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PubMed1998

Properties of horizontal saccades accompanied by blinks.

Using the magnetic search coil technique to record eye and lid movements, we investigated the effect of voluntary blinks on horizontal saccades in five normal human subjects. The main goal of the study was to determine whether changes in the dynamics of saccades with blinks could be accounted for by a superposition of the eye movements induced by blinks as subjects fixated a stationary target and saccadic movements made without a blink. First, subjects made voluntary blinks as they fixed on stationary targets located straight ahead or 20 degrees to the right or left. They then made saccades between two continuously visible targets 20 or 40 degrees apart, while either attempting not to blink, or voluntarily blinking, with each saccade. During fixation of a target located straight ahead, blinks induced brief downward and nasalward deflections of eye position. When subjects looked at targets located at right or left 20 degrees, similar initial movements were made by four of the subjects, but the amplitude of the adducted eye was reduced by 65% and was followed by a larger temporalward movement. Blinks caused substantial changes in the dynamic properties of saccades. For 20 degrees saccades made with blinks, peak velocity and peak acceleration were decreased by approximately 20% in all subjects compared with saccades made without blinks. Blinks caused the duration of 20 degrees saccades to increase, on average, by 36%. On the other hand, blinks had only small effects on the gain of saccades. Blinks had little influence on the relative velocities of centrifugal versus centripetal saccades, and abducting versus adducting saccades. Three of five subjects showed a significantly increased incidence of dynamic overshoot in saccades accompanied by blinks, especially for 20 degrees movements. Taken with other evidence, this finding suggests that saccadic omnipause neurons are inhibited by blinks, which have longer duration than the saccades that company them. In conclusion, the changes in dynamic properties of saccades brought about by blinks cannot be accounted for simply by a summation of gaze perturbations produced by blinks during fixation and saccadic eye movements made without blinks. Our findings, especially the appearance of dynamic overshoots, suggest that blinks affect the central programming of saccades. These effects of blinks need to be taken into account during studies of the dynamic properties of saccades.

Acceleration↗
PubMed2001

Aging of the trigeminal blink system.

This study characterizes trigeminal blinks in normal human subjects between 20 and 80 years of age, 60-year-old Parkinson's disease patients, and young and old guinea pigs. In normal humans over 60 years of age, lid-closing duration, and the excitability and latency of the trigeminal reflex blink increase significantly relative to younger subjects. Aged guinea pigs appear to display similar increases in reflex blink duration and latency. Reflex blink amplitude, however, does not change consistently with age. For subjects less than 70 years of age, a unilateral trigeminal stimulus evokes a 37% larger blink in the eyelid ipsilateral to the stimulus than in the contralateral eyelid, but 70-year-olds exhibit blinks of equal amplitude. In all cases, blink duration is identical for the two eyelids. If normal, age-related loss of dopamine neurons explains these trigeminal blink modifications, then Parkinson's disease should exaggerate age-related changes in these blink parameters. Preliminary data show that Parkinson's disease increases blink duration and excitability relative to age-matched control subjects. Thus, it seems likely that normal, age-related loss of dopamine neurons accounts for increases in trigeminal blink excitability and duration. A previously uncharacterized type of trigeminally evoked blink appears after age 40 in humans and in aged guinea pigs. In subjects less than 40 years old, a single trigeminal stimulus elicits a single reflex blink. In subjects over age 40, however, a single stimulus frequently evokes a reflex blink and additional blinks that occur at a fixed interval relative to the preceding blink. These "blink oscillations" may arise from oscillatory processes within trigeminal reflex blink circuits. The presence of exaggerated blink oscillations in subjects with dry eye and benign essential blepharospasm suggests that an alteration of blink oscillation mechanisms plays a critical role in these disorders.

Adult↗
PubMed1999

Evaluation of three types of blinks with the use of electro-oculogram and electromyogram.

