Acute inflammatory demyelinating polyneuropathy or Guillain-Barré syndrome associated with COVID-19: a case report

Journal of Medical Case Reports volume 15, Article number: 219 (2021) 

Abstract

Background

Coronavirus disease 2019 (COVID-19) is a global pandemic. The disease, typically characterized by bilateral pulmonary infiltrates and profound elevation of inflammatory markers, can range in severity from mild or asymptomatic illness to a lethal cytokine storm and respiratory failure. A number of recognized complications of COVID-19 infection are described in the literature. Common neurological complications include headache and anosmia. Guillain-Barré syndrome (GBS) is an uncommon complication described in isolated case reports. However, a causal relationship has yet to be established. This case report adds to the growing body of evidence that GBS is a potential COVID-19 complication.

Case presentation

A 70-year-old Caucasian woman with recently diagnosed COVID-19 infection presented to the emergency department with 4 days of gradually worsening ascending lower extremity weakness. Exam revealed bilateral lower extremity weakness, mute reflexes, and sensory loss. Soon after starting intravenous administration of immunoglobulin (IVIG), the patient developed respiratory distress, eventually requiring intubation. She remained intubated for the duration of her IVIG treatment. After five rounds of treatment, the patient was successfully extubated and transferred to acute rehab. Following 4 weeks of intense physical therapy, she was able to walk with assistance on room air.

Conclusion

At the present time, this is one of the few reports of acute inflammatory demyelinating polyneuropathy (AIDP) or GBS associated with COVID-19 in the United States. It is unclear whether a causal relationship exists given the nature of the syndrome. However, in light of the growing number of reported cases, physicians should be aware of this possible complication when evaluating COVID-19 patients.

For More Information: https://jmedicalcasereports.biomedcentral.com/articles/10.1186/s13256-021-02831-4

Prevalence of anosmia and ageusia symptoms among long-term effects of COVID-19.

Authors: Moraschini V1Reis D1Sacco R2Calasans-Maia MD3

COVID‐19 is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) that currently presents the greatest, most challenging health concern worldwide. Since the first reports of the disease in December 2019, clinicians and scientists have endeavored to understand the main symptoms, risk factors, and prognosis of the disease (Wynants et al., 2020). Although a significant portion of the infected population remains asymptomatic, many COVID‐19‐infected individuals develop symptoms that vary from mild to severe (Stasi et al., 2020).

Some patients may experience long‐term effects of COVID‐19, which persist for two or more weeks after the onset of the disease (Tenforde et al., 2020). Loss of taste (ageusia) and smell (anosmia) are symptoms that have drawn substantial attention from researchers because of their high prevalence in the early stages of the disease (Eliezer et al., 2020; Gane et al., 2020). However, recent studies have observed persistent dysgeusia and anosmia following recovery from COVID‐19 infection (Andrews et al., 2020; Garrigues et al., 2020; Panda et al., 2020).

The aim of this study was to estimate the prevalence of dysgeusia and anosmia in studies that assessed the long‐term effects of COVID‐19. Four databases (PubMed/MEDLINE, EMBASE, Scopus, and Lilacs) were searched for articles without any restrictions regarding language, and the inclusion criteria were based on the PECO strategy (Morgan et al., 2018). This review included studies that analyzed the prevalence of persistent symptoms (>30 days) of anosmia and dysgeusia in patients who had COVID‐19. There were no language restrictions. Two independent review authors (V.M. and M.D.C.M.) conducted the search‐and‐screening process, commencing with the analysis of titles and abstracts. Next, full papers were selected for careful reading and matched with the eligibility criteria for subsequent data extraction. The search strategy is described in Table S1.

Regarding the quality of the analyzed studies and risk of bias, one study was classified as low quality (Andrews et al., 2020), two as satisfactory (Garrigues et al., 2020; Horvath et al., 2020), and five as of high quality (Carfì et al., 2020; Carvalho‐Schneider et al., 2020; Chopra et al., 2020; Galván‐Tejada et al., 2020; Panda et al., 2020). The analyses can be viewed in Table S2.

The two review authors (V.M. and M.D.C.M.) independently performed risk‐of‐bias and study quality analyses. The Newcastle–Ottawa Scale (Lo et al., 2014) was used in the analysis of non‐randomized studies. For data analysis, the effects reported in one simple arm were estimated by dividing the number of patients with each symptom by the total number of patients with COVID‐19 in the sample and then by multiplying by 100 to estimate the percentage. The prevalence with 95% confidence intervals (CIs) was presented using the software Comprehensive Meta‐Analysis (BioStat).

