Recovery of visual fields in brain-lesioned patients by reaction perimetry treatment

<p>Abstract</p> <p>Background</p> <p>The efficacy of treatment in hemianopic patients to restore missing vision is controversial. So far, successful techniques require laborious stimulus presentation or restrict improvements to selected visual field areas. Due to the large number of brain-damaged patients suffering from visual field defects, there is a need for an efficient automated treatment of the total visual field.</p> <p>Methods</p> <p>A customized treatment was developed for the reaction perimeter, permitting a time-saving adaptive-stimulus presentation under conditions of maximum attention. Twenty hemianopic patients, without visual neglect, were treated twice weekly for an average of 8.2 months starting 24.2 months after the insult. Each treatment session averaged 45 min in duration.</p> <p>Results</p> <p>In 17 out of 20 patients a significant and stable increase of the visual field size (average 11.3° ± 8.1) was observed as well as improvement of the detection rate in the defective visual field (average 18.6% ± 13.5). A two-factor cluster analysis demonstrated that binocular treatment was in general more effective in augmenting the visual detection rate than monocular. Four out of five patients with a visual field increase larger than 10° suffered from hemorrhage, whereas all seven patients with an increase of 5° or less suffered from infarction. Most patients reported that visual field restoration correlated with improvement of visual-related activities of daily living.</p> <p>Conclusion</p> <p>Rehabilitation treatment with the Lubeck Reaction Perimeter is a new and efficient method to restore part of the visual field in hemianopia. Since successful transfer of treatment effects to the occluded eye is achieved under monocular treatment conditions, it is hypothesized that the damaged visual cortex itself is the structure in which recovery takes place.</p

Facial dysmorphopsia: a notable variant of the "thin man" phenomenon?

The aim of this work is to investigate the facial distortion (dysmorphopsia) experienced by patients with homonymous paracentral scotomas and to analyze the interrelationship with the previously described "thin man" phenomenon. Routine neuro-ophthalmological examination and brain MRI in three patients who suffered from small homonymous paracentral scotomas due to infarction or arteriovenous malformations of the occipital lobe. They all complained of distortion and shrinkage of their interlocutor's face contralateral to the brain lesion. The phenomenon appeared some seconds after steady fixation on the interlocutor's nose and was evident with both left and right homonymous scotomas. The patients did not notice a gap in the area corresponding to the scotoma and objects other than faces were perceived normally. Homonymous paracentral scotomas can lead to focal displacement of facial features towards the center of the field defect with resulting distortion of the face on the affected side. This so-called "dysmorphopsia" makes faces appear regionally narrower than they are in reality and may be induced even by visual field defects that remain undetected by conventional perimetry using 6A degrees x 6A degrees grids. Predilection for faces is probably associated with the superior location of scotomas or specific impairment of face processing abilities related to the lesion site. Facial dysmorphopsia is most probably associated with cortical "filling-in" and spatial distortion, and can hence be regarded as a special entity of the "thin man" phenomenon