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PubMed2004

Diagnosis of vestibular imbalance in the blink of an eye.

BACKGROUND: In a recent study, the authors found that blinks in healthy volunteers always triggered ocular torsion quick phases during dynamic roll movements of the head. On the basis of this observation, they hypothesized that blinks in patients with a vestibular tone imbalance would also trigger torsional quick phases. METHODS: Using video-oculography with a fixation target, the authors recorded the ocular torsion position of the left eye of 37 participants while they made voluntary blinks once every 6 to 10 seconds. The participants were recruited from four groups: two age groups of healthy volunteers with a mean +/- SD age of 32 +/- 4 (n = 9) and 65 +/- 11 y (n = 9); patients with a unilateral vestibular disorder in an acute state (n = 12, 53 +/- 17 y); and those in a persisting state in which spontaneous nystagmus had already faded (n = 9, 65 +/- 13 y). RESULTS: In the control groups of healthy volunteers, blinks triggered no or only small quick phases on the order of 0.1 deg. In both patient groups blinks always triggered quick phases with significantly higher amplitudes of 1.85 +/- 1.02 deg and were followed by exponentially decaying slow-phases with time constants on the order of 1 to 2 seconds. Patients in the persisting state clearly differed from patients in the acute state in that their torsional spontaneous nystagmus had already vanished due to vestibular compensation. But surprisingly, these two groups did not show a large difference in terms of the effect of blinks on ocular torsion. The authors always observed torsional quick phases with the upper pole of the eye beating away from the side of the lesion. CONCLUSIONS: Blinks are able to trigger torsional quick phases in patients with both acute and persisting vestibular disorders. The side of the impairment can be determined from the direction in which the eye is rotated after a blink. Thus, ocular torsion recordings during blinks can be used as a simple clinical test for a vestibular tone imbalance, particularly during a persisting failure in which spontaneous nystagmus has resolved and can therefore no longer be used for diagnosis.

Adult↗
PubMed1999

Cortical activation patterns during voluntary blinks and voluntary saccades.

OBJECTIVE: To investigate the activation of frontal, parietal, and occipital areas in normal volunteers during voluntary blinks and during voluntary saccades using functional MRI (fMRI). BACKGROUND: A previous fMRI study revealed the activation of the precentral and posterior middle frontal gyrus ("frontal eye field" [FEF]), the medial part of the superior frontal gyrus ("supplementary eye field" [SEF]), and the visual cortex. The parietal cortex was not included in this study. Frontal and occipital cortical areas involved in voluntary blinking have not been shown previously using fMRI. METHODS: A 1.5-T standard clinical scanner was used for both anatomic and functional studies in 12 observers. To conduct data analyses the authors used voxel-by-voxel cross-correlation. RESULTS: Voluntary blinks led to the activation (p < 0.05) of the FEF, the SEF, the posterior parietal cortex ("parietal eye field" [PEF]), and the visual cortex. Voluntary blinking produced activity in the same cerebral structures as voluntary saccades. However, the number of activated voxels was smaller during voluntary blinking than during voluntary saccades in the visual cortex and in the FEF (p < 0.01). In contrast, the extent of activation was significantly higher (p < 0.003) in the SEF and in the PEF during voluntary blinking. CONCLUSIONS: Voluntary blinks and saccades are associated with similar loci of activation patterns; however, the quantitative distribution of activation suggests that the middle part of the frontal gyrus and posterior parietal cortex are of special significance for voluntary blinks. The results argue for the importance of considering quantitative distributional properties of parallel cortical activities associated with saccades and blinks.

Adult↗
PubMed1999

[Arousal level and blink activity].

The purpose of this study was to investigate the relationship between arousal level and blink activity; blink rate, blink amplitude and blink duration. Blink activity was examined under two different tasks in which arousal level was manipulated. One was a vigilance task (Experiment 1) for comparatively high arousal level. The other was a simple counting task in a dark and quiet room (Experiment 2) for extremely lower arousal level. Results indicated that blink rates and blink durations tended to increase as arousal level got lower in the monotonous vigilance task situations, meanwhile, blink rates and blink amplitudes decreased as a function of negative arousal level in the pre-sleep situation.