A total of eight observational studies were selected for this study. Six cohort studies (Andrews et al., 2020; Carfì et al., 2020; Carvalho‐Schneider et al., 2020; Chopra et al., 2020; Horvath et al., 2020; Panda et al., 2020), one cross‐sectional study (Garrigues et al., 2020), and one case–control study (Galván‐Tejada et al., 2020) were included in this study (Figure S1). The studies analyzed 1,483 patients (773 male and 710 female) with a mean age of 48.3 ± 11.2. All patients were diagnosed with COVID‐19 through reverse transcription polymerase chain reaction (RT‐PCR) and exhibited mild, moderate, or severe symptoms. The mean overall follow‐up time was 60.7 days. The main data for each study are shown in Table ​Table11.

For More Information: https://europepmc.org/article/PMC/PMC8242542

Clinical Outcomes for Patients With Anosmia 1 Year After COVID-19 Diagnosis

Authors: Marion Renaud, MD1Claire Thibault, MD1Floriane Le Normand, MD1et al

Introduction

Since the pandemic was declared in early 2020, COVID-19–related anosmia quickly emerged as a telltale sign of infection.1,2 However, the time course and reversibility of COVID-19–related olfactory disorders, which may persist and negatively affect patients’ lives, require further study. To clarify the clinical course and prognosis, we followed a cohort of patients with COVID-19–related anosmia for 1 year and performed repeated olfactory function evaluations for a subset of patients.Methods

This cohort study follows the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guideline. Participants provided written informed consent. The study was approved by the ethics committee of the University Hospitals of Strasbourg.

In April 2020, we published a study1 about a cohort of patients with polymerase chain reaction–proven COVID-19 with acute smell loss (lasting >7 days). Over the course of 1 year, at 4-month intervals, patients were asked to complete a survey, and their olfactory function was assessed by psychophysical testing (the threshold and identification tests; Sniffin’ Sticks Test; Burghardt).3 Hyposmic or anosmic patients were followed until objective olfactory recovery (normal results were defined as those at or above the 10th percentile). Data analysis was performed from June 2020 to March 2021.Results

We evaluated 97 patients (67 women [69.1%]; mean [SD] age, 38.8 [11.5] years) with acute smell loss beyond 7 days. Of these patients, 51 (52.6%) underwent both subjective and objective olfactory test, and 46 (47.4%) underwent subjective assessment alone (Figure). After subjective assessment at 4 months, 23 of 51 patients (45.1%) reported full recovery of olfaction, 27 of 51 patients (52.9%) reported partial recovery, and 1 of 51 patients (2.0%) reported no recovery. On psychophysical testing, 43 of 51 patients (84.3%) were objectively normosmic, including 19 of 27 (70.0%) who self-evaluated as only partially recovered (all patients who self-reported normal return of smell were corroborated with objective testing) (Table). The remaining 8 patients (15.7%) with persistent subjective or objective loss of smell were followed up at 8 months, and an additional 6 patients became normosmic on objective testing. At 8 months, objective olfactory assessment confirmed full recovery in 49 of 51 patients (96.1%). Two patients remained hyposmic at 1 year, with persistent abnormalities (1 with abnormal olfactory threshold and 1 with parosmia causing abnormal identification). Among those who underwent subjective assessment alone, 13 of 46 patients (28.2%) reported satisfactory recovery at 4 months (7 with total and 6 with partial recovery), and the remaining 33 patients (71.7%) did so by 12 months (32 with total and 14 with partial recovery).

For More Information: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2781319

Anosmia and dysgeusia in SARS-CoV-2 infection: incidence and effects on COVID-19 severity and mortality, and the possible pathobiology mechanisms – a systematic review and meta-analysis

