Cognitive Functions in Children of Persons with Schizophrenia (original) (raw)
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Brain Research Bulletin, 2010
We assessed major cognitive domains in symptom-free children of patients with schizophrenia compared to the healthy children of parents with no psychopathology using neurocognitive tests. We hypothesized that, offspring at high-risk for schizophrenia would have significant impairment in major domains: attention, memory, verbal-linguistic ability and executive functions. Thirty symptom-free children (17males, 13-females; intelligence quotient = 99.6 ± 13.6; age = 12.69 ± 2.32 and education = 5.8 ± 2.3 years) having a parent diagnosed with schizophrenia and 37 healthy children matched for gender (19-males, 18-females), IQ (106.05 ± 14.70), age (12.48 ± 2.58) and years of education (6.0 ± 2.5) were evaluated. The study group showed significant poor performance in cognitive domains, such as working memory (assessed with Auditory consonant trigram test), focused attention (Stroop test), attention speed (Trail making test), divided attention (Auditory consonant trigram test), executive functions (Wisconsin card sorting test), verbal fluency (Controlled word association test) and declarative memory (Rey verbal learning and Short-term memory test). However, no group differences were detected either on verbal attention (Digit span forward test) or sustained attention (TOVA, a continuous performance task); the latter as consistently reported to be a predictor of schizophrenia. In order to determine the cognitive endophenotype of schizophrenia, it seems more rational to conduct comprehensive evaluation of neurocognitive domains in well-matched groups via using sufficiently challenging tests to detect slight deficits. In addition, longitudinal studies with a larger sample size evaluating neurocognitive functions combined with genetic analysis may provide clues about explaining the genetic background of the disorder within the endophenocognitype concept and serve as new targets for early interventions.
Schizophrenia Bulletin, 2000
While it is known that children of schizophrenia parents perform more poorly on tests of cognitive functioning than children of normal parents, less certain is the degree to which such deficits predict schizophrenia outcome, whether cognitive functioning deteriorates during childhood in preschizophrenia individuals, and whether nongenetic etiologic factors (such as obstetric complications) contribute to these deficits. In the present study, 72 patients with schizophrenia or schizoaffective disorder, 63 of their siblings not diagnosed with schizophrenia, and 7,941 controls with no diagnosis were ascertained from a birth cohort whose members had been evaluated with standardized tests of cognitive functioning at 4 and 7 years of age. Adult psychiatric morbidity was ascertained via a longitudinal treatment data base indexing regional public health service utilization, and diagnoses were made by review of all pertinent medical records according to DSAf-TV criteria. Both the patients with schizophrenia and their unaffected siblings performed significantly worse than the nonpsychiatric controls (but did not differ from each other) on verbal and nonverbal cognitive tests at 4 and 7 years of age. Preschizophrenia cases and their siblings were increasingly overrepresented across decreasing quartiles of the performance distributions. There was not significant intra-individual decline, and there were no significant relationships between obstetric complications and test performance among the preschizophrenia subjects. These results suggest that during the period from age 4 to age 7 years, premorbid cognitive dysfunction in schizophrenia represents a relatively stable indicator of vulnerability deriving from primarily genetic (and/or shared environmental) etiologic influences.
Phenotypic markers as risk factors in schizophrenia: neurocognitive functions
Australian and New Zealand Journal of Psychiatry, 2000
There are two approaches that have been used to define at-risk groups for schizophrenia in the neurocognitive area. The first is to assess first-degree relatives of patients with a diagnosis of schizophrenia. Two types of studies fall into this category: (i) prospective studies, which take the form of investigations of children who are at risk of schizophrenia because one parent, usually the mother, has a diagnosis of schizophrenia; and (ii) cross-sectional or family studies that investigate the adult siblings or parents of patients with a diagnosis of schizophrenia. The second Objective: To review the literature on neurocognitive measures as risk markers for schizophrenia and to present data from the Perth family study of schizophrenia. Of all the risk markers that have been identified, the most promising are deficits in sustained attention. Method: Inclusion in the review was determined by whether the research addressed a number of key questions: methods of assessing sustained attention; evidence of sustained attention deficits in patients and first-degree relatives including children; the importance of attentional dysfunction in the schizophrenic process and functional outcome; and the biological basis of sustained attention deficits. Results: Sustained attention deficits are evident in both patients and a proportion of their first-degree relatives, a finding replicated in preliminary data from the Perth family study. The literature suggests that the attention deficit is a stable enduring trait that is independent of clinical state. The neural basis of the deficit may be a functional disconnection between prefrontal and parietal cortex. Attention impairment is an important predictor of functional outcome in patients and the development of social dysfunction in adulthood in the at-risk offspring of patients. However, sustained attention deficits that are measured in childhood results in an unacceptable high false-positive rate (21%) when predicting which at-risk offspring of parents with schizophrenia will develop a schizophrenia spectrum disorder, although the overall classification accuracy (78%) is impressive.
