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Disruption of Neural Systems of Visual Attention in Schizophrenia
Geoffrey F. Potts, PhD;
Brian F. O'Donnell, PhD;
Yoshio Hirayasu, MD, PhD;
Robert W. McCarley, MD
Arch Gen Psychiatry. 2002;59:418-424.
ABSTRACT
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Background Patients with schizophrenia show attention deficits. The frontal P2a
and posterior N2b event-related potential components are early indices of
activity in neural systems supporting attention and they are reduced in schizophrenia
in auditory tasks. However, the auditory P300 is reduced as well. Thus, the
P2a and N2b reductions may simply reflect a general event-related potential
amplitude reduction. The visual P300, however, is often spared in schizophrenia.
If neural systems supporting attention are specifically disrupted in schizophrenia,
the attention-sensitive P2a and N2b should be differentially reduced in patients,
compared with the P300, in a visual attention task.
Methods We analyzed 64-channel event-related potentials from 14 schizophrenic
patients and 14 control subjects in a visual object–spatial attention
task. We examined the amplitude of the P2a, N2b, and P300 components in the
target minus standard difference wave to see if there was a differential reduction
of the P2a and N2b compared with the P300.
Results Both the P2a and N2b waveforms were reduced in the patient group (81%
[control mean, 1.99 µV; patient mean, 0.38 µV] and 95% [control
mean, 0.55 µV; patient mean, 0.03 µV], respectively) while the
P300 was not reduced. Measured at the peak of the frontal P2a, the N2b was
larger dorsally in the spatial task and larger ventrally in the object task
in the control group.
Conclusions The spatial distribution of the P2a and N2b was consistent with activity
in the prefrontal cortex and modality-specific posterior cortex, respectively.
The differential reduction of the P2a and N2b waveforms supports the hypothesis
of specific disruption in neural systems of visual attention in schizophrenia.
INTRODUCTION
DISRUPTION OF attention and working memory are characteristic of patients
with schizophrenia.1-4
Attention allocates resources to task-relevant perceptual representations.
The ability to attend to and process task-relevant stimuli is critical for
generating goal-directed behavior. When attention is disrupted, the ability
to generate goal-directed behavior is impaired. Understanding of the neural
bases of attention and working memory disruption in schizophrenia might provide
insight into the neuropathologic factors of the disorder.
Primate studies suggest that prefrontal cortex and its interactions
with perceptual areas in posterior cortex are important for attention and
working memory.5-8
For visual stimuli, perceptual processing is divided into 2 streams: the dorsal
"where" spatial location stream, projecting to the posterior parietal cortex,
and the ventral "what" object feature stream, projecting to the inferior temporal
cortex.9-10 Interaction between
the posterior parietal cortex and the prefrontal cortex is necessary for visuospatial
working memory8 and similar interaction between
the inferior temporal cortex and the prefrontal cortex is needed in visual
object working memory.11 If the prefrontal
cortex and its connections with the posterior brain support attention and
working memory, then disruptions in these neural networks may underlie those
cognitive disturbances in schizophrenia.12
Event-related potentials (ERPs) have been used to study the neural systems
supporting attention. Early studies focused on the P300 component, a large,
centroparietal positive component, occurring approximately 400 milliseconds
after the presentation of a stimulus.13-15
However, since, in some cases, the P300 can peak after the execution of the
behavioral response,16 it cannot be a direct
index of the allocation of processing resources to relevant stimuli.
There are more specific, earlier posterior negative ERP indices of attention,
including the N2b.17-18 An N2b
has been identified to task-relevant stimuli in auditory,19-20
somatosensory,21-22 and visual
modalities.20, 23 The N2b usually
overlies and has been associated with activity in the cortical areas responsible
for perceptual processing.24-26
Some studies report a positivity over frontal sites at about the same
latency as the N2b.25-29
The frontal positivity, referred to here as the P2a, is due to different neural
generators than the N2b, demonstrated by differences in latency, laterality,
and psychological responsiveness.27-30
While the N2b is modulated both by stimulus properties and task demands, the
P2a is sensitive only to the task relevance of the stimulus.29
Thus, the P2a and N2b may provide an index of interaction between posterior
stimulus representation areas and the frontal executive in the processing
of task-relevant stimuli.