Authors: Endang Mutiawati, Conceptualization, Data Curation, Resources, Validation, Writing – Original Draft Preparation, Writing – Review & Editing,a,1,2Marhami Fahriani, Conceptualization, Data Curation, Investigation, Methodology, Validation, Writing – Original Draft Preparation, Writing – Review & Editing,3Sukamto S. Mamada, Data Curation, Investigation, Validation, Writing – Review & Editing,4Jonny Karunia Fajar, Conceptualization, Formal Analysis, Investigation, Methodology, Writing – Review & Editing,3,5Andri Frediansyah, Data Curation, Investigation, Writing – Original Draft Preparation, Writing – Review & Editing,6Helnida Anggun Maliga, Data Curation, Investigation, Validation, Writing – Review & Editing,7Muhammad Ilmawan, Data Curation, Investigation, Validation, Writing – Review & Editing,7Talha Bin Emran, Validation, Writing – Review & Editing,8Youdiil Ophinni, Investigation, Validation, Writing – Review & Editing,9Ichsan Ichsan, Validation, Writing – Review & Editing,3,10Nasrul Musadir, Validation, Writing – Review & Editing,1,2Ali A. Rabaan, Validation, Writing – Review & Editing,11Kuldeep Dhama, Supervision, Validation, Writing – Review & Editing,12Syahrul Syahrul, Supervision, Validation, Writing – Review & Editing,1,2Firzan Nainu, Data Curation, Investigation, Supervision, Validation, Writing – Review & Editing,4 and Harapan aPreparation, Writing – Review & Editing3,10,13

Abstract

Background: The present study aimed to determine the global prevalence of anosmia and dysgeusia in coronavirus disease 2019 (COVID-19) patients and to assess their association with severity and mortality of COVID-19. Moreover, this study aimed to discuss the possible pathobiological mechanisms of anosmia and dysgeusia in COVID-19.

Methods: Available articles from PubMed, Scopus, Web of Science, and preprint databases (MedRxiv, BioRxiv, and Researchsquare) were searched on November 10th, 2020. Data on the characteristics of the study (anosmia, dysgeusia, and COVID-19) were extracted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline. Newcastle–Ottawa scale was used to assess research quality. Moreover, the pooled prevalence of anosmia and dysgeusia were calculated, and the association between anosmia and dysgeusia in presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was assessed using the Z test.

Results: Out of 32,142 COVID-19 patients from 107 studies, anosmia was reported in 12,038 patients with a prevalence of 38.2% (95% CI: 36.5%, 47.2%); whereas, dysgeusia was reported in 11,337 patients out of 30,901 COVID-19 patients from 101 studies, with prevalence of 36.6% (95% CI: 35.2%, 45.2%), worldwide. Furthermore, the prevalence of anosmia was 10.2-fold higher (OR: 10.21; 95% CI: 6.53, 15.96, p < 0.001) and that of dysgeusia was 8.6-fold higher (OR: 8.61; 95% CI: 5.26, 14.11, p < 0.001) in COVID-19 patients compared to those with other respiratory infections or COVID-19 like illness. To date, no study has assessed the association of anosmia and dysgeusia with severity and mortality of COVID-19.

Conclusion: Anosmia and dysgeusia are prevalent in COVID-19 patients compared to those with the other non-COVID-19 respiratory infections. Several possible mechanisms have been hypothesized; however, future studies are warranted to elucidate the definitive mechanisms of anosmia and dysgeusia in COVID-19.

For More Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7993408/

Parosmia post COVID-19: an unpleasant manifestation of long COVID syndrome

As we begin to slowly unravel the mystery hidden behind the current pandemic, novel clinical manifestations are emerging ceaselessly following SARS-CoV-2. Olfactory dysfunction, which has become one of the sought-after clinical features of COVID-19, has been associated with less severe disease manifestation.1 Yet, the previously deemed ‘fortunate’ patients with olfactory dysfunction who successfully recovered from COVID-19 are now being afflicted by another sinister condition known as parosmia, which is found to be more debilitating than loss of smell. Parosmia or distortion of smell is currently regarded as one of the long COVID-19 syndrome or chronic COVID-19 syndrome. Carfi et al found that 87.4% of patients in their study who recovered from COVID-19 had at least one persistent symptom with loss of smell among them.2 However, recent reports have discovered that a number of patients with loss of smell or anosmia regained their smell, yet surprisingly this time, the smell was distorted. The magical aroma of coffee had turned into a nightmare as coffee began to smell pungent like gasoline and favorite dishes were turning to smell more like rotten food or garbage, which inadvertently affects taste as food becomes almost unpalatable. The word parosmia is taken from the Greek words: para and osme (smell) which is defined as a distortion of smell with the presence of odorant, whereas phantosmia is a condition when there is a distortion of smell with the absence of odorant. Anosmia, on the other hand, means complete loss of smell. As of the latest report, three hypotheses exist to explain the pathophysiology of olfactory dysfunction secondary to COVID-19, which include: (1) Mechanical obstruction ensuing the inflammation around the olfactory cleft, which prevents the odorants from binding with the olfactory receptors,3 (2) infection of the ACE-2 expressing supporting cell, mainly the sustentacular cell of the olfactory epithelium4 and (3) direct invasion of olfactory neurons by SARS-CoV-2, which impedes the olfaction transmission.5

