Search

Language and oculomotor disturbances are 2 of the best replicated findings in schizophrenia. However, few studies have examined skilled reading in schizophrenia (e.g., Arnott, Sali, Copland, 2011; Hayes & O'Grady, 2003; Revheim et al., 2006; E. O. Roberts et al., 2012), and none have examined the contribution of cognitive and motor processes that underlie reading performance. Thus, to evaluate the relationship of linguistic processes and oculomotor control to skilled reading in schizophrenia, 20 individuals with schizophrenia and 16 demographically matched controls were tested using a moving window paradigm (McConkie & Rayner, 1975). Linguistic skills supporting reading (phonological awareness) were assessed with the Comprehensive Test of Phonological Processing (R. K. Wagner, Torgesen, & Rashotte, 1999). Eye movements were assessed during reading tasks and during nonlinguistic tasks tapping basic oculomotor control (prosaccades, smooth pursuit) and executive functions (predictive saccades, antisaccades). Compared with controls, schizophrenia patients exhibited robust oculomotor markers of reading difficulty (e.g., reduced forward saccade amplitude) and were less affected by reductions in window size, indicative of reduced perceptual span. Reduced perceptual span in schizophrenia was associated with deficits in phonological processing and reduced saccade amplitudes. Executive functioning (antisaccade errors) was not related to perceptual span but was related to reading comprehension. These findings suggest that deficits in language, oculomotor control, and cognitive control contribute to skilled reading deficits in schizophrenia. Given that both language and oculomotor dysfunction precede illness onset, reading may provide a sensitive window onto cognitive dysfunction in schizophrenia vulnerability and be an important target for cognitive remediation. (Contains 8 tables, 4 figures and 1 footnote.)

Social communication deficits have been robustly documented in schizophrenia spectrum disorders. Historically, attempts to lessen this dysfunction have focused almost exclusively on modifying the person with schizophrenia's own behaviors and cognition. However, social communication is inherently dyadic, and this approach leaves unaddressed the role of the neurotypical interlocutor in communication breakdown. In this position piece, we review psycholinguistic theories and research in order to propose a more comprehensive and equitable understanding of the social dysfunction that people with schizophrenia experience. We do so by drawing attention to the manner in which neurotypical individuals may drive communication failure in schizophrenia. Stigma is proposed to be a major component of this phenomenon. In addition to an overview of our theoretical framework, we provide a research agenda to test the hypotheses this framework has produced. We hope this piece can inform future research directions within psycholinguistics. [ABSTRACT FROM AUTHOR]

Deficits in smooth pursuit eye movements are well documented in schizophrenia and schizotypic psychopathology. The status of eye tracking dysfunction (ETD) as an endophenotype for schizophrenia liability is relatively robust. However, the relation of ETD to schizophrenia-related deviance in the general population has not been confirmed. This study examined smooth pursuit eye tracking and schizotypal personality features in the general population. Smooth pursuit eye movement and schizotypal features were measured in 300 adult community subjects. The sample included both sexes, subjects with a wide age and educational range, and subjects with no prior history of psychosis. Primary outcome measures were peak gain (eye velocity/target velocity), catch-up saccade rate, and schizotypal feature scores. Total schizotypal features were significantly associated with decreased peak gain and were associated at the trend level with increased catch-up saccade rate. These associations were essentially unchanged after controlling for age, sex, and intellectual level effects. These data confirm a hypothesized association between schizotypal features and poorer eye tracking performance (principally, peak gain) in the general population as well as support the conceptualization of ETD as an endophenotype for schizophrenia liability. Keywords: schizotypy, eye tracking dysfunction, endophenotype, schizotypal, schizophrenia

Converging evidence from clinical, preclinical, neuroimaging, and genetic research implicates dopamine neurotransmission in the pathophysiology of attention deficit hyperactivity disorder (ADHD). The in vivo neuroreceptor imaging evidence also suggests alterations in the dopamine system in ADHD; however, the nature and behavioral significance of those have not yet been established. Here, we investigated striatal dopaminergic function in ADHD using [11C]raclopride PET with a d-amphetamine challenge. We also examined the relationship of striatal dopamine responses to ADHD symptoms and neurocognitive function. A total of 15 treatment-free, noncomorbid adult males with ADHD (age: 29.87±8.65) and 18 healthy male controls (age: 25.44±6.77) underwent two PET scans: one following a lactose placebo and the other following d-amphetamine (0.3 mg/kg, p.o.), administered double blind and in random order counterbalanced across groups. In a separate session without a drug, participants performed a battery of neurocognitive tests. Relative to the healthy controls, the ADHD patients, as a group, showed greater d-amphetamine-induced decreases in striatal [11C]raclopride binding and performed more poorly on measures of response inhibition. Across groups, a greater magnitude of d-amphetamine-induced change in [11C]raclopride binding potential was associated with poorer performance on measures of response inhibition and ADHD symptoms. Our findings suggest an augmented striatal dopaminergic response in treatment-naive ADHD. Though in contrast to results of a previous study, this finding appears consistent with a model proposing exaggerated phasic dopamine release in ADHD. A susceptibility to increased phasic dopamine responsivity may contribute to such characteristics of ADHD as poor inhibition and impulsivity. [ABSTRACT FROM AUTHOR]

Drugs that increase dopamine levels in the brain can cause psychotic symptoms in healthy individuals and worsen them in schizophrenic patients. Psychological stress also increases dopamine release and is thought to play a role in susceptibility to psychotic illness. We hypothesized that healthy individuals at elevated risk of developing psychosis would show greater striatal dopamine release than controls in response to stress. Using positron emission tomography and [11C]raclopride, we measured changes in synaptic dopamine concentrations in 10 controls and 16 psychometric schizotypes; 9 with perceptual aberrations (PerAb, ie positive schizotypy) and 7 with physical anhedonia (PhysAn, ie negative schizotypy). [11C]Raclopride binding potential was measured during a psychological stress task and a sensory-motor control. All three groups showed significant increases in self-reported stress and cortisol levels between the stress and control conditions. However, only the PhysAn group showed significant stress-induced dopamine release. Dopamine release in the entire sample was significantly negatively correlated with smooth pursuit gain, an endophenotype linked to frontal lobe function. Our findings suggest the presence of abnormalities in the dopamine response to stress in negative symptom schizotypy, and provide indirect evidence of a link to frontal function.Neuropsychopharmacology (2008) 33, 2033–2041; doi:10.1038/sj.npp.1301597; published online 24 October 2007 [ABSTRACT FROM AUTHOR]

Examines the relationship between schizophrenia and motor abnormalities in neuroleptic-naive patients and high-risk population. Motor abnormalities associated with schizophrenia; Prevalence of parkinsonian symptoms and neurological soft signs; Link between negative symptoms, motor abnormalities and cognitive dysfunction.