<unk>  is a dysfunction in visual perception, presumably related to diffuse neuronal excitability alterations in the anterior and posterior visual pathways. Because of the drugs that cause<unk> , 5-HT2a receptor excitotoxicity or a disruption of GABAergic transmission have been proposed as possible mechanisms. However, the neuropharmacology of the visual system is probably too complex to pinpoint the visual disturbances to a single neurotransmitter or neurotransmitter receptor. The generation of<unk>  is often dependent on ambient light or motion, and the symptoms could be a pathological exaggeration of normal light perception and motion perception mechanisms. Prolonged indistinct afterimages are symptomatically similar to physiological afterimages, and light streaking and visual trailing are symptomatically similar to motion blur when viewing fast-moving objects. Light and motion perception are dynamic operations involving processing and feedback from structures throughout the central nervous system. A patient frequently has multiple types of diffuse, persistent<unk>  symptoms which represent dysfunctions in both light and motion perception. Light and motion are processed via different pathways, which suggests that there are diffuse or global excitability alterations in the visual pathway. Faulty neural adaptation and feedback between the anterior and posterior visual pathways could cause persistent excitability changes. Movement-related<unk>  could be due to inappropriate or incomplete activation of the motion suppression mechanisms (visual masking/backward masking and corollary discharges) related to visual stability during eye or body movements, which are present in saccadic suppression, blinking, smooth pursuit, etc.<unk>  in migraineurs<unk>  may occur during a migraine aura, as do other diffuse<unk>  symptoms such as halos around objects, visual snow, dysmetropsia, and oscillopsia. In a rare migraine subtype known as persistent visual aura without infarction,<unk>  symptoms (prolonged indistinct afterimages, light streaking, and visual trailing) persist after the migraine has abated. Alternatively, up to 10% of all migraineurs report of formed afterimages that only last a couple seconds and do not occur with other<unk>  symptoms. These momentary afterimages appear at a different location in the visual field than the original stimulus, occur a few times per month, and are affected by external light and motion. (variant image perseveration). Migraineurs with these momentary afterimages report significantly fewer migraine headaches than migraineurs without these afterimages (4.3 vs. 14.4 attacks/year). These afterimages probably represent an overlap in hallucinatory and<unk> . Studying these momentary formed afterimages, in relation to alterations in cortical excitability, could advance our understanding of migraine pathogenesis and mechanisms associated with encoding visual memory.
Illusory palinopsia
Oscillopsia
Facial weakness
Meralgia paraesthetica
Hallucinatory palinopsia
Hemifacial spasm
Akinetopsia
Photopsia