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Unilateral cortical spreading depression and conditioned eye blink responses in rabbits.

Conditioned eye blinking was established in the rabbit by optimally pairing a somatosensory, auditory or visual conditioned stimulus (CS) with air puff to the left eye as the unconditioned stimulus (US). After conditioned response (CR) occurred on 80-90 percent of the presentations, single waves of CSD were triggered by micro-injections of 25 percent KCL into the frontal or occipital cortex of each hemisphere. Slow potential changes (SPC) were recorded via implanted, nonpolarizable electrodes and correlated with the presence or absence of the CR. Frontal KCL injections contralateral to the blinking eye totally abolished the CR when the peak SPC invaded the motor cortex independent of the sensory modality conditioned. Recovery took place in the order: somatosensory CS (13 min), auditory CS (18 min) and visual CS (23 min). Occipital KCL injections contralaterally caused partial supression of aurally and visually conditioned eye blinking when the SPC invaded the parieto-occipital region but no such suppression occurred when using the somatosensory CS. Total abolition of the CR ensued when the wave of CSD reached the motor (frontal) cortex and again was independent of the CS modality. Similar but less striking effects were noted during ipsilateral CSD. The conclusion is drawn that whereas the cortical projection of the CS is important but not indispensable, the motor cortex is essential for the elaboration of conditioned eye blinking. A discussion of cortical localization subserving discrete conditioned reactions, as revealed by the technique of CSD, is presented.

Acoustic Stimulation↗

Seizures triggered by blinking when beginning to speak.

A patient had seizures triggered by spontaneous blinking associated with the act of beginning to speak. Diffuse paroxysmal discharges in the EEG appeared when the patient was blinking in darkness or in bright light. Closing the eyes voluntarily, on command, or as a reflex reaction produced this response very infrequently. During intermittent photic stimulation the epileptic discharges were accompanied by myoclonic jerks. The act of beginning to speak was linked with spontaneous blinking and EEG changes and was accompanied consistently by seizures. These were characterized by a peculiar stuttering and an absencelike impairment of consciousness. Seizures have been controlled well using clonazepam and valproic acid.

Blinking↗

Coexistent Meige's syndrome and myasthenia gravis. A relationship between blinking and extraocular muscle fatigue?

We studied five patients with a combination of Meige's syndrome (blepharospasm-oromandibular dystonia) and myasthenia gravis. The coexistence of two disorders impairing eyelid opening led to diagnostic confusion and delayed appropriate therapy. Detailed oculographic monitoring of one patient indicated that eye position drifting due to myasthenic oculomotor fatigue was corrected by eye blinks, and that blinks tended to occur with slower saccades. Our observations suggest that fatigue of extraocular muscles may lead to synkinetic blinking and perhaps eventually to autonomous blepharospasm.

Aged↗

The blink reflex in patients with idiopathic torsion dystonia.

The blink reflex and its recovery cycle were examined in 57 patients with idiopathic dystonia affecting different parts of the body. The group comprised 9 patients with generalized and 15 with segmental forms, 19 with torticollis, and 14 with focal arm dystonia. None had blepharospasm. The duration and amplitude of the R2 component of the blink reflex showed only minor changes. However, its recovery cycle to paired supraorbital nerve stimuli was abnormal in all groups of patients, except those with focal arm dystonia. These findings may be interpreted as showing abnormal control of the interneuronal networks mediating the blink reflex in patients with dystonia affecting sites other than the facial muscles. The fact that the principal changes were seen in patients with torticollis, and generalized or segmental dystonia, suggests that the extent of dystonia (rather than the severity) and, therefore, the close proximity to the cranial muscles was important in determining the extent of the abnormal interneuron function.

Arm↗

Blink reflexes and the silent period in tetanus.

Abnormalities of the silent period (SP) and blink reflexes occur in diseases that interfere with inhibitory pathways, such as tetanus and stiff-person syndrome (SPS). The SP is abnormal in tetanus but not in SPS. Studies of the blink reflex in tetanus are limited. In this report, a patient with generalized tetanus is described. The masseteric-and mixed-nerve SP was absent or truncated. In contrast to SPS, blink reflex studies revealed no bilateral R1 component, and a discrete R3 was only present ipsilateral to right supraorbital stimulation. This reflects the distinct inhibitory pathways underlying these disorders.

