Paraneoplastic syndrome simulating encephalitis in the course of testicular seminoma.

A case of paraneoplastic syndrome diagnosed post mortem in a 68-year-old man with a single submandibular lymphatic metastasis of testicular seminoma is presented. The syndrome developed 3 years after orchidectomy and clinically combined the features of limbic and bulbar encephalitis together with signs of cerebellar degeneration. Histological examination revealed marked loss of cerebellar Purkinje and granular cells and to a lesser extent of cerebral cortical neurons. Additionally axonal injury (spheroids) and multifocal demyelination with sparse lymphocytic infiltrations was observed. Immunohistochemically, strong reaction with monoclonal anti-human IgG in some neurons of cerebellum was detected whereas the reaction with anti-complement (C3b) receptor in corresponding sections was negative. It is suggested that the presented case may represent a "burn out" stage of paraneoplastic syndrome associated with anti-neuronal antibodies, however the isolation of specific antibodies was not performed.

[Spontaneous spinal epidural hematoma. Report of two cases]. / Nieurazowe krwiaki nadtwardówkowe kanalu kregowego. Opis dwóch przypadków.

In the paper 2 cases of non-traumatic spinal epidural haematomas are presented. The possible aetiological factors--vascular malformation, coagulopathy, anticoagulants and neoplasm are discussed. Neurological state, diagnostic procedure and treatment are described. Taking into account our experience we state that only early diagnosis and operation-surgical decompression of spinal cord, could result in complete recovery.

Immunocytochemical analysis of cellular infiltrates in primary glial and metastatic tumors in human brain.

Forty eight human brain tumors: 31 primary glial tumors and 17 metastasizing neoplasms were submitted for an immunocytochemical characterization of mononuclear cell infiltrates in tumor tissue and in its surroundings, with antibodies CD 68, CD45RO, UHCL1, EMB11, CD21 and OPD4. It was found that cells were mainly marked with CD68 and CD45RO, UHCL1. The counting of the marked and unmarked mononuclear cells proved that there is a high degree of variability in cell density which is tumor type and case depended. The results indicate that there were fewer cells which reacted to the antibody EMB11 as compared with cells marked with other antibodies. With CD21 and OPD4 only single cells were marked. A great number of cells remained unmarked. There was a significant difference between the primary glial and the metastatic tumors as far as the number of marked cells is concerned. It is suggested that the difference between primary and metastatic tumors in the number of mononuclear cell infiltrates can be connected with a possibility that the metastatic tumor will present its antigenicity easier as compared with primary tumors of glial origin.

Vascular endothelial growth factor and its receptor, KDR, in human brain tissue after ischemic stroke.

Ischemic stroke results from a reduction in cerebral blood flow to a focal region of the brain after the occlusion of an artery, causing damage to nervous tissue. There is a region of cerebral ischemic tissue (penumbra) surrounding an acute cerebral infarct that is dysfunctional but potentially viable. Restoration of perfusion in the penumbra may ameliorate the tissue damage. The identity and the role of growth factors that control the extent of tissue damage and its repair are poorly understood. Angiogenesis has been demonstrated to occur in brain tissues of patients surviving an acute ischemic stroke. In this paper we have investigated the status of a potent angiogenesis factor, vascular endothelial growth factor (VEGF), in patients after acute ischemic brain stroke. Western blotting and immunohistochemistry were used to determine protein expression, and in situ hybridization was used to quantify and localize mRNA synthesis. The expression of VEGF protein was increased in the penumbra compared with infarcted brain and contralateral hemisphere. Neurones, endothelial cells, and astrocytes in the penumbra in all patients studied had significant up-regulation of both VEGF165 and VEGF189 mRNA (p < 0.01, Wilcoxon Matched-Pairs Signed-Ranks Test) compared with infarcted tissue and the normal looking contralateral hemisphere that was used as a control. Immunohistochemistry demonstrated that kinase insert domain receptor was present in blood vessels within the infarct/penumbra and absent from the normal contralateral hemisphere. VEGF, which is important in angiogenesis, may also influence long term neuronal survival, and possibly its modulation may prove to be of therapeutic value for patients with ischemic stroke.

A putative role for platelet-derived growth factor in angiogenesis and neuroprotection after ischemic stroke in humans.

BACKGROUND AND PURPOSE: Growth factors control two important processes in infarcted tissue, ie, angiogenesis and gliosis. We recently reported that transforming growth factor-beta1 (TGF-beta1) might be involved in angiogenesis after ischemic stroke in humans; here we present data of an extensive study on platelet-derived growth factor (PDGF) and its receptors. METHODS: We studied brain samples from patients who suffered from ischemic stroke for the expression of mRNA encoding PDGF-A, PDGF-B, and PDGF receptors (PDGF-R). Proteins were examined by Western blotting and immunohistochemistry using the antibodies to PDGF-AB, PDGF-BB, PDGF-R alpha, and PDGF-R beta. RESULTS: At the mRNA level, PDGF-A and PDGF-B were expressed mainly in neurons in penumbra. PDGF-R mRNA was strongly expressed in some astrocytes but mainly in type III/IV neurons in infarct and penumbra. The least expression was seen in the contralateral hemisphere (P<.001). In contrast, both PDGF-AB and PDGF-BB immunoreactive products were present in most cell types: PDGF-R alpha and PDGF-R beta mainly on neurons, and PDGF-R beta on some endothelial cells, with less staining of all the isoforms in the contralateral hemisphere. On Western blots, PDGF-AB and -BB were expressed more within white matter than gray matter of infarct/penumbra, whereas both isoforms of receptor were expressed mainly in gray matter compared with contralateral hemisphere. There was no or very weak expression of the receptor in white matter. CONCLUSIONS: PDGF proteins are highly expressed in white matter, suggesting that PDGF may exert its function in white matter participating either in regeneration of damaged axons or in glial scar formation. PDGF-BB and its receptor expressed on microvessel endothelial cells might be involved in angiogenesis after stroke. Thus, PDGF is likely to be angiogenic and neuroprotective in stroke.