Neurological and Neuropsychiatric Impacts of COVID-19 Pandemic.

BACKGROUND: Albeit primarily a disease of respiratory tract, the 2019 coronavirus infectious disease (COVID-19) has been found to have causal association with a plethora of neurological, neuropsychiatric and psychological effects. This review aims to analyze them with a discussion of evolving therapeutic recommendations. METHODS: PubMed and Google Scholar were searched from 1 January 2020 to 30 May 2020 with the following key terms: "COVID-19", "SARS-CoV-2", "pandemic", "neuro-COVID", "stroke-COVID", "epilepsy-COVID", "COVID-encephalopathy", "SARS-CoV-2-encephalitis", "SARS-CoV-2-rhabdomyolysis", "COVID-demyelinating disease", "neurological manifestations", "psychosocial manifestations", "treatment recommendations", "COVID-19 and therapeutic changes", "psychiatry", "marginalised", "telemedicine", "mental health", "quarantine", "infodemic" and "social media". A few newspaper reports related to COVID-19 and psychosocial impacts have also been added as per context. RESULTS: Neurological and neuropsychiatric manifestations of COVID-19 are abundant. Clinical features of both central and peripheral nervous system involvement are evident. These have been categorically analyzed briefly with literature support. Most of the psychological effects are secondary to pandemic-associated regulatory, socioeconomic and psychosocial changes. CONCLUSION: Neurological and neuropsychiatric manifestations of this disease are only beginning to unravel. This demands a wide index of suspicion for prompt diagnosis of SARS-CoV-2 to prevent further complications and mortality.

Les impacts neurologiques et neuropsychiatriques d'une infection à la COVID-19. CONTEXTE: Bien qu'il s'agisse principalement d'une maladie des voies respiratoires, la maladie infectieuse à coronavirus apparue en 2019 (COVID-19) s'est avérée avoir un lien de causalité avec une pléthore d'impacts d'ordre neurologique, neuropsychiatrique et psychologique. Cette étude entend donc analyser ces impacts tout en discutant l'évolution des recommandations thérapeutiques se rapportant à cette maladie. MÉTHODES: Les bases de données PubMed et Google Scholar ont été interrogées entre les 1er janvier et 30 mai 2020. Les termes clés suivants ont été utilisés : « COVID-19 ¼, « SRAS ­ CoV-2 ¼, « Pandémie ¼, « Neuro ­ COVID ¼, « AVC ­ COVID ¼, « Épilepsie ­ COVID ¼, « COVID ­ encéphalopathie ¼, « SRAS ­ CoV-2 ­ encéphalite ¼, « SRAS ­ CoV-2 ­ rhabdomyolyse ¼, « COVID ­ maladie démyélinisante ¼, « Manifestations neurologiques ¼, « Manifestations psychosociales ¼, « Recommandations thérapeutiques ¼, « COVID-19 et changement thérapeutiques ¼, « Psychiatrie ¼, « Marginalisés ¼, « Télémédecine ¼, « Santé mentale ¼, « Quarantaine ¼, « Infodémique ¼ et « Médias sociaux ¼. De plus, quelques articles de journaux relatifs à la pandémie de COVID-19 et à ses impacts psychosociaux ont également été ajoutés en fonction du contexte. RÉSULTATS: Il appert que les manifestations neurologiques et neuropsychiatriques des infections à la COVID-19 sont nombreuses. Les caractéristiques cliniques d'une implication des systèmes nerveux central et périphérique sautent désormais aux yeux. Ces caractéristiques ont fait l'objet d'une brève analyse systématique à l'aide de publications scientifiques. En outre, la plupart des impacts d'ordre psychologique de cette pandémie se sont révélés moins apparents que les changements réglementaires, socioéconomiques et psychosociaux. CONCLUSION: Les manifestations neurologiques et neuropsychiatriques de cette maladie ne font que commencer à être élucidées. Cela exige donc une capacité accrue de vigilance en vue d'un diagnostic rapide, et ce, afin de prévenir des complications additionnelles et une mortalité accrue.

