Critical illness myopathy and polyneuropathy

Neuromuscular weakness commonly develops in the setting of critical illness. This weakness delays recovery and often causes prolonged ventilator dependence. An axonal sensory-motor polyneuropathy, critical illness polyneuropathy (CIP), is seen in up to one third of critically ill patients with the systemic inflammatory response syndrome (usually due to sepsis). An acute myopathy, critical illness myopathy (CIM), frequently develops in a similar setting, often in association with the use of corticosteroids and/or nondepolarizing neuromuscular blocking agents. These patients are often difficult to evaluate due to the limitations imposed by the critical care setting and may be further complicated by the presence of both CIP and CIM in varying degrees. This paper reviews the clinical and electrophysiologic features of these disorders, as well as the putative pathophysiology. In the case of CIM, an animal model has provided evidence that weakness in this disorder is caused by muscle membrane inexcitability due to altered membrane sodium currents and loss of myosin thick filaments.     

Neuromuscular complications of severe COVID-19 in paediatric patients: Medium-term follow-up

Neuromuscular complications in paediatric patients with severe coronavirus disease 2019 (COVID-19) are poorly characterised. However, adult patients with severe COVID-19 reportedly present with frequent neuromuscular complications that mainly include critical illness polyneuropathy (CIP), critical illness myopathy (CIM), and focal neuropathies. We examined the records of all paediatric patients with severe COVID-19 who were mechanically ventilated and experienced neuromuscular complications from our single tertiary centre between March 2020 and August 2021. During this period, 4/36 (11%) patients admitted to the paediatric ICU who were mechanically ventilated experienced neuromuscular complications (one CIM, two focal neuropathies, and one CIP associated with plexopathy). In three of them, the gamma genetic variant of SARS-CoV-2 was identified. At the 4–5 month follow-up, three of our patients exhibited slight clinical improvement. We conclude that paediatric patients with severe COVID-19 may present neuromuscular complications similar to adults (11%), and their medium-term prognosis seems unfavourable.     

Critical illness polyneuropathy and myopathy: a major cause of muscle weakness and paralysis

Critical illness polyneuropathy (CIP) and myopathy (CIM) are complications of critical illness that present with muscle weakness and failure to wean from the ventilator. In addition to prolonging mechanical ventilation and hospitalisation, CIP and CIM increase hospital mortality in patients who are critically ill and cause chronic disability in survivors of critical illness. Structural changes associated with CIP and CIM include axonal nerve degeneration, muscle myosin loss, and muscle necrosis. Functional changes can cause electrical inexcitability of nerves and muscles with reversible muscle weakness. Microvascular changes and cytopathic hypoxia might disrupt energy supply and use. An acquired sodium channelopathy causing reduced muscle membrane and nerve excitability is a possible unifying mechanism underlying CIP and CIM. The diagnosis of CIP, CIM, or combined CIP and CIM relies on clinical, electrophysiological, and muscle biopsy investigations. Control of hyperglycaemia might reduce the severity of these complications of critical illness, and early rehabilitation in the intensive care unit might improve the functional recovery and independence of patients.     

Neuromuscular involvement in COVID-19 critically ill patients

ObjectiveCoronavirus disease 2019 (COVID-19) has a high incidence of intensive care admittance due to the severe acute respiratory syndrome (SARS). Intensive care unit (ICU)-acquired weakness (ICUAW) is a common complication of ICU patients consisting of symmetric and generalised weakness. The aim of this study was to determine the presence of myopathy, neuropathy or both in ICU patients affected by COVID-19 and whether ICUAW associated with COVID-19 differs from other aetiologies.MethodsTwelve SARS CoV-2 positive patients referred with the suspicion of critical illness myopathy (CIM) or polyneuropathy (CIP) were included between March and May 2020. Nerve conduction and concentric needle electromyography were performed in all patients while admitted to the hospital. Muscle biopsies were obtained in three patients.ResultsFour patients presented signs of a sensory-motor axonal polyneuropathy and seven patients showed signs of myopathy. One muscle biopsy showed scattered necrotic and regenerative fibres without inflammatory signs. The other two biopsies showed non-specific myopathic findings.ConclusionsWe have not found any distinctive features in the studies of the ICU patients affected by SARS-CoV-2 infection.SignificanceFurther studies are needed to determine whether COVID-19-related CIM/CIP has different features from other aetiologies. Neurophysiological studies are essential in the diagnosis of these patients.     

