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人类致命性闭合性颅脑损伤中颅内视觉通路的损伤。

Damage to intracranial optic pathways in fatal closed head injury in man.

作者信息

Perunovic B, Quilty R D, Athanasiou A, Love S

机构信息

Department of Neuropathology, Frenchay Hospital, Bristol BS161LE, UK.

出版信息

J Neurol Sci. 2001 Mar 15;185(1):55-62. doi: 10.1016/s0022-510x(01)00463-4.

Abstract

Head injury is a leading cause of visual impairment. This is partly due to direct trauma to the eye and optic nerve but much of the damage involves the intracranial optic pathways. We have studied the frequency, distribution and nature of the intracranial lesions of the optic pathways at autopsy in 45 cases of severe closed head injury, and examined the correlation between these post-mortem lesions and the ante-mortem clinical findings. Twenty-four of the patients had been involved in road traffic accidents. The ages ranged from 9 to 88 years (mean 46.4), the Glasgow Coma Score (GCS) on admission ranged from 3 to 15 (mean 5), and the survival time after injury from 2.5 h to15 days (mean 3.3 days). Skull fractures were present in 75.6% of the cases. Histological assessment included the use of immunohistochemistry for beta-amyloid precursor protein (beta-APP) and the microglial marker CD68. Axonal injury of varying severity was demonstrable in all cases, and in 39 (87%) the optic chiasm, tracts or radiations were involved, usually in more than one region. The severity of axonal injury was mild in 11 (24%), moderate in 9 (20%) and severe in 19 (42%) cases. The optic radiation at the level of the trigone of the lateral ventricle was particularly frequently and severely affected. The least affected parts of the intracranial optic pathways were the optic chiasm and the posterior segment of the optic nerve. The severity of injury to the optic pathways did not always reflect severity of axonal injury elsewhere in the brain and correlated poorly with the type of trauma (high- or low-velocity), presence of skull fractures or evidence of raised intracranial pressure (ICP). Of the 39 patients who survived more than 6 h, histological evidence of ischaemic injury to the primary optic cortex was present in 26 (67%) and was severe in 12. We conclude that the visual pathways are affected in a high proportion of patients with fatal closed head injury, nerve fibres in the optic radiations being particularly vulnerable. The findings suggest that damage to the posterior parts of the optic pathways may be under-diagnosed among patients with head injury.

摘要

头部损伤是视力障碍的主要原因之一。部分原因是眼球和视神经受到直接创伤,但大部分损伤涉及颅内视神经通路。我们研究了45例严重闭合性头部损伤患者尸检时视神经通路颅内病变的频率、分布和性质,并检查了这些死后病变与生前临床发现之间的相关性。其中24例患者曾遭遇道路交通事故。年龄范围为9至88岁(平均46.4岁),入院时格拉斯哥昏迷评分(GCS)范围为3至15分(平均5分),受伤后存活时间为2.5小时至15天(平均3.3天)。75.6%的病例存在颅骨骨折。组织学评估包括使用β-淀粉样前体蛋白(β-APP)免疫组化和小胶质细胞标志物CD68。所有病例均显示出不同程度的轴突损伤,39例(87%)累及视交叉、视束或视辐射,通常累及多个区域。轴突损伤程度轻度的有11例(24%),中度的有9例(20%),重度的有19例(42%)。侧脑室三角区水平的视辐射尤其频繁且严重地受到影响。颅内视神经通路受影响最小的部位是视交叉和视神经后段。视神经通路的损伤严重程度并不总是反映脑内其他部位轴突损伤的严重程度,与创伤类型(高速或低速)、颅骨骨折的存在或颅内压(ICP)升高的证据相关性较差。在39例存活超过6小时的患者中,26例(67%)有初级视皮质缺血性损伤的组织学证据,其中12例损伤严重。我们得出结论,在致命性闭合性头部损伤患者中,视觉通路受影响的比例很高,视辐射中的神经纤维尤其脆弱。研究结果表明,在头部损伤患者中,视神经通路后部的损伤可能未得到充分诊断。

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