Risk of disease relapse, safety and tolerability of SARS-CoV-2 vaccination in patients with chronic inflammatory neuropathies.

BACKGROUND AND PURPOSE: The aim was to evaluate the risk of relapse after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination, and its safety and tolerability, in patients with chronic inflammatory neuropathies. METHODS: In this multicenter, cohort and case-crossover study, the risk of relapse associated with SARS-CoV-2 vaccination was assessed by comparing the frequency of relapse in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and multifocal motor neuropathy (MMN) patients who underwent or did not undergo vaccination. Frequency of relapse in the 3 months prior to and after vaccination, and safety and tolerability of SARS-CoV-2 vaccination, were also assessed. RESULTS: In all, 336 patients were included (278 CIDP, 58 MMN). Three hundred and seven (91%) patients underwent SARS-CoV-2 vaccination. Twenty-nine patients (9%) did not undergo vaccination. Mild and transient relapses were observed in 16 (5%) patients (13 CIDP, 3 MMN) after SARS-CoV-2 vaccination and in none of the patients who did not undergo vaccination (relative risk [RR] 3.21, 95% confidence interval [CI] 0.19-52.25). There was no increase in the specific risk of relapse associated with type of vaccine or diagnosis. Comparison with the 3-month control period preceding vaccination revealed an increased risk of relapse after vaccination (RR 4.00, 95% CI 1.35-11.82), which was restricted to CIDP patients (RR 3.25, 95% CI 1.07-9.84). The safety profile of SARS-CoV-2 vaccination was characterized by short-term, mild-to-moderate local and systemic adverse events. CONCLUSIONS: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination in CIDP and MMN patients does not seem to be associated with an increased risk of relapse at the primary end-point, although a slightly increased risk in CIDP patients was found compared to the 3 months before vaccination.

Electrophysiological assessment in patients with COVID-19-related peripheral neuropathies and myopathies: a systematic review.

Neurological manifestations associated with Coronavirus Disease-2019 (COVID-19) are commonly reported, but patients were not referred to perform the electrophysiological assessment. We aimed to review the existing literature on clinical studies on COVID-19 peripheral neuropathy to correlate patients' symptoms and characteristics with nerve conduction studies/electromyography (NCS/EMG) outcomes. This protocol is registered in the Open Science Framework (https://www.doi.org/10.17605/OSF.IO/ZF4PK). The systematic search included PubMed, ScienceDirect, and Google Scholar, for articles published from December 2019 to March 2022. A total of 727 articles were collected, and according to our inclusion and exclusion criteria, only 6 articles were included. Of 195 participants, only 175 underwent NCS/EMG assessment. Of these, 44 participants (25.1%) had abnormal EMG, 54 participants (30.8%) had abnormal motor NCS, and only 7 participants (4%) had abnormal sensory NCS. All cases presented with myopathy, while a limited number of cases presented with polyneuropathy. According to motor NCS and EMG, the most affected nerves were the tibial and peroneal in the lower extremities and the ulnar nerve in the upper extremities. Interestingly, the median nerve was reported to be associated with the severity and the rate of motor recovery of patients with COVID-19. COVID-19 generates a demyelinating motor neuropathy and myopathy. Clinicians are encouraged to refer patients with COVID-19 presenting with neurological symptoms to be assessed by electrophysiological methods to objectively determine the nature of their symptoms, follow their prognosis, and plan their rehabilitation.

Atypical myelin oligodendrocyte glycoprotein antibody-associated optic neuritis and acute demyelinating polyneuropathy after SARS-CoV-2 infection: Case report and literature review.

