[The significance of biogenic amines in cerebral infarction (author's transl)].
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Aged↗
Biomedical subjects
K Jellinger
Publications and source records attributed to K Jellinger.
[Bromazepam in the treatment of somatized psychogenic disorders (author's transl)].
The clinical effects are reported of the benzodiazepine derivative, bromazepam (Lexotanil) in the treatment of psychosomatic disorders in the course of neurotic, psychovegetative, and masked depressive syndromes. The drug was administered orally in 301 patients (178 males, and 123 females). Target symptoms were anxiety, tension, and varied organic dysfunction of psychogenic origin. The optimum daily dosage was three times 3 mg; the duration of treatment ranged from 1 week to 34 months. The effect of treatment was considered excellent in 51.5%, good in 42.5%, moderate in 2%, and absent in 4%. The most responsive target symptoms were psychogenic disorders of the cardiovascular system and of the gastrointestinal tract, as well as anxiety, while no true antidepressive effect was observed. Drug tolerance is excellent. Slight fatigue, vertigo or a mild reduction in psychomotor activity were complained of by about 10% of the patients and usually occurred with daily doses of 18 mg or more, whereas no other side effects were observed. There was no obvious tendency to drug dependence even after after long-term treatment of up to 34 months. Bromazepam appears to be a superior compound to other anxiolytic and psychovegetatively active minor tranquillisers on account of its mild hypnotic action. Its anxiolytic effect causes additional indirect sleep induction in the above-mentioned conditions.
Adult↗
Intramedullary spinal cord metastases.
Seven autopsy cases of intramedullary metastases, four in the cervical spinal cord, are reported and the literature reviewed. Whereas lung and breast cancer, malignant melanomas and lymphomas are reported as the most common primary tumors, the present series included three cases of breast carcinoma and two cases each of colon and oat cell carcinoma of the lung. Neither the clinical symptoms nor the neurological signs distinguished intramedullary metastases from the more common extradural deposits, but radiological evidence of vertebral metastases and myelographic stop were present in only one case each, and CSF cytology was negative. Intramedullary deposits in this series were neither associated with extradural tumor nor with spread into the subarachnoid space, while cerebral metastases were present in four cases. This favors hematogenous dissemination rather than direct transdural or perineural spread of these lesions.
Adenocarcinoma↗
Primary malignant lymphoma of the CNS and polyneuropathy in a patient with necrotizing vasculitis treated with immunosuppression.
A woman, aged 58, who had undergone prolonged treatment with corticosteroids for generalized necrotizing vasculitis, and had received azathioprine (Imurel) for 18 months, 4 years after discontinuing the latter treatment, developed peripheral neuropathy and a rapidly progressing cerebral disorder suggesting a basal meningeal process. CSF cytology suggested malignant lymphoma with meningeal involvement. Immunological studies showed an increase of Null-lymphocytes in the peripheral blood. Autopsy disclosed a primary malignant lymphoma of the CNS with the histological appearance of a multilocular immunoblastoma showing almost ubiquitous meningocerebral involvement. Clinical and postmortem examinations failed to demonstrate any systemic extraneural lymphoproliferative disorder. In addition, there was peripheral polyneuropathy of the axonal type with denervation atrophy of skeletal muscle, but without lymphomatous involvement of the neuromuscular system. The possible relations between primary malignant lymphomas of the CNS and previous immunosuppressive treatment of immunoinflammatory disease are discussed in view of the concept of impaired immunoregulation. The pathogenetic background of peripheral polyneuropathy is unknown.
Azathioprine↗
The symptomatology with the most severe clinical course of spontaneous subarachnoid hemorrhage.
The symptomatology of 18 patients with the severest clinical course after subarachnoid hemorrhage (SAH) is described and analyzed. Seventeen patients died, five with an acute bulbar syndrome with cardiac arrest, and 12 with irreversible breakdown of brain function. One patient had an apallic syndrome with minimal signs of remission, who died 4 months after the first rebleeding. The cases are divided into five clinical groups on the basis of the acute brainstem symptomatology which set in instantly or after temporary adaptation, or following a second hemorrhage. Pathological examination revealed that 16 patients had a brainstem pressure cone, 14 with marked edema and signs of herniation; one patient had only cisternal tamponade while another had predominantly brain edema with herniation. There was striking parenchymatous damage of the brain of the patient with the apallic syndrome. There was a marked analogy between the material reported and the symptomatology described by Plum and Posner (1972).
Adult↗
[Familial striatal degeneration (author's transl)].
An extrapyramidal disorder occurring in three generations of a family (only males) is described The clinical features were progressive dementia and extrapyramidal signs without choreiform hyperkinesia. The youngest patient (onset of disease at the age of 22 years) showed tremor, rigidity, ataxia, convulsions, and myoclonus. The neuropathologic findings were characterized by isolated symmetrical degeneration of the corpus striatum and diffuse cortical atrophy without affecting other cerebrospinal neuronal systems. The clinical features of this familial disorder and its relation to other types of familial striatal degeneration and to the juvenile form of Huntington's chorea are discussed.
