Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2026
Changes of motor nerve membrane excitability during the acute phase of critical illness.
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Staub Lula, Exl Matthias Thomas, Hedström Yvette, Larsson Lars, Rodriguez Belén, Schefold Joerg C, Z'Graggen Werner J
Аннотация
OBJECTIVE: To investigate early alterations in motor nerve membrane properties during critical illness using nerve excitability testing.
METHODS: Adult critically ill patients admitted to the intensive care unit were examined within 24 h of intubation (day 1) and on days 2, 5 and 10. Examinations included neurological examination, nerve excitability testing, laboratory analyses and review of medication records; and on day 10 conventional nerve conduction studies, electromyography and a fine needle muscle biopsy.
RESULTS: All critically ill patients (N = 26) showed nerve hypoexcitability within 24 h compared to healthy subjects, which persisted up to day 10. Additional nerve membrane depolarisation was only observed in critically ill patients with acute kidney injury (AKI) (n = 13). Four patients fulfilled the diagnostic criteria for critical illness polyneuropathy (CIP) at day 10 (15.4%), and six (23.1%) had a reduced myosin:actin ratio indicative of myosin loss consistent with critical illness myopathy.
CONCLUSIONS: Nerve hypoexcitability appears to be a key feature of the early phase of critical illness, whereas additional nerve membrane depolarisation is associated with AKI, which may be linked to changes in serum potassium levels.
SIGNIFICANCE: The findings do not support CIP as predominant explanation for nerve membrane depolarisation and muscle weakness seems to be associated with myosin loss.
METHODS: Adult critically ill patients admitted to the intensive care unit were examined within 24 h of intubation (day 1) and on days 2, 5 and 10. Examinations included neurological examination, nerve excitability testing, laboratory analyses and review of medication records; and on day 10 conventional nerve conduction studies, electromyography and a fine needle muscle biopsy.
RESULTS: All critically ill patients (N = 26) showed nerve hypoexcitability within 24 h compared to healthy subjects, which persisted up to day 10. Additional nerve membrane depolarisation was only observed in critically ill patients with acute kidney injury (AKI) (n = 13). Four patients fulfilled the diagnostic criteria for critical illness polyneuropathy (CIP) at day 10 (15.4%), and six (23.1%) had a reduced myosin:actin ratio indicative of myosin loss consistent with critical illness myopathy.
CONCLUSIONS: Nerve hypoexcitability appears to be a key feature of the early phase of critical illness, whereas additional nerve membrane depolarisation is associated with AKI, which may be linked to changes in serum potassium levels.
SIGNIFICANCE: The findings do not support CIP as predominant explanation for nerve membrane depolarisation and muscle weakness seems to be associated with myosin loss.