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Although schizophrenia and developmental dyslexia are considered distinct disorders in terms of clinical presentation and functional outcome, they both involve disruption in the processes that support skilled reading, including language, auditory perception, visual perception, oculomotor control, and executive function. Further, recent work has proposed a common neurodevelopmental basis for the two disorders, as suggested by genetic and pathophysiological overlap. Thus, these lines of research suggest that reading may be similarly impacted in schizophrenia and dyslexia. In this review, we survey research on reading abilities in individuals with schizophrenia, and review the potential mechanisms underlying reading deficits in schizophrenia that may be shared with those implicated in dyslexia. Elucidating the relationship between reading impairment in schizophrenia and dyslexia could allow for a better understanding of the pathophysiological underpinnings of schizophrenia, and could facilitate remediation of cognitive deficits that impact day-to-day functioning. [ABSTRACT FROM AUTHOR]

Abstract: Psychological stress causes dopamine release in the striatum and is thought to play a role in susceptibility to psychotic illness. Previous work suggests that an elevated dopaminergic response to stress may index vulnerability to psychosis in certain individuals. With functional magnetic resonance imaging, we measured stress-induced changes in brain activity in healthy individuals at elevated risk of developing psychosis. Participants were 15 controls and 25 psychometric schizotypes: 12 with positive symptom schizotypy (perceptual aberrations) and 13 with negative symptom schizotypy (physical anhedonia), as determined by questionnaires (). In the scanner, participants performed the Montreal Imaging Stress Task and a matched sensory-motor control task. Measures of self-reported stress and salivary cortisol levels were taken throughout the experiment. All three groups showed significant increases in self-reported stress and significant fMRI signal change in the striatal, limbic and cortical regions. However, the Physical Anhedonia group showed greater stress-induced striatal and limbic deactivation than the other two groups. Deactivation in the striatum was significantly correlated with Physical Anhedonia score across all subjects. Our findings suggest the presence of abnormalities in striatal response to stress in negative symptom schizotypy. [Copyright &y& Elsevier]

Abstract: Schizophrenic patients have well-documented abnormalities in smooth pursuit eye movements and antisaccade performance. In populations at risk for schizophrenia, smooth pursuit abnormalities are also well documented. Antisaccade deficits have been replicated in high-risk populations as well, but the findings are more variable and the reasons for the variability are not clear. Some evidence suggests that antisaccade deficits increase in high-risk populations in relation to the presence of positive symptoms. Whether antisaccade deficits increase in relation to negative symptoms in high-risk populations is relatively uninvestigated. We evaluated antisaccade and pursuit performance in “psychometric schizotypes” who had elevated scores on either the Perceptual Aberration Scale (PerAb; i.e., positive symptoms) or the Physical Anhedonia Scale (PhysAnh; i.e., negative symptoms) but not both, and in normal controls. We used the standard version of the antisaccade task, for which results in positive-symptom schizotypes have previously been reported, and investigated performance on a gap and overlap version. We replicated the finding that a significantly larger percentage of positive-symptom schizotypes than controls have elevated antisaccade error rates on the standard antisaccade task (P=0.03); the percentage of negative-symptom schizotypes with elevated antisaccade error rates did not differ from that of control subjects. Neither schizotypal group was impaired on the gap or overlap versions of the task. On the pursuit task, a higher percentage of positive- and negative-symptom schizotypes were classified as having deviant performance than control subjects (both Ps<0.04). These findings suggest that antisaccade deficits may be better at identifying high-risk subjects with positive symptoms. Pursuit deficits identified both positive- and negative-symptom schizotypes, but was better at identifying the latter. [Copyright &y& Elsevier]

Background: Oculomotor tasks are a well-established means of studying executive functions and frontal-striatal functioning in both nonhuman primates and humans. Attention-deficit/hyperactivity disorder (ADHD) is thought to implicate frontal-striatal circuitry. We used oculomotor tests to investigate executive functions and methylphenidate response in two subtypes of ADHD. Methods: Subjects were boys, aged 11.5–14 years, with ADHD-combined (n = 10), ADHD-inattentive (n = 12), and control subjects (n = 10). Executive functions assessed were motor planning (tapped with predictive saccades), response inhibition (antisaccades), and task switching (saccades-antisaccades mixed). Results: The ADHD-combined boys were impaired relative to control subjects in motor planning (p < .003) and response inhibition (p < .007) but not in task switching (p > .92). They were also significantly impaired relative to ADHD-inattentive boys, making fewer predictive saccades (p < .03) and having more subjects with antisaccade performance in the impaired range (p < .04). Methylphenidate significantly improved motor planning and response inhibition in both subtypes. Conclusions: ADHD-combined but not ADHD-inattentive boys showed impairments on motor planning and response inhibition. These deficits might be mediated by brain structures implicated specifically in the hyperactive/impulsive symptoms. Methylphenidate improved oculomotor performance in both subtypes; thus, it was effective even when initial performance was not impaired. [Copyright &y& Elsevier]

