Disease relevance of Eye Movements

• There is a severe encephalopathy with axial hypotonia, abnormal eye movements and pronounced psychomotor retardation, as well as a peripheral neuropathy, cerebellar hypoplasia and retinitis pigmentosa [1].
• Polysomnography revealed sustained hyperventilation, elevated O2 saturation, and low end-tidal CO2 throughout all stages of non-rapid eye movement (NREM) sleep, and absence of rapid eye movement (REM) sleep [2].
• Dynamic vergence eye movements in strabismus and amblyopia: symmetric vergence [3].
• A younger age of onset was associated with more severe dystonia, bradykinesia, and eye movement abnormalities relative to chorea, supporting the notion that in adult-onset HD, the motor phenotype forms a continuum with respect to age of onset [4].
• Hypotension produced by intraperitoneal administration of hydralazine (2 mg/kg) was associated with reduced SA and PSA expression in nonrapid eye movement sleep in both lean and obese rats [5].

Psychiatry related information on Eye Movements

• Baclofen increased the number of movements but decreased their amplitude during non-rapid eye movement (REM) sleep and shortened the interval between movements [6].
• This syndrome appears to be distinct from more typical non-rapid eye movement dyssomnias and suggests an atypical form of epilepsy [7].
• The author summarizes clinical data showing parallels between REM sleep and depressive phenomena; e.g., patients with endogenous depression show a first REM period that has a shorter than normal latency and a higher density of eye movement [8].
• Individual differences in the nature and magnitude of effects of lithium on eye movements were noteworthy [9].
• Smooth pursuit eye movement (SPEM) dysfunctions in major affective disorder patients have been reported to be associated with lithium treatment [10].

High impact information on Eye Movements

• We judged that the best model contained four variables from the admission examination: motor response, pupillary light response, spontaneous eye movements, and blood glucose (levels below 300 mg per deciliter predicted awakening) [11].
• (2) FUNCTION: Control of eye movements, reaching and grasping, cognitive maps, and the roles of vision receive a functional decomposition in terms of schemas [12].
• By 24 hours after onset, 93 poor-outcome patients were identified by motor responses that were absent, extensor, or flexor and by spontaneous eye movements that were neither orienting nor roving conjugate; only one regained independent function [13].
• We examined the activity of single dopamine neurons during a task in which subjects learned by trial and error when to make an eye movement for a juice reward [14].
• In addition, the compensatory eye movements of L7-PKCI mice were recorded during vestibular and visual stimulation [15].

Chemical compound and disease context of Eye Movements

• We conclude that a higher incidence of PLMD and frequent transient arousals associated with eye movements may be responsible in part for the complaint of insomnia made by patients treated with fluoxetine [16].
• Vasoactive intestinal polypeptide decelerates the non-rapid eye movement-rapid eye movement cycle and advances the occurrence of the cortisol nadir [17].
• Variation of electroencephalographic activity during non-rapid eye movement and rapid eye movement sleep with phase of circadian melatonin rhythm in humans [18].
• Reaction times of arm and eye movements were measured in a formal task in two of the monkeys having a moderate and a more important depletion of striatal dopamine, respectively [19].
• Adenosine levels during non-rapid eye movement sleep did not differ from rapid eye movement sleep [20].

Biological context of Eye Movements

• Unilateral infusion of MPTP into the monkey caudate nucleus produced deficits in task-specific saccades, in addition to the deficits in spontaneous eye movements (preceding article) [21].
• The principal finding of this study is that mutations of the SCA2 and SCA3 gene cause phenotypes which can be distinguished in vivo by recording of eye movements and morphometric MRI analysis [22].
• METHOD: Sensitivity to diazepam was assessed in 51 children of alcoholics by using two eye movement measures: peak saccadic velocity and average smooth pursuit gain [23].
• We therefore compared changes in ventilation, end-tidal carbon dioxide (CO2), upper airway resistance, heart rate, and finger photoplethysmogram pulse wave amplitude after both spontaneous and tone-induced arousal from non-rapid eye movement sleep in 13 men and 13 women [24].
• Because heart rate (HR) behavior may yield information on parasympathetic activity during OSA, we analyzed HR in samples of consecutive apneic cycles in non-rapid eye movement (NREM) sleep, recorded in normotensive patients breathing room air (n = 7) and supplemental O2 (n = 4) [25].

