SERIAL CHANGES OF CEREBRAL GLUCOSE-METABOLISM AND CAUDATE SIZE IN PERSONS AT RISK FOR HUNTINGTONS-DISEASE

被引:123
作者
GRAFTON, ST
MAZZIOTTA, JC
PAHL, JJ
STGEORGEHYSLOP, P
HAINES, JL
GUSELLA, J
HOFFMAN, JM
BAXTER, LR
PHELPS, ME
机构
[1] UNIV CALIF LOS ANGELES,SCH MED,DIV NUCL MED & BIOPHYS,LOS ANGELES,CA 90024
[2] UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024
[3] UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024
[4] UNIV CALIF LOS ANGELES,SCH MED,DEPT ENERGY,NUCL MED LAB,LOS ANGELES,CA 90024
[5] MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114
[6] UNIV OKLAHOMA,DEPT PSYCHIAT,OKLAHOMA CITY,OK
[7] DUKE UNIV,DIV NUCL MED,DURHAM,NC 27706
[8] UNIV TORONTO,DEPT NEUROL,TORONTO M5S 1A1,ONTARIO,CANADA
[9] UNIV TORONTO,DEPT MED,TORONTO M5S 1A1,ONTARIO,CANADA
关键词
D O I
10.1001/archneur.1992.00530350075022
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective.-To determine the rate of change of glucose metabolism and caudate size in persons at risk for Huntington's disease. Design-Eighteen persons at risk for Huntington's disease had two positron emission tomographic glucose metabolic studies and two magnetic resonance imaging scans separated by 42 (+/-9) months. Setting.-Ambulatory research subjects at a teaching hospital with magnetic resonance imaging and positron emission tomographic technology. Subjects.-Seven of the individuals were Huntington' disease gene negative by testing at the polymorphic DNA loci D4S10, D4S43, and D4S125; the remainder were gene positive by genetic testing or onset of chorea after study entry. Interventions.-None. Outcome Measures.-Onset of chorea and imaging results. Results.-The gene-positive group demonstrated a significant 3.1% loss of glucose metabolic rate per year in the caudate nucleus (95% confidence interval [CI], -4.64, -1.48) compared with the gene-negative group. There was a 3.6% per year increase in the magnetic resonance imaging bicaudate ratio (95% CI, 1.81, 5.37), a linear measure of caudate atrophy. The rate of change in caudate size did not correlate with the rate of change in caudate metabolism, suggesting that metabolic loss and atrophy may develop independently. Conclusions.-The results suggest that a reduction in caudate glucose metabolism and atrophy develop rapidly in Huntington's disease. The findings establish a strategy for using serial positron emission tomographic imaging to monitor experimental pharmacologic interventions in presymptomatic individuals who have developed caudate hypometabolism.
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收藏
页码:1161 / 1167
页数:7
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