Selective Impairment of Attentional Networks of Alerting in Wilson's Disease

Han, Yongsheng; Zhang, Fangfang; Tian, Yanghua; Hu, Panpan; Li, Bo; Wang, Kai · 2014 · OpenAlex-citations

DOI: 10.1371/journal.pone.0100454

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Summary

This study investigates the specific attentional deficits associated with Wilson’s disease (WD), a rare genetic disorder of copper metabolism that causes neurological and psychiatric symptoms. While attention impairment is a known symptom of WD, previous research had not determined whether this deficit affects all aspects of attention or specific subcomponents. The authors hypothesized that WD patients would exhibit selective impairments in attentional networks, given the disease's impact on basal ganglia structures which are linked to cognitive functions. The study aimed to identify which of the three independent attentional networks—alerting, orienting, and executive control—were affected in WD patients compared to healthy controls. The researchers conducted a comparative study involving 35 patients with early to moderate neurological WD and 35 healthy controls matched for age, gender, and education. Participants performed the Attention Network Test (ANT), a computerized task designed to measure the efficiency of the three attentional networks through reaction times and accuracy. The study excluded patients with significant liver impairment, mental retardation, or severe anxiety and depression to isolate cognitive effects. Neuropsychological background tests, including measures of intelligence, verbal fluency, and mood, were also administered. Statistical analyses, including nonparametric tests and ratio score transformations to control for global slowing, were used to evaluate differences in network efficiencies. The results revealed a selective impairment in the alerting network among WD patients. While WD patients exhibited significantly longer overall reaction times than healthy controls, there were no significant differences in accuracy. Crucially, the alerting effect was significantly reduced in the WD group (p = 0.007), indicating a diminished ability to maintain response readiness based on warning cues. In contrast, the orienting (p = 0.729) and executive control (p = 0.888) networks showed no significant differences between the two groups. Ratio score analyses confirmed that the alerting deficit was not merely a byproduct of general motor slowing. MRI scans of the patients showed abnormalities in the basal ganglia, thalamus, and brainstem, with thalamic involvement being particularly relevant to the alerting network. The findings demonstrate that WD causes a specific deficit in the alerting attentional network, distinct from orienting and executive control functions. This suggests that WD patients struggle to utilize temporal warning cues to enhance reaction speed, likely due to dysfunction in the thalamic and basal ganglia circuits that regulate alertness. The study highlights the utility of the ANT in dissociating specific cognitive deficits in neurological disorders. By identifying a selective alerting impairment, the research provides insight into the cognitive substrate of WD, linking clinical symptoms to specific neuroanatomical pathways and neuromodulators, such as norepinephrine, which are implicated in alerting processes.

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• attention selective divided