1Department of Neurosurgery, Ramón y Cajal University Hospital.
2Department of Endocrinology, Sureste University Hospital, Francisco de Vitoria University.
Neurosurg Focus. 2019 Sep 1;47(3):E7. doi: 10.3171/2019.6.FOCUS19337.
Establishing the neurological localization doctrine for the contralateral hemispheric control of motor functions in the second half of the 19th century, researchers faced the challenge of recognizing false localizing signs, in particular paradoxical or ipsilateral hemiparesis (IH). Despite tremendous progress in current methods of neuroradiological and electrophysiological exploration, a complete understanding of this phenomenon has yet to be attained.
The authors researched the well-described cases of hemiparesis/hemiplegia ipsilateral to an intracranial lesion published in the scientific literature in the pre-MRI era (before 1980). A comprehensive review of the physiopathological mechanisms proposed for paradoxical hemiparesis throughout this period, as well as the pathological evidence substantiating them, is provided.
A collection of 75 patients with hemiparesis/hemiplegia ipsilateral to the primary intracranial lesion reported between 1858 and 1979 were eligible for analysis. Most cases occurred in adults with supratentorial, slowly developing, extraparenchymatous mass lesions, such as neoplasms (38%) or chronic subdural hematomas (36%). Physiopathological theories proposed by the neurologists who investigated IH can be grouped into 4 major concepts: 1) lack of anatomical decussation of the corticospinal tract; 2) impaired functional activation of the contralateral hemisphere by the lesioned dominant hemisphere through the callosal connections; 3) Kernohan's notch phenomenon, or mechanical injury of the contralateral cerebral peduncle against the free edge of the tentorium; and 4) cerebrovascular dysfunction involving the contralateral hemisphere owing to kinking and mechanical flattening of the carotid artery contralateral to the primary intracranial lesion.
IH represents a still underdiagnosed paradoxical neurological phenomenon. With the aid of modern neuroradiological and neurophysiological methods, Kernohan's peduncle notch mechanism has been confirmed to cause IH in many of the cases reported in recent decades. Nevertheless, alternative functional and/or vascular mechanisms must be investigated further for unexplained IH cases, in particular for transitory IH without evidence of peduncle injury. The historical theories reviewed in this paper represent a conceptual framework that may be helpful for this purpose.
在 19 世纪下半叶，为了建立对大脑半球对运动功能的对侧控制的神经定位学说，研究人员面临着识别错误定位体征的挑战，特别是反常或同侧偏瘫（ IH ）。尽管目前在神经放射学和电生理学探索方面取得了巨大进展，但对这一现象仍未完全理解。
作者研究了在 MRI 时代之前（1980 年之前）发表在科学文献中的颅内病变同侧偏瘫/轻偏瘫的情况描述得很好的病例。综述了在此期间提出的反常性偏瘫的所有生理病理学机制，并提供了支持它们的病理证据。
1858 年至 1979 年间，共收集到 75 例原发性颅内病变同侧偏瘫/轻偏瘫的患者符合分析条件。大多数病例发生在成年人，病变位于幕上，进展缓慢，为非实质肿块病变，如肿瘤（38%）或慢性硬膜下血肿（36%）。调查 IH 的神经病学家提出的生理病理学理论可分为 4 个主要概念：1）皮质脊髓束的解剖性交叉缺失；2）病变优势半球通过胼胝体连接对对侧半球的功能激活受损；3）科恩南氏切迹现象，或对侧大脑脚在幕切迹处对游离缘的机械性损伤；4）由于原发性颅内病变对侧颈内动脉的扭曲和机械性变平，导致对侧半球的脑血管功能障碍。
IH 是一种仍未被充分诊断的反常性神经现象。借助现代神经放射学和神经生理学方法，已证实科恩南氏切迹机制可导致最近几十年报告的许多病例出现 IH 。然而，对于不明原因的 IH 病例，特别是无基底节损伤证据的一过性 IH 病例，需要进一步研究替代的功能和/或血管机制。本文回顾的历史理论为这一目的提供了一个概念框架，可能会有所帮助。
