Jaspers' psychopathology.
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Biomedical subjects
Publications and source records attributed to M Langenbach.
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Congenital, spinal, epidural cysts are rare causes of transverse or radicular spinal lesions. Usually these cysts are located in the thoracal region, are oblong-shaped, and extend over several segments dorsally to the cord. Frequently, they cause no symptoms for years. They are fairly accessible to diagnostics by modern neuro-imaging methods. We report on a 15 year old girl with paraparesis, which showed a slow progression over two years, short-term remissions, and finally impairment of bladder function. Myelogram, computer-assisted tomography and nuclear magnetic resonance tomography showed a large space-occupying mass from D8 to L1 epidural and dorsal of the myelon. Operation disclosed an epidural cyst from D10 to L2. Histologically, the removed material was classified as a meningeal cyst. Post-operatively the girl's condition improved under intensive physio-therapy. For the diagnosis of this spinal dysrhapic disorder CT scanning after intrathecal application of contrast medium and magnetic resonance imaging were most valuable.
The leakage of eight different serum proteins and immunoglobulins across the blood-nerve barrier (BNB) was studied by means of the peroxidase-antiperoxidase method in hereditary and inflammatory neuropathies and graded semiquantitatively with respect to endoneurial staining intensity and distribution. These data were compared with the degree of alterations of the myelinated nerve fibre population evaluated by morphometric analysis. Our series of 18 human sural nerve biopsies included seven hereditary neuropathies (three HMSN I, two HMSN II, two tomaculous neuropathies), nine inflammatory neuropathies (seven polyneuritis, two hypertrophic neuritis) and two normal controls. In HMSN II and in tomaculous neuropathy there was no enhanced endoneurial staining for serum proteins despite of a severe nerve fibre loss, whereas in HMSN I a rise of serum proteins of small and moderate molecular size like albumin and IgG was demonstrated in the endoneurial space indicating an impaired BNB function. Qualitative changes of the BNB with leakage also of high molecular weight proteins were observed in polyneuritis and hypertrophic neuritis, irrespective of the degree of nerve fibre changes. Our results show that fibre loss and alteration of the BNB are not correlated. The unselective leakage of serum proteins through the BNB appears to be a characteristic change in inflammatory neuropathies leading to proteinous edema. With regard to the subperineurial accentuation of the endoneurial edema it will be discussed that the vascular diffusion barrier is more fragile than the perineurial diffusion barrier.