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S Matthysse

Publications and source records attributed to S Matthysse.

At least 19 recordsLinked to original sources
PubMed2003

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.

Adult↗
PubMed2000

Bayesian linkage and segregation analysis: factoring the problem.

Complex segregation analysis and linkage methods are mathematical techniques for the genetic dissection of complex diseases. They are used to delineate complex modes of familial transmission and to localize putative disease susceptibility loci to specific chromosomal locations. The computational problem of Bayesian linkage and segregation analysis is one of integration in high-dimensional spaces. In this paper, three available techniques for Bayesian linkage and segregation analysis are discussed: Markov Chain Monte Carlo (MCMC), importance sampling, and exact calculation. The contribution of each to the overall integration will be explicitly discussed.

Bayes Theorem↗
PubMed1999

Intermittent degradation in performance in schizophrenia.

In a series of repeated trials, schizophrenic patients often fluctuate in performance. Our data suggest that it may be useful, not just to report an increased variance relative to nonschizophrenics, but to model these fluctuations concretely as transitions between a relatively normal and an abnormal cognitive state - an intermittent degradation in performance that may be related to transient abnormalities in CNS functioning. We define 'dialipsis' as a temporary substitution of a less efficient process of task performance. This phenomenon is mentioned in the literature, but the descriptions of dialipsis are heuristic rather than based on a statistical model. We present a mixture model in which the ordinary and degraded states are described by distinct ANOVA structures, each with its own task, subject and interaction effects, with transitions between them occurring at random times. We discuss ways of detecting dialipsis and comparing the mixture model statistically with alternative models.

Analysis of Variance↗
PubMed1999

Psychophysical isolation of a motion-processing deficit in schizophrenics and their relatives and its association with impaired smooth pursuit.

Schizophrenia patients and many of their relatives show impaired smooth pursuit eye tracking. The brain mechanisms underlying this impairment are not yet known, but because reduced open-loop acceleration and closed-loop gain accompany it, compromised perceptual processing of motion signals is implicated. A previous study showed that motion discrimination is impaired in schizophrenia patients. Motion discrimination can make use of position and contrast as well as velocity cues. Here, we report that the motion discrimination deficit, which occurs in both schizophrenic patients and in their first-degree relatives, involves a failure of velocity detection, which appears when judging intermediate target velocities. At slower and faster velocities, judgments of velocity discrimination seemed normal until we experimentally disentangled velocity cues from nonmotion cues. We further report that compromised velocity discrimination is associated with sluggish initiation of smooth pursuit. These findings point to specific central nervous system correlates of schizophrenic pathophysiology.

Adult↗
PubMed1999

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.

Brain↗
PubMed1999

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.

Brain↗
PubMed1999

Polymorphisms of the dopamine D4 receptor and response to antipsychotic drugs.

The dopamine D4 receptor may be a site through which the clinical effects of antipsychotic drugs are mediated. Polymorphisms of a 48 base pair repeat in the third exon of the DRD4 gene code for different length segments in the third intracytoplasmic loop of the D4 receptor. The most common long (seven repeat) form of the D4 receptor has been shown in both physiologic and pharmacologic experiments to respond differently to dopamine agonists and antagonists than do shorter forms of D4. Thus, variants of D4 may partly determine patient response to antipsychotic drugs and, in particular, response to typical neuroleptics, which have a relatively low affinity for the D4 receptor, as compared to clozapine, which has a relatively high affinity for D4. DRD4 polymorphisms in the third intron were characterized in 28 patients with chronic psychosis who responded well to typical neuroleptics, 32 patients who responded well to clozapine, and 57 healthy comparison subjects. Patients responding to typical neuroleptics carried the allele for the long (seven repeat) form of the D4 receptor (allele frequency 8.9%) less frequently than patients responding to clozapine (allele frequency 23.4%, P = 0.046) or healthy comparison subjects (allele frequency 26.3%, P = 0.004). The results of this study suggest that inherited variants of D4 may explain some of the interindividual variation seen in patient response to different classes of antipsychotic medication.

Adult↗
PubMed1994

Obstetrical complications and trail making deficits discriminate schizophrenics from unaffected siblings and controls.