Anatomical context of Eye Movements

• Nitric oxide production by brain stem neurons is required for normal performance of eye movements in alert animals [26].
• To determine the effect of catecholamine depletion on ocular motor pathways in humans, we studied the eye movements of 3 normal subjects who received the drug metyrosine (alpha-methylparatyrosine) [27].
• We also analyzed the level of GAD67 mRNA expression in the superior colliculus, a structure that receives the inhibitory influence of the GABAergic neurons of the SNpr and that is involved in eye movement control [28].
• We studied the eye movements (EM) elicited by electrical stimulation of the frontal lobe in 19 awake patients evaluated with subdural electrodes for epilepsy surgery [29].
• The effects of a transient vestibular nerve blockade, achieved by intra-tympanic instillation of lidocaine, were studied in rats by recording horizontal eye movements in darkness [30].

Associations of Eye Movements with chemical compounds

• In this report, the role of attention in these eye movements is addressed in three experiments (using as subjects schizophrenics, their first-degree relatives, and normals administered chloral hydrate) that recruit focused attention to the task [31].
• Lidocaine inactivation of each integrator results in the eye movement deficits expected if horizontal eye position and velocity signals are processed separately [32].
• Here, we found that mice lacking alpha1(G) T-type Ca(2+) channels showed a loss of the thalamic delta (1-4 Hz) waves and a reduction of sleep spindles (7-14 Hz), whereas slow (<1 Hz) rhythms were relatively intact, when compared with the wild-type during urethane anesthesia and non-rapid eye movement (NREM) sleep [33].
• Prostaglandin D synthase gene is involved in the regulation of non-rapid eye movement sleep [34].
• Saccadic, pursuit, and vestibulo-ocular eye movements were recorded using infrared oculography with subjects both on placebo and on metyrosine [27].

Gene context of Eye Movements

• We report that the magnitude of viral-induced non-rapid eye movement sleep responses in both nNOS KOs and iNOS KOs was less than that of their respective controls [35].
• There was a compensatory reduction in light non-rapid eye movement (NREM) sleep in B/F when compared with CTRL and BOTTLE [36].
• GDNF (500-ng dose) increased the time spent in nonrapid eye movement sleep in both rats and rabbits [37].
• Injection of IL-1 or TNF enhances non-rapid eye movement sleep (NREMS) [38].
• Administration of exogenous IL-1 beta or TNF-alpha induces increased non-rapid eye movement sleep (NREMS) [39].

Analytical, diagnostic and therapeutic context of Eye Movements

• Throughout the entire treatment period the allopregnanolone group exhibited shorter non-rapid eye movement sleep (non-REMS) latencies, prolonged REMS latencies, longer non-REMS episodes, more pre-REMS and less low-frequency, but higher spindle activity in the electroencephalogram (EEG) within non-REMS than the placebo group [40].
• Electromyographic (EMG) activity of antagonist neck extensor (splenius capitis) and flexor (longus capitis) muscles as well as horizontal and vertical eye movements (electro-oculography, EOG) were recorded in these different experimental conditions [41].
• Spontaneous eye movements were recorded before and after a microinjection (0.1-0.2 microliter) of either APV (an NMDA receptor antagonist) or NBQX (a non-NMDA receptor antagonist) into the nucleus prepositus hypoglossi (NPH) of the alert cat [42].
• At each time point, optimal prediction required sets of only three to five features, typically including age in decades, depth and duration of coma as assessed by the Glasgow coma scale, pupil reactivity to light, and spontaneous and reflex eye movements [43].
• In a placebo-controlled, double-blind study of acute L-dopa challenge, videopolysomnography revealed multiple episodes of non-rapid eye movement sleep 60 minutes after L-dopa and none following placebo [44].

References