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A 10 year old girl with benign childhood epilepsy with centrotemporal spikes showed centrotemporal spikes induced by blinking even in a dark room. Spikes could not be induced by photic stimulation, eye closure, eye movement, eye deviation, or passive blinks. There have been no previous reports of spikes induced by blinks in benign childhood epilepsy with centrotemporal spikes.
Our visual experience constitutes an unending chain of transient events, including those caused by saccadic eye movements, by blinks, and by localized or global changes in the external world. The categorical perception of objects is maintained across different classes of transient events, suggesting that the neural circuitry underlying visual perception responds to different transient events in a similar manner. However, different sorts of transients do have different perceptual impacts: for example, the sudden changes in a scene due to a saccade or a blink do not disturb our perceptual continuity of a visual scene as much as an external change does. We recorded the responses of 103 single visual cortical neurons in two rhesus monkeys (V1: n = 38, V2: n = 19, V3V/VP: n = 30, V4V: n = 16) to the onset and offset of a visual stimulus that was elicited by four different conditions: 1) stimulus flashed on and off while the eyes remain fixed; 2) stimulus turned on and off along with the entire scene (external darkening); 3) stimulus constant, onset and offset induced by rapid saccadic eye movements; and 4) offset induced by an eyeblink. For most neurons the onset and offset of a visual stimulus elicited qualitatively similar responses regardless of condition. We found no systematic effect of different conditions across the neuronal population. Previously we have shown that when the visual scene is occluded by a blink V1 neuronal firing declines in a similar manner as when the external scene is darkened and the eyes left open. Here we show that this is also the case in V2, V3V/VP, and V4V. However, for a substantial minority of neurons, the response varied strongly as a function of the transient event. This overall pattern was the same in all four cortical areas studied here. We hypothesize that most neurons in visual cortex constitute a passive "filter bank", analyzing the scene for specific details regardless of condition. However, there are neurons that respond in a qualitatively different manner depending on how a stimulus is presented, and we hypothesize that these signals may be important for determining the perceptual salience of a visual event.
In this study the effect of sleep deprivation on specific components of eye and eyelid movement was investigated in a group of young and healthy subjects. The duration of sleep deprivation was 20 h. Each subject had to execute different saccade tasks: reflexive saccades, voluntary prosaccades and antisaccades. Saccade latency, number of saccade errors and blink rate during the saccade tasks were evaluated as predictors of performance decrements resulting from sleep deprivation. The present study showed no significant deterioration of latency and number of errors in the different saccade tasks. However, the blink rate was significantly higher after a night without sleep than before. It is concluded that the blink rate appears to be a promising psychophysical measurement and a more sensitive parameter than saccade performance to evaluate the effects of 20 h of sleep deprivation. These results encourage further research on this topic.
Blink reflexes, elicited by flashes of light, tone bursts and electrical stimuli, as well as checkerboard reversal visual-evoked potentials and brain stem auditory evoked potentials were investigated in 55 patients with different degrees of diagnostic probability of multiple sclerosis. It is demonstrated that electrically and acoustically elicited blink reflexes are simple but rather sensitive methods of indicating brain stem lesions. They should be used complementarily with brain stem auditory potentials. Flash-elicited blink reflexes, although sensitive, are thought to be of minor importance, since they give only restricted localizing information.
PURPOSE: To examine temporal changes in the optical quality of the air-tear film interface at the anterior cornea after a blink. METHODS: Corneal aberrations were determined in fifteen healthy subjects at 1 second time intervals after a blink, up to a total elapsed time of 15 seconds. Corneal aberrations were obtained from corneal elevation maps measured using a Tomey TMS-2N topographer and custom software. All data were decomposed using Zernike polynomials to yield the root mean square (RMS) wavefront deviations, in micrometers, for two pupil diameters (3 and 7 mm). RESULTS: Total wavefront aberration decreased slightly with time in the first few seconds after a blink for both pupil diameters, reaching a minimum after approximately 6 seconds. Thereafter aberrations increased steadily, exceeding the immediate postblink level after approximately 10 seconds. CONCLUSIONS: In normal subjects, the contribution of the anterior cornea to the overall ocular aberration remains reasonably stable over the normal interblink interval (approximately 4 seconds) but rises to levels which could perceptibly degrade retinal image quality under circumstances where the interblink interval is increased to exceed 10 seconds, as may occur during the use of visual display screens or when performing difficult tasks.
