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 ones own motion appears to be important. Causes
Brain lesions
Akinetopsia may be an acquired deficit from lesions in the posterior side of the visual cortex. Lesions more often cause gross akinetopsia. The neurons of the middle temporal cortex respond to moving stimuli and hence the middle temporal cortex is the motion-processing area of the cerebral cortex. In the case of LM, the brain lesion was bilateral and symmetrical, and at the same time 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
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.
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. "LM"
Most of what is known about akinetopsia was learned from LM, a 43-year-old female admitted into the hospital October 1978 complaining of headache and vertigo. LM was diagnosed with thrombosis of the superior sagittal sinus which resulted in bilateral, symmetrical lesions posterior of the visual cortex. These lesions were 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 a "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.