Abstract：
Following prolonged neglect during the formative decades of behavioural neurology, the temporopolar region has become a site of vibrant research on the neurobiology of cognition and conduct. This turnaround can be attributed to increasing recognition of neurodegenerative diseases that target temporopolar regions for peak destruction. The resultant syndromes include behavioural dementia, associative agnosia, semantic forms of primary progressive aphasia and semantic dementia. Clinicopathological correlations show that object naming and word comprehension are critically dependent on the language-dominant (usually left) temporopolar region, whereas behavioural control and non-verbal object recognition display a more bilateral representation with a rightward bias. Neuroanatomical experiments in macaques and neuroimaging in humans show that the temporoparietal region sits at the confluence of auditory, visual and limbic streams of processing at the downstream (deep) pole of the \'what\' pathway. The functional neuroanatomy of this region revolves around three axes, an anterograde horizontal axis from unimodal to heteromodal and paralimbic cortex; a radial axis where visual (ventral), auditory (dorsal) and paralimbic (medial) territories encircle temporopolar cortex and display hemispheric asymmetry; and a vertical depth-of-processing axis for the associative elaboration of words, objects and interoceptive states. One function of this neural matrix is to support the transformation of object and word representations from unimodal percepts to multimodal concepts. The underlying process is likely to start at canonical gateways that successively lead to generic (superordinate), specific (basic) and unique levels of recognition. A first sign of left temporopolar dysfunction takes the form of taxonomic blurring where boundaries among categories are preserved but not boundaries among exemplars of a category. Semantic paraphasias and coordinate errors in word-picture verification tests are consequences of this phenomenon. Eventually, boundaries among categories are also blurred and comprehension impairments become more profound. The medial temporopolar region belongs to the amygdalocentric component of the limbic system and stands to integrate exteroceptive information with interoceptive states underlying social interactions. Review of the pertinent literature shows that word comprehension and conduct impairments caused by temporopolar strokes and temporal lobectomy are far less severe than those seen in temporopolar atrophies. One explanation for this unexpected discrepancy invokes the miswiring of residual temporopolar neurons during the many years of indolently progressive neurodegeneration. According to this hypothesis, the temporopolar regions become not only dysfunctional but also sources of aberrant outputs that interfere with the function of areas elsewhere in the language and paralimbic networks, a juxtaposition not seen in lobectomy or stroke.
摘要：
在行为神经学的几十年中长期忽视之后，时间极区域已成为对认知和行为的神经生物学进行充满活力的研究的场所。这种转机可以归因于对神经退行性疾病的认识日益提高，这些疾病以颞极区域为峰值破坏目标。由此产生的综合征包括行为痴呆，联想失认症，原发性进行性失语症和语义痴呆的语义形式。临床病理相关性表明，对象命名和单词理解在很大程度上取决于语言主导（通常是左）的时间极性区域，而行为控制和非语言对象识别显示出更多的双边表示，并带有向右的偏向。猕猴的神经解剖学实验和人类的神经影像学显示，颞顶区位于听觉的汇合处，在“什么”路径的下游(深)极处的视觉和边缘处理流。这个区域的功能神经解剖学围绕三个轴旋转，从单峰到异峰和旁皮质的顺行水平轴；视觉（腹侧）的径向轴，听觉（背侧）和旁侧（内侧）区域环绕颞极皮层并显示半球不对称性；以及用于单词联想化的垂直处理深度轴，对象和交互状态。此神经矩阵的一个功能是支持对象和单词表示从单峰感知到多模态概念的转换。基础过程可能会从规范网关开始，这些网关相继导致通用（上级），具体(基本)和独特的识别水平。左颞极功能障碍的第一个迹象采取分类模糊的形式，其中保留了类别之间的边界，但保留了类别示例之间的边界。单词图片验证测试中的语义语态和坐标错误是这种现象的后果。最终,类别之间的界限也变得模糊，理解障碍变得更加深刻。内侧颞极区域属于边缘系统的杏仁核中心成分，可以将外感知力信息与社会互动的感知力状态相结合。对相关文献的回顾表明，由颞极中风和颞叶切除术引起的单词理解和行为障碍远不如在颞极萎缩中看到的严重。对这种意外差异的一种解释是在多年的缓慢进行性神经变性过程中，残余的颞极神经元的错误接线。根据这个假设,时间极区域不仅功能失调，而且还会产生异常输出的来源，这些输出会干扰语言和旁视网络中其他区域的功能，在肺叶切除术或中风中未见到的并置。
