Bureau Britta L, Obeidat Ahmed, Dhariwal Mohan S, Jha Pinky
Internal Medicine/Neurology, Medical College of Wisconsin, Wauwatosa, USA.
Neurology, Medical College of Wisconsin, Wauwatosa, USA.
Cureus. 2020 Nov 12;12(11):e11452. doi: 10.7759/cureus.11452.
Previous reports have shown various neurological manifestations in about 36.4% of patients infected with SARS-Cov-2. However, peripheral neuropathy was only reported once before. A 40-year-old healthy woman presented with two weeks of cough, nasal congestion, sore throat, intermittent fevers, fatigue, and myalgia but no weakness. She tested positive for the SARS-Cov-2. Physical exam showed no neurologic deficit. Two weeks later, respiratory symptoms were improving but she developed sudden leg pain, numbness, and weakness. She described it as a "pain crisis". Neurological exam showed bilateral symmetrical, non-ascending lower extremity weakness and normal, symmetric reflexes. She had normal magnetic resonance imaging of the brain and spine, spinal fluid analysis, serum studies including creatinine kinase and C-reactive protein. She had elevated lactate dehydrogenase, low serum copper (72.9 (ref: 80.0-155.0 ug/dL)) and low vitamin B6 (14.6 (ref: 20.0-125.0 nmol/L)). A diagnosis of SARS-Cov-2-associated peripheral neuropathy was considered. We pursued empiric treatment with intravenous steroids (1000 mg methylprednisolone for three days), followed by a total of 2 g/kg of intravenous immunoglobulins (IVIG) given over five days. Pain management was done with gabapentin and ketorolac. We replaced copper and vitamin B6. Six weeks later, she reported improvement and was closer to baseline, but she endorsed residual, exertional, mild bilateral lower extremity pain, numbness, and weakness. Previous reports of treatment of SARS-Cov-2-associated neuropathy included corticosteroids and IVIG. Our patient saw the most symptomatic improvement with gabapentin. In our case, the preserved reflexes, lack of ascending pattern, sudden onset of symptoms, and normal cerebrospinal fluid (CSF) argued against Guillain-Barre syndrome. Copper deficiency can result in myelopathy but not peripheral neuropathy, so is unlikely the sole explanation. Awareness and early treatment of peripheral neuropathy in SARS-Cov-2 can result in improved clinical outcomes for patients.
先前的报告显示,约36.4%感染严重急性呼吸综合征冠状病毒2(SARS-CoV-2)的患者出现了各种神经表现。然而,外周神经病变此前仅被报道过一次。一名40岁的健康女性出现了两周的咳嗽、鼻塞、咽痛、间歇性发热、疲劳和肌痛,但无肌无力症状。她的SARS-CoV-2检测呈阳性。体格检查未发现神经功能缺损。两周后,呼吸道症状有所改善,但她突然出现腿部疼痛、麻木和无力。她将其描述为“疼痛危机”。神经学检查显示双侧对称性、非上行性下肢无力,反射正常、对称。她的脑部和脊柱磁共振成像、脑脊液分析、包括肌酸激酶和C反应蛋白在内的血清学检查均正常。她的乳酸脱氢酶升高,血清铜水平低(72.9(参考值:80.0 - 155.0微克/分升)),维生素B6水平低(14.6(参考值:20.0 - 125.0纳摩尔/升))。考虑诊断为SARS-CoV-2相关的外周神经病变。我们采用经验性治疗方案,静脉注射类固醇(1000毫克甲泼尼龙,连用三天),随后在五天内总共给予2克/千克静脉注射免疫球蛋白(IVIG)。使用加巴喷丁和酮咯酸进行疼痛管理。我们补充了铜和维生素B6。六周后,她报告症状有所改善,且更接近基线水平,但她仍认可存在残留的、劳累后轻度双侧下肢疼痛、麻木和无力。先前关于SARS-CoV-2相关神经病变治疗的报告包括使用皮质类固醇和IVIG。我们的患者使用加巴喷丁后症状改善最为明显。在我们的病例中,反射保留、无上行性模式、症状突然发作以及脑脊液(CSF)正常可排除吉兰 - 巴雷综合征。铜缺乏可导致脊髓病,但不会导致外周神经病变,因此不太可能是唯一的解释。认识到SARS-CoV-2相关外周神经病变并早期治疗可改善患者的临床结局。