Post-infectious immune-mediated neurological complications of Sars-Cov-2 have been increasingly recognized since the novel pandemic emerged. We describe the case of a 74 years-old patient who developed a Myelin Oligodendrocyte Glycoprotein (MOG) antibody-associated unilateral retrobulbar optic neuritis a few weeks after paucisymptomatic COVID-19 disease and, subsequently, after the resolution of the optic neuritis, an acute inflammatory demyelinating polyneuropathy. So far, no cases of these two neurological manifestations have been reported in the same patient. We herein report a case characterized by both manifestations and review the accumulating literature regarding MOG antibody-associated disease following SarsCov-2 infection.

Multifocal motor neuropathy after SARS-CoV-2 vaccination: a causal or coincidental association?

Multifocal motor neuropathy (MMN) is an immune-mediated and acquired demyelinating motor polyneuropathy. Several cases of polyneuropathy associated with severe acquired respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination have been reported. However, MMN has not been reported as a complication of SARS-CoV-2 vaccination. In this study, we report a case of MMN with progressive muscle weakness following the second dose of the Pfizer-BioNTech mRNA vaccine. It was diagnosed by clinical evaluation and electroneuromyography. SARS-CoV-2 vaccination is increasing rapidly all over the world. Some cases of polyneuropathy, especially Guillain-Barré syndrome, have been reported after vaccination. This is the first case report of MMN after SARS-CoV-2 vaccination.

Recombinant protein subunit COVID-19 Vaccine Induced Guillain-Barre Syndrome in an adolescent: A case report. (preprint)

Guillain- Barre Syndrome (GBS), an autoimmune neurological disease of peripheral nerves has been causally associated with COVID-19 vaccination in adults. However, no such report has been published so far in children. We describe a 13-year old female child who presented to emergency department with complaints of bilateral upper limb, lower limb and truncal weakness over three days following first dose of recombinant protein subunit COVID-19 vaccine (Corbevax). Clinical examination and nerve conduction studies showed pure motor axonal polyneuropathy with absent compound muscle action potential (CMAP) in all sampled nerves of upper and lower limbs which was consistent with the diagnosis of GBS after ruling out possible alternative aetiologies. A temporal association between first dose of protein subunit COVID-19 vaccine administered a day prior and symptom onset was noted. The causality assessment using World Health Organization (WHO) tool for adverse event following immunization (AEFI) assessment indicated vaccine-product related reaction categorized as A1. Patient’s clinical condition improved after seven sessions of plasmapheresis. The purpose of this report is to create awareness among the health care professionals about COVID-19 vaccine induced GBS in children as early diagnosis and management can be critical in avoiding complications and improving patient outcomes.

Recrudescence of severe polyneuropathy after receiving Pfizer-BioNTech COVID-19 vaccine in a patient with a history of eosinophilic granulomatosis with polyangiitis.

A middle age man with a history of diabetes mellitus type 2, hypertension, migraine and eosinophilic granulomatosis with polyangiitis (EGPA) with polyneuropathy in remission presented with paresthesia and motor weakness soon after receiving the Pfizer-BioNTech COVID-19 messanger RNA (mRNA) vaccine. The patient had polyneuropathy 10 years ago secondary to EGPA, which had resolved. EGPA was diagnosed on the basis of typical symptoms and positive sural nerve biopsy. Five days after receiving the first dose of COVID-19 vaccine, he developed heaviness and reduced dexterity of both the upper extremities, which progressed to patchy and asymmetric motor weakness of all four extremities. Given the lack of clear alternative explanation after a thorough work up, recrudescence of underlying asymptomatic polyneuropathy due to a possible reaction to COVID-19 mRNA vaccine was considered although a temporal association with vaccine dose does not prove causality. He was treated with corticosteroids with slow improvement of his symptoms.

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.

Development and early diagnosis of critical illness myopathy in COVID-19 associated acute respiratory distress syndrome.

