The neural relationships between eyelid movements and eye movements during spontaneous, voluntary, and reflex blinking in a group of healthy subjects were examined. Electromyographic (EMG) recording of the orbicularis oculi (OO) muscles was performed using surface electrodes. Concurrently, horizontal and vertical eye positions were recorded by means of the double magnetic induction (DMI) ring method. In addition, movement of the upper eyelid was measured by a specially designed search coil, placed on the upper eyelid. The reflex blink was elicited electrically by supraorbital nerve stimulation either on the right or the left side. It is found that disconjugate oblique eye movements accompany spontaneous, voluntary as well as reflex blinking. Depending on the gaze position before blinking, the amplitude of horizontal and vertical components of the eye movement during blinking varies in a systematic way. With adduction and downward gaze the amplitude is minimal. With abduction the horizontal amplitude increases, whereas with upward gaze the vertical amplitude increases. Unilateral electrical supraorbital nerve stimulation at low currents elicits eye movements with a bilateral late component. At stimulus intensities approximately two to three times above the threshold, the early ipsilateral blink reflex response (R(1)) in the OO muscle can be observed together with an early ipsilateral eye movement component at a latency of approximately 15 ms. In addition, during the electrical blink reflex, early ipsilateral and late bilateral components can also be identified in the upper eyelid movement. In contrast to the late bilateral component of upper eyelid movement, the early ipsilateral component of upper eyelid movement appears to open the eye to a greater degree. This early ipsilateral component of upper eyelid movement occurs more or less simultaneously with the early eye movement component. It is suggested that both early ipsilateral movements following electrical stimulation do not have a central neural origin. Late components of the eye movements slightly precede the late components of the eyelid movement. Synchrony between late components of eyelid movements and eye movements as well as similarity of oblique eye movement components in different types of blinking suggest the existence of a premotor neural structure acting as a generator that coordinates impulses to different subnuclei of the oculomotor nucleus as well as the facial nerve nucleus during blinking independent from the ocular saccadic and/or vergence system. The profile and direction of the eye movement rotation during blinking gives support to the idea that it may be secondary to eyeball retraction; an extra cocontraction of the inferior and superior rectus muscle would be sufficient to explain both eye retraction and rotation in the horizontal vertical and torsional planes.

An overview is provided on the physiological aspects of the brainstem reflexes as they can be examined by use of clinically applicable neurophysiological tests. Brainstem reflex studies provide important information about the afferent and efferent pathways and are excellent physiological tools for the assessment of cranial nerve nuclei and the functional integrity of suprasegmental structures. In this review, the blink reflex after trigeminal and nontrigeminal inputs, corneal reflex, levator palpebrae inhibitory reflex, jaw jerk, masseter inhibitory reflex, and corneomandibular reflex are discussed. Following description of the recording technique, physiology, central pathways, and normative data of these reflexes, including an account of the recording of recovery curves, the application of these reflexes is reviewed in patients with various neurological abnormalities, including trigeminal pain and neuralgia, facial neuropathy, and brainstem and hemispherical lesions. Finally, simultaneous electromyographic recording from the orbicularis oculi and the levator palpebrae muscles is discussed briefly in different eyelid movement disorders.

