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Biomedical subjects

A Hausmann

Publications and source records attributed to A Hausmann.

18 recordsLinked to original sources
PubMed2006

Post-traumatic stress disorder and amygdala-hippocampectomy.

OBJECTIVE: The case report suggests the indispensability of preoperative accurate psychiatric checkups especially in temporal resections. METHOD: A single case was reported. RESULTS: We report the case of a 20-year-old woman suffering for 12 years from primary generalized epilepsy, attributed to left-sided hippocampal sclerosis. Because seizures were resistant to drug therapy, she underwent amygdala-hippocampectomy at the age of 18. Furthermore, she had previously been victim of childhood sexual abuse. Two weeks after epilepsy surgery, she manifested symptoms of post-traumatic stress disorder (PTSD). CONCLUSION: There is evidence that the amygdala-hippocampal region is both functionally and morphologically involved in the aetiology of PTSD. The removal of this marked neuroanatomical region and the resulting disconnection and asymmetry between right and left amygdala-hippocampal region might be seen as an evidence for this region aetiologically being involved in the patient's PTSD symptoms.

Adult↗
PubMed2004

ECT response after relapse during continuation repetitive transcranial magnetic stimulation. A case report.

Research on repetitive transcranial magnetic stimulation (rTMS) indicates that the treatment of non-psychotic depression is comparable to electroconvulsive therapy (ECT) in terms of short-term outcome. We report on a woman who exerted a recurrent moderate major depressive episode, 6 months after discontinuation of maintenance ECT. She responded to acute rTMS treatment which was followed by the rTMS maintenance-protocol. Within 2 months of continuation rTMS she relapsed suffering from a severe non psychotic depressive episode and had to be switched to a successful ECT. In this patient rTMS had a good clinical impact as an acute treatment strategy, but failed to prevent relapse as the continuation ECT previously did in the same patient.

Depressive Disorder↗
PubMed2004

No benefit derived from repetitive transcranial magnetic stimulation in depression: a prospective, single centre, randomised, double blind, sham controlled "add on" trial.

Repetitive transcranial magnetic stimulation (rTMS) has been reported to demonstrate slight effects in the treatment of depression. Hence, a novel bilateral versus unilateral and sham stimulation design was applied to further assess rTMS' antidepressant effects. Forty one medication free patients with major depression, admitted to a psychiatric unit specialising in affective disorders, were consecutively randomised into 3 groups. Group A1 (n = 12) received unilateral active stimulation consisting of high frequency (hf) rTMS over the left dorsolateral prefrontal cortex (LDLPC) and subsequent sham low frequency (lf) rTMS over the right dorsolateral prefrontal cortex (RDLPC). Group A2 (n = 13) received simultaneous bilateral active stimulation consisting of hf-rTMS over the LDLPC and lf-rTMS over the RDLPC. Group C (n = 13) received bilateral sham stimulation. Stimulation was performed on 10 consecutive workdays. All patients received antidepressant medication on the first day of stimulation, which was continued during and after the stimulation period. As no significant difference in antidepressant outcome between group A1 and A2 was found, the two groups were pooled. The time course of the outcome variables Hamilton depression rating scale (HDRS(21)) and Beck depression inventory (days 0, 7, 14, 28) by repeated measures analysis of variance revealed no significant group differences (in terms of a group by time interaction), whereas there was a significant effect of time on all three outcome variables in all groups. The results suggest that rTMS as an "add on" strategy, applied in a unilateral and a bilateral stimulation paradigm, does not exert an additional antidepressant effect.

Major Depressive Disorder↗
PubMed2003

Family study of the aggregation of eating disorders and mood disorders.

