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Akinetopsia, also known as cerebral akinetopsia or motion blindness, is a disorder in visual perception in which the subject can not perceive motion in his/her visual field, despite being able to see stationary objects without issue. Most of what is known about akinetopsia was learned through LM, the most studied case in akinetopsia. There is currently no effective treatment or cure for akinetopsia.

Classification

Neuropsychological disorder: A change in brain structure (through lesions) that affects the psychological process of understanding sensory information (visual)

Disorder in visual perception: Akinetopsia is a deficit in perception of vision, not in the physical sensation of vision.

Akinetopsia is possible due to the separation of visual processing from other functions, anatomically. Like akinetopsia, perception of color can also be selectively disturbed as in achromatopsia.

Characteristics

Akinetopsia is the inability to see motion with normal acuity, stereo and color vision intact. Other intact functions include visual space perrception and visual identification of shapes, objects or faces. Patients with akinetopsia struggle with many issues in their day-to-day life. One patient, LM, described problems with pouring a cup of tea or coffee "because the fluid appeared to be frozen, like a glacier". She did not know when to stop pouring, because she could not perceive the movement of the fluid rising. LM also complained of her trouble following conversations, because she could not see lip movements or changing facial expressions. She felt insecure when more than two people were walking around in a room. She stated, "people were suddenly here or there but I have not seen them moving". Unable to judge the speed of car, she could not cross the street. She stated, "When I'm looking at the car at first, it seems far away. But then, when I want to cross the road, suddenly the car is very near". She could however identify each car without issue.

Causes

Brain lesions

Akinetopsia is an acquired deficit from lesions in posterior side of the visual cortex. In the case of LM, the brain lesion was bilateral and symmetrical, and at the same small enough not to affect other visual functions. 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. Akinetopsia has also been reported as a result of traumatic brain injury.

Transcranial Magnetic Stimulation

Akinetopsia can be selectively and temporarily induced using transcranial magnetic stimulation (TMS) of area V5 in healthy subjects. It is performed on 1 square cm surface of the head, corresponding in position to area V5. With a 800 micro second TMS pulse and a 28 ms stimulus at 11 degrees per second, V5 is incapacitated for about 20-30 ms. It is effective -20ms to +10ms 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 than TMS of V5.

Alzeheimer's

Besides memory problems, Alzeheimer's patients may have varying degrees of motion blindness. This could contribute to their marked disorientation. There has not been much research done on the subject as of yet.

Areas of visual perception

Two relevant visual areas are V5 and V1. V5 is also known as visual area MT (middle temporal), located laterally and ventrally in the occipital lobe, near the intersection of the ascending limb of the inferior temporal sulcus and the lateral occipital sulcus. Evidence of functional specialization of V5 was first found in primates. V1 is known as the primary visual cortex, 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. Contrary to conventional theories of streams, some signals reach V5 without passing through V1 and a return input from V5 to V1 is not required for seeing simple visual motion. V5 can act independently of V1. Inactivating V1 limits motion vision, but does not stop it completely.

Motion related signals arrive at V1 (60-70ms) and V5 (<30ms) at different times.

Case Studies

Potzl and Redlich's patient

In 1911, Potzl and Redlich reported a 58 year old female patient with bilateral damage to her posterior brain. She described motion as if the object remained stationary but appeared at different successive positions. Additionally, She also lost a significant amount of her visual field and had anomic aphasia.

Goldstein and Gelb's patient

In 1918, Goldstein and Gelb reported a 24 year old male who suffered a gunshot wound in the posterior brain. The patient reported no impression of movement. He could state the new position of the object (left, right, up, down), but saw “nothing in between”. While Goldestein and Gelb believed the patient had damaged the lateral and medial parts of the left occipital lobe, it was later indicated that both occipital lobes were probably affected, due to the bilateral, concentric loss of his visual field. He lost his visual field beyond a 30 degree eccentricity and could not identify visual objects by their proper names.

Zihl, Von Cramon, and Mai's patient LM

Case Study: LM Most of what we know about akinetopsia, we learned from LM, a 43 year old female admitted into the hospital October 1978. Thrombosis of the superior sagittal sinus resulted in bilateral, symmetrical lesions posterior of the visual cortex, verified by PET and MRI in 1994. LM had minimal motion perception that was preserved as perhaps a function of V1, as a function of "higher" order visual cortical area, or some functional sparing of V5.

LM found no effective treatment, so she learned to avoid conditions with multiple visual motion stimuli, i.e. by not looking at or fixating them. She developed very efficient coping strategies to do this and nevertheless lived her life. In addition, she estimated the distance of moving vehicles by means of sound detection in order to continue to cross the street.

