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Radboud Universiteit Nijmegen, 31 augustus 2011, Promotores : Buitelaar, J.K., Renier, W.O. Co-promotor : Overeem, S., Contains fulltext : 90831.pdf (publisher's version ) (Open Access)

Contains fulltext : 90677.pdf (publisher's version ) (Closed access), Introduction: Narcolepsy is a primary sleeping disorder with excessive daytime sleepiness and cataplexy as core symptoms. There is increasing interest in the psychiatric phenotype of narcolepsy. Although many authors suggest an overrepresentation of mood disorders, few systematic studies have been performed and conflicting results have been reported. Anxiety disorders in narcolepsy have only received little attention. Methods: We performed a case control study in 60 narcolepsy patients and 120 age- and sex-matched controls from a previous population study. The Schedules for Clinical Assessment in Neuropsychiatry were used to assess symptoms and diagnostic classifications of mood and anxiety disorders. Results: Symptoms of mood disorders were reported by about one third of patients. However, the prevalence of formal mood disorder diagnoses including major depression was not increased. In contrast, more than half of the narcolepsy patients had anxiety or panic attacks. Thirty-five percent of the patients could be diagnosed with anxiety disorder (odds ratio=15.6), with social phobia being the most important diagnosis. There was no influence of age, sex, duration of illness or medication use on the prevalence of mood or anxiety symptoms and disorders. Discussion: Anxiety disorders, especially panic attacks and social phobias, often affect patients with narcolepsy. Although symptoms of mood disorders are present in many patients, the prevalence of major depression is not increased. Anxiety and mood symptoms could be secondary complications of the chronic symptoms of narcolepsy. Recent studies have shown that narcolepsy is caused by defective hypocretin signaling. As hypocretin neurotransmission is also involved in stress regulation and addiction, this raises the possibility that mood and anxiety symptoms are primary disease phenomena in narcolepsy.

Contains fulltext : 81794.pdf (publisher's version ) (Closed access), OBJECTIVE: Patients with narcolepsy often experience pervasive hypnagogic hallucinations, sometimes even leading to confusion with schizophrenia. We aimed to provide a detailed qualitative description of hypnagogic hallucinations and other "psychotic" symptoms in patients with narcolepsy and contrast these with schizophrenia patients and healthy controls. We also compared the prevalence of formal psychotic disorders between narcolepsy patients and controls. METHODS: We used SCAN 2.1 interviews to compare psychotic symptoms between 60 patients with narcolepsy, 102 with schizophrenia and 120 matched population controls. In addition, qualitative data was collected to enable a detailed description of hypnagogic hallucinations in narcolepsy. RESULTS: There were clear differences in the pattern of hallucinatory experiences in narcolepsy vs. schizophrenia patients. Narcoleptics reported multisensory "holistic" hallucinations rather than the predominantly verbal-auditory sensory mode of schizophrenia patients. Psychotic symptoms such as delusions were not more frequent in narcolepsy compared to population controls. In addition, the prevalence of formal psychotic disorders was not increased in patients with narcolepsy. Almost half of narcoleptics reported moderate interference with functioning due to hypnagogic hallucinations, mostly due to related anxiety. CONCLUSIONS: Hypnagogic hallucinations in narcolepsy can be differentiated on a phenomenological basis from hallucinations in schizophrenia which is useful in differential diagnostic dilemmas.

Contains fulltext : 79730.pdf (publisher's version ) (Closed access), Although a clear definition of pseudologia fantastica cannot be found in the literature, there is consensus that this condition differs quantitatively and qualitatively from 'normal lying'. We discuss recognition of pseudologia fantastica based on 2 patients who presented with suicidal ideations at the casualty department following a traumatic event. Early recognition is important in order to break the pattern of lying, to restrict the use of medical resources and, finally, to act in accordance with the general principle of 'primum-non-nocere'. Although a psychiatric diagnostic workup might be worthwhile, it remains difficult to engage these patients for psychiatric treatment.

Contains fulltext : 73473.pdf (publisher's version ) (Open Access), Study Objectives: To study the prevalence of and symptoms of eating disorders in patients with narcolepsy. Design: We performed a case-control study comparing symptoms of eating disorders in patients with narcolepsy versus healthy population controls, using the Schedules for Clinical Assessment in Neuropsychiatry (SCAN 2.1). To study whether an increased body mass index (BMI) could be responsible for symptoms of an eating disorder, we also compared patients with BMI-matched controls, using the SCAN as well as the Eating Disorder Examination-Questionnaire. Setting: University hospital. Patients and participants: Patients with narcolepsy/cataplexy (n = 60) were recruited from specialized sleep centers. Healthy controls (n = 120) were drawn from a population study previously performed in the Netherlands. Separately, 32 BMI-matched controls were recruited. Interventions: N/A. Measurements and Results: In total, 23.3% of the patients fulfilled the criteria for a clinical eating disorder, as opposed to none of the control subjects. Most of these were classified as Eating Disorder–Not Otherwise Specified, with an incomplete form of binge eating disorder. On the symptom level, half of the patients reported a persistent craving for food, as well as binge eating. Twenty-five percent of patients even reported binging twice a week or more often. When compared with BMI matched controls, the significant increases persisted in symptoms of eating disorders among patients with narcolepsy. Except for a higher level of interference in daily activities due to eating problems in patients using antidepressants, medication use did not influence our findings. Conclusions: The majority of patients with narcolepsy experience a number of symptoms of eating disorders, with an irresistible craving for food and binge eating as the most prominent features. Eating disorder symptomatology interfered with daily activities. These findings justify more attention for eating disorders in the treatment o

