Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: A study using positron emission tomography (PET)

被引:94
作者
Kraus, MF
Smith, GS
Butters, M
Donnell, AJ
Dixon, E
Yilong, C
Marion, D
机构
[1] Univ Illinois, Dept Psychiat, Ctr Cognit Med, Chicago, IL 60612 USA
[2] N Shore Long Isl Jewish Hlth Syst, Zucker Hillside Hosp, New York, NY USA
[3] N Shore Long Isl Jewish Hlth Syst, Ctr Neurosci, N Shore Long Isl Jewish Res Inst, New York, NY USA
[4] Univ Pittsburgh, Med Ctr, Dept Psychiat, Pittsburgh, PA USA
[5] Univ Pittsburgh, Med Ctr, Dept Neurosurg, Pittsburgh, PA USA
[6] Boston Univ, Med Ctr, Dept Neurol Surg, Boston, MA USA
关键词
amantadine; traumatic brain injury; frontal lobes; executive function; positron emission tomography; dopamine;
D O I
10.1080/02699050400025059
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Primary objective: This study was performed to assess effects of amantadine (AMH), a dopaminergic agent and NMDA antagonist, on chronic traumatic brain injury (TBI). The primary hypotheses were that amantadine treatment would result in executive function improvement and increased activity in pre-frontal cortex. Research design: An open-label design was used. Methods: Twenty-two subjects underwent neuropsychological testing pre- and post-12 week treatment. Six subjects also underwent PET scanning. Intervention: Amantadine 400 mg was administered per day. Results: Significant improvements on tests of executive function were observed with treatment. Analysis of PET data demonstrated a significant increase in left pre- frontal cortex glucose metabolism. There was a significant positive correlation between executive domain scores and left pre- frontal glucose metabolism. Conclusions: This is the first known study to assess amantadine in chronic TBI using PET and the data are consistent with the hypotheses. The conduction of further studies is warranted.
引用
收藏
页码:471 / 479
页数:9
相关论文
共 47 条
[1]   SPECT brain perfusion abnormalities in mild or moderate traumatic brain injury [J].
Abdel-Dayem, HM ;
Abu-Judeh, H ;
Kumar, M ;
Atay, S ;
Naddaf, S ;
El-Zeftawy, H ;
Luo, JQ .
CLINICAL NUCLEAR MEDICINE, 1998, 23 (05) :309-317
[2]  
Abu-Judeh HH, 1998, J NUCL MED, V39, P1357
[3]   BRAIN-DAMAGE IN FATAL NON-MISSILE HEAD-INJURY [J].
ADAMS, JH ;
GRAHAM, D ;
SCOTT, G ;
PARKER, LS ;
DOYLE, D .
JOURNAL OF CLINICAL PATHOLOGY, 1980, 33 (12) :1132-1145
[4]  
Andersson Stein, 1992, Tidsskrift for den Norske Laegeforening, V112, P2070
[5]   CLINICAL PHARMACOKINETICS OF AMANTADINE HYDROCHLORIDE [J].
AOKI, FY ;
SITAR, DS .
CLINICAL PHARMACOKINETICS, 1988, 14 (01) :35-51
[6]   Verbal and design fluency in patients with frontal lobe lesions [J].
Baldo, JV ;
Shimamura, AP ;
Delis, DC ;
Kramer, J ;
Kaplan, E .
JOURNAL OF THE INTERNATIONAL NEUROPSYCHOLOGICAL SOCIETY, 2001, 7 (05) :586-596
[7]  
Benton A.L., 1994, Multilingual Aphasia Examination: Manual of instructions
[8]  
Benton AL, 1994, CONTRIBUTIONS NEUROP
[9]   Trapping channel block of NMDA-activated responses by amantadine and memantine [J].
Blanpied, TA ;
Boeckman, FA ;
Aizenman, E ;
Johnson, JW .
JOURNAL OF NEUROPHYSIOLOGY, 1997, 77 (01) :309-323
[10]   Functional magnetic resonance imaging of working memory impairment after traumatic brain injury [J].
Christodoulou, C ;
DeLuca, J ;
Ricker, JH ;
Madigan, NK ;
Bly, BM ;
Lange, G ;
Kalnin, AJ ;
Liu, WC ;
Steffener, J ;
Diamond, BJ ;
Ni, AC .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 2001, 71 (02) :161-168