14 h continuously) showed a number of periodic trends in blink rate. Mean rates varied from 2 to 50 blinks/min and periods ranged from 10 min to 2.5 h. Three dominant groupings of mean rates were observed (1) under 6, (2) 8--15 and (3) 20--30 blinks/min; these groups appear to be related to more or less distinct behavioral states of the individual. Blink amplitudes also varied and amplitude and rate showed correlations of possible functional significance. Vision-related behaviors affect both the mean rate of blinking and blink amplitude, and may impose a characteristic strategy on the timing of the individual blinks as well. The latter is referred to as bimodal blinking; this strategy contrasts with the random occurrence of blinks seen normally.

Adult↗

Functional MRI of brain activation by eye blinking.

Functional magnetic resonance imaging (fMRI) was used to map cortical areas that control eye blinking. T2*-weighted asymmetric spin-echo MRI (or BOLD-blood oxygen level dependent-MRI) was used to detect changes caused by focal variations in blood oxygenation. Six normal volunteers and two cases of dry eye (less than 5-mm Schirmer's test) entered the study. The experimental scheme consisted of three cycles of a two-step sequence: (eyes closed)-(blink or blink inhibition). And to minimize contamination from photic activation, the experiments were carried out in a dark environment and the volunteers reported no light perception during the MR scans. In all eight cases, normal blinking (about one blink every 4 sec) activated areas in the orbitofrontal cortex and in some cases, the visual cortex including the anterior portion of the visual cortex and the primary visual cortex. In severe dry eye, blink-inhibition strongly activated the visual cortex even after irritation due to corneal desiccation was removed by topical anesthesia. The blinking process, especially the rate, appears to be controlled in the orbitofrontal cortex. The significance of visual cortex activation in the dark and in the case of severe dry eye still remains unclear; although it may be associated with attention and arousal.

Adult↗

Midbrain 6-hydroxydopamine lesions modulate blink reflex excitability.

The blink reflex abnormalities present in the 6 hydroxydopamine (6-OHDA) lesioned rat model of parkinsonism mimicked those of the human with Parkinson's disease. In alert rats, we monitored the long and short latency components of the orbicularis oculi electromyographic (OOemg) response evoked by electrical stimulation of the supraorbital branch of the trigeminal nerve (SO). Two paradigms, habituation and double pulse, provided a measure of blink reflex excitability. In normal rats, repeated stimulation of the SO produced habituation of the R2 component of the blink. In the double pulse paradigm, presentation of two identical SO stimuli resulted in a reduced or suppressed OOemg response to the second stimulus relative to the first. In rats with complete, unilateral lesions of midbrain dopamine neurons, repeated SO stimulation produced facilitation rather than habituation of the R2 component of the blink reflex. This facilitation occurred only with the eyelid contralateral to the lesion. In the double pulse paradigm, the lesioned rats showed increased excitability rather than suppression. This effect occurred bilaterally, although the increased excitability was strongest contralateral to the lesion. Rats with partial lesions of midbrain dopamine neurons exhibited qualitatively similar, but less pronounced blink reflex abnormalities. The R1 component of the blink reflex was unaffected by either the complete or partial lesions. Thus, modification of the blink reflex by 6-OHDA lesions provides a reproducible parkinsonian-like symptom which is amenable to investigations of increases in reflex excitability.

Amphetamine↗

Marked reduction and distinct patterns of eye blinking in patients with moderately dry eyes during video display terminal use.

PURPOSE: To analyze the spontaneous eye-blink rate (SEBR) and blinking pattern in patients with moderately dry eyes during video display terminal (VDT) use. METHODS: The SEBR of 30 patients with dry eye syndrome (median age 44.8 years, range 18 - 67 years) was measured using a computer-based video analysis system. Only complete eye blinks were recorded during 10 min of conversation, during initial VDT use and again after a preceding work period of 30 min. RESULTS: In comparison with SEBR during conversation (mean value 16.8 blinks/min, standard deviation 16.8 blinks/min) the SEBR significantly decreased during initial VDT use (6.6+/-4.8; P<0.001) and remained significantly decreased during re-measurement after 30 min (5.9+/-4.6; P<0.001). SEBR was not significantly different between initial VDT use and re-measurement after 30 min ( P=0.65). The SEBR was characterized by marked interindividual variability during conversation and VDT use. No significant correlation was found between SEBR (either during conversation or during VDT use), and the quality (tear break-up time) or quantity (Schirmer I test, Jones test) of the tear film. Typical blinking patterns were found to be (1). a relatively time-independent, irregular pattern, (2). an initial phase of 2-4 min with shorter inter-eye-blink intervals, and (3). alternating periods of higher and lower inter-eye-blink intervals. CONCLUSIONS: Reduction of the SEBR during VDT use is primarily determined by marked visual attention, resulting in an exacerbation of dry eye symptoms in predisposed humans. High interindividual variability and distinct patterns of eye blinking may be key factors in further clarification of VDT-eye interactions and develop individually designed solutions to prevent desiccation during VDT use.