Long-term neuromuscular sequelae of critical illness

In this observational study, we analyzed the long-term neuromuscular deficits of survivors of critical illness. Intensive care unit-acquired muscular weakness (ICU-AW) is a very common complication of critical illness. Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are two main contributors to ICU-AW. ICU-AW is associated with an increased mortality and leads to rehabilitation problems. However, the long-term outcome of ICU-AW and factors influencing it are not well known. We analyzed the medical records of 490 survivors of critical illness, aged 18–75 years and located in the area of the study center. Intensive care unit (ICU) survivors with comorbidities that might influence neuromuscular follow-up examinations, muscle strength, or results of nerve conduction studies, such as renal or hepatic insufficiency, diabetes mellitus, or vitamin deficiency were excluded. A total of 51 patients were finally included in the study. Six to 24 months after discharge from the ICU, we measured the Medical Research Council (MRC) sum score, the Overall Disability Sum score (ODSS), and also performed nerve conduction studies and EMG. For all ICU survivors, the median MRC sum score was 60 (range 47–60) and the median ODSS score was 0 (range 0–8). CIP was diagnosed in 21 patients (41 %). No patient was diagnosed with CIM. Patients with diagnosis of CIP showed a higher median ODSS scores 1 (range 0–8) versus 0 (range 0–5); p < 0.001 and lower median MRC sum scores 56 (range 47–60) versus 60 (range 58–60); p < 0.001. The three main outcome variables MRC sum score, ODSS score and diagnosis of CIP were not related to age, gender, or diagnosis of sepsis. The MRC sum score (r = ?0.33; p = 0.02) and the ODSS score (r = 0.31; p = 0.029) were correlated with the APACHE score. There was a trend for an increased APACHE score in patients with diagnosis of CIP 19 (range 6–33) versus 16.5 (range 6–28); p = 0.065. Patients with the diagnosis of CIP had more days of ICU treatment 11 days (range 2–74) versus 4 days (range 1–61); p = 0.015, and had more days of ventilator support 8 days (range 1–59) versus 2 days (range 1–46); p = 0.006. The MRC sum score and the ODSS score were correlated with the days of ICU treatment and with the days of ventilator support. The neuromuscular long-term consequences of critical illness were not severe in our study population. As patients with concomitant diseases and old patients were excluded from this study the result of an overall favorable prognosis of ICU-acquired weakness may not be true for other patient’s case-mix. Risk factors for the development of long-term critical illness neuropathy are duration of ICU treatment, duration of ventilator support, and a high APACHE score, but not diagnosis of sepsis. Although ICU-AW can be serious complication of ICU treatment, this should not influence therapeutic decisions, given its favorable long-term prognosis, at least in relatively young patients with no concomitant diseases.     

Critical illness polyneuropathy and myopathy]

Critical Illness Polyneuropathy (CIP) and Myopathy (CIM), either singly or in combination, are a common complication of critical illness. Both disorders may lead to severe weakness and require mechanical ventilation. CIP, as initially described by Bolton et al., in 1984, is a sensorimotor polyneuropathy that is often a complication of sepsis and multiorgan failure. In Japan, Horinouchi et al., first reported a case in 1994. CIM has been referred to by a number of different terms (acute quadriplegic myopathy, thick filament myopathy, acute necrotizing myopathy of intensive care, rapidly evolving myopathy with myosin-deficiency fibers) in the literature. A variety of serious problems (e.g., pneumonia, severe asthma, and lung or liver transplantation) and the concomitant use of high-dose intravenous corticosteroids and nondepolarizing neuromuscular blocking agents predispose to CIM. In Japan, Kawada et al., reported a first case as acute quadriplegic myopathy in 2000. There is no specific treatment for CIP and CIM. Minimizing the use of corticosteroids and nondepolarizing neuromuscular blocking agents in a critical illness setting may prove helpful in preventing the occurrence of these disorders. The prognosis is directly related to the age of the patient and the seriousness of the underlying illness.     

