Marsh Laura C, Apšvalka Dace, Kikuchi Hirokazu, Abe Nobuhito, Kawaguchi Jun, Kopelman Michael D, Anderson Michael C
MRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
Department of Neurology, Sendai Nakae Hospital, Sendai, Japan.
Psychol Med. 2025 Jan 8;54(16):1-9. doi: 10.1017/S0033291724003040.
The mechanisms underlying generalized forms of dissociative ('psychogenic') amnesia are poorly understood. One theory suggests that memory retrieval is inhibited via prefrontal control. Findings from cognitive neuroscience offer a candidate mechanism for this proposed retrieval inhibition. By applying predictions based on these experimental findings, we examined the putative role of retrieval suppression in dissociative amnesia.
We analyzed fMRI data from two previously reported cases of dissociative amnesia. Patients had been shown reminders from forgotten and remembered time periods (colleagues and school friends). We examined the neuroanatomical overlap between regions engaged in the unrecognized compared to the recognized condition, and the regions engaged during retrieval suppression in laboratory-based tasks. Effective connectivity analyses were performed to test the hypothesized modulatory relationship between the right anterior dorsolateral prefrontal cortex (raDLPFC) and the hippocampus. Both patients were scanned again following treatment, and analyses were repeated.
We observed substantial functional alignment between the inhibitory regions engaged during laboratory-based retrieval suppression tasks, and those engaged when patients failed to recognize their current colleagues. This included significant activation in the raDLPFC and right ventrolateral prefrontal cortex, and a corresponding deactivation across autobiographical memory regions (hippocampus, medial PFC). Dynamic causal modeling confirmed the hypothesized modulatory relationship between the raDLPFC and the hippocampus. This pattern was no longer evident following memory recovery in the first patient, but persisted in the second patient who remained amnesic.
Findings are consistent with an inhibitory mechanism driving down activity across core memory regions to prevent the recognition of personally relevant stimuli.
分离性(“心因性”)遗忘症的全身性形式的潜在机制尚不清楚。一种理论认为,记忆提取是通过前额叶控制来抑制的。认知神经科学的研究结果为这种提出的提取抑制提供了一种可能的机制。通过应用基于这些实验结果的预测,我们研究了提取抑制在分离性遗忘症中的假定作用。
我们分析了之前报道的两例分离性遗忘症患者的功能磁共振成像(fMRI)数据。向患者展示来自被遗忘和被记住时间段的提示(同事和校友)。我们检查了在未识别与已识别状态下参与的区域之间的神经解剖学重叠,以及在基于实验室任务的提取抑制过程中参与的区域。进行了有效连接分析,以测试右前背外侧前额叶皮层(raDLPFC)与海马体之间假设的调节关系。两名患者在接受治疗后再次进行扫描,并重复分析。
我们观察到,在基于实验室的提取抑制任务中参与的抑制区域,与患者未能认出其当前同事时参与的区域之间存在实质性的功能一致性。这包括raDLPFC和右腹外侧前额叶皮层的显著激活,以及自传体记忆区域(海马体、内侧前额叶皮层)相应的失活。动态因果模型证实了raDLPFC与海马体之间假设的调节关系。在第一名患者记忆恢复后,这种模式不再明显,但在仍处于遗忘状态的第二名患者中持续存在。
研究结果与一种抑制机制一致,该机制降低核心记忆区域的活动,以防止识别与个人相关的刺激。