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INTRODUCTION: Complications following COVID-19 are starting to emerge; neurological disorders are already described in the literature. CASE REPORT: This case is about a 20-year old male with a severe COVID-19, hospitalized in a Reanimation and Intensive Care Unit with an Acute Respiratory Distress Syndrome, thromboembolic complication and secondary bacterial infection. This patient had a non-specific neurological disorder with a pseudobulbar palsy, (MRI, ENMG and lumbar puncture were normal), associated 4 months later with persistent left shoulder motor deficit and respiratory failure. Respiratory and neurological check-up led to a diagnosis of the Parsonage-Turner syndrome or neuralgic amyotrophy affecting C5-C6 nerve roots, the lateral pectoral and phrenic nerves at the origin of the scapular belt, amyotrophy and left diaphragm paralysis. CONCLUSIONS: This case shows that persistant dyspnoea after COVID 19 infection should lead to a search for a diaphragmatic cause which is not always the result of Reanimation Neuropathy but may also indicate a neuralgic amyotrophy. It is the fourth case of neuralgic amyotrophy following COVID-19. This brings the medical community to consider the risk of diaphragm paralysis apart from critical illness polyneuropathy. Respiratory muscle evaluation and diaphragmatic ultrasound should be considered in case of persistent dyspnoea.

Paediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2 (PIMS-TS) is a recently detected syndrome whose criteria were first established in May 2020 (Royal College of Paediatrics and Child Health). The clinical course varies from mild to severe, life-threatening cases. This paper presents a case of an extremely severe course of PIMS with symptoms resembling Kawasaki syndrome in a previously healthy 13-year-old boy with obesity. A complication of the severe course of PIMS was the development of critical illness polyneuropathy in the patient.

Myasthenia gravis is an autoimmune neuromuscular disease characterized by pathologically rapid fatigue of striated muscles [1]. The main symptom of myasthenia gravis is the presence of pathological muscle weakness with involvement of the ocular, bulbar and skeletal muscles in the pathological process. The provoking factors for the development of myasthenia gravis can be infectious diseases, surgery, drugs [2, 3]. The main danger is represented by myasthenic and cholinergic crises, which are characterized by a severe course and high mortality; therefore, the problems of treating myasthenia gravis are still of high medical and social significance. The prevalence of myasthenia gravis is 17.5–20.3 per 100 thousand population, and the number of patients is increasing by 5–10% annually [4, 5]. In recent years, there has been a steady increase in morbidity with an increase in age over 50 years [6, 7]. Myasthenia gravis is a serious disease with a high mortality rate of up to 30–40% [3]. There are difficulties in the early differential diagnosis of muscle weakness in patients with respiratory failure between myasthenia gravis, myasthenic syndrome and critical illness polyneuropathy. These difficulties and insufficient awareness of patients and doctors of various specialties about myasthenia gravis can lead to the choice of the wrong treatment tactics and the development of myasthenic crisis, which is manifested by respiratory failure, requiring respiratory support. The progression of respiratory failure against the background of myasthenic crisis may require the use of extracorporeal membrane oxygenation (ECMO).It is necessary to expand the differential diagnosis of muscle weakness in a patient during the period of resolution of respiratory failure, allowing to move away from compulsory respiratory support, termination of ECMO.

The COVID-19 pandemic has affected millions of people worldwide. While coronaviruses typically have low rates of neurotropic effects, the massive transmission of SARS-CoV-2 suggests that a substantial population will suffer from potential SARS-CoV-2-related neurological disorders. The rapid and recent emergence of SARS-CoV-2 means little research exists on its potential neurological effects. Here we analyze the effects of similar viruses to provide insight into the potential effects of SARS-CoV-2 on the nervous system and beyond. Seven coronavirus strains (HCoV-OC43, HCoV-HKU1, HCoV-229E, HCoV-NL63, SARS-CoV, MERS-CoV, SARS-CoV-2) can infect humans. Many of these strains cause neurological effects, such as headaches, dizziness, strokes, seizures, and critical illness polyneuropathy/myopathy. Certain studies have also linked coronaviruses with multiple sclerosis and extensive central nervous system injuries. Reviewing these studies provides insight into the anticipated effects for patients with SARS-CoV-2. This review will first describe the effects of other coronaviruses that have caused severe disease (SARS-CoV, MERS-CoV) on the nervous system, as well as their proposed origins, non-neurological effects, and neurological infection mechanisms. It will then discuss what is known about SARS-CoV-2 in these areas with reference to the aforementioned viruses, with the goal of providing a holistic picture of SARS-CoV-2.

Systemic lupus erythematosus (SLE) is a chronic disease of connective tissue with multi-organ invol­vement. Manifestation in the nervous system is one of the most difficult symptoms to assess and interpret. The aim of the study is to indicate diagnostic problems in patients with SLE in whom neurological symptoms are present at the time of diagnosis of SLE but also with complications that occurred after diagnosis. In the presented case, the appearance of flaccid tetraparesis with areflexia suggested peripheral damage to the nervous system. In the electromyography performed in this patient, acute axonal polyneuropathy was mainly suspected. Further differential diagnosis should consider other acute and subacute developing polyneuropathies. Guillain-Barré polyneuropathy deserves special attention. To our knowledge, this is the first case documented in the literature of the coexistence of critical illness polyneuropathy and SLE.

Critical illness-associated weakness (CIAW) is an umbrella term used to describe a group of neuromuscular disorders caused by severe illness. It can be subdivided into three major classifications based on the component of the neuromuscular system (i.e. peripheral nerves or skeletal muscle or both) that are affected. This includes critical illness polyneuropathy (CIP), critical illness myopathy (CIM), and an overlap syndrome, critical illness polyneuromyopathy (CIPNM). It is a common complication observed in people with critical illness requiring intensive care unit (ICU) admission. Given CIAW is found in individuals experiencing grave illness, it can be challenging to study from a practical standpoint. However, over the past 2 decades, many insights into the pathophysiology of this condition have been made. Results from studies in both humans and animal models have found that a profound systemic inflammatory response and factors related to bioenergetic failure as well as microvascular, metabolic, and electrophysiological alterations underlie the development of CIAW. Current management strategies focus on early mobilization, achieving euglycemia, and nutritional optimization. Other interventions lack sufficient evidence, mainly due to a dearth of large trials. The goal of this Physiology in Medicine article is to highlight important aspects of the pathophysiology of these enigmatic conditions. It is hoped that improved understanding of the mechanisms underlying these disorders will lead to further study and new investigations for novel pharmacologic, nutritional, and exercise-based interventions to optimize patient outcomes.

