Biomedical subjects

Margriet M Sitskoorn

Publications and source records attributed to Margriet M Sitskoorn.

17 recordsLinked to original sources

PubMed2006

Effect of short daily home haemodialysis on quality of life, cognitive functioning and the electroencephalogram.

BACKGROUND: End-stage renal disease patients have a poor quality of life (QoL), suffer from impaired cognitive functioning, and their electroencephalogram (EEG) shows abnormalities. Conventional haemodialysis (CHD) only partially restores these disorders. Short daily haemodialysis (SDHD) has been reported to improve QoL, but effects on cognitive functioning and EEG have yet to be described. METHODS: Of the 13 patients (11 male, 2 female, age 45.5 +/- 8.1 years), 11 completed the Kidney Disease Quality of Life and Affect Balance Scale questionnaires, 10 underwent neuropsychological testing, and all 13 underwent EEG examination. For the neuropsychological assessments, nine patients (six male, three female, age 45.4 +/- 12.6) who remained on the CHD schedule, served as controls. The dialysis schedule of thrice-a-week for 4 h was changed in the experimental group to six times a week for 2 h (SDHD) over a period of 6 months and back to thrice a week for 4 h. RESULTS: When on SDHD, patients rated several dimensions of health-related QoL as being improved. After resuming CHD, one of these dimensions again decreased and several others worsened even lower than baseline. Cognitive functioning did not change when compared with control data. On the EEG, alpha peak frequency increased slightly when on SDHD but decreased significantly after resuming CHD. CONCLUSIONS: SDHD improves health-related QoL, but has no clear effects on cognitive functioning and EEG. Resumption of CHD after SDHD decreases aspects of QoL and EEG alpha peak frequency but has no effect on cognitive functioning.

Adult↗

PubMed2005

Long-term neurocognitive effects of olanzapine or low-dose haloperidol in first-episode psychosis.

BACKGROUND: Neurocognitive deficits are severe in first-episode psychosis. METHODS: Patients (N = 263) with first-episode psychosis (schizophrenia, schizoaffective, or schizophreniform disorders) were randomly assigned to double-blind treatment with olanzapine (mean 11.30 mg/day) or haloperidol (mean 4.87 mg/day) for 104 weeks. A neurocognitive battery was administered at baseline (n = 246) and 12 (n = 167), 24 (n = 126), 52 (n = 89), and 104 (n = 46) weeks during treatment. Weighted principal component and unweighted composite scores were derived from individual tests. RESULTS: Both treatment groups demonstrated significant improvement on both composite scores. On the basis of the weighted composite score, olanzapine had greater improvement than haloperidol only at 12 (p = .014) and 24 (p = .029) weeks. For the unweighted composite, olanzapine had significantly better improvement compared with haloperidol only at week 12 (p = .044). At week 12 only, olanzapine improved performance on the Digit Symbol and Continuous Performance Test significantly more than haloperidol. CONCLUSIONS: Both antipsychotic agents appeared to improve neurocognitive functioning among first-episode psychosis patients with schizophrenia. A significantly greater benefit in terms of neurocognitive improvement was found with olanzapine than with haloperidol at weeks 12 and 24.

Adult↗

PubMed2005

Brain anatomy in non-affected parents of autistic probands: a MRI study.

BACKGROUND: Autism is a neurodevelopmental disorder with an estimated genetic origin of 90%. Previous studies have reported an increase in brain volume of approximately 5% in autistic subjects, especially in children. If this increase in brain volume is genetically determined, biological parents of autistic probands might be expected to show brain enlargement, or at least intracranial enlargement, as well. Identifying structural brain abnormalities under genetic control is of particular importance as these could represent endophenotypes of autism. METHOD: Using quantitative anatomic brain magnetic resonance imaging, volumes of intracranial, total brain, frontal, parietal, temporal and occipital lobe, cerebral and cortical gray and white matter, cerebellum, lateral ventricle, and third ventricle were measured in biological, non-affected parents of autistic probands (19 couples) and in healthy, closely matched control subjects (20 couples). RESULTS: No significant differences were found between the parents of the autistic probands and healthy control couples in any of the brain volumes. Adding gender as a factor in a second analysis did not reveal a significant interaction effect of gender by group. CONCLUSIONS: The present sample of biological, non-affected parents of autistic probands did not show brain enlargements. As the intracranium is not enlarged, it is unlikely that the brain volumes of the parents of autistic probands have originally been enlarged and have been normalized. Thus, increased brain volume in autism might be caused by the interaction of paternal and maternal genes, possibly with an additional effect of environmental factors, or increased brain volumes might reflect phenotypes of autism.

