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Gallagher P.,Northumbria University | Gray J.M.,Northumbria University | Kessels R.P.C.,Donders Institute for Brain | Kessels R.P.C.,Radboud University Nijmegen | Kessels R.P.C.,Vincent Van Gogh Institute for Psychiatry
Psychological Medicine | Year: 2015

Background Previous studies of neurocognitive performance in bipolar disorder (BD) have demonstrated impairments in visuo-spatial memory. The aim of the present study was to use an object-location memory (OLM) paradigm to assess specific, dissociable processes in visuo-spatial memory and examine their relationship with broader neurocognitive performance. Method Fifty participants (25 patients with BD in a current depressive episode and 25 matched healthy controls) completed the OLM paradigm which assessed three different aspects of visuo-spatial memory: positional memory, object-location binding, and a combined process. Secondary neurocognitive measures of visuo-spatial memory, verbal memory, attention and executive function were also administered. Results BD patients were significantly impaired on all three OLM processes, with the largest effect in exact positional memory (d=1.18, p<0.0001). General deficits were also found across the secondary neurocognitive measures. Using hierarchical regression, verbal learning was found to explain significant variance on the OLM measures where object-identity was present (the object-location binding and combined processes) and accounted for the group difference. The group difference in precise positional memory remained intact. Conclusions This study demonstrates that patients with bipolar depression manifest deficits in visuo-spatial memory, with substantial impairment in fine-grain, positional memory. The differential profile of processes underpinning the visuo-spatial memory impairment suggests a form of 'cognitive scaffolding', whereby performance on some measures can be supported by verbal memory. These results have important implications for our understanding of the functional cognitive architecture of mood disorder. © Cambridge University Press 2014. Source

Verhoeven W.M.,Vincent Van Gogh Institute for Psychiatry
BMJ case reports | Year: 2013

Kallmann syndrome (KS) is a genetically heterogeneous and rare disorder characterised by the combination of hypothalamic hypogonadism and anosmia/hyposmia, a variable degree of intellectual disability and several somatic anomalies. In about one-third of the patients, mutations have been identified in at least seven different genes. Virtually no data are available about possible neuropsychiatric symptoms in KS. Here, a young adult male is described with a previous clinical diagnosis of KS and recent paranoid schizophrenia of which positive, but not negative symptoms, fully remitted upon treatment with antipsychotics. Neither genome-wide array analysis nor mutation analyses disclosed imbalances or mutations in any of presently known KS disease genes. This is the first report on a patient with KS and paranoid schizophrenia in whom extensive genetic analyses were performed. It is concluded that further studies are warranted in order to elucidate a possible increased risk for psychiatric symptoms in patients with KS. Source

Ahmed A.I.A.,Vincent Van Gogh Institute for Psychiatry | Ahmed A.I.A.,Radboud University Nijmegen | Ali A.N.A.,Vivaldi Pharmacy | Kramers C.,Radboud University Nijmegen | And 5 more authors.
Journal of Clinical Psychopharmacology | Year: 2013

INTRODUCTION: Over the past years, the impact of varenicline in patients with mental illness has been debated as serious neuropsychiatric adverse events (AEs) have been reported with varenicline use. AIM: To identify and summarize published case reports of neuropsychiatric AEs ascribed to varenicline and to determine potential risk factors for these AEs. METHODS: A literature search of MEDLINE, the Cochrane Library, EMBASE, and PsychInfo database was conducted for case reports concerning the neuropsychiatric AEs of varenicline published in English from 2006 (approval year by the US Food and Drug Administration and the Dutch Medicines Evaluation Board) to January 1, 2012. RESULTS: We identified 25 published cases. In most reports, patients had been admitted to psychiatric hospitals with serious neuropsychiatric AEs due to varenicline. The average patient age was 46.4 years, and 56% were men; 68% of patients had a psychiatric history. The onset of symptoms started 2 days to 3 months after the initiation of varenicline. One report described completed suicide in a man with no psychiatric history. In most cases (84%), the neuropsychiatric symptoms resolved after the discontinuation of varenicline. Analysis of all reports using the Naranjo causality scale, a method for estimating the probability of adverse drug reactions, indicated probable causality in 76% of the cases and definite causality in 12% of cases. CONCLUSION: Varenicline is associated with an increased risk of serious neuropsychiatric AEs, especially in patients with a psychiatric illness. It is strongly recommended that varenicline be administered only to mentally stable patients and under close monitoring. Copyright © 2013 Lippincott Williams &Wilkins. Source

Verhoeven W.M.A.,Vincent Van Gogh Institute for Psychiatry | Verhoeven W.M.A.,Erasmus Medical Center | Egger J.I.M.,Vincent Van Gogh Institute for Psychiatry | Egger J.I.M.,Radboud University Nijmegen
Pharmacopsychiatry | Year: 2015

Introduction: This study includes 28 patients with genetically proven 22q11.2 deletion syndrome referred for treatment-resistant psychoses and aims at the identification of a suitable pharmacological treatment strategy. Methods: Based on standardized diagnostic procedures, key psychiatric symptoms and cognitive status were assessed. Also, data about previous diagnostic vignettes as well as the history of psychotropic medication and medical conditions were collected. Finally, the effect of the subsequent treatment regimen was periodically re-assessed. Results: Since psychotic symptoms had been shown to be non-responsive to conventional antipsychotics including risperidone, treatment with either clozapine or quetiapine was started. In 21 patients, a substantial reduction of psychotic symptoms was achieved with either one, and in 3-quarters of this group remission was attained over a longer follow-up period. In a significant number of patients, valproic acid was added either for mood stabilizing purposes or to avoid epileptic side effects of clozapine. Discussion: Treatment of psychotic symptoms in patients with 22q11DS with the atypical antipsychotic quetiapine or clozapine in combination with the mood-stabilizing anticonvulsant valproic acid, appears likely to be more effective than with other psychotropic compounds. Source

Verhoeven W.M.A.,Vincent Van Gogh Institute for Psychiatry | Verhoeven W.M.A.,Erasmus Medical Center | Kleefstra T.,Radboud University Nijmegen | Egger J.I.M.,Vincent Van Gogh Institute for Psychiatry | Egger J.I.M.,Radboud University Nijmegen
American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics | Year: 2010

The 9q Subtelomeric Deletion Syndrome (9qSTDS) is clinically characterized by mental retardation, childhood hypotonia, and facial dysmorphisms. Haploinsufficiency of the EHMT1 gene has been demonstrated to be responsible for its core phenotype. In a significant number of patients behavioral abnormalities like aggression, impulsivity, and chaotic behaviors are present as well as epileptic phenomena. Reports about the developmental, behavioral, and neuropsychiatric aspects of 9qSTDS are scarce and mostly limited to young patients only. In this report, the behavioral and neuropsychiatric characteristics of one male and one female middle-aged patient are described in whom the genetic diagnosis, interstitial and telomeric 9q deletion, respectively, was established recently. In both patients a remarkable sleep disturbance, characterized by frequent awakenings and daytime sleepiness, was present as well as a prominent apathy syndrome. The observedmotor signs such as rigid flexure of the arms and finger stereotypies persisted over a period of many years and could therefore not be viewed as symptoms of catatonia. It is concluded that the proposed behavioral phenotype of 9qSTDS comprises at least an erratic sleep pattern and an enduring severe apathy. © 2009 Wiley-Liss, Inc. Source

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