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At least 55 records · Page 3Linked to original sources
PubMed2005

Cognition, blinks, eye-movements, and pupillary movements during performance of a running memory task.

INTRODUCTION: Blinks, saccades, and pupil diameter changes are studied for their application as tools to unobtrusively monitor aspects of performance. METHODS: Subjects performed a running memory task for a 60-min period. To evaluate changes in the relationship of blinks to saccades as a function of time on task, the ratio of blinks occurring with and without saccade was calculated for the second following stimulus termination plus the last 0.2 s of stimulus presentation, and also the second preceding stimulus onset plus the initial 0.2 s of stimulus presentation. Changes in pupil diameter following blinks with and without saccades were measured at the beginning, middle, and late in the experiment. RESULTS: Blink frequency increased during both periods as a function of time on task (p < 0.0001). The ratio of blinks concurrent with saccades during the post-stimulus period increased as a function of time on task (p < 0.0001). Pupil diameter increased following blink termination (p < 0.05), regardless of time on task, blink duration, or the presence of a saccade during the blink. CONCLUSION: Our results suggest that the increase in blinking associated with saccades as a function of time on task, and the pupillary dilation following a blink are associated with aspects of information processing. These results provide a framework for future studies assessing higher-order cognitive function in operational environments based on measurements of blink, pupil, and saccades.

Adult↗
PubMed1989

Blinking.

Spontaneous blink rates are controlled by a definable neural system originating in PPRF with facilitatory modulation from SN and superior colliculus and inhibitory modulation provided by cerebellum and occipital cortex. The thalamus may also be involved but the result of its influence is not clear. Reflex blinking is often reduced when spontaneous blink rate is increased and the reverse applies as well. The anatomic control of reflex is primarily in structures in the caudal half of pontine tegmentum and rostral midbrain. However, SN and cerebellum and other structures that regulate blink rate also modulate reflex blinking. Neurochemical control as determined by neuropharmacological experiments is exerted by dopaminergic, cholinergic and GABAergic systems of brain stem. Dopamine activity correlates directly with blink rate whereas agonism of the other two relevant neurotransmitter systems may inhibit blink rate. Clinical implications in central nervous system disease are currently restricted to Parkinson's disease, schizophrenia and autism. In the former illness, reduced blink rate signifies a worsening of the illness and a significant increase in blink rate in patients treated with dopamine agonist may be a harbinger of agonist-induced dyskinesia. In schizophrenia, increased blink rate, even in medication-naive subjects, may signify involvement of the structures that regulate blinking. This is important because these structures are rarely invoked as sites of potential pathophysiological import in schizophrenia. Similar considerations apply to autism except that increased blinking more clearly differentiates this disorder from other forms of retardation.

Animals↗
PubMed1997

The role of blink adaptation in the pathophysiology of benign essential blepharospasm.

OBJECTIVE: To investigate eyelid movements in patients with benign essential blepharospasm (BEB), with an emphasis on the characterization of the kinematics of normal and spastic blinks, assessment of interocular differences, and further delineation of the role of adaptive blink mechanisms in eyelid movement disorders. PATIENTS AND METHODS: The electromagnetic search coil technique was used to record the metrics of blinks bilaterally in 5 patients with untreated BEB. Eyelid kinematics and the main-sequence (peak velocity vs amplitude) relationships were analyzed. RESULTS: Patients with BEB exhibited a decrease in blink amplitude and peak velocity. Moreover, the main-sequence slope was decreased bilaterally. Spasms were bilateral and relatively conjugate. There was no change in the coordination of normal blinking across the 2 eyelids. CONCLUSIONS: These data demonstrate the operation of the adaptive regulation of blinking in an eyelid movement disorder. The findings suggest that the adaptive regulation of blink is a bilateral event. Blink-adaptive control systems can act on the blink reflex excitability and main-sequence relationships, changing these either together or independently. The hyperexcitable blink reflex of BEB is met by what is believed to be an adaptive decrease in the main-sequence slope that would decrease the strength of debilitating spasms. Collectively, these data extend the knowledge of the pathophysiology of BEB and, perhaps more important, establish the role of blink system plasticity in eyelid movement disorders.

Adaptation, Physiological↗
PubMed1999

The influence of eye solutions on blinking and ocular comfort at rest and during work at video display terminals.

