Impaired shifting of attention in Balint's syndrome☆
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Cited by (36)
Bálint syndrome
2021, Handbook of Clinical NeurologyCitation Excerpt :Fig. 13.7 shows the figure copy of patients with nonlateralized Bálint's syndrome to be compared with the same figure copied by a clinical neglect patient with additional rightward orienting bias leading him to mislocalize elements more toward the right side of the copy. In Posner's paradigm, patients with posterior parietal lesion exhibit defects in shifting spatial attention (Verfaellie et al., 1990) or in disengaging attention from fixated objects (Rizzo and Vecera, 2002), a difficulty which may be central for the visual grasp reflex to occur. Michel and Henaff (2004) have provided a comprehensive examination of a patient (AT) with bilateral PPC lesion whose initial Bálint's syndrome had been reduced 20 years post onset to bilateral optic ataxia and a variety of attentional deficits that can be interpreted as a concentric shrinking of the attentional field.
Disorders of Higher Cortical Visual Function
2018, Liu, Volpe, and Galetta's Neuro-Ophthalmology: Diagnosis and ManagementVertical line quadrisection: "What" it represents and who gets the upper hand
2013, Brain and LanguageCitation Excerpt :If this upward bias of spatial attention is mediated by the ventral stream, then our results suggest that, as compared to vertical line bisection, vertical line quadrisection leads to greater activation of the ventral stream. Whereas we have presented evidence that the ventral stream for allocentric visual processing is associated with an upward bias of spatial attention, and previous research has also demonstrated that the dorsal stream for egocentric visual processing is associated with a downward bias of spatial attention (Rapcsak, Cimino, & Heilman, 1988; Verfaellie, Rapcsak, & Heilman, 1990), the relation between the left and right hemispheres, focal and global attention, and biases in the vertical distribution of attention is less well understood. We have proposed that during vertical line quadrisection, the focal attentional demands of the task may have led to greater activation of the ventral stream, and this contributed to the increased upward bias of spatial attention.
Visual attention deficits in Alzheimer's disease: Relationship to HMPAO SPECT cortical hypoperfusion
2011, NeuropsychologiaCitation Excerpt :With bilateral damage, however, the attentional deficit should be minimal, since the loss of competitive weights is more or less symmetrical and consequently neither hemifield has a competitive advantage over the other. This latter prediction is supported by reports of patients with bilateral parietal damage who show no evidence of a bilateral disengage deficit (Coslett & Saffran, 1991; Verfaellie, Rapcsak, & Heilman, 1990). Although various studies have explored attentional processing in AD, there has not been a clear consensus on whether the behavioral alterations are unilateral or bilateral in nature.
Chapter 20 Optic ataxia and Bálint's syndrome: neuropsychological and neurophysiological prospects
2008, Handbook of Clinical NeurologyCitation Excerpt :Copying of images is accordingly composed of tiny elements of the original figure without perception of the whole scene. Using Posner's paradigm, it was shown that parietal patients exhibit a defect in shifting spatial attention (Verfaellie et al., 1990), or in disengaging attention from fixated objects (Rizzo and Vecera, 2002), a difficulty which may be central for the visual grasp reflex to occur. Michel and Hénaff (2004) have provided a comprehensive examination of a patient with bilateral PPC lesion whose initial Bálint's syndrome had been reduced 20 years post onset to bilateral optic ataxia and a variety of attentional deficits that could all be interpreted as a concentric shrinking of the attentional field.
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This work was supported in part by the Medical Research Service of the Veterans Administration.
- 1
Present address: Memory Disorders Research Center at the Boston Veterans Administration Medical Center and Boston University School of Medicine, Boston, MA.
- 2
Present address: Department of Neurology, University of Arizona, Tucson, AZ.