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本文引用的文献

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Hyperpolarized shifts in the voltage dependence of fast inactivation of Nav1.4 and Nav1.5 in a rat model of critical illness myopathy.在危重病性肌病大鼠模型中,Nav1.4和Nav1.5快速失活电压依赖性的超极化移位。
J Physiol. 2004 Sep 15;559(Pt 3):813-20. doi: 10.1113/jphysiol.2004.062349. Epub 2004 Jul 14.
2
Critical illness myopathy serum fractions affect membrane excitability and intracellular calcium release in mammalian skeletal muscle.危重病性肌病血清成分影响哺乳动物骨骼肌的膜兴奋性和细胞内钙释放。
J Neurol. 2004 Jan;251(1):53-65. doi: 10.1007/s00415-004-0272-z.
3
Neuromuscular alterations in the critically ill patient: critical illness myopathy, critical illness neuropathy, or both?危重症患者的神经肌肉改变:危重症性肌病、危重症性神经病,还是两者皆有?
Intensive Care Med. 2003 Sep;29(9):1411-3. doi: 10.1007/s00134-003-1884-y.
4
Propagation velocity in electrically activated muscle fibres in man.人体电激活肌纤维中的传播速度。
Acta Physiol Scand. 1955 Sep 20;34(1):75-89. doi: 10.1111/j.1748-1716.1955.tb01227.x.
5
Critical illness polyneuromyopathy: the electrophysiological components of a complex entity.危重病性多神经肌肉病:一种复杂病症的电生理组成部分
Intensive Care Med. 2003 Sep;29(9):1505-14. doi: 10.1007/s00134-003-1858-0. Epub 2003 Jul 17.
6
Crucial role of sodium channel fast inactivation in muscle fibre inexcitability in a rat model of critical illness myopathy.钠通道快速失活在危重病性肌病大鼠模型中肌肉纤维兴奋性丧失中的关键作用
J Physiol. 2003 Mar 1;547(Pt 2):555-66. doi: 10.1113/jphysiol.2002.035188. Epub 2003 Jan 24.
7
Paresis acquired in the intensive care unit: a prospective multicenter study.重症监护病房获得性轻瘫:一项前瞻性多中心研究。
JAMA. 2002 Dec 11;288(22):2859-67. doi: 10.1001/jama.288.22.2859.
8
Critical illness myopathy.危重病性肌病
Curr Rheumatol Rep. 2002 Oct;4(5):403-8. doi: 10.1007/s11926-002-0085-y.
9
Vecuronium-associated axonal motor neuropathy: a variant of critical illness polyneuropathy?维库溴铵相关轴索性运动神经病:危重病性多发性神经病的一种变异型?
Neuromuscul Disord. 2001 Sep;11(6-7):579-82. doi: 10.1016/s0960-8966(01)00200-0.
10
Electrophysiologic studies in critical illness associated weakness: myopathy or neuropathy--a reappraisal.危重症相关肌无力的电生理研究:肌病还是神经病——重新评估
Clin Neurophysiol. 2001 Sep;112(9):1586-93. doi: 10.1016/s1388-2457(01)00572-7.

通过直接肌肉刺激确定重症监护病房获得性麻痹的起源。

Origin of ICU acquired paresis determined by direct muscle stimulation.

作者信息

Lefaucheur J-P, Nordine T, Rodriguez P, Brochard L

机构信息

Service de Physiologie-Explorations Fonctionnelles, Centre Hospitalier Universitaire Henri Mondor, 51 avenue du Marechal de Lattre de Tassigny, 94010 Creteil, France.

出版信息

J Neurol Neurosurg Psychiatry. 2006 Apr;77(4):500-6. doi: 10.1136/jnnp.2005.070813. Epub 2005 Nov 23.

DOI:10.1136/jnnp.2005.070813
PMID:16306155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2077517/
Abstract

BACKGROUND

Acquired diffuse paresis in an intensive care unit (ICU) can result from critical illness myopathy or polyneuropathy. Clinical examination and conventional neurophysiological techniques may not distinguish between these entities.

OBJECTIVE

To assess the value of direct muscle stimulation (DMS) to differentiate myopathic from neuropathic process in critically ill patients with diffuse severe muscle weakness.

METHODS

30 consecutive patients with ICU acquired diffuse motor weakness were studied. Responses of the right deltoid and tibialis anterior muscles to DMS and to motor nerve stimulation (MNS) were studied and compared with results of conventional nerve conduction studies and concentric needle electromyography (EMG). An original algorithm was used for differential diagnosis, taking into account first the amplitude of the responses to DMS, then the MNS to DMS amplitude ratio, and finally the amplitude of the sensory nerve action potentials recorded at the lower limbs.

RESULTS

Evidence of neuropathy and myopathy was found in 57% and 83% of the patients, respectively. Pure or predominant myopathy was found in 19 patients. Other results were consistent with neuromyopathy (n = 5) and pure or predominant neuropathy (n = 2). Four patients had normal results with stimulation techniques, but spontaneous EMG activity and raised plasma creatine kinase suggesting necrotic myopathy.

CONCLUSIONS

A neurophysiological approach combining DMS and conventional techniques revealed myopathic processes in a majority of ICU patients. Reduced muscle fibre excitability may be a leading cause for this. The diagnosis of myopathy in ICU acquired paralysis can be established by a combination of DMS, needle EMG, and plasma creatine kinase.

摘要

背景

重症监护病房(ICU)获得性弥漫性轻瘫可由危重病性肌病或多发性神经病引起。临床检查和传统神经生理学技术可能无法区分这些情况。

目的

评估直接肌肉刺激(DMS)在鉴别患有弥漫性严重肌无力的危重病患者的肌病性与神经病性过程中的价值。

方法

对30例连续的ICU获得性弥漫性运动无力患者进行研究。研究右侧三角肌和胫前肌对DMS以及运动神经刺激(MNS)的反应,并与传统神经传导研究和同心针肌电图(EMG)结果进行比较。采用一种原始算法进行鉴别诊断,首先考虑对DMS的反应幅度,然后是MNS与DMS的幅度比,最后是下肢记录的感觉神经动作电位的幅度。

结果

分别在57%和83%的患者中发现神经病和肌病的证据。19例患者存在单纯性或主要为肌病。其他结果与神经肌肉病(n = 5)和单纯性或主要为神经病(n = 2)一致。4例患者的刺激技术结果正常,但肌电图自发活动及血浆肌酸激酶升高提示坏死性肌病。

结论

结合DMS和传统技术的神经生理学方法在大多数ICU患者中揭示了肌病性过程。肌纤维兴奋性降低可能是其主要原因。ICU获得性瘫痪中肌病的诊断可通过DMS、针极肌电图和血浆肌酸激酶联合确定。