Autistic Disorder↗

PubMed2005

Verbal memory in first-episode schizophrenia: heterogeneity in performance?

It is unclear if the commonly observed "subcortical" verbal memory profile in schizophrenic patients is present at the onset of the disease. Therefore, the performance of 43 first-episode patients with schizophrenia or schizophreniform disorder on the Dutch version of the California Verbal Learning Test (VLGT) was compared to that of 43 normal comparison participants. We hypothesized that the first-episode patients would exhibit a "subcortical" memory profile, that is, they would show a primary retrieval deficit. This hypothesis was not confirmed: the patients displayed a profile suggestive of a prominent storage deficit, that is, a "cortical" memory profile. Subsequently, patients' VLGT performance was cluster analyzed to determine whether subgroups could be identified exhibiting a cortical, subcortical, and normal profile, respectively. Two subgroups (N=22; N=13) exhibited memory impairments, while one subgroup (N=8) was unimpaired. The memory profiles of the two impaired subgroups differed both qualitatively and quantitatively, but did not conform neatly to a cortical and a subcortical profile. Demographic and verbal fluency data provided limited validation of the subgroup classification. Our results may suggest that combining the verbal memory performance of first-episode patients obscures meaningful heterogeneity. Alternatively, the cluster solution could merely reflect a continuum of severity.

Adolescent↗

PubMed2004

Cognitive deficits in relatives of patients with schizophrenia: a meta-analysis.

BACKGROUND: Schizophrenia is characterized by a generalized cognitive impairment with pronounced deficits in the domains of verbal memory, executive functioning and attention. AIM: To investigate whether cognitive deficits found in patients with schizophrenia are also found in non-affected relatives. METHOD: A meta-analytic review of the published literature on cognitive performance between relatives of schizophrenic patients and healthy controls. RESULTS: The meta-analyses yielded nine weighted effect sizes from 37 studies comprising 1639 relatives of schizophrenia patients and 1380 control subjects. The largest differences were found on verbal memory recall (d=0.54, 95% CI=0.43-0.66) and executive functioning (d=0.51, 0.36-0.67). Attentional functioning showed smaller effect sizes (d=0.28, 0.06-0.50). These effect sizes are in the moderate range. CONCLUSION: Cognitive deficits found in patients with schizophrenia are also found in non-affected relatives. This finding is consistent with the idea that certain cognitive deficiencies in relatives are caused by familial predisposition to schizophrenia and that these deficiencies might be putative endophenotypes for schizophrenia. However, our results do not address genetic causes directly. Further work is needed to determine whether certain cognitive traits are familial and whether there is co-inheritance of these traits with schizophrenia within families.

Cognition Disorders↗

PubMed2004

Memory profiles in parents of patients with schizophrenia.

Recent research shows that categorizing patients with schizophrenia based on frontal-striatal and frontal-temporal memory profiles may yield neurobiologically meaningful disease subtypes. We hypothesize that parents of patients exhibit similar memory profiles. Both parents of 36 patients with schizophrenia (N = 72) and 26 healthy married control couples (N = 52) participated in this study. All subjects were physically healthy and had no history of neurological illness or alcohol/drug abuse. The presence of a psychiatric and/or personality disorder was assessed with the Comprehensive Assessment of Symptoms and History (CASH) interview, the Schedule for Affective Disorders and Schizophrenia-lifetime (SADS-L) interview and the Structured Interview for DSM-IV Personality Disorders (SIDP-IV), respectively. Cluster analysis of selected measures from the Dutch version of the California Verbal Learning Test (CVLT) delineated parents into two subgroups with distinct memory deficits and a third subgroup without impairments. Specific frontal-striatal and frontal-temporal subgroups, however, were not found. In addition, our results indicated that mothers seem to be more protected against the negative effects of genetic liability to schizophrenia than fathers. Furthermore, relatives with a higher level of intelligence may have more cognitive reserve to compensate for the negative impact of implied brain dysfunction on verbal memory than relatives with a low level of intelligence. Although the parents of patients with schizophrenia could be delineated into subgroups with primary memory deficits, frontal-striatal and frontal-temporal subgroups could not be unambiguously identified. The association that emerged between level of intelligence, gender and severity of memory impairment deserves further exploration.

