Қозғалыс қабылдаудың жоғалуы: Акинетопсия ауруы

Loss of visual motion perception

Akinetopsia (from Greek akinesia 'absence of movement' and opsis 'seeing'), also known as cerebral akinetopsia or motion blindness, is a term introduced by Semir Zeki to describe an extremely rare neuropsychological disorder, having only been documented in a handful of medical cases, in which a patient cannot perceive motion in their visual field, despite being able to see stationary objects without issue. There are varying degrees of akinetopsia: from seeing motion as frames of a cinema reel to an inability to discriminate any motion. There is currently no effective treatment or cure for akinetopsia.

Akinetopsia can manifest in a spectrum of severity and some cases may be episodic or temporary. It may range from "inconspicuous akinetopsia" to "gross akinetopsia", based on symptom severity and the amount the akinetopsia affects the patient's quality of life.

Inconspicuous akinetopsia is often described by seeing motion as a cinema reel or a multiple exposure photograph. This is the most common kind of akinetopsia and many patients consider the stroboscopic vision as a nuisance. The akinetopsia often occurs with visual trailing (palinopsia), with afterimages being left at each frame of the motion. It is caused by prescription drugs, hallucinogen persisting perception disorder (HPPD), and persistent aura without infarction. The pathophysiology of akinetopsia palinopsia is not known, but it has been hypothesized to be due to inappropriate activation of physiological motion suppression mechanisms which are normally used to maintain visual stability during eye movements (e. g. saccadic suppression).

Gross akinetopsia is an extremely rare condition. Patients have profound motion blindness and struggle in performing the activities of daily living. Instead of seeing vision as a cinema reel, these patients have trouble perceiving gross motion. Most of what is known about this extremely rare condition was learned through the case study of one patient, LM. LM described pouring a cup of tea or coffee difficult "because the fluid appeared to be frozen, like a glacier". A change in brain structure (typically lesions) disturbs the psychological process of understanding sensory information, in this case visual information. Disturbance of only visual motion is possible due to the anatomical separation of visual motion processing from other functions. Like akinetopsia, perception of color can also be selectively disturbed as in achromatopsia. There is an inability to see motion despite normal spatial acuity, flicker detection, stereo and color vision. Other intact functions include visual space perception and visual identification of shapes, objects, and faces. Besides simple perception, akinetopsia also disturbs visuomotor tasks, such as reaching for objects and catching objects. When doing tasks, feedback of one's own motion appears to be important. Some unilateral lesions have been reported to impair motion perception as well. Akinetopsia through lesions is rare, because damage to the occipital lobe usually disturbs more than one visual function.

Inconspicuous akinetopsia can be selectively and temporarily induced using transcranial magnetic stimulation (TMS) of area V5 of the visual cortex in healthy subjects. It is performed on a 1 cm² surface of the head, corresponding in position to area V5. With an 800 microsecond TMS pulse and a 28 ms stimulus at 11 degrees per second, V5 is incapacitated for about 20–30 ms. It is effective between −20 ms and +10 ms before and after onset of a moving visual stimulus. Inactivating V1 with TMS could induce some degree of akinetopsia 60–70 ms after the onset of the visual stimulus. TMS of V1 is not nearly as effective in inducing akinetopsia as TMS of V5. This could contribute to their marked disorientation. While Pelak and Hoyt have recorded an Alzheimer's case study, there has not been much research done on the subject yet. with vision returning to normal once the dosage is reduced.

Two relevant visual areas for motion processing are V5 and V1. These areas are separated by their function in vision. A functional area is a set of neurons with common selectivity and stimulation of this area, specifically behavioral influences. There have been over 30 specialized processing areas found in the visual cortex.

V5, also known as visual area MT (middle temporal), is located laterally and ventrally in the temporal lobe, near the intersection of the ascending limb of the inferior temporal sulcus and the lateral occipital sulcus. All of the neurons in V5 are motion selective, and most are directionally selective.

V1, also known as the primary visual cortex, is located in Brodmann area 17. V1 is known for its pre processing capabilities of visual information; however, it is no longer considered the only perceptually effective gateway to the cortex. MRI confirmed that the damaged brain areas contained area V5 in both hemispheres. TD experienced problems with perceiving visual motion and also reported that bright colours and sharp contrasts made her feel sick. TD also had problems perceiving objects that were more than ± 5 meters away from her. Although TD had some impairments of lower visual functions, these could not explain the problems she experienced with regard to motion perception. Neuropsychological assessment revealed no evidence of Balint's Syndrome, hemispatial neglect or visual extinction, prosopagnosia or object agnosia. There was some evidence for impaired spatial processing. On several behavioural tests, TD showed a specific and selective impairment of motion perception that was comparable to LM's performance. TD's ability to determine the direction of movement was tested using a task in which small grey blocks all moved in the same direction with the same speed against a black background. The blocks could move in four directions: right to left, left to right, upward and downward. Speed of movement was varied from 2, 4.5, 9, 15 and 24 degrees per second. Speed and direction were varied randomly across trials. TD had perfect perception of motion direction at speed up to 9 degrees per second. When speed of targets was above 9 degrees per second, TD's performance dropped dramatically to 50% correct at a speed of 15 degrees per second and 0% correct at 24 degrees per second. When the blocks moved at 24 degrees per second, TD consistently reported the exact opposite direction of the actual movement.

In 2000, a 70 year old man presented with akinetopsia. He had stopped driving two years prior because he could no longer "see movement while driving". His wife noted that he could not judge the speed of another car or how far away it was. He had difficulty watching television with significant action or movement, such as sporting events or action filled TV shows. He frequently commented to his wife that he could not "see anything going on". When objects began to move they would disappear. He could, however, watch the news, because no significant action occurred. In addition he had signs of Balint's syndrome (mild simultanagnosia, optic ataxia, and optic apraxia).

In 2003, a 60 year old man complained of the inability to perceive visual motion following a traumatic brain injury, two years prior, in which a large cedar light pole fell and struck his head. He gave examples of his difficulty as a hunter. He was unable to notice game, to track other hunters, or to see his dog coming towards him. Instead, these objects would appear in one location and then another, without any movement being seen between the two locations. He had difficulties driving and following a group conversation. He lost his place when vertically or horizontally scanning a written document and was unable to visualize three dimensional images from two dimensional blueprints.