Critical-illness-Polyneuropathie und -Myopathie als neurologische Komplikationen der Sepsis

Intensive care unit acquired weakness (ICUAW) is a frequent and severe complication of intensive care management. Within ICUAW critical illness polyneuropathy (CIP) and myopathy (CIM) can be differentiated. The major symptom of ICUAW is progressive quadriparesis, which makes weaning from the respirator more difficult, can appear early after admission to an ICU and can often be detected several months after discharge from the ICU. The pathophysiology of ICUAW is multifactorial and complex. Potential therapeutic approaches are the early and sufficient therapy of mulitorgan dysfunction, optimal control of glucose levels as well as early and intensive physiotherapy. This review article discusses the data on incidence, pathophysiology, diagnostic approaches and prognosis of ICUAW.     

Critical illness polyneuropathy,myopathy and neuronal biomarkers in COVID-19 patients: A prospective study

ObjectiveThe 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).MethodsAn 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.Results111 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.ConclusionsCIN/CIM was more prevalent among COVID-19 ICU patients with severe illness.SignificanceCOVID-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.     

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

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.     

Neuromuscular manifestations of critical illness

Critical illness, more precisely defined as the systemic inflammatory response syndrome (SIRS), occurs in 20%-50% of patients who have been on mechanical ventilation for more than 1 week in an intensive care unit. Critical illness polyneuropathy (CIP) and myopathy (CIM), singly or in combination, occur commonly in these patients and present as limb weakness and difficulty in weaning from the ventilator. Critical illness myopathy can be subdivided into thick-filament (myosin) loss, cachectic myopathy, acute rhabdomyolysis, and acute necrotizing myopathy of intensive care. SIRS is the predominant underlying factor in CIP and is likely a factor in CIM even though the effects of neuromuscular blocking agents and steroids predominate in CIM. Identification and characterization of the polyneuropathy and myopathy depend upon neurological examination, electrophysiological studies, measurement of serum creatine kinase, and, if features suggest a myopathy, muscle biopsy. The information is valuable in deciding treatment and prognosis.     

Neurological complications of sepsis: critical illness polyneuropathy and myopathy

Sepsis may cause not only failure of parenchymal organs but can also cause damage to peripheral nerves and skeletal muscles. It is now recognized that sepsis-mediated disorders of the peripheral nerves and the muscle, called critical illness polyneuropathy (CIP) and critical illness myopathy, are responsible for weakness and muscle atrophy occurring de novo in intensively treated patients. CIP represents an acute axonal neuropathy that develops during treatment of severely ill patients and remits spontaneously, once the critical condition is under control. The course is monophasic and self-limiting. Among the critical illness myopathies, three main types have been identified: a nonnecrotizing "cachectic" myopathy (critical illness myopathy in the strict sense), a myopathy with selective loss of myosin filaments ("thick filament myopathy") and an acute necrotizing myopathy of intensive care. Clinical manifestations of both critical illness myopathies and CIP include delayed weaning from the respirator, muscle weakness, and prolonging of the mobilization phase. The pathogenesis of these neuromuscular complications of sepsis is not understood in detail but most authors assume that the inflammatory factors that mediate systemic inflammatory response and multiple organ failure are closely involved. In thick filament myopathy and acute necrotizing myopathy, administration of steroids and neuromuscular blocking agents may act as triggers. Specific therapies have not been discovered. Stabilization of the underlying critical condition and elimination of sepsis appear to be of major importance. Steroids and muscle relaxants should be avoided or administered at the lowest dose possible.     