BACKGROUND: Family studies have suggested that eating disorders and mood disorders may coaggregate in families. To study further this question, data from a family interview study of probands with and without major depressive disorder was examined. METHOD: A bivariate proband predictive logistic regression model was applied to data from a family interview study, conducted in Innsbruck, Austria, of probands with (N = 64) and without (N = 58) major depressive disorder, together with 330 of their first-degree relatives. RESULTS: The estimated odds ratio (OR) for the familial aggregation of eating disorders (anorexia nervosa, bulimia nervosa and binge-eating disorder) was 7.0 (95 % CI 1.4, 28; P = 0.006); the OR for the familial aggregation of mood disorders (major depression and bipolar disorder) was 2.2 (0.92, 5.4; P = 0.076); and for the familial coaggregation of eating disorders with mood disorders the OR was 2.2 (1.1, 4.6; P = 0.035). CONCLUSIONS: The familial coaggregation of eating disorders with mood disorders was significant and of the same magnitude as the aggregation of mood disorders alone--suggesting that eating disorders and mood disorders have common familial causal factors.

Adult↗
PubMed2002

Differential diagnosis of depressed mood in patients with schizophrenia: a diagnostic algorithm based on a review.

OBJECTIVE: To review the available literature on depressive symptomatology in schizophrenia in order to establish a diagnostic algorithm of depressive syndromes in schizophrenia. METHOD: A literature search was performed using PubMed and Medline. Additional information was gained by cross-referencing from papers found in the database. Data from controlled studies as well as supplementary information from review articles and psychiatric manuals pertinent to the topic were used. Depressive symptoms were classified with respect to their temporal relationship to acute psychotic symptoms before the background of nosological entities as operationalized by Diagnostic Statistical Manual IV (DSM IV). RESULTS: Depression is a common and devastating comorbid syndrome in patients suffering from schizophrenic disorder. The paper summarizes the relevant diagnostic steps to guide the clinician towards therapeutic interventions, which differ depending on the nature of the depressive syndrome. CONCLUSION: Differentiating depressives states in schizophrenia has consequences in terms of choosing therapeutic strategies. An algorithm which leads the practitioner to a reliable diagnosis and in consequence to a valid therapy is presented.

Algorithms↗
PubMed2002

Immunoregulation during disease progression in prediabetic NOD mice: inverse expression of arginase and prostaglandin H synthase 2 vs. interleukin-15.

Non-obese diabetic (NOD) mice spontaneously develop insulin dependent diabetes due to autoimmune destruction of beta-cells. The progression of insulitis can be accelerated and synchronized in the pancreas by a single injection of 250 mg/kg cyclophosphamide. In this study, we will report on three immune mediators that were not known to be expressed during insulitis until now. Early insulitis in ten-week-old female NOD mice was associated with strong expression of prostaglandin H synthase 2 in the pancreas and of arginase, an antagonist enzyme of the inducible NO synthase. After acceleration of insulitis progression by cyclophosphamide, expression of the two enzymes was downregulated within 24 h. There was strong concomitant upregulation of IL-15 gene expression that preceded lymphocyte invasion of islets and a rise of IFN-gamma mRNA levels by several days. The comparison of individual pancreata showed that the expression of IL-12 and IL-18 mRNA closely correlated with levels of IL-15 gene expression. We conclude that arginase and prostaglandin H synthase 2 expression is associated with peri-insulitis, while IL-15 is a candidate cytokine in driving destructive insulitis, as it elicits Th1-cytotoxic responses in lymphoid as well as in non-lymphoid immune cells and is unusually resistant to downregulation by antagonistic cytokines. This is the first report on arginase, prostaglandin H synthase 2 and IL-15 expression in pancreatic lesions of prediabetic NOD mice.

Animals↗
PubMed2001

Magnetic stimulation induces neuronal c-fos via tetrodotoxin-sensitive sodium channels in organotypic cortex brain slices of the rat.

Repetitive transcranial magnetic stimulation is a novel non-invasive method with antidepressant properties, where electromagnetic fields are applied via an electrode. The aim of the present study was to investigate in an in vitro model if magnetic stimulation may activate the transcription factor c-fos. Organotypic brain slices of the parietal cortex were cultured for 2 weeks and then treated with a magnetic stimulator. Immunohistochemistry was used to detect c-fos like immunoreactivity. We show that magnetic stimulation (1 Hz, 10 min, 75% machine output/magstim 200 rapid stimulator) transiently enhanced c-fos 3-6 h after stimulation. Co-localization experiments revealed that c-fos was expressed in neurons but not astroglia. The activation of c-fos by magnetic stimulation was inhibited by the sodium-channel blocker tetrodotoxin (TTX) (10 microM). It is concluded that magnetic stimulation induces neuronal c-fos via TTX-sensitive sodium channels in organotypic cortex slices.

