Objective Abnormal 50 and 100ms event-related brain activity derived from paired-click procedures are a well established finding in schizophrenia. There is little agreement on whether ratio score (second click/first click) paired-click group differences reflect an encoding or gating abnormality. In addition, the functional implications of the ratio score deficit remain unclear. In the present study, EEG and MEG were used to examine paired-click measures as well as the cognitive correlates of paired-click activity. Method Electroencephalographic (EEG) Cz and whole-cortex magnetoencephalographic (MEG) data were acquired during the standard paired-click paradigm in 73 controls and 79 patients with schizophrenia. Paired-click ratio scores were obtained at 50ms (P50 at Cz, M50 at left and right superior temporal gyrus, STG) and 100ms (N100 at Cz, M100 at left and right STG). Subjects were administered a cognitive battery assessing attention, working memory, and long-delay memory. An IQ estimate was also obtained. Results Groups differed on ratio score and S1 amplitude measures. 50ms and 100ms ratio and S1 amplitude scores predicted variance in attention (primarily S1 amplitude), working memory, and long-delay memory. The attention findings remained after removing variance associated with general cognitive ability (i.e., IQ). Conclusions Associations between paired-click measures and cognitive performance in patients supports 50ms and 100ms ratio and amplitude scores as clinically significant biomarkers of schizophrenia. In general, cognitive performance was better predicted by the ability to encode auditory information rather than the ability to filter redundant information.
A growing body of evidence suggests that moderate to vigorous activity levels can affect quality of life, cognition, and brain structure in patients diagnosed with schizophrenia. However, physical activity has not been systematically studied during the period immediately preceding the onset of psychosis. Given reports of exercise-based neurogenesis in schizophrenia, understanding naturalistic physical activity levels in the prodrome may provide valuable information for early intervention efforts. The present study examined 29 ultra high-risk (UHR) and 27 matched controls to determine relationships between physical activity level, brain structure (hippocampus and parahippocampal gyrus), and symptoms. Participants were assessed with actigraphy for a 5-day period, magnetic resonance imaging (MRI), and structured clinical interviews. UHR participants showed a greater percentage of time in sedentary behavior while healthy controls spent more time engaged in light to vigorous activity. There was a strong trend to suggest the UHR group showed less total physical activity. The UHR group exhibited smaller medial temporal volumes when compared to healthy controls. Total level of physical activity in the UHR group was moderately correlated with smaller parahippocampal gyri bilaterally (right: r=.44, left: r=.55) and with occupational functioning (r=−.36; of negative symptom domain), but not positive symptomatology. Results suggest that inactivity is associated with medial temporal lobe health. Future studies are needed to determine if symptoms are driving inactivity, which in turn may be affecting the health of the parahippocampal structure and progression of illness. Although causality cannot be determined from the present design, these findings hold important implications for etiological conceptions and suggest promise for an experimental trial.
Behavioral inhibition is a temperamental trait that refers to slow approach to novel items, shyness towards new people, and fearfulness in new situations, and individuals may develop inhibited response styles by as early as two years of age. There are important methodological considerations in the assessment of early temperament, with parental report and observational measures providing both corroborative and unique data. The present study examined behavioral inhibition measured by parental report and observational measures in a genetically informative sample to delineate the agreement between the methods and the uniqueness of each method, and to estimate the magnitude of genetic and environmental influences on the common and unique variance. The biometric, psychometric, and rater bias models were conducted to study the covariance between measurement modalities. Overall, the results suggested a common phenotype was assessed by both parents and observers. The latent phenotype underlying parental and observational measures of behavioral inhibition was moderately to substantially heritable.
Background Although gray matter (GM) abnormalities are frequently observed in individuals with schizophrenia (SCZ), the functional consequences of these structural abnormalities are not yet understood. The present study sought to better understand GM abnormalities in SCZ by examining associations between GM and two putative functional SCZ biomarkers: weak 100 ms (M100) auditory responses and impairment on tests of attention. Methods Data were available from 103 subjects (healthy controls=52, SCZ=51). GM cortical thickness measures were obtained for superior temporal gyrus (STG) and prefrontal cortex (PFC). Magnetoencephalography (MEG) provided measures of left and right STG M100 source strength. Subjects were administered the Trail Making Test A and the Connors’ Continuous Performance Test to assess attention. Results A strong trend indicated less GM cortical thickness in SCZ than controls in both regions and in both hemispheres (p=0.06). Individuals with SCZ had weaker M100 responses than controls bilaterally, and individuals with SCZ performed more poorly than controls on tests of attention. Across groups, left STG GM was positively associated with left M00 source strength. In SCZ only, less left and right STG and PFC GM predicted poorer performance on tests of attention. After removing variance in attention associated with age, associations between GM and attention remained significant only in left and right STG. Conclusions Reduced GM cortical thickness may serve as a common substrate for multiple functional abnormalities in SCZ, with structural-functional abnormalities in STG GM especially prominent. As suggested by others, functional abnormalities in SCZ may be a consequence of elimination of the neuropil (dendritic arbors and associated synaptic infrastructure) between neuron bodies.