The most commonly reported ERP finding in schizophrenia is an amplitude
reduction of the auditory P300.31-33
Some studies have shown a left-sided lateralization of this reduction and
this has been linked to structural abnormalities in the left temporal lobe.34 The visual P300 seems to be less affected in schizophrenia,
with most studies showing either no reduction or less reduction of the visual
than the auditory P300.31-32 There
have been a few reports of auditory N2 reduction in schizophrenia.30, 35-36 To our knowledge,
there are only 2 reports of visual N2 reduction in schizophrenia, both of
which found the reduction despite a P300 of normal amplitude.35, 37
The single report, by our group, of the auditory frontal P2a in schizophrenia,
found it reduced.30 We know of no studies of
the visual P2a or related components in schizophrenia. Thus, it is unclear
if there is a specific disruption of the neural networks supporting visual
attention in schizophrenia, or whether the disruption is confined to the auditory
modality.
This study used a visual selective attention task, where targets were
defined either by their spatial location or their visual object features.
This task has been shown to elicit a P2a and N2b with a spatiotemporal distribution
consistent with interaction between prefrontal cortex and the dorsal where
pathway in location selection and the ventral what pathway in object selection.26 We compared the ERPs from a 64-channel recording
array, which provided the spatial resolution needed to assess activity in
specific processing pathways. Reduction of the frontal P2a and posterior N2b
in the patients, despite sparing of the P300, would provide evidence of specific
disruption of the neural systems supporting visual attention in schizophrenia.
SUBJECTS AND METHODS
SUBJECTS
The patients (n = 21) were recruited from outpatient treatment and inpatient
wards at the Brockton Veterans Affairs Medical Center, Brockton, Mass. Diagnoses
were made from the Structured Clinical Interview for DSM-IV (SCID) under the supervision of a licensed clinical psychologist trained
in SCID administration ( interrater reliability in our laboratory has
been 0.99 for schizophrenic vs other diagnoses over the last 5 years). Subjects
were between the ages of 19 and 58 years, had no history of electroconvulsive
treatment or neurological illness, no alcohol or other drug abuse in the last
5 years or a lifetime history of addiction, no alcohol use 24 hours prior
to testing, and the desire to participate as evidenced by giving written informed
consent. Control subjects (n = 22) were recruited by newspaper advertisement
using the same exclusion criteria with the addition of no lifetime history
of mental illness.
Subjects who performed at less than 90% accuracy in any task or who
had fewer than 20 artifact-free electroencephalographic (EEG) trials in any
condition were excluded, leaving 14 patients and 18 control subjects. An additional
4 controls were excluded to make equal-subpopulation (n) groups, selected
such that the groups were not significantly different for age. The groups
did differ on verbal IQ, parental socioeconomic status, and years of education
(Table 1). One control and 2 patients
were left-handed; all were male. The diagnostic conditions of the patients
were as follows: 6 were paranoid, 4 undifferentiated, 2 residual, and 2 schizoaffective.
All patients were medicated at the time of testing, 7 with typical antipsychotic
medications, 6 with atypical antipsychotic medications, and 1 with a combination
therapy. Seven of the patients were also taking anticholinergic medication.
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Demographic and Clinical Data for the Patients and Control Subjects*
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STIMULI AND TASKS
Stimuli were presented using a personal computer (Macintosh Centris
650; Apple Computer, Cupertino, Calif) running PsyScope software40
communicating with the EEG amplifiers via a Button Box (New Micros, Dallas,
Tex). During the experiment, there was a fixation dot at the center of the
screen and 4 boxes at the 4 corners of an invisible square. Each box subtended
approximately 2° of visual angle and was approximately 6° from fixation.
On each trial, 1 of 4 objects would appear in 1 of the boxes and remain onscreen
for 150 milliseconds with a 1250-millisecond intertrial interval. The 4 objects
were an "X," a "T," a "check mark," and a "triangle" (96 pixels per object).
The object and location on any given trial were equiprobable and selected
randomly without replacement from a pool of trial types (Figure 1).
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Figure 1. Six screens from the experiment
illustrating stimulus presentation. The boxes and the fixation dot were onscreen
at all times during a block. One of the 4 objects (a check mark, a diamond,
an "X", or a "T") appeared in 1 of the 4 boxes (stimulus and location selected
randomly and without replacement from f a pool of trial types) every 1250
milliseconds and remained on screen for 150 milliseconds in an object task
block, where the X was the target, and screen 4 f would require a response;
in a spatial task block, where the lower right location was the target, screen
6 would require a response.
