Motion perception in schizophrenia

BACKGROUND: Eye-tracking dysfunction has been found in many patients with schizophrenia and in about 40% of their first-degree biological relatives. We hypothesized that a deficit in motion processing is associated with eye-tracking dysfunction because both motion signals and the brain regions responsible for processing motion signals are implicated in the generation of smooth pursuit. We examined several aspects of visual perception, including motion perception, in patients with schizophrenia. METHODS: To evaluate motion perception, contrast sensitivity for velocity discrimination was measured in patients with schizophrenia (n=15) and normal control subjects (n=18). Contrast sensitivities for orientation discrimination and contrast detection were measured as control tasks. RESULTS: Patients with schizophrenia showed significantly lower contrast sensitivity (ie, higher thresholds) than normal controls for the discrimination of small velocity differences (eg, 11 vs 9 degrees/s). This reduction in contrast sensitivity was severe (up to 10-fold) in about 40% of the patients. No group differences were found on the other tasks. CONCLUSION: The discrimination of small velocity differences is impaired in a subgroup of patients with schizophrenia.     

Bipolar and schizophrenic patients differ in patterns of visual motion discrimination

BACKGROUND: Since Kraepelin's early distinction between bipolar disorder and schizophrenia, it has been assumed that these disorders represent two different pathophysiological processes, although they share many clinical symptoms. Previous studies showed that velocity discrimination, a sensitive psychophysiological measure of the visual motion system, is deficient in schizophrenia. Here we examined whether the motion processing impairment found in schizophrenia also occurs in bipolar disorder. METHODS: We compared 16 bipolar patients, 25 schizophrenic patients, and 25 normal controls on a velocity discrimination task. We measured the psychophysical threshold for velocity discrimination and contrast detection (as a control task) in all subjects. RESULTS: Bipolar patients showed normal velocity discrimination thresholds at intermediate velocities, the range in which velocity cues dominate velocity discrimination, and at low velocities. Schizophrenic patients, however, showed elevated velocity discrimination thresholds at intermediate and low velocities. At higher velocities, both bipolar and schizophrenic patients showed elevated thresholds. All subjects showed normal contrast detection thresholds. CONCLUSIONS: Normal velocity discrimination in the intermediate range of velocity indicates unimpaired motion processing in bipolar disorder. The abnormal velocity discrimination of both schizophrenic and bipolar patients at higher velocities may reflect impaired temporal processing rather than impaired motion processing per se. These results suggest that the pathophysiological processes of bipolar disorder and schizophrenia diverge at the stage of visual motion processing, a sensory component mediated primarily in the extrastriate cortex.     

Aging and visual motion discrimination in normal adults and schizophrenia patients

Motion perception is impaired in many neuropathological conditions, including schizophrenia. Motion perception also declines in the course of normal aging. In this study, we ask whether aging is an additive factor in the motion-discrimination deficits of schizophrenia patients. We examined motion perception in schizophrenia patients (n=44) and non-psychiatric controls (n=40) whose ages ranged from 18 to 55. The tasks included velocity discrimination and contrast detection. Thresholds for each of the two tasks were determined for each subject using psychophysical methods. Schizophrenia patients showed significantly increased thresholds (degraded performance) for velocity discrimination compared with the controls. Degraded performance in patients was not related to age. In controls, however, velocity discrimination thresholds were significantly increased beginning by age 45. Performance on a contrast-detection task, which does not require precise discrimination of motion signals, was not significantly affected by age in either group. Aging, even in its early stages, degrades motion discrimination in normal adults. Aging, however, does not adversely affect motion-discrimination deficits in schizophrenia patients through age 55. A similar motion-discrimination deficit in schizophrenia patients and aging normal adults suggests that the mechanisms underlying motion processing in schizophrenia and normal aging may be associated.     