Three kinds of blinks, spontaneous, reflex, and voluntary, were measured for 11 men using electromyogram (EMG) at the orbicularis oculi muscle on the right side and electro-oculogram (EOG) in the vertical direction to the right eyelid. The amplitude and the duration time were defined here from the raw waves of the EMG and the EOG for the three kinds of blinks. The amplitude of the EMG indicated that the mean value for the spontaneous blinks was significantly smaller than that of the voluntary blinks and the mean duration of the EMG shows the value for the spontaneous blinks was smaller than that for the reflex and the voluntary blinks. The EMG for the spontaneous blinks had a smaller amplitude and a shorter duration time than the other blinks. The EOG amplitude indicated that the mean value for the spontaneous blinks was significantly smaller than that for the voluntary blinks, but there was no significant difference between the spontaneous blinks and the other blinks for the duration of the EOG. The amplitude and the duration for both the EMG and the EOG discriminated any two types of blinks from three blinks by statistical test. Those values for the EMG and the EOG are effective indices for the evaluation of blinks. Moreover, the coefficients of variation of the amplitude and durations of EMG and EOG for three kinds of blinks denote their characteristics. Multiple discriminant analysis distinguished the types of blinks simultaneously. The resultant maximum correct rate for the three blinks reaches to be 81.8%. So far, it has been difficult to discriminate the blinks quantitatively, but the procedures presented here are able to solve the difficulty.

Adult↗
PubMed1997

Blinking is controlled primarily by ocular surface conditions.

PURPOSE: To investigate the relation between blinking and ocular surface conditions and to introduce and examine a new index, the maximum blink interval. METHODS: In a prospective study, the blink rate of subjects under relaxed conditions was determined from a video recording taken by a hidden observer. The maximum blink interval was defined as the longest time subjects can avoid blinking without feeling uncomfortable. RESULTS: Significant changes in the blink rate and maximum blink interval were induced by factors that directly or indirectly affect the ocular surface: topical anesthesia, changing exposed ocular surface area, and wind. Moreover, the blink rate and maximum blink interval were significantly different in dry eye patients compared with healthy volunteers, with the values of the former approaching the values of the latter after use of artificial tears. The maximum blink interval was decreased by the same factors that increased the blink rate, and there was a significant inverse correlation between blink rate and maximum blink interval. Use of video display terminals was associated with decreased maximum blink interval and, hence, the development of dry eye symptoms. CONCLUSIONS: There was an important association among blink rate, maximum blink interval, and ocular surface conditions. The blink rate and our newly introduced measurement, the maximum blink interval, should prove useful in assessing factors that cause dry eye. This prospective study should contribute to the understanding and treatment of dry eyes.

Administration, Topical↗
PubMed2000

Blink-perturbed saccades in monkey. I. Behavioral analysis.

Saccadic eye movements are thought to be influenced by blinking through premotor interactions, but it is still unclear how. The present paper describes the properties of blink-associated eye movements and quantifies the effect of reflex blinks on the latencies, metrics, and kinematics of saccades in the monkey. In particular, it is examined to what extent the saccadic system accounts for blink-related perturbations of the saccade trajectory. Trigeminal reflex blinks were elicited near the onset of visually evoked saccades by means of air puffs directed on the eye. Reflex blinks were also evoked during a straight-ahead fixation task. Eye and eyelid movements were measured with the magnetic-induction technique. The data show that saccade latencies were reduced substantially when reflex blinks were evoked prior to the impending visual saccades as if these saccades were triggered by the blink. The evoked blinks also caused profound spatial-temporal perturbations of the saccades. Deflections of the saccade trajectory, usually upward, extended up to approximately 15 degrees. Saccade peak velocities were reduced, and a two- to threefold increase in saccade duration was typically observed. In general, these perturbations were largely compensated in saccade mid-flight, despite the absence of visual feedback, yielding near-normal endpoint accuracies. Further analysis revealed that blink-perturbed saccades could not be described as a linear superposition of a pure blink-associated eye movement and an unperturbed saccade. When evoked during straight-ahead fixation, blinks were accompanied by initially upward and slightly abducting eye rotations of approximately 2-15 degrees. Back and forth wiggles of the eye were frequently seen; but in many cases the return movement was incomplete. Rather than drifting back to its starting position, the eye then maintained its eccentric orbital position until a downward corrective saccade toward the fixation spot followed. Blink-associated eye movements were quite rapid, albeit slower than saccades, and the velocity-amplitude-duration characteristics of the initial excursions as well as the return movements were approximately linear. These data strongly support the idea that blinks interfere with the saccade premotor circuit, presumably upstream from the neural eye-position integrator. They also indicated that a neural mechanism, rather than passive elastic restoring forces within the oculomotor plant, underlies the compensatory behavior. The tight latency coupling between saccades and blinks is consistent with an inhibition of omnipause neurons by the blink system, suggesting that the observed changes in saccade kinematics arise elsewhere in the saccadic premotor system.