Neurological complications of sepsis: critical illness polyneuropathy and myopathy

Sepsis may cause not only failure of parenchymal organs but can also cause damage to peripheral nerves and skeletal muscles. It is now recognized that sepsis-mediated disorders of the peripheral nerves and the muscle, called critical illness polyneuropathy (CIP) and critical illness myopathy, are responsible for weakness and muscle atrophy occurring de novo in intensively treated patients. CIP represents an acute axonal neuropathy that develops during treatment of severely ill patients and remits spontaneously, once the critical condition is under control. The course is monophasic and self-limiting. Among the critical illness myopathies, three main types have been identified: a non-necrotizing “cachectic” myopathy (critical illness myopathy in the strict sense), a myopathy with selective loss of myosin filaments (“thick filament myopathy”) and an acute necrotizing myopathy of intensive care. Clinical manifestations of both critical illness myopathies and CIP include delayed weaning from the respirator, muscle weakness, and prolonging of the mobilization phase. The pathogenesis of these neuromuscular complications of sepsis is not understood in detail but most authors assume that the inflammatory factors that mediate systemic inflammatory response and multiple organ failure are closely involved. In thick filament myopathy and acute necrotizing myopathy, administration of steroids and neuromuscular blocking agents may act as triggers. Specific therapies have not been discovered. Stabilization of the underlying critical condition and elimination of sepsis appear to be of major importance. Steroids and muscle relaxants should be avoided or administered at the lowest dose possible. Received: 12 April 2001, Accepted: 23 April 2001     

危重病性多发性神经肌病电生理特点及对机械通气的影响

目的 浅析危重病性多发性神经肌病(CIPM)的电生理特点及对机械通气支持时间的影响.方法 应用丹麦Keypoint 4肌电图仪对重症监护病房中17例机械通气时间>1周仍未能脱机的肺部感染致呼吸衰竭患者进行神经电生理检测,观察其电生理特点并比较CIPM与非CIPM患者的机械通气时间.结果 17例患者中CIPM 9例,其中亚型危重病性多发性神经病(CIP)6例,危重病性肌病(CIM)3例.CIPM患者均表现四肢交感神经皮肤反应(SSR)异常和复合肌肉动作电位(CMAP)下降,CIP患者伴有感觉神经动作电位(SNAP)波幅减低而神经传导速度(NCV)正常.除2例CIP和2例CIM患者F波出现率减低外,全部CIPM患者重复神经电刺激、体感诱发电位及瞬目反射检测均正常.CIPM患者机械通气时间中位数(四分位数范围)为30.0 d(20.0～45.0 d),比非CIPM患者13.5 d(9.5～17.5 d)明显延长(U=7.500,P=0.006).结论 CIPM患者主要表现为CMAP和(或)SNAP波幅的减低,而NCV正常,全部患者SSR异常且脱机时间延长.     

Influence of critical illness on axonal loss in Guillain–Barré syndrome

In this study we sought to determine whether axonal damage in severe Guillain–Barré syndrome (GBS) was secondary to critical illness polyneuropathy (CIP) in the intensive care unit (ICU) by reviewing comorbidities in patients who had initial and follow‐up electromyographic (EMG) studies. Patients were classified as demyelinating (EMG‐D) or axonal (EMG‐A) according to findings on the second EMG. A critical illness (CI) score, derived from components of the APACHE II score, assessed the severity of critical illness in the ICU. Forty‐one patients were admitted to the ICU and had a follow‐up EMG. Of these, 28 (68%) developed an EMG‐A pattern. There was no difference in the timing of the second EMG (mean, 23 days) between the two groups. The mean CI score (10.7 for EMG‐A vs. 9.2 for EMG‐D, P = 0.47) and frequency of sepsis (89% vs. 77%, P = 0.36) were similar between the groups. Mean strength (0–100, Medical Research Council scale) and Hughes disability scores for the EMG‐A group were significantly worse at admission, nadir, and discharge. EMG‐A patients had significantly more days on the ventilator (25 vs. 11), in the ICU (26 vs. 15), and in the hospital (29 vs. 18). Sixty‐eight percent of patients with GBS in the ICU developed axon loss, but this was not related to the usual precipitants of CIP. Muscle Nerve 39: 10–15, 2009     