Adult↗
PubMed2004

Cortical potentials associated with voluntary, reflex, and spontaneous blinks as bilateral simultaneous eyelid movement.

Movement-related cortical potentials (MRCPs) associated with the contraction of m. orbicularis oculi related to three types of blinks (voluntary, reflex, and spontaneous) were measured for 12 normal subjects. The purpose of the present study was to estimate the role of the cerebral cortex in close association with the blinks caused by bilateral simultaneous eyelid movements. MRCPs were recorded by surface electrodes placed over the frontal to the parietal regions. The mean amplitude and the duration of the MRCPs for the three types of blinks were evaluated by an averaging technique for each subject. MRCPs for the voluntary blinks were evoked in all subjects. For the reflex and the spontaneous blinks, however, a clear negative rising deflection from the baseline was not obtained. The maximum amplitude of the MRCPs for the voluntary blinks was localized at the vertex region, though there was no significant difference between the durations of the MRCPs for the vertex region and for the other regions. Moreover, the positive potential following the voluntary and the spontaneous blinks was recognized in the parietal region. These results suggest that only the voluntary blinks are caused by the neural activation of the supplementary motor area (SMA), and in addition, the neural activation related to visual recognition is considered to be elicited by the voluntary and the spontaneous blinks.

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↗
PubMed1996

An explanation for reflex blink hyperexcitability in Parkinson's disease. I. Superior colliculus.

Hyperexcitable reflex blinks are a cardinal sign of Parkinson's disease. We investigated the neural circuit through which a loss of dopamine in the substantia nigra pars compacta (SNc) leads to increased reflex blink excitability. Through its inhibitory inputs to the thalamus, the basal ganglia could modulate the brainstem reflex blink circuits via descending cortical projections. Alternatively, with its inhibitory input to the superior colliculus, the basal ganglia could regulate brainstem reflex blink circuits via tecto-reticular projections. Our study demonstrated that the basal ganglia utilizes its GABAergic input to the superior colliculus to modulate reflex blinks. In rats with previous unilateral 6-hydroxydopamine (6-OHDA) lesions of the dopamine neurons of the SNc, we found that microinjections of bicuculline, a GABA antagonist, into the superior colliculus of both alert and anesthetized rats eliminated the reflex blink hyperexcitability associated with dopamine depletion. In normal, alert rats, decreasing the basal ganglia output to the superior colliculus by injecting muscimol, a GABA agonist, into the substantia nigra pars reticulata (SNr) markedly reduced blink amplitude. Finally, brief trains of microstimulation to the superior colliculus reduced blink amplitude. Histological analysis revealed that effective muscimol microinjection and microstimulation sites in the superior colliculus overlapped the nigrotectal projection from the basal ganglia. These data support models of Parkinsonian symtomatology that rely on changes in the inhibitory drive from basal ganglia output structures. Moreover, they support a model of Parkinsonian reflex blink hyper-excitability in which the SNr-SC target projection is critical.

Animals↗
PubMed1996

Differential effects of direct and indirect dopamine agonists on eye blink rate in cynomolgus monkeys.

Spontaneous eye blink rate was assessed in cynomolgus monkeys treated intramuscularly with the high-efficacy dopamine (DA) agonists, (-)-apomorphine, naxagolide, PD 128,907, 2-(N-phenylethyl-N-propyl)amino-5-hydroxytetralin (+/-)-PPHT, quinpirole, SKF 81297 and SKF 82958; the low-efficacy DA agonists, (-)-3-PPP, roxindole, SDZ 208-912, SKF 75670 and terguride; and the indirect DA agonists, d-amphetamine, cocaine, GBR 12935 and methylphenidate. All of the direct DA agonists, with the exception of the partial agonists SDZ 208-912 and terguride, produced significant, dose-related elevations in blink rate. In contrast, none of the indirect agonists increased blink rates when administered over a relatively wide, behaviorally active dose range. These differences suggest either that indirect agonists do not interact with mechanisms involved in eye blinking, or that they have other effects which prevent blink-rate increases. The latter does not appear to be the case because cocaine failed to alter the blink rate-increasing effects of the D1 agonist, SKF 81297, which suggests that indirect agonists do not mask their own ability to induce blinking. Overall, the results further characterize the involvement of DA receptors in the mediation of spontaneous eye blinks, reveal differential effects of direct and indirect agonists and suggest new directions for research into the neuroanatomical basis of DA-mediated spontaneous eye blinks.

