Visuospatial abnormalities have often been reported in PD patients. Early in 1964, Proctor et al. (105) demonstrated that PD patients have difficulty in determining when a rod is vertical if they are in a darkened room. Later, this abnormality was confirmed both in patients seated in a chair that is tilted either to the right or to the left (13), and in patients who are upright (106). Subsequently, as we have already documented, a number of authors reported that PD is associated with disproportionate impairments in visuospatial abilities. However, for a long time, consensus on the specificity and significance of experimental data was lacking. Part of the debate stemmed from methodological inadequacies of early studies that did not account for factors such as motor speed, dexterity, and presence or absence of pharmacological treatment. On this basis, it was suggested (107) that impaired visuospatial ability in PD patients may be owing to "generic" increase in reaction time or other aspects of attentional disorders.
More refined neuropsychological studies both in de novo PD patients (88) and using tasks either requiring no motor response or minimizing the dexterity, speed, and coordination, provided insight into the existence of visuospatial disturbances free of such confounding motor factors. In addition, statistical techniques were used to explore relationships between motor and visuospatial deficits and helped to determine whether or not spatial deficits are of the same magnitude as, or in excess of, those attributable to motor abnormalities.
Since degeneration of dopaminergic neurons constitutes the main biochemical abnormality found in PD, dopamine depletion has been considered to account for most of the symptoms, including behavioral abnormalities and cognitive deficits (89). If striatal dopamine deficiency plays a role in PD patients' cognitive deficit, specialized hemispheric functions contralateral to the motor symptoms should be altered in patients with hemiparkinsonism, providing a unique opportunity to study the effect of asymmetrical subcortical degeneration on cognitive functions (108). Yet, the results of these studies have been controversial. A number of studies were not able to demonstrate a specific pattern of difference between patients with predominantly left and right symptoms (9,109-111). However, a number of more recent studies (43,44) did find a specific directional bias related to the side of the predominant symptoms. On the other hand, Pillon et al. (112) demonstrated that cognitive impairment is poorly correlated with symptoms responding well to levodopa treatment (e.g., akinesia and rigidity) and is strongly related to axial symptoms (such as gait disorders and dysarthria), which respond little if at all to levodopa treatment. This finding was interpreted as suggesting that cognitive impairment in PD patients is, to a great extent, a result of dysfunction of non-dopaminergic neuronal systems. A further suggestion that the visuospatial deficits of PD patients do not always depend on the same mechanisms subserving motor impairments derives from the observation that patients treated with bilateral deep brain stimulation of the subthalamic nucleus, despite obtaining clinical motor benefits, show a significant decline in their ability to encode visuospatial material (113). According to this study, the decline was more consistently observed in patients over the age of 69 yr and it led to a mental state that the authors describe as similar to that observed in progressive supranuclear palsy (PSP) patients.
In conclusion, it is still possible that striatal dopamine deficiency, even if it is not the major determinant of visuospatial deficits, could play a role in determining attentional bias underlying the subtle neglect phenomena that are encountered in predominant left-sided PD patients.
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