Cluster Analysis↗

PubMed2004

Effects of recurrent major depressive disorder on behavior and cognitive function in female depressed patients.

Little is known about the effects of recurring depressive episodes on cognition and behavior. The objective of the study was to compare cognitive function and depression-related behavior between healthy female subjects and female outpatients with early-onset DSM-IV recurrent major depressive disorder and to investigate the effect of cumulative depressive duration. Neuropsychological tests and scales for apathy, anhedonia and psychomotor retardation were assessed in 23 female patients and 60 healthy age-matched female controls. Significantly higher levels of apathy, anhedonia and psychomotor retardation, and worse performance on tests of executive function were found in the patient group compared with the healthy controls. In the patient group, cumulative depression duration was not significantly correlated with cognitive function, apathy, anhedonia or psychomotor retardation. The deficits in executive function were not related to the actual level of depression. Mild executive dysfunction may be the effect of the illness process underlying recurrent depressive disorder. Repeated or extensive depressive episodes do not seem to additionally affect cognitive deficits or behavior in depressed patients.

Aged↗

PubMed2004

Elevated levels of schizotypal features in parents of patients with a family history of schizophrenia spectrum disorders.

There is some evidence that schizotypal traits are related to a genetic or familial liability to develop schizophrenia. However, it is unclear whether the number of schizotypal traits is elevated in parents of schizophrenia patients compared with controls. This study used the Schizotypal Personality Questionnaire to investigate the difference in number of schizotypal traits between both parents of 36 patients with schizophrenia (n = 72 persons) and 26 healthy married control couples (n = 52 persons). Parents of patients had a lower score on the positive dimension of schizotypy than healthy controls. There was no difference on the negative or disorganization dimension between groups. The difference on the positive dimension might have been caused by a difference in response style between parents of patients and controls due to the fact that parents are more familiar with schizophrenia than controls. Of interest, parents with a family history of schizophrenia spectrum disorders had more positive and negative schizotypal traits than parents without a family history of schizophrenia spectrum disorders. Because these two groups of parents differ in only genetic risk, not familiarity with schizophrenia, results suggest that the negative and positive dimension of schizotypy are related to a familial or genetic vulnerability to schizophrenia.

Demography↗

PubMed2004

Comparative effect of atypical and conventional antipsychotic drugs on neurocognition in first-episode psychosis: a randomized, double-blind trial of olanzapine versus low doses of haloperidol.

OBJECTIVE: The effect of antipsychotic medication on neurocognitive function remains controversial, especially since most previous work has compared the effects of novel antipsychotic medications with those of high doses of conventional medications. This study compares the neurocognitive effects of olanzapine and low doses of haloperidol in patients with first-episode psychosis. METHOD: Patients with a first episode of schizophrenia, schizoaffective disorder, or schizophreniform disorder (N=167) were randomly assigned to double-blind treatment with olanzapine (mean modal dose= 9.63 mg/day) or haloperidol (mean modal dose=4.60 mg/day) for the 12-week acute phase of a 2-year study. The patients were assessed with a battery of neurocognitive tests at baseline and 12 weeks after beginning treatment. RESULTS: An unweighted neurocognitive composite score, composed of measures of verbal fluency, motor functions, working memory, verbal memory, and vigilance, improved significantly with both haloperidol and olanzapine treatment (effect sizes of 0.20 and 0.36, respectively, no significant difference between groups). A weighted composite score developed from a principal-component analysis of the same measures improved to a significantly greater degree with olanzapine, compared with haloperidol. Anticholinergic use, extrapyramidal symptoms, and estimated IQ had little effect on the statistical differentiation of the medications, although duration of illness had a modest effect. The correlations of cognitive improvement with changes in clinical characteristics and with side effects of treatment were significant for patients who received haloperidol but not for patients who received olanzapine. CONCLUSIONS: Olanzapine has a beneficial effect on neurocognitive function in patients with a first episode of psychosis. However, in a comparison of the effects of olanzapine and low doses of haloperidol, the difference in benefit is small.