The aim of this work was to study blink frequency changes and levels of ocular discomfort during work at a video display terminal, and the effects on these parameters of augmented or reduced humidification of the ocular surface. Blink rate was measured from recordings of the electrical signal evoked by the contraction of the orbicularis oculi muscle. Blink rate and interblink intervals were analyzed at rest and during performance of a task with a computer (playing a card game) for 10 or 30 min in steady environmental conditions and during application of a continuous stream of air to the face. In two separate sessions, the effect of pretreatment with humidifying ocular solutions of different elastoviscosity (balanced salt solution or elastoviscous 0.1% Hylan A solution) was assayed. At the end of each experimental period, the subjects marked the level of ocular discomfort experienced on a 0-10 cm visual analogue scale. The blink frequency at rest (12.4+/-1.2 blinks min-1) was reduced significantly (to 10.3+/-1.1 blinks min-1) by pretreatment with elastoviscous eyedrops both with and without air applied to the face. This effect was not obtained with balanced salt solution. During performance of the visual task for 10 or 30 min, basal blink rate decreased significantly, to about 40% of the control value. Neither application of an air jet on the face nor application of eye solutions of different viscosity modified this reduced blink rate.A low degree of ocular discomfort developed after performance of the visual task that was enhanced by air application to the face. This discomfort was reduced by pretreatment with ocular solutions, the elastoviscous eye solution being more efficient than the balanced salt solution. Interblink interval duration was also more regular after treatment with the elastoviscous solution. These data suggest that blink rate at rest is maintained in part by activation of sensory receptors of the cornea and conjunctiva, which are stimulated by desiccation of the ocular surface. Reduction of eye blink frequency elicited by the performance of a visual task with a computer appears to depend on central neural mechanisms that are quite independent of peripheral sensory inputs. The reduction of blink frequency consecutive to computer use was associated with a sensation of discomfort that was attenuated more effectively by elastoviscous eyedrops than by regular balanced salt solution.

Adult↗
PubMed2005

Modification of cornea-evoked reflex blinks in rats.

Although maintaining the tear film on the cornea is the most important role of blinking, information about the organization and modification of cornea-evoked blinks is sparse. This study characterizes cornea-evoked blinks and their modification in urethane-anesthetized rats. Cornea-evoked blinks typically begin 16.2 ms after an electrical stimulus to the cornea and last an average of 50.2 ms. In anesthetized rats, the blink only occurs ipsilateral to the stimulus. In response to cornea stimulation, the orbicularis oculi EMG activity typically exhibits two bursts that correlate with the arrival of A delta and C-fiber inputs to the spinal trigeminal complex. In the paired-stimulus paradigm, suppression of the blink evoked by the second cornea stimulus occurs for interstimulus intervals less than 300 ms and is exclusively unilateral. Stimulation of the contralateral cornea does not affect subsequent blinks evoked from stimulation of the ipsilateral cornea. To determine whether activation of cornea-related neurons in the border region between the spinal trigeminal caudalis subdivision and the C1 spinal cord (Vc/C1) inhibits the second blink in the paired-stimulus paradigm, we examine the suppression of cornea-evoked blinks caused by microstimulation in this region. This suppression of orbicularis oculi EMG activity begins 8.3 ms after Vc/C1 stimulation. Activation of this region, however, is unlike suppression in the paired-stimulus paradigm because Vc/C1 activation bilaterally inhibits cornea-evoked blinks. Thus, activation of Vc/C1 is a previously unidentified mechanism for modulating cornea-evoked blinks.

Afferent Pathways↗
PubMed1993

Quantitative analysis of eyelid movement metrics reveals the highly stereotyped nature of monkey blinks.

Blink movement metrics were studied in three alert cynomolgus monkeys using electromagnetic search coils attached to the eyelids bilaterally. Monkey blinks averaged approximately 24 degrees. Down-phase peak velocities were approximately twice those of the corresponding up phases. Most blinks were symmetrical with close temporal linkage of onset and offset between the two eyelids. Monkey blinks exhibited higher peak velocities and shorter durations than have been previously described for similar amplitude movements in humans. Peak velocity vs. amplitude plots were linear and non-saturating within a 45 degrees range for both up and down phases. The relationship between blink peak velocity and average velocity was linear with a slope of approximately 2.0. These values were very similar to those obtained by others, not only for blinks, but also for saccadic eye and ballistic limb movements. Down-phase amplitude-duration behavior could be best described by a linear function with slope < 0.7, while amplitude-duration slope of up phases was best described by a second-order polynomial. Unlike saccadic eye movements, larger amplitude blinks are obtained primarily via increases in peak velocity rather than through extension of blink duration. These data provide mathematical descriptions of monkey blink behavior that indicate the stereotypical nature of blinks. This will serve as a normative data base with which to better understand the neural processing that goes into blinks and will allow the assessment of eyelid movement disorders and evaluation of potential treatments of these disorders.

