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H Beckmann

Publications and source records attributed to H Beckmann.

At least 73 records · Page 4Linked to original sources
PubMed1997

Specific P300 features in patients with cycloid psychosis.

In previous studies, low amplitudes and asymmetrical topography with right-sided peaks of the P300-evoked response have been repeatedly described in schizophrenic patients. A sample consisting of 18 patients with cycloid psychosis fulfilling the criteria of Perris and Brockington and 18 controls was investigated with a standard auditory odd-ball paradigm and multichannel evoked potential recordings. Patients had normal P300 topographies and latencies but significantly higher amplitudes than the controls. Higher than normal P300 amplitudes have not been described in any other psychiatric disorder until now, and indicate an enhanced level of arousal. Future studies are expected to shed light on the question of whether high P300 amplitudes are transitory sequelae of the acute psychotic episode or a trait of cycloid psychosis.

Adult↗
PubMed1997

First-trimester maternal gestational infection and cycloid psychosis.

Using a structured interview, the mothers of patients with cycloid psychosis, manic depression and controls (40 mothers in each case) were investigated in order to assess the occurrence of maternal gestational infection and other obstetric complications during pregnancy with the affected child. The cycloid psychoses with low heritability and a good long-term prognosis were found to be significantly associated with first-trimester respiratory infection (i.e. influenza and febrile cold). Furthermore, maternal infection seems to predict an early onset in cycloids. In manic depression, we failed to identify a significant link with maternal gestational infection or other obstetric complications. These findings are discussed in the light of our previous reports of an excess of maternal gestational infections during the second trimester in chronic schizophrenics. Our results suggest that the exogenously induced disturbances of fetal brain maturation during the first trimester of gestation caused by maternal respiratory infection via live virus or disturbed maternal immune response are involved in the aetiology of cycloid psychoses.

Adult↗
PubMed1997

Parkinson's disease and depression: evidence for an alteration of the basal limbic system detected by transcranial sonography.

OBJECTIVES: Depression is a frequent symptom in Parkinson's disease. Compelling evidence suggests a role of the brainstem in the control of mood and cognition. In patients with unipolar depression transcranial sonography (TS) studies have shown structural alteration of the mesencephalic brainstem raphe which could suggest an involvement of the basal limbic system in the pathogenesis of primary mood disorders. The objective of the present study was to evaluate whether a similar alteration could be found in depressed patients with Parkinson's disease using TS. METHODS: Thirty patients with Parkinson's disease and 30 age and sex adjusted controls were examined by TS. Raphe echogenicity was rated semiquantitatively. The severity of motor symptoms and depression was rated using standard research instruments. RESULTS: Raphe echogenicity was significantly reduced in depressed patients with Parkinson's disease compared with nondepressed patients with Parkinson's disease and control subjects. Raphe echogenicity correlated negatively with degree of motor impairment, and differences in raphe echo between depressed and non-depressed patients with Parkinson's disease were upheld when motor impairment was controlled for. CONCLUSION: These preliminary findings suggest that, as in unipolar depression, a morphological alteration of the brainstem raphe might be involved in the pathogenesis of depression in Parkinson's disease. This raphe alteration may reflect involvement in the basal limbic system in the pathogenesis of secondary depression. This concept is in line with current knowledge on the pathogenesis of both depression in Parkinson's disease and primary depressive disorders.

Aged↗
PubMed1996

Is computerized tomography ventricular abnormality related to cycloid psychosis?

Twenty-eight psychiatric patients with computerized tomography (CT) findings of ventricular abnormality most likely to result from prenatal/perinatal lesions (VA group) were compared to 28 sex- and age-matched psychiatric patients with normal neuroradiological findings (NCT group). The neuroradiological rater was blind to clinical psychiatric diagnoses and, vice versa, clinical diagnoses were established without knowledge of neuroradiological findings. A polydiagnostic approach (DSM-III-R, ICD-10, Leonhard Classification) was used for psychiatric diagnostic workup. Significantly more patients with cycloid psychoses (according to Leonhard's original description) were found in VA as compared to NCT patients. According to DSM-III-R and ICD-10, VA and NCT groups did not differ significantly regarding diagnostic distribution. Ventricular abnormalities that may reflect sequels of birth complications and/or adverse events during pregnancy may constitute one of the risk factors for developing cycloid psychosis as originally described by Leonhard.