Magnocellular contributions to impaired motion processing in schizophrenia

Patients with schizophrenia show impairments in motion processing, along with deficits in lower level processing primarily involving the magnocellular visual pathway. The present study investigates potential magnocellular contributions to impaired motion processing in schizophrenia using a combined neurophysiological and behavioral approach. As compared to prior motion studies in schizophrenia, thresholds were determined for both incoherent and coherent visual motion. In this study, velocity discrimination thresholds were measured for schizophrenia patients (n=14) and age-matched normal control subjects (n=16) using a staircase procedure. Early visual processing was evaluated using steady-state visual evoked potentials (ssVEP), with stimuli biased toward activation of either the magnocellular or parvocellular visual pathways through luminance contrast manipulation. Patients with schizophrenia showed poor velocity discrimination for both incoherent and coherent motion, with no significant group x task interaction. Further, when coherent motion performance was measured at individually determined incoherent motion thresholds, accuracy levels for patients were similar to controls, also indicating similarity of deficit for incoherent vs. coherent motion discrimination. Impairments in velocity discrimination correlated significantly with reduced amplitude of ssVEP elicited by magnocellular -- but not parvocellular -- selective stimuli. This study demonstrates that deficits in motion processing in schizophrenia are significantly related to reduced activation of the magnocellular visual system. Further, this study supports and extends prior reports of impaired motion processing in schizophrenia, and indicates significant bottom-up contributions to higher-order cognitive impairments.     

Bipolar and schizophrenic patients differ in patterns of visual motion discrimination

BackgroundSince Kraepelin's early distinction between bipolar disorder and schizophrenia, it has been assumed that these disorders represent two different pathophysiological processes, although they share many clinical symptoms. Previous studies showed that velocity discrimination, a sensitive psychophysiological measure of the visual motion system, is deficient in schizophrenia. Here we examined whether the motion processing impairment found in schizophrenia also occurs in bipolar disorder.MethodsWe compared 16 bipolar patients, 25 schizophrenic patients, and 25 normal controls on a velocity discrimination task. We measured the psychophysical threshold for velocity discrimination and contrast detection (as a control task) in all subjects.ResultsBipolar patients showed normal velocity discrimination thresholds at intermediate velocities, the range in which velocity cues dominate velocity discrimination, and at low velocities. Schizophrenic patients, however, showed elevated velocity discrimination thresholds at intermediate and low velocities. At higher velocities, both bipolar and schizophrenic patients showed elevated thresholds. All subjects showed normal contrast detection thresholds.ConclusionsNormal velocity discrimination in the intermediate range of velocity indicates unimpaired motion processing in bipolar disorder. The abnormal velocity discrimination of both schizophrenic and bipolar patients at higher velocities may reflect impaired temporal processing rather than impaired motion processing per se. These results suggest that the pathophysiological processes of bipolar disorder and schizophrenia diverge at the stage of visual motion processing, a sensory component mediated primarily in the extrastriate cortex.     

Smooth pursuit eye movements to extra-retinal motion signals: deficits in patients with schizophrenia

In order to understand mechanisms underlying the smooth pursuit abnormality(ies) in schizophrenia, new methods, which independently evaluated predictive smooth pursuit responses to extra-retinal motion signals, were developed and tested. The study compared responses to only extra-retinal motion signals in normal volunteers (n = 25), and individuals with a chronic (n = 21) and a recent onset (n = 18) schizophrenia. Subject groups with chronic schizophrenia and recent onset schizophrenia had significantly poorer predictive pursuit than normal subjects in response to only extra-retinal motion signals. The poor predictive pursuit was evident even at low target velocity when the closed-loop pursuit gain was normal in patients with schizophrenia. Ten of the 18 recent onset patients were drug-free at the time of testing and had no or minimum previous exposure to anti-psychotic medications. Re-analyses of the data showed that on most measures of predictive pursuit, drug-free patients were not significantly different from patients who received anti-psychotic drug treatment. Both patient groups had significantly poorer predictive pursuit than normal subjects. These results suggest that a deficit in processing extra-retinal motion may underlie the abnormal smooth pursuit response in schizophrenia. At low target velocities, patients with schizophrenia were able to compensate for the low extra-retinal gain by increasing the gain of response to the retinal slip velocity. This indicates that patients were able to process retinal slip velocity and generate smooth pursuit eye movements, but experienced a specific deficit in processing and/or integrating extra-retinal motion information for the smooth pursuit response.     

