Acute quadriplegic myopathy

Hirano, Michio; Ott, Bernhard; Raps, Eric C.; Minetti, Carlo; Lennihan, Laura; Libbey, N. P.; Bonilla, E.; Hays, Arthur P.

doi:10.1212/wnl.42.11.2082

Cited by 216 publications

(89 citation statements)

References 12 publications

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“…In this study the agents more commonly related with myopathy were corticosteroids that can be associated either with acute or chronic myopathy; the latter was more common as had also been reported in other series 1,3,8,9 . This form of myopathy can occur in up to 60% or more of patients in chronic use of corticosteroids 3 .…”

Section: Discussionsupporting

confidence: 73%

Toxic myopathies: muscle biopsy features

Scola

Pereira

Lorenzoni

et al. 2007

Arq. Neuro-Psiquiatr.

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-Several drugs and toxic substances can cause muscular abnormalities and are frequent causes of acquired myopathies. We present a series of 32 patients, predominance of young adult patients, diagnosed with toxic myopathy. The most common substances inducing myopathy were corticosteroids (56.2%) followed by the propoxyphene, neuroleptics, zidovudine and drug-induced hypokalemia. The investigation showed normal serum creatine kinase levels in 65.4%, myopathic pattern of the needle electromyography in 40% and the more frequent histological diagnosis of the muscle biopsy was type 2 fiber atrophy (59.3%). Clinical features, etiology, course of the disease, serum levels of muscular enzymes, electromyographic features and, especially, muscle biopsy features are discussed.KEY WORDS: myopathy, drug, iatrogenic myopathy, toxic myopathy, muscle biopsy.Miopatia tóxica: biópsia muscular RESUMO -Diversos medicamentos e substâncias tóxicas podem causar alterações musculares e são causas freqüentes de miopatia adquirida. Apresentamos uma série de 32 pacientes, predomínio de pacientes adulto jovens, com miopatia tóxica. As substâncias mais relacionadas com a miopatia foram os corticosteróides (56,2%) seguidos pelo propoxifeno, neurolépticos, zidovudina e drogas indutoras de hipocalemia. A investigação mostrou níveis normais de creatino quinase sérica em 65,4%, eletromiografia de agulha com padrão miopático em 40% e o mais freqüente diagnóstico histológico da biópsia muscular foi atrofia de fibras do tipo 2 (59,3%). As manifestações clínicas, etiologia, tempo de evolução, nível sérico das enzimas musculares, alterações da eletroneuromiografia e, especialmente, da biópsia muscular são discutidos. PALAVRAS-CHAVE: miopatias, drogas, miopatia iatrogênica, miopatia tóxica, biópsia muscular.

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Section: Discussionsupporting

confidence: 73%

Toxic myopathies: muscle biopsy features

Scola

Pereira

Lorenzoni

et al. 2007

Arq. Neuro-Psiquiatr.

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“…Several other authors, by use of muscle biopsies, confirmed the occurrence of an acute myopathy in the intensive care unit, associated with the use of corticosteroids and neuromuscular blocking agents (37, 141,165,314,382). These patients exhibited preferential myosin loss and also demonstrated flaccid weakness and failure to wean from the respirator.…”

Section: History Time Course and Clinical Features Of Icu-relatmentioning

confidence: 85%

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

292

329

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Critical illness polyneuropathies (CIP) and myopathies (CIM) are common complications of critical illness. Several weakness syndromes are summarized under the term intensive care unit-acquired weakness (ICUAW). We propose a classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data. Triggers include sepsis, mechanical ventilation, muscle unloading, steroid treatment, or denervation. Some ICUAW forms require stringent diagnostic features; CIM is marked by membrane hypoexcitability, severe atrophy, preferential myosin loss, ultrastructural alterations, and inadequate autophagy activation while myopathies in pure sepsis do not reproduce marked myosin loss. Reduced membrane excitability results from depolarization and ion channel dysfunction. Mitochondrial dysfunction contributes to energy-dependent processes. Ubiquitin proteasome and calpain activation trigger muscle proteolysis and atrophy while protein synthesis is impaired. Myosin loss is more pronounced than actin loss in CIM. Protein quality control is altered by inadequate autophagy. Ca 2ϩ dysregulation is present through altered Ca 2ϩ homeostasis. We highlight clinical hallmarks, trigger factors, and potential mechanisms from human studies and animal models that allow separation of risk factors that may trigger distinct mechanisms contributing to weakness. During critical illness, altered inflammatory (cytokines) and metabolic pathways deteriorate muscle function. ICUAW prevention/treatment is limited, e.g., tight glycemic control, delaying nutrition, and early mobilization. Future challenges include identification of primary/secondary events during the time course of critical illness, the interplay between membrane excitability, bioenergetic failure and differential proteolysis, and finding new therapeutic targets by help of tailored animal models.

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“…Finally, the combination of mechanical ventilation with muscle-relaxing agents and/or high-dose steroids was reported to be associated with significant myopathy [19][20][21][22][23]24]. Muscle weakness varied from mildto-severe.…”

Section: Patient Studiesmentioning

confidence: 99%

Effects of mechanical ventilation on diaphragm function and biology

Gayan‐Ramirez¹,

Decramer²

2002

Eur Respir J

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The pathophysiological mechanisms of weaning from mechanical ventilation are not fully known, but there is accumulating evidence that mechanical ventilation induces inspiratory muscle dysfunction.Recently, several animal models have provided potential mechanisms for mechanical ventilation-induced effects on muscle function. In patients, weaning difficulties are associated with inspiratory muscle weakness and reduced endurance capacity. Animal studies demonstrated that diaphragm force was already decreased after 12 h of controlled mechanical ventilation and this worsened with time spent on the ventilator.Diaphragmatic myofibril damage observed after 3-days controlled mechanical ventilation was inversely correlated with maximal diaphragmatic force. Downregulation of the diaphragm insulin-like growth factor-I and MyoD/myogenin messenger ribonucleic acid occurred after 24 h and diaphragmatic oxidative stress and increased protease activity after 18 h. In keeping with these findings, diaphragm fibre atrophy was shown after 12 h and reduced diaphragm mass was reported after 48 h of controlled mechanical ventilation.These animal studies show that early alterations in diaphragm function develop after short-term mechanical ventilation. These alterations may contribute to the difficulties in weaning from mechanical ventilation seen in patients. Strategies to preserve respiratory muscle mass and function during mechanical ventilation should be developed. These may include: adaptation of medication, training of the diaphragm, stabilisation of the catabolic state and pharmacotherapy.

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Acute quadriplegic myopathy

Cited by 216 publications

References 12 publications

Toxic myopathies: muscle biopsy features

Toxic myopathies: muscle biopsy features

The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

Effects of mechanical ventilation on diaphragm function and biology

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