Adult↗

Masseter reflex and blink reflex abnormalities in Chiari II malformation.

Masseter reflex and blink reflex were evaluated in 64 patients with a myelomeningocele and Chiari II malformation. In 46 patients, no brainstem signs or symptoms were present. Brainstem dysfunction related to Chiari II malformation occurred in 18 patients. The masseter reflex was more frequently abnormal in the symptomatic than asymptomatic patients (P = 0.02). Although the blink reflex was similarly affected in the two groups of patients (P > 0.1), it was very sensitive, being abnormal in 83% of symptomatic and 65% of asymptomatic patients. Concomitant abnormality of masseter reflex and the late contralateral blink reflex component (R2c) was almost exclusively found in symptomatic patients and reached the highest significance in separating the two groups (P = 0.002).

Adolescent↗

Blink-induced saccadic oscillations.

A patient with a neurodegenerative disease had abnormal saccades only when he blinked. These saccades were hypermetric and were followed immediately, without any intersaccadic interval, by a large, oppositely directed saccade (dynamic overshoot). To explain these findings, we hypothesize that a blink-related neural signal can modulate the activity of pause cells that normally inhibit saccadic burst neurons during fixation. In pathological circumstances, abnormal function of pause cells could lead to large-amplitude saccadic oscillations. In normal subjects, blinks could induce short bursts of low-amplitude flutter.

Adult↗

Analysis of blink rate in patients with blepharospasm.

The blink rate (BR) during rest, conversation, and reading was assessed in 50 patients with blepharospasm (BS) and in 150 healthy subjects. BR at rest and during conversation was higher in patients with BS. Moreover, 76% of patients had BR higher at rest than during conversation, whereas in 74% of controls, BR was higher during conversation than at rest. The sensitivity and specificity of two parameters (value of BR at rest and pattern rest-BR higher than conversation-BR) in discriminating patients and controls were computed. The best fit was obtained with a rest-BR above 27 blinks per minute. When the two parameters were combined (rest-BR above 27 blinks per minute together with the pattern rest-BR higher than conversation-BR), we obtained a 92.3% sensitivity and a 82.0% specificity in discriminating between BS patients and controls. These findings indicate that specific features of BR can be associated with BS, suggesting that the analysis of BR might be helpful for the diagnosis of BS in early stages.

Blepharospasm↗

Corneal and blink reflexes in Parkinson's disease with "on-off" fluctuations.

In 13 patients with Parkinson's disease and "on-off" fluctuations and in a control group, the electrically evoked blink (R1 and R2 component) and corneal reflexes (CR), the habituation of the glabellar reflex, and the blink rate were studied. Latency, amplitude, and recovery cycle of R1 was normal. CR latency, but not R2 latency, was significantly shorter in patients than in normal subjects. R2 recovery cycle, but not CR recovery cycle, was facilitated in "off" patients in comparison to normal subjects. CR and R2 duration was longer in "off" than in "on" patients. R2 recovery cycle became similar to that of normal subjects after fluctuation from "off" to "on" period, but CR recovery cycle varied only slightly. The habituation of the glabellar reflex and the blink rate were decreased in "off" patients. These findings indicate that the enhanced excitability of R2 is related to the central dopamine activity levels. The differences between the recovery cycles of CR and R2 may be explained with the smaller number of interneurons subserving CR than R2 circuit. The shorter latency of CR, but not of R2, both in "on" and "off" patients, may suggest that in Parkinson's disease basal ganglia exert a different control of incoming sensory input transmitted via beta and delta fibers.

Adult↗

Unilateral injection of botulinum toxin in blepharospasm: single fiber electromyography and blink reflex study.

We studied six patients affected with blepharospasm (BSP). We injected botulinum toxin (BTX) around only one eye and saline solution around the other. Clinical rating of BSP was performed. Single fiber electromyography (SFEMG), compound motor action potential (cMAP) at the orbicularis oculi muscle by stimulation of the facial nerve, blink reflex, and blink reflex recovery curve were recorded. All clinical and electrophysiological investigations were carried out before, and 1, 2, and 4 weeks after treatment. Evidence of bilateral clinical benefit was provided. Following therapy, facial cMAP decreased bilaterally and SFEMG revealed statistically significant changes on both sides while the excitability curve of blink reflex remained unmodified. The results confirm that BTX affects merely the neuromuscular junctions. The clinical and neurophysiological effects are present on both sides also for unilateral injection probably because of toxin spreading.