Adult↗
PubMed1996

Systematic search for variation in the human norepinephrine transporter gene: identification of five naturally occurring missense mutations and study of association with major psychiatric disorders.

The complete coding region of the norepinephrine transporter (NET) gene was systematically screened for genetic variants in 137 unrelated individuals (including 46 probands with bipolar affective disorder and 45 schizophrenic probands, as well as 46 blood donors) using single-strand conformation analysis. We identified 13 DNA sequence variants, among them five missense substitutions. The missense substitutions Val69Ile, Thr99Ile, Val245Ile, Val449Ile, and Gly478Ser are located at putative transmembrane domains (TMD) 1, 2, 4, 9, and 10, respectively. The Thr99Ile substitution is at the 5th position of the putative leucine-zipper in TMD2. In a case-control study distribution of missense substitutions was found to be similar in 103 patients with bipolar affective disorder, in 228 schizophrenia patients and in 187 controls, indicating that presence of these variants is not causally related to major psychiatric diseases. The detection of a highly polymorphic silent 1287G/A polymorphism was utilized to demonstrate biallelic expression of the NET in adult human brain.

Adult↗
PubMed1996

Confirmation of reduced temporal limbic structure volume on magnetic resonance imaging in male patients with schizophrenia.

A structural deficit in the temporal lobes has been implicated in the pathogenesis of schizophrenia. A prospective magnetic resonance imaging (MRI) study was carried out in 20 young male patients with schizophrenia and 20 age-matched healthy male volunteers. Volumetric measurements were performed in all slices with temporal lobe cross-sections from the temporal pole to the tip of the Sylvian fissure. Volumetric assessment included the temporal lobe as a whole, hippocampal formation and amygdala complex, temporal horn and cella media of the lateral ventricle, the third ventricle, and hemispheric volume in all slices that showed temporolimbic structures. Brain structural deficit in the patients was most conspicuous in the posterior portion of the hippocampal formation. Significant effects of diagnosis were also found for the total temporal lobe and the third ventricle. Multiple regression analysis revealed posterior hippocampal volume to be significantly determined by diagnosis, but not by age or by temporal lobe or hemispheric volume. Significant correlations of morphologic and clinical parameters were restricted to negative correlations of temporal lobe volume with the global rating and sum score of the Scale for the Assessment of Negative Symptoms. The study confirms subtle temporolimbic deficit reported in previous MRI studies in patients with schizophrenia.

Adult↗
PubMed1996

Genetic heterogeneity in catatonic schizophrenia: a family study.

In family study concentrating on 139 probands with chronic DSM-III-R schizophrenia, catatonic type, 83 probands (41 women, 42 men) met the criteria for periodic catatonia and 56 probands (14 women, 42 men) for systematic catatonia according to the Leonhard classification. The reliability and stability of this subclassification were tested by 2 experienced psychiatrists working independently of each other. Both diagnosticians were kept blind as to the probands' family history. The 139 probands had a total of 543 first-degree relatives. Only those hospitalized for schizophrenia were allocated to the group of afflicted family members. Diagnostic reliability was kappa statistic 0.93 and diagnostic stability during catamnesis reached 97% and kappa of 0.93. Life-table analyses revealed that the age-corrected risks were significantly different in periodic and systematic catatonia. In systematic catatonia mothers had a risk of 6.8%, fathers 2%, and randomly selected sibs 3%. IN periodic catatonia an excess of homologous psychoses was apparent: There was a risk of 33.7% for mothers, 15.4% for fathers, and 24.4% for sibs. The quota of afflicted parents (33 of 161) was higher than that of sibs (26 of 162). In periodic catatonia, 59% of the families were multiple afflicted with pronounced unilineal vertical transmission. In 10% of the families 3 successive generations suffered from the disease and were treated in hospital. The results of the study led to the following hypotheses: Periodic and systematic catatonia are valid subgroups of DSM-III-R schizophrenia. In systematic catatonia heritability is very low. Periodic catatonia is a familial disorder. Homogeneity of familial psychoses and unilineal vertical transmission with anticipation are consistent with a major gene effect. Periodic catatonia seems to be a promising candidate for molecular genetic evaluation.

