Visual-spatial neglect after right-hemisphere stroke: behavioral and electrophysiological evidence
Visual-spatial neglect (VSN), also known as hemispatial neglect, hemineglect, or hemi-inattention, is a neuropsychological syndrome that occurs after brain injury, characterized by asymmetric spatial behavior. In most cases, VSN is contralateral to the damaged brain hemisphere, although ipsilesional VSN has also been rarely reported. Visual neglect commonly involves the left side of space, with spatial neglect caused by right hemisphere damage accounting for approximately 13% to 82% of all spatial neglect cases. The pathogenetic mechanism of VSN remains unclear, though previous neuroimaging studies suggest that deficits in visual processing may be a major contributor to unilateral spatial neglect.
Currently, the most widely used tool for behavioral assessment of VSN is the paper-and-pencil task. However, its diagnostic sensitivity is limited, as some patients with subclinical VSN may show normal performance on these tasks. Event-related potentials (ERPs) provide a non-invasive and objective method for recording the brain’s response to specific sensory, cognitive, and motor events. ERPs have been increasingly used to evaluate attention function in patients with VSN, with the most commonly used components being P1, N1, and P300. P1 represents the early processing stage of spatial attention, essential for maintaining attention and regulated by endogenous attention. Previous studies have found that VSN is associated with increased latencies of visual evoked potentials, with the latency of P1 evoked by contralesional stimuli being longer than that evoked by ipsilesional stimuli. The N1 component is attenuated in neglect patients, indicating an impairment in processing left-side visual input. The P300 component represents the late processing stage of spatial attention and has been found to be associated with the number of missed contralesional targets.
This study aimed to investigate the behavioral and ERP changes in patients with or without VSN following right-hemisphere stroke. The visual processing function in these patients was compared to that in normal controls through analysis of behavioral and electrophysiological parameters, providing new insights into the pathogenesis of VSN.
The study was approved by the Ethics Committee of Xuanwu Hospital of Capital Medical University, and written informed consent was obtained from each participant. A total of 22 patients diagnosed with right-hemisphere stroke were enrolled, with 11 patients developing VSN allocated to the VSN group and the other 11 patients allocated to the non-VSN group. Additionally, 11 age- and gender-matched healthy participants were recruited as controls. The inclusion criteria included right-handedness, age within the range of 18 to 80 years, normal or corrected visual acuity, and first-onset ischemic or hemorrhagic stroke restricted within the right hemisphere with a clinical course of at least two weeks. Exclusion criteria included achromatopsia or hemianopsia, previous history of stroke, severe psychiatric disorders, neuropsychological diseases, brain tumor, severe cardiac, pulmonary, or kidney diseases, and disturbance of consciousness.
The individual visual-spatial function was evaluated using several behavioral tests, including the line bisection task, line cancellation task, star cancellation task, clock drawing task, gap detection task, and text reading task. These tests assessed various aspects of visual-spatial attention and neglect, such as the ability to mark the midpoint of line segments, identify and mark specific targets, and read text columns. The neglect degree was calculated based on the distance from the marked point to the actual midpoint in the line bisection task, and the percentage of missed targets was documented in the cancellation tasks.
Electrophysiological evaluation was performed using a Neuroscan 64-lead ERP workstation. Participants were tested in a quiet, electromagnetic interference-free testing room, sitting 57.5 cm away from the display screen. During the examination, participants were instructed to press the left mouse button when left-side target stimulation was observed and the right mouse button when right-side target stimulation was observed. The ERP task consisted of 16 blocks, each with 40 trials, and the electrical signals were collected using the International EEG system and processed using E-prime software.
The ERP signals were analyzed between 200 ms before stimulation and 800 ms after stimulation, with artifacts beyond 100 mV removed. The waveforms of standard stimuli and deviant stimuli were averaged and digitally filtered, respectively. P300 referred to the positive wave occurring 300 ms after stimulation onset, N1 was the negative wave occurring 130 to 230 ms after stimulation onset, and P1 was the positive wave presenting 90 to 160 ms after target onset. The amplitude and latency of P300, N1, and P1 components were measured using Neuroscan 4.5 software.
The results showed that the response times in the VSN and non-VSN groups were both prolonged compared with those of normal controls. In response to either valid or invalid cues in the left side, the accuracy in the VSN group was lower than that in the non-VSN group, and the accuracy in the non-VSN group was lower than that in controls. The P1 latency in the VSN group was significantly longer than that in the control group, and the N1 amplitude in the VSN group was significantly lower than that in the control group. When responding to right targets, the left-hemisphere P300 amplitude in the VSN group was significantly lower than that in the control group. With either left or right stimuli, the bilateral-hemisphere P300 latencies in the VSN and non-VSN groups were both significantly prolonged, while the P300 latency did not differ significantly between the VSN and non-VSN groups.
The line bisection mean score of patients in the VSN group was significantly higher than that of the control participants, suggesting that the left-side spatial attention function may be impaired even in the absence of apparent VSN. In the neuroelectrophysiological task, the left-target accuracy in the non-VSN group was significantly lower than that in the normal controls, and ERPs showed abnormalities as well, supporting the behavioral manifestations. The accuracy for both left and right targets in the VSN group was significantly lower than that in the other two groups, and the response times for both left and right targets were prolonged, indicating that the right-side spatial attention function may be impaired.
In the ERP monitoring, significant heterogeneity was found in the early-stage ERP components (P1 and N1) between bilateral hemispheres, with the response of the left hemisphere to valid cues being more severely impaired than that of the right hemisphere. This provides neuroelectrophysiological evidence for the lateralization of VSN. There was no significant difference in the P1 amplitude among the three groups, but the P1 latency responding to the right stimuli in the VSN group was significantly longer than those in the non-VSN and control groups. The right-hemisphere amplitude for responding to the left stimuli in the VSN group was significantly lower than that in the control group, consistent with previous reports. There was no significant difference in the N1 latency among the three groups.
P300 is a late component of ERPs that reflects the late stage of cognitive processing. In this study, bilateral P300 in response to the right stimuli had a lower amplitude and longer latency in patients with VSN compared with normal controls, indicating that the responses of bilateral hemispheres to right-sided targets were both impaired. In the non-VSN group, even though the patients performed well on the paper-and-pencil task, the ERPs were abnormal, including inter-hemispheric heterogeneity of P1 and N1 components as well as reduced amplitude and prolonged latency of P300, indicating potential visual-spatial impairment.
In conclusion, visual-spatial attention function is impaired after right-hemisphere stroke, independent of the presentation of apparent clinical neglect symptoms. Clinicians should be aware of subclinical VSN. This study provides neuroelectrophysiological evidence for the lateralization of VSN, and both the early (P1 and N1) and late (P300) ERP components were altered in patients with VSN after right-hemisphere stroke.
doi.org/10.1097/CM9.0000000000000218
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