Tags

Type your tag names separated by a space and hit enter

Clinical and neuropathological correlates of Lewy body disease.
Acta Neuropathol. 2003 Apr; 105(4):341-50.AN

Abstract

We investigated distribution of neuronal and glial inclusions in 30 brains obtained at autopsy from patients with Lewy bodies (LBs) disease, which was clinically diagnosed as Parkinson's disease (PD), dementia with Lewy bodies (DLB), or pure autonomic failure (PAF). The cases were classified, according to the guidelines for the pathological diagnosis of DLB, into three types: the neocortical type, the limbic type, and the brain stem-predominant type. All postmortem brains had coil-like glial inclusions as well as LBs, and the distribution pattern and density of glial inclusions and LBs varied. The distribution of glial inclusions was strikingly similar to that of LBs. In the cerebral cortex in particular, the number of glial inclusions was fairly well correlated with the number of LBs, irrespective of the three pathological types. In the brain stem, distribution was similar between glial inclusions and LBs, and there was no distinct pathological difference among the three types. Glial inclusions and LBs were immunohistopathologically similar with respect to ubiquitin, alpha-synuclein, and Gallyas-Braak staining. The clinical features of the three types of LB disease were also similar; i.e., parkinsonism, some dementia, and/or autonomic failure. The inclusions in neurons and glial cells occurred in parallel with respect to tissue distribution and immunohistochemical features, suggesting that accumulation of neuronal and glial inclusions in the LB diseases have a common pathological feature. Our findings suggest that DLB, PD with and without dementia, and PAF share one clinicopathological entity.

Authors+Show Affiliations

Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, 466-8550 Nagoya, Japan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

12624787

Citation

Hishikawa, Nozomi, et al. "Clinical and Neuropathological Correlates of Lewy Body Disease." Acta Neuropathologica, vol. 105, no. 4, 2003, pp. 341-50.
Hishikawa N, Hashizume Y, Yoshida M, et al. Clinical and neuropathological correlates of Lewy body disease. Acta Neuropathol. 2003;105(4):341-50.
Hishikawa, N., Hashizume, Y., Yoshida, M., & Sobue, G. (2003). Clinical and neuropathological correlates of Lewy body disease. Acta Neuropathologica, 105(4), 341-50.
Hishikawa N, et al. Clinical and Neuropathological Correlates of Lewy Body Disease. Acta Neuropathol. 2003;105(4):341-50. PubMed PMID: 12624787.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Clinical and neuropathological correlates of Lewy body disease. AU - Hishikawa,Nozomi, AU - Hashizume,Yoshio, AU - Yoshida,Mari, AU - Sobue,Gen, Y1 - 2003/01/14/ PY - 2002/08/21/received PY - 2002/10/22/revised PY - 2002/10/22/accepted PY - 2003/3/8/pubmed PY - 2003/5/13/medline PY - 2003/3/8/entrez SP - 341 EP - 50 JF - Acta neuropathologica JO - Acta Neuropathol VL - 105 IS - 4 N2 - We investigated distribution of neuronal and glial inclusions in 30 brains obtained at autopsy from patients with Lewy bodies (LBs) disease, which was clinically diagnosed as Parkinson's disease (PD), dementia with Lewy bodies (DLB), or pure autonomic failure (PAF). The cases were classified, according to the guidelines for the pathological diagnosis of DLB, into three types: the neocortical type, the limbic type, and the brain stem-predominant type. All postmortem brains had coil-like glial inclusions as well as LBs, and the distribution pattern and density of glial inclusions and LBs varied. The distribution of glial inclusions was strikingly similar to that of LBs. In the cerebral cortex in particular, the number of glial inclusions was fairly well correlated with the number of LBs, irrespective of the three pathological types. In the brain stem, distribution was similar between glial inclusions and LBs, and there was no distinct pathological difference among the three types. Glial inclusions and LBs were immunohistopathologically similar with respect to ubiquitin, alpha-synuclein, and Gallyas-Braak staining. The clinical features of the three types of LB disease were also similar; i.e., parkinsonism, some dementia, and/or autonomic failure. The inclusions in neurons and glial cells occurred in parallel with respect to tissue distribution and immunohistochemical features, suggesting that accumulation of neuronal and glial inclusions in the LB diseases have a common pathological feature. Our findings suggest that DLB, PD with and without dementia, and PAF share one clinicopathological entity. SN - 0001-6322 UR - https://www.unboundmedicine.com/medline/citation/12624787/Clinical_and_neuropathological_correlates_of_Lewy_body_disease_ L2 - https://dx.doi.org/10.1007/s00401-002-0651-4 DB - PRIME DP - Unbound Medicine ER -