Algorithms↗
PubMed1994

Conjugacy of spontaneous blinks in man: eyelid kinematics exhibit bilateral symmetry.

PURPOSE: To provide a quantitative description of the conjugacy of human eyelid movements during spontaneous blinks. METHODS: Eyelid movements occurring during spontaneous blinks were recorded bilaterally using a modification of the electromagnetic search coil technique. In off-line analyses, covariation of amplitude, peak velocity, and duration of blink down phases were determined for the two eyelids. Interocular differences in the timing of blink onset and offset, and time to peak velocity, also were evaluated. RESULTS: Human blink motor control systems act to link tightly the spatial and temporal characteristics of movements of the two eyelids. Data show that human spontaneous blinks are conjugate. Analysis of interocular covariation of blink amplitude, peak velocity, and duration yielded linear functions with high correlation coefficients. Interocular comparison of eyelid movement durations during blinks showed a particularly high correlation. There were negligible interocular differences in blink down-phase onset time, termination time, and time to peak velocity. A small percentage of blinks exhibited interocular differences in amplitude and peak velocity of > 20%; however, even in these cases, blink duration remained tightly linked. CONCLUSION: Spatial and temporal properties of eyelid movements occurring during spontaneous blinks are conjugate. These data support the hypothesis that a bilateral gating mechanism regulates blink duration. Elements downstream from the gate may differentially and unilaterally alter blink amplitude and peak velocity, but the duration of blinks remains time-locked for the two eyelids.

Adult↗
PubMed2004

Blink effects on ongoing smooth pursuit eye movements in humans.

Blinks are known to affect eye movements, e.g., saccades, slow and fast vergence, and saccade-vergence interaction, in two ways: by superimposition of blink-associated eye movements and changes of the central premotor activity in the brainstem. The goal of this study was to determine, for the first time, the effects of trigeminal evoked blinks on ongoing smooth pursuit eye movements which could be related to visual sensory or premotor neuronal changes. This was compared to the effect of a target disappearing for 100-300 ms duration during ongoing smooth pursuit (blank paradigm) in order to control for the visual sensory effects of a blink. Eye and blink movements were recorded in eight healthy subjects with the scleral search coil technique. Blink-associated eye movements during the first 50% of the blink duration were non-linearly superimposed on the smooth pursuit eye movements. Immediately after the blink-associated eye movements, the pursuit velocity slowly decreased by an average of 3.2+/-2.1 degrees /s. This decrease was not dependent on the stimulus direction. The pursuit velocity decrease caused by blinks which occluded the pupil more than 50% could be explained mostly by blanking the visual target. However, small blinks that did not occlude the pupil (<10% of lid closure) also decreased smooth pursuit velocity. Thus, this blink effect on pursuit velocity cannot be explained by blink-associated eye movements or by the blink having blanked the visual input. We propose that part of this effect might either be caused by incomplete visual suppression during blinks and/or a change in the activity of omnipause neurons.

Adult↗
PubMed2001

Long-term potentiation of the human blink reflex.

