Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage.

Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage.
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DOI:
10.1002/acn3.44
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发表时间:
2014-03-01
影响因子:
5.3
通讯作者:
Hinson, Holly E.
Hinson, Holly E.
中科院分区:
医学2区
文献类型:
--
作者:
Gao, Billy;Pollock, Jeffrey A.;Hinson, Holly E.

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阵发性交感神经亢进 (PSH) 是一种肾上腺素能亢进综合征,可能发生在急性脑损伤后,其特征是生命体征发生阵发性肾上腺素能亢进改变。确定 PSH 患者病变定位的共性具有挑战性,但脑实质内出血 (IPH) 代表的局灶性损伤可能提供见解。我们描述了一系列出现 PSH 的 IPH 患者,并回顾了文献。出现 PSH 的 IPH 患者是从 OHSU 医院记录中确定的。通过 PUBMED、OVID 和 Google Scholar 进行文献综述以识别类似案例。确定了三例符合 PSH 标准的病例。出血量范围为 70 至 128 mL,颅内出血评分范围为 2 至 3。每位患者的出血偏侧性和显着出血量相似,特别是所有出血均较大、皮质下且位于右侧。文献检索发现了另外 6 例病例,其中一半报告右半球出血,大多数也有皮质下定位。我们的文献综述发现了 6 例与 PSH 相关的 IPH 病例,其中 5 例具有皮质下病变位置,与我们的 3 例病例中的破坏区域相呼应。基于这些观察,我们假设从岛叶皮层到下游交感中枢的路径上的损伤可能会消除强直性抑制,导致不受控制的交感神经流出。有必要对 IPH 和 PSH 患者的病变位置进行前瞻性研究来检验这一假设,特别是使用先进的神经影像技术。
Paroxysmal sympathetic hyperactivity (PSH) is a hyperadrenergic syndrome that may follow acute brain injury characterized by episodic, hyperadrenergic alterations in vital signs. Identifying commonality in lesion localization in patients with PSH is challenging, but intraparenchymal hemorrhage (IPH) represents a focal injury that might provide insight. We describe a series of patients with IPH that developed PSH, and review the literature. Patients with IPH who developed PSH were identified from OHSU hospital records. A literature review was conducted to identify similar cases through PUBMED, OVID, and Google Scholar. Three cases meeting criteria for PSH were identified. Hemorrhage volume ranged from 70 to 128 mL, and intracranial hemorrhage score ranged from 2 to 3. The laterality of the hemorrhage and significant volume of hemorrhage was similar in each of the patients, specifically all hemorrhages were large, subcortical, and right-sided. A literature search identified six additional cases, half of whom reported a right hemisphere hemorrhage and the majority also had subcortical localization. Our literature review identified six cases of IPH associated with PSH with five cases having subcortical lesion locations, echoing the areas of disruption in our three cases. On the basis of these observations, we hypothesize that injuries along the pathway from the insular cortex to downstream sympathetic centers may remove tonic inhibition leading to unchecked sympathetic outflow. Prospective investigations of lesion location in patients with IPH and PSH are warranted to test this hypothesis, especially with advanced neuroimaging techniques.
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