BACKGROUND: The COVID-19 pandemic has greatly increased the incidence and clinical importance of critical illness myopathy (CIM), because it is one of the most common complications of modern intensive care medicine. Current diagnostic criteria only allow diagnosis of CIM at an advanced stage, so that patients are at risk of being overlooked, especially in early stages. To determine the frequency of CIM and to assess a recently proposed tool for early diagnosis, we have followed a cohort of COVID-19 patients with acute respiratory distress syndrome and compared the time course of muscle excitability measurements with the definite diagnosis of CIM. METHODS: Adult COVID-19 patients admitted to the Intensive Care Unit of the University Hospital Bern, Switzerland requiring mechanical ventilation were recruited and examined on Days 1, 2, 5, and 10 post-intubation. Clinical examination, muscle excitability measurements, medication record, and laboratory analyses were performed on all study visits, and additionally nerve conduction studies, electromyography and muscle biopsy on Day 10. Muscle excitability data were compared with a cohort of 31 age-matched healthy subjects. Diagnosis of definite CIM was made according to the current guidelines and was based on patient history, results of clinical and electrophysiological examinations as well as muscle biopsy. RESULTS: Complete data were available in 31 out of 44 recruited patients (mean [SD] age, 62.4 [9.8] years). Of these, 17 (55%) developed CIM. Muscle excitability measurements on Day 10 discriminated between patients who developed CIM and those who did not, with a diagnostic precision of 90% (AUC 0.908; 95% CI 0.799-1.000; sensitivity 1.000; specificity 0.714). On Days 1 and 2, muscle excitability parameters also discriminated between the two groups with 73% (AUC 0.734; 95% CI 0.550-0.919; sensitivity 0.562; specificity 0.857) and 82% (AUC 0.820; CI 0.652-0.903; sensitivity 0.750; specificity 0.923) diagnostic precision, respectively. All critically ill COVID-19 patients showed signs of muscle membrane depolarization compared with healthy subjects, but in patients who developed CIM muscle membrane depolarization on Days 1, 2 and 10 was more pronounced than in patients who did not develop CIM. CONCLUSIONS: This study reports a 55% prevalence of definite CIM in critically ill COVID-19 patients. Furthermore, the results confirm that muscle excitability measurements may serve as an alternative method for CIM diagnosis and support its use as a tool for early diagnosis and monitoring the development of CIM.

Nervous system involvement after infection with COVID-19 and other coronaviruses.

Viral infections have detrimental impacts on neurological functions, and even to cause severe neurological damage. Very recently, coronaviruses (CoV), especially severe acute respiratory syndrome CoV 2 (SARS-CoV-2), exhibit neurotropic properties and may also cause neurological diseases. It is reported that CoV can be found in the brain or cerebrospinal fluid. The pathobiology of these neuroinvasive viruses is still incompletely known, and it is therefore important to explore the impact of CoV infections on the nervous system. Here, we review the research into neurological complications in CoV infections and the possible mechanisms of damage to the nervous system.

Critical Illness Polyneuropathy and Functional Outcome in Subjects with Covid-19: Report on Four Patients and a Scoping Review of the Literature.

Patients with COVID-19 may develop a range of neurological disorders. We report here 4 COVID-19 subjects with intensive care unit-acquired weakness and their functional outcome. In addition, a scoping review of COVID-19 literature was performed to investigate this issue. Of the post-COVID-19 patients admitted to our Neuro-Rehabilitation Unit, 4 (3 males, 1 female; mean age 59.2 ± 8.62 years) had intensive care unit-acquired weakness, diagnosed with electromyography. Muscle strength and functional evaluation were performed on all patients with Medical Research Council, Disability Rating Scale and Functional Independence Measure, respectively, at admission, discharge and 6-month follow-up after discharge. Electromyography revealed that 3 subjects had critical illness polyneuropathy and 1 had critical illness polyneuropathy/critical illness myopathy. At follow-up, the 3 subjects with critical illness polyneuropathy reached full recovery. The patient with critical illness polyneuropathy/critical illness myopathy showed moderate disability requiring bilateral ankle foot-orthosis and support for ambulation. The scoping review retrieved 11 studies of COVID-19 patients with intensive care unit-acquired weakness, concerning a total of 80 patients: 23 with critical illness myopathy (7 probable), 21 with critical illness polyneuropathy (8 possible), 15 with critical illness polyneuropathy and myopathy (CIPNM) and 21 with intensive care unit-acquired weakness. Of 35 patients who survived, only 3 (8.5%) reached full recovery. All 3 had critical illness myopathy, but 2 of these had a diagnosis of probable critical illness myopathy. Intensive care unit-acquired weakness commonly occurred in subjects with COVID-19. Recovery was variable and a low percentage reached full recovery. However, the heterogeneity of studies did not allow definitive conclusions to be drawn.

