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At least 19 recordsLinked to original sources
PubMed1979

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

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

Adolescent↗
PubMed1990

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

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

Blinking↗
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↗
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↗
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↗
PubMed1989

Blinking and corneal sensitivity.

We have investigated the relationship between corneal sensitivity and blinking patterns. Using a group of 9 young normal subjects, measurements were made of blink patterns, central and peripheral corneal sensitivity and lid margin sensitivity both before and after use of topical corneal anaesthetic, proxymetacaine hydrochloride (Alcaine). Blink patterns were recorded through concealed filming and were later analysed in terms of blink frequency and the type of blinks (proportion of complete, incomplete, twitch and forced blinks). Blink rate was significantly lower following anaesthetic administration, but the relative proportion of blink types remained unchanged. We speculate that one of the factors responsible for normal involuntary blinks is the imminent break-up of the tear film which is sensed by the cornea.

Adult↗
PubMed1988

Physiology of normal and abnormal blinking.

Blink rate is determined by many factors, including local eye irritation, the state of the corneal tear film, factors related to general visual function, the amount of general facial movement, cognitive variables, and the level of arousal. These factors appear to be mediated by several neuroanatomic structures (Table 2). The timing and the nature of the interrelationship between neuroanatomic structures during blinking remains to be determined. Dopamine is the neurotransmitter that is most strongly linked to blinking, exerting its effect on blinking primarily through the D2 receptor. The reduced rate in Parkinson's disease seems to implicate the nigrostriatal system. Perhaps efferents of the nigrostriatal system, such as those to the superior colliculus, are primarily involved, as suggested by the reduced blinking in PSP. Changes in blinking produced in the sylvian aqueduct syndrome further suggest involvement of the periaqueductal structures. At best, however, these conclusions are tentative, as the biochemical neuroanatomy will probably prove more complicated than suggested by the initial studies using the dopaminergic paradigm. Nevertheless, insofar as blink rate represents a noninvasive probe of CNS dopamine activity, the failure to associate dyskinesias (except levodopa-induced dyskinesia) with increased blinking, indicates that the pathophysiology of these conditions may not involve hyperactivity of CNS dopamine systems. Fittingly, the current clinical potential of blink rate seems maximal in parkinsonism, both to follow the severity of the illness and to monitor side effects of dopamine agonist treatment.

Animals↗
PubMedDate not supplied

Effects of general anesthesia on the human blink reflex.

The blink reflex was studied in 10 patients undergoing elective procedures under general anesthesia. Anesthetic agents were isoflurane, halothane, nitrous oxide, methohexital, and thiopental in various combinations. At induction, blink reflexes were diminished by low-dose thiopental (1-1.5 mg/kg) and abolished by high-dose thiopental (4-8 mg/kg) and methohexital (1.5 mg/kg). Blink reflexes were absent during halogenated volitile inhalational anesthesia and did not return until patients were in the recovery room, well after end-tidal anesthetic levels were zero by mass spectroscopy. Recovery of consciousness and the ability to blink on command often preceded return of any blink reflex activity, indicating that the blink reflex is not useful as a postoperative test of facial nerve function in the operating room after anesthesia. In six patients, blink reflexes were still diminished 2-3 hours after cessation of anesthesia, at a time when patients were fully oriented and corneal and eyelid reflexes were clinically normal. This finding suggests that the blink reflex might be a sensitive test of subtle CNS dysfunction after inhalational anesthesia and potentially could serve as a useful objective indicator of recovery from anesthesia for outpatient surgery.

Adult↗
PubMed1992

Effect of task difficulty and interstimulus interval on blink parameters.

The effects of task difficulty and interstimulus interval (ISI) on blink rate, blink latency and blink duration, were studied in a modified Sternberg memory task in which either two or six characters were to be memorized. Stimuli were presented in ISI blocks at either 5.3 or 9.3 s (SOAs of 6 or 10 s). While blink rate and blink duration declined prior to each stimulus, the difficulty of the expected task (the length of the memory set) did not affect the rate of decline or the final prestimulus level. Concerning ISI, blink rate declined more rapidly during shorter ISIs but the final prestimulus level, as was the case with task difficulty, was unaffected by the ISI duration. Presentation of the 6-character memory set produced a marked immediate inhibition of blinking. The data suggest that the encoding of visual stimuli is more akin to processes invoked in preparation for input than to ensuing processing stages since both encoding as well as preparation are accompanied by inhibition of blinking.

Adolescent↗
PubMed1990

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↗
PubMed1978

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↗
PubMed1991

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↗
PubMed1989

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↗
PubMed1989

The relationship between eye-winking tics, frequent eye-blinking and blepharospasm.