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↗
PubMed2006

Eyelid movements during blinking in patients with Parkinson's disease.

We examined eyelid movements during spontaneous, voluntary, and trigeminal reflex blinks in 16 patients with mild to moderate Parkinson's disease (PD) off medication and 14 controls. Voluntary and reflex blink amplitudes tended to be smaller than normal for PD patients, whereas eyelid kinematics (amplitude-maximum velocity relationship) for all three blink types were normal. Spontaneous blink rate was less than normal for 10 patients and abnormally high for 6 patients. A significant positive correlation between spontaneous blink amplitude and blink rate was found. These observations suggest that PD modifies the gain of a premotor blink circuit shared by spontaneous, voluntary, and reflex blinks.

Adult↗
PubMed1986

Anatomical observations on the afferent projections to the retractor bulbi motoneuronal cell group and other pathways possibly related to the blink reflex in the cat.

In the cat retractor bulbi (RB) muscle reflexively retracts the eye ball into the orbit. This reflex action is called the nictitating membrane response which, together with the reflex contraction of the orbicularis oculi muscle, constitutes the blink reflex. The retractor bulbi (RB) motoneuronal nucleus is a small cell group located in the lateral tegmentum of the caudal pons, just dorsal to the superior olivary complex. The nucleus is identical to the accessory abducens nucleus and sends its fibers through the abducens nerve. Autoradiographical tracing results indicate that the RB nucleus receives some fibers from the principal and rostral spinal trigeminal nuclei and from the dorsal red nucleus and dorsally adjoining tegmentum. The same areas project to the intermediate facial subnucleus, containing motoneurons innervating the orbicularis oculi muscle. It is suggested that the trigeminal projections take part in the anatomical framework for the R1 component of the blink reflex. Two other brainstem areas i.e.: a portion of the caudal pontine ventrolateral tegmental field and the medullary medial tegmentum at the level of the hypoglossal nucleus were also found to project to the RB motoneuronal cell group and to the intermediate facial subnucleus. These projections were much stronger than those derived from the trigeminal nuclei and red nucleus. Moreover, the medullary premotor area projects not only to the blink motoneuronal cell groups but also to the pontine premotor area. It is suggested that both areas are involved in the R2 blink reflex component. The medullary blink premotor area receives afferents especially from oculomotor control structures in the reticular formation of the brainstem while the pontine blink premotor area receives afferents from the olivary pretectal nucleus and/or the nucleus of the optic tract and from the dorsal red nucleus and its dorsally adjoining area. Because the oculomotor control structures in the reticular formation (by way of the superior colliculus) and the red nucleus receive afferents from trigeminal nuclei, they may play an important role in tactually induced reflex blinking, while the pretectum could take part in the neuronal framework of the visually induced blink reflex.

Afferent Pathways↗
PubMed1983

Relationships between characteristics of electrical stimulation, muscle pain and blink responses in man.

The present research was undertaken in 11 healthy volunteers with the aim of investigating the relationship between blink response, a feature of the startle reaction, and muscular pain evoked by muscle electrical stimulation (train of stimuli). At a repetition rate of 0.1 Hz, a close relationship was found between the threshold for muscle pain and that for the blink response, without apparent habituation. At the same rate and with stimulation intensity maintained at pain threshold, the subject could voluntarily inhibit the blink response, but not pain. Under the same conditions both pain and blink response were inhibited during a mental task. By increasing the current intensity pain became more intense and the blink response tended to increase in amplitude and to decrease in latency. Similar effects were achieved by increasing the repetition rate with the current intensity maintained at pain threshold. Habituation of the blink response, but not of pain, was found at repetition rates of 1 Hz or more. Present results indicate that nociceptive inputs from muscle have a facilitatory effect on central mechanisms subserving the blink response. It is suggested that the comparative analysis of pain sensation and the blink response may be a useful tool for pain research in man.

Adult↗
PubMed1995

Spectral characteristics of blink suppression in normal observers.

