Neuropatologia polska最新文献

The effect of a subtoxic level of quinolinic acid (QUIN) on the morphological picture of the rat hippocampus in dissociated cultures was investigated. Addition of 50 microM of QUIN to the culture medium induced only slight advanced and reversible changes of the postsynaptic elements, whereas the majority of pyramidal neurons were undamaged. The results suggest that subtoxic concentration of QUIN is insufficient to produce stable depolarization of cell membranes and severe neuronal damage.

An analysis of heavy metals content in the brain of a clinically unusual case of hepatolenticular degeneration was performed with the use of paramagnetic resonance. The studies established a manyfold increase of copper content in the brain in the form of free ions, and, less significant, also in the form of copper multi-ion clusters. The content of iron in the studied brain was lower than in controls. These results confirmed significantly the neuropathological diagnosis of hepato-lenticular degeneration.

Allogenic adrenal medullary tissue was implanted into the striatum of 68 rats. The material was evaluated by routine histological, histochemical, immunocytochemical as well as histofluorescence techniques 1, 3, 7, 14, 21 and 42 days after implantation. The viability of chromaffin cells continued through the 21st day after the implantation. The host brain tissue responded in two ways. First, by macrophagic resorption of the progressively necrotic graft in the experimental group and of the damaged area along the needle tract, noted both in experimental and control animals. This was accompanied by demarcation by proliferating reactive astrocytes and microglial cells. Second, by lymphocyte infiltration in the graft and around it, detected only in the experimental group which suggested immunological rejection.

A 21-year-old oligophrenic man developed after upper respiratory tract infection, quadriplegia with sphincter and respiratory disturbances. Lumbar punction revealed subarachnoid bleeding and elevated cerebrospinal protein level. Guillain-Barré syndrome and subarachnoid hemorrhage were diagnosed. At autopsy intraspinal angioma (C2-D6) and diastematomyelia (D11-lumbar segments) were found. Beside, intraspinal hemorrhage was present. Morphological examination of posterior and anterior spinal roots as well as peripheral nerves was done. Spheroids, axonal degeneration and prominent loss of myelinated fibers were observed in the proximal parts of the spinal roots. Axonal degeneration of myelinated fibers and regenerated fibers were noted in the distal parts of spinal roots and in peripheral nerves. Abnormal, fetal-like vessels were present in the spinal roots. Two mechanisms of acute and chronic changes (transneuronal and Wallerian degeneration) are discussed.

We report 2 cases of subacute sensory neuropathy (SSN) in small cell cancer of the lung. In both cases motor disturbances were caused by motor neuropathy and neuropathy as well. In both cases we observed altered immunoreactivity of the nervous tissue, suggesting the participation of humoral immunity in the tissue damage.

A 30-year-old man suffered for a year of a typical syndrome of cerebellar tumor. At suboccipital craniectomy a soft tumor infiltrating both hemispheres and vermis, filling up part of the IV ventricle was found. After subtotal removal of the neoplasm the postoperative course was poor and the patient died 5 weeks later. Biopsy material consisted of three types of tissue: 1. large nests of carrot-shaped, hyperchromatic cells, 2. fields of "halo" cells presenting myelin basic protein (MBP) immunoreactivity and 3. fields and scattered strongly GFAP-positive cells. The histological and immunocytochemical pattern of the neoplasm indicates differentiation of the tumor into oligodendrogliomatous and astrocytomatous line being an uncommon example of dual glial differentiation capability in medulloblastoma.

Neuropathological examination of six brains of newborns and infants who died in the course of congenital cyanotic cardiac anomalies showed focal brain lesions. The material included five cases from two weeks to two months of age, and one two-year-old infant. In two of them, the periventricular ischemic infarcts were found, in one multifocal encephalomalacia due to multiple vascular occlusions, and in three the necrotic foci corresponded to the supply of large cerebral arteries. The character and topography of severe brain lesions, particularly within the hemispheric white matter, were clearly influenced by the immaturity of the cerebral structures.

Effective doses of sodium valproate (200 mg/kg) applied in rats chronically (1, 3, 6, 9 and 12 months) evoked the first morphological changes in the brain hemispheres after 9 months of drug administration. Structural abnormalities of the brain tissue consisted in disseminated nonspecific neuronal lesions and patchy nerve cell loss, more pronounced in the final phase of the experiment. The neuronal lesions were localized predominantly in the 3rd and 5th layers of the neocortex and in the pyramidal cell layer of the hippocampus. They were accompanied by vascular wall alterations, perivascular tissue damage, as well as by microvacuolar changes and spongy degeneration of the subpial and periventricular regions. Vasogenic character of parenchymal changes is stressed by the authors. The possible influence of liver damage on the development of brain pathology is discussed.

The aim of the study is to present the damaging influence of toxoplasmic encephalitis on newborn brains. The material consisted of six cases of toxoplasmosis who died during the first months of life. The neuropathological picture indicated indirectly the mechanism of spread of the inflammatory-necrotic process. In the first stage of pathologic process intensive inflammatory infiltrations in the periventricular white matter were seen. In the next stage the necrotic changes involved the majority of the hemispheric white matter. Further development of the disease transformed the brain hemispheres into thin-walled sacs composed of meninges and remnants of the nervous system. Finally, the inflammatory process resulted in hydranencephaly. Proliferation of subependymal glia evident in all cases and blocking the pathways of the cerebro-spinal fluid circulation, may have played a role in this process.

Among the chronic idiopathic inflammatory myopathies inclusion body myositis (IBM) has emerged as a clinicopathologic variant. Slowly progressive weakness of the distal and the proximal muscle groups, the presence of rimmed vacuoles with basophilic granules as well as 15-18-nm filamentous inclusions in affected muscle confirm the clinical and histopathological distinction between inclusion body myositis and chronic polymyositis.