Psychoeducation for patients with a psychotic disorder: effects on knowledge and coping.

OBJECTIVE: Psychoeducation is an essential and promising element in the nonpharmacologic treatment of patients with a psychotic disorder. This study examined the effects of patient-directed psychoeducation on knowledge and coping. METHOD: This study included 99 primary care patients with a psychotic disorder according to DSM-IV-TR criteria who completed a knowledge questionnaire before and a knowledge and coping questionnaire halfway through, immediately after, and 6 months after a 20-session group psychoeducation program. The first time the program was given was between April and October 2007, and the final time the program was given was between October 2009 and April 2010. Results were analyzed with multilevel analysis. RESULTS: Knowledge increased significantly from the beginning of the program to halfway through the program (P < .001), even after correction for baseline scores, but not any further thereafter. Coping improved from halfway through the program to the end of the program (P = .02), also after correction for baseline scores, but not thereafter. Only at 6 months after the program was knowledge related to coping (P = .01). There were no differences in knowledge and coping between male and female patients. Halfway through (P = .001) and at the end of the program (P = .02), the increase in knowledge was significantly lower for patients taking atypical antipsychotic medication than for patients taking typical antipsychotic medication. CONCLUSIONS: In patients with a psychotic disorder, psychoeducation results in more knowledge immediately and several months after the program and contributes to better coping only immediately after the program. Patients with more knowledge several months after psychoeducation may also be patients who then cope better with the disorder.

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.

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.

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.

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.

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.

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.