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Biomedical subjects

M Weller

Publications and source records attributed to M Weller.

At least 271 records · Page 15Linked to original sources
PubMed1992

Humoral CSF parameters in the differential diagnosis of hematologic CNS neoplasia.

Cerebrospinal fluid (CSF) and serum samples of 20 patients with central nervous system manifestations of hematological malignancies including primary cerebral lymphoma (n = 5) and disseminated non-Hodgkin lymphoma (n = 7) were examined for albumin, IgG, IgM, fibronectin, beta 2-microglobulin, interleukin-6, soluble interleukin-2 receptor, tumor necrosis factor alpha, and oligoclonal immunoglobulin bands. Although a broad range of abnormalities were detected, no reliable CSF parameter for the diagnosis of leptomeningeal spread from hematological neoplasias could be identified. An analysis of 61 repeat lumbar punctures added little to the findings of the first CSF examinations. Currently, immunochemical studies of CSF cell surface markers and early biopsy have probably more clinical value than the determination of the humoral CSF parameters included in this study. However, analysis of cytokine synthesis by single CSF cells using molecular biology techniques may improve the differential diagnosis of hematological neoplasia of the brain and spinal cord in the future.

Biomarkers, Tumor↗
PubMed1992

CSF and serum ganglioside antibody patterns in MS.

The authors determined CSF and serum IgG and IgM antibodies to seven gangliosides in 48 patients with multiple sclerosis. Differing ganglioside antibody patterns in CSF but not serum allowed to reclassify 93% of MS patients correctly when compared to patients with Guillain-Barré syndrome or neuroborreliosis. This suggest that the antibody patterns are neither random nor alike in inflammatory diseases of the nervous system. CSF ganglioside antibody titres were found to be different for patients with relapsing remitting (RRMS; n = 35) and chronic progressive (CPMS; n = 13) multiple sclerosis. Our study reveals characteristic ganglioside antibody patterns in MS and confirms previous evidence of disturbed immunoregulation in MS.

Adult↗
PubMed1992

Clozapine rechallenge after an episode of 'neuroleptic malignant syndrome'.

Nine out of 4044 patients admitted to our institution between 1987 and 1990 suffered an episode of NMS. Neuroleptic rechallenge using clozapine for persisting psychiatric illness was tolerated by eight patients. Clozapine was discontinued in one older, high-risk patient because recurrence of NMS was anticipated. Clozapine should be considered a drug of choice for psychotic patients with a history of NMS.

Adult↗
PubMed1992

Very-late-onset adrenoleukodystrophy: possible precipitation of demyelination by cerebral contusion.

We report the clinical history, neuroradiology, and autopsy findings in a patient with very late onset, at age 57, of adrenoleukodystrophy (ALD) presenting with dementia, hemianopia, and gait apraxia. Open brain biopsy, elevated plasma very-long-chain fatty acids, and autopsy confirmed the diagnosis of ALD. Demyelinative lesions were most extensive at the site of a recent cerebral contusion. CNS trauma may have precipitated or accelerated demyelination in this patient carrying the ALD gene.

Adrenoleukodystrophy↗
PubMed1992

[Idiopathic proliferative vitreoretinopathy. Activation of microglial cells as the deciding factor].

Mononuclear phagocytes are considered pacemakers in the pathogenesis of proliferative vitreoretinopathy (PVR), but their precise biological origin in preretinal PVR traction membranes has remained obscure. This study presents a combined immunohistochemical protocol for the detection of microglial cells, which was applied to 37 membranes of patients with idiopathic and traumatic PVR and with proliferative diabetic retinopathy (PDR). Microglial cells may be labeled by staining for LN-1, ricinus communis agglutinin-(RCA)-1, vimentin, HLA-DR-II, and nucleoside diphosphatase, but are negative for Leu-M1, Leu-M3, EBM-11, von Willebrand factor, CD22, cytokeratin, and glial fibrillary acidic protein (GFAP). Significant proliferation of microglial cells was found in idiopathic PVR while classical macrophages were typical of traumatic PVR. Only rarely were microglial cells detected in PDR. These findings bring into question previous concepts of the pathobiology of idiopathic PVR and support the hypothesis of idiopathic PVR as a specific disease entity.

Cicatrix↗
PubMed1992

[Pathophysiology and therapy of malignant neuroleptic syndrome].

Rigidity, hyperthermia, and elevated levels of creatine phosphokinase are the essential features of "neuroleptic malignant syndrome" (NMS), a clinical condition caused either by pharmacological treatment with dopamine receptor antagonists or by the withdrawal of dopamine receptor agonists. An acute dopaminergic transmission block in the basal ganglia and the hypothalamus is thought to be the pathophysiological mechanism of NMS. NMS, the "malignant dopamine depletion syndrome", and the akinetic Parkinsonian crisis may be considered identical conditions with regard to their presumptive pathogenesis. Centrally acting dopamine receptor agonists and the peripheral calcium antagonist, dantrolene, are the most common adjunctive pharmacological approaches to NMS, although their efficacy has been questioned. The motor symptoms and the autonomic nervous system disturbances of NMS may be related to a relative glutamatergic transmission excess, as a consequence of a dopaminergic block. Therefore, we recommend the application of N-methyl-D-aspartate (NMDA) receptor antagonists such as amantadine or memantine for the management of NMS. These drugs counteract excitatory amino acid neurotransmission and exhibit hypothermic and central muscle relaxant properties. However, identification and reversal of the causative event, such as neuroleptic drug therapy or change of anti-parkinsonian medication, remain the cornerstones for reducing the incidence and mortality of NMS.

