Critically ill polyneuropathy: electrophysiological studies and differentiation from Guillain-Barre syndrome.

Bolton, C F; Laverty, D A; Brown, Jason; Witt, Norbert; Hahn, Angelika F.; Sibbald, William J.

doi:10.1136/jnnp.49.5.563

Cited by 271 publications

(174 citation statements)

References 10 publications

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“…However, it took another century before this syndrome was described in more detail and was labeled as CIP (67). Almost simultaneously, several authors reported the occurrence of profound flaccid and symmetrical weakness after a severe disease (35,66,68,134,590,812). The weakness was accompanied by muscle wasting and often, but not necessarily, by reduction or loss of tendon reflexes but with a relative sparing of the facial muscles.…”

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

confidence: 99%

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

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

291

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

confidence: 99%

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

Friedrich

Reid

Berghe

et al. 2015

Physiological Reviews

291

329

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“…Myopathy is due to both structural abnormalities, which include loss of myosin thick filament and atrophy, and physiologic abnormalities caused by reduced excitability (5)(6)(7). It has appeared that neuropathy is accounted for by degeneration of axons (8)(9)(10) such that physiologic problems do not contribute. However, 2 studies suggest that physiologic problems may contribute to neuropathy in critically ill patients.…”

Section: Introductionmentioning

confidence: 99%

Inactivation of sodium channels underlies reversible neuropathy during critical illness in rats

Novak¹,

Nardelli²,

Cope³

et al. 2009

J. Clin. Invest.

100

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Neuropathy and myopathy can cause weakness during critical illness. To determine whether reduced excitability of peripheral nerves, rather than degeneration, is the mechanism underlying acute neuropathy in critically ill patients, we prospectively followed patients during the acute phase of critical illness and early recovery and assessed nerve conduction. During the period of early recovery from critical illness, patients recovered from neuropathy within days. This rapidly reversible neuropathy has not to our knowledge been previously described in critically ill patients and may be a novel type of neuropathy. In vivo intracellular recordings from dorsal root axons in septic rats revealed reduced action potential amplitude, demonstrating that reduced excitability of nerve was the mechanism underlying neuropathy. When action potentials were triggered by hyperpolarizing pulses, their amplitudes largely recovered, indicating that inactivation of sodium channels was an important contributor to reduced excitability. There was no depolarization of axon resting potential in septic rats, which ruled out a contribution of resting potential to the increased inactivation of sodium channels. Our data suggest that a hyperpolarized shift in the voltage dependence of sodium channel inactivation causes increased sodium inactivation and reduced excitability. Acquired sodium channelopathy may be the mechanism underlying acute neuropathy in critically ill patients.

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“…7 The presence of sensory involvement, in addition to motor impairment, is well described in the axonal variant of GBS, known as acute motor-sensory axonal neuropathy (AMSAN). However, sensory involvement can also be seen in CiN.…”

Section: Discussionmentioning

confidence: 99%