The trigeminal reflex blink is an ideal system to investigate whether stimulus paradigms that produce long-term potentiation (LTP) in vitro modify motor learning in humans. Presentation of 12 trains of low-intensity, high-frequency stimuli (HFS) to the supraorbital branch of the trigeminal nerve (SO) modified subsequent reflex blinks of human subjects. When HFS occurred concurrently with reflex blinks, the procedure potentiated subsequent blinks for >1 hr. Combining HFS with feedback from the lid movement was critical for this facilitation because presenting HFS immediately after the blink did not alter subsequent blinks. When HFS preceded the blink, however, this treatment suppressed subsequent blinks for 30 min. These effects appear to occur within the trigeminal reflex blink circuits rather than at motoneurons, because stimulation of the previously HFS-treated SO evoked altered blinks in both eyelids, whereas stimulation of the untreated SO elicited unaltered blinks in both eyelids. The modified blink amplitude resulted from altering the response to A-fiber inputs to the trigeminal nerve because all stimuli were too weak to activate C-fibers. The data suggest that HFS produce LTP- and long-term depression (LTD)-like effects on wide dynamic range neurons in the trigeminal reflex blink circuit. The data also support the hypothesis that LTP and LTD mechanisms play a role in adaptive modification of human reflex blinks.

Blinking↗
PubMed1997

Age-related changes in human blinks. Passive and active changes in eyelid kinematics.

PURPOSE: The authors analyzed eyelid kinematics in normal aging subjects to test the hypothesis that eyelid movements exhibit age-related changes and that blink disorders prevalent among the elderly, in turn, represent an outcome of normal aging processes. METHODS: The electromagnetic search coil technique was used to study blinks in normal human subjects for each decade from 40 to 89 years. Blink metrics (amplitude, peak velocity, and duration), main sequence relationships, and conjugacy were assessed. RESULTS: Mean amplitude and peak velocity of blinks decreased with age for spontaneous blinks and, to a lesser extent, for voluntary blinks. Some but not all, of this decline could be attributed to a peripheral phenomenon, narrowed palpebral fissure width. The spontaneous blink down phase main sequence slope also declined with age. By contrast, blink rate and the coordination of movements of the two eyelids--blink conjugacy--exhibited no change. CONCLUSIONS: These data demonstrate that disorders of blink systems typically seen in persons 50 years of age or older occur on a background of normal age-dependent changes in eyelid kinematics. Alterations in main sequence slope imply the operation of central adaptive systems during aging. Reduction in main sequence slope is interpreted as a reduction in aggregate orbicularis oculi motoneuron activity. Such a central neurologic adjustment in the motor output of blink systems may serve to compensate for an age-related increase in blink reflex excitability. Compensatory reduction in the main sequence relationship may offset a potentially hyperexcitable blink reflex, thereby reducing the likelihood of disorders such as blepharospasm. The authors conclude that although there are changes in the kinematics of blinking with age, such changes do not necessarily predispose an aging population to eyelid motility disorders.

Adult↗
PubMed2005

Two distinct neural effects of blinking on human visual processing.

Humans blink every few seconds, yet the changes in retinal illumination during a blink are rarely noticed, perhaps because visual sensitivity is suppressed. Furthermore, despite the loss of visual input, visual experience remains continuous across blinks. The neural mechanisms in humans underlying these two phenomena of blink suppression and visual continuity are unknown. We investigated the neural basis of these two complementary behavioural effects using functional magnetic resonance imaging to measure how voluntary blinking affected cortical responses to visual stimulation. Two factors were independently manipulated in a blocked design; the presence/absence of voluntary blinking, and the presence/absence of visual stimulation. To control for the simple loss of visual input caused by eyelid closure, we created a fifth condition where external darkenings were dynamically matched to each subjects' own blinks. Areas of lateral occipital cortex, including area V5/MT, showed suppression of responses to visual stimulation during blinking, consistent with the known loss in visual sensitivity. In contrast, a medial parieto-occipital region, homologous to macaque area V6A, showed responses to blinks that increased when visual stimulation was present. Our data are consistent with a role for this region in the active maintenance of visual continuity across blinks. Moreover, both suppression in lateral occipital and activation in medial parieto-occipital cortex were greater during blinks than during matched external darkenings of the visual scene, suggesting that they result from an extra-retinal signal associated with the blink motor command. Our findings therefore suggest two distinct neural correlates of blinking on human visual processing.

Adolescent↗
PubMed2000

EOG correction of blinks with saccade coefficients: a test and revision of the aligned-artefact average solution.

