Primary motor cortex involvement in Alzheimer disease

被引:82
作者
Suvà, D [1 ]
Favre, I
Kraftsik, R
Esteban, M
Lobrinus, A
Miklossy, J
机构
[1] CHU Vaudois, Inst Pathol, Div Neuropathol, CH-1011 Lausanne, Switzerland
[2] Univ Lausanne, Inst Biol Cellulaire & Morphol, Lausanne, Switzerland
关键词
Alzheimer disease; associative cortex; neurofibrillary tangle; primary motor cortex; primary sensory cortex; pyramidal signs; senile plaques;
D O I
10.1097/00005072-199911000-00002
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
In Alzheimer disease (AD) the involvement of entorhinal cortex, hippocampus, and associative cortical areas is well established. Regarding the involvement of the primary motor cortex the reported data are contradictory. In order to determine whether the primary motor cortex is involved in AD, the brains of 29 autopsy cases were studied, including, 17 cases with severe cortical AD-type changes with definite diagnoses of AD 7 age-matched cases with discrete to moderate cortical AD-type changes, and 5 control cases without any AD-type cortical changes. Morphometric analysis of the cortical surface occupied by senile plaques (SPs) on beta-amyloid-immunostained sections and quantitative analysis of neurofibrillary tangles (NFTs) on Gallyas-stained sections was performed in 5 different cortical areas including the primary motor cortex. The percentage of cortical surface occupied by SPs was similar in all cortical areas, without significant difference and corresponded to 16.7% in entorhinal cortex, 21.3% in frontal associative, 16% in parietal associative, and 15.8% in primary motor cortex. The number of NFTs in the entorhinal cortex was significantly higher (41 per 0.4 mm(2)), compared with those in other cortical areas (20.5 in frontal, 17.9 in parietal and 11.5 in the primary motor cortex). Our findings indicate that the primary motel cortex is significantly involved in AD and suggest the appearance of motor dysfunction in late and terminal stages of the disease.
引用
收藏
页码:1125 / 1134
页数:10
相关论文
共 42 条
[21]   SELECTIVE DISCONNECTION OF SPECIFIC VISUAL ASSOCIATION PATHWAYS IN CASES OF ALZHEIMERS-DISEASE PRESENTING WITH BALINTS SYNDROME [J].
HOF, PR ;
BOURAS, C ;
CONSTANTINIDIS, J ;
MORRISON, JH .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1990, 49 (02) :168-184
[22]   AMYOTROPHIC-LATERAL-SCLEROSIS AND PARKINSONISM-DEMENTIA FROM GUAM - DIFFERENCES IN NEUROFIBRILLARY TANGLE DISTRIBUTION AND DENSITY IN THE HIPPOCAMPAL-FORMATION AND NEOCORTEX [J].
HOF, PR ;
PERL, DP ;
LOERZEL, AJ ;
STEELE, JC ;
MORRISON, JH .
BRAIN RESEARCH, 1994, 650 (01) :107-116
[23]   DISTRIBUTION OF CORTICAL NEUROFIBRILLARY TANGLES IN PROGRESSIVE SUPRANUCLEAR PALSY - A QUANTITATIVE-ANALYSIS OF 6 CASES [J].
HOF, PR ;
DELACOURTE, A ;
BOURAS, C .
ACTA NEUROPATHOLOGICA, 1992, 84 (01) :45-51
[24]   QUANTITATIVE-ANALYSIS OF A VULNERABLE SUBSET OF PYRAMIDAL NEURONS IN ALZHEIMERS-DISEASE .1. SUPERIOR FRONTAL AND INFERIOR TEMPORAL CORTEX [J].
HOF, PR ;
COX, K ;
MORRISON, JH .
JOURNAL OF COMPARATIVE NEUROLOGY, 1990, 301 (01) :44-54
[25]   FOCAL ALZHEIMERS-DISEASE [J].
JAGUST, WJ ;
DAVIES, P ;
TILLERBORCICH, JK ;
REED, BR .
NEUROLOGY, 1990, 40 (01) :14-19
[26]  
Kemper T., 1984, CLIN NEUROLOGY AGING, P9
[27]   DIAGNOSIS OF ALZHEIMERS-DISEASE [J].
KHACHATURIAN, ZS .
ARCHIVES OF NEUROLOGY, 1985, 42 (11) :1097-1104
[28]  
MCKHANN G, 1984, NEUROLOGY, V34, P939, DOI 10.1212/WNL.34.7.939
[29]   Curly fiber and tangle-like inclusions in the ependyma and choroid plexus - A pathogenetic relationship with the cortical Alzheimer-type changes? [J].
Miklossy, J ;
Kraftsik, R ;
Pillevuit, O ;
Lepori, D ;
Genton, C ;
Bosman, FT .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1998, 57 (12) :1202-1212
[30]   THE CONSORTIUM TO ESTABLISH A REGISTRY FOR ALZHEIMERS-DISEASE (CERAD) .2. STANDARDIZATION OF THE NEUROPATHOLOGIC ASSESSMENT OF ALZHEIMERS-DISEASE [J].
MIRRA, SS ;
HEYMAN, A ;
MCKEEL, D ;
SUMI, SM ;
CRAIN, BJ ;
BROWNLEE, LM ;
VOGEL, FS ;
HUGHES, JP ;
VANBELLE, G ;
BERG, L .
NEUROLOGY, 1991, 41 (04) :479-486