PubMed Health⌕ Search

Biomedical subjects

G Hamann

Publications and source records attributed to G Hamann.

At least 19 recordsLinked to original sources
PubMed2003

Neurological and neuropsychological examination and outcome after use of an intra-aortic filter device during cardiac surgery.

Cerebral embolization of particles after cardiac surgery is frequently associated with neurological deficits. Aortic crossclamp manipulation seems to be the most significant cause of emboli release during cardiac surgery. The goal of this study was to demonstrate whether the use of an intra-aortic filter device has an effect on the magnet resonance imaging (MRI) and functional neurological outcome. Twenty-four patients undergoing cardiosurgical procedures using cardiopulmonary bypass (CPB) were selected: coronary artery bypass graft (CABG) surgery (n = 17), aortic valve replacement (AVR) surgery (n = 4) or combined procedures (n = 3). Patients were evaluated by diffusion weighted MRI of the brain, neurological examination and neuropsychological assessment regarding alertness as well as divided and selective attention before and five to seven days after surgery. The patients were divided into two groups. In group I, 12 patients received a filter through a modified 24 F arterial cannula immediately before the aortic crossclamp was released. Filters remained in the aorta until CPB was discontinued. Intraoperatively, bilateral middle cerebral artery transcranial Doppler (TCD) was monitored at baseline, at the beginning of CPB, at a timepoint when the aorta was crossclamped, when the filter was inserted and while the crossclamp was switched to partial clamping until the CPB was discontinued. TCD was used for detection of microembolic signals (MES). The captured material in the filter was examined histologically. Twelve patients served as controls without aortic filtration (group II). The MRI of the brain did not show any diffusion alterations in either group before or after surgery. No patient developed a focal neurological deficit or stroke. Intraoperative quantitative MES detection revealed a four to tenfold increase in patients of group I compared with group II (5-6 versus 0.5-1 MES/min) during the filter dwell time. There was no consistent pattern regarding the neurobehavioural sequelae. Filters showed arteriosclerotic debris in 75% of the patients. The use of the intra-aortic filter device did not show a positive effect on neurological, neuroradiographical and neuropsychological outcomes. The increase of the MES rate in group I patients may be due to microbubbles generated as microcavitations by the filter or the aortic filter cannula. The intra-aortic filter was able to capture atheromatous material in 75% of the patients.

Aorta, Thoracic↗
PubMed2002

RXR acts as a coregulator in the regulation of genes of the hypothalamo-pituitary axis by thyroid hormone receptors.

Thyroid hormone receptors (TRs) often modulate transcriptional activity of target genes by heterodimerization with the 9-cis retinoic acid receptor (RXR). On positive thyroid response elements (TREs), RXR favors binding of the TR-RXR complex to DNA and stimulates transcription. RXR action on negative TREs is unclear. Furthermore, the single half-site configuration of many negative TREs does not favor the binding of a classic TR-RXR heterodimer. In a comparative study using CV-1 cells (relatively RXR- and TR-deficient) and JEG-3 cells (relatively TR-deficient), we demonstrate the importance of RXR in the negative transcriptional regulation of genes of the hypothalamo-pituitary axis by tri-iodothyronine. While RXR has variable effects on ligand-independent activation produced by TRs, it was required for efficient ligand-dependent repression of the TRH gene for TRalpha1 and TRbeta1 and of the TSH genes by all TRs. Using different RXR constructs we also observed the importance of the C-terminus of RXR but not of the N-terminus nor the DNA-binding domain, in the potentiation of negative regulation. We thus suggest that, with regard to negative regulation of the TRH and TSH genes by thyroid hormones, RXR behaves more like a cofactor than a classic heterodimerization partner.

Animals↗
PubMed2001

In vitro effect of Triac on resistance to thyroid hormone receptor mutants: potential basis for therapy.

Resistance to thyroid hormone (RTH) is a syndrome caused by a mutation in the carboxyl-terminal domain of the thyroid hormone receptor beta (TRbeta) gene. 3,5,3'-triiodothyroacetic acid (Triac) has been used on an empirical basis to treat RTH but its efficacy is still controversial. In previous studies, we demonstrated that Triac has TR isoform- and TRE-specific effects. In this report, we used five natural RTH mutations of the ligand-binding domain in both TRbeta1 and TRbeta2 isoforms for the evaluation of the effect of T3 and Triac on regulation of transcription and binding affinity. We show that Triac has superior activity on negatively and positively regulated promoters and higher binding affinity than T3 for a majority of TRbeta1 and TRbeta2 mutants. However, the difference of transcriptional activity and binding affinity between both ligands is less for RTH mutants than for wild type receptors. These results suggest that Triac could be a potential treatment for RTH patients.