Animals↗
PubMed2004

Endogenous eye blinks in preadolescents: relationship to information processing and performance.

Endogenous blinks--those occurring without apparent provocation--are regulated in adults with respect to the presentation, cognitive loading, and response demands of stimuli. This investigation determined the extent to which similar regulatory and response-related relationships were evident in preadolescents during a visual continuous performance task (CPT). As in adults, increased blink incidence on task, longer blink deferral following stimuli with greater cognitive loading, and blink-facilitated motor responses to imperative stimuli were observed. Reaction times significantly decreased when the button press (BP) occurred near (+/- 200 ms) blink onset and increased across the task period on blink-free but not blink-associated trials. More blinks occurred before motor responses in females, and a reaction time (RT) advantage for males on blink-free trials was maintained across blink-associated conditions. From these results, an interpretation is developed arguing that endogenous blinks are a meaningful and integral component of sensory-motor processing, indexing times of facilitated attentional and motor response capability.

Adolescent↗
PubMed1998

An electroencephalographic study comparing maximum blink rates in schizophrenic and nonschizophrenic psychiatric patients and nonpsychiatric control subjects.

BACKGROUND: We did a retrospective electroencephalographic (EEG) analysis of blink rates in patients with psychiatric disorders and control subjects to determine whether maximum blink rates under different conditions were higher in patients with psychiatric disorders. METHODS: Maximum blink rates in those with schizophrenia (n = 23), those with nonschizophrenic psychiatric illnesses (n = 21), and nonpsychiatric control subjects (n = 35) were obtained from patients' EEGs and compared with one-way analysis of variance and post hoc tests. In addition, correlation analysis was performed to determine if patients' medications affected maximum blink rates. RESULTS: Patients with schizophrenic and nonschizophrenic psychiatric disorders had twofold higher maximum resting blink rates compared to controls (p < .05 respectively). No difference was found between those with schizophrenic and nonschizophrenic psychiatric disorders. The maximum blink rate during cognitive testing was also twofold higher in those with nonschizophrenic psychiatric disorders (n = 11) compared to controls (n = 16; p < .05). Within each group, maximum blink rates during quiet rest and cognitive testing did not differ, nor were there differences between groups in the duration of high-frequency blinking (greater than 40 blinks per minute) during quiet rest. In psychiatric patients, none of the medications taken at the time of EEG recording correlated with maximum blink rates. CONCLUSIONS: High maximum blink rates recorded by EEG may suggest the presence of a psychiatric disorder.

Adult↗
PubMedDate not supplied

Role of cerebellum in adaptive modification of reflex blinks.

We investigated the involvement of the cerebellar cortex in the adaptive modification of corneal reflex blinks and the regulation of normal trigeminal reflex blinks in rats. The ansiform Crus I region contained blink-related Purkinje cells that exhibited a complex spike 20.4 msec after a corneal stimulus and a burst of simple spike activity correlated with the termination of orbicularis oculi activity. This occurrence of the complex spike correlated with trigeminal sensory information associated with the blink-evoking stimulus, and the burst of simple spike activity correlated with sensory feedback about the occurrence of a blink. Inactivation of the inferior olive with lidocaine prevented all complex and significantly reduced simple spike modulation of blink-related Purkinje cells, but did not alter orbicularis oculi activity evoked by corneal stimulation. In contrast, both acute and chronic lesions of the cerebellar cortex containing blink-related Purkinje cells blocked adaptive increases in orbicularis oculi activity of the lid ipsilateral but not contralateral to the lesion. These data are consistent with the hypothesis that the cerebellum is part of a trigeminal reflex blink circuit. Changes in trigeminal signals produce modifications of the cerebellar cortex, which in turn, reinforce or stabilize modifications of brainstem blink circuits. When the trigeminal system does not attempt to alter the magnitude of trigeminal reflex blinks, cerebellar input has little or no effect on reflex blinks.

