A positive significant relationship (p<0,01) is found between a psychiatric judgement on autonomic nervous system complaints and a “blind” neurological judgement on paroxysmal EEG phenomena. Classification: Somatization Disorder (DSM-III-R; IV 300.81). Diagnoses: nervous functional complaints, hyperventilation syndrome, Da Costa's disease (irritable heart syndrome, neurocirculatory asthenia) and irritable bowel syndrome. A positive significant relationship (p<0,001) is found between a diagnosis of “Da Costa's disease” and a “blind” neurological judgement on PEF. A positive significant relationship (p<0,001) is found between a psychiatric judgement on neurasthenia (atypical headache and atypical tiredness) classified as dysthymia DSM-IH-R 300.40 and a neurological judgement on localised (cortical) abnormalities by “blind” EEG evaluation. No medication in the last half year. Logistic regression analysis (n=116) revealed that sex and age are of no importance. No medication in the last half year before EEG registration.

In this first part of a review on recent insights into the structure and function of the γ-aminobuty rie acid type A - benzodiazepine receptor system, the γ-aminobutyric acid type A (GABAA) receptor and the different types of benzodiazepine (BDZ) receptors known at this moment are dicussed. GABAA- and BDZ receptors are coupled in a supramolecular GABAA-BDZ-ionophore receptor complex, each consisting of five acidic glycoprotein molecules called subunits. These subunits can be classified into five groups: α, β, γ, σ and ρ. Present evidence indicates the existence of multiple subtypes of these subunits. Multiple GABAA-BDZ receptors exist in the brain that show differential distribution and developmental patterns. These receptors differ from their subunit composition. The final functional properties of the receptor are determined by the different subunits constituting this receptor. Heterogeneity among α- subunits may determine the diversity of BDZ pharmacology in different regions of the nervous system.

This article describes the use of non-invasive magnetic resonance (MR) methods for the characterization and monitoring of the pathophysiology of experimental brain injury in laboratory animals as a function of time and treatment. The impact of MR in brain research is primarily due to its non-invasive nature, thereby enabling repeated measurements in long-term studies, and due to the type of information that it provides. MR imaging (MRI) enables the measurement of the morphology/anatomy as well as the functional status of tissues under in vivo conditions. Compared to other in vivo imaging modalities, MRI has a high spatial resolution and allows for a remarkable soft tissue differentiation. MR spectroscopy (MRS) provides information on the biochemical/metabolic status of tissues. MR methods which have proven valuable in animal studies, can be readily translated to the clinical situation where MR-based diagnosis and treatment planning play a rapidly increasing role.

After a short introduction into the principles of MR, we will illustrate the remarkable versatility of MR in research on brain injury from recent animal studies. Examples will be mainly drawn from experiments on early injury in focal cerebral ischemia and from research on mechanical brain trauma and excitotoxic lesions. The article ends with a brief description of the perspectives of MR in neuropsychiatry.

Severe schizophrenics as a group show subtle abnormalities of cerebral structure. Cerebral ventricular enlargement is the best replicated finding, and this tends to be associated with impairment of neuropsychological performance. The idea that these abnormalities have a neurodevelopmental origin gains indirect support from the, admittedly less consistent, evidence of abnormalities of cerebral asymmetry and of neuronal migration in adult schizophrenics, as well as from the behavioural, psychomotor, and cognitive impairments reported in preschizophrenic children. However, the relationship between childhood and adult neuropsychological and brain structural findings has not been proven, and we do not know whether only some schizophrenics have a developmental origin, or whether patients differ only in the degree of developmental impairment that they show.

In contrast to the research in panic disorder, not much neurobiological studies have been conducted in social phobia. In challenge-tests using lactate or pentagastrin general anxiety and anxiety symptoms were induced in social phobies, although not as frequent is in panic disorder patients, but no specific social phobic anxiety was induced. The role of neurotransmitters such as serotonin, dopamine and noradrenalin is, as yet, unclear. There are no indications for abnormal hypothalamic-pituitary-adrenal-axis activity or abnormal hypothalamic-pituitary-thyroid-axis activity in social phobia. To the present, preliminary findings in neuroimaging studies show no differences between patients and controls, except a possibly diminished and reversible metabolic activity.

Three principles of neuronal interaction within cortically distributed networks are discussed. PET-rCBF activation methods provide an opportunity to acquire insight in the distribution of functionally related areas of the human brain in vivo. The distinction of visual areas, activated by either motion or color within an observed scenery, points at a segregation in neuronal information processing. Such a segregation extends into both a dorsal and a ventral route towards consequently the parietal and temporal cortex.

Simultaneous activation over the dorsal and ventral route, which for example occurs in relation to the perception of complex motion (optic flow), or motion perception after lesion of V5, suggests integration by means of cross-connectivity. The third principle, i.e. “top-down” integration, appears by analysis of V5-V1 interaction, attentional effects on V4, frontal activation in prosopagnosia, and by analysis of hallucinations. Such “top-down” integration indicates the presence of momentaneous effect on cortical areas, intimately related to the primary sensory cortex, by neuronal activity of remote “association” cortex, the latter being connected by direct (synaps-restricted) bypass from early stations of information processing.

Aim: Translation of a specific instrument to measure psychomotor retardation, the “Widlöcher Retardation Rating Scale” and validation of this Dutch translation (Widlöcher remmingsschaal, WRS). Method: In three separate studies, we studied reliability (n = 26), concurrent and divergent validity (n = 25) and predictive validity (n = 28) of the WRS. In- and outpatients with a depressive disorder or schizophrenia participated, and scores on the WRS were compared with those on the Montgomery Asberg Depression Rating Scale (MADRS) and retardation items of the Comprehensive Psychopathological Rating Scale (CPRS).

Results: The internal consistency was good (Cronbach alpha = 0.86), interrater reliability was sufficient to good, the correlation between the sumscores of both raters was r = 0.84, n = 23, p <0.01 and the kappa's were between 0.23 and 0.80. Convergent and divergent validity showed in comparing the correlation between the sum scores on the WRS and the CPRS retardation items (r = 0.91, n = 25, p < 0.01 ) with the correlation between the sumscores on the WRS and the MADRS (r = 0.40, n = 25, p = 0.1). The decrease of the sum scores on the WRS after two weeks of treatment with antide-pressants predicted remission after six weeks. A subgroup of the patients who were not in remission after six weeks, showed a predominance of retardation signs over mood disturbances. The same clinical picture was seen in a group of patients with a chronic disorder.

Conclusion: De Widlöcher Retardation Rating Scale in this Dutch translation is a usefull instrument to measure psychomotor retardation. The connection between remaining retardation symptoms and longterm prognosis deserves further investigation.

An attempt is made to relate drug and non-drug antidepressive interventions to brain processes. In the present context two concepts are proposed: vulnerability towards depressogenic factors and depression as a state of the brain. Accordingly, it is assumed that the current antidepressants make the brain less vulnerable by inhibiting monoaminergic neurons and by reducing the number or efficacy of their postsynaptic receptors. In contrast, electroconvulsive therapie and sleep-deprivation affect primarily the state of the brain and can produce spectacular (but often short lasting) improvements. It is proposed that the combination of the two aspects may lead to fast and lasting antidepressive effects.

A considerable amount of patients with panic disorder (25 – 30%) is refractory for the first line of treatment, mostly antidepressants, and for psychotherapy. Augmentation and combination strategies are discussed; and a protocol for the treatment of refractory patients with panic disorder is proposed with consists of five steps.

No patients is considered treatment refractory until they have had a trial with monoamine oxidase inhibitors.

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.