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      Facial nerve neurographies in intensive care unit-acquired weakness

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          Abstract

          Background

          Patients with an intensive care unit-acquired weakness (ICU-AW) often present clinically with severe paresis of the limb and trunk muscles while facial muscles appear less affected. To investigate whether the facial nerves are partially spared from this condition, we performed both peripheral and cranial nerve conduction studies in critically ill patients.

          Methods

          In patients requiring prolonged ICU therapy, the motor and sensory nerve conduction velocities of the peroneal, ulnar and facial nerves and the muscle action potentials of the associated muscles, as well as the orbicularis oculi reflexes were assessed shortly after admission, and on ICU days 7 and 14.

          Results

          Eighteen patients were included in the final data analysis (average age 54.2 ± 16.8 years, 8 females). The amplitudes of the peroneal nerve compound muscle action potentials (CMAPs) were reduced in all patients at ICU days 7 and 14 (F(1.39; 23.63) = 13.85; p < 0.001). There was no similar decrease in the CMAP amplitudes of the ulnar or facial nerve. Other parameters of nerve function (latencies, sensory and motor nerve conduction velocities, sensory nerve action potentials) remained unchanged. The reproducibility of the orbicularis oculi reflex was reduced during the disease course, while its latencies did not change significantly during the disease course.

          Conclusions

          There is a relative preservation of CMAPs in facial and hand as opposed to foot muscles. This is compatible with the clinical observation that the facial muscles in patients with ICU-AW are less severely affected. This may be primarily a function of the nerve length, and consequently more robust trophic factors in shorter nerves.

          Trial registration This study was prospectively registered in the German Clinical Trial Register on April 20th 2020 (DRKS00021467).

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s42466-023-00275-3.

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          Most cited references19

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          Clinical review: intensive care unit acquired weakness

          A substantial number of patients admitted to the ICU because of an acute illness, complicated surgery, severe trauma, or burn injury will develop a de novo form of muscle weakness during the ICU stay that is referred to as “intensive care unit acquired weakness” (ICUAW). This ICUAW evoked by critical illness can be due to axonal neuropathy, primary myopathy, or both. Underlying pathophysiological mechanisms comprise microvascular, electrical, metabolic, and bioenergetic alterations, interacting in a complex way and culminating in loss of muscle strength and/or muscle atrophy. ICUAW is typically symmetrical and affects predominantly proximal limb muscles and respiratory muscles, whereas facial and ocular muscles are often spared. The main risk factors for ICUAW include high severity of illness upon admission, sepsis, multiple organ failure, prolonged immobilization, and hyperglycemia, and also older patients have a higher risk. The role of corticosteroids and neuromuscular blocking agents remains unclear. ICUAW is diagnosed in awake and cooperative patients by bedside manual testing of muscle strength and the severity is scored by the Medical Research Council sum score. In cases of atypical clinical presentation or evolution, additional electrophysiological testing may be required for differential diagnosis. The cornerstones of prevention are aggressive treatment of sepsis, early mobilization, preventing hyperglycemia with insulin, and avoiding the use parenteral nutrition during the first week of critical illness. Weak patients clearly have worse acute outcomes and consume more healthcare resources. Recovery usually occurs within weeks or months, although it may be incomplete with weakness persisting up to 2 years after ICU discharge. Prognosis appears compromised when the cause of ICUAW involves critical illness polyneuropathy, whereas isolated critical illness myopathy may have a better prognosis. In addition, ICUAW has shown to contribute to the risk of 1-year mortality. Future research should focus on new preventive and/or therapeutic strategies for this detrimental complication of critical illness and on clarifying how ICUAW contributes to poor longer-term prognosis.
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            ICU-acquired weakness

            Critically ill patients often acquire neuropathy and/or myopathy labeled ICU-acquired weakness. The current insights into incidence, pathophysiology, diagnostic tools, risk factors, short- and long-term consequences and management of ICU-acquired weakness are narratively reviewed. PubMed was searched for combinations of “neuropathy”, “myopathy”, “neuromyopathy”, or “weakness” with “critical illness”, “critically ill”, “ICU”, “PICU”, “sepsis” or “burn”. ICU-acquired weakness affects limb and respiratory muscles with a widely varying prevalence depending on the study population. Pathophysiology remains incompletely understood but comprises complex structural/functional alterations within myofibers and neurons. Clinical and electrophysiological tools are used for diagnosis, each with advantages and limitations. Risk factors include age, weight, comorbidities, illness severity, organ failure, exposure to drugs negatively affecting myofibers and neurons, immobility and other intensive care-related factors. ICU-acquired weakness increases risk of in-ICU, in-hospital and long-term mortality, duration of mechanical ventilation and of hospitalization and augments healthcare-related costs, increases likelihood of prolonged care in rehabilitation centers and reduces physical function and quality of life in the long term. RCTs have shown preventive impact of avoiding hyperglycemia, of omitting early parenteral nutrition use and of minimizing sedation. Results of studies investigating the impact of early mobilization, neuromuscular electrical stimulation and of pharmacological interventions were inconsistent, with recent systematic reviews/meta-analyses revealing no or only low-quality evidence for benefit. ICU-acquired weakness predisposes to adverse short- and long-term outcomes. Only a few preventive, but no therapeutic, strategies exist. Further mechanistic research is needed to identify new targets for interventions to be tested in adequately powered RCTs.
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              The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill.

              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(2+) dysregulation is present through altered Ca(2+) 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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                Author and article information

                Contributors
                CStephani@med.uni-goettingen.de
                Journal
                Neurol Res Pract
                Neurol Res Pract
                Neurological Research and Practice
                BioMed Central (London )
                2524-3489
                21 September 2023
                21 September 2023
                2023
                : 5
                : 50
                Affiliations
                [1 ]GRID grid.411984.1, ISNI 0000 0001 0482 5331, Department of Anesthesiology, , University Medical Center Göttingen, ; Robert-Koch-Straße 40, 37075 Göttingen, Germany
                [2 ]GRID grid.411984.1, ISNI 0000 0001 0482 5331, Department of Urology, , University Medical Center Göttingen, ; Robert Koch-Str. 40, 37075 Göttingen, Germany
                [3 ]GRID grid.411984.1, ISNI 0000 0001 0482 5331, Department of Neurology, , University Medical Center Göttingen, ; Robert Koch-Str. 40, 37075 Göttingen, Germany
                Author information
                http://orcid.org/0000-0002-2989-8251
                Article
                275
                10.1186/s42466-023-00275-3
                10512492
                37730657
                6b1be2f4-2291-491b-bcf6-00300c3fe227
                © Deutsche Gesellschaft für Neurologie e.V. 2023

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 21 May 2023
                : 20 July 2023
                Funding
                Funded by: Georg-August-Universität Göttingen (1018)
                Categories
                Research Article
                Custom metadata
                © Deutsche Gesellschaft für Neurologie e.V. 2023

                nerve conduction studies,critical illness,intensive care unit acquired weakness,orbicularis oculi reflex,facial nerve

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