Adult↗
PubMed1996

A null mutation allele in the CNTF gene and schizophrenic psychoses.

The maldevelopmental theory postulates disturbances in neural development as crucial factors in the aetiopathogenesis of schizophrenia. Neurotrophic factors, including ciliary neurotrophic factor (CNTF), play a central role in the regulation of such development. A mutation has been described for the CNTF gene, whereby subjects homozygous for the mutation lack CNTF. The polymerase chain reaction was used to amplify the CNTF gene region containing this mutation in whole blood genomic DNA. The mutation was detected by analysis of restriction fragment length polymorphisms. Patients suffering from schizophrenic psychosis (ICD-10 criteria) (51 from Würzburg, 83 from Barcelona), and healthy controls (62 from Würzburg, 50 from Barcelona) were investigated. In the Würzburg group, the frequency of subjects homozygous or heterozygous for the mutation was significantly higher among schizophrenic patients than in controls. However, no difference could be detected in the Spanish sample; the possible reasons for the different allele distribution in the two patient groups is discussed. It is concluded that the CNTF null mutation may be relevant to the aetiopathogenesis of schizophrenia in some patients, but further work is required to identify specifically the patient group for which it is important.

Adult↗
PubMed1996

Association between a null mutation in the human ciliary neurotrophic factor (CNTF) gene and increased incidence of psychiatric diseases?

We report a possible association between a null mutation in the human ciliary neurotrophic factor (CNTF) gene and psychiatric diseases. Prior findings that the mutant allele frequency is not significantly elevated in patients suffering from neurological diseases are confirmed. The frequency of the mutant allele was higher among psychiatric patients (0.192, n = 297) than among healthy controls and neurological patients (0.142, n = 267). This difference (one-tailed 2 x 2 chi-square test, P < 0.05) might be evidence that disturbances in the neurotrophic factor system could play a crucial role in the etiopathogenesis of psychiatric disorders, mainly psychoses.

Adult↗
PubMed1996

[Manneristic catatonia. A psychotropic drug refractory chronic progressive course].

Manneristic catatonia, one form of Leonhard's systematic schizophrenias, is illustrated in nine case notes. The essential syndrome of this rare disorder (described by Leonhard in the preneuroleptic era) consisted in mannerisms and progressive stiffness of psychomotor activity. Mannerisms often developed from obsessive and compulsive ideas; whereas distress disappeared, repetitive behavior developed into a stereotype. Complex movements (e.g. not to shake hands; mutism) became mannerisms. With disease progression stiffness of facial expression and gestures and an impairment of voluntary motor activity became increasingly prominent. There were no signs of (neuroleptic-induced) parkinsonism. Manneristic catatonia affects preponderantly men and exhibits an early age of onset (median: 23 years). In none of the cases a family history of psychiatric illness was noted. Severe obstetric and birth complications as well as the high prevalence of supratentorial and cerebellar CT/MR abnormalities in this patient group point to deviations of prenatal brain maturation. The median yearly dose of neuroleptics was 83.1 g chlorpromazin equivalents. The characteristic psychopathology was not essentially influenced by modern psychopharmacological treatment neither in the beginning nor in the long run irrespective of the time of onset of the disease. Continuous high-dose neuroleptic treatment is not efficacious in this distinct group of systematic schizophrenias. Behavioural training in a rehabilitation unit is the treatment of choice from the early beginning.

Adolescent↗
PubMed1996

Specific P300 features in patients with cycloid psychosis.

In previous studies, low amplitudes and asymmetrical topography with right-sided peaks of the P300-evoked response have been repeatedly described in schizophrenic patients. A total of 18 patients with cycloid psychosis fulfilling the criteria of Perris and Brockington and 18 controls were investigated with a standard auditory odd-ball paradigm and multichannel-evoked potential recordings. Patients had normal P300 topographies and latencies but significantly higher amplitudes than controls. Higher than normal P300 amplitudes have not been described in any other psychiatric disorder until now, and indicate an enhanced level of arousal. Future studies are expected to shed light on the question of whether high P300 amplitudes are transitory sequelae of the acute psychotic episode or a trait of cycloid psychosis.