Electromyographic (EMG) recording was performed synchronously from the levator palpebrae superioris (LP) and the orbicularis oculi (OO) muscles in 28 patients referred to us for treatment of blepharospasm with botulinum A toxin. At the time of this study, 19 patients were under the treatment with botulinum, four started treatment shortly after the EMG recording and five patients had not yet been treated. Based on the EMG patterns, we were able to classify five major groups of abnormalities. Group 1 (blepharospasm): consisted of 10 patients with dystonic discharges limited to OO, normal LP tonic activity, intact reciprocal inhibition between LP and OO and dense bursts of action potentials with high amplitude preceding the return of LP tonic activity, i.e. 'postinhibition potentiation' of LP, brought about by a brief contraction of OO. Group 2 (combined dystonic activities of LP and OO): seven patients belonged to this group. The EMG recording revealed alternating tremulous discharges in both LP and OO muscles, and short intervals of co-contractions due to moderately disturbed reciprocal inhibition. Group 3 (combination of blepharospasm, LP motor impersistence): the EMG patterns, observed in three patients, were characterized by a gradual cessation of LP activity, followed by a brief contraction of OO, which facilitated the return of LP activity, resulting in opening of the eyes. The EMG recordings, thus, revealed the crucial, beneficial role of postinhibition potentiation as a compensatory mechanism in this type of eyelid movement disorder. The EMG patterns were also characterized by short or prolonged periods of dystonic discharges limited to the OO muscles. Group 4 (combination of blepharospasm, involuntary LP inhibition): this group consisted of four patients. In addition to episodes of dystonic activities of OO, the EMG also showed some periods of involuntary inhibition of LP without any concomitant activities of OO. Two patients also exhibited a failure of inhibition of OO muscle activity, following the voluntary contraction of this muscle. The postinhibition potentiation was often not observed. Group 5 (involuntary LP inhibition): consisted of four patients with EMG patterns of involuntary inhibition of LP activity, without any dystonic discharges in OO. The postinhibition potentiation was not observed in this group. The response to the treatment with botulinum toxin was good in the first group and gradually worsened towards the fifth group. Application of botulinum into multiple sites of OO, especially its pretarsal portion, resulted in better response to the treatment in the second and fourth groups.(ABSTRACT TRUNCATED AT 400 WORDS)

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We report on five patients with involuntary eyelid closure, diagnosed as blepharospasm and referred to use for treatment with botulinum A toxin. Synchronous electromyographic (EMG) recording was performed from the levator palpebrae superioris (LP) and the orbicularis oculi (OO) muscles. In the first two cases, EMG registration showed alternating, semirhythmic dystonic activities in both the LP and OO, clinically perceptible as "flickering" of the eyelids. While the eyelids were lowered, one of them also showed involuntary upper eyelid tractions due to dystonic activities of LP. In the third patient, EMG patterns were characterized by a gradual decrease in the level of LP activity, followed by the contraction of OO, which facilitated the return of LP to its tonic activity, termed "postinhibition potentiation" of LP. In the fourth patient, EMG recording showed involuntary inhibition of LP in combination with blepharospasm. Involuntary closure of the eyelids in the fifth patient was caused by short or prolonged periods of involuntary LP inhibition, whereas OO activity remained normal. Our results provide further evidence that LP muscle activities are regulated by burst-tonic motoneurons, and we suggest that these motoneurons, and/or the input signals regulating their activities, can be involved independently in a pathological process. Clinical symptoms are discussed that may be helpful to recognize those cases with LP motor dysfunction, whether or not accompanied by OO activity disorders. Because the term blepharospasm indicates an abnormal motor function of OO, we propose "blepharospasm-plus" to designate those cases with a combined motor dysfunction of LP and OO muscles.

We report on a blink reflex abnormality observed in two patients, which provides additional information on the central pathways mediating this reflex. Autopsy was performed in one patient and MRI in the other. In the first patient there was a small lesion at the dorsal middle third of the lateral tegmental field and in the second patient at the level of the dorsal lower third of the medulla oblongata. In both patients the common finding was the absence of the late response (R2) ipsilateral to the side of the lesion, while the R2 response on the unaffected side was normal regardless of the side of the supraorbital nerve stimulation. The R1 responses were normal. This type of blink reflex abnormality has not been reported before and is referred to by us as 'tegmental type' of R2 abnormality. The results led to the conclusions that: (i) the crossed and uncrossed ascending trigeminofacial connections are mediated through the lateral tegmental field; (ii) the uncrossed trigeminofacial connection originates at the level of at least the lower medulla oblongata; (iii) the contralateral R2 response is established by way of an ascending pathway, which crosses the midline at the level of at least the lower third of the medulla oblongata.