ArticleIntensive care medicine experimental2016
Critical illness polyneuropathy in ICU patients is related to reduced motor nerve excitability caused by reduced sodium permeability.
Article in Intensive care medicine experimental, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 24 citations in OpenAlex.
- Temporary and highly variable recovery of neuromuscular dysfunction by electrical stimulation in the follow-up of acute critical illness neuromyopathy: a pilot study.Neurological research and practice · 2023Article
- Development and early diagnosis of critical illness myopathy in COVID-19 associated acute respiratory distress syndrome.Journal of cachexia, sarcopenia and muscle · 2022Article
- Article
- Impact of prolonged sepsis on neural and muscular components of muscle contractions in a mouse model.Journal of cachexia, sarcopenia and muscle · 2021Article
- Muscular weakness and muscle wasting in the critically ill.Journal of cachexia, sarcopenia and muscle · 2020Review
- Approach to critical illness myopathy and polyneuropathy in the older SARS-CoV-2 patients.Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia · 2020Review
- [Sepsis impairs aggregation of nicotinic acetylcholine receptors on murine skeletal muscle cell membranes by inhibiting AKT/GSK3β phosphorylation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Pneumonia and hypercapnic respiratory failure.Breathe (Sheffield, England) · 2019Article
- Electrophysiologic alterations in the excitability of the sciatic and vagus nerves during early stages of sepsis.Journal of pain research · 2018Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundReduced motor and sensory nerve amplitudes in critical illness polyneuropathy (CIP) are characteristic features described in electrophysiological studies and due to dysfunction of voltage-gated sodium channels. Yet, faulty membrane depolarization as reported in various tissues of critically ill patients may cause reduced membrane excitability as well. The aim of this study was to compare the pathophysiological differences in motor nerve membrane polarization and voltage-gated sodium channel function between CIP patients and critically ill patients not developing CIP during their ICU stay (ICU controls).
methodsICU patients underwent electrophysiological nerve conduction studies and were categorized as either ICU controls or CIP patients. Subsequently, excitability parameters were recorded as current-threshold relationship, stimulus-response behavior, threshold electrotonus, and recovery of excitability from the abductor pollicis brevis following median nerve stimulation.
resultsTwenty-six critically ill patients were enrolled and categorized as 12 ICU controls and 14 CIP patients. When compared to 31 healthy subjects, the ICU controls exhibited signs of membrane depolarization as shown by reduced superexcitability (p = 0.003), depolarized threshold electrotonus (p = 0.007), increased current-threshold relationship (p = 0.03), and slightly prolonged strength-duration time constant. In contrast, the CIP patients displayed a significantly reduced strength-duration time constant (p < 0.0001), which indicates an increased inactivation of voltage-gated sodium channels.
conclusionsAbnormal motor nerve membrane depolarization is a general finding in critically ill patients whereas voltage-gated sodium channel dysfunction is a characteristic of CIP patients.
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