Neuropatologia polska最新文献

The effect of the organic calcium channel blocker, verapamil, on quinolinic acid (QUIN) neurotoxicity in rat hippocampal cultures was studied. Verapamil and QUIN, both in 100 microns concentration, were added simultaneously to the culture medium. Ultrastructural analysis showed that verapamil was able to reduce typical QUIN-induced tissue damages. Especially, 3 and 7 days after exposure to the two agents, majority of both neurons and postsynaptic dendrites revealed normally appearing morphological features. The results support the suggestion of the important role of calcium entry in the development of QUIN neurotoxicity.

The authors report the clinical course and neuropathological findings in the case of hemiballismus due to leukemic infiltration of the subthalamic nucleus. The symptoms were observed in a 19-year-old patient with blastic phase of chronic myelogenous leukemia, two weeks before death, when what is called the "critical point" developed (white cell count beyond 100 G/l and thrombocytopenia less than 50 G/l). The investigation are considered to confirm the role of the "critical point" in the development of central nervous system leukemic complications.

Neuronal changes in Ammon's horn were examined immunocytochemically in 20 patients aged from 51 to 101 years, deceased in the course of ischemic lesions localized within the area supplied by vessels derived from other then Ammon's horn vascularization (middle cerebral artery). Numerous neurons within various sector of the pyramidal layer, in the dentate gyrus, subiculum and entorhinal cortex were immunopositive in reaction with antibodies to serum proteins (albumin, IgG, alpha-1-antitrypsin), indicating their damage. The distribution of damaged Ammon's horn pyramidal cells differed from the location of injured Ammon's horn neurons in experimental investigations of brain ischemia and did not indicate a selective vulnerability of pyramidal cells in the human h1 area, corresponding to the CA1 sector in animals. Contrary to experimental material, changes in the human Ammon's horn are caused by numerous overlapping factors.

The development processes coinciding in formation of cerebral cortex were presented. On this background may arise the cortical developmental abnormalities. The review of principal cortical malformations include the 1) agyria-pachygyria - lissencephaly type I, 2) polymicrogyria, 3) disorganized cortical structure - lissencephaly type II, 4) minor cortical developmental anomalies and 5) other cortical dysplasia syndromes. It will help to reconstruct the pathomechanism of cortical abnormal development from early occurring primary errors to late changes in which coincide necrotic lesions. The presented material illustrate the role of time of occurrence and intensity of damage in final result of pathologic developmental processes.

We report a comparison of the ultrastructural pathology of bovine spongiform encephalopathy, experimental scrapie in hamsters and a panencephalopathic model of Creuzfeldt-Jakob disease (CJD) in mice. Vacuoles in dendrites, intramyelinic vacuoles (myelin ballooning), dystrophic axons, phagocytic astrocytes and macrophages, differing in extent, were found in all three models. We conclude, that this axonal and myelin pathology is a phenomenon common to the three models of SSVE studied, and the differences between panencephalophatic CJD and polioencephalopathic BSE and scrapie are only quantitative.

Changes of inositol 1,4,5-trisphosphate content in the rat brain have been evaluated by means of the radioimmunologic method during 5-min clinical death and up to 2 hrs after resuscitation. Ischemia produced a decrease of IP3 content in the brain on the average to 63% of the control values. IP3 concentration in the brain increased on the average to 197% of the control values at the 15th min after resuscitation, and decreased to 127% at the 60 min. Two hours after resuscitation the IP3 content in the brain again increased on the average to 187%. The new data on brain metabolism in the ischemic conditions and the role of IP3 as the second messenger and mediator of neuromodulation processes are discussed.

Changes of cGMP content in the rat brain and plasma have been evaluated by means of the radioimmunologic method after 5-min clinical death and up to 2 hours after resuscitation. Ischemia produced a decrease of cGMP in the brain, however, at the 15th min after resuscitation a reversible significant rise of nucleotide concentration was noted. In plasma at the end of ischemia and in the postischemic period a significant decrease of cGMP level was observed. The mechanisms of cGMP regulation in the central nervous system and the significance of the obtained results are discussed.

Coexistence of several developmental abnormalities in adults is very rare and often asymptomatic. In many instances appearance of clinical symptomatology is evoked by some additional factors, not related directly with the basic pathological process. In a 21-year-old oligophrenic man a progressive paresis of inferior limbs appeared in the course of the upper respiratory tract infection. During 5 days of hospitalization transient peripheral paresis of the right facial nerve, tetraplegia, sphincter and respiratory disturbances occurred. Guillain-Barré syndrome and subarachnoid hemorrhage were diagnosed. On autopsy hemorrhagic focus in the medulla and in the cervical and upper thoracic parts of the spinal cord was found. Microscopic examination revealed hypocellularity of the 2nd and 4th layers of the temporal cortex, presence of the central canal within the brain stem, and hemorrhagic focus in the medulla. Two malformations in spinal cord were revealed: intraspinal angioma extending from the C2 to the Th6 segments and diastematomyelia within Th11 and lumbar segments. Diastematomyelia, cortical hypocellularity and angioma composed of fetal, lacunar artery- and vein-like vessels, are related with different periods of the ontogenic development. Coexistence of these malformations indicates prolonged action of the pathogenic factor(s), both in the embryonic and fetal life.

The frequency and distribution of intravascular coagulation (IVC) were studied in brains of 121 patients who had died due to acute myeloblastic leukemias type M1 or M2. The IVC within the brain was observed in 59% of cases, more frequently in patients treated with polychemotherapy, especially according to TAD or VAPA protocols. The microthrombi were found predominantly in capillaries and small venous vessels. IVC was more frequent in cerebral and cerebellar white matter and in the neighbourhood of lateral ventricles (hippocampus, thalamus). In patients who had developed brain hemorrhage in the course of primary neoplasmic disease IVC was very frequent phenomenon, thus IVC is considered to be an important factor in the development of CNS hemorrhages in myeloblastic leukemias, irrespective of thrombocytopenia related to bone marrow involvement.