<unk>  is a dysfunction of visual memory, caused by localized cortical hyperexcitability or hyperactivity in the posterior visual pathway. Post-geniculate cortical lesions or seizures may cause cortical deafferentation, focal cortical irritation, and epileptic discharges, the proposed mechanisms of<unk> . Cortical deafferentation Palinopsia can occur from posterior visual pathway (post-geniculate) deafferentation, which causes homonymous visual field deficits. This mechanism is thought to be similar to the deafferentation hyperexcitability seen in visual release hallucinations (Charles Bonnet syndrome), which are distinguished from palinopsia by whether the formed image or scene previously occurred. It is hypothesized that deafferentation hyperexcitability is the cause of neuropathic pain. Molecular changes from deafferentation include an increase in presynaptic neurotransmitter vesicles and heightened post-synaptic receptor sensitivity. Epileptic discharges Palinopsia from epileptic discharges, confirmed by electroencephalogram, have been reported during a seizure aura, during the seizure, or post-ictally. The seizures can originate anywhere in the posterior visual pathway, depending on the location of the pathology. Palinoptic seizures rarely generalize, and there are case reports of palinopsia as the only symptom of a visual seizure. If seizures are persistent, then continual palinoptic episodes often occur. Focal cortical irritation Palinopsia, which occurs after neurosurgical procedures or cerebrovascular accidents, has been partly attributed to focal cortical irritation. Symptoms are associated with perilesional hyperperfusion, which may reflect focal cortical instability and subsequent hyperactivity. While there are reports of palinopsia from each individual mechanism, there is usually a combination of the aforementioned mechanisms. For example,<unk>  may present in a patient with seizure symptoms and visual field deficits, after a neurosurgical procedure. This suggests that the cortical hyperactivity from each mechanism is additive.<unk> , once considered a disorder of the nondominant parieto-occipital lobe, has since been shown to occur from lesions in the dominant or non-dominant temporal, parietal, or occipital lobes. … The predominance of lesions in certain cortical areas is more likely due to the uneven distribution or functional variation of visual cortex-hippocampal neurons. ... All of the<unk>  symptoms occur concomitantly in a patient with one lesion, which supports current evidence that objects, features, and scenes are all units of visual memory, perhaps at different levels of processing. This alludes to neuroanatomical integration in visual memory creation and storage."
Hallucinatory palinopsia
Lexical–gustatory synesthesia
Illusory palinopsia
Agraphesthesia
Homonymous hemianopsia
Hemifacial spasm
Facial toning
Binocular dysphoria