Animals↗
PubMed2000

Chronic repetitive transcranial magnetic stimulation enhances c-fos in the parietal cortex and hippocampus.

Repetitive transcranial magnetic stimulation (rTMS) is a novel non-invasive method with anti-depressant properties. However, the mechanism of activation on the cellular level is unknown. Twelve hours after the last chronic rTMS treatment (14 days, once per day, 20 Hz, 10 s, 75% machine output, the transcription factor c-fos was markedly increased in neurons in layers I-IV and VI of the parietal cortex and in few scattered neurons in the hippocampus of Sprague-Dawley rats. The cortical activation was not blocked by the NMDA antagonist MK-801. The increase of c-fos was not paralleled by an increased glial response and activation of cortical growth factors. Thus, it is concluded that chronic rTMS differentially activates parietal cortical layers and this might be involved in mediating anti-depressant activity in other brain areas.

Animals↗
PubMed2000

A single five-step desaturase is involved in the carotenoid biosynthesis pathway to beta-carotene and torulene in Neurospora crassa.

Phytoene desaturase Al-1 from Neurospora crassa was expressed in Escherichia coli and an active enzyme was isolated which catalyzed the stepwise introduction of up to five double bonds into the substrate phytoene. The major reaction products were 3, 4-didehydrolycopene and lycopene. Several of the desaturation intermediates, zeta-carotene, neurosporene, and lycopene, were also accepted as a substrate by Al-1. In contrast to the structurally related bacterial enzymes, the cofactor involved in the dehydrogenation reaction was NAD for Al-1. In situ competition with a neurosporene- and lycopene-converting hydratase and cyclase indicated that these enzymes can divert intermediates of the desaturation sequence. Based on the in vitro and in vivo results, the organization of the phytoene desaturase from N. crassa was proposed as an assembly of identical protein units which are responsible for the multistep reaction. However, the spatial arrangement should be loose enough to allow an exchange of individual intermediates in both directions in and out of this complex. Since gamma-carotene is not accepted as a substrate by Al-1, the formation of torulene must proceed exclusively by the cyclization of 3,4-didehydrolycopene.

Carotenoids↗
PubMed2000

The implications of intergenic polymorphism for major histocompatibility complex evolution.

A systematic survey of six intergenic regions flanking the human HLA-B locus in eight haplotypes reveals the regions to be up to 20 times more polymorphic than the reported average degree of human neutral polymorphism. Furthermore, the extent of polymorphism is directly related to the proximity to the HLA-B locus. Apparently linkage to HLA-B locus alleles, which are under balancing selection, maintains the neutral polymorphism of adjacent regions. For these linked polymorphisms to persist, recombination in the 200-kb interval from HLA-B to TNF must occur at a low frequency. The high degree of polymorphism found distal to HLA-B suggests that recombination is uncommon on both sides of the HLA-B locus. The least-squares estimate is 0.15% per megabase with an estimated range from 0.02 to 0.54%. These findings place strong restrictions on possible recombinational mechanisms for the generation of diversity at the HLA-B.

Animals↗
PubMed2000

Transcranial magnetic stimulation induces 'pseudoabsence seizure'.

OBJECTIVE: Several studies support the hypothesis of an antidepressive or mood-enhancing effect of repetitive transcranial magnetic stimulation (rTMS) on depressive patients. The most acute concern regarding rTMS is possible seizure induction; therefore, reports on seizure during rTMS are of special significance. METHOD: We describe a case in which high frequency rTMS over the left dorsolatero-prefrontal cortex (DLPC) applied as an add-on antidepressive strategy may have induced a frontal lobe complex partial seizure in a female patient affected by drug-resistant depression. RESULTS: The epileptic seizure was self-limited, and the patient did not report any physical sequelae. The psychopathological improvement, observed immediately after the incident in question, did not last. CONCLUSION: In this case train duration in rTMS, combined with drugs modulating the norepinephrine turnover, may have contributed to the occurrence of this complex partial seizure, which neuroanatomically seems to be localized in the DLPC.