Background Critical illness polyneuropathy and myopathy (CIPNM) is a frequent neurological manifestation in patients with acute respiratory distress syndrome (ARDS) from coronavirus disease 2019 (COVID‐19) infection. CIPNM diagnosis is usually limited to clinical evaluation. We compared patients with ARDS from COVID‐19 and other aetiologies, in whom a neurophysiological evaluation for the detection of CIPNM was performed. The aim was to determine if there were any differences between these two groups in frequency of CINPM and outcome at discharge from the intensive care unit (ICU). Materials and Methods This was a single‐centre retrospective study performed on mechanically ventilated patients consecutively admitted (January 2016‐June 2020) to the ICU of Careggi Hospital, Florence, Italy, with ARDS of different aetiologies. Neurophysiological evaluation was performed on patients with stable ventilation parameters, but marked widespread hyposthenia (Medical Research Council score

INTRODUCTION Data are consistent on the benefits of inpatient rehabilitation for intensive care unit-acquired weaknesses (ICUAW), including critical illness myopathy, critical illness polyneuropathy, critical illness polyneuromyopathy, and disuse atrophy. This study focuses on the effects of inpatient rehabilitation on patients with ICUAW, specifically those with a clinical pattern of proximal muscle weakness and sensory sparing. OBJECTIVES To evaluate the impact of inpatient rehabilitation on patients with ICUAW versus other medically complex patients, and to identify comorbidities associated with poor rehabilitation outcomes. DESIGN Retrospective cohort study. SETTING Institutional, inpatient rehabilitation hospital. PATIENTS Two hundred seventy adult patients (≥18 years) divided into two groups: diagnosis of ICUAW (N = 55) or otherwise medically complex (N = 215), and admitted under the care of one physiatrist. INTERVENTIONS Not applicable. MAIN OUTCOME MEASURES For all patients we compared functional independence measure (FIM) gain, FIM efficiency, rehabilitation length of stay (RLOS), discharge disposition, and major medical comorbidities. RESULTS Patients with ICUAW had significantly greater FIM gain (P = .015) and RLOS (P = .02). There was no significant difference in FIM efficiency (P = .15). Patients with ICUAW had a significantly lower odds of acute hospital transfer (odds ratio [OR] = 0.52, with 95% confidence interval [CI] 0.47, 0.58) and skilled nursing facility discharge (OR = 0.19, with 95% CI 0.038, 0.95). However, patients with ICUAW did have a higher percent of acute hospital transfers than other medically complex patients (P = .017). In addition, patients with ICUAW were more medically complex, as evidenced by a significantly higher Charlson Comorbidity Index (P

Objective To report clinical and electroneuromyographic (ENMG) characteristics of patients affected by severe COVID-19 infection, evaluated for muscular weakness. Materials and methods ENMGs performed for evaluation of diffuse weakness in patients who could not be discharged from semi-intensive care COVID unit because of difficulties in ventilation weaning were reviewed. Patients with severe COVID-19 infection who had undergone endotracheal intubation and able to co-operate were considered. ENMG protocol was focused on neurophysiological items that excluded or confirmed critical illness polyneuropathy (CIP), myopathy (CIM), or polyneuromyopathy (CIPM). Standardized clinical evaluation was performed using Medical Research Council (MRC) sum score. Results Eight patients were included in the study. All presented known risk factors for intensive care unit-acquired weakness (ICU-AW), and none of them had history of underlying neuromuscular disorders. ENMG findings were normal in two patients, while only two patients had an altered MRC sum score (< 48). Neuromuscular involvement was diagnosed in 6/8 patients (75%): 2 had CIP, 1 had possible CIM, 1 had CIPM, while 1 patient, with clinically evident weakness but equivocal ENMG findings, was classified as ICU-AW. Finally, 1 patient was diagnosed with acute demyelinating neuropathy. Patients with neuromuscular involvement were those with longer intubation duration and higher levels of IL-6 at admission. Conclusion Neuromuscular complications are frequent in severe COVID-19 and cannot be excluded by MRC sum scores above 48. Standardized ENMG is helpful in guiding diagnosis when clinical evaluation is not reliable or possible. Elevated IL-6 at admission may be a predictor biomarker of ICU-AW in COVID-19.

Background Around 20% of patients hospitalized for COVID-19 need mechanical ventilation (MV). MV may be prolonged, thus warranting tracheostomy. Methods Observational cohort study enrolling patients admitted due to COVID-19. Demographic and clinical data at hospital and ICU admission were collected. The primary endpoint was to identify parameters associated with a need for tracheostomy; secondary endpoints were to analyze the clinical course of patients who needed tracheostomy. Results 118 patients were enrolled; 37 patients (31.5%) were transferred to ICU, of which 11 (29.72%) needed a tracheostomy due to prolonged MV. Sequential Organ Failure Assessment (SOFA) score at ICU admission (OR 0.65, 95% CI 0.47–0.92, p 0.015) was the only variable found to be associated with increased risk of the need for tracheostomy, with a cut-off point of 4.5 (sensitivity 0.72, specificity 0.73, positive predictive value 0.57 and negative predictive value 0.85). The main complications were nosocomial infection (100%), supraventricular cardiac arrhythmia (45.5%), agitation (54.5%), pulmonary thromboembolism (9.1%) and depression (9.1%). All patients presented with hypoalbuminemia and significant critical illness polyneuropathy. Conclusion SOFA at ICU admission is associated with an increased risk of tracheostomy in patients with COVID-19. Moreover, they present clinical features similar to those with chronic critical illness and suffer SARS-CoV-2-related complications.

Introduction:The aim of this study was to determine the frequency of patients with critical illness polyneuropathy/myopathy followed by mechanical ventilator in the intensive care unit, and to determine the risk factors associated with this condition and discuss them with the literature.Methods:This study was performed retrospectively (August 2012 to August 2017), at a tertiary university hospital in Turkey. A total of 31 patients who were on mechanical ventilation and diagnosed with polyneuropathy/myopathy by electroneuromyography (ENMG) during pediatric intensive care unit follow-up were included in the study. Data were collected from patient files and computer system. Demographic characteristics of the patients, causes of hospitalization, underlying disease, length of the pediatric intensive care unit and hospital stay, length of mechanical ventilation, and treatment modalities were recorded. Patients without respiratory support and patients on mechanical ventilation without ENMG procedures were excluded.Results:A total of 31 patients were included in the study. Myopathy was present in 5/31 (16.1%) and polyneuropathy in 26/31 (83.9%) patients. Respiratory distress/failure was the most common cause of respiratory support (n=10, 32.3%) and the second most common cause was post cardiac surgery (n=9, 29%). The diagnosis of 18 (58%) patients were sepsis and 2 (6.4%) patients had multiple organ failure. The mean duration of mechanical ventilation was 27.4±14.1 days, length of pediatric intensive care unit stay was 41.5±24 days, length of hospital stay was 57.5±27.5 days. Mortality was observed in 5 (16.1%) of 31 patients.Conclusion:Critical illness polyneuropathy and myopathy in intensive care practice is a condition with increasing frequency and importance. Increased attention to this matter allows to take the necessary preventions, early recognition and to make the appropriate approach.