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Subjects performed 2 blocked target detection tasks: selection by location
and selection by object. In the location task, 1 of the 4 boxes was designated
the target location. Subjects were instructed to press a key whenever any
object appeared at the target location. In the object task, 1 of the 4 objects
was designated the target. Subjects were instructed to press a key any time
the target object appeared at any location. The target objects and target
locations were randomly selected for each subject. Halfway through each run,
a new location and object were selected as targets, constrained such that
each subject had a target location in each visual field. Each subject participated
in 4 task blocks of 200 trials each, 2 location and 2 object blocks, with
a break every 100 trials. Task order and response hand were counterbalanced
across subjects.
EEG RECORDING AND PROCESSING
The EEG was referenced to the vertex and sampled at 250 Hz using 2 linked
32-channel EEG amplifiers (SynAmps; Neuroscan Labs, Herndon, Va) and 64-channel
electrode nets (Geodesic Sensor Nets; Electrical Geodesics Inc, Eugene, Ore).
Epochs were 1000 milliseconds, including a 200-millisecond prestimulus baseline.
The epochs were scanned by an artifact detection algorithm and trials with
eye blinks or out-of-range data (0 ± 75 µV) excluded from further
analysis. The EEG was digitally low-pass filtered at 30 Hz to eliminate high-frequency
noise. The EEG epochs were averaged by stimulus type (nontarget, target),
visual field (left, right), and task block (spatial, object) to create the
ERP waveforms, then transformed into an average reference representation to
attenuate spatial distortions due to choice of reference sensor.41
Grand average waveforms were created by averaging together the individual
subject averages for each group (schizophrenic, control) in each condition.
Since the psychological operation of interest was the detection of the task-relevant
targets, the ERP components in common to both the targets and nontargets were
removed by creating target minus nontarget difference waves. Target and nontarget
waveforms comparing the spatial and object tasks for the control and patient
groups at the frontal, dorsal, and ventral regions of interest (ROIs) are
shown in Figure 2. Target minus
nontarget waveforms are shown in Figure 3.
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Figure 2. Grand-average event-related potentials
to the target and nontarget stimuli in the right visual field (left visual
field stimuli event-related potentials are similar) in the spatial and object
tasks from the patient and control groups.
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Figure 3. Target minus nontarget difference
waves for the frontal, dorsal, and ventral regions of interest.
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DATA ANALYSES
Temporal windows were selected around the P2a, N2b, and P300 peaks in
the difference wave by inspection of the waveforms and a peak latency analysis
was performed. Where significant effects on latency were found between groups
or conditions, latency adjustments were made to the windows and the mean amplitude
was extracted (latencies below). To reduce the dimensionality of an electrode
factor, ROIs were identified containing subsets of the electrodes.42-43 These ROIs were frontal (bilateral
electrode pairs 2-59, 4-62, and 5-58) for the P2a; dorsal (8-34, 13-46, and
61-49) and ventral (20-38, 26-37, and 27-32) for the N2b; and centroparietal
(8-34, 20-38, 24-33) and temporal (15-47, 16-45, 18-43, and 23-42) for the
P300. The frontal, dorsal, and ventral ROIs are shown on a map of the electrode
locations in Figure 4. Six independent
repeated-measures analysis of variances (ANOVAs) were performed, a peak latency
and a mean amplitude analysis for each component window, with the within factors
task (spatial, object), visual field (left, right), and hemisphere (left,
right), plus an ROI factor (dorsal, ventral) in the N2b analysis, and a between
factor group (control, schizophrenic). A seventh ANOVA was performed on the
amplitude only at the temporal lobe ROI to test for laterality differences
as seen in the auditory P300 with the same electrode array.30
An ANOVA was also performed on the reaction time data. Correlations were computed
between the frontal P2a and the N2b at the 2 posterior ROIs and probabilities
computed with the Fisher r-to-z test. Tests for differences between groups on demographic variables
were performed using 2-tailed t tests. An  -level
of .05 was used for all comparisons.
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Figure 4. Electrode position map. The nose
is at the top, back of the head at the back, and the vertex at the center
of the figure. Standard positions from the 10/20 system are marked in circles.
The region of interest electrodes are identified by squares (frontal), diamonds
(dorsal), and triangles (ventral). FP indicates prefrontal electrode; F, lateral
frontal electrode; Fz, superior frontal electrode; T, midtemporal electrode;
Cz, central electrode; Pz, parietal electrodes; O, cccipital electrode; and
Oz, midline occipital electrode.