Dose-Response Relationship, Drug↗
PubMed2001

Transcranial color-coded sonography of a vein of Galen arteriovenous malformation in an adult.

The case of an adult harboring a vein of Galen arteriovenous malformation (VGAM) is reported. Diagnosis was established by computed tomography (CT) and digital subtraction angiography and confirmed afterwards by transcranial color-coded sonography (TCCS). The patient's course after endovascular treatment was then consecutively monitored by TCCS until complete occlusion was achieved. The results of TCCS were validated by angiography, with which they showed good correlation. Thus, it can be concluded that TCCS may be a useful adjunct to CT and angiography to noninvasively monitor adults with VGAM.

Adult↗
PubMed1999

Heparin-mediated extracorporeal LDL/fibrinogen precipitation--H.E.L.P.--in coronary and cerebral ischemia.

Cerebral and myocardial infarctions share common aspects of pathobiochemistry. The central problem is the oxygen supply of the infarcted region. To maintain this supply, H.E.L.P.-apheresis (Heparin-mediated Extracorporeal LDL/Fibrinogen Precipitation) has already proven beneficial in the prevention and therapy of myocardial infarction. Since H.E.L.P.-apheresis can lower significantly plasma viscosity and erythrocyte aggregation without reducing the oxygen transport capacity, patients with cerebral infarction (stroke) may also benefit from our experiences in myocardial ischemia. The system is designed to remove selectively plasma fibrinogen, LDL-cholesterol and lipoprotein(a) from blood circulation, simultaneously. The removal of the plasma compounds is achieved by extracorporeal precipitation with heparin at low pH. Excess heparin is completely removed by an adsorber before the plasma is given back to the patient. H.E.L.P.-apheresis has proved to be safe in patients with coronary heart disease and allows a controlled reduction of thrombogenic plasma compounds. It is therefore hoped to be effective also in patients with acute ischemic stroke.

Blood Component Removal↗
PubMed1999

[Cerebral ischemia as initial manifestation of neoplastic low-malignancy changes. 2 case reports and review of the literatures].

Thrombembolic events as paraneoplastic complications in malignant disease account for severe morbidity and mortality in these patients. In some cases disturbance in hemostasis is the first manifestation of a neoplastic process. We report the cases of two patients with cerebral and extracerebral vessel occlusions, in whom epithelial tumors of low malignant potential (borderline-tumors) of ovary and peritoneum were diagnosed later on. In one case the removal of the tumor stopped the coagulation problems. The second patient died a few days after the first symptoms with devastating multiple vessel occlusion. In stroke of unknown aetiology a paraneoplastic process should be kept in mind. The diagnosis is more probable with recurrent thrombembolism in different body regions and when warfarin therapy was ineffective. Thoughtful coagulation studies and a tumor search program is recommended in these cases.

Adult↗
PubMed1997

Molecular forms of somatostatin-like immunoreactivity in the cerebrospinal fluid of patients with senile dementia of the Alzheimer type.

In the cerebrospinal fluid (CSF) of 53 patients with senile dementia of the Alzheimer type (SDAT) and 12 elderly controls, we measured somatostatin (SLI) and its molecular forms: high-molecular weight form (HMV-SST), somatostatin-14 (SST-14), somatostatin-25/28 (SST-28/25), and des-ala-somatostatin (des-ala-SST) using high pressure liquid chromatography (HPLC) and a radioimmunoassay. In SDAT, SLI was significantly decreased (p < 0.05) and correlated with dementia scores (r = -0.65, p < 0.05). HPLC separation showed a marked heterogeneity of SLI in the CSF with a preponderance of SST-14 and SST-25/28. The significant loss of SST-14 (p < 0.05) in SDAT was found to be correlated with dementia scores (r = 0.65). Moreover, qualitative and quantitative changes in the molecular pattern of SLI in SDAT indicated dysregulated synthesis and/or processing of somatostatin relating to the severity of dementia. The long-term administration of neuroleptics in severe cases of SDAT caused a significant increase of SLI (p < 0.05) and influenced the ratio of HMV-SST/SST-14 and SST25/28/SST-14.