Dependence of impaired eye tracking on deficient velocity discrimination in schizophrenia

BACKGROUND: Abnormal smooth pursuit eye movements have been found in many schizophrenic patients and in about 40% of their first-degree biological relatives. A velocity discrimination deficit has also been demonstrated in schizophrenic patients. In this study, we address the relation between deficient velocity discrimination and impaired smooth pursuit eye movements, inasmuch as the brain regions responsible for processing velocity signals are implicated in generating and maintaining smooth pursuit. METHODS: Horizontal eye movements of 15 schizophrenic patients and 8 normal controls were recorded in response to sine wave (predictable) and step-ramp (nonpredictable) targets. Smooth pursuit eye movements were assessed during both the initiation and maintenance periods. Correlations were computed between measures of smooth pursuit (qualitative rating, peak gain, saccade frequency, and initial acceleration) and contrast sensitivity for velocity discrimination. RESULTS: Contrast sensitivity for fine velocity discrimination was significantly correlated both with initial acceleration of smooth pursuit and with peak gain, but was not significantly correlated with saccade frequency and qualitative ratings of pursuit integrity. No significant correlations were found within the normal control group. CONCLUSION: Deficient processing of velocity information seems to be one component that contributes to a dysfunction in the initiation and maintenance of smooth pursuit in schizophrenia.     

Processing of global,but not local,motion direction is deficient in schizophrenia

Visual motion processing is compromised in a substantial proportion of schizophrenic patients, but precise neural mechanisms underlying the motion-processing deficit have not yet been elaborated. The visual motion pathway includes a local and a global processing stage, each of which has distinct neural substrates. Here, we attempt to identify the stage(s) that are implicated in impaired motion processing of schizophrenia-local, global, or both. For schizophrenia patients (n=23) and normal controls (n=26), we measured (1) the thresholds for detecting the motion direction of a random dot pattern, a task that requires global motion processing, and (2) the thresholds for detecting the motion direction of a grating, a task that requires only local motion processing, using psychophysical methods. Schizophrenia patients showed elevated thresholds for detecting the direction of coherent motion, particularly for the high dot-density target. In contrast, schizophrenia patients showed normal thresholds for detecting the direction of motion of a grating. The results indicate that the global, but not the local, processing stage of the visual motion system is compromised in schizophrenia patients, thus implicating motion-sensitive brain areas that possess large receptive fields for spatial and temporal integration, such as Middle Temporal Area/Medial Superior Temporal Area.     

The face and its emotion: right N170 deficits in structural processing and early emotional discrimination in schizophrenic patients and relatives

Previous studies have reported facial emotion recognition impairments in schizophrenic patients, as well as abnormalities in the N170 component of the event-related potential. Current research on schizophrenia highlights the importance of complexly-inherited brain-based deficits. In order to examine the N170 markers of face structural and emotional processing, DSM-IV diagnosed schizophrenia probands (n=13), unaffected first-degree relatives from multiplex families (n=13), and control subjects (n=13) matched by age, gender and educational level, performed a categorization task which involved words and faces with positive and negative valence. The N170 component, while present in relatives and control subjects, was reduced in patients, not only for faces, but also for face-word differences, suggesting a deficit in structural processing of stimuli. Control subjects showed N170 modulation according to the valence of facial stimuli. However, this discrimination effect was found to be reduced both in patients and relatives. This is the first report showing N170 valence deficits in relatives. Our results suggest a generalized deficit affecting the structural encoding of faces in patients, as well as the emotion discrimination both in patients and relatives. Finally, these findings lend support to the notion that cortical markers of facial discrimination can be validly considered as vulnerability markers.     

Early stage vision in schizophrenia and schizotypal personality disorder

Previous studies of visual perception have reported deficits in contrast sensitivity and dot motion discrimination in schizophrenia. We tested whether these deficits also appear in schizotypal personality disorder (SPD). SPD appears to be genetically and symptomatically related to schizophrenia, but without the marked psychosocial impairment associated with psychotic disorders. The present study investigated contrast sensitivity for moving and static gratings, form discrimination and dot motion discrimination in 24 patients with schizophrenia or schizoaffective disorder (SZ), 16 individuals with SPD, and 40 control subjects. SZ, but not SPD subjects, showed impairments on tests of contrast sensitivity for static and moving gratings, form discrimination in noise, and dot motion discrimination. Visual performance did not differ between medicated SZ patients and patients withdrawn from medication. These results confirm early stage visual deficits in schizophrenia regardless of medication status. SPD subjects, in contrast, show intact early stage visual processing despite the presence of marked schizotypal symptoms.     

