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. Alzheimers disease
Besides memory problems, Alzheimers patients may have varying degrees of akinetopsia. This could contribute to their marked disorientation. While Pelak and Hoyt have recorded an Alzheimers case study, there has not been much research done on the subject yet. Antidepressants
Inconspicuous akinetopsia can be triggered by high doses of certain antidepressants with vision returning to normal once the dosage is reduced. Areas of visual perception
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
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. Evidence of functional specialization of V5 was first found in primates. Patients with akinetopsia tend to have unilateral or bi-lateral damage to the V5. V1
V1, also known as the primary visual cortex, is located in Brodmann area 17.
Stereochemistry
Midodrine contains a stereocenter and consists of two enantiomers, making it a racemate; i.e., a 1:1 mixture of (R)- and (S)-forms:

Synthesis
Acylation of 1,4-dimethoxybenzene with chloroacetyl chloride gives the chloroketone 2. The halogen is then converted to the amine 3 by any set of standard schemes, and the ketone reduced to an alcohol with borohydride (4). Acylation of the amino group in this last intermediate with chloroacetyl chloride affords the amide 5. The halogen is then displaced with azide and the resulting product 6 reduced catalytically to the glycinamide, midodrine (7). References
External links
 Media related to Midodrine at Wikimedia Commons

"Midodrine". Drug Information Portal. U.S. National Library of Medicine.