Numerous studies have reported that both obstetrical complications (OCs) and deficits on the Trail Making Test show elevated prevalences in schizophrenics. Trail Making deficits have also been reported to be more common in schizophrenics' relatives than in controls, suggesting poor Trail Making performance may be a behavioral indicator of a familial risk factor for schizophrenia. Few studies, however, have investigated how these two variables co-vary in samples of schizophrenics and non-schizophrenics. In this study, DSM-III-R diagnoses, OCs noted in birth records, and Trail Making performance were independently assessed in 30 subjects: 9 schizophrenics, 8 of their non-schizophrenic siblings, and 13 comparison subjects with neither a personal nor a family history of schizophrenia. Results supported two key predictions of a two-factor etiologic model of schizophrenia: (a) the combination of perinatal OCs and poor Trail Making performance discriminated schizophrenics extremely well from non-schizophrenics, including their own non-schizophrenic sibs, and (b) perinatal OCs and Trail Making errors manifested a significant inverse association among schizophrenics' non-schizophrenic sibs, but not among other subjects.

Adult↗
PubMed1994

Eye tracking and schizophrenia: a selective review.

The replications of the finding of eye tracking dysfunction (ETD) in schizophrenia patients and their first-degree relatives suggest that ETD may be informative in studies of a schizophrenia genotype having broadly defined phenotypes. We review and critically assess the literature on ETD with respect to syndrome and familial specificity and discuss the quantitative assessment of eye tracking.

Attention↗
PubMed1993

Eye tracking dysfunction and schizophrenia: a critical perspective.

Eye tracking dysfunction (ETD) has been found in large numbers of schizophrenia patients and their first-degree relatives. Because of the many replications of the central findings, ETD has been proposed as a useful way of expanding the schizophrenia phenotype in genetic studies. We critically review the literature on ETD with respect to issues of measurement and the search for quantitative indices of ETD; syndrome and familial specificity of ETD for schizophrenia; statistical, interpretive, and methodological considerations in the use of mixture analysis; the association of ETD with clinically and psychometrically defined schizotypy; and the questions of trait stability and medication effects.

Arousal↗
PubMed1992

Extending the phenotype of schizophrenia: implications for linkage analysis.

On the basis of simulation studies, we suggest that most existing designs for studying linkage in schizophrenia do not have sufficient power to detect a major contributing locus, even if one is present. For this reason, recent failures to replicate reports of linkage in schizophrenia are not surprising. Inclusion in the linkage design of phenotypes genetically related to schizophrenia, but more commonly found in the relatives of schizophrenics than schizophrenia itself, may increase the power of linkage analysis substantially.

Computer Simulation↗
PubMed1992

Gene expression in mental illness: a navigation chart to future progress.

An initial course in disentangling complex causal interactions in psychiatric illnesses, we suggest, is finding co-familial traits with classical Mendelian segregation. Starting with non-Mendelian traits, three methods can be used to find underlying Mendelian phenotypes. (1) Statistically-inferred latent traits, with more nearly Mendelian transmission than the measures from which they are derived, can serve as pointers to concrete Mendelian phenotypes. (2) Linkage of non-Mendelian traits to genetic markers, if it can be established, can be followed by searching for phenotypes that discriminate carriers from non-carriers of the imputed trait gene. (3) In the long run, the most successful method is likely to be direct refinement of non-Mendelian behavioral and physiological traits into more fundamental components.

Bipolar Disorder↗
PubMed1991

Spontaneous generation of selectable variation in the brain.

Selection models of behavior presuppose "selectable variation", diversity in the brain that is stable over time. Diversity can arise spontaneously through the mutual interactions of cell assemblies, which are postulated to align or disalign their neighbors into processing modes conforming to or opposite from their own. These processes are similar to magnetization and crystallization. If aligning and disaligning influences are distributed at random, a state resembling a spin glass can arise, where processing modes are highly varied in space but stable in time. If disalignment occurs regularly at the points of a two-dimensional lattice, and elsewhere the interactions are aligning, a pattern emerges with properties remarkably similar to visual orientation columns. These patterns are maintained dynamically, and emerge statistically without detailed genetic specification.

Animals↗
PubMed1990

Genetic latent structure analysis of dysmorphology in attention deficit disorder.

Dysmorphology--in the form of minor physical anomalies--has been frequently reported in children with attention deficit disorder (ADD). The authors report an overrepresentation of minor physical anomalies in both ADD probands and their first-degree relatives. Further, ADD probands who are not dysmorphic have non-ADD relatives who are dysmorphic; this familial pattern suggests that a single underlying factor may influence transmission of both traits. A genetic latent structure model was fit to these data to describe the factor's mode of transmission. In this analysis, an autosomal dominant model emerged. Successfully fitting this model is not equivalent to testing the validity of the model itself. Meaningful tests of the model will require larger samples than available at present, and would benefit from diagnostic refinement of the ADD and dysmorphic phenotypes.

Attention Deficit Disorder with Hyperactivity↗