For More Information: https://pmj.bmj.com/content/postgradmedj/early/2021/03/31/postgradmedj-2021-139855.full.pdf

Age-dependent appearance of SARS-CoV-2 entry sites in mouse chemosensory systems reflects COVID-19 anosmia-ageusia symptoms

Authors: Julien Brechbühl,Ana Catarina Lopes,Dean Wood,Sofiane Bouteiller,Aurélie de Vallière,Chantal Verdumo, and Marie-Christine Broillet

Abstract

COVID-19 pandemic has given rise to a collective scientific effort to study its viral causing agent SARS-CoV-2. Research is focusing in particular on its infection mechanisms and on the associated-disease symptoms. Interestingly, this environmental pathogen directly affects the human chemosensory systems leading to anosmia and ageusia. Evidence for the presence of the cellular entry sites of the virus, the ACE2/TMPRSS2 proteins, has been reported in non-chemosensory cells in the rodent’s nose and mouth, missing a direct correlation between the symptoms reported in patients and the observed direct viral infection in human sensory cells. Here, mapping the gene and protein expression of ACE2/TMPRSS2 in the mouse olfactory and gustatory cells, we precisely identify the virus target cells to be of basal and sensory origin and reveal the age-dependent appearance of viral entry-sites. Our results propose an alternative interpretation of the human viral-induced sensory symptoms and give investigative perspectives on animal models.

Introduction

The Corona Virus Disease 2019 (COVID-19) has federated worldwide scientific efforts for understanding the viral epidemiological mechanisms of the coronavirus 2 (SARS-CoV-2) that causes this severe acute respiratory syndrome. In humans, the viral syndrome is characterized by an increased mortality rate in aged and/or comorbidity patients associated with the upper respiratory infection symptoms, such as severe respiratory distress13. In addition to its major impact, COVID-19 is associated by its direct alteration of human olfaction and gustation, in absence of substantial nasal inflammation or coryzal signs, resulting to anosmia and ageusia in up to 77% of the patients47. While these sensory symptoms are well established and intensely affect everyday behaviors8,9, the precise related mechanisms remain elusive10.

The target cells of the virus share a molecular signature: the concomitant cellular expression of the angiotensin-converting enzyme 2 (ACE2) and of its facilitating transmembrane serine protease 2 (TMPRSS2), which plays a crucial role for the interaction of viral spike proteins with the host cell1113. Paradoxically, these entry sites seem to be lacking in sensory cells1418, while a direct SARS-CoV-2 contamination has been observed both in humans and rodents19,20, requesting further investigations to explain the sensory-associated symptoms2124. Therefore, the characterization of the animal model is necessary prior to its use to understand the causality underling the viral-induced sensory symptoms.

The use of mice is indeed limited for epidemiological studies due to their absence of hands, which, with aerosols, are the foremost passages of interindividual viral transmission25, as well as their published lack of SARS-CoV-2 ACE2-spike protein affinity26,27. Nevertheless, the ease of production of genetically modified mice and their scientific availability, as well as their well-studied and specialized chemosensory systems2830, make them a valuable ally for the development of potential prophylactic and protective treatments related to these sensory symptoms.

Thus, we aimed here at characterizing the potential viral entry sites across mouse sensory systems. We found SARS-CoV-2 entry cells to be of different origins depending on the sensory systems. In summary, the virus could target cells involved in tissue regulation such as the supporting cells of the olfactory receptor neurons and the regenerative basal cells but also, specifically, the chemosensory cells of both gustatory and olfactory systems. We finally revealed that the emergence of viral entry sites in sensory and basal cells only occurs with age, which could explain both, the observed COVID-19 long-lasting effects and the age-dependent sensory-symptomatology in human.

