RESUMO
BACKGROUND: Wallenberg syndrome was first reported by Adolf Wallenberg as arising due to the obstruction of the posterior inferior cerebellar artery (PICA), which caused an infarct in the lateral medulla oblongata (MO). METHOD: This study was carried out on brain tissue from 2 patients with typical Wallenberg syndrome and 10 autopsy cases without central nervous system disturbances. RESULTS: Patient 1 exhibited the 3 major neurological symptoms of right crossed sensory disturbance, right cerebellar ataxia and bulbar palsy. There was the pathological obstruction of the right vertebral artery (VA). Regarding the histopathlogical distribution, the infarct extended on the right side to the lateral spinothalamic tract, nucleus of the spinal tract of the trigeminal nerve, spinal tract of the trigeminal nerve, inferior cerebellar peduncle, spinocerebellar tract and nucleus ambiguous. Moreover, a clear infarct in the left lateral MO was pathologically identified, but pathological obstruction of the left PICA or left VA could not be found. The left cerebellar ataxia and bulbar palsy were observed among these 3 major symptoms. Patient 2 showed the 3 major symptoms of right crossed sensory disturbance, right cerebellar ataxia and bulbar palsy. A pathological luminal occlusion was identified in the right PICA. Regarding the histopathological lesion, the infarct disturbed on the right side the lateral spinothalamic tract, nucleus of the spinal tract of the trigeminal nerve, spinal tract of the trigeminal nerve, spinocerebellar tract, inferior cerebellar peduncle and nucleus ambiguus. CONCLUSION: Based on our investigation of pathological lesions using our 2 autopsies, we suggest calling the cases that satisfy the following 3 criteria "definite pathologic Wallenberg syndrome": i) identifiable pathological obstruction of the PICA or VA; ii) infarction in the lateral MO based on PICA or VA obstruction; and iii) a 1-to-1 correspondence between clinical symptoms and neuropathological lesions.
RESUMO
We have produced a novel rat IgG(2a) monoclonal antibody against a stage-specific fetal brain glycoprotein of 68 kDa (FGP68), and succeeded in applying it to staining paraffin sections. To gain some insight into the pathobiological significance of this FGP68, this monoclonal antibody was used in immunohistochemical studies to compare the expression of FGP68 and Ki-67 antigen (MIB-1) in 235 primary brain tumors. Approximately half of the glioblastomas multiforme (GBMs) (44/75) and anaplastic astrocytomas (9/17) as well as some astrocytomas (5/30), medulloblastomas (2/14) and primitive neuroectodermal tumors (2/10) had tumor cells that expressed FGP68; however, pilocytic astrocytomas (0/7), oligodendrogliomas (0/15), ependymomas (0/6), schwannomas (0/21), meningiomas (0/22) and pituitary adenomas (0/18) did not express FGP68. The values of the MIB-1 labeling index were statistically higher in GBMs (0.005< P<0.01, Wilcoxon rank-sum test) and anaplastic astrocytomas (0.025< P<0.05) that expressed FGP68 than in those that did not. Normal brain tissue from 20 individuals aged 3-75 years was negative for FGP68 and MIB-1. We conclude that primary brain tumors express FGP68, one of the oncofetal proteins derived from fetal brain, and that FGP68 expression in certain brain tumor cells may depend, in part, on proliferation potential. Based on the possibility that the stage-specific FGP68 plays an important role in brain embryogenesis, some of FGP68-expressing tumor cells might phylogenetically revert to more primitive cells.
