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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 43 (1978), S. 217-226 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has been shown that 5 or 10 mg (-)deprenyl after i.v. application inhibited platelet MAO within 30 min. This effect correlated with the improvement of parkinsonian patients disability. Platelet MAO is purely of type B, thus resembling the human brain enzyme, which is 80% of type B. In other organs of the human MAO-A is of higher activity, thus it can oxidatively deaminate 5-HT, noradrenaline and tyramine in the periphery. The rather low peripheral side effects of (-)deprenyl can be explained by this fact. In vitro studies demonstrated that (-)deprenyl in comparison to d, l-tranylcypromine, clorgyline and harmaline is by far the most potent inhibitor of human brain MAO. Post-mortem studies in different human brain areas showed that there are differences in the behaviour of (-)deprenyl (10 mg) between short- and long-term treatment. Both show sufficient inhibition of DA-sensitive MAO (85–90%). However, when 5-HT is used as a substrate short-term treatment inhibits by about 40–50% whereas long-term treatment inhibits by about 65% which is higher than that mentioned before but not sufficient to increase brain 5-HT or decrease 5-HIAA. Therefore, long-term treatment with more than 1 mg/10 kg body weight could result in an accumulation of (-)deprenyl in the brain. Evidence for this derives from one parkinsonian patient, who was treated with 100 mg (-)deprenyl in which case both forms of the enzyme were inhibited sufficiently to increase DA and 5-HT in several brain regions.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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 chromatographie technique.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 212 (1976), S. 55-64 
    ISSN: 1432-1459
    Keywords: Sézary syndrome ; Mycosis fungoides, CNS involvement ; CSF cytology ; Lymphomas malignant
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Fallbericht über einen 45jährigen Mann, bei dem es im Rahmen einer histologischen verifizierten Mycosis fungoides offensichtlich im Verlauf eines leukämischen Schubes zur Hirnbeteiligung mit zwei Herden in der linken Parietal- bzw. Parieto-Temporalregion kam. Bioptisch fanden sich lymphomartige Gefäß- und Gewebsinfiltrate mit einzelnen Riesenzellen (Lutzner-Zellen) ohne sichere Meningealaussaat. Die Liquorcytologie ergab präund postoperativ vereinzelt atypische Lymphocyten und Mononucleäre, darunter eine ultrastrukturell charakteristische Sézary-Zelle. Im peripheren Blut waren nach postoperativem Rückgang der hohen Leukocytenzahl die in den Hautinfiltraten vorhandenen atypischen Lymphocyten (Sézary-Zellen) morphologisch und an Hand cytochemischer (β-Glucuronidase) und immunologischer (Rosetten mit Schafserythrocyten) Marker nachweisbar. Das Krankheitsbild wird als cerebrale Manifestation in der leukämischen Phase einer Mycosis fungoides im Sinne eines Sézary-Syndroms angesehen.
    Notes: Summary Two foci of histologically verified mycosis fungoides were found in the left parietal region of a 45-year-old man with involvement of the brain during an exacerbation of leukemia. There was perivascular and diffuse infiltration with lymphoma-like cells and occasional giant (Lutzner) cells but no involvement of the meninges. Both before and after operation the CSF contained a few atypical lymphocytes and mononuclear cells, one of which showed ultrastructurally the deeply clefted nucleus of Sézary cells. Atypical cells were confirmed morphologically in the peripheral blood, as well as by cytochemical (β-glucuronidase) and immunological (rosettes with SRBC) markers, after the postoperative leucocytosis had subsided. It is suggested that this CNS involvement during a leukemic conversion phase of mycosis fungoides is consistent with the Sézary syndrome.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Virchows Archiv 370 (1976), S. 345-362 
    ISSN: 1432-2307
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A retrospective histologic study of 145 consecutive autopsy cases of systemic malignant lymphomas (including lymphatic leukemias) was performed. The classification followed the Kiel Classification (Gérard-Marchant et al., 1974). There was an overall secondary CNS involvement in 26.2% of the total or in 30.4% of the non-Hodgkin's lymphomas including ALL, with intracranial lesions in 21.4 and 26.1%, respectively, and spinal epidural spread in 5.5 (5.1)%. Peripheral nerve involvement was seen in almost 40% of the examined cases. Ten further cases were isolated (“primary”) intracranial lymphomas without evidence of extraneural deposits or systemic lymphatic disease. The CNS complications in non-Hodgkin's lymphomas were diffuse meningeal and/or perivascular infiltration with or without invasion of the nervous parenchyma, and did not differ from those in CNS leukemia. Isolated solid mass lesions in the brain were only present in 7% of the secondary CNS lymphomas, but were seen in all instances of “primary” cerebral lymphomas. The incidence of CNS complications was highest in lymphoblastic lymphomas including ALL (39%), CLL (31%), immunocytic