Adult↗
PubMed1999

IL-18 inhibits diabetes development in nonobese diabetic mice by counterregulation of Th1-dependent destructive insulitis.

The development of type 1 diabetes in animal models is T cell and macrophage dependent. Islet inflammation begins as peripheral benign Th2 type insulitis and progresses to destructive Th1 type insulitis, which is driven by the innate immune system via secretion of IL-12 and IL-18. We now report that daily application of IL-18 to diabetes-prone female nonobese diabetic mice, starting at 10 wk of age, suppresses diabetes development (p < 0.001, 65% in sham-treated animals vs 33% in IL-18-treated animals by 140 days of age). In IL-18-treated animals, we detected significantly lower intraislet infiltration (p < 0.05) and concomitantly an impaired progression from Th2 insulitis to Th1-dependent insulitis, as evidenced from IFN-gamma and IL-10 mRNA levels in tissue. The deficient progression was probably due to lesser mRNA expression of the Th1 driving cytokines IL-12 and IL-18 by the innate immune system (p < 0.05). Furthermore, the mRNA expression of inducible NO synthase, a marker of destructive insulitis, was also not up-regulated in the IL-18-treated group. IL-18 did not exert its effect at the levels of islet cells. Cultivation of islets with IL-18 affected NO production or mitochondrial activity and did not protect from the toxicity mediated by IL-1beta, TNF-alpha, and IFN-gamma. In conclusion, we show for the first time that administration of IL-18, a mediator of the innate immune system, suppresses autoimmune diabetes in nonobese diabetic mice by targeting the Th1/Th2 balance of inflammatory immune reactivity in the pancreas.

Animals↗
PubMed1998

Hippocampal volume reduction in male schizophrenic patients.

Using magnetic resonance imaging of the brain, we examined volumetric measurements of total brain, hemispheres, lateral ventricles and the hippocampus/amygdala complex in male subjects (41 first-episode schizophrenics, 30 chronic schizophrenic patients and 32 healthy controls). We found significantly smaller total brain size in the chronic schizophrenic group, significantly larger lateral ventricles in both patient groups and hippocampal volume reduction bilaterally in first-episode patients (-13.2% left, -12.05% right) and chronic patients (-10.6% left, -10.5% right) compared to controls--irrespective of diagnostic subtype, family history for psychiatric diseases, psychopathology, duration of illness or age at onset.

Adult↗
PubMedDate not supplied

Body image and psychopathology in male bodybuilders.

BACKGROUND: To compare male bodybuilders to men with eating disorders and control men regarding body image, psychopathology and sexual history. METHOD: We compared 28 male bodybuilders, 30 men with eating disorders (anorexia nervosa, bulimia or binge eating disorder defined by DSM-IV), and 30 controls, using a battery of questionnaires covering weight history, eating behavior, body image, lifetime history of psychiatric disorders, and sexuality. Eating-disordered and control men were recruited from a college student population and studied during the course of an earlier investigation. RESULTS: Bodybuilders exhibited a pattern of eating and exercising as obsessive as that of subjects with eating disorders, but with a 'reverse' focus of gaining muscle as opposed to losing fat. Bodybuilders displayed rates of psychiatric disorders intermediate between men with eating disorders and control men. In measures of body image, the bodybuilders closely resembled the men with eating disorders, but significantly differed from the control men, with the former two groups consistently displaying greater dissatisfaction than the latter. Sexual functioning did not distinguish the three groups except for the item 'lack of sexual desire' which was reported significantly more often by both bodybuilders and men with eating disorders. CONCLUSION: On measures of body image and eating behavior, bodybuilders share many features of individuals with eating disorders.

Adult↗