Adult↗
PubMed1996

Gene-environment interaction in schizophrenia: season-of-birth effect reveals etiologically different subgroups.

Compared to the general population, one consistent finding in schizophrenia research is a significant surplus of schizophrenic births in the winter/spring months. There is little evidence that this is attributed to statistical artefacts. The "harmful effects' hypothesis offers the most plausible explanation for this phenomenon. Exogenous harmful effects, predominant during the cold season, may affect the developing immature fetal brain and thus constitute some of the factors predisposing to schizophrenic breakdown in adulthood. Neuropathological and epidemiological studies point to the second trimenon of gestation as the crucial period of fetal brain maturation. Recently, some studies found that the surplus in schizophrenic winter/spring births is mainly due to sporadic forms. In contrast, patients with high genetic risk of the disease even tended to have a birth deficit during this period. This suggests that schizophrenia is not a disease entity but consists of etiologically distinct subgroups on which the influence of genes and/or environment has to be weighted differently. On the one hand, in sporadic forms of the disease exogenous noxious agents may be of major etiological importance. On the other hand, in fetuses at high genetic risk neurodevelopment may already be disturbed due to a genetic defect and additional environmentally noxious agents can cause abortions, stillbirths and sudden infant deaths.

Embryonic and Fetal Development↗
PubMed1996

[Genetic heterogeneity of schizophrenia. Results of a systematic twin study].

One reason for the inconsistent findings in schizophrenia research is the lack of diagnostic conformity. In the face of modern operational "atheoretical" diagnostic systems, this dilemma is still present. In order to examine specificity and validity of diagnoses, we carried out a systematic twin study with index twins suffering from schizophrenic spectrum psychoses. We compared the diagnostic systems of DSM-III-R, which is based on consensus of international experts, with Leonhards' nosology developed on sophisticated clinical observation and description of psychopathological phenomena occurring during the long-term course of psychiatric diseases. We examined twin concordance, family history, and the frequency and severity of complications of pregnancy and child-birth. The results suggest that the schizophrenic spectrum has to be divided into clinically and etiologically heterogeneous subgroups. This was much more striking when Leonhard's diagnostic criteria were used than with DSM-III-R diagnostic criteria. There seem to be three valid and etiologically different groups: cycloid psychoses, unsystematic schizophrenias and systematic schizophrenias as proposed by Leonhard. In cycloid psychoses genetic loading seems to be low (proband concordance MZ 38%, DZ 29%), but pregnancy and birth complications may have an important role in the etiology. On the other hand, unsystematic schizophrenias are obviously predominantly inherited (proband concordance MZ 88%, DZ 17%) and "environmental" factors are not very prominent. It is striking that MZ twins with a diagnosis of systematic schizophrenia have not yet been found, whereas 32% of DZ index twins (6 out of 19) were diagnosed as having systematic schizophrenia. Further, all DZ twins with the diagnosis of systematic schizophrenia were discordant and the affected twins had threetimes as many and as severe pregnancy and birth complications in the history than their healthy co-twins.

Adult↗
PubMed1995

Coactivator and promoter-selective properties of RNA polymerase I TAFs.

Human ribosomal RNA synthesis by RNA polymerase I requires the activator UBF and the promoter selectivity factor SL1, which consists of the TATA binding protein (TBP) and three associated subunits, TAFI110, TAFI63, and TAFI48. Here it is shown that both TAFI110 and TAFI63 contact the promoter, whereas TAFI48 serves as a target for interaction with UBF and is required to form a transcriptionally active SL1 complex responsive to UBF in vitro. TAFI48 also alters the ability of TBP to interact with TATA box elements, and the resulting complex fails to support transcription by RNA polymerase II. Thus, TAFI48 may function both as a target to mediate UBF activation and as a class-specific promoter selectivity factor.

DNA-Binding Proteins↗