Critical illness polyneuropathy in ICU patients is related to reduced motor nerve excitability caused by reduced sodium permeability

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.Electronic supplementary materialThe online version of this article (doi:10.1186/s40635-016-0083-4) contains supplementary material, which is available to authorized users.

Electrophysiologic alterations in the excitability of the sciatic and vagus nerves during early stages of sepsis

“… 8 , 9 Preliminary findings have suggested that, rather than degeneration of axons, the reduction in the excitability of motor and sensory fibers is due to a hyperpolarized shift in the voltage dependence of sodium caused by inactivation of sodium channels in peripheral nerves during the acute phase of critical illness. 10 …”

Approach to critical illness myopathy and polyneuropathy in the older SARS-CoV-2 patients

“…Another theory is that the chronic inflammation in CIP patients increases vascular permeability and leads to vasogenic edema [27]. Fenzi et al biopsied the superficial peroneal nerve of critically ill patients with CIP and found decreased myelin density and axonal degeneration.…”

Neurophysiological study of critical illness polyneuropathy and myopathy in mechanically ventilated children; additional aspects in paediatric critical illness comorbidities

“…On the other hand, the explanation of the reduced motor and sensory nerve amplitudes in CIP is reported to be due to dysfunction of voltage-gated sodium channels, as abnormal membrane depolarization found in different tissues of critically ill patients may cause reduced membrane excitability [35]. Also, Z'Graggen et al [36] described membrane depolarization of motor nerves in patients with CIP.…”