The acoustic startle response (ASR) and a range of psychophysiological parameters were evaluated during a continuous intravenous administration of cholecystokinin-tetrapeptide (CCK-4) in healthy volunteers. Subjects (n=28) were randomly assigned to double-blind infusion of either CCK-4 (0.5 mg/60 min) or placebo. The ASR sessions were performed prior to infusion and at 20 min and 50 min after the onset of infusion by recording eye-blink response to a series of acoustic stimuli (110 dB, 40 ms). An effect of CCK-4 on the eye-blink startle was observed in the first half of infusion. CCK-4 produced an increase of eye-blink startle amplitude from baseline values in contrast to the decrease observed at this time point with placebo. A mild increase in anxiety and heart rate followed by fatigue was reported with CCK-4. Administration of CCK-4 produced increases in plasma concentrations of adrenocorticotropic hormone, cortisol, prolactin and growth hormone. The results of this study show that a prolonged intravenous administration of CCK-4 may be a useful challenge method for further studies on the role of CCK system in the modulation of human anxiety and stress response.
Twenty-three patients diagnosed as depressed and a matched group of normal subjects were interviewed on three occasions using standardised procedures. Their behaviour was quantified from video recordings. The results indicate that blink rate is increased in depression and falls to normal levels during treatment. The effect on blink rate was found to be independent of medication, but was related to the degree of improvement in the patients' condition. By contrast a sample of schizophrenic patients seen on one occasion showed a reduced blink rate which was probably a result of neuroleptic administration.
The effect of blinks on the saccade frequency before the onset of step ramp smooth pursuit was assessed in healthy controls. Blinks elicited before smooth pursuit onset suppressed saccades in contrast to a control and a gap paradigm. The source of blink associated suppression of saccades remains unclear but is probably not caused by visual signals or the omnipause neurons.
We studied two patients who could make saccades of normal velocity and amplitude only in association with a simultaneous blink. In one patient, the initiation of saccades was also facilitated by blinks. Both patients had signs of cerebellar or brainstem dysfunction, suggesting a posterior fossa localization for blink facilitation of saccadic velocity and amplitude.
We studied 12 patients with spasmodic dysphonia (SD) and 12 healthy control subjects. The patients, who had no symptomatic involvement of the eyes, were evaluated for increased excitability of blink reflexes, which is characteristic of blepharospasm and generalized dystonia. We measured symptom severity from sound spectrograms of five sentences, including sentence production time, number of pitch phonatory breaks, and percentage of aperiodic phonation. We evoked blink reflexes by electrical and mechanical stimulation, and assessed excitability by obtaining excitability recovery curves and responses to trains of stimuli. Patients and controls differed from each other in test R2 amplitude attenuation across all intervals from 150 to 1,000 msec to electrical and mechanical stimulation. Our results indicate that patients with SD have increased excitability of blink reflexes, which suggests that the dystonia involves not only the larynx but also other anatomical structures.
Compulsive behavior in Prader-Willi syndrome is well-documented, though the neurochemical basis of these behaviors remains unknown. We studied a group of 16 people with Prader-Willi syndrome and a comparison group of 19 people with intellectual disability. Using eye-blink rate as an indirect measure of central nervous system dopamine, we found a higher eye-blink rate in the Prader-Willi syndrome group and a relationship between compulsive behavior and eye-blink rate across both groups. Our findings indicate a relationship between compulsions and an indirect measure of dopamine in people with intellectual disability. Our findings may provide evidence for a gene-brain-behavior link between dopamine levels and GABAergic mechanisms in individuals with Prader-Willi syndrome.
Damage to the peripheral nervous system is particularly frequent in leprosy patients. Trigeminal and facial nerves are among the most commonly affected. The aim of our study was to evaluate the efficacy of the blink reflex as a method for diagnosis of cranial nerve involvement in people affected by leprosy. We studied 37 affected people (mean age: 38 yrs, 20 female and 17 male) and 35 age-matched healthy subjects (mean age: 34 yrs, 20 female and 15 male). Blink reflexes were obtained after unilateral electrical stimulation of the supraorbital nerve for quantitative analysis of 3 responses, early ipsilateral phasic component (R1), late ipsilateral tonic component (R2i), and late contralateral tonic component (R2c). Nerve conduction parameters were studied in all subjects. The latencies of both the ipsilateral early phasic component (R1) and bilateral late tonic components (R2i and R2c) in people affected by leprosy were significantly prolonged compared with the controls. Out of 37 people affected by leprosy, 22 (59%) showed abnormalities R1 latency, 28 (75%) R2i latency and 31 (83%) R2c latency. No correlation was observed between prolonged latencies and duration of the disease. We conclude that blink reflex testing, which can be easily and rapidly performed in an EMG laboratory using standard equipment, can provide useful and objective information for the diagnosis of cranial nerve lesions and for the determination of the degree thereof.
Laser belonging to class 2 emit in the visible part of the spectrum. The power is limited to 1 mW in the CW mode. Up to now the protection of the eyes has been supposed to be given by the blink reflex for incidentally intrabeam viewing in many regulations. In 3 field trials with 519 test persons we have shown that only 15.9% at 670 nm, 17.2% at 635 nm, and 20.3% at 532 nm had a blink reflex under laser irradiation. An analysis of the results showed neither significant differences concerning the age and the gender of the test persons nor whether they were wearer of glasses or right sighted. The frequent lack of the blink reflex demands organizational measures like instruction using laser class 2 in medical and other applications.