Used to study filtering abnormalities in schizophrenia, the paired-click paradigm suffers from poor test-retest reliability of the gating ratio, calculated from the P50 component of the ERP recorded at Cz approximately 50 ms following each of two stimuli. This study sought to improve reliability by assessing 50-ms gating at primary auditory cortices (PAC), the main generators of the P50 Cz component. MEG source modeling was used, taking advantage of the tangentially oriented PAC sources. Ten healthy subjects underwent three sessions, during which Cz-based and PAC-derived gating was measured. Unlike Cz P50, gating ratios at bilateral PACs achieved an intraclass coefficient of .8 or greater. Variability of gating within the same subject was also significantly smaller for bilateral PACs than for Cz P50. Paired-click gating ratio reliability can be improved by examining the individual PACs rather than composite scalp-recorded activity.
Recent evidence suggests that changes in brain structure associated with alcohol abuse are compounded in individuals dually diagnosed with alcohol abuse and schizophrenia. To investigate the separate, and possibly interacting, effects of these diagnoses, an event-related brain potential (ERP) measure of auditory information processing (P50 sensory gating paradigm) and neuropsychological measures were administered to healthy control participants with either (1a) no history of alcohol abuse/dependence, or (1b) a remote history of alcohol abuse/dependence, and patients with schizophrenia with either (2a) no history of alcohol abuse/dependence, or (2b) a remote history of alcohol abuse/dependence. Schizophrenia was associated with impaired P50 sensory gating and poorer performance across neuropsychological scores compared to measurements in healthy control participants. Those with a positive alcohol history had impaired gating ratios in contrast to those with a negative alcohol history. There were additive effects of schizophrenia diagnosis and alcohol history for P50 sensory gating and for neuropsychological scores: attention, working memory, and behavioral inhibition. For executive attention and general memory there was an interaction, suggesting that the combination of schizophrenia and history of alcohol abuse results in greater impairment than that predicted by the presence of either diagnosis alone.
Background Current observational literature on the mental health impact of the COVID-19 pandemic has focused on anxiety, depression, and sleep-disturbance among the public, healthcare workers, and COVID-19 patients. Case reports suggest catatonia and psychosis may be presenting symptoms of COVID-19 disease with a mechanism postulated to involve central nervous system changes in response to inflammation. There is a lack of robust evidence examining catatonia in this context. We sought to systematically review available case data and contextualize our findings. Case Presentations We present three cases of patients with catatonia seen at a large metropolitan tertiary care hospital in which their catatonia was likely attributable to SARS-CoV-2 infection. Ms. A is a female in her 50s with no psychiatric history who presented with self-inflicted stab wounds following her COVID-19 diagnosis. Ms. B is a female in her 50s with a history of schizophrenia, but no history of catatonia, who presented with akinetic catatonia, SARS-CoV-2 infection, and Clostridium difficile infection, without respiratory manifestations of COVID-19. Ms. C is a female in her 20s with a history of bipolar disorder (type 1) without catatonic features who presented with akinetic catatonia without the physical symptoms of SARS-CoV-2 infection. Discussion We present a brief review of six case reports detailing co-occurring catatonia and SARS-CoV-2 infection and one case report of catatonia attributed to the psychological stress of the COVID-19 pandemic in a patient without SARS-CoV-2 infection. We note one additional case of co-occurring catatonia and SARS-CoV-2 infection for which details are not available. COVID-19-associated catatonia may develop secondary to psychological and physical factors. Cases often report anxiety preceding catatonic symptoms. Developing evidence also suggests SARS-CoV-2 may act directly on the central nervous system or via a systemic inflammatory response. One of our cases featured significant anxiety preceding symptoms, and two had co-occurring elevated serum inflammatory markers. We suggest that clinicians should keep a high index of suspicion for both clinically significant anxiety disorders and catatonia.
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