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Background: Versive seizures, consisting of forced, involuntary, sustained and unnatural turning of eyes and head toward one side, lateralize to the hemisphere contralateral to the direction of the eye and head turn. The characteristics of eye and head movements in version have been rarely and incompletely studied in spontaneous epileptic seizures as opposed to direct cortical stimulation studies.Methods: We performed a single center retrospective analysis of a cohort of 28 patients with 43 seizures, who had been admitted to the adult epilepsy monitoring unit at University Hospitals Cleveland Medical Center between January 2009 and August 2020. We only included patients with clear, high-resolution seizure videos and interpretable EEG.Results: The eye movements were conjugate and contralateral to the hemisphere of seizure onset in 100% of the focal-onset seizures. The eye movements were saccadic in 89.3% with a predominant vector in oblique upward direction in 86.8% of the seizures. Head deviation was present in 100% of the seizures and the eyes and head deviated in the same direction in 97.6% of the seizures. In addition to deviation along the horizontal meridian, there was a vertical component to the head deviation as well, as evidenced by movement of the chin upward along the vertical axis in 93% of the seizures, thus indicating strong activation of the sternocleidomastoid muscle ipsilateral to the hemisphere of seizure onset. Concomitant facial motor activity ipsilateral to the direction of version was seen in 93% of the seizures. The most common pattern was a clonic superimposed on tonic facial contraction.Discussion: Version remains a reliable and highly lateralizing sign. The majority of the eye movements during version occur in a saccadic fashion rather than one smooth movement, mostly in an oblique upward direction. Head deviation is very closely associated with eye deviation, thus indicating a common symptomatogenic zone for both, which is most likely the frontal eye field. A high concurrence of ipsilateral facial motor activity with version is likely because of close proximity of the frontal eye field to the face area in the primary motor cortex. [ABSTRACT FROM AUTHOR]

Background: Spontaneity is a unique feature of the nervous system. One of the fundamentally critical and recognized forms of spontaneous motor activity is witnessed in the visuomotor system. Microsaccades, the miniature spontaneous eye movements, are critical for the visual perception. We hypothesized that microsaccades follow specific temporal patterns that are modulated by the basal ganglia output. Methods: We used high-resolution video-oculography to capture microsaccades in 48 subjects (31 healthy and 17 with Parkinson's disease) when subjects were asked to hold their gaze on a straight-ahead target projected on white background. We analyzed spontaneous discharge patterns of microsaccades. Results: The first analysis considering coefficient of variation in intersaccadic interval distribution demonstrated that microsaccades in Parkinson's disease are more dispersed than the control group. The second analysis scrutinized microsaccades' temporal variability and revealed 3 distinct occurrence patterns: regular rhythmic, clustered, and randomly occurring following a Poisson-like process. The regular pattern was relatively more common in Parkinson's disease. Subthalamic DBS modulated this temporal pattern. The amount of change in the temporal variability depended on the DBS-induced volume of tissue activation and its overlap with the subthalamic nucleus. The third analysis determined the autocorrelations of microsaccades within 2-second time windows. We found that Parkinson's disease altered local temporal organization in microsaccade generation, and DBS had a modulatory effect. Conclusion: The microsaccades occur in 3 temporal patterns. The basal ganglia are one of the modulators of the microsaccade spontaneity. [ABSTRACT FROM AUTHOR]

Synchronous movements of the 2 eyes in the opposite direction, disconjugate movements such as vergence, facilitate depth perception. The vergence eye movements are affected in Parkinson disease (PD). Visual blur (accommodation) and fusion (retinal disparity) are important triggers for the vergence. The neural circuit responsible for blur-driven and disparity-driven vergence is tightly coupled. We investigated the effect of PD on these 2 vergence paradigms. In the experiment involving 14 patients with PD and 6 healthy controls, substantial differences between blur-driven and disparity-driven vergence were found. The gain (ratio of actual vs desired eye movements) was reduced in patients with PD in case of disparity-driven vergence but not in blur-driven vergence. The latency of disparity-driven vergence onset was significantly longer for patients with PD compared with healthy controls. Four strategies were used to drive disparity-driven vergence: a) pure disconjugate vergence, b) conjugate saccadic movements, c) disconjugate vergence followed by saccadic movements, and d) conjugate saccades followed by disconjugate vergence movements. Blur-driven vergence had only 2 strategies: a) conjugate saccades followed by disconjugate vergence and b) conjugate saccadic movements only. The results are consistent with the prediction that PD primarily affects disparity-driven vergence, but there are some effects on the strategies to execute blur-driven vergence. We speculate that the deep cerebellar nuclei and the supraoculomotor area of the midbrain that carry the disparity-driven and blur-driven vergence are affected in PD. It is possible to modulate their function through projections to the subthalamic nuclei. [ABSTRACT FROM AUTHOR]