Aged↗
PubMed1997

Cerebrospinal fluid neuropeptides and monoaminergic transmitters in patients with trigeminal neuralgia.

The pathogenesis of trigeminal neuralgia remains largely unknown. "Peripheral" as well as "central" causes have been suggested. To investigate the role of serotonergic, noradrenergic, dopaminergic, and peptidergic systems, we determined the concentrations of epinephrine, norepinephrine, and their breakdown product, vanillylmandelic acid, in the cerebrospinal fluid of 16 patients (55.3 +/- 8.3 years) with trigeminal neuralgia. As a marker for the dopaminergic system, we determined cerebrospinal fluid concentrations of dopamine and its metabolite, homovanillic acid. As a marker for the serotonergic system, we measured cerebrospinal fluid levels of the serotonin metabolite, 5-hydroxyindoleacetic acid. In addition, levels of the neuropeptides, substance P and somatostatin, were determined. The concentration of norepinephrine (P < 0.01) and its metabolite, vanillylmandelic acid, (P < 0.05) were significantly decreased in our patients. The level of the dopamine metabolite, homovanillic acid, was also significantly reduced (P < 0.01). Also significantly decreased was 5-hydroxyindoleacetic acid (P < 0.01). Substance P was significantly elevated (P < 0.05). Somatostatin was significantly decreased (P < 0.05). We hypothesize that the sum of complex neurochemical changes plays a role in the pathogenesis of trigeminal neuralgia. The elevated substance P could support the concept of a neurogenic inflammation in the trigeminovascular system, whereas changes in the monoaminergic transmitters and their metabolites seem to reflect a more central dysfunction possibly due to a longer duration of the disease and an accompanying depression.

Biogenic Monoamines↗
PubMed1997

[Faulty regulation of the hypothalamo-hypophyseal-adrenal axis and chronobiological manifestations in cluster headache].

Cluster headache is a rare very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. Although peripheral structures are postulated to be involved in triggering the pain attacks, chronobiological changes like the cluster period and the complex dysbalance of the sympathetic and parasympathetic nervous system point to a "central" genesis of cluster headache. To check neuroendocrine changes in cluster headache, in 12 patients (43.4 +/- 6.3 years) during the cluster period cortisol and ACTH were determined four-times a day (7.00, 12.00, 17.00, 23.00) in the plasma. To prove the central genesis of cluster headache, in the cerebrospinal fluid (CSF) the neurotransmitters norepinephrine, epinephrine, dopamine and the metabolites 5-hydroxyindolacetic acid (5-HIAA), homovanillic acid (HVA) and vanillymandelic acid (VMA) were determined. The values of cortisol and ACTH were significantly elevated in the morning (p < 0.01, p < 0.05) and at night (p < 0.01, p < 0.01) in comparison to the control patients. The daily mean value of cortisol was significantly increased compared to controls (p < 0.01). In the CSF norepinephrine (p < 0.05), HVA (p < 0.01) and 5-HIAA (p < 0.01) decreased to significant low levels compared to control patients. We found significant correlations between cortisol/ACTH and norepinephrine and 5-HIAA. Moreover, our results indicate that the higher cortisol the longer the duration of the cluster period. The results of this study confirm changes of the hypothalamic-pituitary-adrenal axis due to the chronobiological changes in cluster headache. The reduced values of neurotransmitters in the CSF are compatible with the hypothesis of a central genesis of cluster headache.

Adrenocorticotropic Hormone↗
PubMed1996

CSF substance P somatostatin and monoaminergic transmitter metabolites in patients with narcolepsy.

