Neuropathology : official journal of the Japanese Society of Neuropathology
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Comparative Study
Early metabolic reactivation versus antioxidant therapy after a traumatic spinal cord injury in adult rats.
Disability after traumatic spinal cord injury (TSCI) results from physical trauma and from "secondary mechanisms of injury" such as low metabolic energy levels, oxidative damage and lipid peroxidation. In order to prove if early metabolic reactivation is a better therapeutic option than antioxidant therapy in the acute phase of TSCI, spinal cord contusions were performed in adult rats using a well-characterized weight drop technique at thoracic 9 level. After TSCI, pyrophosphate of thiamine or non-degradable cocarboxylase (NDC) enzyme was used to maintain energy levels, antioxidants such as superoxide dismutase and catalase (ANT) were used to decrease oxidative damage and methylprednisolone (MP), which has both therapeutic properties, was used as a control. ⋯ In contrast, NDC treatment increased lipid peroxidation, measured through thiobarbituric acid reactive substances (TBARS) levels, as well as spinal cord tissue destruction and functional deficit. Early metabolic reactivation after a TSCI may be deleterious, while natural early metabolic inhibition may not be a "secondary mechanism of injury" but a "secondary neuroprotective response". While increased antioxidant defence after a TSCI may currently be an ideal therapeutic strategy, the usefulness of metabolic reactivation should be tested in the sub-acute or chronic phases of TSCI and new strategies must continue to be tested for the early ones.
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Case Reports
Primary central nervous system lymphoma initially mimicking lymphomatosis cerebri: an autopsy case report.
A 59-year-old immunocompetent man was admitted to our hospital because of progressive dementia with concomitant bilateral uveitis. The first brain MRI revealed diffuse hyperintense lesions in the cerebral white matter of both hemispheres on a T2-weighted image and fluid-attenuated inversion recovery image. However, another MRI taken more than 1 month later revealed enhanced cohesive mass lesions in the bilateral thalami, in addition to the white matter lesions. ⋯ Pathological diagnosis was diffuse large B-cell lymphoma with perivascular proliferation and diffuse scattered infiltration in the cerebrum and brainstem. Microscopically, cohesive mass lesions in the bilateral thalami were a massive cluster of lymphoma cells. This is a case of primary CNS lymphoma (PCNSL) mimicking 'lymphomatosis cerebri (LC)' at first but later exhibiting typical mass lesions, giving rise to the possibility that cases of LC might unmask features of regular lymphomas in their later course more often than believed thus far.
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Up to February 2008, a total of 132 patients with dura mater graft-associated Creutzfeldt-Jakob disease (dCJD) have been identified in Japan, accounting for a majority of the world's patients with dCJD. The patients received dura mater grafts from 1978 to 1993. Lyodura (B. ⋯ The plaque type accounted for one-third of the pathologically confirmed or clinically diagnosed cases of dCJD. The non-plaque type was associated with methionine homozygosity at codon 129 (129M/M) of the PrP gene in all patients, except for in one patient with the 129M/valine (V) genotype and type 1 protease-resistant PrP (PrP(res)), whereas the plaque type was always associated with the 129M/M genotype and the intermediate type between types 1 and 2 of PrP(res) in all cases. Thus, the clinicopathological and molecular features of the plaque type are distinct from those of the non-plaque type, suggesting contamination of the dura mater grafts with different prion strains.
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J1-31 is one of the astrocytic proteins, the expression of which has not been evaluated in astrocytomas. In the present study, we studied the expression of J1-31 protein in astrocytes and astrocytomas in comparison with GFAP, p53 and Ki-67. Materials consisted of formalin-fixed paraffin-embedded tissue specimens that included five cases of normal brain, 17 of gliosis, 15 of pilocytic astrocytoma (WHO grade I), 26 of low-grade diffuse astrocytoma (WHO grade II), four of anaplastic astrocytoma (WHO grade III), and eight of glioblastoma (WHO grade IV). ⋯ In conclusion, down-regulation of J1-31 expression correlates with advancing grade of astrocytomas. The result suggests this protein plays some role in astrocytes that is progressively lost in malignant progression. The anti-J1-31 antibody may help further our understanding of astrocytes in disease and may be useful as an aid in the pathologic diagnosis of astrocytic lesions.