Motor cortex excitability correlates with an anxiety-related personality trait

被引:104
作者
Wassermann, EM
Greenberg, BD
Nguyen, MB
Murphy, DL
机构
[1] NINDS, Brain Stimulat Unit, NIH, Bethesda, MD 20892 USA
[2] Brown Univ, Dept Psychiat & Human Behav, Providence, RI 02912 USA
[3] NIMH, Clin Sci Lab, NIH, Bethesda, MD 20892 USA
关键词
transcranial magnetic stimulation; motor cortex; obsessive-compulsive disorder; anxiety disorders; GABA; sex differences;
D O I
10.1016/S0006-3223(01)01210-0
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background: In an earlier study comparing obsessive-compulsive disorder (OCD) patients to psychiatrically screened normals, we found lowered motor evoked potential (MEP) threshold to transcranial magnetic stimulation (THS) and decreased intracortical inhibition in OCD. We sought to determine whether this pattern was specific to OCD. Methods: We measured the threshold and amplitude of MEPs to single and paired (subthreshold-suprathreshold; 3, 4, 10, 15 msec intervals) TMS in 46 healthy volunteers (23 women, 23 men) who were given the NEO-PI-R personality inventory. Nineteen of the men also received cognitive and motor tests. Results: The paired-pulse conditioned/unconditioned MEP amplitude ratios correlated with Neuroticism (N), a stable measure of trait-level anxiety and other negative emotions, in the whole sample (r = 0.48; p = 0.0006), and in the men (r = 0.63; p = 0.0009). There were no other significant correlations. Conclusions: This relationship reflects a factor that contributes to both personality and cortical regulation. It was not statistically significant in women, probably because of confounding hormonal influences on excitability. Decreased intracortical inhibition may be related more to trait anxiety and depression, which are high in OCD, than to OCD itself. However, the MEP threshold (significantly lowered in OCD) was unrelated to N. Biol Psychiatry 2001;50:377-382 (C) 2001 Society, of Biological Psychiatry.
引用
收藏
页码:377 / 382
页数:6
相关论文
共 34 条
[1]   5-HT2 receptor regulation of extracellular GABA levels in the prefrontal cortex [J].
Abi-Saab, WM ;
Bubser, M ;
Roth, RH ;
Deutch, AY .
NEUROPSYCHOPHARMACOLOGY, 1999, 20 (01) :92-96
[2]   The genetics of Tourette syndrome [J].
Alsobrook, JP ;
Pauls, DL .
NEUROLOGIC CLINICS, 1997, 15 (02) :381-+
[3]   The central 5-HT3 receptor in CNS disorders [J].
Bloom, FE ;
Morales, M .
NEUROCHEMICAL RESEARCH, 1998, 23 (05) :653-659
[4]  
Breidt F, 1996, BIOTECHNOL SOFTW J, V13, P8
[5]  
Costa P. T., 1992, PROFESSIONAL MANUAL
[6]   THE RELATIONSHIP BETWEEN BENZODIAZEPINE RECEPTOR SENSITIVITY AND NEUROTICISM [J].
GLUE, P ;
WILSON, S ;
COUPLAND, N ;
BALL, D ;
NUTT, D .
JOURNAL OF ANXIETY DISORDERS, 1995, 9 (01) :33-45
[7]  
Greenberg BD, 2000, AM J MED GENET, V96, P202, DOI 10.1002/(SICI)1096-8628(20000403)96:2<202::AID-AJMG16>3.0.CO
[8]  
2-J
[9]   Altered cortical excitability in obsessive-compulsive disorder [J].
Greenberg, BD ;
Ziemann, U ;
Corá-Locatelli, G ;
Harmon, A ;
Murphy, DL ;
Keel, JC ;
Wassermann, EM .
NEUROLOGY, 2000, 54 (01) :142-147
[10]  
John O. P., 1999, HDB PERSONALITY THEO, P102, DOI [10.1525/fq.1998.51.4.04a00260, DOI 10.1525/FQ.1998.51.4.04A00260]