强迫症的脑功能障碍(5)
[32] McFarland N R, Haber S N. Thalamic relay nuclei of the basal ganglia form both reciprocal and nonreciprocal cortical connections, linking multiple frontal cortical areas. Journal of Neuroscience, 2002, 22: 8117~8132
[33] Horvitz J C. Mesolimbocortical and nigrostriatal dopamine responses to salient non-reward events. Neuroscience, 2000, 96: 651~656
[34] Nieoullon A. Dopamine and the regulation of cognition and attention. Progress in Neurobiology, 2002, 67: 53~83
, http://www.100md.com
[35] Lucki I. The spectrum of behaviors influenced by serotonin. Biological Psychiatry, 1998, 44: 151~162
[36] Kapur S, Remington G. Serotonin-dopamine interaction and its relevance to schizophrenia. American Journal of Psychiatry, 1996, 153: 466 ~ 476
[37] Bergqvist P B, Bouchard C, Blier P. Effect of long-term administration of antidepressant treatments on serotonin release in brain regions involved in obsessive–compulsive disorder. Biological Psychiatry, 1999, 45: 164 ~ 174
, 百拇医药
[38] Breiter H C, Rauch S L, Kwong K K, et al. Functional magnetic resonance imaging of symptom provocation in obsessive–compulsive disorder. Archives of General Psychiatry, 1996, 53: 595~606
[39] Adler C M, McDonough-Ryan P, Sax K W, et al. fMRI of neuronal activation with symptom provocation in unmedicated patients with obsessive compulsive disorder. Journal of Psychiatry Research, 2000, 34: 317~324
[40] Mataix-Cols D, Rauch S L, Baer L, et al. Symptom stability in adult obsessive–compulsive disorder: Data from a naturalistic two-year follow-up study. American Journal of Psychiatry, 2002, 159:263~268
, 百拇医药
[41] Schwartz J M, Stoessel P W, Baxter Jr. L R, et al. Systematic changes in cerebral glucose metabolic rate after successful behavior modification treatment of obsessive– compulsive disorder. Archives of General Psychiatry, 1996, 53: 109~113
[42] Rauch S L, Shin L M, Dougherty D D, et al. Predictors of fluvoxamine response in contamination-related obsessive compulsive disorder: A PET symptom provocation study. Neuropsychopharmacology, 2002, 27: 782~ 791
, 百拇医药
[43] Brody A L, Saxena S, Schwartz J M, et al. FDG–PET predictors of response to behavioral therapy and pharmacotherapy in obsessive compulsive disorder. Psychiatry Research, 1998, 84: 1~6
[44] Hoehn-Saric R, Schlaepfer T E, Greenberg B D, et al. Cerebral blood flow in obsessive–compulsive patients with major depression: Effect of treatment with sertraline or desipramine on treatment responders and non-responders. Psychiatry Research, 2001, 108: 89~100
, http://www.100md.com
[45] Rauch S L, Dougherty D D, Cosgrove G R, et al. Cerebral metabolic correlates as potential predictors of response to anterior cingulotomy for obsessive compulsive disorder. Biological Psychiatry, 2001, 50:659~667
[46] Modell J G, Mountz J M, Curtis G C, et al. Neurophysiologic dysfunction in basal ganglia/limbic striatal and thalamocortical circuits as a pathogenetic mechanism of obsessive–compulsive disorder. Journal of Neuropsychiatry and Clinical Neurosciences, 1989, 1: 27~36
[ 上 页 ]
, http://www.100md.com(蔡厚德)
[33] Horvitz J C. Mesolimbocortical and nigrostriatal dopamine responses to salient non-reward events. Neuroscience, 2000, 96: 651~656
[34] Nieoullon A. Dopamine and the regulation of cognition and attention. Progress in Neurobiology, 2002, 67: 53~83
, http://www.100md.com
[35] Lucki I. The spectrum of behaviors influenced by serotonin. Biological Psychiatry, 1998, 44: 151~162
[36] Kapur S, Remington G. Serotonin-dopamine interaction and its relevance to schizophrenia. American Journal of Psychiatry, 1996, 153: 466 ~ 476
[37] Bergqvist P B, Bouchard C, Blier P. Effect of long-term administration of antidepressant treatments on serotonin release in brain regions involved in obsessive–compulsive disorder. Biological Psychiatry, 1999, 45: 164 ~ 174
, 百拇医药
[38] Breiter H C, Rauch S L, Kwong K K, et al. Functional magnetic resonance imaging of symptom provocation in obsessive–compulsive disorder. Archives of General Psychiatry, 1996, 53: 595~606
[39] Adler C M, McDonough-Ryan P, Sax K W, et al. fMRI of neuronal activation with symptom provocation in unmedicated patients with obsessive compulsive disorder. Journal of Psychiatry Research, 2000, 34: 317~324
[40] Mataix-Cols D, Rauch S L, Baer L, et al. Symptom stability in adult obsessive–compulsive disorder: Data from a naturalistic two-year follow-up study. American Journal of Psychiatry, 2002, 159:263~268
, 百拇医药
[41] Schwartz J M, Stoessel P W, Baxter Jr. L R, et al. Systematic changes in cerebral glucose metabolic rate after successful behavior modification treatment of obsessive– compulsive disorder. Archives of General Psychiatry, 1996, 53: 109~113
[42] Rauch S L, Shin L M, Dougherty D D, et al. Predictors of fluvoxamine response in contamination-related obsessive compulsive disorder: A PET symptom provocation study. Neuropsychopharmacology, 2002, 27: 782~ 791
, 百拇医药
[43] Brody A L, Saxena S, Schwartz J M, et al. FDG–PET predictors of response to behavioral therapy and pharmacotherapy in obsessive compulsive disorder. Psychiatry Research, 1998, 84: 1~6
[44] Hoehn-Saric R, Schlaepfer T E, Greenberg B D, et al. Cerebral blood flow in obsessive–compulsive patients with major depression: Effect of treatment with sertraline or desipramine on treatment responders and non-responders. Psychiatry Research, 2001, 108: 89~100
, http://www.100md.com
[45] Rauch S L, Dougherty D D, Cosgrove G R, et al. Cerebral metabolic correlates as potential predictors of response to anterior cingulotomy for obsessive compulsive disorder. Biological Psychiatry, 2001, 50:659~667
[46] Modell J G, Mountz J M, Curtis G C, et al. Neurophysiologic dysfunction in basal ganglia/limbic striatal and thalamocortical circuits as a pathogenetic mechanism of obsessive–compulsive disorder. Journal of Neuropsychiatry and Clinical Neurosciences, 1989, 1: 27~36
[ 上 页 ]
, http://www.100md.com(蔡厚德)