Animals↗
PubMed2005

Blink rate in boys with fragile X syndrome: preliminary evidence for altered dopamine function.

BACKGROUND: Dopamine, a neurotransmitter involved in motor and cognitive functioning, can be non-invasively measured via observation of spontaneous blink rates. Blink rates have been studied in a number of clinical conditions including schizophrenia, autism, Parkinsons, and attention deficit/hyperactivity disorder with results implicating either hyper or hypo dopaminergic states. METHODS: This study examined spontaneous blink rate in boys with fragile X syndrome (FXS). Blink rates of boys (4-8 years old) with FXS (n = 6) were compared with those of age-matched typically developing boys (n = 6) during active and passive tasks. Blink rates (blinks per minute) for each task were compared between the two groups. Then, the relation between blink measures and core FXS-related features [problem behaviours, arousal, fmr 1 protein (FMRP)] were examined within the group of boys with FXS. RESULTS: Blink rate in boys with FXS was significantly higher than typically developing boys during passive tasks. Within the FXS group, there were significant correlations between blink rate and problem behaviours and physiological arousal (i.e. heart activity) but not with FMRP. CONCLUSIONS: Observed differences in spontaneous blink rate between boys with and without FXS and the relation between blink rate and physiological and behavioural measures in boys with FXS suggests that further work examining dopamine dysfunction as a factor in the pathophysiology of FXS may be warranted.

Arousal↗
PubMed2005

Tear-film lipid layer morphology and corneal sensation in the development of blinking in neonates and infants.

The aim of the study was to evaluate the role of lipid layer thickness and corneal sensation in the development of blinking in neonates. The study group comprised sixty-four neonates and infants (mean age 27.5 +/- 15 (sd) weeks, range 3.4-52) whose mothers were attending a general practice healthy baby clinic. Spontaneous eye-blink activity was determined from digital videographic recordings; tear film lipid layer morphology wasexamined using interference patterns produced by the Keeler Tearscopetrade mark Plus over a five-point grading scale (higher grades are associated with thick and stable lipid films); corneal sensation threshold was assessed with the Non-Contact Corneal Aesthesiometer (NCCA), using the eye-blink response as an objective indication that the cooling stimulus had been felt; palpebral aperture dimensions were measured using calibrated digital still images of the eye in the primary position. The overall mean spontaneous blink-rate was found to be 3.6 (+/- 0.3) blinks min(-1), and the mean interblink time was 21.6 (+/- 2.8) s. The lowest blink-rates were observed in the 0-17-week age group (average 2 blinks min(-1)). The blink-rate showed a highly significant correlation with age (r = 0.46, P < 0.01). The overall mean lipid layer grading was 3.6 (+/- 0.2 SE) arbitrary units. Higher grades were found in the newborn and the mean grading score reduced with age (P < 0.01). The mean sensation threshold to blink (TTB) was 0.69 (0.04 SE) mbar, which did not differ from a control group of older subjects (P > 0.05). There was a rapid increase in palpebral aperture length and width from birth to 1 year old, with surface area increasing by 50% over the same period. We concluded that the low rate of spontaneous eye blink activity in neonates is associated with a thick stable lipid layer that may be a function of a small palpebral aperture. Furthermore, neonates appear to have the capacity to detect ocular surface cooling, which is a major trigger for spontaneous blinking.

Blinking↗
PubMed1991

D1 and D2 dopamine receptors independently regulate spontaneous blink rate in the vervet monkey.

Previous studies have revealed the involvement of a dopaminergic link in the regulation of spontaneous eye blink rate in primates. Based on the effect of dopamine D2 receptor-selective drugs and the anecdotal failure of the partial D1 agonist, SKF 38393, to alter blink rate in monkeys, it was assumed that D1 dopamine receptors did not control blink rate. The recent availability of dihydrexidine, a full D1 agonist, prompted us to reevaluate the role of D1 and D2 receptors in the regulation of blink rate. African green monkeys (n = 5) were used in all studies. Dihydrexidine produced a rapid and dose-dependent (up to 1 mg/kg, i.m.) increase in blink rate. The elevation in blink rate elicited by 0.3 mg/kg dihydrexidine was completely reversed by prior administration of a specific D1 antagonist, SCH 23390 (0.01 mg/kg, i.m.), but was unaffected by prior administration of a specific D2 antagonist, remoxipride (1 mg/kg, i.m.). Treatment with the specific D2 agonist, (+)-4-propyl-9-hydroxynaphthoxazine, led to a rapid and dose-dependent (up to 0.01 mg/kg, i.m.) increase in blink rate. The raised blink rate produced by (+)-4-propyl-9-hydroxynaphthoxazine (0.001 mg/kg) was abolished by pretreatment with remoxipride, but was not influenced by pretreatment with SCH 23390. These data indicate that spontaneous blink rate in the primate can be regulated by both D1 and D2 dopamine receptors. Furthermore, the receptor subtypes appear to affect blink rate in the same direction, yet function independently. Measurement of blink rate may provide a noninvasive method to assess the potency and selectivity of dopamine agonists and antagonists in primates.

