曲唑酮治疗心理性勃起功能障碍的功能磁共振研究

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目的用功能磁共振技术结合药物磁共振技术研究正常男性和心理性勃起功能障碍患者中枢神经系统激活的差异,探讨曲唑酮治疗心理性勃起功能障碍的可能机制。方法A组为30例健康成年男性志愿者,均为右利手;30例心理性勃起功能障碍患者单盲、随机分为B组(用曲唑酮治疗7周)和C组(用安慰剂治疗7周),每组15个患者,所有患者人均为右利手。A组仅进行一次功能磁共振检查;B组和C组在治疗前后均进行功能磁共振检查,治疗前B组和C组不服用任何药物;治疗后B组患者在磁共振扫描前60分钟服用曲唑酮100mg;C组服用安慰剂100mg。所有参与者均用色情录像和非色情录像刺激,用GE1.5TMR扫描系统进行血氧水平依赖的功能磁共振扫描。结果在色情录像的刺激下,与正常男性相比,心理性勃起功能障碍(ED)患者(B组+C组)双侧前扣带回激活范围明显增大(t=6.715,P<0.001),两者存在显著性差异。B组经曲唑酮治疗后,在曲唑酮的干预下,心理性ED患者的双侧前扣带回激活被抑制与正常人接近,而双侧海马激活范围较前增大,双侧脑岛的激活被抑制;B组病人治疗前后前扣带回激活体积存在显著性差异(t=1.930,P<0.05);双侧海马激活较前明显,前后激活体积存在显著性差异(左侧:t=3.790,P<0.001;右侧:t=4.203,P<0.001);脑岛的激活被抑制。C组病人治疗前后在安慰剂的干预下,脑激活图前后无明显改变。结论心理性ED患者在中枢神经系统可能存在潜在的病因;脑岛、前扣带回、海马可能富含5-HT受体;曲唑酮对心理性ED的治疗可能在于调节了脑岛、前扣带回、海马的神经元生物活性;曲唑酮对不同亚型的5-HT受体的调节具有多肽性。 Objective To investigate the differences of central nervous system activation between normal men and psychological erectile dysfunction patients by using functional magnetic resonance imaging and magnetic resonance imaging and to explore the possible mechanism of trazodone in treating psychological erectile dysfunction. Methods A group of 30 healthy adult male volunteers were right hand; 30 patients with mental erectile dysfunction were single blind, were randomly divided into group B (with trazodone for 7 weeks) and group C (placebo Treatment for 7 weeks), each group of 15 patients, all patients were right hand. Group A received only functional magnetic resonance imaging (FMRI); Group B and Group C underwent FMRI before and after treatment. Patients in groups B and C did not take any medication before treatment. After treatment, patients in Group B were given 60 minutes before magnetic resonance Trazodone 100mg; C group taking placebo 100mg. All participants were stimulated by pornographic and non-pornographic recordings using a magnetic resonance (MR) -based magnetic resonance scan of the GE 1.5 TMR scanning system. Results In the stimulation of the pornographic video, the activation range of bilateral anterior cingulate gyrus in ED patients (group B + C) was significantly higher than that of normal men (t = 6.715, P <0.001) , There is a significant difference between the two. After trazodone treatment in tramadol group, the activation of bilateral anterior cingulate gyrus in patients with psychological ED was inhibited by trazodone intervention, and the activation range of bilateral hippocampus was increased compared with that of the normal subjects. The bilateral brain The activation of the island was inhibited. There was a significant difference in the activation volume of anterior cingulate cortex before and after treatment in group B (t = 1.930, P <0.05). The activation of bilateral hippocampus was more obvious than before, t = 3.790, P <0.001; right: t = 4.203, P <0.001); activation of insula was inhibited. C group before and after treatment in the placebo intervention, brain activation before and after no significant change. Conclusions There may be a potential etiopathogenisis in the central nervous system in patients with psychic ED. The insula, anterior cingulate gyrus and hippocampus may be enriched in 5-HT receptors. Trazodone treatment of psychological ED may lie in the regulation of insula, Cingulate gynecological neurons, hippocampus neurons; Trazodone modulates the 5-HT receptors in different subtypes.
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