Gállego Culleré Jaime, Erro Aguirre María Elena
Servicio de Neurología, Complejo Hospitalario de Navarra, C/ Irunlarrea 3, 31008, Pamplona Navarra, Spain,
Curr Treat Options Cardiovasc Med. 2011 Jun;13(3):247-60. doi: 10.1007/s11936-011-0125-x.
During the past few years, the branch syndromes have been ascribed to pontine lesions, and the development of neuroimaging techniques has renewed the interest in exploring their clinical-radiological correlation. Brain imaging via MRI has helped in the diagnosis and accurate localization of lesions. From classic studies it is now accepted that the pathogenic mechanism of lacunar pontine infarction (LPI) is perforating small arterial disease or microangiopathy caused by lipohyalinosis, whereas paramedian pontine infarction (PPI) are caused by paramedian or circumferential basilar branch disease due to atheromatous branch occlusion. The importance of basilar artery disease not only in severe posterior circulation infarcts but also in minor brainstem strokes is known from previous reports. The mechanism of PPI is probably local occlusion of the mouths of paramedian perforators through the atheromatous basilar artery (basilar branch occlusion). Infrequent basilar artery diseases such as dissection, aneurysm and hypoplasia, dolichoectatic basilar artery, embolism, or vasospasms are known to block the orifices of penetrating branch arteries and cause an infarct in the territory of the obstructed branches. An association between basilar artery branch disease and isolated pontine infarction exists; moreover, the enlargement of pontine lesion seems to be associated with neurologic worsening and fluctuating symptoms, but we know little about stroke mechanisms in patients with fluctuating symptoms and about the role of branch atherosclerotic disease. The treatment remains controversial, even in acute cases. Implementation of new neuroimaging techniques, such as high-resolution MRI, could be helpful in identifying pathogenetic mechanisms of isolated pontine infarction, thus improving therapeutic strategy and secondary prevention.
在过去几年中，脑桥分支综合征一直被归因于脑桥病变，而神经影像技术的发展重新激发了人们探索其临床与影像学相关性的兴趣。通过磁共振成像（MRI）进行脑成像有助于病变的诊断和精确定位。从经典研究中可知，目前公认腔隙性脑桥梗死（LPI）的发病机制是由脂质透明变性引起的穿支小动脉疾病或微血管病，而脑桥旁正中梗死（PPI）是由动脉粥样硬化分支闭塞导致的旁正中或环行基底动脉分支疾病引起的。先前的报道已表明基底动脉疾病不仅在严重的后循环梗死中，而且在轻微的脑干卒中中都很重要。PPI的机制可能是动脉粥样硬化的基底动脉（基底动脉分支闭塞）导致旁正中穿支开口局部闭塞。已知罕见的基底动脉疾病，如夹层、动脉瘤、发育不全、基底动脉延长扩张症、栓塞或血管痉挛，会阻塞穿支动脉的开口并导致阻塞分支区域的梗死。基底动脉分支疾病与孤立性脑桥梗死之间存在关联；此外，脑桥病变的扩大似乎与神经功能恶化和症状波动有关，但我们对症状波动患者的卒中机制以及分支动脉粥样硬化疾病的作用了解甚少。即使在急性病例中，治疗仍存在争议。采用新的神经影像技术，如高分辨率MRI，可能有助于识别孤立性脑桥梗死的发病机制，从而改善治疗策略和二级预防。
