Saccadic Reaction Times in Patients With Frontal and Parietal Lesions

Braun, Doris I.; Weber, Heike; Mergner, Thomas; Schulte‐Mönting, Jürgen

doi:10.1093/brain/115.5.1359

Cited by 181 publications

(80 citation statements)

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“…The existence of express saccadeenhanced persistent neurons in LIP supports the findings from lesion study of posterior parietal cortex in human and nonhuman primates in which the number of express saccades decreased and the SRT distribution of regular saccade shifted to the right (Lynch and McLaren, 1989;Braun et al, 1992;Li et al, 1999). Our results also support the findings of a more recent human EEG study in which authors found the increased activity in occipital-parietal network during mid-gap and lategap intervals preceding express saccades (Hamm et al, 2010).…”

Section: Preparatory Activity Plays Crucial Role In Determining Srtsupporting

confidence: 62%

“…Notably, this hypothesis excluded the involvement of the higher cortical regions in express saccade generation. In contrast, another line of experiments observed that, following lesions of posterior parietal cortex in both human and nonhuman primates, express saccades were rare and saccade reaction times (SRTs) increased (Lynch and McLaren, 1989;Braun et al, 1992;Li et al, 1999). Consistent with this, EEG studies in humans found increased activity in an occipital-parietal network during the gap interval preceding express saccades (Hamm et al, 2010), further suggesting that parietal areas might be specifically involved in generation of express saccades.…”

Section: Introductionmentioning

confidence: 99%

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Parietal Cortical Neuronal Activity Is Selective for Express Saccades

et al. 2013

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Saccadic eye movements are central to primate behavior and serve to move the eyes to visual objects of interest. Express saccades, unlike regular saccades, occur with very short reaction times, a behavior necessary for speeded reactions in goal-directed behavior. Previous studies have shown that introduction of a blank interval (gap) between the fixation point offset and the saccadic target onset leads to an increase in the number of express saccades and that the superior colliculus plays a crucial role in the generation of express saccades. A longstanding hypothesis asserted that express saccades are mediated largely by a subcortical circuit, circumventing extrastriate visual cortex. An alternative "posterior pathway" hypothesis proposed the involvement of posterior parietal cortex. In the present study, using a gap saccade task, we investigated the role of nonhuman primate's lateral intraparietal cortex (LIP) in generation of express saccades. We show that roughly half of recorded LIP neurons were modulated during the gap interval. Moreover, a group of neurons with persistent activity in a memory-guided saccade task enhanced their activity during express saccades relative to that during regular saccades. After reducing the target's certainty by increasing the potential target locations, neuronal activity remained in the similar level during express saccades but markedly reduced during regular saccades that correlated with the increase of saccadic reaction time in the regular saccade. Our results suggest that area LIP is directly involved in generating saccades in express mode.

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Section: Preparatory Activity Plays Crucial Role In Determining Srtsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Parietal Cortical Neuronal Activity Is Selective for Express Saccades

et al. 2013

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“…In general, patients with lesions encompassing the FEF seem to have difficulty inhibiting saccades to inappropriate stimuli (Braun et al 1992;Guitton et al 1985;Machado and Rafal 2004a). More specifically for fixation-related inhibition, such patients can show abnormally small fixation-offset effects on their contralesional side (Machado and Rafal 2004b).…”

Section: Discussionmentioning

confidence: 99%

Which Visual Pathways Cause Fixation-Related Inhibition?

Sumner

Nachev²,

Castor-Perry³

et al. 2006

Journal of Neurophysiology

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Sumner, Petroc, Parashkev Nachev, Sarah Castor-Perry, Heather Isenman, and Christopher Kennard. Which visual pathways cause fixation-related inhibition? J Neurophysiol 95: 1527-1536, 2006. First published November 30, 2005 doi:10.1152/jn.00781.2005. Visual stimuli can both inhibit and activate motor mechanisms. In one well-known example, the latency of saccadic eye movements is prolonged in the presence of a fixation stimulus, relative to the case in which the fixation stimulus disappears before the target appears. This automatic sensory-motor effect, known as the gap effect or fixationoffset effect, has been associated with inhibitory connections within the superior colliculus (SC). Visual information is provided to the SC and other oculomotor areas, such as the frontal eye fields (FEF), mainly by the magnocellular geniculostriate pathway, and also by the retinotectal pathway. We tested whether signals in these pathways are necessary to create fixation-related inhibition, by using stimuli invisible to them. We found that such stimuli, visible only to short-wavesensitive cones (S cones), do produce fixation-related inhibition (including when warning effects were equated). We also demonstrate that this fixation-related inhibition cannot be explained by residual activation of luminance pathways and must be caused by a route separate from that of luminance fixation signals. Thus there are at least two routes that cause fixation-related inhibition, and direct sensory input to the SC or FEF by the magnocellular or retinotectal pathways is not required. We discuss the implications that there may be both cortical and collicular mechanisms.

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“…Indeed a recent review has highlighted the predominant role of the parietal eye field in 'reflexive' saccades, and the frontal eye fields in 'voluntary' saccades (Leigh and Kennard 2004). In particular, parietal eye field lesions in humans cause increased latency of visually triggered saccades, which does not seem to occur after frontal eye field lesions (Pierrot-Deseilligny et al 1991;Braun et al 1992). Furthermore, lesion of the parieto-collicular tract can cause isolated impairment of reflexive but not memoryguided saccades (Gaymard et al 2003).…”

Section: The Site Of Action Of Dopaminementioning

confidence: 99%

Saccadic latency distributions in Parkinson’s disease and the effects of l-dopa

Michell

Fritz

et al. 2006

Exp Brain Res

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Parkinson's disease (PD) is associated with a loss of central dopaminergic pathways in the brain leading to an abnormality of movement, including saccades. In PD, analysis of saccadic latency distributions, rather than mean latencies, can provide much more information about how the neural decision process that precedes movement is affected by disease or medication. Subject to the constraints of intersubject variation and reproducibility, latency distribution may represent an attractive potential biomarker of PD. Here we report two studies that provide information about these parameters, and demonstrate a novel effect of dopamine on saccadic latency, implying that it influences the neural decision process itself. We performed a detailed cross-sectional study of saccadic latency distributions during a simple step task in 22 medicated patients and 27 agematched controls. This revealed high intersubject variability and an overlap of PD and control distributions. A second study was undertaken on a different population specifically to investigate the effects of dopamine on saccadic latency distributions in 15 PD patients. L-dopa was found to prolong latency, although the magnitude of the effect varied between subjects. The implications of these observations for the use of saccadic latency distributions as a potential biomarker of PD are discussed, as are the effects of L-dopa on neural decision making, where it is postulated to increase the criterion level of evidence required before the decision to move is made.

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Saccadic Reaction Times in Patients With Frontal and Parietal Lesions

Cited by 181 publications

References 0 publications

Parietal Cortical Neuronal Activity Is Selective for Express Saccades

Parietal Cortical Neuronal Activity Is Selective for Express Saccades

Which Visual Pathways Cause Fixation-Related Inhibition?

Saccadic latency distributions in Parkinson’s disease and the effects of l-dopa

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