lymphoma (29%), less frequent in immunoblastic (18.7%), and centrocytic lymphomas (16.6%). No intracranial lesion was observed in centroblastic-centrocytic and centroblastic lymphomas which only produced epidural spread. Bone marrow involvement was present in 92.8% of the cases with secondary CNS lesions, and in 83.2% of the epidural lymphomas. Leukemic conversion, present in 44% of the total (52% with ALL), was demonstrated in 83.3% of the cases with secondary brain lesions, but was hardly combined with epidural spread. The histologic pattern of CNS lesions in non-Hodgkin's lymphomas and their frequent association with leukemic conversion suggest the importance of hematogenous dissemination rather than of direct spread from bone marrow or local manifestation in multisystem disease. Isolated (“primary”) lymphomas of the CNS which are morphologically identical with the extraneural lymphomas may represent a primary, often lethal manifestation of a multisystem disease with or without secondary generalization.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 35 (1976), S. 247-259 
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Seven cases are reported of anaplastic cerebral gliomas with metastases outside the neuraxis, seen among about 1500 gliomas. There were two children with anaplastic ependymomas, one adult with oligodendroglioma, and four young to middle-aged adults with astrocytomas grade III and IV. All patients had one or more craniotomies, and four had radiotherapy prior to the appearance of distant tumour deposits. The survival times ranged from 7 to 31 months in cases with gliomas grade II, and from 8 to 18 months with high grade astrocytomas. All seven tumours showed invasion of the meninges, ventricular walls, or both, and in four cases they transgressed the dura and surrounding bone or soft tissues. In six autopsy cases there was widespread dissemination of gliomas through the CSF pathways. Distant metastases involved regional or distant lymph nodes in six patients, the lungs in two, and the vertebrae, pleura, liver, or mediastinum in one patient each. The possible pathways for distant spread of intracranial gliomas and the factors which are considered responsible are briefly discussed.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 41 (1978), S. 173-176 
    ISSN: 1432-0533
    Keywords: Cerebral infarct ; Cerebral edema ; Monoamines ; Dopamine ; Serotonin ; Neurotransmitters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Dopamine (DA), serotonin (5-HT), and 5-hydroxyindole acetic acid (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 infarcts 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 5-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 edena.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 43 (1978), S. 63-68 
    ISSN: 1432-0533
    Keywords: Monoamines ; Indoleamines ; Serotonin ; Hepatic encephalopathy ; Metabolic coma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Dopamine (DA) serotonin (5-HT), 5-hydroxyindole acetic acid (5-HIAA), and tryptophan (Trp) were assayed spectrofluorometrically in various brain regions of 10 patients with acute hepatic coma, in 3 cases of uremic coma, 4 cases of diabetic coma, in three patients with liver cirrhosis without coma, and in 5 cases of hepatic coma treated by parenteral nutrition withi-valine a branched-chain amino acid. The results were as follows: 1. In all types of coma, brain DA showed a mild general decrease, the average reduction being 20 to 30% of the controls. 2. In hepatic and other metabolic comata, brain 5-HT and 5-HIAA were generally increased, most significantly in the brainstem tegmentum and parts of the limbic system. 3. Brain Trp was significantly increased in hepatic coma, with the highest elevation in the brainstem tegmentum. 4. In liver cirrhosis without coma, brain 5-HT was within normal range, while Trp and 5-HIAA were elevated in the brainstem, their increase being much less than in untreated hepatic coma. 5. In hepatic coma treated by parenterali-valine, brain Trp showed slight elevation similar to non-comatose cirrhosis, while 5-HIAA showed almost normal values, and 5-HT was even decreased in most brain areas. These preliminary results in human postmortem brains confirm previous CSF and brain findings in experimental and human hepatic and uremic encephalopathies, indicating considerable derangement in central monoamine neurotransmitters which are attributed, at least in part, to amino acid imbalance in plasma and brain. Increased 5-HT synthesis or turn-over in the ascending serotonergic brainstem systems might represent one biochemical substrate of clinical disorders of consciousness in hepatic failure and other metabolic catastrophes. Manipulation of plasma and hence brain amino acids may influence neurological symptoms of hepatic encephalopathy by changing the brain neurotransmitter profile.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 36 (1977), S. 117-138 
