EEG-Veränderungen bei einer INH-bedingten Psychose und nach einem Suicidversuch mit Nicoteben

Zusammenfassung Es werden 2 Fälle von INH-Intoxikationen geschildert. Einmal handelt es sich um ein psychotisches Bild, das bei einem Patienten mit einer kavernösen Lungentuberkulose und einer Lebercirrhose bei einer Dosierung von 5 mg/kg Körpergewicht/die auftrat. Anfälle stellten sich jedoch trotz einer alten traumatischen Epilepsie vom Jacksontyp mit sehr seltenen Iktus nicht ein.Im EEG zeigten sich zum Zeitpunkt der Psychose 1–2/sec-Wellen, die mehr an Formen beim Leberkoma erinnern. Anfallsmerkmale traten dagegen nicht auf.Im zweiten Fall handelt es sich um ein 15jähriges Mädchen, das mit 10 g INH einen Suicidversuch unternahm und in einen Status epilepticus kam. Zeichen einer erhöhten cerebralen Anfallsbereitschaft fanden sich im EEG noch 26 Tage nach der Intoxikation.Die unterschiedlichen EEG-Bilder wurden mit zweierlei Wirkungsweisen des INH, einmal über den Leberstoffwechsel, das andere Mal direkt auf das Zentralnervensystem, in Zusammenhang gebracht.Herrn Prof. Dr.Hans Frhr. v.Kress zum 60. Geburtstag gewidmet.     

Max Nonne zum Gedächtnis 13. 1. 1860–12. 8. 1959

Ohne Zusammenfassung     

MR imaging of the pericardial cyst.

Findings obtained with magnetic resonance (MR) imaging in four patients with pericardial cyst are reported. MR imaging allowed not only localization and diagnosis in all four cases but characterization of cystic content. MR imaging, including RARE (rapid acquisition with relaxation enhancement) MR hydrography, which shows only liquids with T2s greater than 500 msec, proved to be useful in characterizing the fluid content of a mediastinal lesion and monitoring follow-up. In one case, MR imaging allowed differentiation of a pericardial cyst from a suspected necrotic lymph node in a patient with colic carcinoma, with subsequent correction of staging and therapy. The authors conclude that MR imaging is the method of choice for diagnosis (especially in unusual locations) and monitoring of pericardial cysts and for differential diagnosis of malignant mediastinal cystic tumors that show a solid part.     

Almitrine prevents some hypoxia-induced metabolic injury in rat astrocytes

During reperfusion of ischemic brain tissue, the production of reactive oxygen species initiates several modifications of the astroglial functional and ultrastructural integrity. During 24 h after ischemic treatment, modification of cellular superoxide free radical scavenging systems have been observed in primary culture of rat astroglial cell. Mitochondrial Mn superoxide dismutase activity (Mn-SOD) gradually decreases, whereas that of the cytosolic Cu,Zn form of the enzyme remains unaffected. We observed in parallel a significant decrease of glutamine synthetase (GS), an astrocyte specifically located enzyme. Addition of almitrine (dialylamine-4′,6′-triazinyl 2′)-l-(bis-parafluorobenzydryl)-4-piperazine or dibucaine (a phospholipase A₂ inhibitor) antagonizes the decrease of Mn-SOD activity, but does not affect modification of GS activity. Combined effects are observed by simultaneous addition of both drugs. Our data demonstrate that almitrine may increase the synthesis of some mitochondrial proteins, like Mn-SOD, and provide support for further study on the therapeutic potential of almitrine in ischemic astroglial cell injury.     

Cells with neuronal properties in permanent cultures of quail embryo neuroretinas infected with rous sarcoma virus

Neuroretina cells from 7-day quail embryos infected 'in vitro' with the mutant ts NY-68 of Rous sarcoma virus, were established into permanent cultures. An initial stage of cellular proliferation was followed by a period of minimal multiplication. After recovery from this crisis, cell proliferation resumed. About 30% of the cells had binding sites for tetanus toxin and the monoclonal antibody A2B5 which seem to be specific for neurons, and an ultrastructural study suggested the presence of neurons and Müller (astroglial) cells. The specific activity of glutamic acid decarboxylase, the enzyme responsible for the synthesis of the neurotransmitter gamma-aminobutyric acid was high (10-30 nmol CO2/h/mg of protein) and electrophysiology showed that some cells had 'active' membranes. After about 18 months in culture, approximately 20% of the cells were able to respond to electrical stimulation by producing action potentials which were inhibited by 10(-7) M tetrodotoxin. These electrophysiological properties are stable: they have been repeatedly found at regular intervals throughout a 20 months period. Furthermore, a clone in which all tested cells are excitable, has been derived from the mass culture. Quail embryo neuroretina cells with typical neuronal properties can thus be established into permanent cultures after infection with Rous sarcoma virus.     

Relative contribution of intrinsic lung dysfunction and hypoventilation to hypoxemia during hemodialysis

Two mechanisms have been proposed to explain hemodialysis (HD)-induced hypoxemia: reversible lung damage due to intrapulmonary leukostasis as a consequence of the contact of blood with the dialyzer membrane, or alveolar hypoventilation due to the loss of carbon dioxide through the dialyzer. To assess the role of these factors, seven chronically uremic patients were studied before and during 4-hr HD sessions using a cuprophane membrane and either acetate (AHD) or bicarbonate (BHD) dialysate. In AHD only we observed, by comparison with predialysis values, a significant hypoxemia, and a decrease of alveolar ventilation (VA), lung carbon dioxide output, and respiratory exchange ratio. In both the AHD hypoxemic group and BHD nonhypoxemic group, there was a similar decrease in lung carbon dioxide diffusing capacity (DLCO) and of white blood cells (WBC), and a positive correlation between arterial oxygen pressure and VA without modification of alveolo arterial PO2 difference, an argument against the existence of ventilation-perfusion or ventilation-diffusion mismatching. We conclude that, although WBC sequestration induced a lung damage evidenced by DLCO impairment, the key factor of hypoxemia observed in AHD was the hypoventilation.