Department of Psychology, University of California, Los Angeles (UCLA), Los Angeles, California 90095-1563, USA.
J Abnorm Psychol. 2010 Feb;119(1):31-9. doi: 10.1037/a0018265.
Schizophrenia is associated with deficits in P50 suppression to the second stimulus in a pair, a process often conceptualized as a preattentive index of sensory gating. This study assessed the malleability of the deficit by determining whether early attentional control can influence P50 gating across different phases of schizophrenia. Participants included 28 patients in the recent-onset (n = 16) or chronic (n = 12) phase of illness and 28 healthy comparison subjects. During the standard paradigm, chronic schizophrenia patients exhibited impaired P50 suppression relative to healthy subjects, whereas recent-onset schizophrenia patients were intermediate. Directing voluntary attention toward the initial stimulus yielded substantial improvements in the P50 ratio; recent-onset schizophrenia patients achieved ratio scores comparable to those of healthy participants, whereas chronic patients also improved and could no longer be distinguished clearly from the healthy comparison sample. Directing attention toward the second stimulus enhanced P50 amplitude to the second stimulus across groups, possibly because activation of the inhibitory mechanism was overridden or circumvented by task demands. Thus, P50 suppression may be primarily preattentive under standard conditions, but manipulation of early attention can exert a modulatory influence on P50, indicating that the suppression deficit is malleable in schizophrenia without pharmacological agents.
精神分裂症与对一对刺激中的第二个刺激的 P50 抑制缺陷有关,这个过程通常被概念化为感觉门控的前注意指数。本研究通过确定早期注意力控制是否可以跨精神分裂症的不同阶段影响 P50 门控,来评估该缺陷的可塑程度。参与者包括处于疾病近期发作(n=16)或慢性(n=12)阶段的 28 名患者和 28 名健康对照者。在标准范式中,慢性精神分裂症患者的 P50 抑制相对于健康受试者受损,而近期发作的精神分裂症患者则处于中间状态。将自愿注意力引导至初始刺激会显著改善 P50 比值;近期发作的精神分裂症患者的比值分数可与健康参与者相媲美,而慢性患者也有所改善,并且不再与健康对照组样本明显区分开来。将注意力引导至第二个刺激会在所有组中增强第二个刺激的 P50 振幅,这可能是因为抑制机制的激活被任务要求所覆盖或绕过。因此,在标准条件下,P50 抑制可能主要是前注意的,但早期注意力的操纵可以对 P50 产生调节影响,表明精神分裂症中的抑制缺陷是可塑的,而无需药物干预。