Plowman P N
Department of Radiotherapy, St Bartholomew's Hospital, London, UK.
Br J Neurosurg. 1999 Jun;13(3):256-64. doi: 10.1080/02688699943655.
Postradiation reactions in the CNS are well described and catalogued in the conventional radiotherapy literature; acute, subacute and late CNS reactions are recognized. Tumours predispose to these normal tissue reactions by the oedema and pressure epiphenomena that occur in their environs, and probably by other mechanisms associated with tissue breakdown. That late normal tissue reactions (particularly permanent late sequelae--universally referred to as 'necrosis') occur in the normal nervous system is in the complication list of every radiosurgery centre. This article, for the first time, places postradiosurgery observations within or without the existing classification of reactions, and draws attention to the fact that previous 'radiosurgery risk factor' papers in the literature may be wrong to pool different 'reactions' in the formulation of risk formulae for normal brain damage following single shot radiotherapy. Acute reactions occur in the same manner as described for conventional radiotherapy, being a transient swelling phenomenon that occurs 12-48 h after therapy; they are fully reversible and do not usually augur late problems; routine administration of short duration steroids around the time of radiosurgery may prevent or delay the clinical signs. Subacute reactions occur 3-10 months later (a later time than the subacute reactions following conventionally fractionated radiotherapy), and may prove fully or partially reversible, or progress to permanent sequelae; the difference between these and late sequelae (which tend to be permanent themselves) then becomes blurred. That tumour swelling occurs in the subacute phase and is associated with oedema in the surrounding normal brain is an interesting observation (occurring in extra- and intra axial slow-growing tumours); it denotes tumour damage and has not been encountered in the conventionally-fractionated radiotherapy literature. Tumour shrinkage occurs later, with subsidence of the surrounding oedema, and this phenomenon may therefore be regarded (paradoxically) as a good prognostic sign, a point about which the referring clinician should be made aware. Similarly, contrast enhancement in the tumour perimeter at this time reflects a host reactive response and not tumour activity. Persistent clinical neurological signs and MRI changes (best seen on the T2 weighted sequences) beyond 2 years, indicate late damage or reaction. Usually, this represents scarring or coagulative necrosis without mass effect, but if there is a low signal area with mass effect and considerable surrounding oedema, liquefactive necrosis has occurred and (as in the brachytherapy literature) surgical decompression is very occasionally needed.
中枢神经系统的放射后反应在传统放射治疗文献中有详尽描述和分类;急性、亚急性和晚期中枢神经系统反应已得到确认。肿瘤因其周围出现的水肿和压迫性附加现象,可能还通过与组织破坏相关的其他机制,引发这些正常组织反应。正常神经系统会出现晚期正常组织反应(尤其是永久性晚期后遗症,普遍称为“坏死”),这在每个放射外科中心的并发症列表中都有。本文首次将放射外科术后观察结果纳入或不纳入现有的反应分类,并提请注意这样一个事实,即以往文献中关于“放射外科风险因素”的论文在制定单次放疗后正常脑损伤风险公式时,将不同的“反应”合并在一起可能是错误的。急性反应的发生方式与传统放射治疗中描述的相同,是治疗后12 - 48小时出现的短暂肿胀现象;它们完全可逆,通常不会预示后期问题;在放射外科手术前后常规给予短疗程类固醇可能会预防或延迟临床症状的出现。亚急性反应在3 - 10个月后出现(比传统分次放射治疗后的亚急性反应出现时间晚),可能完全或部分可逆,也可能发展为永久性后遗症;那么这些与晚期后遗症(本身往往是永久性的)之间的区别就变得模糊了。肿瘤在亚急性期出现肿胀并与周围正常脑组织的水肿相关,这是一个有趣的观察结果(发生在轴外和轴内生长缓慢的肿瘤中);它表明肿瘤受到损伤,而在传统分次放射治疗文献中未见过这种情况。肿瘤缩小稍后出现,周围水肿消退,因此这种现象(看似矛盾地)可被视为一个良好的预后指标,转诊医生应了解这一点。同样,此时肿瘤周边的对比增强反映的是机体的反应性反应而非肿瘤活性。超过2年持续存在的临床神经学体征和MRI变化(在T2加权序列上最明显)表明晚期损伤或反应。通常,这表现为无占位效应的瘢痕形成或凝固性坏死,但如果存在有占位效应且周围有大量水肿的低信号区,则发生了液化性坏死,并且(如近距离放射治疗文献中所述)极少数情况下需要进行手术减压。