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The parietal cortex and saccade planning: lessons from human lesion studies.

Ptak R, Müri RM - Front Hum Neurosci (2013)

Bottom Line: The parietal cortex is a critical interface for attention and integration of multiple sensory signals that can be used for the implementation of motor plans.Many neurons in this region exhibit strong attention-, reach-, grasp- or saccade-related activity.However, these patients also show bilateral impairments of saccade initiation and control that are difficult to explain in the context of their lateralized deficits of visual attention.

View Article: PubMed Central - PubMed

Affiliation: Division of Neurorehabilitation, University Hospitals Geneva Geneva, Switzerland ; Laboratory of Cognitive Neurorehabilitation, Faculty of Medicine, University of Geneva Geneva, Switzerland ; Faculty of Psychology and Educational Sciences, University of Geneva Geneva, Switzerland.

ABSTRACT
The parietal cortex is a critical interface for attention and integration of multiple sensory signals that can be used for the implementation of motor plans. Many neurons in this region exhibit strong attention-, reach-, grasp- or saccade-related activity. Here, we review human lesion studies supporting the critical role of the parietal cortex in saccade planning. Studies of patients with unilateral parietal damage and spatial neglect reveal characteristic spatially lateralized deficits of saccade programming when multiple stimuli compete for attention. However, these patients also show bilateral impairments of saccade initiation and control that are difficult to explain in the context of their lateralized deficits of visual attention. These findings are reminiscent of the deficits of oculomotor control observed in patients with Bálint's syndrome consecutive to bilateral parietal damage. We propose that some oculomotor deficits following parietal damage are compatible with a decisive role of the parietal cortex in saccade planning under conditions of sensory competition, while other deficits reflect disinhibition of low-level structures of the oculomotor network in the absence of top-down parietal modulation.

No MeSH data available.


Related in: MedlinePlus

Average latency of saccades (upper row) and manual reaction times (lower row) as a function of distracter location, shown separately for healthy controls, brain injured patients without neglect, and neglect patients. Positive numbers indicate distracter locations (in degrees) in the same hemifield as the target (for left targets distracters in the left hemifield are shown on the right side and distracters in the right hemifield on the left side of each graph). The straight horizontal lines show average latency/reaction time when no distracter was presented. Note the increase of saccade latency for neglect patients when the distracter was presented at fixation (position 0). Figure adapted from Ptak et al. (2007) by permission from Oxford University Press.
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Figure 2: Average latency of saccades (upper row) and manual reaction times (lower row) as a function of distracter location, shown separately for healthy controls, brain injured patients without neglect, and neglect patients. Positive numbers indicate distracter locations (in degrees) in the same hemifield as the target (for left targets distracters in the left hemifield are shown on the right side and distracters in the right hemifield on the left side of each graph). The straight horizontal lines show average latency/reaction time when no distracter was presented. Note the increase of saccade latency for neglect patients when the distracter was presented at fixation (position 0). Figure adapted from Ptak et al. (2007) by permission from Oxford University Press.

Mentions: Compared to healthy controls and control patients with right-hemisphere lesions neglect patients had only slightly increased saccade latencies for contralesional targets when no distracter was present (Figure 2). However, the pattern of response changed when a distracter was added: distracters in the right hemifield strongly captured the gaze of neglect patients, resulting in up to 60% directional errors. The capture of gaze by ipsilesional distracters is a robust finding and has been observed in patients with post-acute neglect (Müri et al., 2009) as well as in clinically recovered neglect (Harvey et al., 2002; Olk et al., 2002; Pflugshaupt et al., 2004). More interestingly, in those trials where no directional error was made remote distracters did not increase contralesional saccade latencies of neglect patients more than of control participants. These results suggest that an ipsilesional distracter interferes at two different levels with saccade programming: it either interacts with processes involved in the selection of the saccade target (the where-process; eventually resulting in a directional error) or it delays the onset of the saccade once the correct target has been selected (when-process). The first type of interference appears to be pathologically increased in spatial neglect, while the second type is unaffected.


