2011
DOI: 10.1016/j.neuropsychologia.2011.03.002
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Initiation and inhibitory control of saccades with the progression of Parkinson's disease – Changes in three major drives converging on the superior colliculus

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Cited by 130 publications
(134 citation statements)
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“…Altered oculomotor performance in PD Significant differences between PD patients and controls were demonstrated for all of the investigated eye movement parameters (Table 2), in agreement with previous studies (Helmchen et al 2012;Mosimann et al 2005;Pinkhardt et al 2012;Terao et al 2011). The only exception was peak eye velocity.…”
Section: Resultssupporting
confidence: 90%
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“…Altered oculomotor performance in PD Significant differences between PD patients and controls were demonstrated for all of the investigated eye movement parameters (Table 2), in agreement with previous studies (Helmchen et al 2012;Mosimann et al 2005;Pinkhardt et al 2012;Terao et al 2011). The only exception was peak eye velocity.…”
Section: Resultssupporting
confidence: 90%
“…Nonetheless, a dysfunctional inhibitory system was consistently proposed to be responsible for a disturbed suppression of unwanted gaze shifts both in the absence of any targets (Lemos and Eggenberger 2013) and in the presence of a distracting stimulus (Munoz and Everling 2004). This 'hyper-reflexive' behavior observed for patients with PD in the present study has been previously attributed to a disturbed triggering of the 'input gate', the superior colliculus, due to abnormal firing patterns mediated by the basal ganglia (Terao et al 2011). However, this proposed model is not satisfactory to explain the full spectrum of oculomotor dysfunction including executive eye movement dysfunctions such as interrupting saccades during smooth pursuit, fixational periods as well as a high distractability in anti-saccade performance. Fig.…”
Section: Discussionsupporting
confidence: 58%
“…A more detailed cognitive status would have been particularly important for the PD patients who presented executive deficits in oculomotor functions that were correlated with volume loss of the cerebrum, since volumetric studies demonstrated that GM atrophy in PD is modest in cognitively “normal” patients but becomes marked in the presence of cognitive deficits [35]. Oculomotor abnormalities worsen when PD patients present with cognitive difficulties [22] as investigated in detail with respect to cognitive status [19] and overall disease stage [36]. Moreover, the analysis was correlational per se so that direct conclusions about causal relationships between regional volume loss and oculomotor performance are not possible.…”
Section: Discussionmentioning
confidence: 99%
“…Additionally, the structures and connections underlying oculomotor neurophysiology have been well characterized (Gaymard et al, 1998;Leigh and Zee, 1999;Munoz and Everling, 2004;Munoz et al, 2000). Eye movement tasks have provided powerful insight into neurological dysfunction in clinical disorders such as Parkinson's disease (Terao et al, 2011), attention-deficit/ hyperactivity disorder (ADHD) (Mahone et al, 2009) and schizophrenia (Reuter et al, 2011). For example, deficits in eye movement control are measurable in both children and adults with ADHD, and are consistent with frontostriatal pathophysiology (Munoz et al, 2003).…”
mentioning
confidence: 99%