Aged↗

Topodiagnostic value of blink reflex R1 changes: a digital postprocessing MRI correlation study.

The aim of the study was to investigate the relation of the blink reflex R1 arc to known anatomical brainstem structures. Acute vascular brainstem lesions as identified by magnetic resonance imaging (MRI) of patients with isolated R1 pathology were superimposed into a stereotactic anatomical atlas using a new method of digital postprocessing. Isolated acute brainstem lesions were documented by diffusion-weighted MRI in 12 of 24 patients with unilateral R1 pathology. The lesions were located in the ipsilateral mid- to lower pons. In three patients only, the lesion had partial contact with the principal sensory nucleus of the trigeminal nerve (PSN) on at least one level. In two patients, the lesion involved the medial longitudinal fasciculus. Most lesions were located medially and ventrally to the PSN on transverse slices. Our results underline the high localizing value of changes in the R1 component of the blink reflex in patients with ipsilateral pontine functional deficits. Although available physiological evidence suggests that the R1 component of the blink reflex traverses an oligosynaptic pathway, this MRI study does not support the view that synaptic transmission in the PSN subserves R1. The reflex arc probably descends more medially and ventrally on its course to the facial nucleus.

Adult↗

Validity of Listing's law during fixations, saccades, smooth pursuit eye movements, and blinks.

In its original formulation, Listing's law referred only to eye positions during steady fixation. In recent years, however, several studies have suggested that Listing's law can be extended to the movements of the eyes, including during saccades and smooth pursuit. A major problem in deciding whether or not Listing's law is obeyed during eye movements is the influence of any spontaneous fluctuations in torsional eye position. To try to settle this question, the three-dimensional position of the eyes (around the three axes: horizontal, vertical, and torsional) was recorded with dual search coils in five normal subjects during fixations, 20 degrees saccades, blinks, and 20 degrees pursuit movements with a 20 degrees/s stimulus velocity. Eye movements across a wide range of horizontal positions were measured at different elevations of gaze during 11 min. Variability (as reflected in the standard deviation of torsional eye position) was used as a measure of the validity of Listing's law. After linear detrending single trials, each lasting 21.5 s, to remove the effects of drift over minutes, the reduction in the standard deviation of torsional position in tertiary eye positions was 54% assuming a planar and 58% assuming a second-order curved Listing's surface. We attributed this long-term fluctuation of the torsional signal to slippage of the coil on the eye. The remaining variability was mainly due to short-term fluctuation of eye torsion over seconds. The impact of hysteresis, associated with consecutive centrifugal-centripetal horizontal movements, on the variability of torsional eye position appeared negligible. Peak increases in the standard deviation from the fixation baseline after fitting individual Listing's planes for each trial were 348% during blinks, 141% during saccades, and 72% during pursuit movements (median value of five subjects). In conclusion, Listing's law during blinks, saccades, and pursuit is less valid than during fixations, which raises doubts about the existence of an internal "Listing's law operator" for eye movements. Possibly, central eye velocity commands do not comply with Listing's law.

Blinking↗

A model system for motor learning: adaptive gain control of the blink reflex.

An important aspect of the control of movement is how the nervous system produces adaptive gain modification. To investigate this problem in a simple motor system, we studied lid movement and orbicularis oculis muscle activity in human and rabbit subjects during adaptation of reflex eye blinks. The gain of the reflex could be increased or decreased, depending upon the nature of the adaptive stimulus. Since these gain changes could persist upon removal of the adapting stimulus, adaptation appears to result from a modification of the neural program subserving the blink reflex. The orbicularis oculis electromyogram revealed that the neural modifications producing adaptive gain changes predominantly altered the longer latency components of the reflex, while the short latency components remained unchanged. Moreover, in two other paradigms that modulate the gain of reflexes, habituation and reflex modification, similar changes also occurred primarily in the longer latency components of the blink reflex. This result suggests that modification of neurons in longer latency, indirect pathways, may underlie different forms of motor learning.

Adaptation, Physiological↗

The blink reflex in neonates with a subsequent poor outcome.

