Über Polyopie und Palinopsie; pp. 154–164

Bekény, Georg; Péter, Ágnes

doi:10.1159/000131159

Cited by 6 publications

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“…Palinopsia usually occurs in a defective but not blind hemifield or field quadrant, sometimes as monocular diplopia, sometimes bilateral, and on occasions associated with polyopia, in which multiple afterimages are superimposed on the background picture after the visual stimulus has disappeared (Bender and Sobin, 1963;Bender et al, 1968). The images may move in the direction of gaze (Cummings et al, 1982), and may be associated with the illusion of movement or other disturbances in visuospatial perception (Bekeny and Peter, 1961;Meadows and Munro, 1977;Cleland et al, 1981). Palinopsia is most often the result of a right posterior cerebral lesion that interferes with mechanisms of visual synthesis (Bender and Kanzer, 1941;Le Beau et al, 1952, 1954, 1958Kinsbourne and Warrington, 1963;Meadows and Munro, 1977;Michel and Troost, 1980;Koelmel, 1982;Cummings et al, 1982).…”

Section: S Sveinbjornsdottir and J S Duncanmentioning

confidence: 99%

Parietal and Occipital Lobe Epilepsy: A Review

1993

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There has been considerable recent interest in frontal lobe epileptic syndromes, and less attention paid to occipital and parietal epilepsies. The occipital and parietal lobes have arbitrary anatomical borders. The prinicpal seizure symptomatology includes somatosensory (paresthetic, painful, thermal, sexual, apraxia, disturbances of body image); visual (amaurotic, elementary and complex hallucinations, illusions) and other phenomena (anosognosia, apraxia, acalculia, alexia, aphemia, confusional states, gustatory, vertiginous, adversive, oculoclonic and eyelid flutter). The seizure symptoms are of varying localizing and lateralizing value and seizure discharges may spread rapidly and perceived symptoms may reflect secondary spread rather than the primary site of seizure onset. Recognized parietal and occipital epilepsy syndromes include benign epilepsy of childhood with centrotemporal spikes, benign epilepsy of childhood with parietal evoked spikes, benign occipital epilepsy of childhood, migraine/epilepsy syndromes, and epilepsy with bilateral occipital calcification. In addition, occipital and parietal epilepsy may be on the basis of any underlying structural lesion. There is frequently a poor correlation between clinical and EEG features. MRI and functional imaging often reveals underlying pathology. There have been no specific trials of different antiepileptic drugs for occipital and parietal seizures. Surgical treatment has its place, with attention to the risk of causing a fixed neurological deficit.

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