W.M.A. Verhoeven

Catatonia: Disappeared or Under-Diagnosed?

Background: Over the last century, especially during the latter half, the prevalence of the diagnosis of catatonic schizophrenia decreased considerably. Several explanations for this phenomenon have been put forward. Sampling and Methods: The present study investigated the frequency of the diagnosis of catatonic schizophrenia in a large sample of admitted psychiatric patients (n = 19,309). In addition, the presence of catatonic symptoms was studied in a sample of patients with schizophrenia (n = 701) and in a group of consecutively admitted psychotic patients (n = 139). In these two groups the effect of the diagnostic procedures on the recognition of catatonia was examined. Results: The diagnosis of catatonic schizophrenia dropped from 7.8% in 1980–1989 to 1.3% in 1990–2001 (p < 0.001). In addition, a possible under-diagnosis of catatonic schizophrenia was found in an independent sample of patients with schizophrenia. Application of a systematic catatonia rating scale in patients admitted with acute psychosis identified a bimodally distributed catatonic dimension. At least 18% of these patients fulfilled the criteria for catatonia. Interestingly, the catatonic subgroup used atypical antipsychotic compounds more frequently (p < 0.05). Conclusions: The results suggest that changes in diagnostic criteria and the diagnostic procedure itself are responsible for the under-recognition of catatonia.

Cerebrospinal fluid 5-hydroxyindolacetic acid and aggression : a critical reappraisal of the clinical data

Over the past 15 years several clinical studies have been published dealing with the hypothesis that disturbances in central serotonergic functioning could be related to outward directed aggression and impulsivity. Close reading of the 22 relevant reports, however, raises doubt about the unequivocality of the results across diagnostic boundaries and in comparison with normal controls. Only eight of the studies are methodologically acceptable and seem to support the hypothesis. Taking all data together, it is concluded that some relationship exists between decreased serotonin metabolism, as reflected by lowered cerebrospinal fluid 5-hydroxyindolacetic acid, and certain aspects of aggressive behavior in a subgroup of young, male, personality-disordered subjects with seriously deviant behavior.

Naltrexone attenuates self-injurious behavior in mentally retarded subjects

The effect of naltrexone on the frequency of self-injurious behavior (SIB) was investigated in 6 male subjects with profound mental retardation. Following a double-blind placebo-controlled crossover design, naltrexone was administered in a dose of 50 mg once daily for 3 consecutive weeks. In 2 of 5 subjects, a significant decrease of SIB frequency could be demonstrated, and in 1, a tendency to a reduction was found. No effect on duration of restrain time was found in 3 subjects. These data suggest that disturbances of the endogenous opioid systems may be involved in the pathophysiology of SIB of certain patients.

Meditation-Induced Psychosis

Background:Meditation is a self-regulatory psychological strategy that is frequently applied in Western as well as non-Western countries for different purposes; little is known about adverse events. Sampling and Methods: A male patient is described who developed an acute and transient psychosis with polymorphic symptomatology after meditating. A literature search for psychotic states related to meditation was carried out on PubMed, Embase and PsycInfo. Results: In the case presented a diagnosis of acute polymorphic psychotic disorder was made. Other case reports dealt with either a relapse of a pre-existent psychotic disorder or with a brief psychotic reaction in patients without a psychiatric history. Conclusion:Meditation can act as a stressor in vulnerable patients who may develop a transient psychosis with polymorphic symptomatology. The syndrome is not culture bound but sometimes classified in culture-bound taxonomies like Qi-gong Psychotic Reaction.

Endorphins and schizophrenia

Clinical endorphin research in schizophrenia has so far fanned out in the following directions: (a) studies of endorphin concentration in body fluids, and (b) studies of the effects in schizophrenic patients of opiate (endorphin) antagonists, and of endorphins and endorphin derivatives. The main results are reviewed in this paper. The conclusions drawn are: (1) Body fluid research has so far yielded no conclusive evidence of disrupted endorphin metabolism in schizophrenia. Technology for the measurement of small quantities of endorphins is, however, still deficient. (2) The opiate antagonist issue is controversial. One of the major problems is that the studies undertaken differ considerably from each other in patient selection, dose and route of administration, making comparisons difficult. Furthermore, only single dose studies have been reported; the results of repeated administrations may be different. (3) To date only β-endorphin, DTγE (a fragment of γ-endorphin) and FK33-824 (a synthetic met-enkephalin derivative) have been studied therapeutically. Of these, DTγE is the most interesting in scientific terms, firstly because, pharmacologically, it seems to be related to the ‘true’ neuroleptics, and secondly because its lacks morphinomimetic properties. The therapeutic potential of this substance, if confirmed, would therefore not be related to morphine-like activity but to a ‘genuine’ opiate-receptor-independent anti-psychotic action.

