In this review, we explore current literature and assess evidence linking secondary (acquired) alexithymia to aberrant humor processing, in terms of their neurobiological underpinnings. In addition, we suggest a possible common neuropathological substrate between secondary alexithymia and deficits in humor appreciation, by drawing on neurophysiologic and neuroradiological evidence, as well as on a recent and unique single-case study showing the cooccurrence of secondary alexithymia and deficit in humor appreciation. In summary, what emerges from the literature is that the cortical midline structures, in particular the medial prefrontal cortex (mPFC), the anterior cingulate cortex (ACC), and the insular cortex, seem to play a crucial role in the expression of both alexithymia and defective humor processing, while though to a lesser extent, a right hemisphere and bilateral frontoparietal contribution becomes evident. Neurobiological evidence of secondary alexithymia and aberrant humor processing points to the putative role of ACC/mPFC and the insular cortex in representing crucial processing nodes whose damage may produce both the above clinical conditions. We believe that the association of secondary alexithymia and aberrant humor processing, especially humor appreciation deficit, and their correlation with specific brain regions, mainly ACG/mPFC, as emerged from the literature, may be of some heuristic importance. Increased awareness on this topic may be of aid for neurosurgeons when accessing emotion-relevant structures, as well as for neuropsychologists to intensify their efforts to plan evidence-based neurorehabilitative interventions to alleviate the deleterious effects of such interpersonal communication deficits.

中文翻译：

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解决将继发性述情障碍与异常幽默处理联系起来的证据。


在这篇综述中，我们探讨了当前的文献，并评估了继发性（获得性）述情障碍与异常幽默处理之间的神经生物学基础。此外，通过利用神经生理学和神经放射学证据，以及最近一项显示继发性述情障碍和幽默欣赏缺陷同时发生的独特单例研究，我们提出继发性述情障碍和幽默欣赏缺陷之间可能存在共同的神经病理学基础。总之，从文献中得出的结论是，皮质中线结构，特别是内侧前额叶皮质（mPFC）、前扣带皮层（ACC）和岛叶皮质，似乎在述情障碍的表达中发挥着至关重要的作用。和有缺陷的幽默处理，虽然程度较小，但右半球和双侧额顶叶的贡献变得明显。继发性述情障碍和异常幽默处理的神经生物学证据表明 ACC/mPFC 和岛叶皮质在代表关键处理节点中的假定作用，这些节点的损伤可能会产生上述两种临床状况。我们认为，继发性述情障碍和异常的幽默处理之间的关联，尤其是幽默欣赏缺陷，以及它们与特定大脑区域（主要是 ACG/mPFC）的相关性，如文献中所显示的那样，可能具有一定的启发意义。提高对这一主题的认识可能有助于神经外科医生了解情绪相关结构，也有助于神经心理学家加紧努力规划基于证据的神经康复干预措施，以减轻此类人际沟通缺陷的有害影响。