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.     

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.     

Early detection of evolving critical illness myopathy with muscle velocity recovery cycles

ObjectiveTo 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).MethodsTwenty-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.ResultsMVRC 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.ConclusionsAltered 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.SignificanceCIM is often under-recognized by intensivists, and large-scale longitudinal studies are needed to determine its incidence and pathogenesis.     

Neuromuscular disorders in critically ill patients: review and update

Neuromuscular disorders that are diagnosed in the intensive care unit (ICU) usually cause substantial limb weakness and contribute to ventilatory dysfunction. Although some lead to ICU admission, ICU-acquired disorders, mainly critical illness myopathy (CIM) and critical illness polyneuropathy (CIP), are more frequent and are associated with considerable morbidity. Approximately 25% to 45% of patients admitted to the ICU develop CIM, CIP, or both. Their clinical features often overlap; therefore, nerve conduction studies and electromyography are particularly helpful diagnostically, and more sophisticated electrodiagnostic studies and histopathologic evaluation are required in some circumstances. A number of prospective studies have identified risk factors for CIP and CIM, but their limitations often include the inability to separate CIM from CIP. Animal models reveal evidence of a channelopathy in both CIM and CIP, and human studies also identified axonal degeneration in CIP and myosin loss in CIM. Outcomes are variable. They tend to be better with CIM, and some patients have longstanding disabilities. Future studies of well-characterized patients with CIP and CIM should refine our understanding of risk factors, outcomes, and pathogenic mechanisms, leading to better interventions.     

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.     

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.     

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.     

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.     

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.     

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.     

Optimizing testing methods and collection of reference data for differentiating critical illness polyneuropathy from critical illness MYOPATHIES

Introduction: In severe acute quadriplegic myopathy in intensive care unit (ICU) patients, muscle fibers are electrically inexcitable; in critical illness polyneuropathy, the excitability remains normal. Conventional electrodiagnostic methods do not provide the means to adequately differentiate between them. In this study we aimed to further optimize the methodology for the study of critically ill ICU patients and to create a reference database in healthy controls. Methods: Different electrophysiologic protocols were tested to find sufficiently robust and reproducible techniques for clinical diagnostic applications. Results: Many parameters show large test–retest variability within the same healthy subject. Reference values have been collected and described as a basis for studies of weakness in critical illness. Conclusions: Using the ratio of neCMAP/dmCMAP (response from nerve and direct muscle stimulation), refractory period, and stimulus–response curves may optimize the electrodiagnostic differentiation of patients with critical illness myopathy from those with critical illness polyneuropathy. Muscle Nerve 53 : 555–563, 2016     

Prevalence and prospective evaluation of cognitive dysfunctions after SARS due to SARS-CoV-2 virus. The COgnitiVID study

ObjectiveCOVID-19 due to SARS-CoV-2 virus is a new cause of severe acute respiratory syndrome (SARS). Little is known about the short-term cognitive prognosis for these patients. We prospectively evaluated basic cognitive functions shortly after care in the intensive care unit (ICU) and three months later in post-ICU COVID-19 patients.Material and methodsWe performed a prospective single-center study in our institution in Paris. Patients with SARS-CoV-2 SARS were prospectively recruited via our ICU. Patients were evaluated using standardized cognitive tests at baseline and at three months’ follow-up. Our primary endpoint was the evolution of the following five global tests: MMSE, FAB, oral naming test, Dubois five words test and MADRS.ResultsWe explored 13 patients at baseline and follow-up. All patients had cognitive impairment at baseline but they all improved at three months, significantly on two of the five global tests after Bonferroni correction for multiple testing: MMSE (median 18 (IQR [15–22]) and 27 (IQR [27–29]) respectively, P = 0.002) and FAB test (median 14 (IQR [14–17]) and 17 (IQR [17,18]) respectively, P = 0.002).ConclusionsWe report here the first longitudinal data on short-term cognitive impairment after intensive care in COVID-19 patients. We found acute and short-term cognitive impairment but significant improvement at three months. This pattern does not seem to differ from other causes of post-intensive care syndrome.     