Anhedonia, suicide ideation and Dexamethasone nonsuppression in depressed patients

In the search for a valid analysis of a number of operationalised symptoms common to depressive behaviour, a study was performed comprising 46 patients showing depressive symptoms, according to operationalised criteria and as part of which all agreed to undergo the following tests: (a) psychiatric: Present State Examination; (b) psychological: Hamilton Rating Scale, Montgomery-Asberg Rating Scale, State-Trait Anxiety Inventory, Beck Suicide Ideation Scale, Chapman Anhedonia Scale, Mood Scale, Sleep Quality Scale, Activities Scale, Social Support Scale, Questionnaire on Recently Experienced Events and the Paykel Life Events Interview; and (c) biochemical: Dexamethasone Suppression (DEX) Test. After gathering different depressive subgroups, based on operationalised symptoms, a dichotomy was made in the distributions of the (an)hedonia, suicide ideation and DEX-(non) suppression scores. This study may indicate that anhedonia, suicide ideation and DEX-nonsuppression are the opening to the identification of a subgroup of depressed patients. This symptom complex could not definitely be identified on the basis of existing DSM-III diagnostic entities, because of the known fact that this method of classification is not appropriate for our purposes in revealing pathophysiological processes. It is suggested, therefore, that these symptoms might prove to be the anchor-point from which to reach a better insight into the aetiology and pathogenesis (i.e. the final common pathway) of depression.

HLA, AND THE RESPONSE TO TREATMENT WITH γ‐TYPE ENDORPHINS IN SCHIZOPHRENIA

In order to investigate whether genetic factors are involved in the response of schizophrenic patients to treatment with γ‐type endorphins, we typed 32 Dutch schizophrenic patients for the HLA‐A, ‐B, ‐C and ‐DR antigens. The total patient group showed an increase of HLA‐Bw4 and HLA‐Cw1. A subgroup of 20 paranoid patients showed an increase of HLA‐Cw1 and a significant heterogeneity for the HLA‐C locus. In 16 patients who responded moderately or markedly to treatment with γ‐type endorphins, an increase of HLA‐B15/Cw3 and a decrease of HLA‐B17 were found as compared to 16 patients with no or a slight response. Moreover, HLA‐B15 was particularly increased in those patients who responded markedly and remained free of psychotic symptoms for a period of at least 6 months after treatment with γ‐type endorphins (RR = 24.6, Puncorr.= 0.0015).Our results suggest that genetic factors coded for within the HLA region are associated with paranoid schizophrenia, and that HLA‐B15/Cw3 is associated with a marked and prolonged response to treatment with γ‐type endorphins.

Nonschizophrenic psychotic disorders: The case of cycloid psychoses

Background: Cycloid psychosis is a psychiatric disorder known for about 100 years. This disorder is at present partly and simplified represented in the ICD-10. Sampling and Methods: Over a period of 15 months, 139 consecutively acutely admitted psychotic patients were assessed, by means of different diagnostic instruments, in order to investigate the prevalence and the symptom profile of cycloid psychoses. In addition, the concordance between the diagnoses cycloid psychosis, brief psychotic disorder, and acute polymorphic psychotic disorder with or without symptoms of schizophrenia was calculated. Results: Cycloid psychoses were present in 13% of the patients. There was a significant but small overlap with the DSM brief psychotic disorder and the ICD acute polymorphic psychotic disorder. Conclusions: This study demonstrates that cycloid psychoses can be identified with the proper diagnostic instruments in a proportion that is also found in other studies. Since this type of psychosis entails a distinct prognosis and may require a specific treatment, its identification is of clinical importance. Limitations are the nature of the psychiatric facility with an inherent bias in the selection of patients and the lack of a long-term evaluation.

Serotonin and Disruptive Behaviour; A Critical Evaluation of the Clinical Data

Over the past two decades, several clinical studies have addressed the relationship between aggression, impulsivity and other aspects of disruptive behaviour and indicators of central serotonergic function, particularly hormonal challenge tests and CSF 5‐HIAA measurements. Analysis of the 23 studies on CSF 5‐HIAA and the 11 studies using challenge tests does not reveal unequivocal support for the serotonin–aggression hypothesis. Taking all the data together, it appears the disturbances in central serotonin neurotransmission, as reflected by lower CSF 5‐HIAA levels or blunted prolactin response to a serotonergic challenge compound, may be present in a subgroup of relatively young, male, personality‐disordered patients.

Use of Naloxone in Schizophrenic Psychoses and Manic Syndromes

Since 1975, different morphinomimetic peptides have been isolated from hypophyseal-hypothalamic extracts: the pentapeptides methionine-enkephalin and leucine-enkephalin, and the longer peptides alpha-, beta- and gamma-endorphin. The primary structure of most of these peptides is also present in that of beta-lipotropin. The morphinomimetic properties of endorphins can be blocked with opiate-antagonists. In rats, moreover, the endorphins influence behavior which cannot be blocked with opiate antagonists. On the basis of the hypothesis that hyperactivity of endorphin systems may be involved in the pathogenesis of schizophrenia and manic syndromes, the effect of opiate antagonists on psychotic and manic symptoms has been examined in a number of clinical studies in the past few years. A transient therapeutic effect has been demonstrated in about 30% of the patients so treated. Our own double-blind controlled study of 5 schizophrenic and 5 manic patients in the context of a World Health Organization project failed to reveal any therapeutic effect after subcutaneous injection of 20 mg naloxone. The possible reasons of the negative results are discussed.