We have measured the concentrations of substance P, somatostatin, homovanillic acid (HVA), vanillyl mandelic acid (VMA) and 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF) of six patients suffering from narcolepsy and 12 age- and gender-matched controls using high pressure liquid chromatography (HPLC) and radioimmunoassay (RIA). Substance P and somatostatin were significantly decreased in our patients compared to controls (36.9 +/- 9.1 fmol/ml versus 52.5 +/- 9.9 fmol/ml, P < 0.05 and 30.3 +/- 7.8 fmol/ml versus 43.9 +/- 9.8 fmol/ml, P < 0.05, respectively). 5-HIAA (P < 0.05) and VMA (P < 0.05) were also significantly decreased. HVA was significantly increased (P < 0.01). The CSF concentrations of substance P and somatostatin correlated with the clinical parameters duration of disease (r = -0.68, P < 0.05 and r = -0.72, P < 0.05, respectively) and severity of cataplectic symptoms (r = -0.71, P < 0.05 and r = -0.78, P < 0.01). In addition, substance P correlated with the intensity of sleepiness and the frequency of day-sleep attacks (r = -0.69, P < 0.05 and r = -0.68, P < 0.05, respectively). Substance P affects the amount of dopamine release in the nigra-striatal region, and decreased amounts could contribute to the pathogenesis of narcolepsy. Reduced levels of substance P, which affects serotonin release, may be responsible for diminished release of serotonin which in turn could affect sleep cycles. Because somatostatin affects motor behavior through dopaminergic mechanisms and since the levels of somatostatin correlate with the intensity of cataplectic symptoms, we speculate that an interaction between somatostatin and dopaminergic neurons plays a role in the pathogenesis of narcolepsy.

Adult↗
PubMed1996

[Substance P, somatostatin and monoaminergic transmitters in the cerebrospinal fluid of patients with chronic idiopathic trigeminal neuralgia].

The etiology of trigeminal neuralgia is unknown, but both peripheral and central causes have been suggested. To investigate the role of central neurochemical mechanisms we measured epinephrine, norepinephrine and their breakdown product, vanilly mandelic acid (VMA), in the cerebrospinal fluid (CSF) of 16 patients (53.3 +/- 8.3 years) suffering from trigeminal neuralgia. As markers for the dopaminergic system, we determined CSF levels of dopamine and its metabolite homovanillic acid (HVA). As a marker for the serotonergic system, we measured CSF levels of serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA). In addition, levels of the neuropeptides substance P and somatostatin were determined. The concentration of norepinephrine (P < 0.01), VMA (P < 0.05) and HVA (P < 0.05) were significantly decreased in patients with trigeminal neuralgia and correlated with the duration of the disease and depression scores. 5-HIAA was also significantly decreased (P < 0.05) compared to control patients. Whereas substance P was significantly elevated (P < 0.05), somatostatin was significantly decreased (P < 0.05). Various correlations between the classical neurotransmitters and the neuropeptides could be established. We hypothesize than the sum of complex neurochemical changes plays a role in the etiology of trigeminal neuralgia, which can be separated in local and more central proceedings. The increase in substance P, a major nociceptive neuromodulator, supports the concept of a local neurogenic inflammation, possibly located in the trigeminovascular system. Depending on the duration of the disease and depression, the loss of serotonergic, dopaminergic and noradrenergic innervation seems to reflect more central changes, possibly due to alterations in their antinociceptive descending pathways.

English Abstract↗
PubMed1996

Autonomic nervous system and neuroendocrine changes in patients with idiopathic trigeminal neuralgia.

To investigate sympathetic nervous system and neuroendocrine changes in idiopathic trigeminal neuralgia, we determined the plasma level of the catecholamines norepinephrine and epinephrine, as well as cortisol and ACTH in 16 patients (55.3 +/- 8.3 years) with trigeminal neuralgia at four different times during the day (7.00, 13.00, 17.00 and 23.00). Morning and evening values of plasma norepinephrine as well as the daily mean value (dmv) were significantly higher (p < 0.01) in patients with trigeminal neuralgia than in an age- and gender-matched control group. Moreover, morning, afternoon and dmv epinephrine values were also significantly elevated. The dmv norepinephrine levels correlated with the intensity of the attacks (r = 0.68, p < 0.01), the frequency of the attacks (r = 0.75, p < 0.01) and the duration of the disease (r = 0.78, p < 0.01). In addition to elevated catecholamines, trigeminal neuralgia patients also demonstrated significantly increased morning, evening and daily mean values of plasma cortisol. Thus, patients with trigeminal pain have an increased sympathetic nervous system activity for an extended period of time without a direct link to pain attacks, which suggests that the sympathetic nervous system itself is at least co-activated in trigeminal neuralgia and perhaps plays a role in the induction and maintenance of trigeminal pain. The neuroendocrine changes are similar to cluster headache and point to a central dysregulation of the hypothalamic-pituitary-adrenal axis, possibly due to the cyclic phenomena in idiopathic trigeminal neuralgia.