OBJECTIVE: The 'aligned-artefact average' (AAA) procedure was advanced by the authors as a technique suitable for removing eye movement-related artefacts from the EEG. It was proposed that this method would correct both blink and non-blink artefact from the EEG, using the same set of correction coefficients (Bs). However, recent evidence suggests that this simplification is not always accurate. Thus, we test here a revision of the AAA, including an appropriate allowance for the radial EOG (REOG) component, that does allow the use of the same Bs for the correction of blink and non-blink artefact. METHODS: Blink (and saccade) ERP data from 15 subjects were corrected using the AAA method, with Bs calculated from the same blink (and saccade) data set (referent waveforms), or a different set of blink (and saccade) data, or using the new revised AAA procedure (RAAA). RESULTS: AAA Bs calculated from saccades corrected blinks poorly (and vice versa). However, the RAAA Bs corrected blink ERPs better than blink-derived Bs, and saccade ERPs better than saccade-derived Bs. It was also found that irrespective of correction type, inclusion of REOG improved correction. CONCLUSION: EOG correction is more accurate when the radial channel is included, but inclusion of REOG (and/or HEOG) is not sufficient to resolve the discrepancy between blink and saccade correction. Using the RAAA procedure, both blink and non-blink data can be corrected using the same set of Bs.

Adolescent↗
PubMed1996

An explanation for reflex blink hyperexcitability in Parkinson's disease. II. Nucleus raphe magnus.

Hyperexcitable reflex blinks are a cardinal sign of Parkinson's disease. The first step in the circuit linking the basal ganglia and brainstem reflex blink circuits is the inhibitory nigrostriatal pathway (Basso et al., 1996). The current study reports the circuits linking the superior colliculus (SC) to trigeminal reflex blink circuits. Microstimulation of the deep layers of the SC suppresses subsequent reflex blinks at a latency of 5.4 msec. This microstimulation does not activate periaqueductal gray antinociceptive circuits. The brainstem structure linking SC to reflex blink circuits must suppress reflex blinks at a shorter latency than the SC and produce the same effect on reflex blink circuits as SC stimulation, and removal of the structure must block SC modulation of reflex blinks. Only the nucleus raphe magnus (NRM) meets these requirements. NRM microstimulation suppresses reflex blinks with a latency of 4.4 msec. Like SC stimulation, NRM microstimulation reduces the responsiveness of the spinal trigeminal nucleus. Finally, blocking the receptors for the NRM transmitter serotonin eliminates SC modulation of reflex blinks, and muscimol inactivation of the NRM transiently prevents SC modulation of reflex blinks. Thus, the circuit through which the basal ganglia modulates reflex blinking is (1) the substantia nigra pars reticulata inhibits SC neurons, (2) the SC excites tonically active NRM neurons, and (3) NRM neurons inhibit spinal trigeminal neurons involved in reflex blink circuits.

Animals↗
PubMed1975

Blinking and thinking.

Blinking is related to certain cognitive processes. For example, individuals "punctuate" their speech by blinking between phrases and at the end of sentences. Daydreaming is associated with low rates of blinking. Blinking occurs between fixations and may be timed so as not to interfere with significant visual input. Apparently, blinking occurs at transitions between internal events and is inhibited at other times. In the experiment reported here, blinking was measured while the activity of operational memory was manipulated with mental load kept constant. The rate of blinking was significantly reduced when the cognitive operation of internal counting was being performed. It is inferred that the blink rate is low when information in memory is being operated on. To suspend blinking during certain cognitive activities would be adaptive if blinking disrupts them. Since the blackout period of the blink produces a rapid change in visual level, blinking disrupts those cognitive processes utilizing display areas accessible to visual input. Operational memory and the visual imagination may share components with the visual perceptual system. To protect these vulnerable processes from interference, blinking may be inhibited when they are active.

Acoustic Stimulation↗
PubMed2005

Blinking suppresses the neural response to unchanging retinal stimulation.