For More Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8282876/

COVID-19-Associated Bronchiectasis and Its Impact on Prognosis

Authors: Aasir M. SulimanBassel W. BitarAmer A. FarooqiAnam M. ElarabiMohamed R. AboukamarAhmed S. Abdulhadi

Abstract

Coronavirus disease 2019 (COVID-19), which initially emerged in Wuhan, China, has rapidly swept around the world, causing grave morbidity and mortality. It manifests with several symptoms, on a spectrum from asymptomatic to severe illness and death. Many typical imaging features of this disease are described, such as bilateral multi-lobar ground-glass opacities (GGO) or consolidations with a predominantly peripheral distribution. COVID-19-associated bronchiectasis is an atypical finding, and it is not a commonly described sequel of the disease. Here, we present a previously healthy middle-aged man who developed progressive bronchiectasis evident on serial chest CT scans with superimposed bacterial infection following COVID-19 pneumonia. The patient’s complicated hospital course of superimposed bacterial infection in the setting of presumed bronchiectasis secondary to COVID-19 is alleged to have contributed to his prolonged hospital stay, with difficulty in weaning off mechanical ventilation. Clinicians should have high suspicion and awareness of such a debilitating complication, as further follow-up and management might be warranted.

Introduction

Beginning in December 2019, a series of pneumonia cases were reported in Wuhan City, Hubei Province, China. Further investigations revealed that it was a new type of viral pneumonia caused by severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), which was termed coronavirus disease 2019 (COVID-19). Symptoms are variable, nonspecific, and include dry cough, fever, fatigue, myalgia, dyspnea, anosmia, and ageusia [1]. The real-time reverse transcription-polymerase chain reaction (rRT-PCR) test is the current gold standard for confirming infection and is performed using nasal or pharyngeal swab specimens.

Computerized tomography of the thorax (CT thorax), as a routine imaging tool for pneumonia diagnosis, is of great importance in the early detection and treatment of patients affected by COVID-19. Chest CT may detect the early parenchymal abnormalities in the absence of positive rRT-PCR at initial presentation [2]. Since chest CT was introduced as a diagnostic tool for COVID-19 pneumonia, many typical features of this disease were described such as bilateral multi-lobar ground-glass opacification (GGO) with a prevalent peripheral or posterior distribution, mainly in the lower lobes; sometimes, consolidative opacities superimposed on GGOs could be found [3]. To our knowledge, bronchiectasis is not a classical finding in COVID-19 pneumonia, with a paucity of reporting on its development and progression during the disease course.

For More Information: https://www.cureus.com/articles/59350-covid-19-associated-bronchiectasis-and-its-impact-on-prognosis

How COVID-19 Affects the Brain

Authors: Maura Boldrini, MD, PhD1,2Peter D. Canoll, MD, PhD3Robyn S. Klein, MD, PhD4,5,6

COVID-19 has resulted in more than 120 million cases and 2.6 million deaths to date. Respiratory and gastrointestinal symptoms are accompanied by short- and long-term neuropsychiatric symptoms (NPs) and long-term brain sequelae.

Some patients present with anosmia, cognitive and attention deficits (ie, brain fog), new-onset anxiety, depression, psychosis, seizures, and even suicidal behavior.1,2 These present before, during, and after respiratory symptoms and are unrelated to respiratory insufficiency,1 suggesting independent brain damage. Follow-ups conducted in Germany and the United Kingdom found post–COVID-19 NPs in 20% to 70% of patients, even in young adults, and lasting months after respiratory symptoms resolved,1 suggesting brain involvement persists.

Entering through angiotensin-converting enzyme 2 receptors,2 SARS-CoV-2 can damage endothelial cells leading to inflammation, thrombi, and brain damage. Moreover, systemic inflammation leads to decreased monoamines and trophic factors and activation of microglia, resulting in increased glutamate and N-methyl-d-aspartate (NMDA)3 and excitotoxicity (Figure). These insults induce new-onset or re-exacerbation of preexisting NPs.

Brain Vascular Injury, Neurotransmitter System Dysfunction, Thrombotic Events, Neuronal Damage, and Neuropsychiatric Symptoms

A, SARS-CoV-2 invades endothelial cells via transmembrane angiotensin-converting enzyme 2 (ACE2) receptor, enabled by transmembrane protease, serine 2 (TMPRSS2). B, Cytokine elevation and microglia activation result in increased kynurenine, quinolinic acid, and glutamate, and neurotransmitter depletion. C, Coagulation cascade and elevation of von Willebrand factor (vWF) lead to thrombotic events. D, Altered neurotransmission, excitotoxicity by increased glutamate, and hypoxic injury contribute to neuronal dysfunction and loss. E, Neuropsychiatric symptoms differ depending on the Brodmann area involved. IL indicates interleukin; NMDA, N-methyl-d-aspartate; TNF, tumor necrosis factor.

