辐射诱发的中枢性脱髓鞘白质脑病

E. Eruyar, C. Irkech
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摘要

背景。白质脑病出现在照射后相当规律的延迟之后,它们选择性地累及内皮细胞,导致血脑屏障破坏、纤维素坏死、血管周围渗出和单核浸润,从而导致不同年龄的髓鞘破坏灶。病例。一位 63 岁的男性患者在 20 个月前被诊断为转移性小细胞肺癌,并开始接受顺铂+维甲酸化疗,在治疗的第 6 个月,患者接受了 3 次预防性颅内放疗,每次间隔 2 个月。治疗后,他出现过度睡眠、呆滞和癫痫发作,在头颅 MRG 中观察到弥漫性 T2 高密度,在患者的血液化验中没有病理解释,脑电图也出现弥漫性减慢。结论在我们的病例中,明显的白质病变主要发生在桥脑,桥脑-小脑纤维受到环形脱髓鞘区域的影响,而桥脑核的神经元却幸免于难。与 De Vivo 等人、Rosemberg 和 Bleyer 以及 Griffin 的病例一样,白质脑病也是在照射后相当规律的延迟后出现的,病变仅限于受照射的大脑,而未受照射的脊髓则不受影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
RADIATIONINDUCED CENTRAL DEMYELINATING LEUKOENCEPHALOPATHY
Background. Great improvement in survival has resulted from the contemporary treatment of cancer.However, this has been associated with the appearance of various previously unobserved neurological complications that have recently been reviewed.That radiotherapy is responsible is suggested by many features.Leukoencephalopathy appears after a quite regular delay following irradiation.They electively involve the endothelial cells with a break down of the blood-brain barrier, fibrinoid necrosis, perivascular exudation and mononuclear infiltration leading to foci of myelin destruction of different ages. Case. A 63 year old male patient was diagnosed with metastatic small cell lung cancer 20 months ago, and cisplatin+vepesid chemotherapy is started.At the 6th month of the treatment, prophylactic intracranial radiotherapy is given 3 times with an interval of 2 months. After the treatment,he had oversleeping,sluggishness, and epileptic seizures.Diffuse T2 hyperintensities were observed in the Cranial MRG taken.There was no pathology to explain the situation in the blood tests of the patient with diffuse slowing in his EEG.The patient was started on antiepileptic and steroid treatment and was followed up. Conclusion. Clinically there is progressive psychomotor deterioration.Convulsions are very rare and were seen in our patient.The MRG pattern was also very characteristic in our case especially affecting the white matter.In our case,the striking white matter predominance of the lesions was clearly shown in the pons where circumscribed areas of demyelination affected the ponto-cerebellar fibres whereas the neurons of the pontine nuclei were spared.That radiotherapy is responsible is suggested by many features.As in the cases of De Vivo et al,Rosemberg and Bleyer and Griffin,leukoencephalopathy appears after a quite regular delay following irradiation.The lesions are limited to the irradiated brain and spare the unirradiated spinal cord.The frequency of leukoencephalopathy increases with increasing doses of irradiation.This case suggests Demyelinating Leukoencephalopathy with clinical and radiological findings, biopsy is required for definitive diagnosis.
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