Benign essential blepharospasm (BEB) is a focal cranial dystonia affecting eye closure. Here, we tested the hypothesis that BEB is associated with abnormal plasticity of the neuronal circuits mediating reflex blinks. In patients with BEB and healthy age-matched controls, we used the conditioning protocol introduced by Mao and Evinger (2001) to induce long-term potentiation (LTP)-like plasticity in trigeminal wide dynamic range neurons of the blink reflex circuit. High-frequency trains of electrical stimuli were repeatedly given over the right supraorbital nerve (SO) and timed to coincide with the R2 response elicited by a preceding SO stimulus. High-frequency stimulation (HFS) resulted in a long-lasting and input-specific potentiation of the R2 response in both groups, yet the facilitation of the R2 response was markedly increased in patients relative to controls. Botulinum toxin (BTX) injections in both orbicularis oculi muscles normalized the previously enhanced LTP-like plasticity of the R2 response. The increased responsiveness to HFS provides first-time evidence that LTP-like plasticity is increased in the trigeminal reflex circuit of patients affected by BEB. The results also show that the enhanced modifiability is not fixed in BEB, because BTX injections can transiently restore normal LTP-like plasticity. We propose that an abnormal corneal input induced by excessive blinking exacerbates increased LTP-like plasticity in BEB. BTX treatment removes the latter and restores plasticity toward normal values. Our results support the concept that maladaptive reorganization contributes to the pathophysiology of focal dystonias.
We applied a new microswitch-based stimulation procedure for eye-blinking responses with a young woman with profound multiple disabilities, and compared effects of this procedure on the eye-blinking responses and smiling with the effects of a caregiver-based stimulation condition. Analysis showed that the microswitch-based stimulation procedure, with stimulation occurring contingent on eye-blinking responses, increased the frequencies of these responses significantly above the levels recorded in baseline and caregiver-based stimulation conditions. No changes in smiling frequencies occurred. Implications of the findings in terms of alertness, learning, and quality of life are discussed.
The effect of a preceding brief interruption in the illumination of a small numeral eight on the auditory startle blink was investigated in human subjects. In Exp. 1 (n = 9) trials were given in which a 20-msec. interruption of the visual stimulus preceded elicitation of the startle blink by a loud tone at intervals from 80 to 200 msec. Compared to trials on which the digit was continuously lit but the reflex was elicited, the blink was augmented at 80 msec. and depressed at longer intervals. Exp. 2 (n = 24) showed that the depressive effect peaked at about 200 msec. and did not depend upon requiring subjects to make judgements concerning the stimuli. In Exp. 3 (n = 17) dark intervals ranged from 1.25 msec. to 40 msec. and preceded the loud tone by 200 msec. Reflex effects paralleled subjects' reports: dark intervals of 10 msec. or greater reliably inhibited the reflex and subjects reported seeing the dark interval at least 50% of the time at intervals of 8 msec. or greater, suggesting that the reflex method may be useful as an alternative objective technique for measuring visual temporal resolution.
Blink reflexes were evoked at distinct times during a 3 sec foreperiod (FP) between a warning stimulus (WS) and a reaction signal (RS). Sixteen well-trained, right-handed subjects participated in the experiment. Following RS, they reacted instantaneously with a blink of the right eye. In the electrically evoked blink reflex, an early ipsilateral component (R1) with a latency of +/- 10 msec and a late bilateral component (R2) with a latency of +/- 25-40 msec could be distinguished. The peak-to-peak amplitude of R1 and the integral of R2 were computed. In the beginning of FP, R1 was enlarged as compared to control values. Toward the end of FP, a continuous rise of R1 amplitudes was seen. This increment was most pronounced in the muscle involved in the reaction following RS. R2 was inhibited immediately after WS, while no significant inhibition could be seen near the end of FP. The conclusion is that the facilitation of R1 and the disinhibition of R2 towards the end of FP reflect the preparation on the reaction after RS. The extra increment of R1 might be due to a selective extra preparation of the motoneurons of the involved muscle, although an effect of motor dominance cannot be excluded.
The involuntary blink rate is a clinical monitor of dopaminergic activity. Since there is disagreement in the literature on the relative neurochemical hemispheric asymmetry or laterality of dopamine, we studied the effects of differential forced unilateral nostril breathing on blink rate. This technique has been demonstrated to induce selective contralateral hemispheric stimulation as measured by relative increases in the EEG amplitude as well as alternating lateralization of plasma catecholamines. We used the artifact of the two-channel electro-oculogram to measure the endogenous eyeblink in an N = 1 design with 11 reversals of left vs. right hemisphere activation. There was a significant increase in blink rate (p less than .01) with right hemisphere activation, and this suggests that dopamine may be lateralized to the right cerebral hemisphere.