JAMA Psychiatry, 2018
IMPORTANCE Children at familial high risk of schizophrenia spectrum disorders (FHR-SZ) or bipolar disorder (FHR-BP) exhibit neurocognitive impairments. Large studies of neurocognition in young children at familial high risk at the same age are important to differentiate the pathophysiology and developmental trajectory of these 2 groups. OBJECTIVE To characterize neurocognitive functions in 7-year-old children with FHR-SZ or FHR-BP and a control population. DESIGN, SETTING, AND PARTICIPANTS This multisite population-based cohort study collected data from January 1, 2013, to January 31, 2016, in the first wave of the Danish High Risk and Resilience Study VIA 7 at 2 university hospital research sites in Copenhagen and Aarhus using Danish registries. Participants (n = 514) included 197 children with FHR-SZ, 118 with FHR-BP, and 199 controls matched with the FHR-SZ group for age, sex, and municipality. Assessors were blinded to risk status. EXPOSURES Parents with schizophrenia, bipolar disorder, or neither diagnosis. MAIN OUTCOMES AND MEASURES Neurocognitive functions were measured across 23 tests. Four neurocognitive domains were derived by principal component analysis, including processing speed and working memory, verbal functions, executive and visuospatial functions, and declarative memory and attention. RESULTS A total of 514 children aged 7 years were included in the analysis (46.3% girls), consisting of 197 children with FHR-SZ (46.2% girls), 118 with FHR-BP (46.6% girls), and 199 controls (46.2% girls). Children with FHR-SZ were significantly impaired compared with controls on processing speed and working memory (Cohen d = 0.50; P < .001), executive and visuospatial functions (Cohen d = 0.28; P = .03), and declarative memory and attention (Cohen d = 0.29; P = .02). Compared with children with FHR-BP, children with FHR-SZ performed significantly poorer in processing speed and working memory (Cohen d = 0.40; P = .002), executive and visuospatial functions (Cohen d = 0.35; P = .008), and declarative memory and attention (Cohen d = 0.31; P = .03). Children with FHR-BP and controls did not differ. CONCLUSIONS AND RELEVANCE Children with FHR-SZ had widespread neurocognitive impairments, supporting the hypothesis of neurocognitive functions as endophenotypes of schizophrenia. The absence of neurocognitive deficits in children with FHR-BP suggests distinct neurodevelopmental manifestations in these familial high-risk groups at this age. Early detection of children with FHR-SZ and cognitive impairments is warranted to investigate associations of neurocognition with transition to psychosis, add to the knowledge of their developmental pathophysiology, and inform early intervention programs.
Journal of Postgraduate Medicine
Cognitive impairment is said to be a core feature of schizophrenia. Executive function is an important cognitive domain. This study was undertaken to assess cognitive impairment among Indian patients with schizophrenia (Sz) or schizoaffective disorder (SzA), compared with their parents and unaffected individuals (controls). Executive functions as measured by Trail-making Test (TMT), of patients and their parents were compared with controls. The patients were recruited from the Outpatients' Department (OPD) of a government hospital. Patients diagnosed as Sz or SzA (n=172) and their parents (n=196: families n=132, 119 fathers and 77 mothers) participated. We also included 120 persons with no history of psychiatric illness. Cognitive function was assessed with the TMT. The Information Score of the Post Graduate Institute Battery of Brain Dysfunction test, developed in India for Indian subjects was used as a proxy for general fixed knowledge. Logistic and linear regression was used ...
Neurocognitive Profile in Adolescents with Early-Onset Schizophrenia: Clinical Correlates
Background: Neurocognitive impairments have been documented in adolescents with early-onset schizophrenia (EOS; onset by age 18) and are important treatment targets. Information concerning the severity, pattern, and clinical correlates of these deficits in EOS remains limited. Methods: Tests assessing motor skills, attention, memory, visuospatial abilities and executive functioning were administered to 54 clinically stabilized adolescents with EOS and 52 age-and sex-matched healthy controls. Childhood-onset patients (onset by age 13) were compared to those with an adolescent onset of illness. Patients' neurocognitive profiles were compared to those of controls. Relationships between neurocognitive deficits and demographic and clinical characteristics were explored. Results: Neurocognitive profiles did not differ between childhood-and adolescent-onset participants. Patients showed a generalized neurocognitive deficit of 2.0 SDs compared to controls, with relative deficit in executive functioning and relative sparing of language and visuospatial abilities. Degree of generalized neurocognitive impairment was associated with premorbid adjustment and negative symptom severity (Adjusted R 2 ϭ .39). Conclusions: Results document both a significant generalized deficit and a relative deficit of executive functioning in adolescents with EOS. The overall pattern is similar to that observed in severely ill first-episode adult patients. The impairments across multiple neurocognitive domains suggest widespread brain dysfunction in EOS.
Neurocognitive profile of adolescents with early-onset schizophrenia and their unaffected siblings
World Journal of Biological Psychiatry , 2022
Background: We investigated the neurocognitive profiles of Early-Onset Schizophrenia (EOS; onset before age 18) and paired unaffected siblings and the little-studied effect of age-of-onset and duration of illness on cognitive performance. Methods: 31 EOS probands, and 31 of their siblings, had four cognitive domains assessed: (a) Memory: California Verbal Learning Test, and the Wechsler Memory Scale-Revised; (b) Working memory: Digit Span; (c) Attention: Degraded-Stimulus Continuous Performance Test, Span of Apprehension (SPAN), and Trail Making Test (TMT) part A; (d) Executive function: Wisconsin card sorting task, and TMT part B. Diagnosis was confirmed using the structured clinical interview for DSM-IV. Results: While EOS showed a generalised neurocognitive deficit (0.25-0.50 effect size) compared with siblings, across all cognitive domains, significantly greater patient deficits were observed with, working memory, attention, and executive function and minimal differences for digit span forward, block design and false alarms on the SPAN-12 confirmed by repeated measures MANOVA. Patients with earlier onset (12-15) showed greater deficits on false alarm and digits backward scores. Siblings showed individual cognitive task profiles similar to patients, confirming familial effects. EOS showed much more variable scores than siblings with more individual tasks showing 2 SD deficits than siblings. Long duration patients had greater z-score variability across tasks. Conclusions: Duration of illness was a more important characteristic in patients with onset 16 and over than in younger onset patients with comparable durations. Both the similarity of sibling pair profiles and greater patient variability across task provide further support for neurobiological heterogeneity in schizophrenia.