Putamen hypertrophy in nondemented patients with human immunodeficiency virus infection and cognitive compromise

被引:47
作者
Castelo, J. Mimi Boer
Courtney, Maureen G.
Melrose, Rebecca J.
Stern, Chantal E.
机构
[1] Boston Univ, Ctr Memory & Brain, Neuroimaging Lab, Boston, MA 02215 USA
[2] Harvard Univ, Sch Med, Charlestown, MA USA
[3] Massachusetts Gen Hosp, Ctr Biomed Imaging, Charlestown, MA USA
关键词
D O I
10.1001/archneur.64.9.1275
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Documented death and dysfunction of basal ganglia cells in patients seropositive for human immunodeficiency virus (HIV) suggest that the virus may cause structural compromise to these regions. Objectives: To examine subcortical volumes in non-demented patients seropositive for HIV (HIV+) by means of a novel automated neuroanatomic morphometric analysis tool, and to investigate relationships among cognitive function, immune health, and subcortical volumes. Design and Setting: Cross-sectional study of subcortical morphometry and cognitive function conducted at the Boston University Center for Memory and Brain and the Massachusetts General Hospital Athinoula A. Martinos Center for Biomedical Imaging. Patients: Twenty-two nondemented HIV+ patients and 22 age- and education-matched healthy control participants. Main Outcome Measures: Subcortical segmentation volumes, neuropsychological performance, and immunological variables. Results: Nondemented HIV+ patients demonstrated relative and isolated putamen hypertrophy compared with control participants. Putamen volume enlargement in HIV+ patients was related to motor slowing and immune status, such that higher CD4 lymphocyte levels were associated with larger putamen volumes. There were no other subcortical volume differences between the groups. Conclusions: This study suggests that basal ganglia hypertrophy accompanies HIV-related mild cognitive compromise. These findings may represent a structural imaging parallel to functional imaging studies demonstrating basal ganglia hypermetabolism in HIV+ patients with mild cognitive compromise and early HIV-associated brain disease.
引用
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页码:1275 / 1280
页数:6
相关论文
共 27 条
[1]  
[Anonymous], 1992, MMWR Recomm Rep, V41, P1
[2]   Influence of HAART on HIV-related CNS disease and neuroinflammation [J].
Anthony, IC ;
Ramage, SN ;
Carnie, FW ;
Simmonds, P ;
Bell, JE .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2005, 64 (06) :529-536
[3]   MOTOR DYSFUNCTION IN HIV-INFECTED PATIENTS WITHOUT CLINICALLY DETECTABLE CENTRAL-NERVOUS DEFICIT [J].
ARENDT, G ;
HEFTER, H ;
ELSING, C ;
STROHMEYER, G ;
FREUND, HJ .
JOURNAL OF NEUROLOGY, 1990, 237 (06) :362-368
[4]   REDUCED BASAL GANGLIA VOLUME IN HIV-1 ASSOCIATED DEMENTIA - RESULTS FROM QUANTITATIVE NEUROIMAGING [J].
AYLWARD, EH ;
HENDERER, JD ;
MCARTHUR, JC ;
BRETTSCHNEIDER, PD ;
HARRIS, GJ ;
BARTA, PE ;
PEARLSON, GD .
NEUROLOGY, 1993, 43 (10) :2099-2104
[5]   HIV dementia: the role of the basal ganglia and dopaminergic systems [J].
Berger, JR ;
Arendt, G .
JOURNAL OF PSYCHOPHARMACOLOGY, 2000, 14 (03) :214-221
[6]  
BLAIR J, 1989, NEW ADULT READING TE
[7]   A multicenter in vivo proton-MRS study of HIV-associated dementia and its relationship to age [J].
Chang, L ;
Lee, PL ;
Yiannoutsos, CT ;
Ernst, T ;
Marra, CM ;
Richards, T ;
Kolson, D ;
Schifitto, G ;
Jarvik, JG ;
Miller, EN ;
Lenkinski, R ;
Gonzalez, G ;
Navia, BA .
NEUROIMAGE, 2004, 23 (04) :1336-1347
[8]   Different effects of typical and atypical antipsychotics on grey matter in first episode psychosis:: the ÆSOP study [J].
Dazzan, P ;
Morgan, KD ;
Orr, K ;
Hutchinson, G ;
Chitnis, X ;
Suckling, J ;
Fearon, P ;
McGuire, PK ;
Mallett, RM ;
Jones, PB ;
Leff, J ;
Murray, RM .
NEUROPSYCHOPHARMACOLOGY, 2005, 30 (04) :765-774
[9]   Whole brain segmentation: Automated labeling of neuroanatomical structures in the human brain [J].
Fischl, B ;
Salat, DH ;
Busa, E ;
Albert, M ;
Dieterich, M ;
Haselgrove, C ;
van der Kouwe, A ;
Killiany, R ;
Kennedy, D ;
Klaveness, S ;
Montillo, A ;
Makris, N ;
Rosen, B ;
Dale, AM .
NEURON, 2002, 33 (03) :341-355
[10]  
Heaton R K, 1995, J Int Neuropsychol Soc, V1, P231