Background Diagnosis of intensive care unit acquired weakness (ICUAW) is challenging. Pathogenesis of underlying critical illness polyneuromyopathy (CIPNM) remains incompletely understood. This exploratory study investigated whether longitudinal neuromuscular ultrasound examinations and cytokine analyses in correlation to classical clinical and electrophysiological assessment contribute to the understanding of CIPNM. Methods Intensive care unit patients were examined every 7 days until discharge from hospital. Clinical status, nerve conduction studies, electromyography as well as ultrasound of peripheral nerves and tibial anterior muscle were performed. Cytokine levels were analyzed by a bead-based multiplex assay system. Results Of 248 screened patients, 35 patients were included at median of 6 days (IQR: 8) after admission to intensive care unit. Axonal damage was the main feature of CIPNM. At the peak of CIPNM (7 days after inclusion), nerve ultrasound showed cross-sectional area increase of tibial nerve as a sign of inflammatory edema as well as hypoechoic nerves as a possible sign of inflammation. Cytokine analyses showed signs of monocyte and macrophage activation at this stage. Fourteen days after inclusion, cytokines indicated systemic immune response as well as profiles associated to neovascularization and regeneration. Conclusions Exploratory neuromuscular ultrasound and cytokine analyses showed signs of inflammation like macrophage and monocyte activation at the peak of CIPNM followed by a systemic immune response parallel to axonal damage. This underlines the role of both axonal damage and inflammation in pathogenesis of CIPNM.

Neurological manifestations are increasingly reported in a subset of COVID-19 patients. Previous infections related to coronaviruses, namely Severe Acute Respiratory Syndrome (SARS) and Middle Eastern Respiratory Syndrome (MERS) also appeared to have neurological effects on some patients. The viruses associated with COVID-19 like that of SARS enters the body via the ACE-2 receptors in the central nervous system, which causes the body to balance an immune response against potential damage to nonrenewable cells. A few rare cases of neurological sequelae of SARS and MERS have been reported. A growing body of evidence is accumulating that COVID-19, particularly in severe cases, may have neurological consequences although respiratory symptoms nearly always develop prior to neurological ones. Patients with preexisting neurological conditions may be at elevated risk for COVID-19-associated neurological symptoms. Neurological reports in COVID-19 patients have described encephalopathy, Guillain-Barré syndrome, myopathy, neuromuscular disorders, encephalitis, cephalgia, delirium, critical illness polyneuropathy, and others. Treating neurological symptoms can pose clinical challenges as drugs that suppress immune response may be contraindicated in COVID-19 patients. It is possible that in some COVID-19 patients, neurological symptoms are being overlooked or misinterpreted. To date, neurological manifestations of COVID-19 have been described largely within the disease trajectory and the long-term effects of such manifestations remain unknown.

Highlights • Critical illness myopathy/neuropathy often go under-diagnosed. • Over 70% of patients hospitalized for SARS-CoV-2 were ≥50 years old. • Older populations are at higher risk of suffering from ICU acquired weakness. • Early mobilization is a mainstay of treatment for ICU acquired weakness., One of the major concerns of the health care community and the public surrounding the SARS-CoV-2 pandemic is the availability and use of ventilators. Unprecedented surges of patients presented to intensive care units across the country, with older adults making up a large proportion of the patient population. This paper illustrates contemporary approaches to critical illness myopathy (CIM), critical illness polyneuropathy (CIP), and critical illness polyneuromyopathy (CIPNM) in older patients, including incidence, risk factors, mechanisms for pathology, diagnosis, contemporary treatment approaches, and outcomes. We hope that the following analysis may help educate clinicians and ultimately decrease the duration of the mechanical ventilation required by these patients, resulting in improved clinical outcomes and an increase in ventilator availability for other patients in need.

The new COVID-19 coronavirus infection, which has become a pandemic, is a very dangerous disease, the clinical picture of which can vary from mild to extremely severe forms of the course. Currently, there are no complete data on the pathogenetic mechanism of SARS-CoV-2, but there are extensive data on the probable risk factors for the development of extremely severe forms of COVID-19. The study of such factors becomes most suitable in terms of preventing their development and influence on the course of the disease in individuals with compromised immune systems and patients with impaired neuromuscular transmission. The article describes two clinical cases of extremely severe COVID-19 in patients with impaired neuromuscular transmission. Based on the analysis of the course of diseases, the conclusions are made about the possible aggravation and mutual activation of the immunopathological process with the launch of the cascade mechanism of the “cytokine storm”. An assumption has been made about the influence of human leukocyte antigen (HLA) on the severity of COVID-19, which is confirmed by a positive dynamics against the background of administration of IVIG, glucocorticosteroids (GCS), virusinactivated plasma and extracorporeal detoxification methods.

The spectrum of neuromuscular diseases encountered in the ICUs today has rapidly evolved over the last decades. Multiple predisposing factors are involved in the development of neuromuscular complications in intensive care patients. Those complications broadly classified into weakness from the preexisting neuromuscular disease exacerbated by critical illness or the complication of the critical illness itself. Patients, when unresponsive, confused, or sedated precludes careful clinical examination. A careful schematic approach that involves acquiring extensive history, any underlying infections, use of any offending medications, and the course of presenting illness will help in delineating the underlying etiology. Here in this review, we describe many causes and the pathophysiology that contribute to the development of neuromuscular weakness in the ICU. A comprehensive investigation protocol must strictly be adhered to all the cases in the ICU settings to reduce the mortality and morbidity.

Although the exact pathophysiology of critical illness polyneuropathy (CIP) is still unknown, there are several hypotheses, some of which are increased inflammation and oxidative stress. We used rodent sepsis model in which we induced sepsis through cecal ligation followed by cecal puncture. We then administered ascorbic acid (AA) and evaluated outcomes. The levels of malondialdehyde (MDA), tumor necrosis factor α (TNF-α), interleukins (IL)-6 in the plasma, and heat shock protein-70 (HSP-70) levels in the sciatic nerve were measured, and also electromyography analyses were performed. While plasma MDA, TNF-α, and IL-6 levels were decreased significantly with AA treatment, sciatic nerve levels of HSP-70 were significantly elevated in the AA group. A significant increase in compound muscle action potential (CMAP) amplitude and a significant decrease in CMAP latency were detected in the AA group. We observed healing effects of AA on a rat model of CIP and these effects seem to be related to its anti-inflammatory and antioxidant properties.

