Edelstyn Nicola M J, John Christopher M, Shepherd Thomas A, Drakeford Justine L, Clark-Carter David, Ellis Simon J, Mayes Andrew R
School of Psychology, Keele University, Staffordshire, UK.
School of Psychology, Keele University, Staffordshire, UK.
Cortex. 2015 Oct;71:85-101. doi: 10.1016/j.cortex.2015.06.021. Epub 2015 Jul 2.
Medicated, non-dementing mild-to-moderate Parkinson's disease (PD) patients usually show recall/recollection impairments but have only occasionally shown familiarity impairments. We aimed to assess two explanations of this pattern of impairment. Recollection typically improves when effortful planning of encoding and retrieval processing is engaged. This depends on prefrontally-dependent executive processes, which are often disrupted in PD. Relative to an unguided encoding and retrieval of words condition (C1), giving suitable guidance at encoding alone (C2) or at encoding and retrieval (C3) should, if executive processes are disrupted, improve PD recollection more than control recollection and perhaps raise it to normal levels. Familiarity, being a relatively automatic kind of memory, whether impaired or intact, should be unaffected by guidance. According to the second explanation, PD deficits are amnesia-like and caused by medial temporal lobe dysfunction and although poorer recollection, which is caused by hippocampal disruption, may be improved by guidance, it should not improve more than control recollection. Familiarity impairment will also occur if the perirhinal cortex is disrupted, but will be unimproved by guidance. Without guidance, recollection/recall was impaired in thirty PD patients relative to twenty-two healthy controls and remained relatively equally impaired when full guidance was provided (C1 vs C3), both groups improving to broadly the same extent. Although impaired, and markedly less so than recollection, familiarity was not improved by guidance in both groups. The patients showed elevated rates of subclinical depressive symptoms, which weakly correlated with recall/recollection in all three conditions. PD executive function was also deficient and correlated with unguided/C1 recollection only. Our results are consistent with a major cause of the patients' recall/recollection impairments being hippocampal disruption, probably exacerbated by subclinical depressive symptoms. However, the results do not exclude a lesser prefrontal cortex contribution because patient executive functions were impaired and correlated solely with unguided overall recollection.
接受药物治疗、无痴呆症状的轻至中度帕金森病（PD）患者通常存在回忆/再认障碍，但仅有偶尔出现熟悉度障碍的情况。我们旨在评估对这种障碍模式的两种解释。当进行编码和检索过程的刻意规划时，回忆通常会得到改善。这依赖于前额叶依赖的执行过程，而这些过程在PD中常常受到干扰。相对于单词的无引导编码和检索条件（C1），仅在编码时（C2）或在编码和检索时（C3）给予适当指导，如果执行过程受到干扰，应该比对照组的回忆更能改善PD患者的回忆，甚至可能将其提高到正常水平。熟悉度作为一种相对自动的记忆类型，无论受损与否，都不应受指导的影响。根据第二种解释，PD缺陷类似失忆，是由内侧颞叶功能障碍引起的，尽管由海马体破坏导致的较差回忆可能会因指导而改善，但不应比对照组的回忆改善得更多。如果嗅周皮质受到破坏，也会出现熟悉度障碍，但不会因指导而改善。在没有指导的情况下，3０名PD患者的回忆/再认相对于22名健康对照者受损，在提供全面指导时（C1与C3），两组的受损程度仍相对相当，且改善程度大致相同。尽管两组的熟悉度受损，且明显不如回忆受损严重，但均未因指导而改善。患者亚临床抑郁症状的发生率较高，在所有三种情况下，这些症状与回忆/再认呈弱相关。PD患者的执行功能也存在缺陷，且仅与无引导/C1回忆相关。我们的结果与患者回忆/再认障碍的主要原因是海马体破坏一致，可能因亚临床抑郁症状而加剧。然而，结果并不排除前额叶皮质的较小贡献，因为患者的执行功能受损，且仅与无引导的整体回忆相关。