Zoster Cranial Polyneuropathy in a COVID-19 Patient.

BACKGROUND Ramsay Hunt syndrome is a rare form of herpes zoster caused by the reactivation of the varicella-zoster virus in the geniculate ganglion. The main clinical manifestations are peripheral facial palsy, vesicular rash in the ear, and ipsilateral auricular pain, and sometimes vertigo. COVID-19 is a new multisystemic infectious disease that, in addition to common respiratory manifestations, it is known to affect the immune system, primarily depressing cellular immunity. CASE REPORT A 54-year-old woman was admitted to our hospital with an acute vestibular syndrome and diplopia. She had been diagnosed 3 years prior with interstitial lung disease for which she was taking methylprednisolone. At admission, she tested positive for SARS-CoV-2. In the following days, she developed a sixth nerve palsy on the left side and a right peripheral facial palsy on the right side, followed by a typical zoster rash on the ipsilateral ear. One month later, she developed acute severe hearing loss on the right side. There were no COVID-19 symptoms during her stay in our hospital. The MRI showed Gd enhancement of both facial nerves. Under antiviral and corticoid treatment, the evolution was favorable, with marked improvement at 6 months. CONCLUSIONS COVID-19 increases the risk for herpes zoster infection, probably through induced depression of the cellular immunity. Our case suggests Ramsay Hunt syndrome can be the presenting symptom and sometimes the only symptom of COVID-19. This also seems to be true for other cranial neuropathies, and we recommend testing these patients even if there are no other manifestations.

Post-coronavirus disease 2019 polyneuropathy with significant response to immunoglobulin therapy: a case report.

BACKGROUND: The symptoms of coronavirus disease 2019, caused by the novel severe acute respiratory syndrome coronavirus 2, were originally assumed to be mainly respiratory. With increasing knowledge, however, it turned out that the spectrum of complaints varies broadly with age and concomitant diseases. While many neurological symptoms were reported in the context of the disease, ranging from permanent fatigue to recurrent headaches and concentration disturbance, treatment approaches are still in development. This case discusses a possible treatment approach with immunoglobulin therapy and its outcomes. CASE PRESENTATION: We present the case of a 56-year-old Caucasian female patient who, following coronavirus disease 2019, developed peripheral sensory and autonomic disturbances that fell within subacute demyelinating neuropathy. Because a significant improvement in symptoms as well as in the results of clinical and electrophysiological examination was reported after immunoglobulin therapy, long-term therapy does not appear to be necessary. CONCLUSION: Given the significant subjective and objective improvement reported, this case provides additional evidence that immunoglobulin therapy can be considered in post-coronavirus disease 2019 syndrome.

Pure sensitive chronic inflammatory axonal polyneuropathy following Pfizer COVID-19 vaccine.