Adolescent↗

Changes in eye blink frequency as a measure of trigeminal stimulation by exposure to limonene oxidation products, isoprene oxidation products and nitrate radicals.

OBJECTIVES: To measure eye blink frequency as a measure of trigeminal stimulation of the eye. Human subjects were exposed to oxidation mixtures representative of reactive indoor pollutants and clean air, from which relative changes in blink frequencies were measured. METHOD: Male subjects ( n=8) were exposed for 20 min to limonene oxidation products (LOPs), isoprene oxidation products (IOPs), nitrate radicals (NO(3)), their residual reactants, and clean air at 20% relative humidity. A baseline blink frequency was measured prior to and following each exposure (2 x 8 min). The subjects were exposed locally in the non-dominant eye and single blind in random order. Blinking was video-recorded and evaluated for full sessions of 36 min while the subjects viewed an educational film. The initial terpene concentrations were one to two orders of magnitude higher than mean indoor concentrations. RESULTS: The mean blink frequency increased significantly during subjects' exposure to gas-phase oxidation products at lower part-per-billion (ppb) levels of LOPs, 42% ( P<0.0001) and NO(3), 21% ( P<0.022), compared with that at baseline. Neither the residual reactants nor clean air changed the blink frequency significantly. The findings coincided with qualitative reporting of weak eye irritation symptoms. CONCLUSIONS: Changes in blink frequency appear to be a promising measure of trigeminal stimulation from exposure to eye irritants in ppb levels. Gaseous products of limonene and ozone, and reactive radicals may cause eye irritation indoors.

Adult↗

Blink rate, neurocognitive impairments, and symptoms in schizophrenia.

This study addresses the relationship between blink rate (as a measure of central dopaminergic activity), symptoms, neuropsychological performance, as well as neurological signs in schizophrenia. Blink rate between schizophrenic patients and a matched control group was compared in both "relaxed" and "attentive" conditions. Blink rate was increased in schizophrenic patients in the "relaxed" condition but not in the "attentive" condition. The relationship between blink rate and clinical variables was examined in a larger sample of 204 patients. In both "relaxed" and "attentive" conditions, blink rate was related to "hallucinations," "anxiety," negative symptoms, and neuroleptic dosage. Attention was a significant predictor only in the "relaxed" condition. No other significant correlation was found between blink rate, neuropsychological impairments, and neurological signs. These findings suggest that blink rate is not related to neurocognitive impairments in schizophrenia.

Adolescent↗

The instruction to refrain from blinking affects auditory P3 and N1 amplitudes.

Often subjects have been instructed to refrain from blinking lest their evoked EEG potentials should be distorted. We studied whether these very instructions have any impact on P3 amplitude. Two tones were presented in random order, and subjects had to count the high-pitched tones. Half the subjects were instructed not to blink, whereas this instruction was omitted for the other subjects. Target tones evoked larger P3s than non-targets in the latter group but not in the former, in particular not in those subjects that actually blinked rarely. The groups also differed in their N1 amplitudes. These findings might be relevant to P3 studies working with patients and controls: the harder some frequently blinking subjects try to refrain from blinking, the smaller might become their P3 amplitudes. Omitting the instruction and using off-line blink subtraction procedures seems a viable alternative. This study was actually motivated by discrepant findings on the effects of the preceding tone sequence on P3. These discrepancies could be largely resolved by the instructional variable, in conjunction with different tone intensities. It is suggested that subjects who are discouraged from blinking try to protect themselves against the arousing effects of stimuli.

Adult↗

Eye movements and blinks: their relationship to higher cognitive processes.

Information about the timing of spontaneous eye blinks was abstracted while subjects performed a detection and identification task. We found blinks to be time-locked to saccadic eye movements involved in the identification of peripherally presented stimuli. The larger the required eye movement, the greater the likelihood of blink occurrence. Blink latencies were found to be significantly shorter for centrally, as compared to peripherally presented stimuli, and blinks were more likely to be associated with eye movement returning gaze to a central location than with movements associated with the identification of peripherally presented information. Thus, we conclude that the spontaneous or endogenous eye blink is triggered by aspects of information processing, and that blink latencies can be used as one tool for evaluating the level of complexity of such processing under a wide variety of task demands.

Blinking↗