精神分裂症患者听感觉门控抑制功能的脑磁图研究

摘要

Objective To explore the neural mechanism of auditory sensory gating function in schizophrenia using magnetoencephalography (MEG).Methods Whole-head MEG data were acquired during the standard paired-click paradigm in 20 schizophrenia patients and 20 healthy controls.The M50,M100 and M200 responses were investigated,and dipole source localization was performed.Sensory gating ratios were determined by measuring the strength of the M50,M100 and M200 response to the second click divided by that of the first click (S2/S1).Results In every subject,M50,M100 and M200 dipolar sources localized to the left and right posterior portion of superior temporal gyrus (STG).The bilateral M50 gating ratios and M50 S2 source strengths were significantly higher in the schizophrenia group compared to the control group (patients,M50 gating left (0.87 ± 0.39),right (0.82 ± 0.34) ; M50 S2 strengths left (15.47±7.81) nAm,right (14.26±4.54) nAm; controls,M50 gating left (0.53 ±0.28),right (0.53 ± 0.34) ; M50 S2 strengths left (10.38 ± 5.55) nAm,right (9.76 ± 5.77)nAm,P ＜ 0.05).The bilateral M100 gating ratios and M100 S2 source strengths were significantly higher in the schizophrenia group compared to the control group (patients,M100 gating left (0.98 ±0.40),right (0.86 ±0.42) ; M100 S2 strengths left (28.17 ± 18.96) nAm,right (33.36 ± 16.06) nAm; controls,M100 gating left (0.55 ±0.22),right (0.52 ± 0.16) ; M100 S2 strengths left (15.93 ± 8.25) nAm,right (16.07 ± 5.98) nAm,P ＜ 0.05).The left hemispheric M200 gating ratio was significantly higher in the schizophrenia group compared to the control group (patients 0.95 ±0.51 ; controls 0.51 ±0.22,P ＜0.01).The left hemispheric S1-M50 latency was significantly shorter in the schizophrenia group compared to the control group (patients,(53.44 ± 13.67) ms ; controls,(62.46 ± 9.89) ms,P ＜ 0.05).No significant correlations were found between PANSS scores and bilateral M50,M100,M200(r =-0.351,r =0.206,r =-0.287,r =0.361,r =-0.265,r =-0.093,all P ＞ 0.05).Conclusions Schizophrenia patients have auditory gating deficits at both preattentive and early attentive levels,which might be related to STG structural/functional abnormality.%目的 利用脑磁图技术探讨精神分裂症患者听感觉门控抑制功能的神经机制.方法 对20例精神分裂症患者(患者组)和20名年龄、性别、受教育时间均匹配的健康对照者(对照组),采用听觉条件(S1)-测试(S2)刺激范式,用脑磁图设备记录刺激后产生的感觉门控相关的听觉诱发磁场M50、M100、M200,并将脑磁图资料叠加到MRI以获得磁源性影像.以S2强度与S1强度的比值表示感觉门控功能的缺失程度,分别记作M50 S2/S1比值、M100S2/S1比值、M200 S2/S1比值.同时采用PANSS评定患者的临床症状.结果 (1)所有受试者诱发的M50、M100、M200的等效电流偶极位置源均位于双侧颞上回中后部.(2)患者组双侧M50 S2/S1比值(左:0.87±0.39,右:0.82±0.34)高于对照组(左:0.53±0.28,右:0.53±0.34),双侧S2-M50强度[左:(15.47±7.81) nAm,右:(14.26±4.54)nAm]高于对照组[左:(10.38±5.55) nAm,右:(9.76±5.77) nAm](均P＜0.05).患者组双侧M100 S2/S1比值(左:0.98±0.40,右:0.86±0.42)高于对照组(左:0.55±0.22,右:0.52±0.16),双侧S2-M100强度[左:(28.17±18.96) nAm,右:(33.36±16.06) nAm]高于对照组[左:(15.93±8.25)nAm,右:(16.07±5.98)nAm](均P＜0.05).患者组左侧M200 S2/S1比值(0.95±0.51)高于对照组(0.51 ±0.22) (P ＜0.01).患者组左侧S1-M50潜伏期[(53.44±13.67) ms]短于对照组[(62.46±9.89) ms](P＜0.05).(3)患者组PANSS总分与双侧M50、M100、M200比值无相关性(r=-0.351、r=0.206、r=-0.287、r =0.361、r=-0.265、r=-0.093,均P＞0.05).结论 精神分裂症患者感觉门控缺损可能与颞上回结构和(或)功能异常有关,听感觉门控缺损可能影响了后期注意参与的认知加工处理过程.