Adolescent↗

PubMed2003

Brain volumes as predictor of outcome in recent-onset schizophrenia: a multi-center MRI study.

Gray matter brain volume decreases have been found in patients with schizophrenia as compared to healthy control subjects measured by using Magnetic Resonance Imaging (MRI). An association has been suggested between decreased gray matter volume and poor outcome in chronically ill patients with schizophrenia. The present longitudinal multi-center study investigated whether gray matter volume at illness onset can predict poor outcome in recent-onset schizophrenia after a follow-up of approximately 2 years. An MRI calibration study was performed since scans of patients with recent-onset psychosis were conducted at three sites with 1.5 T MR scanners from two different manufacturers. Applying a linear scaling procedure on the histogram improved comparability between volume measurements acquired from images from the different scanners. Brain scans were obtained from 109 patients with recent-onset schizophrenia. Volumes of intracranium, total brain, cerebral gray and white matter, third and lateral ventricles, and cerebellum were measured. After a mean follow-up period of approximately 2 years, measurements of symptoms, functioning, need for care, and illness history variables were assessed. No significant correlations were found between the brain volume measures and any of these measures. Gray matter volume at illness onset does not predict outcome after 2 years in recent-onset schizophrenia.

Adolescent↗

PubMed2003

Cognitive dysfunctions in parents of schizophrenic patients parallel the deficits found in patients.

Schizophrenia is characterized by a global cognitive impairment, with varying degrees of deficit in all ability domains. Since genetic factors are important in the etiology of schizophrenia we investigated whether parents of schizophrenic patients also show cognitive deficits, particularly on those cognitive ability domains that are most severely affected in patients. Both biological parents of 37 patients with schizophrenia (N=74 subjects) and 28 comparable healthy married control couples (N=56 subjects) were included. A comprehensive and standardized cognitive battery was used including tests measuring verbal memory, executive functioning, language, attention, and psychomotor functioning. Parents of patients differed from control couples on those cognitive constructs that are generally considered to be most impaired in schizophrenic patients, i.e. global verbal memory, bilateral motor skill, continuous performance, and word fluency. In addition, parents differed significantly from control couples on some other cognitive constructs on which patients show a smaller but also significant difference compared to healthy controls, i.e. unilateral motor skill and digit span. Results suggest that the cognitive constructs on which patients show relatively most severe impairment may prove suitable as endophenotypic markers in schizophrenia.

Cognition Disorders↗

PubMed2003

Long-term memory deficits in schizophrenia: primary or secondary dysfunction?

Long-term memory impairment is often found in schizophrenia. The question remains whether this is caused by other cognitive deficits. One hundred eighteen first-episode patients were compared with 45 control participants on several memory tasks. The role of processing speed and central executive functions on memory performance was examined with regression analysis for all participants and for patients separately. Deficits were found in general verbal learning performance and retrieval in episodic memory and semantic memory. Processing speed reduced disease-related variance in all memory variables. Coordination, organization of information, and speed of processing were the best predictors for long-term memory deficits in patients. The amount of explained variance, however, is small, especially in general verbal learning performance.

Adult↗

PubMed2003

Global intellectual impairment does not accelerate with age in patients with schizophrenia: a cross-sectional analysis.

Neuropsychological studies show impairment in intellectual functions in schizophrenia patients. It is still unclear, however, whether intelligence scores decline progressively during the illness as compared to healthy subjects' scores. Longitudinal studies conducted so far have been restricted to relatively short time spans. The aim of this study is to investigate whether changes in intelligence scores accelerate with age in schizophrenia patients. In a cross-sectional design, performance of four subtests of the Wechsler Adult Intelligence Scale (WAIS) was analyzed in 112 schizophrenia patients and compared to that of 70 healthy subjects, across an age span of 40 years (16-56 years). A linear regression analysis was performed. A main effect on the total ratio score of the four tests was demonstrated between the two groups. No main effect of age and no interaction effect of age with group for the total ratio score were found. The results confirm that there is global intellectual impairment in schizophrenia patients at the onset of illness but no age-accelerated decline and are consistent with the neurodevelopmental hypothesis of schizophrenia.