Does the Virus Invade the Brain?

SARS-CoV-2 is known to penetrate the olfactory mucosa, causing loss of smell, and may enter the brain, migrating from the cribriform plate along the olfactory tract2 or through vagal or trigeminal pathways; however, definitive evidence for this is lacking. SARS-CoV-2 could pass the blood-brain barrier (BBB) because inflammatory cytokines induce BBB instability or via monocytes.4 It could reach brain tissue via circumventricular organs (CVOs), midline structures around the third and fourth ventricles, that monitor blood and cerebral spinal fluid content via fenestrated capillaries lacking the junctional proteins expressed in the BBB. Viral RNA was detected by reverse transcription–quantitative real-time polymerase chain reaction but not by in situ hybridization in medulla and cerebellum,2 located next to the area postrema, a CVO that controls emetic responses to toxins. SARS-CoV-2 protein has been found in brain vascular endothelium but not in neurons or glia.2 Thus, detected viral RNA may represent contamination by vasculature in leptomeninges and Virchow-Robin spaces. Histopathologic analysis of whole human brain showed microglial nodules and phagocytosis of neurons (neuronophagia) in brain stem and less frequently in cortex and limbic structures, associated with sparse lymphocytic infiltration, and no correlations between histopathologic findings and levels of viral messenger RNA in the same brain.5 While ageusia, nausea, and vomiting may be related to CVO and brain stem viral invasion, other short-term and long-lasting NPs are more likely due to neuroinflammation and hypoxic injury. Brain stem involvement may explain persistent autonomic abnormalities and anxiety.

For More Information: https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2778090

Neurology and neuropsychiatry of COVID-19: a systematic review and meta-analysis of the early literature reveals frequent CNS manifestations and key emerging narratives

Authors:

  1. Jonathan P Rogers1,2, Cameron J Watson3, et.al

Abstract

There is accumulating evidence of the neurological and neuropsychiatric features of infection with SARS-CoV-2. In this systematic review and meta-analysis, we aimed to describe the characteristics of the early literature and estimate point prevalences for neurological and neuropsychiatric manifestations.

We searched MEDLINE, Embase, PsycINFO and CINAHL up to 18 July 2020 for randomised controlled trials, cohort studies, case-control studies, cross-sectional studies and case series. Studies reporting prevalences of neurological or neuropsychiatric symptoms were synthesised into meta-analyses to estimate pooled prevalence.

13 292 records were screened by at least two authors to identify 215 included studies, of which there were 37 cohort studies, 15 case-control studies, 80 cross-sectional studies and 83 case series from 30 countries. 147 studies were included in the meta-analysis. The symptoms with the highest prevalence were anosmia (43.1% (95% CI 35.2% to 51.3%), n=15 975, 63 studies), weakness (40.0% (95% CI 27.9% to 53.5%), n=221, 3 studies), fatigue (37.8% (95% CI 31.6% to 44.4%), n=21 101, 67 studies), dysgeusia (37.2% (95% CI 29.8% to 45.3%), n=13 686, 52 studies), myalgia (25.1% (95% CI 19.8% to 31.3%), n=66 268, 76 studies), depression (23.0% (95% CI 11.8% to 40.2%), n=43 128, 10 studies), headache (20.7% (95% CI 16.1% to 26.1%), n=64 613, 84 studies), anxiety (15.9% (5.6% to 37.7%), n=42 566, 9 studies) and altered mental status (8.2% (95% CI 4.4% to 14.8%), n=49 326, 19 studies). Heterogeneity for most clinical manifestations was high.

Neurological and neuropsychiatric symptoms of COVID-19 in the pandemic’s early phase are varied and common. The neurological and psychiatric academic communities should develop systems to facilitate high-quality methodologies, including more rapid examination of the longitudinal course of neuropsychiatric complications of newly emerging diseases and their relationship to neuroimaging and inflammatory biomarkers.

This article is made freely available for use in accordance with BMJ’s website terms and conditions for the duration of the covid-19 pandemic or until otherwise determined by BMJ. You may use, download and print the article for any lawful, non-commercial purpose (including text and data mining) provided that all copyright notices and trade marks are retained.

For More Information: https://jnnp.bmj.com/content/92/9/932