Literature DB >> 11960806

Effects of cortical lesions on saccadic: eye movements in humans.

Ch Pierrot-Deseilligny1, C J Ploner, R M Muri, B Gaymard, S Rivaud-Pechoux.   

Abstract

Our knowledge of the cortical control of saccadic eye movements (saccades) in humans has recently progressed mainly because of lesion and transcranial magnetic stimulation (TMS) studies, but also because of functional imaging. It is now well known that the frontal eye field is involved in the control of intentional saccades, the parietal eye field in that of reflexive saccades, the supplementary eye field (SEF) in the initiation of motor programs comprising saccades, the pre-SEF in the learning of these programs, and the dorsolateral prefrontal cortex (DLPFC) in saccade inhibition, prediction and spatial working memory. Saccades may also be used as a convenient model of motricity to study general cognitive processes such as motivation and spatial memory. Thus, it has been shown that the posterior part of the anterior cingulate cortex, called the cingulate eye field, is involved in motivation and the preparation of all intentional saccades, but not in reflexive saccades. Recently, our understanding of the cortical control of spatial memory has noticeably progressed by using the simple visuo-oculomotor model represented by the memory-guide saccade paradigm, in which a single saccade is made to the remembered position of a unique visual item presented a while before. Transcranial magnetic stimulation studies have determined that after a brief stage of spatial integration in the posterior parietal cortex (inferior to 300 ms), short-term spatial memory (i.e., up to 15-20 seconds) is controlled by the DLPFC. Behavioral and lesion studies have shown that medium-term spatial memory (between 15 and 20 seconds and a few minutes) is specifically controlled by the parahippocampal cortex, before long-term memorization (i.e., after a few minutes) in the hippocampal formation. These different but complementary study methods used in humans have thus contributed to a better understanding of both eye movement physiology and general cognitive processes preparing motricity as whole.

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Year:  2002        PMID: 11960806     DOI: 10.1111/j.1749-6632.2002.tb02821.x

Source DB:  PubMed          Journal:  Ann N Y Acad Sci        ISSN: 0077-8923            Impact factor:   5.691


  47 in total

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2.  Gap effects on saccade and vergence latency.

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Journal:  Exp Brain Res       Date:  2003-10-14       Impact factor: 1.972

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5.  Visual exploration of emotional facial expressions in Parkinson's disease.

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6.  Influence of gap and overlap paradigms on saccade latencies and vergence eye movements in seven-year-old children.

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Journal:  Exp Brain Res       Date:  2005-02-23       Impact factor: 1.972

7.  Behavioral plasticity of antisaccade performance following daily practice.

Authors:  Kara A Dyckman; Jennifer E McDowell
Journal:  Exp Brain Res       Date:  2004-11-13       Impact factor: 1.972

8.  Saccades to the seeing visual hemifield in hemidecorticate patients exhibit task-dependent reaction times and hypometria.

Authors:  Troy M Herter; Daniel Guitton
Journal:  Exp Brain Res       Date:  2007-05-22       Impact factor: 1.972

Review 9.  A new neural framework for visuospatial processing.

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Journal:  Nat Rev Neurosci       Date:  2011-04       Impact factor: 34.870

10.  Aberrant brain activation during gaze processing in boys with fragile X syndrome.

Authors:  Christa Watson; Fumiko Hoeft; Amy S Garrett; Scott S Hall; Allan L Reiss
Journal:  Arch Gen Psychiatry       Date:  2008-11
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