Blinks profoundly interrupt visual input but are rarely noticed, perhaps because of blink suppression, a visual-sensitivity loss that begins immediately prior to blink onset. Blink suppression is thought to result from an extra-retinal signal that is associated with the blink motor command and may act to attenuate the sensory consequences of the motor action. However, the neural mechanisms underlying this phenomenon remain unclear. They are challenging to study because any brain-activity changes resulting from an extra-retinal signal associated with the blink motor command are potentially masked by profound neural-activity changes caused by the retinal-illumination reduction that results from occlusion of the pupil by the eyelid. Here, we distinguished direct top-down effects of blink-associated motor signals on cortical activity from purely mechanical or optical effects of blinking on visual input by combining pupil-independent retinal stimulation with functional MRI (fMRI) in humans. Even though retinal illumination was kept constant during blinks, we found that blinking nevertheless suppressed activity in visual cortex and in areas of parietal and prefrontal cortex previously associated with awareness of environmental change. Our findings demonstrate active top-down modulation of visual processing during blinking, suggesting a possible mechanism by which blinks go unnoticed.

Adult↗
PubMed2005

The spontaneous eye-blink as sleepiness indicator in patients with obstructive sleep apnoea syndrome-a pilot study.

BACKGROUND AND PURPOSE: To evaluate the spontaneous eye-blink as drowsiness/sleepiness indicator in patients with obstructive sleep apnoea (OSA) syndrome. PATIENTS AND METHODS: Using a contact-free sensor for the recording of spontaneous eye-blinks, we investigated the diagnostic value of spontaneous blink parameters in 21 OSA patients. Before the study, all patients underwent a night of polysomnography. Eye-blinks were studied the following morning before therapy, and again after the first therapy night with nasal continuous positive airway pressure (nCPAP), to investigate whether blink parameters reflected changes of alertness pre- and post-nCPAP treatment. General daytime sleepiness was assessed using the Epworth Sleepiness Scale (ESS). The current subjective state was determined by means of standardised questionnaires directly before recording the eye-blinks. Studies were conducted in two sleep laboratories in hospitals. RESULTS: In OSA patients with excessive daytime sleepiness (EDS; ESS >10, respiratory disturbance index [RDI]=42.4) several parameters proved informative for sleepiness diagnostics. Reduction of blink duration and reopening time as well as increase in blink frequency were significant; furthermore, proportion of long-closure duration blinks indicated reduced sleepiness. OSA patients without EDS (ESS < or =10, RDI=33.5) did not reveal systematic changes of the blink parameters registered after one night of nCPAP intervention. CONCLUSIONS: Specific parameters of the spontaneous eye-blink may be applied as a sleepiness index for diagnostics in OSA patients. Further studies are needed to prove the diagnostic value of blink parameters and their advantages in comparison to subjective measures commonly used in clinical studies.

Adult↗
PubMed2003

Automatic blink detection: a method for differentiation of wake and sleep of intellectually disabled and healthy subjects in long-term ambulatory monitoring.

OBJECTIVES: To develop a method for automatic detection of blinks in electrooculograms and to evaluate reliability of blink rate as an indicator of wake and sleep in subjects with developmental brain disorders. DESIGN: Categorization of wake and sleep by blink rate was compared with visual sleep scoring of the polysomnograms. SETTING: Ambulatory polysomnographic recordings at home or in the sleep laboratory. PARTICIPANTS: Nine healthy volunteers for calibration, 10 for validation; 7 intellectually disabled patients for calibration, 10 for validation of the method. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Blinks were detected from electrooculograms using a weighted finite impulse response median hybrid filtering and the criterion of minimum duration at amplitude threshold. More than 80% of the visually identified electrooculographic blinks were detected in most subjects. When 30-second epochs of electrooculograms with 1 or more blinks were defined as wake and those without blinks as sleep, the average agreement with polysomnographic scoring was 95% in healthy subjects and 84% in patients. The mismatch was mostly due to the 30-second epochs without blinks during waking. A contextual redefinition of wake and sleep by expanding the inspected electrooculographic span from 1 to 20 epochs (10 minutes) increased the agreement to 93% in patients. The agreement is comparable to that of actigraphy with polysomnography. The linear correlation coefficient of the proportions of sleep epochs between visual scoring and the contextual blink rate method was 0.869. The main sleep periods detected by the blink-rate method were an average of 7 minutes longer than those determined by visual scoring. This was caused by differences in the detection of sleep onsets: blinking ceased before the first stage 1 sleep period was scored. The absolute period lengths obtained by the 2 methods did not differ significantly from each other in unpaired t-tests, and the linear correlation between the values was 0.999. CONCLUSIONS: The blinks extracted from the electrooculographic signal can be used to reliably determine the main sleep and wake periods in both healthy subjects and patients with developmental brain disorders.