BACKGROUND: During the worldwide mass vaccination campaign against SARS-CoV-2, multiple side effects have been observed. We described the case of a patient who developed pure sensitive chronic inflammatory axonal polyneuropathy (CIAP) in a close temporal relationship with the administration of the BNT162b2 (Pfizer®) vaccine. CASE REPORT: An 82-year-old woman developed lower limb sensory loss and "pricking" associated with marked gait imbalance after she had received her second dose of Pfizer-BioNTech COVID-19 vaccine. At the electroneurographic examination, the motor nerves conduction study was normal. Median, ulnar, and sural nerves sensory compound nerve action potential (CNAP) were bilaterally absent. Somatosensory evoked potentials (SSEPs) were not recordable. Spine MRI demonstrated roots enhancement from C3 to Th2 and diffuse enhancement of cauda equina nerve roots. She was treated with IV methylprednisolone whit benefit. A follow-up visit was made 4 months after the disease onset; a diagnosis of pure sensitive CIAP has been made. DISCUSSION: To the best of our knowledge, this is the first description of CIAP occurring in a close temporal relationship with the administration of Pfizer-BioNTech COVID-19 vaccine.

Stridor Due to Cranial Nerve X Palsy Progressing to Polyneuropathy in a Teenager With COVID-19.

The neurologic manifestations of coronavirus disease 2019 (COVID-19) are wide-ranging, including various cranial neuropathies, beyond anosmia and dysgeusia, the exact neuropathological mechanism of which are yet unknown. Acute cranial nerve (CN) X neuritis with vocal cord paralysis has not been reported in COVID-19 and is a rare presentation of neuropathy in general. A girl aged 14 years was admitted with stridor. She was diagnosed with symptomatic COVID-19 8 days before. By presentation, fever had resolved, but she had developed stridor; sore throat with dysphagia; chest, shoulder, and back pain; and generalized weakness. Neurologic examination and laryngoscopy were consistent with isolated left CN X palsy. Steroids were started, but neurologic disease progressed with subjective pain, right lower face numbness, and eye fatigability. Respiratory distress increased, and she was intubated for airway protection. MRI revealed abnormal enhancement of CNs III, V, XII, and X. Cerebrospinal fluid studies were normal. Nasopharyngeal severe acute respiratory syndrome coronavirus 2 polymerase chain reaction test result was positive. She was treated with intravenous immunoglobulin, a total of 2 g/kg, and steroids were continued. She made a full neurologic recovery and was discharged after 9 days of hospitalization. This is a case of a teenager who presented with an acute, life-threatening CN X palsy and development of a progressive polyneuropathy in the setting of COVID-19. Although there was concern for Guillain-Barre syndrome, a definitive diagnosis could not be made, and the unusual features of this case, including presentation with stridor and predominate CN involvement seem to indicate a separate symptomatic COVID-19-associated polyneuritis.

Critical illness neuropathy in severe COVID-19: a case series.

INTRODUCTION: Neurological complications of SARS-CoV-2 disease have received growing attention, but only few studies have described to date clinical and neurophysiological findings in COVID patients during their stay in intensive care units (ICUs). Here, we neurophysiologically assessed the presence of either critical illness neuropathy (CIP) or myopathy (CIM) in ICU patients. MATERIALS AND METHODS: Patients underwent a neurophysiological assessment, including bilateral examination of the median, ulnar, deep peroneal and tibial motor nerves and of the median, ulnar, radial and sural sensory nerves. Needle electromyography (EMG) was performed for both distal and proximal muscles of the lower and upper limbs. In order to differentiate CIP from CIM, Direct Muscle Stimulation (DMS) was applied either to the deltoid or tibialis anterior muscles. Peak to peak amplitudes and onset latencies of the responses evoked by DMS (DMSamp, DMSlat) or by motor nerve stimulation (MNSamp, MNSlat) were compared. The ratio MNSamp to DMSamp (NMR) and the MNSlat to DMSlat difference (NMD: MNSlat - DMSlat) were also evaluated. RESULTS: Nerve conduction studies showed a sensory-motor polyneuropathy with axonal neurogenic pattern, as confirmed by needle EMG. Both MNSamp and NMR were significantly reduced when compared to controls (p < 0.0001), whereas MNSlat and NMD were markedly increased (p = 0.0049). CONCLUSIONS: We have described COVID patients in the ICU with critical illness neuropathy (CIP). COVID-related CIP could have implications for the functional recovery and rehabilitation strategies.

