Vincent Van Gogh Institute for Psychiatry

Venray, Netherlands

Vincent Van Gogh Institute for Psychiatry

Venray, Netherlands

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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.

Michielsen L.A.,Vincent van Gogh Institute for Psychiatry | van der Heijden F.M.M.A.,Vincent van Gogh Institute for Psychiatry | Janssen P.K.C.,VieCuri Medical Center | Kuijpers H.J.H.,Vincent van Gogh Institute for Psychiatry
Neuropsychiatric Disease and Treatment | Year: 2014

Background: The aim of this retrospective study was to explore the relationship between psychotropic medication dosage and birth outcomes. Methods: A total of 136 women were enrolled, who had an active mental disorder, were taking medication to prevent a relapse, or had a history of postpartum depression or psychosis. Medication use was evaluated for the three trimesters and during labor. Based on the defined daily dose, medication use was classified into three groups. Primary outcome variables included the infant gestational age at birth, birth weight, and Apgar scores at one and 5 minutes. Results: Our study showed a significantly higher incidence of Apgar score ≤7 at and 5 minutes in women taking psychotropic drugs as compared with the group taking no medication, respectively (16.3% versus 0.0%, P=0.01). There was no significant difference between the two groups in Apgar score at one minute or in gestational age and birth weight. The results showed no significant differences in gestational age, birth weight, or Apgar scores for a low-intermediate or high dose of a selective serotonin reuptake inhibitor and for a low or intermediate dose of an antipsychotic. Conclusion: This study does not indicate a relationship between doses of selective serotonin reuptake inhibitors and antipsychotics and adverse neonatal outcomes. © 2014 Michielsen et al.

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.

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.

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 | And 6 more authors.
Parkinsonism and Related Disorders | Year: 2014

Neurodegeneration with brain iron accumulation (NBIA) comprises a group of rare neuropsychiatric syndromes characterized by iron accumulation in the basal ganglia. The pantothenate kinase-associated neurodegeneration (PKAN) was the first NBIA form to be genetically identified almost 15 years ago. Nowadays, eight types can be genetically distinguished. More recently, a novel NBIA was delineated and termed Static Encephalopathy of childhood with Neurodegeneration in Adulthood (SENDA), characterized by early intellectual disability followed by delayed progressive motor and cognitive deterioration with an onset in the second to third decade. Very recently, mutations in the WD repeat-containing protein 45 (WDR45) gene located on Xp11.23 were shown to be the causal factor. The protein encoded by WDR45 propels protein interaction important for autophagy. This form was therefore retermed Beta-propeller Protein Associated Neurodegeneration (BPAN). Here, the first three Dutch patients with genetically proven BPAN are comprehensively described with respect to course and neurological as well as neuropsychiatric phenotypes. All three showed a characteristic delayed progression of neurological symptoms with parkinsonism and prominent dystonia. Treatment with levodopa/carbidopa had limited effects only. Neuropsychiatric symptoms within the autistic and affective spectrum were present in the early phase of the disease. The specific course and prognosis should implicate restrained psychopharmacological interventions.The clinical picture and imaging hallmarks are often highly suggestive and should lead to suspect this specific disorder. However, the identification of a WDR45 mutation is needed for a definite diagnosis of BPAN. © 2013 Elsevier Ltd.

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.

Van Geldorp B.,Radboud University Nijmegen | Bergmann H.C.,Radboud University Nijmegen | Robertson J.,Vincent Van Gogh Institute for Psychiatry | Wester A.J.,Vincent Van Gogh Institute for Psychiatry | And 2 more authors.
Brain Research | Year: 2012

Both neuroimaging work and studies investigating amnesic patients have shown involvement of the medial temporal lobe during working memory tasks, especially when multiple items or features have to be associated. However, so far no study has examined the relationship between working memory and subsequent episodic memory in patients using similar tasks. In this study, we compared patients with amnesia due to Korsakoff's syndrome (n = 19) with healthy controls (n = 18) on an associative working memory task followed by an unexpected subsequent episodic memory task. The computerized working memory task required participants to maintain two pairs of faces and houses for either short (3 s) or long (6 s) delays. Approximately 5 minutes after completion of the working memory task, an unexpected subsequent recognition task with a two-alternative forced choice paradigm was administered. By directly comparing working memory and subsequent episodic memory, we were able to examine long-term encoding processes that may take place after longer delays. As expected, patients performed at chance level on the episodic memory task. Interestingly, patients also showed significantly impaired working memory performance (p <.01), even at short delays. Longer delays did not result in better subsequent memory, indicating that they do not facilitate long-term encoding processes. Our results are discussed in relation to Baddeley's working memory model as the episodic buffer is assumed to be a short-term store for maintaining bound representations. In light of these results, the long-standing view that working memory and long-term memory are strictly dissociated may need to be revisited. © 2011 Elsevier B.V. All rights reserved.

Berry C.J.,University of Plymouth | Kessels R.P.C.,Radboud University Nijmegen | Kessels R.P.C.,Vincent van Gogh Institute for Psychiatry | Wester A.J.,Vincent van Gogh Institute for Psychiatry | Shanks D.R.,University College London
Journal of Neuroscience | Year: 2014

We challenge the claim that there are distinct neural systems for explicit and implicit memory by demonstrating that a formal single- system model predicts the pattern of recognition memory (explicit) and repetition priming (implicit) in amnesia. In the current investigation, human participants with amnesia categorized pictures of objects at study and then, at test, identified fragmented versions of studied (old) and nonstudied (new) objects (providing a measure of priming), and made a recognition memory judgment (old vs new) for each object. Numerous results in the amnesic patients were predicted in advance by the single-system model, as follows: (1) deficits in recognition memory and priming were evident relative to a control group; (2) items judged as old were identified at greater levels of fragmentation than items judged new, regardless of whether the items were actually old or new; and (3) the magnitude of the priming effect (the identification advantage for old vs new items) overall was greater than that of items judged new. Model evidence measures also favored the single-system model over two formal multiple-systems models. The findings support the single-system model, which explains the pattern of recognition and priming in amnesia primarily as a reduction in the strength of a single dimension of memory strength, rather than a selective explicit memory system deficit. © 2014 the authors.

Verhoeven W.M.,Vincent Van Gogh Institute for Psychiatry | Egger J.I.M.,Vincent Van Gogh Institute for Psychiatry
Pharmacopsychiatry | Year: 2015

In their letter to the editor, Boot and colleagues comment on the results of treatment with atypical antipsychotics in patients with 22q11.2 deletion syndrome and relapsing psychoses. They identify 3 issues (i.'e., description of study rationale and assessments, the importance of endocrine dysfunctions and possible effects of sample bias) and conclude that until strong evidence to the contrary [is available], standard pharmacological management of psychotic illness in 22q11DS remains recommended. In our reply, we will illustrate the erroneous nature of their conjectures. © Georg Thieme Verlag KG Stuttgart. New York.

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.

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