A variety of neuropsychiatric complications has been described in association with Covid-19 infection. Large scale studies presenting a wider picture of these complications and their relative frequency are lacking. The objective of our study was to describe the spectrum of neurological and psychiatric complications in patients with Covid-19 seen in a multidisciplinary hospital center over six months. We conducted a retrospective, observational study on all patients showing neurological or psychiatric symptoms in the context of Covid-19 seen in the medical and university neuroscience department of Assistance Publique Hopitaux de Paris -Sorbonne University. We collected demographic data, comorbidities, symptoms and severity of Covid-19 infection, neurological and psychiatric symptoms, neurological and psychiatric examination data and, when available, results from CSF analysis, MRI, EEG and EMG. A total of 249 Covid-19 patients with a de novo neurological or psychiatric manifestation were included in the database and 245 were included in the final analyses. One-hundred fourteen patients (47%) were admitted to the intensive care unit and 10 (4%) died. The most frequent neuropsychiatric complications diagnosed were encephalopathy (43%), critical illness polyneuropathy and myopathy (26%), isolated psychiatric disturbance (18%), and cerebrovascular disorders (16%). No patients showed CSF evidence of SARS-CoV-2. Encephalopathy was associated with older age and higher risk of death. Critical illness neuromyopathy was associated with an extended stay in the intensive care unit. The majority of these neuropsychiatric complications could be imputed to critical illness, intensive care and systemic inflammation, which contrasts with the paucity of more direct SARS-CoV-2-related complications or post-infection disorders., Graphical Abstract Graphical Abstract

Background: Intensive care unit acquired weakness (ICUAW), embraces an array of disorders labeled “critical illness polyneuropathy” (CIP), “critical illness myopathy” (CIM) or “critical illness polyneuromyopathy” (CIPNM). Several studies have addressed the various characteristics of CIPNM, but the recovery is still unclear. Objective: The present review investigated the recovery and the long-term functional outcome of subjects with CIPNM, whether the types of CIPNM have different outcomes and whether there is any supporting evidence. Methods: Literature search was performed from MEDLINE/PubMed, CINAHL, EMBASE, PeDro, Web of Science and Scopus. Inclusion criteria were: i) sample size including five or more subjects; ii) subjects who suffered from CIPNM and/or CIP, CIM and CIP/CIM; iii) CIPNM ascertained by EMG. Follow-ups longer than one year were defined as long-term.Results: Twenty-nine studies met the inclusion criteria. In total, 788 subjects with CIPNM were enrolled: 159 (20.1%) died and 588 (74.6%) were followed. Of all the included patients, 613 (77.7%) had CIP, 82 (10.4%) CIM and 56 (7.1%) CIP/CIM. Overall, 70.3% of the subjects with CIPNM fully recovered. Seven (24.1%) studies had a follow-up longer than 1 year (range 2-8) with 173 (21.9%) subjects enrolled globally and 108 followed. Of these subjects, 88.8% gained full recovery. Most of the studies did not use proper functional scales and only 4 and 3 studies employed the Barthel scale and the FIM scale. Differentiation between the types of CIPNM was performed in 7 studies, but only 3 studies reported that subjects with CIM had a better prognosis and earlier recovery than subjects with CIP/CIM.Conclusions: Subjects with CIPNM could achieve good recovery and could further improve at follow-up. The quality of the published studies due to short follow-ups and the paucity of defined outcome measures limit the evidence.

Purpose of review This article discusses the pathophysiology, presentation, diagnosis, treatment, and prognosis of common neuromuscular disorders seen in the intensive care unit, including Guillain-Barre syndrome, myasthenia gravis, and intensive care unit-acquired weakness. Recent findings Guillain-Barre syndrome can have an excellent prognosis if patients are diagnosed early, appropriately treated, and monitored for complications, including respiratory failure and dysautonomia. Intensive care unit-acquired weakness increases overall mortality in patients who are critically ill, and distinguishing between critical illness myopathy and critical illness polyneuropathy may have important prognostic implications. Summary Neuromuscular disorders are not rare in the intensive care unit setting, and precise identification and treatment of these conditions can greatly impact long-term outcomes.

There has been tremendous growth in patients requiring critical care with severe infections. During a prolonged stay in the intensive care unit (ICU), patients develop critical illness polyneuropathy (CIP). The early identification of neurological involvement requires special attention during ICU care. We describe two cases who developed complete motor weakness after a prolonged stay in ICU. Patients were successfully managed with pyridostigmine and testosterone hormonal therapy initially and later with pyridostigmine only. The present case series highlights the need for early recognition, assessment, and novel management of CIP in ICU patients. However, the role of nutrition, physiotherapy, and supportive care is equally essential for the successful outcome in these patients.

The still ongoing COVID-19 pandemic has exposed the medical community to a number of major challenges. A significant number of patients require admission to intensive care unit (ICU) services due to severe respiratory, thrombotic and septic complications and require long-term hospitalization. Neuromuscular weakness is a common complication in critically ill patients who are treated in ICUs and are mechanically ventilated. This complication is frequently caused by critical illness myopathy (CIM) or critical illness polyneuropathy (CIP) and leads to difficulty in weaning from the ventilator. It is thought to represent an important neurologic manifestation of the systemic inflammatory response syndrome (SIRS). COVID-19 infection is known to trigger strong immune dysregulation, with an intense cytokine storm, as a result, the frequency of CIP is expected to be higher in this setting. The mainstay in the diagnosis of this entity beside the high level of clinical awareness is the electrophysiological examination that provides evidence of axonal motor and sensory polyneuropathy. The present article presents the case of a 54-year-old woman with severe COVID 19 infection who developed neuromuscular weakness, which turned out to be secondary to CIP and was treated successfully with a high dose of human intravenous immunoglobulins. Related to this case, we reviewed the relevant literature data regarding the epidemiology, pathophysiology and clinical features of this important complication and discussed also the treatment options and prognosis.

