孤立性第三脑神经麻痹与缺血性垂体卒中继发低渗性低钠血症突然恶化相关

Emanuele Varaldo, Alessandro Maria Berton, Mauro Maccario, Valentina Gasco
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摘要

垂体性中风(PA)是一种罕见的急症。蝶鞍内压力的突然增加可能导致周围结构受到压迫,从而导致相关的典型症状,特别是视野损害和/或眼麻痹和垂体功能减退;低渗性低钠血症也可能发生,即使它并不常见。虽然在文献中已有描述,但孤立性III型脑神经麻痹的病例极为罕见。我们报告一例60岁左右的男性垂体腺瘤患者,因头痛加重,对止痛药无反应而进入急诊科(ED),形态学图像与缺血性PA一致,尽管垂体病变未见尺寸增加;在ED进入后,还观察到轻度无症状低钠血症。地塞米松、甘露醇经经验应用于神经外科指征,曲马多、酮乐酸也及时应用,但均无疗效。在接下来的几天里,出现了严重的低渗性低钠血症,并出现了明显的左III型脑神经麻痹,但没有观察到明显的脑出血或缺血迹象,也没有观察到明显的同外侧海绵窦压迫。在排除了其他可能的原因后,对液体限制的快速反应证实了不适当抗利尿综合征(SIAD)的可能诊断。总的来说,由于钠水平的正常化与III型脑神经麻痹的快速和完全逆转有关,因此,强直性血浆水平的突然下降似乎有助于神经功能障碍的加剧。
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Isolated Third Cranial Nerve Palsy Associated with Sudden Worsening of Hypotonic Hyponatremia Secondary to Ischemic Pituitary Apoplexy
Pituitary apoplexy (PA) is a rare medical emergency. The sudden pressure increase in the sella turcica may determine compression on the surrounding structures determining the classical symptomatology associated, especially visual field impairment and/or ocular palsies and hypopituitarism; hypotonic hyponatremia may occur too, even if it is not common. Although already described in the literature, cases of isolated III cranial nerve palsies are extremely rare events. We report the case of a mid-60-year-old man with a known pituitary adenoma accessing the Emergency Department (ED) for worsening headaches unresponsive to analgesics, with a morphological picture consistent with ischemic PA, despite no dimensional increase of the pituitary lesion; upon ED access, a mild paucisymptomatic hyponatremia was also observed. Dexamethasone and mannitol were empirically introduced upon neurosurgical indication and tramadol and ketorolac were promptly administered as well, but without benefit. In the next days, a severe hypotonic hyponatremia was evidenced and a clear left III cranial nerve palsy developed, but no clear signs of cerebral bleeding or ischemia, nor a significant compression on the homolateral cavernous sinus, were observed. Upon ruling out other possible causes, a likely diagnosis of syndrome of inappropriate antidiuresis (SIAD) was made, confirmed by the quick response to fluid restriction. Overall, the sudden fall in tonicity plasma levels seemed to contribute to the exacerbation of the neurological deficit since the normalization of sodium levels was associated with a rapid and complete reversion of the III cranial nerve palsy.
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