Adrenocorticotropic Hormone↗
PubMed1996

[Primary cerebral non-Hodgkin's lymphomas. The results of radiotherapy].

BACKGROUND: In the last years many therapeutic attempts were made to improve the poor prognosis of primary cerebral non Hodgkin's lymphoma. The aim of this study was to report on own experiences concerning this rare disease. PATIENTS AND METHODS: In 1986 to 1994 26 patients were treated for primary cerebral non Hodgkin's lymphoma. 15% were HIV-positive. High-grade non-Hodgkin's lymphomas were diagnosed in 62%. 46% of all cases showed multiple lesions. 23% of our patients received a dose less than 25.5 Gy, 27% received 37.5 Gy (whole brain) and 39% were treated with 51 Gy (37.5 Gy whole brain and 13.5 Gy boost dose). Radiation technique included regular and irregular fields (single dose: 1.5 Gy). RESULTS: 62% of patients achieved a complete or partial remission directly after irradiation, in 4% no change or progression was seen. 31% could not be examined due to their bad status or death. The mean follow-up time for all patients was 19.6 months, the median survival was 3.6 months. The 1-year-survival rate was 41%, 3-year survival rate was 28%. Patients who received a tumor dose of 51 Gy had better survival times in comparison to patients who received less (p = 0.01). Prognostic parameters (Cox regression analysis) were: tumor dose, grading and local result after irradiation. The Karnofsky performance status was not an independent parameter (p = 0.12). Side effects were low. Long-term survivors had relatively good quality of life. CONCLUSION: Taking into consideration the small numbers of patients in all studies all results or conclusions have to be made with great reservations. Despite the high proportion of HIV-positive patients our results are in compliance with other authors using similar therapy protocols. Reports dealing with combined radio-chemotherapy have published good results concerning survival time. But long-term morbidity due to these protocols needs further investigation and has to be awaited.

Adult↗
PubMed1995

[Intracerebral hemorrhage and multiple brain abscesses caused by Bacillus cereus within the scope of acute lymphatic leukemia].

Multiple hematogenic brain abscesses in immunosuppression are occasionally caused by rare and primary apathogenic causative agents. We report a first case of an isolated CNS infection by Bacillus cereus, which led to death from multiple brain abscesses and an intracerebral hemorrhage, probably caused by the infection, within 4 days. The underlying disease leading to immunosuppression was acute lymphatic leukemia in complete remission. In spite of antibiotic therapy the chemotherapy-induced neutropenia enabled unhindered spreading of the necrotizing infection, which was verified by histological analysis. The production of potent toxins such as hemolysin and cerelolysin by B. cereus leads to rapid and fulminant tissue destruction usually involving the walls of blood vessels.

Adult↗
PubMed1994

[The value of various transcranial color doppler tests for determining cerebrovascular reserve capacity].

One of the techniques for the assessment of the cerebrovascular reserve capacity is the so-called "breath-holding" test. In order to minimise haemodynamic changes following deep inspiration the patients should hold their breath at the end of a normal inspiration. We studied three different ways (breath holding following normal inspiration [NI], deep inspiration [DI], hyperventilation [HV]), of performing this test in 20 healthy volunteers. The acetazolamide test was taken as a reference. The mean flow velocity (FVmean) in the middle cerebral artery was recorded continuously using a TCD monitoring system. Blood pressure, cardiac output and heart rate were measured simultaneously. Breath holding after deep inspiration resulted in longer apnoea (DI: 68.1 +/- 24.1 s; NI: 44.8 +/- 18.4 s; p < 0.01), produced the highest increase of FVmean (DI: +72.2 +/- 29.8%; NI: +69.2 +/- 29.0%) and was the least inconvenient to the patients. Following HV apnoea was longest (93.0 +/- 33.5 s; p < 0.01), but resulted in the lowest increase of FVmean were not significant. A significantly lower increase of FVmean (44.2 +/- 13.4%, p < 0.01 resp.) could be observed after intravenous injection of 1 g acetazolamide. There were no significant haemodynamic changes in any case. Thus, this bedside test does not appear to be influenced by variations in breath holding.

Acetazolamide↗