Background Lung transplantation (LT) requires complex multidisciplinary organization and constitutes a therapeutic option and a life-saving procedure. Although the number of lung recipients continues to increase, neurological complications and death rates following lung transplantation are still higher than desirable. Purpose This study aims to analyse the neuroimaging findings in a cohort of adult patients with LT. Material and Methods A retrospective cohort study of all lung transplant recipients (344 patients: 205 men and 139 women) at a single institution from January 2011 to January 2020. The collected data included demographic features, clinical data and evaluation of the imaging findings. We also recorded the date of neurological complication(s) and the underlying disease motivating lung transplantation. Results We found an elevated rate of neuroimaging findings in patients following LT with 32.6% of positive studies. In our cohort, the average time after LT to a neurological complication was 4.9 months post-transplant. Encephalopathy, critical illness polyneuropathy and stroke, in that order, were the most frequent neurological complications. Structural abnormalities in brain imaging were more often detected using MRI than CT for indications of encephalopathy and seizures. Conclusions LT recipients constitute an especially vulnerable group that needs close surveillance, mainly during the early post-transplant period.

Critical illness myopathy (CIM), critical illness polyneuropathy (CIP), and critical illness polyneuromyopathy (CIPNM) are the group of disorders that are commonly presented as neuromuscular weakness in intensive care unit (ICU) settings. They are responsible for prolonged ICU stay and failure to wean off from mechanical ventilation. We report a case of young female who was admitted with undiagnosed type I diabetes mellitus with diabetic ketoacidosis, severe hypokalemia, sepsis developed acute onset quadriplegia, and diaphragmatic palsy within 72 hours of ICU admission. On detailed investigation, CIPNM was diagnosed. In view of high morbidity, mortality, and poor prognosis, a guided approach to diagnose and treat in earliest possible duration might give better improvement and outcome of the illness. Despite all the odds, our patient showed good clinical improvement and finally got discharged. How to cite this article Mahashabde M, Chaudhary G, Kanchi G, Rohatgi S, Rao P, Patil R, et al. An Unusual Case of Critical Illness Polyneuromyopathy. Indian J Crit Care Med 2020;24(2):133–135.

Our goal was to establish electrophysiological features of critical illness polyneuropathy in children with infectious diseases. Materials and Methods: We evaluated peripheral nervous system involvement in 67 critically ill children, admitted in ICU with different types of infectious diseases (viral encephalitis, meningoencephalitis, meningitis, acute gastroenteritis). Age of the group varied from 4 months to 17 years. All patients underwent conduction studies and neurological investigation. Sensory and motor fibers of n. ulnaris et n. medianus, motor fibers of n. Tibialis and sensory fibers of n. Suralis were tested. Lowering of the amplitudes, conduction velocity slowing and asymmetry were accounted for the motor and sensory fibers. Results: In 47 cases (n=71) diagnosis of critical illness polyneuropathy (CIP) was established. Lesions mostly involved lower limbs nerves. According to our data, severe course of CIP was seen in 40% of all cases. Average time of CIP onset in children was 5-7 days from the beginning of mechanical ventilation. Conclusions: Critical illness polyneuropathy in children with infectious diseases is a severe condition which may lead to the disability of the patients. Average time of its onset is the 5-7 days from the beginning of the mechanical ventilation in 71% of the patients. More often sensory and motor fibers of lower limbs nerves are affected. Conduction studies is a valuable tool in diagnostic process in establishing the critical illness polyneuropathy in children with infectious diseases. Keywords: Critical illness, critical illness polyneuropathy, children, electromyography.

Objective: To provide an overview of the muscle weakness development in intensive care units (ICU), summarize clinical trials on the role of neuromuscular electrical stimulation for muscle weakness rehabilitation in ICU and highlight recent strategies that may prevent or minimize this condition.Methodology: Literature review. Results: Some recent studies have shown that an increasing number of survivors of critical illness develop significant functional impairment; one of the common impairments being ICU acquired muscle weakness. Prolonged immobilization and mechanical ventilation likely contribute to the development of ICU-acquired weakness. Several novel therapeutic strategies have been used to overcome the impairment, including neuromuscular electrical stimulation. This neuromuscular electrical stimulation, a kind of physical therapy, is known to stimulate the nerves and thus increase muscle contraction. Conclusion: Neuromuscular electrical stimulation for rehabilitation in ICU-related muscle weakness has shown some promise, but more efforts are needed to detect the development of ICU-acquired weakness as early as possible and rigorously evaluate novel rehabilitation interventions.Abbreviations: ICU (Intensive Care Unit); ICU-Acquired Weakness (ICU-AW); CIP (Critical Illness Polyneuropathy); CIM (Critical Illness Myopathy), CIPM (Critical Illness Polyneuropathy and Myopathy)Citation: Kusumawardani MK, Poerwandari D, Narasinta I, Hidayati HB, Subadi I. The role of neuromuscular electrical stimulation for rehabilitation in ICU acquired weakness. Anaesth Pain & Intensive Care 2018;22 Suppl 1:S164-S169

Objectives To determine the prevalence of critical illness polyneuropathy and its risk factors in critically ill children mechanically ventilated for 7 days or more. Design Observational cohort study. Setting PICU of a tertiary care hospital from North India. Patients Children 1-15 years old admitted in PICU from June 2016 to September 2017, mechanically ventilated for 7 days or more, excluding those with diagnosed neuromuscular disease, stroke, or spinal pathology. Intervention Demographic details, diagnosis, treatment details, and anthropometry at admission and enrolment were recorded. Nerve conduction studies were performed after enrolment and repeated a week later, if the child was still in PICU. Medical Research Council scoring for muscle strength was performed in survivors. Risk factors including Pediatric Index of Mortality-2 score, sepsis, multiple organ dysfunction, hypoalbuminemia, use of steroids, neuromuscular-blocking agents, and vasopressors were recorded. Samples for the level of micronutrients (copper, zinc, folate, and vitamin B12) were collected at the time of enrolling the child and at the time of discharge. Measurements and main results Thirty-two children were enrolled, of whom 29 had features of critical illness polyneuropathy on evaluation at day 8 of mechanical ventilation (prevalence, 90.6% [95% CI, 80.5-100%]). The polyneuropathy was axonal in 26 (81.2%), mixed in one patient (3.1%), and uncharacterized in two (6.2%). Sepsis and multiple organ dysfunction were present in 31 subjects (96.9%). No risk factors for critical illness polyneuropathy could be identified although the study was not sufficiently powered to do so. The difference between serum micronutrient levels (copper, zinc, folate, and vitamin B12) between patients who developed polyneuropathy, and those who did not, was statistically insignificant. Conclusions We observed a high prevalence of critical illness polyneuropathy in children in PICU, mechanically ventilated for 7 days or more; almost all of whom had underlying sepsis.