A family is reported in which three generations were affected with eye-winking tics and/or blepharospasm. The proband developed eye-winking tics in childhood and then developed excessive blinking progressing to blepharospasm by the age of 21 years. His mother presented with Meige's syndrome and spasmodic torticollis at the age of 59 years; his uncle had blinked excessively from his early forties. His eldest son developed an eye-winking tic with facial grimacing at the age of 8 years, and in another son, a self-limiting period of eye-blinking occurred at the age of 4 years. The recovery cycle of the blink reflex was abnormal in all three generations. Three other children with eye-winking tics have a parent or close relative with frequent eye-blinking or blepharospasm. Five patients with adult-onset blepharospasm or Meige's syndrome are also described who had excessive eye-blinking dating back to childhood. It is suggested that eye-winking tics, frequent blinking and blepharospasm may share common pathophysiological mechanisms; the clinical expression may be age-related.

Adolescent↗
PubMed1978

A simple device to improve blinking.

A blink beeper was devised to remind patients with incomplete or infrequent blinking to blink completely and at normal intervals; the beeper worked by transmitting an audible tone every ten seconds through an earphone. In three postkeratoplasty patients, this simplistic approach not only resulted in a complete blink at regular intervals, but seemed to condition this response to continue when the blink beeper was taken away; this resulted in healing of large chronic epithelial defects. The blink beeper has also proved valuable in patients with either punctate epithelial erosions or those who wore hard contact lenses unsuccessfully because of infrequent or incomplete blinking.

Adolescent↗
PubMed1990

Seasonal independence of low prolactin concentration and high spontaneous eye blink rates in unipolar and bipolar II seasonal affective disorder.

Twenty-four subjects with seasonal affective disorder (SAD: bipolar II, n = 14; unipolar, n = 10) and 20 normal controls were assessed for early follicular basal serum prolactin (PRL) concentration in winter and summer. Luteal basal PRL concentration was assessed in winter. The PRL values represented the mean of three values derived during a 45-minute period. A subset of 17 subjects with SAD and 11 controls were also assessed for spontaneous eye blinking via a polygraphic recording in winter and summer. In winter, compared with controls, subjects with SAD were characterized by significantly lower follicular (10.1 vs 4.5 micrograms/L, respectively) and luteal (14.4 vs 7.4 micrograms/L, respectively) PRL values and by significantly higher eye blink rates (30 vs 61 blinks per 3 minutes, respectively). In summer, controls and subjects with SAD showed similar significant differences in follicular PRL values (9.3 vs 3.9 micrograms/L, respectively) and eye blink rates (25 vs 67 blinks per 3 minutes, respectively). No significant differences in PRL values or eye blink rates were found between the bipolar II and unipolar forms of SAD in either season. Results were discussed in terms of dopamine functioning.

Adult↗
PubMedDate not supplied

Blinks as an index of cognitive activity during reading.

Horizontal and vertical EOG recordings of eye movements were analyzed to determine the spatial and temporal distribution of blinks and the patterns of eye movements (saccades and fixation pauses) exhibited by six subjects during the reading of stories presented in two formats (on paper and on a VDT). The frequency and placement of blinks was not affected by the presentation condition. Blinks were determined to be non-randomly distributed during reading. Significantly more blinks (36%) occurred in conjunction with saccades than the proportion of time consumed by saccades (12%) would predict. Significantly more blinks (36%) occurred in the vicinity of line change saccades, which accounts for 15% of reading time, and with fixation pauses associated with regressions (42%), which accounts for 26% of reading time, than with fixation pauses during normal reading (22%), which accounts for 60% of reading time. The results of the study suggest that blink behavior during reading is under perceptual and cognitive control.

Adult↗
PubMed1991

MPTP lesions and dopaminergic drugs alter eye blink rate in African green monkeys.

Eye blink rates were studied in African green monkeys following relatively specific destruction of substantia nigra and its dopamine projections with the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Monkeys treated with MPTP had a significantly lower blink rate than controls over a period from two to five and a half months after treatment. Furthermore, the degree of parkinsonism expressed in treated animals was inversely correlated with blink rate. Pharmacologic studies further supported the role of dopamine receptors in the regulation of blink rate. PHNO (4-propyl-9-hydroxynaphoxazine), a potent and highly specific D2 agonist, effective in alleviating parkinsonism, caused a significant transient increase in blink rate, while sulpiride, a D2 antagonist, caused a decrease and blocked the effect of PHNO. Apomorphine and haloperidol, although less specific, had potent and predictable effects based on their interactions with dopamine systems. Blink rate may provide a nonintrusive measure of central dopamine activity that would help to evaluate the progress of Parkinson's disease or treatments which attempt to restore dopamine function.

Animals↗