Impaired detection of visual motion in schizophrenia patients

PURPOSE: A recent report demonstrated impaired auditory detection and discrimination in schizophrenia patients. It is suggested that a deficit in attention resulted in flatter slopes of the psychometric functions. Here, we investigated whether these patients showed a similar deficit in another sensory modality. Specifically, we examined a subset of the schizophrenia patients in a visual task involving motion detection. METHODS: A total of 13 schizophrenia patients and 14 normal controls detected the presence of a group of random dots moving in a coherent direction among other dots moving in random directions. Signal intensity varied from trial to trial. Detection sensitivity and bias were computed using signal detection theory. RESULTS: The schizophrenia patients were less sensitive in detecting motion stimuli, compared to normal subjects. The decrement in sensitivity varies with signal-to-noise ratio. The two groups did not differ in response bias. CONCLUSION: Schizophrenics were impaired in visual, as well as in auditory, attention, in accordance with the idea that attention impairment may represent a core deficit in schizophrenia.     

Naive theory impairment in schizophrenia: is it domain-specific?

The ability to represent mental states of self and others to account for behavior is called theory of mind (ToM). This study examined whether ToM deficit in schizophrenia patients is a specific deficit in the cognitive component of interpersonal skills or a more global deficit, involving impaired information processing skills. Schizophrenia inpatients (N = 41) were compared with a control group of healthy subjects (N = 22) and to nonschizophrenia psychiatric patients (24 with affective disorders, seven with other psychosis) over a range of ToM tasks and another naive theory (theory of biology; ToB). Psychiatric inpatients as a whole showed significant deficit compared with the control group of healthy subjects in ToM tasks. The schizophrenia patients showed significantly larger deficits compared with patients suffering from affective disorder, while the performance of patients with nonschizophrenia psychosis was intermediate. In contrast, no difference was observed in the performance of the different groups on the ToB tasks. The fact that a deficit was found in ToM but not in ToB suggests a specific deficit in a cognitive component of interpersonal skills in schizophrenia rather than a general deficit in information processing skills. Naive theories deficits in schizophrenia seem to be domain-dependent.     

Specific motion processing pathway deficit during eye tracking in schizophrenia: a performance-matched functional magnetic resonance imaging study.

BACKGROUND: The neural mechanisms underlying smooth pursuit eye movement (SPEM) abnormalities in schizophrenia are not well understood. Previous evidence suggests that a deficit in the processing of internal representations of object motion (extraretinal motion) contributes to SPEM deficits in patients. Functional magnetic resonance imaging (fMRI) activation was compared between patients and control subjects to determine whether schizophrenia patients exhibit abnormal cerebral activation in regions associated with extraretinal motion processing during SPEM. METHODS: Patients and control subjects were selected based on matched performance in the closed-loop gain. Despite similar performance on closed-loop pursuit gain, patients showed consistent deficits in extraretinal motion based on predictive pursuit. In the magnet, subjects were tested using a traditional smooth-pursuit task that elicits closed-loop response. RESULTS: Patients had reduced pursuit-related activation in several known extraretinal motion processing areas including frontal and supplemental eye fields, medial superior temporal cortex, and anterior cingulate. Patients also showed increased activation in medial occipitotemporal cortex. CONCLUSIONS: These results provide functional anatomic evidence supporting reduced function in the extraretinal motion processing pathway in schizophrenia. Increased activation in medial occipitotemporal cortex suggests an increased dependence on immediate retinal motion information, which may be used to compensate for reduced extraretinal signaling during sustained visual tracking.     