Background:Intensive care unit-acquired weakness (ICU-AW) is associated with poorer outcome of critically ill patients. Microcirculatory changes and altered vascular permeability of skeletal muscles might contribute to the pathogenesis of ICU-AW. Muscular ultrasound (MUS) displays increased muscle echogenicity, although its pathogenesis is uncertain.Objective:We investigated the combined measurement of serum and ultrasound markers to assess ICU-AW and clinical patient outcome.Methods:Fifteen patients and five healthy controls were longitudinally assessed for signs of ICU-AW at study days 3 and 10 using a muscle strength sum score. The definition of ICU-AW was based on decreased muscle strength assessed by the muscular research council-sum score. Ultrasound echogenicity of extremity muscles was assessed using a standardized protocol. Serum markers of inflammation and endothelial damage were measured. The 3-month outcome was assessed on the modified Rankin scale.Results:ICU-AW was present in eight patients, and seven patients and the control subjects did not develop ICU-AW. The global muscle echogenicity score (GME) differed significantly between controls and patients (mean GME, 1.1 ± 0.06 vs. 2.3 ± 0.41;p= 0.001). Mean GME values significantly decreased in patients without ICU-AW from assessment 1 (2.30 ± 0.48) to assessment 2 (2.06 ± 0.45;p= 0.027), which was not observed in patients with ICU-AW. Serum levels of syndecan-1 at day 3 significantly correlated with higher GME values at day 10 (r= 0.63,p= 0.012). Furthermore, the patients’ GME significantly correlated with mRS at day 100 (r= 0.67,p= 0.013).Conclusion:The combined use of muscular ultrasound and inflammatory biomarkers might be helpful to diagnose ICU-AW and to predict long-term outcome in critical illness.

Intensive care units’ acquired muscle weakness is present in approximately 50% of the patients. Although active muscle training can attenuate weakness, a large proportion of critical patients cannot participate in any active mobilization. Neuromuscular electrical stimulation may be an alternative strategy to reverse muscle weakness. The objective of the study was to review the scientific publications on the use of neuromuscular electrical stimulation and its parameters and the main results in patients hospitalized in intensive care units. This is an integrative review surveying studies in online databases. The studies were selected from the following descriptors: neuromuscular electrical stimulation AND parameters AND intensive care units AND muscle weakness. The inclusion criteria included articles that addressed the topic of neuromuscular electrical stimulation and the parameters used in patients admitted to intensive care units, aged 18 years or older. Exclusion criteria were studies involving animals, case reports, letters to the editor and book chapters. The search comprised articles in the Portuguese, English and Spanish languages from January 2013 to March 2019. Of the 185 articles identified, nine met the eligibility criteria. The studies were evaluated assessing the level of evidence, and the relevant information was presented in the table and discussed. The parameters of the neuromuscular electrical stimulation employed in the studies showed positive results for the maintenance of strength and muscle mass. There was evidence of benefits in the local and systemic microcirculation, potentially mobilizing endothelial stem cells, to prevent atrophy, to reduce mechanical ventilation time and stay in intensive care unit; and when incorporated into the usual physiotherapy care, proved to be more effective than usual care. Its use is safe and viable in critically ill patients.

Intracranial hemorrhage (ICH) is rarely seen in patients with thalassemia. A seven-year-old male, known case of beta-thalassemia major, on irregular packed cell transfusions (elsewhere) and non-compliant with chelation therapy, presented with congestive cardiac failure (Hb-3 gm/dl). He received three packed red cell transfusions over 7 days (cumulative volume 40 cc/kg). On the 9th day, he developed projectile vomiting and two episodes of generalized tonic-clonic convulsions with altered sensorium. He had exaggerated deep tendon reflexes and extensor plantars. CT-scan of brain revealed bilateral acute frontal hematoma with diffuse subarachnoid hemorrhage (frontal and parietal). Coagulation profile was normal. CT-angiography of brain showed diffuse focal areas of reduced caliber of anterior cerebral, middle cerebral, and basilar and internal carotid arteries (likely to be a spasmodic reaction to subarachnoid hemorrhage). He required mechanical ventilation for 4 days and conservative management for the hemorrhage. However, on the 18th day, he developed one episode of generalized tonic-clonic convulsion and his sensorium deteriorated further (without any new ICH) and required repeat mechanical ventilation for 12 days. On the 28th day, he was noticed to have quadriplegia (while on a ventilator). Nerve conduction study (42nd day) revealed severe motor axonal neuropathy (suggesting critical illness polyneuropathy). He improved with physiotherapy and could sit upright and speak sentences at discharge (59th day). The child recovered completely after 3 months. It is wise not to transfuse more than 20 cc/kg of packed red cell volume during each admission and not more than once in a week (exception being congestive cardiac failure) for thalassemia patients.

Hypoxemic respiratory failure caused by coronavirus disease 2019 (COVID-19) may lead to prolonged intensive care unit stay and mechanical ventilation. Critically ill patients often develop intensive care unit acquired weakness (ICUAW), which is an umbrella term that encompasses critical illness polyneuropathy and critical illness myopathy. The aim of this paper is to report the clinical, neurophysiological, and radiological findings suggesting critical illness myopathy in three patients with critical COVID-19. Muscle magnetic resonance imaging may serve as a diagnostic tool for critical illness myopathy. Weaning failure and generalized muscle weakness with preserved sensation and cranial nerve function should alert physicians for ICUAW.

Coronavirus disease 2019 (COVID-19) is associated with multiple neurological complications including Guillain-Barre syndrome (GBS). While there are reports of COVID-19 -related GBS cases, much remain unknown. We report two cases of GBS-associated COVID-19, which started about eight weeks after the initial COVID-19 infection. Such a long duration between infection and symptom onset of GBS is unusual for post-infectious GBS. Moreover, severely ill patients with COVID-19 may have prolonged hospital stay leading to critical illness myoneuropathy. Diagnosing superimposed GBS can be challenging in such cases. Clinical suspicion, nerve conduction studies with electromyography, and cerebrospinal fluid analysis can help in making the correct diagnosis. Both presented cases responded to intravenous immunoglobulin therapy.

Organized anatomically into categories spanning from the lower motor neuron to muscle, this chapter describes the neuromuscular complications of systemic medical disease. The text focuses on diagnosis and treatment of the disorders. The neuromuscular effects of toxic exposures are also discussed. Numerous tables are included to help with the diagnostic process.