Adult↗
PubMed2002

Effects of voluntary blinks on saccades, vergence eye movements, and saccade-vergence interactions in humans.

Blinks are known to change the kinematic properties of horizontal saccades, probably by influencing the saccadic premotor circuit. The neuronal basis of this effect could be explained by changes in the activity of omnipause neurons in the nucleus raphe interpositus or in the saccade-related burst neurons of the superior colliculus. Omnipause neurons cease discharge during both saccades and vergence movements. Because eyelid blinks can influence both sets of neurons, we hypothesized that blinks would influence the kinematic parameters of saccades in all directions, vergence, and saccade-vergence interactions. To test this hypothesis, we investigated binocular eye and lid movements in five normal healthy subjects with the magnetic search coil technique. The subjects performed conjugate horizontal and vertical saccades from gaze straight ahead to targets at 20 degrees up, down, right, or left while either attempting not to blink or voluntarily blinking. While following the same blink instruction, subjects made horizontal vergence eye movements of 7 degrees and combined saccade-vergence movements with a version amplitude of 20 degrees. The movements were performed back and forth from two targets simultaneously presented nearby (38 cm) and more distant (145 cm). Small vertical saccades accompanied most vergence movements. These results show that blinks change the kinematics (saccade duration, peak velocity, peak acceleration, peak deceleration) of not only horizontal but also of vertical saccades, of horizontal vergence eye movements, and of combined saccade-vergence eye movements. Peak velocity, acceleration, and deceleration of eye movements were decreased on the average by 30%, and their duration increased by 43% on the average when they were accompanied by blinks. The blink effect was time dependent with respect to saccade and vergence onset: the greatest effect occurred 100 ms prior to saccade onset, whereas there was no effect when the blink started after saccade onset. The effects of blinks on saccades and vergence, which are tightly coupled to latency, support the hypothesis that blinks cause profound spatiotemporal perturbations of the eye movements by interfering with the normal saccade/vergence premotor circuits. However, the measured effect may to a certain degree but not exclusively be explained by mechanical interference.

Adult↗
PubMed2006

Cerebellar modulation of trigeminal reflex blinks: interpositus neurons.

Because of its simplicity, blinking is a prominent model system in analysis of adaptation and conditioning with the cerebellum. Nevertheless, data on the role of the cerebellum in modulation of normal reflex blinks are limited. We correlated the discharge of interpositus (IP) neurons with normal trigeminal reflex blinks and blink adaptation in urethane-anesthetized rats. Two groups of IP neurons responded to cornea stimulation. One group, pause neurons, showed a long cessation of their tonic discharge beginning 6 ms before the end of lid closure. The second group, burst neurons, exhibited a transient increase in firing frequency at a constant interval after the cornea stimulus. The cessation of pause neuron activity appeared to contribute to the termination of blinks. The tonic discharge rate increased and the cessation of pause neuron activity was delayed coincident with increased amplitude and duration of reflex blinks produced by blink adaptation. There was a coincident increase in the amplitude and duration of reflex blinks with increased tonic activity and delayed pause in pause neurons treated with the GABA(A) antagonist, gabazine. Burst neurons did not appear to modulate reflex blinks. Burst neuron discharge correlated neither with blink characteristics normally nor with blink adaptation. These findings indicated that pause neurons affect reflex blinks by providing a tonic excitatory input to facial motoneurons during lid closure and then disfacilitating those motoneurons to adjust the termination of lid closure. Burst neurons may play a role in eyelid conditioning.

Action Potentials↗