LM was tested in three areas against a 24 year old female subject with normal vision:

Visual functions other than movement vision

LM had no evidence of a color discrimination deficit in either center or periphery of visual fields. Her recognition time for visual objects and words was slightly higher than the control, but not statistically significant. There was no restriction in her visual field and no scotoma.

Disturbance of movement vision

With circular light targets as stimuli, LM reported some impression of horizontal movement when the target's velocity was approximately 14 deg/s while fixating in the middle of the motion path. She had difficulty seeing motion below and above this velocity. When allowed to track the moving spot, she had some movement vision up to 18 deg/s for horizontal movement. For vertical movement direction, the patient could only see the target in motion when stimulus velocity was below 10 deg/s or 13 deg/s when tracking the target. The patient described her perceptual experience for stimulus velocities higher than 18 and 13 deg/s, respectively as "one light spot left or right" or "one light spot up or down" and "sometimes at successive positions in between", but never as motion.

Motion in depth, detection of movement in the inner and outer visual fields, prediction of velocity, motion aftereffect, and Phi phenomenon were also tested.

To determine perception of motion in depth, studies were done monocularly and binocularly in which the experimenter moved a black painted wooden cube on a tabletop either towards the patient or away in line of sight. After 20 trials with a 100 cm movement at 3 or 6 deg/s, the patient had no clear impression of movement. However she knew the object had changed in position, she knew the size of the cube, and she could correctly judge the distance of the cube in relation to other nearby objects.

Detection of movement in the inner and outer visual fields was tested binocularly for the inner visual field with a best performance of 85% correct, with horizontal motion more easily distinguished than vertical motion. In the patient's peripheral visual field, the patient was never able to detect any direction of movement. LM's ability to judge velocities was also tested. LM was asked the velocity of several targets moving at 3, 6, 12, or 24 deg/s. Speed was underestimated at velocities of 12 to 24 degrees (with a stated estimation less than 10 deg/s for both).

Motion aftereffects of vertical stripes moving in a horizontal direction and a rotating spiral were tested. She was able to detection motion in both patterns, but reported motion aftereffect in only 3 of the 10 trials for the stripes, and no effect for the rotating spiral. She also never reported any impression of motion in depth of the spiral. In Phi phenomenon two circular spots of light appear alternating. It appears that the spot moves from one location to the other. The distance between the spots varied 2.5 to 15 deg and the interstimulus interval was varied from 0 to 200 ms. Under no combination of conditions did the patient report any apparent movement. She always reported two independent light spots.

Visually guided pursuit eye and finger movements

LM was to follow the path of a wire mounted onto a board with her right index finger. The test was performed under purely tactile (blindfolded), purely visual (glass over the board), or tactile-visual condition. The patient performed best in the purely tactile condition and very poorly in the visual condition. She did not benefit from the visual information in the tactual-visual condition either. The patient reported that the difficulty was between her finger and her eyes. She could not follow her finger with her eyes if she moved her finger too fast.

Shipp's Experiments

Using a stimulus with a random distribution of light squares on a dark background that moved coherently, several other observations of LM's capabilities were made in 1994. Under these conditions, LM could always determine the axis of motion (vertical, horizontal), but not always the direction. If a few static squares were added to the moving display, identification of direction fell to chance, but identification of the axis of motion was still accurate. If a few squares were moving opposite and orthogonal to the predominant direction, her performance on both direction and axis fell to chance. She was also unable to identify motion in oblique directions, such as 45, 135, 225, and 315 degrees, and always gave answers in cardinal directions, 0, 90, 180, and 270 degrees.

Pelak and Hoyt's Alzheimer's patient

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 televisions 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).

Pelak and Hoyt's TBI patient

In 2003, a 60 year old man complained of the inability to perceive visual motion following a TBI, 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 see his dog, notice game, or track other hunters. 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 is place when vertically or horizontally scanning a written document and was unable to visualize three-dimensional images from two-dimensional blueprints.

In pop culture

Akinetopsia was mentioned in the TV show House in season 3, episode 7, entitled “Son of a Coma Guy”. When a young man walks into the hospital room, House begins to flash the room lights on and off to induce a seizure. He then throws a bag of potato chips into the young man's face who makes no attempt to avoid it or catch it. House asks if he wants to see something cool. He then proceeds to stand up, disappear, and does not reappear until he stops moving in front of the man's face. House tells the man he cannot see motion, a condition called akinetopsia, preceding his seizures.