Posterior cortical atrophy: clinical characteristics and differences compared to Alzheimer's disease

BACKGROUND: Predominant and progressive complex visual disorders are often due to posterior cortical atrophy (PCA), a rare early-onset dementing syndrome presenting with visual complaints. In clinicopathological studies, PCA is most commonly considered a form of Alzheimer's disease (AD); no prior study has evaluated clinical differences between PCA and AD. METHODS: This study identified 15 patients who presented with progressive complex visual disorders and predominant occipitoparietal hypoperfusion on SPECT. These patients were retrospectively compared on clinical variables with 30 patients with clinically probable AD matched for gender, age and duration of illness. RESULTS: The PCA patients presented with alexia, elements of Balint's syndrome, apperceptive visual agnosia, dressing apraxia and environmental disorientation along with elements of Gerstmann's syndrome. Compared to the AD patients, the 15 PCA patients (mean age of onset 58 years, range 51-64) had significantly better verbal fluency, less memory difficulty, more depression and greater insight into their illness but similar familial and apolipoprotein E risk factors. In the PCA patients, MRI often showed occipitoparietal atrophy without detectable mesiotemporal atrophy. CONCLUSIONS: PCA is a distinct clinical syndrome and not just AD with prominent visual deficits. Compared to AD controls, PCA patients have better language and memory but more insight and depression and more posterior atrophy on MRI. These results indicate clinical criteria for the diagnosis of PCA and recommend specific interventions such as visual aids and antidepressant medications. Similar risk factors and course suggest that PCA is most commonly an early-onset posteriorly shifted AD variant.     

Approach to neuromuscular disorders in the intensive care unit

Neuromuscular disorders increasingly are recognized as a complication in patients in the intensive care unit (ICU) and represent a common cause of prolonged ventilator dependency. The distinct syndromes of critical illness myopathy, prolonged neuromuscular blockade, and critical illness polyneuropathy (CIP) may arise as a consequence of sepsis, multi-organ failure, and exposure to various medications—notably, intravenous corticosteroids and neuromuscular blocking agents—but the pathophysiology of these disorders remains poorly understood. More than one syndrome may occur simultaneously, and the distinctions may be difficult in a particular patient, but a specific diagnosis usually can be established after careful clinical, electrodiagnostic, and, when necessary, histological evaluation. For example, asthmatics requiring treatment with corticosteroids and neuromuscular blocking agents may develop an acute myopathy characterized by generalized weakness, preserved eye movements, elevated creatine kinase levels, and myopathic motor units on electromyography (EMG). Muscle biopsy demonstrates distinctive features of thick (myosin) filament loss on ultrastructural studies. Conversely, those with a prolonged ICU course that is complicated by episodes of sepsis with failure to wean from the ventilator, distal or generalized flaccid limb weakness, and areflexia probably have CIP. EMG in these patients demonstrates reduced or absent motor and sensory potentials with neurogenic motor units. Prolonged neuromuscular blockade most commonly occurs in patients with renal failure who have received prolonged infusions of neuromuscular blockers. There is severe flaccid, areflexic paralysis with normal sensation, facial weakness, and ophthalmoparesis that persists for days or weeks after the neuromuscular blockers have been discontinued. Repetitive nerve stimulation shows a decrement of the compound muscle action potential and, in most cases, establishes a disorder of neuromuscular transmission. With the recent epidemic of West Nile virus infection, a clinical syndrome of acute flaccid paralysis with several features indistinguishable from poliomyelitis has emerged. This article critically examines the clinical, electrophysiological, and pathological features of these and other acute neuromuscular syndromes that arise in the context of ICU care and summarizes the current understanding of the pathophysiology and treatment of these disorders.     

