The writers of this paper made an inventory of the studies on the use of thyroid hormone in the treatment of depression. Fifteen clinical trials (353 patients), published between 1969 and 1987. were found, that can be described, as to their design, in two seperate groups:

One group (7 studies) administers thyroid hormone simultaneously with a tricyclic antidepressant to reach a faster effect of the antidepressant. The other group (8 studies) adds thyroid hormone to a tricyclic antidepressant in patients who fail to respond to this treatment, with the aim to convert therapeutic failure to success. After studying the literature we think we are able to conclude that it can be usefull to combine the antidepressant with thyroid hormone in view of the fact that, in a number of depressed patients, it shortens the duration of the illness. The augmentation of tricyclics by thyroid hormone needs further study.

Several studies have demonstrated that psychomotor retardation is an important sign of the major depressive episode, both from a diagnostic point of view and as a predictor of treatment outcome. However, it is uncertain to what extent psychomotor retardation is specific for the major depressive episode. A heterogeneous group of psychiatric patients (n=26) was studied using a rating scale developed specifically to assess psychomotor retardation (RRS). The 13 patients suffering from a major depressive episode had a significantly higher RRS score than patients with another diagnosis. Furthermore, in the depressive subjects the severity of the depression (measured by means of Hamilton's depression rating scale) appeared to correlate with the severity of the psychomotor retardation. Cognitive features of psychomotor retardation were mainly responsible for the more severe psychomotor retardation in the depressive patients. Surprisingly. Hamilton's depression scale which was used in this study does not pay much attention to these aspects.

A concise review is given of the importance of the atypical antipsychotic drugs clozapine, sulpiride, remoxipride and raclopride. Both the concept of atypicality and the pharmacological profile of these compounds is discussed. The newly developed atypical antipsychotic remoxipride has been studied in several double blind studies. In virtually all of these studies a reduced propensity for the induction of extrapyramidal symptoms was found.

These findings implicate that atypical antipsychotics may also not induce tardive dyskinesia. In addition to the treatment of acute schizophrenia, these compounds might be of use in the treatment of treatment resistent schizophrenia (clozapine), tardive dyskinesia and psychosis during the course of Parkinson's disease.

A case report is presented of a 72 year old woman, who has been treated for a depression with amitriptyline. During the treatment an orofacial dyskinesia develloped. Data in the literature concerning a possible link between the manifestation of orofacial dyskinesia and treatment with antidepressants were mainly found to be case reports. A closer study of the total in all of 25 case reports reveals that the antidepressant is often at most one of more possible determinants of the movement disorder. Particularly, it was frequently noted that patients were treated with other drugs or that the use of other drugs was not specified. A controverse exists in the literature whether or not a so called spontaneous orofacial dyskinesia is found in high frequency in elderly people. For clinical practice the advice is given that, in case an orofacial dyskinesia arises during antidepressant treatment, attention should be paid to other provoking factors in the first place.

The controversy concerning the concept ‘alcoholic dementia’ is reviewed in brief. Evidence from neuroradiological and neuropathological studies contribute little to the solution of this controversy, if dementia is considered as a clinical syndrome. From clinical descriptions it can be concluded that a sub-population of alcoholics suffers from a syndrome typified by psychologic disturbances other than amnesia alone. These patients fulfill the criteria for the syndromal diagnosis of ‘dementia’.

The nosologic concept of ‘alcoholic dementia’ implies a direct neurotoxic effect of alcohol and it raises questions concerning pathogenetic mechanisms which can not be answered. The DSM-III-R category ‘dementia associated with alcoholism’ represents a solution for this controversy, because it gives a correct and complete (radically syndromal) clinical description without making assumptions on the relative contribution of multiple factors causing cognitive disturbances in alcoholics.

The study of the biological determinants of abnormal behavior is not anymore psychiatry's stepchild, but a respected branch of that discipline. There is every reason to be optimistic over the future of biological psychiatry. The brain sciences are developing with astounding speed and the systematic attention for psychiatric-diagnosis and differential diagnosis renders biological psychiatry an unprecedented vitality.

One should, however, not ignore some disquieting prospects. The following points of concern are discussed: the alarming shortage of young research psychiatrists; the deficiencies in the teaching of biological psychiatry; the hesitancy to utilize the fruits of brain and behavior research in clinical practice; the shortcomings in psychiatric diagnosing; nosological tunnel vision and, finally, the danger of overrating biological psychiatry with the inevitable disappointment reaction that will follow. The scientific maturation of psychiatry is contingent on a balanced development of its constituents.

The narcoleptic syndrome in its most specific way is characterized by a set of clinical symptoms, including cataplexy, irresistable sleep episodes, hypnagogic hallucinations and sleepparalysis; the syndrome has been defined by the association of excessive day-time somnolence and REM-sleep abnormalities. In principle, anamnestic information is sufficient to establish the clinical diagnosis, although neuro-physiological and biochemical data(CSF monoamine metabolites and HLA-typology) are sometimes needed to support the diagnostic procedure. Treatment of excessive daytime somnolence is still primarily based upon CNS stimulants, while treatment of cataplexy and related symptoms rests on antidepressants with a primarily serotonergic mode of action.