We examined maturational changes in the electrical blink reflex in 11 handicapped children, i.e., 4 cases of developmental delay, 4 of cerebral palsy, 2 of congenital hydrocephalus, and 1 of congenital cytomegalovirus infection. The developmental delay and cerebral palsy cases were all born at 25-36 weeks' gestation. In all cases, prolonged latency, low amplitude, or the absence of the late component of the blink reflex was observed in the follow-up study. These results indicate that prematurity and some congenital impairment mainly influence the maturation of the long-loop reflex arc in the blink reflex.

Blinking↗

A pharmacological distinction between the long and short latency pathways of the human blink reflex revealed with tobacco.

In three, normal, human subjects, tobacco smoking was used as a pharmacological probe to modify differentially the direct and indirect pathways underlying the blink reflex. The latency of the indirect R2 component of the orbicularis oculis electromyogram evoked by electrical stimulation of the trigeminal supraorbital nerve transiently increased 20-80% after smoking, while the latency of the shorter latency, direct R1 component remained constant. The magnitude of both components of the blink reflex transiently decreased. The data demonstrate that tobacco smoking can differentially alter the long and short latency components of the blink reflex, and suggest that these effects result from modifications of central pathways sensitive to nicotine.

Adult↗

Blink reflex in patients with an ischaemic lesion of the brain-stem verified by MRI.

The electrically elicited blink reflex was investigated in 25 patients with ischaemic lesions of the pons or the medulla oblongata. Only patients with a lesion on MRI appropriate to the clinical syndrome were included. Twenty patients had an infarction of the pons, bilateral in 5. Additional 5 patients had an infarction of the dorsolateral medulla oblongata. Patients with hemispheric lesions were excluded. Four of the 5 patients with Wallenberg's syndrome showed delayed R2 components to stimulation ipsilateral to the lesion. Additional loss of the ipsilateral R1 component was observed in 1 patient. Fifteen of the 20 patients with pontine infarctions had pathological blink reflexes. All 6 patients with a unilateral pons lesion and an abnormality of R1 had this abnormality on the side contralateral to the lesion. In 3 cases with bilateral pontine infarction R1 was abnormal on one side or on either side. Of 11 patients with a normal R1, 6 had isolated abnormalities of R2 without consistent correlation to the side of the lesion. We conclude that abnormalities of the blink reflex are of minor localizing value in pontine infarction. This may be explained by the fact that a pontine infarction affects either the reflex arch itself or descending pathways that have a modulating influence on the reflex arch. Infarctions of the medulla oblongata, however, have characteristic abnormalities that have already been described.

Adult↗

The blink reflex before and after percutaneous glycerol rhizotomy in patients with trigeminal neuralgia--a prospective study of 28 patients.

The blink reflex was prospectively studied in 28 patients with trigeminal neuralgia, prior-to and following percutaneous glycerol rhizotomy to the Gasserian ganglion. Fifteen patients (54%) had varying degrees of sensory loss in the trigeminal nerve distribution already before glycerol injection. Three more patients developed sensory loss following glycerol injection. Thus following glycerol injection 18 patients had graded sensory loss. Pre-injection the blink reflex showed abnormal R1 wave in 57% patients, while direct and consensual R2 waves were abnormal in 43% and 48%, respectively. Post-injection R1 wave was abnormal in 64% patients. Direct R2 waves were abnormal in 33% patients. Thus clinical findings of sensory loss correlated well with pre-and post-injection blink reflex abnormality. Postoperatively R1 and ipsilateral R2 latencies from the side of the injection deteriorated and consensual R2 latency improved, thus, signifying better function on the contralateral side following relief of pain by glycerol rhizotomy.

Adult↗

Creation of a defense dominant during the functioning of a blink dominant in the rabbit.

The possibility of creating (through serial electrodermal stimulation of the limb) a defense dominant during, the formation and functioning of a blink dominant was investigated in chronic experiments in rabbits. The formation of a motor dominant against the background of a blink dominant was difficult. Sequential, but not simultaneous, manifestation of the dominants under investigation was observed when the motor defense dominant was created against the background of a formed blink dominant. Difficulty in the formation of the motor dominant was also observed in the presence of transition to an inhibitory state, as a result of the repeated summation of the initial dominant focus, created via the reflex route, and in the presence of induction activation of a secondary dominant focus in symmetrical structures.

Aggression↗