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脱髓鞘疾病脊髓病变所致顽固性呃逆

Intractable hiccup caused by spinal cord lesions in demyelination disease.

作者信息

Hao Xiao-ting, Wang Lu, Yan Bo, Zhou Hong-yu

机构信息

Department of Neurology, West China Hospital, Sichuan University, Chengdu, China.

出版信息

J Spinal Cord Med. 2013 Nov;36(6):711-4. doi: 10.1179/2045772313Y.0000000148. Epub 2013 Jun 13.

DOI:10.1179/2045772313Y.0000000148
PMID:24090474
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3831336/
Abstract

OBJECTIVE

This study aimed to summarize the clinical features of patients who presented intractable hiccup (IH) without brain and medulla oblongata (MO) lesions.

METHOD

This study included six patients who were diagnosed with inflammatory demyelinating myelitis, categorized as neuromyelitis optica (NMO), multiple sclerosis (MS), and myelitis. Patients who presented IH with cervical lesions but without MO lesions were also included. Clinical profiles, laboratory data, and magnetic resonance imaging findings were analyzed.

RESULTS

Three out of six patients were diagnosed with NMO, whereas the remaining three were diagnosed with acute myelitis, recurrent myelities, and MS, respectively. The duration of hiccup was from 2 to 23 days (average = 9.33 ± 8.64 days). Five patients (83.33%, patients 1-5) had long segmental lesions and one had a patchy lesion. None of these patients had any MO lesions. Half of them were successfully treated with high-dose methylprednisolone combined with gamma-aminobutyric acid (GABA) inhibitor.

CONCLUSION

IH occurred in patients without MO lesion. However, the mechanism remained unclear. Immune factors of demyelinating neuropathy stimulated the hiccup reflex arch. Cervical cord lesions may activate the hiccup center. In general, IH can be controlled by IVMP combined with GABA inhibitor. Unilateral phrenic nerve block may elicit no effect.

摘要

目的

本研究旨在总结无脑和延髓(MO)病变的顽固性呃逆(IH)患者的临床特征。

方法

本研究纳入6例被诊断为炎性脱髓鞘性脊髓炎的患者,分类为视神经脊髓炎(NMO)、多发性硬化症(MS)和脊髓炎。纳入有颈部病变但无MO病变的IH患者。分析临床资料、实验室数据和磁共振成像结果。

结果

6例患者中有3例被诊断为NMO,其余3例分别被诊断为急性脊髓炎、复发性脊髓炎和MS。呃逆持续时间为2至23天(平均=9.33±8.64天)。5例患者(83.33%,患者1-5)有长节段病变,1例有斑片状病变。这些患者均无任何MO病变。其中一半患者通过大剂量甲基强的松龙联合γ-氨基丁酸(GABA)抑制剂成功治疗。

结论

无MO病变的患者可发生IH。然而,其机制仍不清楚。脱髓鞘性神经病的免疫因素刺激呃逆反射弧。颈髓病变可能激活呃逆中枢。一般来说,IH可通过静脉注射甲基强的松龙联合GABA抑制剂得到控制。单侧膈神经阻滞可能无效。

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