Importance:. Dysphagia is a common complication of critical illness, and many known risk factors are also present in critically ill coronavirus disease 2019 victims. Objectives:. To investigate dysphagia in patients with severe coronavirus disease 2019. Design, Setting, and Participants:. In this case series, we report results of dedicated evaluation of swallowing function in six consecutive, tracheotomized coronavirus disease 2019 patients after they had survived acute respiratory distress syndrome and were weaned from the respirator. Main Outcomes and Measures:. Dysphagia was assessed with flexible endoscopic evaluation of swallowing. Results:. Three patients suffered from severe dysphagia and airway compromise precluding decannulation, whereas in the other, three swallowing was less critically impaired, and the tracheal cannula could be removed. Four patients presented with additional laryngeal dysfunctions not typically seen in acute respiratory distress syndrome survivors. Conclusion and Relevance:. Dysphagia with impaired airway protection is a key feature in coronavirus disease 2019 acute respiratory distress syndrome survivors. Apart from critical illness polyneuropathy, coronavirus disease 2019–related involvement of the peripheral and central nervous system may contribute to swallowing impairment and laryngeal dysfunction.

COVID-19 may potentially increase the incidence of persisting pain syndromes and worsen symptoms of preexisting chronic pain., Pain is a common symptom accompanying the coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Nonspecific discomfort such as sore throat and body ache are frequent. Parainfectious pain such as headache, myalgia, or neuropathic pain has also been reported. The latter seems to be associated with an autoimmune response or an affection of the peripheral neuromuscular system or the central nervous system because of the viral infection. Furthermore, chronic pain can be a complication of intensive care unit treatment due to COVID-19 itself (such as intensive care–acquired weakness) or of secondary diseases associated with the SARS-CoV-2 infection, including Guillain–Barré syndrome, polyneuritis, critical illness polyneuropathy, or central pain following cerebrovascular events. Data on long-lasting painful symptoms after clinically manifest COVID-19 and their consequences are lacking. In addition, preexisting chronic pain may be exacerbated by limited and disrupted health care and the psychological burden of the COVID-19 pandemic. Medical providers should be vigilant on pain during and after COVID-19.

Objective To investigate the sensitivity of muscle velocity recovery cycles (MVRCs) for detecting altered membrane properties in critically ill patients, and to compare this to conventional nerve conduction studies (NCS) and quantitative electromyography (qEMG). Methods Twenty-four patients with intensive care unit acquired weakness (ICUAW) and 34 healthy subjects were prospectively recruited. In addition to NCS (median, ulnar, peroneal, tibial and sural nerves) and qEMG (biceps brachii, vastus medialis and anterior tibial muscles), MVRCs with frequency ramp were recorded from anterior tibial muscle. Results MVRC and frequency ramp parameters showed abnormal muscle fiber membrane properties with up to 100% sensitivity and specificity. qEMG showed myopathy in 15 patients (63%) while polyneuropathy was seen in 3 (13%). Decreased compound muscle action potential (CMAP) amplitude (up to 58%) and absent F-waves (up to 75%) were frequent, but long duration CMAPs were only seen in one patient with severe myopathy. Conclusions Altered muscle fiber membrane properties can be detected in patients with ICUAW not yet fulfilling diagnostic criteria for critical illness myopathy (CIM). MVRCs may therefore serve as a tool for early detection of evolving CIM. Significance CIM is often under-recognized by intensivists, and large-scale longitudinal studies are needed to determine its incidence and pathogenesis.

OBJECTIVE: The aim was to characterize the electrophysiological features and plasma biomarkers of critical illness polyneuropathy (CIN) and myopathy (CIM) in coronavirus disease 2019 (COVID-19) patients with intensive care unit acquired weakness (ICUAW). METHODS: An observational ICU cohort study including adult patients admitted to the ICU at Uppsala University Hospital, Uppsala, Sweden, from March 13th to June 8th 2020. We compared the clinical, electrophysiological and plasma biomarker data between COVID-19 patients who developed CIN/CIM and those who did not. Electrophysiological characteristics were also compared between COVID-19 and non-COVID-19 ICU patients. RESULTS: 111 COVID-19 patients were included, 11 of whom developed CIN/CIM. Patients with CIN/CIM had more severe illness; longer ICU stay, more thromboembolic events and were more frequently treated with invasive ventilation for longer than 2 weeks. In particular CIN was more frequent among COVID-19 patients with ICUAW (50%) compared with a non-COVID-19 cohort (0%, p = 0.008). Neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAp) levels were higher in the CIN/CIM group compared with those that did not develop CIN/CIM (both p = 0.001) and correlated with nerve amplitudes. CONCLUSIONS: CIN/CIM was more prevalent among COVID-19 ICU patients with severe illness. SIGNIFICANCE: COVID-19 patients who later developed CIN/CIM had significantly higher NfL and GFAp in the early phase of ICU care, suggesting their potential as predictive biomarkers for CIN/CIM. De två första författarna delar förstaförfattarskapet

Background: Although early identification of critical illness polyneuropathy (CIP) is necessary, the established diagnostic criteria have several limitations in the intensive care unit (ICU) setting. The purpose of this study was to define simplified diagnostic criteria of CIP that best predict clinical outcomes. Methods: This prospective, single-center study included 41 ICU patients with prolonged mechanical ventilation (&ge, 21 days). We applied three different sets of diagnostic criteria (combining the results of the Medical Research Council (MRC) sum score and nerve conduction studies (NCS)) for CIP in order to identify the criteria with the best predictive power for clinical outcomes. Results: The simplified diagnosis of CIP meeting the criteria, i.e., that the MRC sum score &lt, 48 and amplitudes of the tibial and sural nerve &lt, 80% of the lower limit of normal, showed the strongest association with 0 ventilator-free days at day 60 (odds ratio, 6.222, p = 0.029). Conclusions: The diagnostic criteria combining the MRC sum score and the tibial and the sural NCS were identified as the simplified criteria of CIP that best predicted the clinical outcomes. The implementation of these simplified criteria may allow for early identification of CIP in the ICU, thereby contributing to prompt interventions for patients with a poor prognosis.

Rationale: Stiff-person syndrome (SPS) is an uncommon neurological disorder with autoimmune features. Here, we report a 60-year-old man with SPS associated with critical illness polyneuropathy (CIP). CIP was diagnosed during an episode of acute respiratory failure secondary to muscular rigidity and spasms, which has rarely been reported in this condition. The overlapping of CIP and SPS complicated the case. Patient concerns: A 60-year-old man presented with gradual onset of cramps, stiffness, and rigidity in his lower limbs 1 year before admission, which eventually led to inability to stand and walk. The persistent nature of his symptoms progressed to frequent acute episodes of dyspnea and he was admitted to intensive care unit (ICU). Diagnosis: SPS had been diagnosed after 2 tests of electromyography (EMG) and the detection of an elevated anti-GAD65 antibody titer. During the first EMG, low or absent compound muscle action potentials (CMAP), and sensory nerve action potentials (SNAP) were shown. Therefore, the diagnosis of SPS coexisting with CIP was made. Interventions: Symptomatic treatment was initiated with oral clonazepam (0.5 mg Bid) and baclofen (5 mg Bid). Intravenous immunoglobulin (IVIG) (0.4 g/kg/d) was administered for the patient for 5 days after admission. We observed a significant clinical improvement during the administration period, and the patient became ambulatory. Outcomes: On follow-up, the patient reported complete relief of his pain and rigidity. Lessons: We report this special case to address the varied clinical features of SPS. Electrophysiological testing is an important diagnostic approach. Accurate recognition of the disease ensures that the patients can be given appropriate treatment without delay.