The mechanism for stable gaze-holding requires a neural integrator that converts pulse of neural discharge to steady firing rate. The integrator is feedback-dependent, impaired feedback manifests as either "unstable" integration when it is too much or "leaky" when it is too little. The "unstable" integrator is known to cause sinusoidal oscillations of the eyes called pendular nystagmus, whereas the "leaky" integrator causes jerky eye oscillations called gazeevoked nystagmus. We hypothesized that integrator can be simultaneously leaky and unstable. Mechanistically, some parts of network are served by increased feedback gain (unstable network), while other part would be decreased feedback gain (leaky). Both leaky and unstable, the network converges on the ocular motor plant, leading to simultaneously present gaze-evoked jerk and sinusoidal nystagmus. We tested our hypothesis by measuring eye movements with search coil technique in 7 multiple sclerosis patients. Five of these patients had gaze-evoked nystagmus and superimposed pendular nystagmus. The gazeevoked nystagmus depicted all the features of "leaky" integrator, that is, the drifts were always toward the null that was located at the central eye-in-orbit orientation, there were no drifts at null, and the drift velocity increased as the eyes moved farther away from the null. The pendular nystagmus had all the features of "unstable" integrator, that is, constant 4- to 6-Hz frequency, eye-in-orbit position dependence of the oscillation amplitude, and the voluntary saccade causing an oscillatory phase reset. These features were then simulated in a computational model conceptualizing our hypothesis of simultaneously leaky and unstable neural integrator. [ABSTRACT FROM AUTHOR]

Supplemental Digital Content is Available in the Text. [ABSTRACT FROM AUTHOR]

Highlights • Oculogyric crises and epilepsy have similar phenomenology with different mechanisms. • OGC in patients with diffuse cerebral lesions can be difficult to diagnose from epilepsy. • Video EEG monitoring is essential in differentiating OGC from epilepsy. Abstract Ictal gaze deviation and oculogyric crisis (OGC) can show identical clinical manifestations. We report a case of repeated drug induced OGCs in a 38 year old patient with secondary progressive multiple sclerosis. He was referred to our center for treatment of "intractable" epilepsy manifesting as episodic eye and head deviations with apparent unresponsiveness. In the epilepsy monitoring unit, ten typical spells were captured without epileptiform electroencephalographic correlates, but we discovered chronic exposure to metoclopramide. A diagnosis of OGC was suspected and Metoclopramide was stopped. This robustly improved the frequency of his spells. In a setting of usage of antidopaminergic medications and/or pontomesencephalic lesions, a low threshold should be kept for the diagnosis of oculogyric crisis, thus avoiding seizure diagnoses and inappropriate treatment of the phenomenon. Video-EEG monitoring is essential for teasing apart epilepsy and OGC. [ABSTRACT FROM AUTHOR]

Purpose To quantitatively characterize eye and head oscillations in patients with infantile nystagmus syndrome (INS). Methods Vertical and horizontal eye and head position in INS patients were measured simultaneously at a sampling frequency of 500 Hz. Eye and head movements were measured continuously for 180 seconds. The data was calibrated and converted to angular vectors, which were further analyzed with custom software. Results A total of 10 patients with INS were included: 3 with pseudo-jerk, 3 with pure-jerk, 2 with pseudo-pendular with foveating saccade form of jerk, 1 with bidirectional jerk, and 1 with asymmetric pendular nystagmus waveforms. None of the patients had periodic, aperiodic, or a superimposed latent nystagmus component. Two types of head oscillations were observed: one with a frequency of 1–3 Hz, present in all patients; and another with a frequency range of 5–8 Hz, present in only 7 patients. High-frequency oscillations were episodic, whereas low-frequency oscillations were constantly present. Peak velocity of the high-frequency head oscillations and eye velocity of nystagmus were not correlated, suggesting that these oscillations did not influence foveation. Conclusions Two types of head oscillations were found in INS patients: a constant, low-frequency and an episodic, high–frequency. Lack of correlation between the foveation period of nystagmus and peak head velocity during high-frequency oscillations suggests a coexisting pathological phenomenon rather than a compensatory mechanism used to improve the visual acuity. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The motion perception and the vestibulo-ocular reflex (VOR) each serve distinct functions. The VOR keeps the gaze steady on the target of interest, whereas vestibular perception serves a number of tasks, including awareness of self-motion and orientation in space. VOR and motion perception might abide the same neurophysiological principles, but their distinct anatomical correlates were proposed. In patients with cerebellar stroke in distribution of medial division of posterior inferior cerebellar artery, we asked whether specific location of the focal lesion in vestibulocerebellum could cause impaired perception of motion but normal eye movements. METHODS/RESULTS: Thirteen patients were studied, 5 consistently perceived spinning of surrounding environment (vertigo), but the eye movements were normal. This group was called 'disease model.' Remaining 8 patients were also symptomatic for vertigo, but they had spontaneous nystagmus. The latter group was called 'disease control.' Magnetic resonance imaging in both groups consistently revealed focal cerebellar infarct affecting posterior cerebellar vermis (lobule IX). In the 'disease model' group, only part of lobule IX was affected. In the disease control group, however, complete lobule IX was involved. CONCLUSIONS: This study discovered a novel presentation of cerebellar stroke where only motion perception was affected, but there was an absence of objective neurologic signs. [ABSTRACT FROM AUTHOR]

