Search

Objective: The aim of the present study was to ascertain the extent of impairment of position error and velocity error processing in eye tracking dysfunction in schizophrenic and depressive patients., Method: A total of 21 schizophrenic and 19 unipolar depressive patients and 21 healthy controls were subjected to an eye tracking test with electro-oculography using horizontal sinusoidal stimuli with frequencies of 0.2-0.7 Hz. Position error and velocity error were measured over a saccade-free range of 200 ms before catch-up saccades at 50 ms intervals., Results: For position error, the schizophrenia patients displayed increased values particularly compared to controls, more rarely compared to depressive patients, depending on the stimulus frequency used. The increase in stimulus frequency did not lead to an increase in position error in any group of subjects over a prolonged period. For velocity error, in contrast, the study groups differed only in a few, isolated pre-saccadic intervals. The increase in stimulus frequency, however, led to an increase in velocity error in the schizophrenia patients over the entire 200 ms interval. The depressive patients did not differ notably from the controls, neither in terms of position error nor velocity error., Conclusions: Eye tracking dysfunction in schizophrenia can be described as follows with regard to position error and velocity error: On the one hand, there is an increased position error tolerance largely independent of stimulus frequency, possibly due to an impairment of processing localization information. On the other hand, velocity processing is more severely impaired by an increase in stimulus frequency.

The high pathogenetic relevance of genetic factors in schizophrenia is beyond doubt based on the findings of epidemiological studies. By means of a complex mode of transmission, it is likely that several genes with weak to moderate effect jointly constitute a genetic basis for a vulnerability to schizophrenia that may well vary for different individuals. Other organic and psychosocial factors also play an individually different -- in some cases significant -- role in terms of pathogenesis, as a result of which an oligogenic/polygenic multifactor model is assumed from the standpoint of aetiopathogenetics. Molecular genetic methods consist in linkage analyses and association analyses. Positive linkage findings accumulate particularly for the chromosomes 1q, 6p, 8p, 13q and 22q. By themselves, individual mutations contribute little to the range of schizophrenic feature characteristics, it was not possible -- irrespective of some subtypes -- to replicate genes of major effect. From the large number of possible candidate genes, although studies on DRD3, DRD2 and HTR2A produced positive results, the magnitudes of effect were low. The findings for alleles of dysbindin, neuregulin 1, DAO, COMT, PRODH, ZDHHC and DISC are less clear. The search for schizophrenia-relevant mutations is hampered by the possibility of a heterogeneous phenotype of schizophrenia in case of a homogeneous genotype as much as by the possibility of inter-individually homogeneous phenotypical characteristics in case of schizophrenia-relevant heterotype in the genome. With the aid of the concept of endo-phenotypes, based on neurobiological phenomena, it might be possible to take a more direct approach that leads from relevant mutations to the risk of schizophrenias. However, replacing schizophrenic alienation with neurobiological aspects leads to difficulties in explaining these complex disorder profiles. Schizophrenic diseases require an explanatory approach that also incorporates personality and developmental psychological aspects from the outset, if the aim is not to restrict type of schizophrenic disease exclusively to loci of molecular genetic changes.

Panic disorder and epilepsy usually are distinct entities which require different and specific therapeutic strategies. While anticonvulsant medication is the treatment of choice for seizure disorders, behavioral methods have proven to be effective in panic disorder. We here report a case of comorbidity between panic disorder and photosensitive epilepsy. Special attention is given to the different symptomatic presentations of the disorders, because a thorough knowledge of both disorders may save unnecessary diagnostic procedures. Therefore, the necessity of taking a careful patient's history is underlined. Furthermore the different possible relationship between panic disorder and epilepsy are discussed., (Copyright 2000 S. Karger AG, Basel.)

Immunological examinations in schizophrenic patients have shown that there are many alterations in both arms of the immune system, i.e. cellular and humoral activities. The results are quite heterogeneous, as not even all schizophrenics show these pathological changes. Immunological findings are assumed to be etiopathogenetically related to the disease process or to be an epiphenomenon. The present study supposes that immunological alterations as they can be found during the course of schizophrenia may be an indicator for somatic vulnerability or an epiphenomenon. 60 male inpatients, fulfilling DSM-IV criteria of schizophrenia where examined during their acute phases of psychosis and during their phases of clinical improvement, by means of a serological profile including cellular and humoral parameters. The control group consisted of 42 healthy male volunteers. It was the aim of this study to find out if there were (a) overall differences in the immune profiles between patients and control group and (b) differences between different categories of schizophrenic disorder. During the acute phase nearly half of the schizophrenic patients showed pathologic immunological parameters, whereas none of the controls did. During the phase of clinical improvement the number of patients with normal immunological findings predominated. Furthermore there was a difference between the Paranoid and the Disorganized Subtype, the latter showing more immunological abnormalities. The results of this study give further support to the hypothesis that immunological aberrations should not be seen as closely etiopathogenetically related to schizophrenic disorders, but rather as an epiphenomenon (e.g. as a stress marker) and/or as indicators for somatic vulnerability.

The current pharmacotherapeutic approaches to alcohol dependence, together with the results of a number of clinical trials, are reviewed in this article. Despite the somewhat disappointing clinical results, pharmacotherapeutic interventions did lead to some small, but significant, improvements in alcohol abstinence rates.

36 elderly outpatients (mean age 68.6 years) with depression and increased blood urea level were treated with mianserin (60 mg every evening). All patients were ordered to drink additionally 11 of mineral water per day, which only 30 patients complied with. The patients who complied with the ordered increase in fluid intake (responder, n = 30) showed in comparison to those who did not comply (non-responder, n = 6) a significant improvement in depression (i.e., HAM-D, p < 0.001) after a four week period of treatment (t2). The responders' blood urea level normalized whereas the non-responders' level, although lowered, still remained in the pathological range.

30 right-handed male and female inpatients with Major Depression diagnosed with the Diagnostic and Statistical Manual of Mental Disorders, revised Third Edition, (DSM-III-R) were investigated with reference to the retarded motor activity of their dominant hand. The treatment included antidepressants, neuroleptics and tranquilizers. The tests (handedness test, HDT; a test showing evaluation for the degree of depression, TSD; a test for mood disturbance, EWL) were carried out at the onset of drug treatment (t1) and after improvement of the depression (t2). Both motor retardation and the scores of the depressivity-tests ameliorated significantly.