Post-Traumatic Stress Disorder in Medical Settings: Focus on the Critically Ill

The relevance of the post-traumatic stress disorder (PTSD) concept to medically ill patients is becoming increasingly clear. Some medical conditions (e.g., rheumatologic diseases) are likely related to PTSD indirectly. Others, such as myocardial infarction and critical illness/intensive care unit (ICU) treatment, are likely traumatic stressors. Importantly, PTSD seems to be a potent risk factor for fatal and nonfatal cardiac events. Risk factors for medical illness–related PTSD appear similar to risk factors for PTSD in general. PTSD is particularly common among survivors of critical illness and ICU treatment. Further research is needed to determine how specific ICU interventions (e.g., administration of benzodiazepines, corticosteroids, and catecholamines) affect PTSD risk. In the meantime, given the negative impact of PTSD on patients’ quality of life, it is important for psychiatrists and other clinicians to be aware of the syndrome in survivors of critical illness so as to ensure that such patients receive the care that they deserve.     

Single-fiber electromyography,nerve conduction studies,and conventional electromyography in patients with critical-illness polyneuropathy: Evidence for a lesion of terminal motor axons

Nine patients at risk for critical illness polyneuropathy (CIP) were included in a prospective study. We performed nerve conduction studies, electromyography, and a stimulation single-fiber electromyography (SFEMG). Five of 9 patients were diagnosed as CIP because they developed abnormal spontaneous activity during the follow-up period. Their SFEMG revealed a significant increase in mean jitter (25%, P < 0.005). In 4 patients without abnormal spontaneous activity there was no significant increase in the mean jitter, although 1 of the latter 4 patients showed an increased jitter, indicating that abnormal SFEMG may precede abnormal spontaneous activity. Nerve conduction studies did not show any significant changes in both patient groups. Our findings suggest that CIP is a primarily axonal motor neuropathy. The increased jitter in patients with CIP indicates that CIP is a primarily axonal neuropathy with a lesion of terminal motor axons. © 1997 John Wiley & Sons, Inc. Muscle Nerve, 20, 696–701, 1997.     

Anxiety symptoms and syndromes in bipolar children and adolescents

Anxiety disorders are relatively common in children and adolescents with bipolar disorder. Research to date indicates they may impact the onset, course, and treatment response of bipolar illness in children. Anxiety disorders often precede the onset of pediatric bipolar disorder. Family studies suggest first-degree relatives of bipolar patients are at increased risk for developing mood and anxiety disorders compared with relatives of individuals without mood disorders. Childhood adversity has been associated with higher rates of comorbid anxiety disorders and more severe illness course in bipolar patients. Preliminary study of the neurobiology of bipolar disorder with comorbid anxiety disorders suggests it may be neurophysiologically distinct from bipolar disorder without comorbid anxiety. Bipolar disorder with comorbid anxiety disorders has been associated with greater functional impairment and slower recovery. Prospective, longitudinal studies are needed to help us better understand the relationship between bipolar disorder and comorbid anxiety disorders so that opportunities for early intervention and effective treatment can be realized.     

Causes of neuromuscular weakness in the intensive care unit: A study of ninety-two patients

The spectrum of neuromuscular disorders among intensive care unit (ICU) patients has shifted toward disorders acquired within the ICU and away from “traditional” neuromuscular disorders that lead to ICU admission. We sought to assess this spectrum by determining the causes and relative frequencies of neuromuscular disorders that led to electromyography (EMG) examinations in our ICU population. Ninety-two patients were studied over a 4½-year period. Twenty-six (28%) had neuromuscular disorders (mainly Guillain–Barré syndrome, myopathy, and motor neuron disease) that led to ICU admission. Among patients who developed weakness in the ICU, there was a predominance of organ transplant patients and patients with the systemic inflammatory response syndrome and multiorgan dysfunction. Thirty-nine (42%) developed acute myopathy (consistent with critical illness myopathy in most), and 13% developed acute axonal sensorimotor polyneuropathy (mainly critical illness polyneuropathy). Patients with acute myopathy and acute axonal sensorimotor polyneuropathy had similar functional outcomes. We conclude that among patients who underwent EMG in our ICU population, acute myopathy is three times as common as acute axonal polyneuropathy, and the outcomes from acute myopathy and acute axonal polyneuropathy may be similar. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:610–617, 1998.