The parietal cortex and saccade planning: lessons from human lesion studies.

Ptak R, Müri RM - Front Hum Neurosci (2013)

Average latency of saccades (upper row) and manual reaction times (lower row) as a function of distracter location, shown separately for healthy controls, brain injured patients without neglect, and neglect patients. Positive numbers indicate distracter locations (in degrees) in the same hemifield as the target (for left targets distracters in the left hemifield are shown on the right side and distracters in the right hemifield on the left side of each graph). The straight horizontal lines show average latency/reaction time when no distracter was presented. Note the increase of saccade latency for neglect patients when the distracter was presented at fixation (position 0). Figure adapted from Ptak et al. (2007) by permission from Oxford University Press.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3675316&req=5

Figure 2: Average latency of saccades (upper row) and manual reaction times (lower row) as a function of distracter location, shown separately for healthy controls, brain injured patients without neglect, and neglect patients. Positive numbers indicate distracter locations (in degrees) in the same hemifield as the target (for left targets distracters in the left hemifield are shown on the right side and distracters in the right hemifield on the left side of each graph). The straight horizontal lines show average latency/reaction time when no distracter was presented. Note the increase of saccade latency for neglect patients when the distracter was presented at fixation (position 0). Figure adapted from Ptak et al. (2007) by permission from Oxford University Press.
Mentions: Compared to healthy controls and control patients with right-hemisphere lesions neglect patients had only slightly increased saccade latencies for contralesional targets when no distracter was present (Figure 2). However, the pattern of response changed when a distracter was added: distracters in the right hemifield strongly captured the gaze of neglect patients, resulting in up to 60% directional errors. The capture of gaze by ipsilesional distracters is a robust finding and has been observed in patients with post-acute neglect (Müri et al., 2009) as well as in clinically recovered neglect (Harvey et al., 2002; Olk et al., 2002; Pflugshaupt et al., 2004). More interestingly, in those trials where no directional error was made remote distracters did not increase contralesional saccade latencies of neglect patients more than of control participants. These results suggest that an ipsilesional distracter interferes at two different levels with saccade programming: it either interacts with processes involved in the selection of the saccade target (the where-process; eventually resulting in a directional error) or it delays the onset of the saccade once the correct target has been selected (when-process). The first type of interference appears to be pathologically increased in spatial neglect, while the second type is unaffected.

Bottom Line: The parietal cortex is a critical interface for attention and integration of multiple sensory signals that can be used for the implementation of motor plans.Many neurons in this region exhibit strong attention-, reach-, grasp- or saccade-related activity.However, these patients also show bilateral impairments of saccade initiation and control that are difficult to explain in the context of their lateralized deficits of visual attention.

View Article: PubMed Central - PubMed

Affiliation: Division of Neurorehabilitation, University Hospitals Geneva Geneva, Switzerland ; Laboratory of Cognitive Neurorehabilitation, Faculty of Medicine, University of Geneva Geneva, Switzerland ; Faculty of Psychology and Educational Sciences, University of Geneva Geneva, Switzerland.

ABSTRACT
The parietal cortex is a critical interface for attention and integration of multiple sensory signals that can be used for the implementation of motor plans. Many neurons in this region exhibit strong attention-, reach-, grasp- or saccade-related activity. Here, we review human lesion studies supporting the critical role of the parietal cortex in saccade planning. Studies of patients with unilateral parietal damage and spatial neglect reveal characteristic spatially lateralized deficits of saccade programming when multiple stimuli compete for attention. However, these patients also show bilateral impairments of saccade initiation and control that are difficult to explain in the context of their lateralized deficits of visual attention. These findings are reminiscent of the deficits of oculomotor control observed in patients with Bálint's syndrome consecutive to bilateral parietal damage. We propose that some oculomotor deficits following parietal damage are compatible with a decisive role of the parietal cortex in saccade planning under conditions of sensory competition, while other deficits reflect disinhibition of low-level structures of the oculomotor network in the absence of top-down parietal modulation.

No MeSH data available.


Related in: MedlinePlus