Sejvar James J, Leis A Arturo, Stokic Dobrivoje S, Van Gerpen Jay A, Marfin Anthony A, Webb Risa, Haddad Maryam B, Tierney Bruce C, Slavinski Sally A, Polk Jo Lynn, Dostrow Victor, Winkelmann Michael, Petersen Lyle R
Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
Emerg Infect Dis. 2003 Jul;9(7):788-93. doi: 10.3201/eid0907.030129.
Acute weakness associated with West Nile virus (WNV) infection has previously been attributed to a peripheral demyelinating process (Guillain-Barré syndrome); however, the exact etiology of this acute flaccid paralysis has not been systematically assessed. To thoroughly describe the clinical, laboratory, and electrodiagnostic features of this paralysis syndrome, we evaluated acute flaccid paralysis that developed in seven patients in the setting of acute WNV infection, consecutively identified in four hospitals in St. Tammany Parish and New Orleans, Louisiana, and Jackson, Mississippi. All patients had acute onset of asymmetric weakness and areflexia but no sensory abnormalities. Clinical and electrodiagnostic data suggested the involvement of spinal anterior horn cells, resulting in a poliomyelitis-like syndrome. In areas in which transmission is occurring, WNV infection should be considered in patients with acute flaccid paralysis. Recognition that such weakness may be of spinal origin may prevent inappropriate treatment and diagnostic testing.
先前认为与西尼罗河病毒(WNV)感染相关的急性肌无力是由外周脱髓鞘过程(格林-巴利综合征)引起的;然而,这种急性弛缓性麻痹的确切病因尚未得到系统评估。为了全面描述这种麻痹综合征的临床、实验室和电诊断特征,我们对在路易斯安那州圣塔曼尼教区和新奥尔良以及密西西比州杰克逊的四家医院连续确诊的7例急性WNV感染患者所出现的急性弛缓性麻痹进行了评估。所有患者均急性起病,表现为不对称肌无力和无反射,但无感觉异常。临床和电诊断数据提示脊髓前角细胞受累,导致类似脊髓灰质炎的综合征。在正在发生病毒传播的地区,急性弛缓性麻痹患者应考虑WNV感染。认识到这种肌无力可能源于脊髓,可避免不恰当的治疗和诊断检查。