Color discrimination in schizophrenia

Neuropsychiatric conditions that involve dopaminergic depletion have been associated with color discrimination deficits along the blue-hue (tritan, or short-wavelength-sensitive) axis. Because dopamine dysregulation may be a major factor in schizophrenia, we investigated color vision in this disorder. The performance of males with schizophrenia (SZ, n = 16) and normal male control subjects (CS, n = 14) was evaluated on five measures of color discrimination. SZ made more hue discrimination errors than CS, but no pattern emerged regarding a hue-specific axis of deficit. Dosage of anti-psychotic medication was not correlated with performance on hue discrimination. These results suggest that in medicated patients with schizophrenia, the dopaminergic disturbance, which may involve system hyperactivity, does not produce tritan-specific color deficits that have been observed in disorders involving dopaminergic hypoactivity.     

Visual perception and working memory in schizotypal personality disorder

OBJECTIVE: Patients affected by schizophrenia show deficits in both visual perception and working memory. The authors tested early-stage vision and working memory in subjects with schizotypal personality disorder, which has been biologically associated with schizophrenia. METHOD: Eleven subjects who met DSM-III-R criteria for schizotypal personality disorder and 12 normal comparison subjects were evaluated. Performance thresholds were obtained for tests of visual discrimination and working memory. Both form and trajectory processing were evaluated for each task. RESULTS: Subjects with schizotypal personality disorder showed intact discrimination of form and trajectory but were impaired on working memory tasks. CONCLUSIONS: These data suggest that subjects with schizotypal personality disorder, unlike patients affected by schizophrenia, have relatively intact visual perception. Subjects with schizotypal personality disorder do show specific deficits on tasks of comparable difficulty when working memory demands are imposed. Schizotypal personality disorder may be associated with a more specific visual processing deficit than schizophrenia, possibly reflecting disruption of frontal lobe systems subserving visual working memory operations.     

Cortical intercorrelations of temporal area volumes in schizophrenia

BACKGROUND: Abnormal temporal connections with other cortical areas may underlie some of the most prominent cognitive deficits described in schizophrenia. In order to evaluate the relationship between temporal and other cortical regions in schizophrenia, we examined the intercorrelations of volumetric measures of gray and white matter for each Brodmann's area of the temporal lobe with volumes in the rest of the cortex in patients with schizophrenia and normal comparison subjects. METHODS: MR images were acquired in normal subjects (n=46) and patients with schizophrenia (n=106), divided into good-outcome (n=52) and poor-outcome (Kraepelinian; n=54) subtypes; and correlational patterns between the volumes of individual Brodmann's areas were compared and examined in relation to outcome. RESULTS: Positive frontotemporal intercorrelations were significantly stronger while negative frontotemporal intercorrelations were weaker in schizophrenia patients as compared to normal subjects. Correlations between the right temporal pole and other temporal regions were significantly weaker in schizophrenia patients than in controls. When compared to normal controls and good-outcome patients, schizophrenia patients with poor outcomes showed a selective pattern of stronger gray matter correlations between the medial temporal vs. primary visual and between primary auditory vs. dorsolateral prefrontal cortices, all in the left hemisphere. CONCLUSIONS: Strengthening of positive associations among the temporal and extratemporal (mainly frontal and occipital) regions as well as weakening of regional intercorrelations within the temporal lobe in patients appear to constitute the major differences of correlational patterns in schizophrenia patients and normal subjects. Present findings may be implicated in object recognition deficits seen in patients with schizophrenia, as well as in purportedly deficient spatial and semantic processing of both auditory and visual information that may be associated with poor outcome.     

Facial expression and sex recognition in schizophrenia and depression.

BACKGROUND: Impaired facial expression recognition in schizophrenia patients contributes to abnormal social functioning and may predict functional outcome in these patients. Facial expression processing involves individual neural networks that have been shown to malfunction in schizophrenia. Whether these patients have a selective deficit in facial expression recognition or a more global impairment in face processing remains controversial. OBJECTIVE: To investigate whether patients with schizophrenia exhibit a selective impairment in facial emotional expression recognition, compared with patients with major depression and healthy control subjects. METHODS: We studied performance in facial expression recognition and facial sex recognition paradigms, using original morphed faces, in a population with schizophrenia (n=29) and compared their scores with those of depression patients (n=20) and control subjects (n=20). RESULTS: Schizophrenia patients achieved lower scores than both other groups in the expression recognition task, particularly in fear and disgust recognition. Sex recognition was unimpaired. CONCLUSION: Facial expression recognition is impaired in schizophrenia, whereas sex recognition is preserved, which highly suggests an abnormal processing of changeable facial features in this disease. A dysfunction of the top-down retrograde modulation coming from limbic and paralimbic structures on visual areas is hypothesized.     