Previous studies of the characteristics of suppression occurring under various visual conditions show similarities and differences which may indicative of the mechanism of suppression. The primary purpose of this study was to determine if the suppression that occurs in response to an eyelid blink (blink suppression) is similar to that which occurs during a saccade (saccadic suppression). In addition, the characteristics of blink suppression and other forms of suppression (i.e. permanent and binocular rivalry suppression) are compared. A test probe paradigm was utilized to determine the effect of blink suppression on the spectral sensitivity function in three normal observers. Employing a two alternative forced choice technique, thresholds were determined for wavelengths from 420 to 680 nm in 20 nm steps. At each wavelength, the threshold was determined at 0 and 400 msec after the onset of a voluntary blink. The magnitude of suppression was taken as the difference between the 0 and 400 msec thresholds. Similar to saccadic suppression, the magnitude of blink suppression increased as the stimuli biased detection towards the luminance channel. These results suggest that blink suppression and saccadic suppression are the result of a single mechanism. Similarities between blink suppression and other forms of visual suppression are also considered.

Blinking↗
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↗
PubMed2006

The blink reflex in "chronic migraine".

OBJECTIVES: Activation of the trigeminovascular system and sensitisation of brainstem trigeminal nuclei are thought to play an important role in migraine. The aim of this study was to investigate the blink reflex and its habituation in patients with "chronic migraine". METHODS: We studied 35 patients suffering from "chronic migraine" (IHS classification criteria) outside and during a spontaneous attack, and 35 control subjects. An EMG device with a specific habituation test program was used to elicit and record blink reflex responses and to randomly repeat stimulations at different time intervals so as to induce habituation. RESULTS: The R(1) and R(2) latencies, amplitudes and areas of the basal blink reflex were similar in patients studied both outside and during an attack as well as in control subjects, whereas the blink reflex habituation responses were markedly reduced in patients studied outside an attack. The percent changes in the R(2) areas from the baseline values, obtained when stimuli were delivered at time intervals of 10, 5, 4, 3, 2 and 1s, were statistically different (p<0.01-p<0.001) from those of the same patients studied during a migraine attack and of those of control subjects. There was a significant correlation between decreased habituation of the blink reflex and a higher frequency of attacks. The stimulus intensities of the blink reflex (multiples of the detection threshold intensities) were significantly lower (p<0.001) on the side affected, or more severely affected, by headache in patients studied during a migraine attack. CONCLUSIONS: The decreased habituation of the blink reflex outside an attack reflects abnormal excitability in "chronic migraine", which normalizes during the attacks. The inverse correlation between the frequency of attacks and habituation responses confirms the abnormal excitability induced by the high frequency of attacks. Central sensitisation mechanisms (allodynia) may explain the lower detection thresholds observed on the side affected by headache in patients during the attacks. SIGNIFICANCE: The blink reflex and its habituation may help shed light on the subtle neurophysiological changes that occur in migraine patients between and during attacks.

Adult↗
PubMed1997

A comparison of saccadic and blink suppression in normal observers.

Recent research suggests that blink and saccadic suppression are produced by the same mechanism (Volkmann, 1986; Uchikawa & Sato, 1995; Ridder & Tomlinson, 1993, 1995). These studies demonstrated that blink and saccadic suppression have the same effect on various visual functions. However, none of these studies made a comparison of blink and saccadic suppression in the same individual. The purpose of this study was to compare the effects of blink and saccadic suppression on contrast sensitivity functions in the same subject. The effect of saccadic suppression on the contrast sensitivity function in three normal observers was determined. Employing a two-alternative, forced-choice technique, thresholds were measured for seven spatial frequencies. At each spatial frequency, the threshold was determined immediately following detection of a voluntary saccade. The magnitude of suppression was taken as the log ratio of the contrast sensitivities obtained while foveating the stimulus and those obtained during saccades. The magnitude of saccadic suppression was found to increase as the saccade amplitude increased and to be spatial-frequency dependent. Low spatial frequencies were suppressed more than high spatial frequencies. The blink suppression data have been measured previously (Ridder & Tomlinson, 1993). Saccadic and blink suppression were qualitatively similar. A vertical shift of the data brought the saccadic and blink suppression data into register. These results suggest that blink and saccadic suppression are produced by the same or similar mechanisms.