Animals↗
PubMed1999

Spontaneous blink rates correlate with dopamine levels in the caudate nucleus of MPTP-treated monkeys.

Previous studies have suggested a dopaminergic regulation of eye blink rates in human and nonhuman primates. Blockade of either dopamine (DA) D1 or DA D2 receptors or DA depletion induced by the dopaminergic neurotoxin MPTP both decrease spontaneous eye blink rates in monkeys. MPTP-induced decreases in blink rates can be reversed by administration of the full efficacy D1 agonist dihydrexidine, which has also been found to have dramatic antiparkinsonian effects in MPTP-treated animals. Increases in blink rates can also be induced by D1 and D2 agonists in normal animals. In the current study, we have investigated whether blink rates correlate with concentrations of DA or HVA and/or HVA:DA ratios in specific brain regions in MPTP-treated monkeys. Furthermore, the potential relationship between the severity of behavioral indices of parkinsonism and blink rates were examined. We found that (1) blink rates significantly correlate positively with concentration of DA and inversely with HVA:DA ratios in the rostral portion of the ventromedial body of the caudate nucleus (CD), but not other subcortical regions, and (2) that severity of parkinsonism was inversely correlated with blink rate. These data support a dopaminergic regulation of blink rate and suggest that the ventromedial region of the body of the CD may be critically involved in regulation of blink rate.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1994

Not looking while leaping: the linkage of blinking and saccadic gaze shifts.

Many vertebrates generate blinks as a component of saccadic gaze shifts. We investigated the nature of this linkage between saccades and blinking in normal humans. Activation of the orbicularis oculi, the lid closing muscle, EMG occurred with 97% of saccadic gaze shifts larger than 33 degrees. The blinks typically began simultaneously with the initiation of head and/or eye movement. To minimize the possibility that the blinks accompanying saccadic gaze shifts were reflex blinks evoked by the wind rushing across the cornea and eye-lashes as the head and eyes turned, the subjects made saccadic head turns with their eyes closed. In this condition, orbicularis oculi EMG activity occurred with all head turns greater than 17 degrees in amplitude and the EMG activity began an average of 39.3 ms before the start of the head movement. Thus, one component of the command for large saccadic gaze shifts appears to be a blink. We call these blinks gaze-evoked blinks. The linkage between saccadic gaze shifts and blinking is reciprocal. Evoking a reflex blink prior to initiating a voluntary saccadic gaze shift dramatically reduces the latency of the initiation of the head movement.

Blinking↗
PubMed1993

A role for the basal ganglia in nicotinic modulation of the blink reflex.

In humans and rats we found that nicotine transiently modifies the blink reflex. For blinks elicited by stimulation of the supraorbital branch of the trigeminal nerve, nicotine decreased the magnitude of the orbicularis oculi electromyogram (OOemg) and increased the latency of only the long-latency (R2) component. For blinks elicited by electrical stimulation of the cornea, nicotine decreased the magnitude and increased the latency of the single component of OOemg response. Since nicotine modified only one component of the supraorbitally elicited blink reflex, nicotine must act primarily on the central nervous system rather than at the muscle. The effects of nicotine could be caused by direct action on lower brainstem interneurons or indirectly by modulating descending systems impinging on blink interneurons. Since precollicular decerebration eliminated nicotine's effects on the blink reflex, nicotine must act through descending systems. Three lines of evidence suggest that nicotine affects the blink reflex through the basal ganglia by causing dopamine release in the striatum. First, stimulation of the substantia nigra mimicked the effects of nicotine on the blink reflex. Second, haloperidol, a dopamine (D2) receptor antagonist, blocked the effect of nicotine on the blink reflex. Third, apomorphine, a D2 receptor agonist, mimicked the effects of nicotine on the blink reflex.