Schizophrenia is a neurobiological developmental disorder of basic neuro-integrative functions, resulting in failures of cognitive selfregulation. Neurophysiological and psychophysiological dysfunctions should be considered in connection with the ubiquitous cognitive dysfunctions. Schizophrenic patients have problems with the integration of information, resulting in deficits of perceptual organization, and in ‘metacognitive’ deficits of executive functions in the area of behavior and experience. The biological basis of these cognitive functions is in the frontal cortex, but the primary dysfunction seems to be a subcortical one. Negative symptoms can be understood as a secondary exhaustion mechanism, and partly as an adaptive process, corresponding with energetic deficits in information processing. Psychophysiological studies of regional cerebral blood flow, positron emission tomography, electrophysiological recordings and measures of eye tracking point to frontal dysfunction and hypoactivation in patients with negative symptoms. This agrees well with the results of cognitive studies. Psychophysiologists and cognitive psychologists are studying different aspects of the same systems disorder.

Lithium was added to imipramine in case of a 55-year old depressed woman who didn't respond to imipramine alone. There was a clear improvement within a few days on 900 mg lithium carbonate a day (lithium plasmalevel 0.9 mmol/l). However when after two weeks the lithium dose was reduced to 600 mg a day (lithium plasmalevel 0.5 mmol/l), an almost immediate relapse followed. On resuming lithium in the old dose the depression disappeared again. After four weeks the second attempt at reducing and eventually stopping the lithium appeared to be successful. Half a year after cessation of lithium imipramine was also stopped. More than a year afterwards there hasn't been a depression again.

In this case, after a fast potentiation of imipramine by lithium, a relapse followed when the lithium dose was reduced. It seems to be that even a high and successful starting dose of lithium needs to be continued for some time in order to prevent a relapse.

To answer the question if it is possible for specific psychiatric illnesses to influence the thyroxine-concentration, a group of 376 patients admitted to a psychiatric hospital was studied retrospectively.

13.5% had an elevated thyroxine-concentration and only 0.6% had a low concentration.

Of the group of 145 men, 22.8% was found to have an elevated thyroxine-concentration. In the group of 196 women we found 6.6% to be elevated. A low thyroxine was found in only 0.5% of the women and 0.7% of the men.

In the group with an elevated thyroxine the psychiatric diagnoses of schizophrenia and psychotic disorders NOS are more common (19.6% and 17.4% respectively) than in the group with a normal thyroxine (4.4% and 6.5% respectively).

In deze rubriek zal worden ingegaan op recente observaties betreffende de psychofarmakologie in de breedst mogelijke zin. Vaak zullen zaken uit de Literatuur worden behandeld. De gekozen onderwerpen dienen altijd klinische relevantie te hebben. Ook zal deze rubriek gaan over gewoontes die in psychofarmakologische behandeling of in onderzoek zijn geslopen die volgens de auteur lang niet altijd logisch zijn. Soms zal deze rubriek een oproep bevatten om te reageren op een bijdrage gepubliceerd in dit of in een ander tijdschrift. Ook zal de lezer worden aangemoedigd hier zijn eigen ervaringen mee te delen. Het is niet de bedoeling in deze rubriek onderzoeken uitvoerig te rapporteren. Daarvoor staan andere pagina's van de Acta Neuropsychiatrica voor u open.

The influence of propofol on mood was evaluated, considering the potential use of propofol as an anesthetic for electroconvulsive therapy. The mood state of 80 psychologically healthy subjects was assessed before and from 1/2 hour till 4 hours after surgery under anesthesia with either propofol or methohexitone. The mood was assessed with the Profile of Mood States (POMS). The propofol group was more elated from one hour until 4 hours after anesthesia (p<0,01 )(factor 1). 1 hour after anesthesia the propofol group was continuously more composed than the methohexitone group (p<0,01) (factor 4) and after two hours the propofol group was more agreeable (p<0,05) (factor 2). Moreover, patients, who received propofol, were less tired (factor 3) and confused (factor 5). It can be concluded that, compared with methohexitone, propofol has a favorable influence on different aspects of mood.

The dexamethasone suppression test has been carried out in 111 depressed inpatients. Fasting, 8 a.m. plasma levels of Cortisol and adrenocorticotropic hormone (ACTH) were determined before and after administration of 1 mg dexamethasone. In 64 subjects multisequential (1-17,1-24,1-39) ACTH, and in 47 subjects intact (1-39) ACTH has been determined. Patients with melancholia exhibited significantly higher postdexamethasone Cortisol and intact ACTH values as compared with minor and simple major depressives. Severity of illness was significantly and positively related to postdexamethasone intact ACTH - but not to multisequential ACTH. Cortisol nonsuppressors showed higher postdexamethasone (only intact) ACTH values than Cortisol suppressors. Both postdexamethasone ACTH values were significantly and positively related with the postdexamethasone Cortisol values. We have established that Cortisol nonsuppression during melancholia is determined by an augmented escape of ACTH from suppression by dexamethasone. Intact ACTH showed the most significant clinical relevance for depression and Cortisol nonsuppression. In the clinical practice we advize the use of postdexamethasone intact ACTH in stead of plasma Cortisol or multisequential ACTH.