Muscular weakness and/or muscle wasting is recognized as a key medical problem in critically ill patients on intensive care units (ICUs) worldwide.Intensive care unit-acquired weakness (ICUAW) results from various diseases leading to critical illness and is observed in about 40% [1080/2686 patients, 95% confidence interval (CI): 38-42%] of mixed (medical-surgical) ICU patients. Muscle strength at ICU discharge is directly associated with mortality 5 years after discharge [hazard ratio 0.946, 95% CI: 0.928-0.968 per point increase in Medical Research Council (MRC) scores, P = 0.001]. ICUAW serves as umbrella term for the subgroups ‘critical illness myopathy’, ‘critical illness polyneuropathy’, and ‘critical illness polyneuromyopathy’, the latter distinguished using electrophysiology and/or biopsy studies. Diagnosing, studying, and developing treatments for ICUAW among the critically ill seems challenging due to the acuity and severity of the underlying heterogeneous diseases. Ventilator-induced diaphragmatic dysfunction occurs in up to 80% (n = 32/40) of ICUAW patients after mechanical ventilation and mostly results from distinct muscular pathologies, disuse, underlying critical illness, and/or effects imposed directly by mechanical ventilation. Swallowing disorders/dysphagia likely represent an additional (local) neuromuscular dysfunction/ICUAW sequelae and presents in 10.3% (n = 96/933) of mixed medical-surgical ICU survivors, with 60.4% (n = 58/96) of patients remaining dysphagia positive until hospital discharge. Key independent risk factors for dysphagia following mechanical ventilation are baseline neurological disease [odds ratio (OR) 4.45, 95% CI: 2.74-7.24, P 0.01], emergency admission (OR 2.04, 95% CI: 1.15-3.59, P 0.01), days on mechanical ventilation (OR 1.19, 95% CI: 1.06-1.34, P 0.01), days on renal replacement therapy (OR 1.1, 95% CI: 1-1.23, P = 0.03), and disease severity (Acute Physiology and Chronic Health Evaluation II score within first 24 h; OR 1.03, 95% CI: 0.99-1.07, P 0.01). Dysphagia positivity independently predicts 28-day and 90-day mortality (90-day univariate hazard ratio: 3.74; 95% CI, 2.01-6.95; P 0.001) and is associated with a 9.2% excess (all-cause) mortality rate.Neuromuscular weakness and muscle wasting is observed in many survivors of critical illness. ICUAW, ventilator-induced diaphragmatic dysfunction, and dysphagia are associated with complicated and prolonged ICU stay, impaired weaning from mechanical ventilation, impeded rehabilitative measures, and a considerable impact on morbidity and mortality is noted. Future research strategies should further explore underlying pathomechanisms and lead to development of causal treatment strategies.

Introduction. Critical Illness Polyneuropathy (CIP) is a frequent complication of critical illness, acutely and primarily affecting the motor and sensory axons. CIP delays weaning from mechanical ventilation, increases the length of stay at the intensive care unit, compromises rehabilitation and may result in a lifelong loss of function and in a reduction in quality of life. Greater than 50% of patients mechanically ventilated for more than 7 days will develop electrophysiological abnormalities with 25-33% developing clinically overt weakness. Until recently, no therapeutic measures had been proven to affect its incidence, and apart from supportive treatment. Results. A 52-year-old chinese lady presented to ED with shortness of breath due to SIRS et. causa pneumonia was consulted to neurology department because of loss of conciousness. After being intubated, patient awakened within stable condition. On neurological examination, there were bilateral ptosis, bilateral ophthalmoplegia, flaccid over all extremities, decrease of tendon reflexes and sensory were intact. There were leukocytosis and respiratory acidosis on laboratory findings. Chest X-ray noticed bilateral minimal pleural effusion and cardiomegaly. Bronchoscopy and Thorax CT-scan found inflammation. Abdominal ultrasound and head CT scan were within normal limits. Lumbar puncture was not done due to rejection from the family. On EDX findings, NCS found axonal loss pattern in motor and sensory, RNS was within normal limits and needle EMG findings noted distal pattern of decreased recruitment with denervation. After 18 months being hospitalised in ICU and using mechanical ventilator, the patient died. Conclusion. There is no direct treatment for CIP. CIP results in substantial morbidity, mortality, costs and could likely be improved with earlier diagnosis and more timely intervention. To achieve this goal, however, more awareness on the part of medical establishment is needed, as well as further research into the causes of treatments for CIP.

ObjectiveTo describe the spectrum of neurological and psychiatric complications in patients with Covid-19 seen in a multidisciplinary center over six months.MethodsWe conducted a retrospective, observational study on all patients showing neurological or psychiatric symptoms in the context of Covid-19 seen in the Department of Neurology and Psychiatry of the APHP-Sorbonne University. We collected demographic data, medical and treatment history, comorbidities, symptoms, date of onset, and severity of Covid-19 infection, neurological and psychiatric symptoms, neurological and psychiatric examination data and, when available, results from cerebrospinal fluid (CSF) analysis, brain magnetic resonance (MRI) imaging, 18-fluorodesoxyglucose-position emission computed tomography (FDG-PET/CT)), electroencephalography (EEG) and electroneuromyography (ENMG).Results245 patients were included in the analysis. One-hundred fourteen patients (47%) were admitted to the intensive care unit (ICU) and 10 (4%) died. The most frequently reported neuropsychiatric symptoms were motor deficit (41%), cognitive disturbance (35%), impaired consciousness (26%), psychiatric disturbance (24%), headache (20%) and behavioral disturbance (18%). The most frequent syndromes diagnosed were encephalopathy (43%), critical illness polyneuropathy and myopathy (26%), isolated psychiatric disturbance (18%), and cerebrovascular disorders (16%). No patients showed evidence of SARS-CoV-2 in their CSF. Encephalopathy was associated with greater age and higher risk of death. Critical illness neuromyopathy was associated with an extended stay in the ICU.ConclusionsThe majority of the neuropsychiatric complications recorded could be imputed to critical illness, intensive care and systemic inflammation, which contrasts with the paucity of more direct SARS-CoV-2-related complications or post-infection disorders.