19 He had presented a case with an exact temporal correspondence of visual loss and the onset of figure and landscape hallucinations.

Morax’s derived a theory of their cause based on positive scotoma, dark areas of the visual field related to retinal lesions. He argued that positive scotoma occurred when aberrant retinal impulses were conducted to the brain, and were absent when such conduction could not take place, for example through retinal fiber loss. Visual hallucinations Inhibitors,research,lifescience,medical in eye disease were simply a more elaborate form of positive scotoma in which the aberrant retinal signals were conducted beyond the visual cortex to its associative centers. Other ophthalmologists joined Morax with further reports of temporal associations (eg, Truc20) and two psychiatrists, Brunerie and Cloche, presented a case in which visual hallucinations resolved after a cataract operation.21 Arthur Ormond, an ophthalmologist at Guy’s hospital in London, Inhibitors,research,lifescience,medical published his own cases in 192522 and, influenced by Galton’s work on visual imagery, concluded that visual hallucinations

Inhibitors,research,lifescience,medical were related to a hypersensitivity of specialized visual cortical areas, triggered in some cases by eye disease. Yet not all ophthalmologists agreed with the ocular theory. In France, Terson summarized in a single phrase the seemingly incontrovertible evidence against the eye as a primary cause of visual hallucinations: “[...]consider the vast number of cases of eye disease without hallucinations and hallucinations without eye disease.”23 In his view, additional toxic or inflammatory brain factors were invariable in such patients. Eye disease Inhibitors,research,lifescience,medical itself could not be an important factor as visual hallucinations could occur without it, in its presence or after it had resolved. L’Hermitte and de Ajuriaguerra’s 1936 paper added further weight to Terson’s counterargument with post-mortem evidence of a patient with visual hallucinations in which thalamic lesions were found in addition to eye disease.2 They also argued that aberrant retinal signals could at best only engender simple hallucinatory Inhibitors,research,lifescience,medical forms and should cease with

eye closure, a maneuver that only seemed to influence hallucinations in a few patients. They did not dismiss the possible role of the eye but believed it, at best, a secondary why factor. De Morsier incorporated this view into his 1936 and 1938 papers, citing L’Hermitte as having disproved the ocular theory For de Morsier, eye disease was not the cause of CBS, or indeed visual hallucinations under any circumstances, and was specifically excluded from his classification. However, it is clear that in 1938 at least, de Morsier’s opposition to the eye was specific to the aberrant retinal impulse theory In response to the commentary on his 1938 paper, he agreed with Velter that a reduction in MEK inhibitor clinical trial acuity through eye disease might provoke visual hallucinations,24 a view that differs little from modern deafferentation theory (see below).