Adult↗
Combination chemotherapy (COMP protocol) and radiotherapy of anaplastic supratentorial gliomas.
Postoperative survival time and recurrence-free intervals in 116 consecutive patients with supratentorial grade III and IV gliomas (glioblastomas, gliosarcomas, anaplastic astrocytomas, and ependymomas) were compared in unselected groups receiving different forms of treatment. Postoperative high-voltage radiotherapy (31 patients, dosage 4,000--6,000 rads) and combined chemotherapy consisting of CCNU, vincristine, amethopterine, and procarbazine in 15-day circles (COMP protocol) (12 patients) showed the same median survival time of 10.6 months and comparable recurrence-free intervals of 6.8 and 7.0 months, respectively. These results were significantly different from a control group (39 patients) receiving best postoperative supportive (conventional) care (median survival 5.4 months, free interval 3.7 months). Combination of postoperative radiotherapy with simultaneous polychemotherapy (COMP protocol), evaluated in 18 patients, did not significantly change the recurrence-free interval (median 7.0 months), but increased the median survival time to 12.9 months, which was significantly superior to the two other treatment groups. The toxic side effects of COMP therapy were moderate and essentially haematological. In general, simultaneous radiation and chemical treatment was well tolerated after major tumour resection. These preliminary results of postoperative combination of radiation and polychemotherapy for anaplastic supratentorial gliomas appear encouraging, but further trials for optimization of combined therapeutic strategies are warranted.
Adult↗
Primary brain tumour presenting as spontaneous intracerebral haemorrhage.
In an autopsy series of 430 spontaneous intracerebral haematomas 44 cases, or 10.2 percent, were caused by a proved neoplasm, including 21 anaplastic gliomas, 17 metastases, 2 oligodendrogliomas, 2 malignant lymphomas, and one meningioma. These instances of massive bleeding into brain tumour represented 2.4 percent of about 1,800 primary and secondary cerebral neoplasms proved by necropsy. In only four of the patients with primary brain tumours (two glioblastomas, one oligodendroglioma invading the leptomeninges, and one primary malignant lymphoma), three of them with a history of arterial hypertension, were the presenting symptoms these of a spontaneous intracerebral haemorrhage, and the tumour itself was not diagnosed until surgery or necropsy. One patient with acute haemorrhage into a glioblastoma of the basal ganglia showed a rapidly lethal course, while the others demonstrated one or more episodes before the onset of the acute fatal illness and a prolonged period from the time of the bleed until death. The clinical features and the pathogenesis of spontaneous haemorrhage into cerebral neoplasms are briefly reviewed.
Aged↗
Primary intracranial malignant lymphomas a fine structural cytochemical and CSF immunological study.
Cytochemical and electron microscopical studies in six cases of primary intracranial malignant lymphomas, four of which were diagnosed by biopsy, confirmed their ultrastructural identity with extraneural malignant lymphomas classified as immunoblastomas and immunocytomas. Demonstration of transformation of 'blast-like' cells (immunoblasts) toward rough E. R. developing cells in all these tumours argue for the B-dell origin of these types of cerebral lymphomas, previously referred to as reticulum cell sarcomas/microgliomas. CSF studies showed increased levels of B cells with surface IgG in two cases of immunoblastoma, and increased IgG levels with light chains in two cases each immunoblastoma and of pleomorphic immunocytoma, while one case of immunoblastoma showed a normal T cell to B cell ratio with increased monoclonal and surface, IgM suggesting some morphological and immunological heterogeneity of these lymphomas.
B-Lymphocytes↗
[Metabolic factors in the pathogenesis of consciousness disorders and coma].
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Aged↗
Brain monoamines in human hepatic encephalopathy.
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Aged↗
[Ultrastructure of intracellular storage materials in an autopsy case of adult-onset metachromatic leucodystrophy (MLD) (author's transl)].
Formalin-fixed samples from the demyelinated frontal white matter of an autopsy case of adult-onset MLD were studied by electron microscopy. The intracellular storage materials exhibited the following types of structural patterns: (I) ordinary myelin figures; (II) pleated myelin figures; (III) narrow stacks of lamellar discs which were most likely components of formerly compact "prismatic" inclusions; (IV) paired lamellae, either arranged in loose parallel arrays or scattered about in random directions; (V) piles of parallel lamellae with alternating electron-dense and electron-lucent inter-spaces; and (VI) collections of structures resembling fragments of so-called pentalaminar membranes. Types I to IV have already been described in early-onset as well as late-onset forms of MLD, but types V and VI have not. Postmortem autolysis had possibly altered the structural organization of some cytoplasmic deposits and given rise to the formation of those lamellar patterns which were hitherto not known to occur in MLD.
Cell Membrane↗
Brain monoamines in human cerebral infarcts. A preliminary study.
