Eye movement - Wikipedia
These involuntary eye movements can occur from side to side, up and down, or in a circular pattern. As a result, both eyes Generally, nystagmus is a symptom of another eye or medical problem. Fatigue and system diseases. [back to top] . I think what OP is experiencing is a split second, back and forth eye movement that is really rapid. I also have experienced this a few times in. The claimed link between lying and eye movements is a key element about the relationship between their eye movements and their thoughts.
No relationships were found in the group of healthy subjects, but, in the group of schizophrenic patients, the total points of neurological subtle signs were positively correlated with three variable saccades. Finally, negative correlations were found for the estimation rate of anticipated saccades. The researchers also analyzed individuals with alterations in their prefrontal areas, such as schizophrenic patients; the results showed that these subjects had difficulty initiating voluntary saccades toward the contralateral side in response to a visual stimulus and difficulty in suppressing reflexive saccades.
The authors also reported that FEF was not essential to generate the saccade.
Lesions in this area only produced transient and subtle deficiencies in eye movement generation. Combined lesions to the superior colliculus and FEF produced more significant and permanent changes, distorting the execution of eye movements.
The researchers hypothesized that first-degree relatives of schizophrenic patients are vulnerable to these changes because they present the same phenotype. The authors reported that in addition to the patients, their first-degree relatives also had a high number of errors for saccadic re-fixation tasks and guided memory saccadic tasks, reflecting a failure to inhibit reflexive saccades directed to a visible target.
A different experiment compared the reaction time to execute a visually guided saccade of 53 schizophrenic patients and 1, control subjects. The researchers concluded that this difference in the distribution could be attributed to a basic difference in information processing, leading to the decision to move the eyes to the visually presented target. The results showed that patients with BD have difficulty in performing antisaccadic tasks due to a dysfunction in the activation of the prefrontal cortex, which is responsible for movement planning.
This failure occurs because of alterations in the sensory transmission measures of P50, which supports the auditory system and the integrity of the interneuronal cholinergic modulation in the hippocampus, often altered in bipolar patients. The schizophrenic patients demonstrated moderately stable reaction times, accuracy, and mistakes over time.
In contrast, bipolar patients do not show temporal stability and accuracy in the task or for the latencies of correct or incorrect answers. Gooding et al 37 researched 34 schizophrenic patients, 20 bipolar patients, and 30 non-patient controls. The objective of their study was to harmonize the discrepant results verified in previous studies about visual fixation performance in schizophrenic subjects.
The patients were presented with central fixation targets. Analysis of variance of the number of saccades produced during fixation revealed that the three groups did not differ in terms of ratings of fixation quality.
Mueller et al 12 studied young bipolar patients, comparing 20 youths with BD and 23 healthy subjects on a mixed pro-antisaccade task with monetary incentives.
The participants were presented with three types of incentives: Impaired reward processing was found in youths with BD compared with controls, particularly on antisaccades.
Saccadic eye movement applications for psychiatric disorders
This difference was reflected in lower error rates during incentive trials in the control but not in the BD group. By comparison, no group differences were found in terms of prosaccade movements. Kathmann et al 38 hypothesized a possible impairment of SPEM in unaffected family members of patients with affective disorders. To verify this hypothesis, 54 patients with schizophrenia or schizoaffective disorder, 46 patients with an affective disorder, 43 unaffected first-degree relatives of the schizophrenic patients, 36 unaffected first-degree relatives of the affective disorder patients, and 84 healthy subjects were compared when executing an eye movement task.
A significantly lower pursuit gain was observed in the schizophrenia and affective disorder patients than in the healthy subjects.
Moreover, the relatives of both the schizophrenia and affective disorder patients showed significant gain deficits. However, a gain deficit was observed in patients and in their unaffected biological relatives. This finding supports the existence of eye movement impairment in the relatives, but the sensitivity of this marker is too weak to be considered a genetic factor in schizophrenia and affective disorder patients. Depression Sweeney et al 39 assessed depressed subjects through a battery of oculomotor tasks selected to evaluate the functional integrity of frontostriatal circuits and cerebellar vermis.