Objective: The motion perception and the vestibulo-ocular reflex (VOR) each serve distinct functions. The VOR keeps the gaze steady on the target of interest, whereas vestibular perception serves a number of tasks, including awareness of self-motion and orientation in space. VOR and motion perception might abide the same neurophysiological principles, but their distinct anatomical correlates were proposed. In patients with cerebellar stroke in distribution of medial division of posterior inferior cerebellar artery, we asked whether specific location of the focal lesion in vestibulocerebellum could cause impaired perception of motion but normal eye movements. Methods/Results: Thirteen patients were studied, 5 consistently perceived spinning of surrounding environment (vertigo), but the eye movements were normal. This group was called “disease model.” Remaining 8 patients were also symptomatic for vertigo, but they had spontaneous nystagmus. The latter group was called “disease control.” Magnetic resonance imaging in both groups consistently revealed focal cerebellar infarct affecting posterior cerebellar vermis (lobule IX). In the “disease model” group, only part of lobule IX was affected. In the disease control group, however, complete lobule IX was involved. Conclusions: This study discovered a novel presentation of cerebellar stroke where only motion perception was affected, but there was an absence of objective neurologic signs. [Copyright &y& Elsevier]

Saccadic oscillations threaten clear vision by causing image motion on the retina. They are either purely horizontal (ocular flutter) or multidimensional (opsoclonus). We propose that ion channel dysfunction in the burst cell membrane is the underlying abnormality. We have tested this hypothesis by simulating a neuromimetic computational model of the burst neurons. This biologically realistic model mimics the physiologic properties and anatomic connections in the brainstem saccade generator. A rebound firing after sustained inhibition, called post-inhibitory rebound (PIR), and reciprocal inhibition between premotor saccadic burst neurons are the key features of this conceptual scheme. PIR and reciprocal inhibition make the circuits that generate the saccadic burst inherently unstable and can lead to oscillations unless stabilized by external inhibition. Our simulations suggest that alterations in membrane properties that lead to an increase in PIR, a reduction in external glycinergic inhibition, or both can cause saccadic oscillations. [ABSTRACT FROM AUTHOR]

Cerebellar lesions may present with gravity-dependent nystagmus, where the direction and velocity of the drifts change with alterations in head position. Two patients had acute onset of hearing loss, vertigo, oscillopsia, nausea, and vomiting. Examination revealed gravity-dependent nystagmus, unilateral hypoactive vestibulo-ocular reflex (VOR), and hearing loss ipsilateral to the VOR hypofunction. Traditionally, the hypoactive VOR and hearing loss suggest inner-ear dysfunction. Vertigo, nausea, vomiting, and nystagmus may suggest peripheral or central vestibulopathy. The gravity-dependent modulation of nystagmus, however, localizes to the posterior cerebellar vermis. Magnetic resonance imaging in our patients revealed acute cerebellar infarct affecting posterior cerebellar vermis, in the vascular distribution of the posterior inferior cerebellar artery (PICA). This lesion explains the gravity-dependent nystagmus, nausea, and vomiting. Acute onset of unilateral hearing loss and VOR hypofunction could be the manifestation of inner-ear ischemic injury secondary to the anterior inferior cerebellar artery (AICA) compromise. In cases of combined AICA and PICA infarction, the symptoms of peripheral vestibulopathy might masquerade the central vestibular syndrome and harbor a cerebellar stroke. However, the gravity-dependent nystagmus allows prompt identification of acute cerebellar infarct. [Copyright &y& Elsevier]