Division of Mood Disorder, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China.
Chin Med J (Engl). 2009 Dec 20;122(24):2956-60.
Depressive disorder is a well-known chronic, recurrent and disabling mental disease with high direct and indirect costs to society in both western and eastern cultures. Approximately 40% of depressed patients show only partial or no response to initial or even multiple antidepressant medications and are usually called treatment-resistant depression (TRD) patients. The present work was to measure the features of sensory gating (SG) P50 in TRD patients with the intent of understanding the characteristics of this disease.
In 50 TRD patients, 39 non-treatment-resistant depression (NTRD) patients and 51 healthy controls (HC), auditory evoked potential P50 was measured using the conditioning/testing paradigm presented with auditory double clicks stimuli, and 36 TRD patients had repeated measurements after an 8-week venlafaxine treatment course.
All the depressive disorder patients, including the TRD and NTRD groups, showed an increased testing stimulus wave (S2-P50) amplitude compared to controls (P < 0.01 and P < 0.05), but there was no significant difference between the TRD and NTRD groups (P > 0.05). There were significant differences in the ratio of testing stimulus (S2) and conditioning stimulus (S1) (S2/S1) and in the value of 100 x (1 - S2/S1) among the three groups. Compared to the baseline, TRD patients had no significant changes of features and different expression of P50 after acute treatment (P > 0.05). Meanwhile, a statistically significant positive correlation of S2/S1 with the scores of the 17-item Hamilton Rating Scale for Depression (HAMD-17) (P < 0.01), and a significantly negative correlation of S1 - S2, 100 x (1 - S2/S1) with the scores of HAMD-17 (P < 0.01) were observed in the TRD patients' baseline measurement, but there was no correlation after venlafaxine treatment (P > 0.05).
Both the TRD and NTRD patients had obvious SG deficits, with a more severe deficit in TRD patients. Although, with a correlated relationship to the severity of depressive symptoms, SG P50 deficit might be suggested as a trait marker for TRD, and a combination of S2/S1 ratio, S1 - S2 and 100 x (1 - S2/S1), was recommended for electrophysiological measurement in TRD patients.
抑郁障碍是一种在西方和东方文化中都具有较高直接和间接社会成本的、众所周知的慢性、复发性和致残性精神疾病。大约 40%的抑郁患者对初始甚至多次抗抑郁药物治疗仅部分或无反应，通常被称为难治性抑郁（TRD）患者。本研究旨在测量 TRD 患者感觉门控（SG）P50 的特征，以了解该疾病的特征。
在 50 名 TRD 患者、39 名非难治性抑郁（NTRD）患者和 51 名健康对照者（HC）中，使用听觉双点击刺激呈现的条件/测试范式测量听觉诱发电位 P50，并在 8 周文拉法辛治疗后对 36 名 TRD 患者进行重复测量。
所有抑郁障碍患者，包括 TRD 和 NTRD 组，与对照组相比，测试刺激波（S2-P50）振幅均升高（P < 0.01 和 P < 0.05），但 TRD 和 NTRD 组之间无显著差异（P > 0.05）。三组之间 S2/S1 比值和 100 x（1-S2/S1）值均有显著差异。与基线相比，TRD 患者在急性治疗后 P50 的特征无明显变化，表达也不同（P > 0.05）。同时，在 TRD 患者的基线测量中，S2/S1 与 17 项汉密尔顿抑郁量表（HAMD-17）评分呈显著正相关（P < 0.01），S1-S2、100 x（1-S2/S1）与 HAMD-17 评分呈显著负相关（P < 0.01），但文拉法辛治疗后无相关性（P > 0.05）。
TRD 和 NTRD 患者均存在明显的 SG 缺陷，TRD 患者更为严重。尽管与抑郁症状严重程度相关，SG P50 缺陷可能被认为是 TRD 的特征性标志物，但建议在 TRD 患者中进行电生理测量时，结合 S2/S1 比值、S1-S2 和 100 x（1-S2/S1）。