Dopamine (DA), serotonin (5-HT), and 5-hydroxyindole acetic aced (5-HIAA) were assayed spectrofluorometrically in various brain regions of 8 human patients who died after acute and old cerebral infarction. In both recent and older infarct a total depletion of DA and 5-HT was associated with slight reduction of DA and 5-HT levels in remote nonischemic areas and various nuclei of both the injured and contralateral hemispheres. 5-HIAA was significantly reduced in acute ischemic necrosis, while the perifocal edema zone showed considerable accumulation of both 5-HT and 5-HIAA. The degradation zone surrounding old infarcts showed a mild decrease of both 5-HT and 5-HIAA, indicating normalization of K-HT metabolism and turnover after decrease of cerebral edema. These preliminary data which confirm previous findings in experimental cerebral ischemia and infarct indicate that disorders of brain monoamine metabolism are contributing to the development of postischemic brain damage and the complicating cerebral edema.
Aged↗
On the mode of action of L-deprenyl in the human central nervous system.
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Blood Platelets↗
Amphetamine and 2-phenylethylamine in post-mortem Parkinsonian brain after (-)deprenyl administration.
Deprenyl is an inhibitor of monoamine oxidase type B, the enzyme responsible for 2-phenylethylamine oxidation, and is used in conjunction with L-Dopa therapy in Parkinson's disease. Post-mortem studies in human brain tissue have shown that after (-)deprenyl administration to parkinsonian patients amphetamine is present in concentrations up to 56 ng/g. It also could be shown that phenylethylamine concentrations are substantially increased in such patients. Phenylethylamine and amphetamine have been investigated using a gas chromatographic technique.
Amphetamines↗
Glioblastoma multiforme: morphology and biology.
Glioblastoma multiforme, representing about 50% of all gliomas, encompasses a group of intrinsic tumours of the brain in later years (age peak around 50 years), the morphological hallmarks of which are an ensemble of variations in tumour cell and tissue structure featuring its biological malignancy. Glioblastoma, while sometimes appearing as a distinct "primary" tumour type, is usually accepted as an extreme manifestation of anaplasia and dedifferentiation of glia, mostly astrocytic. The astrocytic nature of most glioblastomas has been confirmed by ultrastructural studies and progressive differentiation of tumours maintained in organotypic tissue culture. Reproducible experimental models are particularly induced by oncogenic RNA (oncorna) viruses. The cell kinetic parameters are similar to those of other solid malignant tumours except for a comparatively low growth fraction of glioblastoma. The frequent occurrence of giant cells as well as of regressive changes with necrosis and vascular responses are indirect (secondary) indicators of malignancy which coincide with histochemical (enzymatic anisochronia) and biochemical data (lower level of glia specific S100 protein than in differentiated gliomas). Vascular proliferation, a characteristic feature of glioblastoma, may occasionally progress to sarcomatous transformation with development of gliosarcomas (mixed glial-mesenchymal tumours). While dissemination of glioblastoma through the cerebrospinal pathways is not uncommon, extraneural distant metastatic spread is rare, and usually observed after craniotomy. The results of modern neuro-oncology support the pathogenetic view that glioblastoma results from neoplastic transformation of glial elements with continuing dedifferentiation. This transformation can be experimentally induced by various factors including oncogenic DNA (oncorna) viruses by using a reverse transcriptase, while there is indirect evidence for an oncorna-virus information in human glioblastoma. The significance of immunological factors in the pathogenesis of brain tumours and in the course of neoplastic transformation of glia is not yet understood, but both morphological and immunological data are in favour of a cell mediated immunological reaction against tumour-specific antibodies. Since immunological factors and changes in cytokinetics are apparently active after the transformed tumour cells proliferate, all available therapeutic methods, including radiation, chemotherapy, and immunotherapy of glioblastoma only influence the final stages of neoplastic development with clinical manifestation of the tumour. In spite of modern combination and multimodality therapy schemes the prognosis of glioblastoma is still poor.
Adult↗
Pathology of brain tumors with relation to prognosis.
In a brief survey, the classification of cerebral tumours preferred at present is dealt with (WHO classification Geneva 1976) and the prognostic relation is established for the various cases. Special consideration is devoted to the questions of the conformity of the histologic picture, grading by means of microscopic examination, and the tendency of certain tumours to become malignant and their relapses. The statistical frequency of occurrence of the various kinds of tumours and their preferred localisation are also discussed.
Brain Neoplasms↗
Dopamine-sensitive adenylate cyclase activity in the caudate nucleus and adrenal medulla in Parkinson's disease and in liver cirrhosis.
In human caudate nucleus and adrenal medulla dopamine-stimulated adenylate cyclase was measured. At a concentration of 100 microM dopamine, liver cirrhosis, carcinoma and therapy resistent parkinsonian patients showed decreased stimulation or even a reduction compared to controls. Therapy responding parkinsonian patients showed a decreased stimulation compared to controls, but this stimulation was significantly higher than in drug resistent patients.
Adenylyl Cyclases↗