Anesthesia↗
PubMed1986

Different forms of blinks and their two-stage control.

The purpose of this paper is to examine blink kinematics and the neural basis of blinks evoked reflexively by different kinds of stimuli. The kinematics of the upper lid movement and the electromyographic response of lid muscles levator palpebrae and orbicularis oculi were recorded in the rabbit during trigeminally and visually-evoked blinks. We find that there is a basic, kinematic difference between blinks. A blink in response to an airpuff is more rapidly accomplished and achieves a higher velocity than does an equal amplitude blink in response to a flash of light. The two forms of the reflex blink result from differences in the nature and timing of activity in antagonistic lid muscle motoneurons. Nevertheless, most characteristics of blink neural control are common to both reflex blinks. Most importantly, it appears that blinks are produced by two-stage neural control, an early component that is preprogrammed and a late component that is under stimulus control.

Animals↗
PubMed2004

Differential effects of blinks on horizontal saccade and smooth pursuit initiation in humans.

Blinks executed during eye movements affect kinetic eye movement parameters, e.g., peak velocity of saccades is decreased, their duration is increased, but their amplitude is not altered. This effect is mainly explained by the decreased activity of premotor neurons in the brainstem: omni-pause neurons (OPN) in the nucleus raphe interpositus. Previous studies examined the immediate effect of blinks directly on eye movements but not their effect when they are elicited several hundred milliseconds before the eye movements. In order to address this question we tested blinks elicited before the target onset of saccades and pursuit and compared the results to the gap effect: if a fixation light is extinguished for several hundred milliseconds, the reaction time (latency) for subsequent saccades or smooth pursuit eye movements is decreased. Monocular eye and lid movements were recorded in nine healthy subjects using the scleral search-coil system. Laser stimuli were front-projected onto a tangent screen in front of the subjects. Horizontal step-ramp smooth pursuit of 20 deg/s was elicited in one session, or 5 deg horizontal visually guided saccades in another experimental session. In one-third of the trials (smooth pursuit or saccades) the fixation light was extinguished for 200 ms before stimulus onset (gap condition), and in another third of the trials reflexive blinks were elicited by a short airpuff before the stimulus onset (blink condition). The last third of the trials served as controls (control condition). Stimulus direction and the three conditions were randomized for saccades and smooth pursuit separately. The latency of the step-ramp smooth pursuit in the blink condition was found to be decreased by 10 ms, which was less than in the gap condition (38 ms). However, the initial acceleration and steady-state velocity of smooth pursuit did not differ in the three conditions. In contrast, the latency of the saccades in the gap condition was decreased by 39 ms, but not in the blink condition. Saccade amplitude, peak velocity, and duration were not different in the three conditions. There was also no difference in blink amplitude and duration of pupil occlusion in the blink condition, neither in saccades nor in smooth pursuit. The latency reduction of smooth pursuit, but not of saccades, may neither be explained by the brief pupil occlusion nor by visual suppression, warning signals, or the startle response. Whether the effects are caused by the influence of blinks on OPNs or other premotor structures remains to be tested.

Adult↗
PubMed1993

Suppression of contrast sensitivity during eyelid blinks.

Each blink of the eyelids is associated with a concurrent suppression of vision that lasts as long as 200 msec. Saccadic eye movements are also associated with a concurrent suppression of vision. Previous studies suggested that blink and saccadic suppression may be the result of a single mechanism. Volkmann, Riggs, White and Moore [(1978) Vision Research, 18, 1193-1199] demonstrated that saccadic suppression is most evident for low spatial frequency stimuli. However, the effect of stimulus spatial frequency on blink suppression has not been evaluated. If blink suppression and saccadic suppression result from a single mechanism, then blink suppression should also exhibit its greatest effect at low spatial frequencies. The purpose of this study was to determine the effect of stimulus spatial frequency on blink suppression. The stimulus was a sine-wave grating presented at different times after the blink. Psychometric functions were produced from the data for each post-blink, stimulus onset time and a Weibull function was fit to the data to determine threshold. The magnitude and duration of blink induced contrast sensitivity suppression was found to depend on the spatial frequency of the stimulus employed (similar to saccadic suppression). This is further evidence that a single mechanism may produce both blink induced visual suppression and saccadic suppression.

Blinking↗