Acute Hepatitis B Associated Neuromyopathy (preprint)

A 67 year old man presented with abdominal discomfort and jaundice for 1 month with difficulty in walking with severe pain in both thighs of 3 days duration. He was a diabetic and hypertensive on medications. There was no history of HMG CoA reductase inhibitor use. On examination he had icterus and grade 2 power in the proximal upper and lower limbs. Deep tendon reflexes were inelicitable. On day 1, CRP was 37mg/L and liver function tests were deranged [ Total Bilirubin 16 mg%, direct 14.3mg%, SGOT [920 U/L], SGPT [590 U/L], Alkaline Phosphatase 276.5 U/L. Serum CPK levels [9768 U/L], LDH [979 U/L] and Ferritin [7264 ng/ml] were elevated on day 2. ANA profile was negative. Leptospiral antibody, dengue serology and SARS-CoV2 RT-PCR were negative. Hepatitis B serology was compatible with an acute infection. On day 3, nerve conduction studies showed an axonal sensory-motor polyneuropathy predominantly involving the lower limbs. F waves were absent. Fibrillations and positive waves were picked up from the Tibialis anterior muscles bilaterally. He was started on IVIG 2gm/kg x 5 days. On day 4, his CPK levels increased to >42,000 U/L and he was shifted to the ICU and started on forced alkaline diuresis. Urine myoglobin was positive.. On day 6, MRI whole body muscle STIR imaging showed patchy ill-defined STIR hyperintensities involving the muscles of the gluteal, pelvic girdle muscles, both thighs and leg muscles with fascial edema. The muscles of the upper limbs and shoulder girdles also showed patchy STIR hyperintensities. Diffuse subcutaneous oedema was noted in the soft tissue of the thighs, legs and abdominal wall. Over the next few days, the weakness in the upper limbs worsened and he developed a weak cough. He did not consent to a lumbar puncture or muscle biopsy. Over the next 9 days, his liver function tests and CPK levels gradually normalised. He was also started on Entacavir. By day 10, his upper limb and distal lower limb had improved to grade 4/5 power and he was able to stand with support and he was discharged.

Polyneuropathy following COVID-19 infection: the rehabilitation approach.

A range of neurological manifestations associated with COVID-19 have been reported in the literature, but the pathogenesis of these have yet to be fully explained. The majority of cases of peripheral nervous system disease published thus far have shown a symmetrical pattern. In contrast, we describe the case of a patient with asymmetrical predominantly upper-limb sensorimotor polyneuropathy following COVID-19 infection, likely due to a multifactorial pathological process involving critical illness neuropathy, mechanical injury and inflammatory disease. His presentation, management and recovery contribute to the understanding of this complex condition and informs rehabilitation approaches.

Electrodiagnostic findings in patients with non-COVID-19- and COVID-19-related acute respiratory distress syndrome.

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 <48). Creatine phosphokinase (CPK), lactic dehydrogenase (LDH) and mean morning glycaemic values were collected. RESULTS: From a total of 148 patients, 23 with COVID-19 infection and 21 with ARDS due to other aetiologies, underwent electroneurography/electromyography (ENG/EMG) recording. Incidence of CIPNM was similar in the two groups, 65% (15 of 23) in COVID-19 patients and 71% (15 of 21) in patients affected by ARDS of other aetiologies. At ICU discharge, subjects with CIPNM more frequently required ventilatory support, regardless the aetiology of ARDS. CONCLUSION: ENG/EMG represents a useful tool in the identification of the neuromuscular causes underlying ventilator wean failure and patient stratification. A high incidence of CIPNM, with a similar percentage, has been observed in ARDS patients of all aetiologies.