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 Balints 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 LMs performance.TDs 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, TDs 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. Pelak and Hoyts Alzheimers patient
In 2000, a 70-year-old man presented with akinetopsia.
Side effects
Common side effects include:
Nausea
Bone marrow suppression, including
Decreased white blood cell count causing increased risk of infection
Decreased platelet count causing increased risk of bleedingLess common side effects include:

Severe allergic reactions
Pulmonary fibrosis (scarring of lung tissue) including fatal outcomes (usually only with prolonged use)
Hair loss
Interstitial pneumonitis
Rash
Itching
Irreversible bone marrow failure due to melphalan not being withdrawn early enough
Cardiac arrest

Mechanism of action
Melphalan chemically alters the DNA nucleotide guanine through alkylation, and causes linkages between strands of DNA. This chemical alteration inhibits DNA synthesis and RNA synthesis, functions necessary for cells to survive. These changes cause cytotoxicity in both dividing and non-dividing tumor cells. Tumor cells spend less time in resting phases than normal cells so at any given time, they are more likely to be metabolically active than most normal host cells. The rationale behind incorporating an alkylating function in a molecule resembling a primary cellular metabolite was to get a greater safety margin by fooling tumor cells into taking up the toxin preferentially. Synthesis
4-Nitro-L-phenylalanine (1) was converted to its phthalimide by heating with phthalic anhydride, and this was converted to its ethyl ester (2). Catalytic hydrogenation produced the corresponding aniline. Heating in acid with oxirane, followed by treatment with phosphorus oxychloride provided the bischloride, and removal of the protecting groups by heating in hydrochloric acid gave melphalan (3). Society and culture
Legal status
On 17 September 2020, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for melphalan.