Contains fulltext : 53466.pdf (publisher's version ) (Open Access)

Contains fulltext : 48956.pdf (publisher's version ) (Closed access), Narcolepsy is associated with lowered vigilance. Diurnal variation in vigilance appears altered, but the exact nature of this change is unclear. It was hypothesized that the homeostatic sleep drive is increased in narcolepsy. Decreased levels of vigilance are reflected in low frequency band power in the electroencephalogram (EEG), so these frequencies were expected to be increased in the narcolepsy group. Furthermore, it was expected that low frequency power should increase over the day. Narcoleptic patients and healthy controls participated (36 participants in total); they were not allowed to take medication or naps on the experimental day. EEG was measured at 9:00, 11:00, 13:00, 15:00, and 17:00 hours, during rest and during reaction time tasks. In the narcolepsy group, alpha power was lower at rest at all times. Delta and theta power during rest and task performance increased steadily over the day in this group, from 11:00 hours onwards. Additionally, in the narcolepsy group beta1 and beta2 power during rest appeared increased at the end of the day. The effects in the lower frequency bands strongly suggest that vigilance is low at all times. The progressive increase in low frequency power indicates that the sleep drive is enhanced. It is not clear whether this pattern reflects an extreme state of low vigilance, or a pathological brain condition. The effects in the higher frequencies suggest that narcoleptic patients may make an effort to counteract their low vigilance level.

Contains fulltext : 48164.pdf (publisher's version ) (Closed access), OBJECTIVE: To report serious psychiatric symptoms after standard chloroquine treatment following human malaria infection induced for research. CASE SUMMARY: A 34-year-old healthy woman volunteered to participate in a study of malaria treatment. She was infected on day 0 with a chloroquine-susceptible strain of Plasmodium falciparum and was treated with a standard 3-day course of chloroquine from day 9 onward, following a positive blood smear (parasitemia 0.001%). On day 10, the blood smear became negative. On day 11, she developed a psychotic disorder not otherwise specified, most probably caused by chloroquine use, with symptoms of depersonalization and anxiety. The diagnosis of delirium was considered but ruled out because of clear consciousness with lack of diurnal fluctuations. She refused to take antipsychotic medication. Three weeks later, the woman still encountered serious concentration problems. All complaints gradually subsided over the next 4 months, after which she felt completely recovered. Plasma chloroquine concentrations were within the therapeutic range. DISCUSSION: Chloroquine may achieve high concentrations in the brain and has a long half-life. As quinolines, the antimalarials may have the same pathologic activity as the fluoroquinolone antibiotics in acting as N-methyl-d-aspartate agonists and gamma-aminobutyric acid antagonists. Application of the Naranjo probability scale indicated that, in this patient, chloroquine was the probable cause of the serious psychiatric symptoms. CONCLUSIONS: Our unique observation demonstrates that serious psychiatric symptoms can emerge as a rare occurrence during standard chloroquine therapy. This adverse effect may persist for several months.

Contains fulltext : 59356.pdf (publisher's version ) (Closed access), Adenosine is an endogenous purine with vasodilating and cardioprotective properties. Animal experiments have shown that some benzodiazepine-induced effects can be explained by potentiation of adenosine effects, via inhibition of the nucleoside transport system. The objective of this study was to determine whether the frequently used benzodiazepines diazepam and midazolam increase adenosine-induced vasodilation in the human forearm vascular bed, measured by venous occlusion plethysmography. Adenosine (0.6, 6, 20, and 60 nmol/min/dl ForeArm Volume) was infused into the brachial artery with and without concomitant separate infusion of diazepam (21 nmol/min/dl, n = 9) and midazolam (23 nmol/min/dl, n = 8). Plasma concentrations of diazepam resp. midazolam at the end of the infusion protocol averaged 0.5 +/- 0.2 microg/ml plasma (1.6 microM) for diazepam versus 1.2 +/- 0.4 microg/ml plasma (3 microM) for midazolam. Intra-arterial infusion of the benzodiazepines did not alter baseline vascular tone, and had no significant influence on the forearm vasodilator response to adenosine. The adenosine-induced relative change in Forearm Vascular Resistance (FVR) was -3 +/- 7, -48 +/- 8, -75 +/- 6, and -85 +/- 3% in the absence and 3.5 +/- 11, -54 +/- 5, -74 +/- 5, and -82 +/- 3% resp. in the presence of diazepam (P > 0.1, repeated measures ANOVA, n = 9). Likewise, in the absence resp. presence of midazolam, FVR fell by 1 +/- 6, 55 +/- 5, 74 +/- 3, and 84 +/- 2% resp. 11 +/- 11, 59 +/- 2, 80 +/- 3, and 87 +/- 2% (P > 0.1, n = 7). Intra-brachial infusion of diazepam and midazolam resulting in forearm concentrations in the high therapeutic range does not augment adenosine-induced forearm vasodilation. A possible interaction at supra-therapeutic levels of the benzodiazepines can not be excluded from the present study, but lacks clinical significance.

Contains fulltext : 58623.pdf (publisher's version ) (Closed access), Peripheral benzodiazepine receptor (PBR) density in blood platelets and plasma allopregnanolone concentration in humans were determined following acute stress as represented by PhD examination. Fifteen healthy PhD students participated. Heart rate, blood pressure, plasma allopregnanolone, plasma cortisol, and PBR density were measured at different time points. Allopregnanolone and cortisol concentration and PBR density were significantly increased during examination. A positive correlation between allopregnanolone and PBR density was found.

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Contains fulltext : 22439.pdf (publisher's version ) (Open Access)