Acute quadriplegic myopathy following autologous peripheral blood stem cell transplantation for breast cancer

Samuelsson, Jan; Zackrisson, Håkan; Tokics, L.; Ljungman, Per; Lidbrink, Elisabet; Pircher, P; Larsson, Lars

doi:10.1038/sj.bmt.1701661

Cited by 7 publications

(3 citation statements)

References 10 publications

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“…Furthermore, the complete "mechanical silencing," unique for ICU patients, has been shown to play an important role in the development of CIM in experimental and clinical studies (435,517,574). An additional factor that needs to be taken into account is the relatively long delay between exposure to trigger factors and the phenotype characterizing CIM, i.e., severe muscle wasting and preferential myosin loss (399,511,610). The preferential and significant myosin loss is the result of both a decreased synthesis at the transcriptional level and increased myofibrillar protein degradation (399,434,496,513,517).…”

Section: A the Problem Of Choosing The Right Animal Model: Matching mentioning

confidence: 99%

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

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

274

308

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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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Section: A the Problem Of Choosing The Right Animal Model: Matching mentioning

confidence: 99%

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

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

274

308

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“…This preparation in combination with biochemical and molecular biological methods has been of particular importance for our understanding of the mechanisms underlying generalized muscle weakness in patients with acute quadriplegic myopathy (AQM), i.e. the weakness observed in mechanically ventilated patients given massive doses of corticosteroid in combination with non-depolarizing neuromuscular blocking agents (NMBA) and sepsis [59,60,65]. This condition was initially regarded as rare and of limited clinical significance.…”

Section: Resultsmentioning

confidence: 99%

“…We have found the skinned fibre preparation to be very useful in the study of various neuromuscular disorders [56,[58][59][60]65]. This preparation in combination with biochemical and molecular biological methods has been of particular importance for our understanding of the mechanisms underlying generalized muscle weakness in patients with acute quadriplegic myopathy (AQM), i.e.…”

Section: Resultsmentioning

confidence: 99%

Regulation of human muscle contraction at the cellular and molecular levels

Larsson

Höök

Pircher

1999

Neurological Sciences

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The rat is the most extensively characterized species with regard to regulation of muscle contraction and myofibrillar protein isoform expression, but there is reason to question whether results from small mammals, such as the rat, can be extrapolated directly to larger mammals, such as man. Studies of human muscle contraction have primarily used different in vivo muscle function measurements, i.e. measurements of force at different speeds of movement during electrical stimulation or voluntary activation. These measurements give important information on overall muscle function, but they are of limited value for our understanding of regulation of muscle contraction. In basic science, cellular-and molecular-physiological methods have been used for many years, but these techniques have so far only rarely been used in studies of human muscle contraction. Detailed studies of human muscle contraction can be performed in the short muscle fibre segments obtained by the percutaneous muscle biopsy technique both at the cellular and molecular level. The skinned fibre preparation in combination with a novel in vitro motility assay offers a unique possibility to investigate regulation of human muscle contraction at the cellular and molecular levels in the same muscle cell segment in both health and disease, i.e. in muscle cells characterized according to the type and amount of expressed myofibrillar protein isoforms.

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Complications neuromusculaires des patients transplantés

Echaniz‐Laguna

2007

Revue Neurologique

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Acute quadriplegic myopathy following autologous peripheral blood stem cell transplantation for breast cancer

Cited by 7 publications

References 10 publications

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

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

Regulation of human muscle contraction at the cellular and molecular levels

Complications neuromusculaires des patients transplantés

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