Amantadine↗
PubMed1992

The effects of basic fibroblast growth factor on bovine retinal pigment epithelium in vitro.

Basic fibroblast growth factor (bFGF) has been reported to initiate DNA synthesis in a variety of cells involved in the pathogenesis of proliferative vitreoretinal disorders, e.g., glial cells and fibroblasts. We analyzed the mitogenic effects of bFGF on cultured bovine retinal pigment epithelial cells in relation to time and dose response regulations and culture conditions. Maximum stimulatory effect of bFGF (+70% compared to control group) was found on day 3 following treatment of cultures with 80 ng/ml bFGF. The action of bFGF seems to depend on the serum concentration in the culture media, which means that cofactors may be present in the serum and potentiate the effects of bFGF on cell proliferation.

Animals↗
PubMed1992

[Differential neuroleptic treatment of schizophrenic psychoses in puerperium: advantages of the atypical neuroleptic clozapine].

Clozapine is an atypical neuroleptic drug characterised by specific pharmacological properties and clinical side effects, which are different from those observed with conventional neuroleptics such as drugs of the phenothiazine or butyrophenone classes. This report suggests a new clinical indication for clozapine, based on its negligible influence on plasma prolactin levels: the pharmacotherapy of schizophrenic psychoses in the post-partum period and in patients suffering from acute mastitis.

Adult↗
PubMed1992

[Proliferative vitreoretinopathy. Activation of the complement system].

The complement system is a principal constituent of humoral immune reactions. Because of the multitude of biological effects related to complement activation, we analyzed its potential pathophysiological importance in the development of proliferative vitreoretinopathy (PVR). Vitreous aspirates from patients with idiopathic PVR (n = 7) and traumatic PVR (n = 11) were examined for total vitreal protein, complement components C3, C3d, and C1q-fixed immunoglobulins using enzyme-linked immunosorbent assay (ELISA), SDS-Page and Western blotting. Total vitreal protein and C3 components were significantly elevated both in traumatic and idiopathic PVR. Elevated levels of C3d titers in both PVR forms reflect an activation of the complement system. C1q-fixed IgG suggests complement activation via the classic pathway as a result of a humoral antibody-dependent immune reaction.

Autoimmune Diseases↗
PubMed1992

[Contractile elements in proliferative retinal diseases].

Contraction of epiretinal membranes remains the leading cause of failure in retinal surgery. The mechanism of contraction of cellular units is as yet unknown. We have used immunohistochemical methods to demonstrate the intracellular localization of the proteins actin, myosin, tropomyosin and vinculin, which are thought to be responsible for cellular contraction, in 26 surgically obtained epiretinal traction membranes from patients with traumatic (n = 12) and idiopathic (n = 7) proliferative vitreoretinopathy, and proliferative diabetic retinopathy (n = 7). The use of cell marker proteins for glial cells (GFAP) and retinal pigment epithelium (cytokeratin) demonstrates that the prevalence of contractile components is independent of cellular construction. We suggest that an intracellular mechanism is responsible for the contraction of epiretinal membranes in proliferative vitreoretinal disorders.

Contractile Proteins↗
PubMed1992

[Intrathecal immune response in meningeosis neoplastica: IgG, IgM, oligoclonal bands and cytokines].

Owing to improved systemic control of widespread malignancy, neurological complications have become a major outcome factor and determinant of life quality in oncological patients. While solitary cerebrospinal metastases are often amenable to surgical and radiological treatment, the management of diffuse leptomeningeal neoplasia, mostly using combined radiochemotherapy, is still very difficult. Immunomodulative approaches represent a therapeutic alternative with increasing potential. We have analysed the natural immune response to leptomeningeal tumor invasion in 43 Patients by assessing cerebrospinal fluid (CSF) levels of albumin, IgG, IgM, interleukins (IL) 1, 2, 4 and 6, soluble IL-2 receptor (sIL-2R), interferon gamma (IFN gamma), tumor necrosis factor alpha (TNF alpha), and the tumor markers, carcinoembryonic antigen (CEA) and alphafetoprotein (AFP). In most patients, either elevated IgG index, IgM index, CSF IL-6, or detection of CSF oligoclonal immunoglobulin bands indicated a host reaction against tumor cells. IL-1, IL-2, and IL-4 were never detected in CSF or serum. sIL-2R and IFN gamma were rarely detected and were not associated with specific malignancies. CSF TNF alpha was only detected in melanoma patients and may be a specific indicator of that neoplasm. No correlation was found between levels of the tumor markers, CEA and AFP, and parameters of the immune response such as IgG, IgM or IL-6. The demonstration of intrathecal immune activation in a majority of patients with leptomeningeal neoplasia may offer a new option for immunomodulative oncological therapy.

Biomarkers, Tumor↗
PubMed1992

[Electroconvulsive therapy in treatment of acute life threatening catatonia in toxic epidermal necrolysis (Lyell syndrome)].

Toxic epidermal necrolysis (Lyell syndrome) developed in a 43-year woman treated with carbamazepine, perazine, and sulpiride for recurrent manic bipolar disorder. Five days after withdrawal of all psychotropic medication her psychiatric illness was exacerbated and a syndrome of lethal catatonia developed which was promptly treated with unilateral electroconvulsive therapy (ECT). Rapid remission of lethal catatonia after the first ECT treatment and of her affective disorder within days was achieved. According to clinical observations of the preneuroleptic era, early improvement of lethal catatonia following ECT may have been supported by concurrent high dose corticosteroid therapy for toxic epidermal necrolysis.

Adult↗