Blinking↗
PubMed2001

Kalman filter detection of blinks in video-oculography: applications for VVOR measurement during locomotion.

A Kalman filter algorithm was implemented for automatic detection of blink artifacts in video-oculography (VOG) data, and a cubic spline used to patch the eliminated data. The algorithm was tested by randomly introducing artificial blinks into eye movement data and computing the errors introduced by the patches. We also computed visual vestibulo-ocular reflex (VVOR) gain and phase in healthy and vestibulopathic subjects during a locomotor task, before and after blink removal, to demonstrate the interpretive importance of eliminating blink artifacts. The error introduced by the patched data was small (0.50+/-0.32 degrees ) and within the resolution of head angle measurements. Comparison of gain and phase shift before and after removing blinks revealed that even when calculated values are within expected limits, coherence of the VVOR signal was significantly (p=0.003) lower prior to blink removal (0.51+/-0.37) compared to that after blink removal (0.92+/-0.08). Comparison of VVOR calculations between healthy and vestibulopathic subjects (after removal of blinks) revealed that vestibulopathic subjects had significantly decreased gains (p=0.018) and increased phase shifts (p=0.009): these results agree with data reported in literature. We conclude that the Kalman filter detection and cubic spline patching algorithms are useful tools for VOG and should enable reliable VVOR measurements during unconstrained, ecologically meaningful locomotor activities.

Adult↗
PubMed2003

Lead stimulus modality change and the attentional modulation of the acoustic and electrical blink reflex.

Two experiments investigated the effects of the sensory modality of the lead and of the blink-eliciting stimulus during lead stimulus modality change on blink modulation at lead intervals of 2500 and 3500 ms. Participants were presented with acoustic, visual, or tactile change stimuli after habituation training with lead stimuli from the same or a different sensory modality. In Experiment 1, latency and magnitude of the acoustic blink were facilitated during a change to acoustic or visual lead stimuli, but not during a change to tactile lead stimuli. After habituation to acoustic lead stimuli, blink magnitude was smaller during tactile change stimuli than during habituation stimuli. The latter finding was replicated in Experiment 2 in which blink was elicited by electrical stimulation of the trigeminal nerve. The consistency of the findings across different combinations of lead stimulus and blink-eliciting stimulus modalities does not support a modality-specific account of attentional blink modulation. Rather, blink modulation during generalized orienting reflects modality non-specific processes, although modulation may not always be found during tactile lead stimuli.

Acoustics↗
PubMed2000

Habituation of the blink reflex in first-episode schizophrenia, psychotic depression and non-psychotic depression.

OBJECTIVE: Electrophysiological recording of the electrically elicited blink reflex is the most reliable method of investigating habituation of the startle reflex. The purpose of this study was to compare the habituation and the late R3-component of the blink reflex between control subjects (N=19) and first-episode patients with schizophrenia (N=17), psychotic depression (N=23), and severe non-psychotic depression (N=25). METHODS: The blink reflex was evoked by electrical stimulation of the supraorbital nerve, and the deficient habituation of the R2i-component was measured with a computer-assisted integral area measurement. Prefrontal executive function of the patients was assessed with the Wisconsin Card Sorting Test. Current psychiatric symptoms were assessed with the Brief Psychiatric Rating Scale, the Hamilton Depression Scale, the Positive and Negative Syndrome Scale, and the Calgary Depression Scale. RESULTS: Deficient habituation of the blink reflex and occurrence of the late R3 component were associated both with a previous diagnosis of psychotic disorder and with the presence of current psychosis. The sensitivity and specificity of the abnormal habituation of the blink reflex in detecting psychotic disorder were 0.50 and 0.80, respectively. The abnormalities of the blink reflex were not associated with psychotropic medication. In schizophrenic patients, defective habituation of the blink reflex was associated with negative and cognitive symptoms, and in depressive patients with the presence of delusions. CONCLUSIONS: The deficient habituation of the blink reflex and occurrence of the late R3 component seem to be both trait and state markers of a psychotic disorder. The results suggest that schizophrenia and psychotic depression share some common neurobiological mechanisms involved in the modulation of the startle reflex.

Adult↗