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RESULTS
BEHAVIORAL MEASURES
The groups differed on reaction time, F1,23 = 19.32, P<.001, with the patient group (mean [SD], 593.99 [92.32]
milliseconds) about 120 milliseconds slower than the control group (mean,
471.41 [83.04] milliseconds). There was also a significant difference in reaction
time between the tasks, F1,23 = 89.95, P<.001,
with the reaction time in the spatial task (mean, 488.43 [84.05] milliseconds)
about 93 milliseconds faster than in the object task (mean, 580.91 [108.79]
milliseconds). Mean accuracy was 99% (792/800) for controls in the spatial
task and 97% (776/800) in the object task; the patients were 97% (775/800)
in the spatial task and 94% (750/800) in the object task.
ELECTROPHYSIOLOGICAL MEASURES
Latency
Effects for task and group were used for latency correction. The latency
window for the P2a and N2b was from 160 to 400 milliseconds For the P2a there
was a main effect for task, F = 46.93, P<.001,
with the spatial task peak (mean, 263.26 [73.12] milliseconds) about 51 milliseconds
earlier than the object task peak (mean, 313.96 [60.19] milliseconds). There
was an effect for task on the N2b, F = 81.37, P<.001,
showing a faster latency in the spatial task (mean, 248.82 [56.360] milliseconds)
than in the object task (mean, 296.67 [68.16] milliseconds). The latency window
for the P300 was from 320 to 600 milliseconds. There was an effect for task,
F = 78.43, P<.001, showing shorter peak latency
in the spatial task (mean, 455.81 [69.64] milliseconds) than in the object
task (mean, 520.12 [63.13] milliseconds). There was also an effect for group,
F = 5.10, P = .03, showing a faster latency in the
control group (mean, 469.26 [75.66] milliseconds) than in the patient group
(mean, 506.67 [66.95] milliseconds).
Amplitude
Figure 5 shows ERP from a
midline electrode between Cz and Pz (electrode 21) comparing the patient and
control groups with the amplitude windows for the P2a/N2b and P300. The latency
corrected amplitude windows for the P2a and N2b were 160 to 300 milliseconds
for the spatial task and 228 to 368 milliseconds for the object task. There
was an effect on the P2a for group, F = 34.25, P<.001,
showing reduced amplitude in the patient group. For the N2b, there was a main
effect for group, F1,26 = 10.13, P = .004,
showing a smaller amplitude in the patient group and an effect for hemisphere,
F = 31.97, P<.001, which was modified by group,
F = 26.89, P<.001, showing a larger amplitude
over the left hemisphere in the controls only. Task x ROI x Group
was significant, F = 14.22, P<.001, showing a
larger N2b in the ventral path in the object task and a larger N2b in the
dorsal path in the spatial task in the control group (Figure 6). Task x ROI x Field was significant, F = 7.67, P = .01, as were the Task x ROI x Field x
Group, F = 6.63, P = .016, and Task x ROI x
Hemisphere x Group, F = 4.77, P = .04 interactions,
indicating that the larger dorsal N2b in the spatial task and ventral N2b
in the object task in the control group was mostly for stimuli in the left
visual field and over the left hemisphere.
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Figure 5. Difference waves at a posterior
midline site, near parietal electrode 21 showing the N2b reduction despite
amplitude sparing of the P300 in the patient group compared with the control
subjects. The amplitude windows are shown here, the object windows on the
object, left visual field plot, and the spatial windows on the spatial left
visual field plot. The N2b windows are in long dashes, the P300 windows for
the controls are in the light dots, and the P300 window for the patients is
in the dark dots.
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Figure 6. Task x ROI x Group
interaction. Bars denote SE. Amplitude of the N2b at the dorsal and ventral
regions of interest (ROIs) in the spatial and object tasks for the controls
and patients. Note the larger N2b dorsally in the spatial condition and ventrally
in the object condition for the controls only.
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The P300 amplitude window was latency corrected for differences in group
and task. For the spatial task the window was from 360 to 520 milliseconds
for the controls and 392 to 552 milliseconds for the patients; for the object
task the window was from 416 to 576 milliseconds for the controls and 464
to 624 milliseconds for the patients. In the centroparietal ROI there was
an effect for task, F = 6.10, P = .02, showing a
larger P300 in the spatial task. The Field x Hemisphere x Group
interaction was significant, F = 7.29, P = .01, suggesting
a larger P300 contralateral to the visual field of the stimulus for the control
subjects. In the temporal lobe ROI, there was a Field x Hemisphere interaction,
F = 5.00, P = .03, showing the P300 larger contralateral
to the visual field of the stimulus. Task x Hemisphere x Group
interaction was significant, F = 6.30, P = .02, indicating
that, for the controls, the P300 in the spatial task was larger over the left
hemisphere and in the object task was larger over the right hemisphere.