Origin of ICU acquired paresis determined by direct muscle stimulation

BACKGROUND: Acquired diffuse paresis in an intensive care unit (ICU) can result from critical illness myopathy or polyneuropathy. Clinical examination and conventional neurophysiological techniques may not distinguish between these entities. OBJECTIVE: To assess the value of direct muscle stimulation (DMS) to differentiate myopathic from neuropathic process in critically ill patients with diffuse severe muscle weakness. METHODS: 30 consecutive patients with ICU acquired diffuse motor weakness were studied. Responses of the right deltoid and tibialis anterior muscles to DMS and to motor nerve stimulation (MNS) were studied and compared with results of conventional nerve conduction studies and concentric needle electromyography (EMG). An original algorithm was used for differential diagnosis, taking into account first the amplitude of the responses to DMS, then the MNS to DMS amplitude ratio, and finally the amplitude of the sensory nerve action potentials recorded at the lower limbs. RESULTS: Evidence of neuropathy and myopathy was found in 57% and 83% of the patients, respectively. Pure or predominant myopathy was found in 19 patients. Other results were consistent with neuromyopathy (n = 5) and pure or predominant neuropathy (n = 2). Four patients had normal results with stimulation techniques, but spontaneous EMG activity and raised plasma creatine kinase suggesting necrotic myopathy. CONCLUSIONS: A neurophysiological approach combining DMS and conventional techniques revealed myopathic processes in a majority of ICU patients. Reduced muscle fibre excitability may be a leading cause for this. The diagnosis of myopathy in ICU acquired paralysis can be established by a combination of DMS, needle EMG, and plasma creatine kinase.     

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     

A family with adult-onset myofibrillar myopathy with BAG3 mutation (P470S) presenting with axonal polyneuropathy

We report a family with adult-onset myofibrillar myopathy with BAG3 mutation who presented peroneal weakness and axonal polyneuropathy, mimicking axonal Charcot-Marie-Tooth disease. The male proband noticed difficulty in tiptoeing at age 34. At age 42, the examination showed muscle weakness and atrophy in distal lower extremities with diminished patellar and Achilles tendon reflexes. Thermal and vibration sensations were also impaired in both feet. The serum CK level was 659 U/L. On muscle imaging, predominant semitendinosus muscle atrophy coexisted with atrophies in the quadriceps, gastrocnemius and lumbar paraspinal muscles. The muscle biopsy showed myofibrillar myopathy with fiber type grouping. His 68-year-old mother also had suffered from distal leg weakness and sensory impairment since her forties. A heterozygous mutation in BAG3 (P470S) was identified in both patients. Clinical features of myofibrillar myopathy with axonal polyneuropathy were consistent with BAG3-related myopathy. Our patients showed remarkably mild presentations without cardiomyopathy, unlike the majorities of previously reported cases.     

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.     

Neuromuscular function in survivors of the acute respiratory distress syndrome

BACKGROUND: Survivors of acute respiratory distress syndrome (ARDS) report generalized weakness and reduced exercise tolerance up to two years following discharge from the intensive care unit (ICU). Persistent neuromuscular complications of ARDS may contribute to the functional disability observed in these patients. METHODS: Sixteen ARDS survivors underwent comprehensive neurological evaluation and standardized electrodiagnostic testing 6 to 24 months after ICU discharge. Four of these patients agreed to open muscle biopsy. RESULTS: Seven of sixteen patients had clinically significant focal compressive mononeuropathies. Electrodiagnostic testing failed to reveal any changes attributable to critical illness polyneuropathy or myopathy. All four muscle biopsies were abnormal, and although the pathological features were structurally non-specific, the presence of an acquired myopathy remains possible. Four patients had persistent mixed sensory complaints but had normal electrodiagnostic evaluation. CONCLUSIONS: The high frequency of mononeuropathies highlights the need for vigilance in daily ICU care. The findings also suggest that complaints of weakness and reduced exercise capacity in ARDS survivors may be related to combined effects of compressive neuropathies and generalized longstanding structural changes in muscle and may support an organic basis for long-term functional disability.     

The Effects of COVID-19 on Patients with Acute Ischemic and Hemorrhagic Stroke

ObjectiveThe objective of this study was to evaluate how COVID-19 affects patients with acute ischemic or hemorrhagic stroke outcome.Materials and methodsThis retrospective study was performed on adult patients (> 18 years old) with stroke (ischemic or hemorrhagic) who were admitted to hospital with or without COVID-19. The primary outcome was stroke-related disability, which was measured by mRS at baseline and discharge. Hospital duration, intensive care unit (ICU) admission, and mortality were considered the secondary outcomes.ResultsFrom February 2019 until August 2020, we recruited and analyzed 151 patients, 42 of whom had COVID-19 based on RT-PCR tests or lung CT scan findings. COVID-19 positive patients had higher baseline and final mRS scores than the control group (4.46 ± 0.67 vs 4.79 ± 0.61, P: 0.001, 3.83 ± 1.22 vs 4.46 ± 0.67, P: 0.001). Moreover, stroke patients with COVID-19 experienced a more severe disease and required a higher rate of ICU admission (17 vs 0, P:0.001) and longer hospitalization compared to those without COVID-19 (8.50 ± 7.86 vs 7.5 ± 11.20, P: 0.021). Also, mortality was higher in the COVID-19 group (19 vs 13, P:0.001). There was not any significant differences between the two groups in terms of the involvement of cerebral arteries and type of stroke. Male sex, COVID-19, and ICU admission were the main independent risk factors for death.ConclusionThe results of the study showed stroke patients (ischemic or hemorrhagic) with COVID-19 can have more disabilities and incur more hospital complications and mortality than non-COVID-19 patients.