Facial emotion discrimination: III. Behavioral findings in schizophrenia.

Emotional discrimination was studied in patients with schizophrenia (n = 20) and matched controls. Performance of the emotion-discrimination tasks in the schizophrenic patients was impaired, relative to their performance of an age-discrimination task. Performance patterns in the patient group could also be reliably distinguished from those of normal controls. The impairment was associated with the severity of both emotional and nonemotional symptoms specific to schizophrenia, but not with the severity of nonspecific symptoms. The deficit associated with schizophrenia is more marked than that reported for depression (Gur et al., 1992), particularly for the emotion-discrimination tasks, and showed no difference between "happy" discrimination and "sad" discrimination. The main difficulty in patients with schizophrenia is the assignment of emotional valence to neutral faces. The magnitude of the deficit underscores the salience of emotional impairment in schizophrenia, and its relation to cognitive dysfunction in this disorder merits further scrutiny.     

Reaction time and sustained attention in schizophrenia and its genetic predisposition

Sustained attention is affected by schizophrenia. The simplest form of Continuous Performance Test (CPT-X) is a purer test of vigilance than more demanding variants but widely thought too insensitive to detect abnormalities in those with genetic predisposition to schizophrenia. We used a 7-minute CPT to compare 61 patients diagnosed with schizophrenia, 45 of their never-psychotic relatives, and 47 control subjects. We found a significant impairment in stimulus discrimination in both patients (p=0.001) and their relatives (p=0.006). There was no difference in stimulus discrimination between relatives of patients with impaired and unimpaired stimulus discrimination. Relatives of patients with unimpaired stimulus discrimination were still inferior to controls (p=0.02). Reactions slowed in all groups equally as the test progressed. Patients showed increased mean reaction time (p<0.0001) and interquartile range (p=0.003). Relatives showed slower reaction times (p=0.01) but normal interquartile range. Groups did not differ in respect of individuals' fastest reaction times. We conclude that genetic predisposition to schizophrenia reduces performance even during a task placing minimal cognitive load on working memory and perceptual processing, suggesting impaired vigilance. Increased reaction time in the disease and its predisposition appear to be due to changes in response distribution rather than by a limitation of maximum speed. Our results raise the possibility of separating the cognitive components of vigilance, working memory and perceptual processing tapped by more demanding variants of the CPT, and draw attention to the need for consideration of dynamic neurocognitive processes in schizophrenia.     

Abnormal patterns of regional cerebral blood flow in schizophrenia with primary negative symptoms during an effortful auditory recognition task.

OBJECTIVE: Using functional brain imaging, the authors sought to replicate their earlier finding of low metabolism in the middle frontal and inferior parietal cortices of schizophrenic patients with primary negative symptoms. METHOD: According to the presence or absence of enduring negative symptoms, patients with schizophrenia were classified as having deficit or nondeficit schizophrenia, respectively. Twelve normal volunteers and 18 drug-free schizophrenic volunteers (deficit, N=8; nondeficit, N=10) were trained in a tone discrimination task. They were trained to perform with 70%-80% accuracy and were then scanned with positron emission tomography with [(15)O]H(2)O during three conditions: rest, sensory-motor control task, and decision task. RESULTS: Levels of performance of the auditory recognition task were similar in the three groups. An initial hypothesis-driven analysis revealed that across tasks the deficit group failed to show significant activation in the middle frontal cortex. This was in contrast to both the normal volunteers and nondeficit patients. When the patient groups were contrasted, the deficit patients showed significantly less activation in the middle frontal cortex bilaterally during the control task and in the right middle frontal cortex and inferior parietal cortex during the decision task. An exploratory analysis contrasting deficit and nondeficit patients across conditions did not reveal further differences between groups. CONCLUSIONS: This study replicated the finding of low activation in the middle frontal cortex and inferior parietal cortex in deficit schizophrenia. This deficit was observed without performance confound and may provide a marker of primary negative symptoms and a target for new therapies.