Poor performance on the antisaccade (AS) task has been interpreted as a potential indicator of genetic liability that may enhance the power of linkage studies of a multidimensional phenotype for schizophrenia. Every study has replicated the finding of significantly worse performance in schizophrenia patients regardless of which specific antisaccade paradigm was employed. In some studies involving a standard version of the antisaccade task, relatives of schizophrenia patients made an increased number of errors, but in other studies that used this same paradigm, relatives of schizophrenia patients did not differ from controls. In this paper, we report the results of a meta-analysis on studies that used the standard antisaccade paradigm. The meta-analysis shows that those studies that reported large effect sizes and statistically significant differences between relatives of schizophrenia patients and controls used inclusion/exclusion criteria that were not symmetrical between the two groups, whereas those studies that reported small and nonsignificant differences between relatives of schizophrenia patients and controls used symmetrical inclusion/exclusion criteria. Specifically, studies that applied stricter psychopathology exclusion criteria to controls than to relatives of schizophrenia patients had larger effect sizes than studies that applied comparable exclusion criteria to both groups, suggesting that antisaccade performance is compromised by psychopathology in general rather than by schizophrenia per se. Since symmetrical inclusion/exclusion criteria between relatives of schizophrenia patients and controls are essential for a genetic analysis, and those studies that did apply symmetrical criteria had small effect sizes, the available data suggest that poor antisaccade performance is unlikely to be useful in identifying clinically unaffected carriers of genes for schizophrenia. [ABSTRACT FROM AUTHOR]

Schizophrenia, a debilitating psychiatric disorder, has a long-term impact on social and occupational functioning. While negative symptoms, notably amotivation, are recognized as poor prognostic factors, the positive force of patient motivation (autonomous motivation) remains underexplored. This systematic review, guided by Self-Determination Theory (SDT), investigated the impact of motivation on clinical presentation, and treatment engagement and response in schizophrenia-spectrum disorders. Fifty-five independent studies (N = 6897), using 23 different motivation scales, met inclusion criteria. Results were categorized into cross-sectional and longitudinal correlates of autonomous motivation, and the effects of motivational interventions. Cross-sectionally, autonomous motivation was positively associated with social/occupational functioning, and negatively associated with negative and positive symptom severity. In longitudinal studies, baseline autonomous motivation predicted engagement in and response to social/occupational treatments, with mixed results in cognitive interventions. In the 16 randomized controlled trials (RCTs), the most common motivational interventions were individualized goal setting and goal attainment support, followed by increasing sense of competence by challenging defeatist beliefs, and enhancing relatedness by increasing contact time. Motivational interventions consistently increased autonomous motivation, treatment engagement and response. More studies are needed, particularly studies that monitor motivation during treatment: proximal assessments could facilitate the identification of treatment elements that impact motivation and engagement and inform treatment modifications to enhance the patient experience and improve treatment efficacy. • Motivation is important in schizophrenia treatment, not only in its absence but as a positive force that can be fostered. • Baseline motivation linked to clinical status, with the magnitude of response to treatments targeting social/work functioning. • Motivation changes over time, with increases in motivation associated with treatment response. • RCTs showed motivational interventions to established treatments increase motivation, treatment engagement, and response. • More studies are needed that monitor motivation during treatment and antecedents of motivation. [ABSTRACT FROM AUTHOR]

To determine whether two groups of schizophrenic patients representing the two extremes of the neuroleptic response-spectrum (consistent responders vs. consistent nonresponders) differ with respect to their neuropsychological profile. Neuroleptic-responder (R; n=36) and -nonresponder (NR; n=39) schizophrenic patients were recruited according to a priori defined criteria of responsiveness to typical neuroleptics. Seven neuropsychological domains were assessed and compared between groups: attention-vigilance, abstraction-flexibility, spatial organization, visual-motor processing, visual memory, verbal abilities, and verbal memory and learning. All measures were standardized using the scores of 36 healthy volunteers. NR schizophrenic patients performed worse in all neuropsychological domains compared to normal controls and R schizophrenic patients. However, only performances on visual memory, verbal abilities, and verbal memory and learning were significantly poorer in NR compared to R patients. Only the latter domain significantly differentiated NR patients from the other two groups. R patients performed at an intermediate level in all domains. This report of differences in neuropsychological profile between neuroleptic-responder and -nonresponder schizophrenic patients adds to the growing evidence supporting the value of distinguishing schizophrenic patients on the basis of their therapeutic response to neuroleptics. [ABSTRACT FROM AUTHOR]