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Wirkung anuneoplastisdier Behandlung auf Gliome ist abhängig von der Tumorzeil- und Proliferationskinetik, der Gliomarchitektur und dem umgebenden Hirngewebe. Durch Strahlen- und Chemotherapie induzierte morphologische Veränderungen sind gekennzeichnet durch Zellnekrosen sowie schwere Zell- und Kernschäden durch Eingriffe in die Zellkinetik, doch können diese auch spontan in unbehandelten anaplastischen Gliomen auftreten. Vergleichsuntersuchungen von zytologischen Abstrichen und histologischen Routinepräparaten an Biopsie- und Autopsiematerial von 4 Gruppen anaplastischer Astrozytome und Glioblastome (78 Fälle) wurden nach postoperativer Strahlenbehandlung, Polychemotherapie und CCNU-Behandlung sowie ohne spezifische postoperative Therapie (Kontrollgruppe) vorgenommen. Nach Strahlen- und Chemotherapie fanden sich neben gesteigerter Nekrose und Gefäßreaktion verschiedene charakteristische, aber unspezifische Zell- und Kernveränderungen mit gesteigerter Neigung zur Bildung vielkerniger Riesen- und Monsterzellen, Kernhyperchromasie sowie schwerer Zytoplasmadegeneration als Hinweise auf Mitosestörungen und Zellschädigung. Nach antineoplastischer Therapie fand sich eine statistisch signifikante Zunahme von Riesen- und vielkernigen Monsterzellen sowie Abnahme der Mitosen, wobei diese Veränderungen nach Chemotherapie stärker ausgeprägt waren als nach Bestrahlung. Zwischen Polychemo- und CCNU-Behandlung ergaben sich keine wesentlichen Abweichungen. Die Bedeutung dieser zytologischen Spätbefunde auf die Effekte antineoplastischer Behandlung anaplastischer Gliome wird diskutiert.
    Notes: Summary The effects of antineoplastic treatment on gliomas are related to tumour cell cycle and proliferation kinetics, glioma tissue architecture, and the surrounding environment. Morphological changes induced by radiation and chemotherapy are characterized by cell necrosis and severe alterations in cell and nuclear morphology caused by changes in the cell kinetic parameters which, however, may also occur spontaneously in untreated anaplastic gliomas. Comparative studies of cytological imprints and routine histological preparations of biopsy and autopsy specimens were performed in four groups of anaplastic astrocytomas and glioblastomas (78 cases) with postsurgical irradiation, combination chemotherapy, and CCNU treatment, and without specific postsurgical treatment (control group). Following radiation and chemotherapy, in addition to increased necrosis and vascular response, a variety of characteristic but nonspecific changes were observed in cell and nuclear morphology with prominent formation of multinucleated giant and monstrous cells, irregular and hyperchromatic nuclei, and severe cytoplasmic degeneration indicating both inhibition of cell division and cell damage. Statistically significant findings were a posttreatment increase in the number of multinucleated giant and monstrous cells and a decrease in the number of mitoses. These changes were more pronounced after chemotherapy than after radiation, while no significant dissimilarities were found between combination chemotherapy and CCNU. The implications of these changes on the mechanisms of antitumour treatment in anaplastic gliomas are discussed.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 35 (1976), S. 261-269 
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A 28 year old woman suffered from lumbar radicular signs and sensory deficit for three years before death. A progressive illness with increased intracranial pressure, cerebellar signs, and multiple cranial nerve palsies appeared one year after the onset of symptoms, but craniotomy of the posterior fossa was negative. After development of spastic paraparesis, an intramedullary oligodendroglioma of the lower thoracic cord was partly removed. Death occurred two months later from raised intracranial pressure. At autopsy a diffuse oligodendroglioma was found involving the periventricular regions of the brain, the entire subarachnoid space, the cerebral parenchyma, and the whole length of the thoracic cord. There was a small lumbar syrinx. It is suggested in this case that the dorsal intramedullary oligodendroglioma was the source from which tumour spread diffusely through the cerebrospinal fluid pathways and secondarily invaded the cerebrum. The diagnostic difficulties of diffuse meningeal gliomatosis are discussed.
    Notes: Zusammenfassung Beschreibung des klinischen Verlaufs und autoptischen Befundes bei einem Fall mit diffusem Oligodendrogliom, das die periventrikulären Regionen des Gehirns und den gesamten zerebro-spinalen Subarachnoidalraum befallen hat mit diffuser Infiltration des zerebralen Parenchyms. Außerdem war die ganze Länge des Thorakalmarkes befallen und die spinalen Meningen waren breit von Tumor infiltriert. Zusätzlich fand sich eine kleine lumbale Syringomyelie. Ausgangspunkt der diffusen Aussaat des Tumors entlang den äußeren und inneren Liquorräumen und mit sekundärer Invasion des Hirngewebes war wahrscheinlich ein thorakales intramedulläres Oligodendrogliom. Die diagnostischen Schwierigkeiten bei diffusen meningealen Gliomen und Gliomatosen, auch bezüglich der Bestimmung des Ausgangsbereiches, werden diskutiert.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 42 (1978), S. 5-32 
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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
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