Adolescent↗

PubMed2002

Schizophrenic patients without neuropsychological deficits: subgroup, disease severity or cognitive compensation?

Some schizophrenic patients do not show clinically relevant cognitive deficits. The question remains whether this represents the existence of an etiologically different subgroup, a general effect of disease severity or whether their cognitive deficits do not reach a clinical threshold due to a greater cognitive compensation ('brain reserve') capacity. A group of 23 out of 118 first onset patients was identified as cognitively normal (CN). The cognitive profile of these patients was compared with that of 45 healthy controls. Next these patients were compared with the cognitively impaired (CI) patients on obstetric complications (OCs), premorbid adjustment, age at onset, Positive and Negative Syndrome Scale ratings, social functioning and substance abuse. In addition both groups were compared on intelligence and educational level as indirect indicators of cognitive compensation capacity. There were no differences in OCs, premorbid adjustment, age at onset, psychopathology or substance abuse between the two patient groups. There was a significant difference in social functioning, which is a consequence rather than a cause of cognitive deficits. However, the CN patients scored significantly higher on measures of intelligence and educational level than the CI patients. This suggests that a difference in cognitive compensation capacity could explain the existence of a CN patient group.

Adolescent↗

PubMed2002

Neurological signs in parents of schizophrenic patients.

The importance of neurological abnormalities in relatives of schizophrenic patients is not completely clear and has been questioned. The hypothesis that neurological abnormalities are trait markers for a vulnerability to develop schizophrenia was tested in 32 parents of patients with schizophrenia and 34 healthy controls. A comprehensive and standardized neurological assessment battery was used. The examiners were blind as to whether they tested a parent of a patient or a healthy control. Four function domains were investigated; higher cerebral functions, cranial nerve functions, general motor functions and gait. There were no significant differences between parents of patients and healthy controls on any of the neurological function domains, or on the total number of neurological abnormalities. No difference was found between parents with a positive family history of schizophrenia spectrum disorders, parents with a negative family history and controls. Results suggest that the neurological functions investigated are not related to a genetic liability to develop schizophrenia.

Female↗

PubMed2002

Release from proactive inhibition in schizophrenia and its potential as a genotypic marker.

Release from proactive inhibition (RPI) in first-episode (FE) schizophrenic patients and the potential of RPI as a genotypic marker of schizophrenia was investigated in two studies. The first study showed that FE patients ( n=35) exhibited weaker RPI than matched obsessive compulsive disorder (OCD) patients (n=20) as well as healthy controls (n=34). OCD patients and controls showed similar RPI. The second study showed that RPI is similar in both parents of patients (n=64) and matched controls (n=52). Results were explained in terms of additional evidence for impairment in the inhibition of irrelevant information in schizophrenia. Combination of our data and literature review suggests that diminished RPI can be attributed to a combination of dorsolateral-prefrontal and dorsomedial-thalamic impairment. RPI may not be a genotypic marker for schizophrenia but rather related to the illness or its treatment. An alternative explanation in terms of insufficient power of the parent-sample, due to unilineal inheritance of schizophrenia is, however, possible.

Adult↗

PubMed2002

School performance as a premorbid marker for schizophrenia: a twin study.

Evidence is accumulating that developmental abnormalities, poor neuromotor function, and increased problem behavior precede the manifestation of schizophrenia itself. Information on school performance and behavioral development was obtained for 49 pairs of twins in which at least one twin suffered from schizophrenia (20 monozygotic [MZ], 29 dizygotic [DZ]) and for 43 pairs of healthy control twins (25 MZ, 18 DZ). Cox regression was used to analyze the contribution of schizophrenia, zygosity, sex, and year of birth to the age at which developmental divergence occurred. In both MZ and DZ twin pairs with schizophrenia, divergence in school performance occurred about 7.5 years earlier than it did in control twins, at 12 years of age, preceding the onset of psychosis by 10 years. This suggests that the first prodromal signs of schizophrenia manifest themselves as cognitive symptoms at the onset of puberty. Underperformance at school might therefore be considered one of the first signs of an until then latent vulnerability for schizophrenia.

Adult↗