Woischneck D, Schmitz B, Kapapa T
Department of Neurosurgery, Hospital Landshut, Robert-Koch-Straße 1, 84034 Landshut, Germany.
Section Neuroradiology, University Ulm, Albert-Einstein-Allee 23, 89081 Ulm, Germany.
Clin Radiol. 2017 May;72(5):426.e7-426.e15. doi: 10.1016/j.crad.2016.11.011. Epub 2017 Jan 7.
To identify whether increased numbers of brainstem lesions are found in the presence of a post-traumatic pupillary function disturbance and classify them anatomically.
In this study, a diagnostic magnetic resonance imaging (MRI) examination was performed within 8 days after traumatic brain injury (TBI) in patients who had been unconscious for more than 24 hours post-TBI. The Glasgow Outcome Scale was evaluated 6 months after TBI. The data obtained from 140 consecutively enrolled patients between 2005 and 2011 were analysed. The clinical study parameter comprised the development of post-traumatic anisocoria at least once over the course between onset of trauma and diagnostic MRI, as a yes/no decision. Significance was presumed at p≤0.05.
A total of 57 patients (41%) were found to have a lesion at MRI without involvement of the brainstem; in 83 (59%) the brainstem was (multiple) affected. Of the latter, 66 (46%) of patients had lesions in the midbrain, 38 (27%) in the pons, and seven (5%) in the medulla oblongata. By the time of MRI, anisocoria had been diagnosed in 45 (32%) patients. Mortality was highest, at 58%, in patients with anisocoria and a midbrain lesion, whilst it was 23% in those with anisocoria and no lesion in the midbrain. Mortality was 33% in relation to a midbrain lesion without anisocoria.
Overall, the study demonstrated that there is a significant correlation between midbrain lesions and post-traumatic anisocoria in unconscious trauma patients. A brainstem lesion in this case can be assumed to be a pathomorphological correlate of anisocoria. The rate of damage to the midbrain was approximately 50% in cases of transient anisocoria. It can be assumed in this situation that there are functional disorders of the peripheral oculomotor nerve or identifiable/unidentifiable lesions of the brainstem.
确定创伤后瞳孔功能障碍患者脑干病变数量是否增加，并对其进行解剖学分类。
在本研究中，对创伤性脑损伤（TBI）后昏迷超过24小时的患者，于创伤性脑损伤后8天内进行诊断性磁共振成像（MRI）检查。在创伤性脑损伤6个月后评估格拉斯哥预后量表。分析了2005年至2011年连续纳入的140例患者的数据。临床研究参数包括在创伤发作至诊断性MRI期间至少出现一次创伤后瞳孔不等大，以是/否判定。p≤0.05时认为具有显著性。
共发现57例（41%）患者MRI有病变但未累及脑干；83例（59%）脑干（多处）受累。在后者中，66例（46%）患者中脑有病变，38例（27%）脑桥有病变，7例（5%）延髓有病变。到MRI检查时，45例（32%）患者已诊断为瞳孔不等大。瞳孔不等大且中脑有病变的患者死亡率最高，为58%，而瞳孔不等大但中脑无病变的患者死亡率为23%。无瞳孔不等大的中脑病变患者死亡率为33%。
总体而言，该研究表明无意识创伤患者中脑病变与创伤后瞳孔不等大之间存在显著相关性。在这种情况下，脑干病变可被认为是瞳孔不等大的病理形态学关联。短暂性瞳孔不等大病例中脑损伤率约为50%。在这种情况下，可以假定存在外周动眼神经功能障碍或脑干可识别/不可识别的病变。