How your eyes betray your thoughts | Science | The Guardian
Twenty-nine non-medicated depressed inpatients and an age-and sex-matched healthy comparison group of 19 subjects were analyzed. The study verified that these patients presented an increased rate of error suppression in response to an antisaccadic task, a less accurate memory for spatial information, dysmetria in visually guided saccades and an increased rate of saccadic intrusion during visual fixation.
Winograd-Gurvich et al 4041 observed that depression patients exhibited greater latency and a higher number of errors when performing saccadic tasks.
They also demonstrated a reduction in movement precision and difficulty suppressing peripheral target stimuli. These studies have determined that it is possible to differentiate motor disorders in melancholic and non-melancholic depression. Melancholic patients exhibit motor slowness, having difficulty in initiating movements without external cues.
It leads to increased latency, reduced peak velocity, and hypometric primary saccades. The increase of reprogrammed saccadic latencies and the severity of melancholic symptoms may reflect a deficiency in the ability to select or inhibit the responses to competing targets. The researchers observed similar control results in patients with non-melancholic depression, but the peak velocity as well as the amplitudes of the reflexive saccade increased.
Further, melancholic patients present a higher latency and a lower peak velocity in the execution of a memory-guided saccade, replicating results observed in stimulus-guided saccades. An experiment using therapeutic repetitive transcranial magnetic stimulation rTMS was conducted to examine the influence of this on different types of saccades in patients treated for major depression. The latency and directional error were analyzed in reflexive and voluntary saccades ie, prosaccades and antisaccades.
The tasks were studied in eleven depressed patients before and after rTMS. The eye movement was registered by infrared oculography. After applying ten sessions of rTMS on the left dorsolateral prefrontal cortex, new measures were adopted to observe modifications.
A decrease in the antisaccade task latency occurred after rTMS application, but the stimulation in this cortex seemed to have no important effectiveness on reflexive saccades.
Nystagmus - 5 Main Types, Plus Causes and Treatments
The voluntary prosaccades were also not influenced. These results suggest that rTMS might differentially affect specific aspects of saccade behavior. The precision, peak velocity, and reaction time were considered for comparison. The velocity peak significantly increased in schizophrenic patients.
Depressive patients had a longer reaction time. The patients exhibited more corrective saccades than controls. In contrast, Flechtner and colleagues 44 evaluated schizophrenic patients and patients with affective disorders major depression during clinical treatment. Subjects were evaluated during execution of eye movement tasks; specifically, the velocity gain was evaluated in different saccadic categories.
How your eyes betray your thoughts
No significant correlations were found between psychopathological status, neuroleptic medications, and eye movement variables. The ADHD adult subjects, unmedicated for at least 48 hours, and normal comparison adults were studied by means of a comprehensive battery of ocular motor paradigms.
During a prosaccade task, the ADHD subjects generated significantly more anticipatory premature saccades with reaction time of less than 90 milliseconds. In the antisaccade task, the ADHD subjects made significantly more directional errors than the normal adults.
However, the performance of the adults with ADHD was consistent with deficits in saccadic inhibition. Therefore, the study concluded that there is interdependence between the brain systems mediating visual attention and ocular motor behavior. One of the main uses for these saccadic eye movements is to be able to scan a greater area with the high-resolution fovea of the eye.
Vestibulo-ocular reflex The visual system in the brain is too slow to process that information if the images are slipping across the retina at more than a few degrees per second.
Another specialisation of visual system in many vertebrate animals is the development of a small area of the retina with a very high visual acuity. This area is called the foveaand covers about 2 degrees of visual angle in people. To get a clear view of the world, the brain must turn the eyes so that the image of the object of regard falls on the fovea.
Eye movement is thus very important for visual perception, and any failure can lead to serious visual disabilities. To see a quick demonstration of this fact, try the following experiment: Keep your head still, and shake your hand from side to side, slowly at first, and then faster and faster. At first you will be able to see your fingers quite clearly. But as the frequency of shaking passes about 1 Hzthe fingers will become a blur. Now, keep your hand still, and shake your head up and down or left and right.
No matter how fast you shake your head, the image of your fingers remains clear. This demonstrates that the brain can move the eyes opposite to head motion much better than it can follow, or pursue, a hand movement.
When your pursuit system fails to keep up with the moving hand, images slip on the retina and you see a blurred hand.