CORRELATIONS
For the controls, the strongest correlations were between the frontal
and ventral ROIs in both tasks (object task: r = -0.34, P<.001; spatial task: r = -0.39, P<.001). However, the P2a was significantly correlated
with the dorsal N2b only in the spatial task, r = -0.23, P = .003; in the object task the correlation only approached
significance, r = -0.15, P = .06. In the patients, the correlation was actually stronger between
the frontal P2a and ventral N2b in the object task that for the controls, r = -0.48, P<.001. However,
for the patients, the correlation between the P2a and ventral N2b in the spatial
task was reduced compared with the controls, r = -0.22, P = .005, and the correlation between the P2a and dorsal
N2b was not significant in the spatial task, r = -0.12, P = .11.
COMMENT
In this visual attention study, the patients with schizophrenia showed
a reduced P2a and a reduced N2b, despite a P300 of normal amplitude and spatial
distribution. This suggests that the neural systems and cognitive operations
indexed by the P2a and the N2b were differentially affected in the patient
group.
Attention requires the direction of processing resources to task-relevant
perceptual representations. Prior research indicates that the N2b indexes
the formation of a perceptual representation in modality specific areas of
posterior cortex.44 The P2a, with its inferior
prefrontal distribution and enhancement to target stimuli, may index activity
in orbitofrontal cortical areas of task-relevance computation or salience
evaluation.26 One of the functions of orbitofrontal
cortex appears to be to evaluate the motivational value of a stimulus, independent
of its physical features.45 The topographic
distribution and psychological responsiveness of the P2a and N2b are consistent
with simultaneous activity in posterior cortical areas of perceptual representation
and prefrontal cortical areas of salience evaluation.26, 29
For the controls, at the peak of the P2a, the N2b was larger at the ventral
ROI when target detection was based upon object feature and larger at the
dorsal ROI when target detection was based upon stimulus location (Figure 3 and Figure 6). This relationship was not true for the patients, indicating
a disruption in the visual attention network between prefrontal cortex and
stimulus-specific posterior cortex. The patients were able to perform the
task, thus, there had to be some level of activity in the network. However,
if the activity was sufficiently degraded, it might be unable to generate
a scalp detectable P2a and N2b. In a more difficult task, the performance
of the patients might start to decline more precipitously than that of the
controls as the network became more challenged.
From the data presented here it is impossible to determine if the location
of the physiological dysfunction is in one of the contributing cortical areas
(prefrontal cortex or multiple posterior areas) or in the connections between
the areas. There is substantial evidence that structural and functional abnormality
in the frontal brain contributes to cognitive disruption in schizophrenia.46-52
There are also hypotheses that posit functional disconnections in the brain
in schizophrenia,53-55
one of which proposes a disruption in communication between prefrontal and
posterior cortex.56-57 There is
less evidence of distributed posterior dysfunction. The correlation analysis
here is ambiguous, suggesting disrupted communication in the spatial task
but not in the object task, consistent with behavioral data suggesting differential
disruption in the dorsal pathway in schizophrenia.58
This study used a heterogenous group of long-term, medicated patients,
and there were significant differences between the control and patient groups.
The ERP effects might be medication induced, although a prior study found
visual N2 reduction in unmedicated patients.50, 59
Despite these limitations, the large and differential degradation of the P2a
and N2b in the patient group provides evidence of specific disruption of the
neural system supporting detection of task relevant visual stimuli in schizophrenia.
AUTHOR INFORMATION
Submitted for publication October 4, 2000; final revision received September
7, 2001; accepted October 1, 2001.
This study was supported by a young investigator's award from the National
Alliance for Research on Schizophrenia and Depression, Great Neck, NY (Dr
Potts). Additional support was provided by grant MH40799-09 from the National
Institutes of Health, Bethesda, Md (Dr McCarley) and by the Veterans Administration
through the Research Center for Basic and Clinical Neuroscience Studies of
Schizophrenia, Washington, DC (Dr McCarley).
Corresponding author and reprints: Geoffrey F. Potts, PhD, Psychology,
MS-25, Rice University, 6100 Main St, Houston, TX 77005 (e-mail: gpotts{at}rice.edu).
From Rice University, Houston, Tex (Dr Potts); University of Indiana,
Bloomington (Dr O'Donnell); Kyorin University School of Medicine, Tokyo, Japan
(Dr Hirayasu); Harvard Medical School, Boston, Mass, and Brockton Veterans
Affairs Medical Center, Brockton, Mass (Dr McCarley).
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