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Objectives: Examine the long-term incident neurologic sequelae post COVID recovery and assess relationship with COVID severity using real-world data. Method(s): This retrospective cohort study was conducted using Optum Research Database between 01July2019 to 30Sep2022. Patients included were >=18 years with COVID diagnosis (index date) between 01Jan2020 and 31Oct2020, with continuous enrollment 6 months before and >=12 months after index date, known demographics, not pregnant, and with no baseline neurologic conditions. Patients were stratified into COVID severity cohorts as mild (index diagnosis), moderate (inpatient visit within 15 days of index), or severe (evidence of acute respiratory distress) and followed for a minimum of 12-months post-index. Neurologic sequelae examined were persistent headache, migraine, anosmia, sleep disturbance, cognitive dysfunction, post-traumatic stress disorder, suicidality, anxiety, depression, attention deficit hyperactivity disorder, cerebrovascular disease (CVD), fatigue/myalgia and tremors. Descriptive statistics and incidence rate ratios (IRR) were calculated to assess outcomes. Result(s): Of 534,843 patients, 107,656 (Mild 96,637;Moderate 3,371;Severe 7,648) met the study inclusion criteria. Median follow up time was 750, 774 and 768 days in the mild, moderate and severe cohorts, respectively. About 20% of patients in the mild, 32% in moderate and 35% in the severe cohort experienced >=3 neurologic sequelae during the follow-up period. A significantly higher incidence of any neurologic sequelae was observed in moderate and severe cohorts compared with the mild cohort (IRR 3.1 and 3.0, respectively;p<0.001). Cognitive dysfunction (moderate IRR 5.4, severe IRR 5.7;p<0.001), and CVD (moderate IRR 4.8, severe IRR 4.0;p<0.001) were the most commonly occurring manifestations in moderate and severe cohorts compared with the mild cohort. Conclusion(s): These results highlight the need for long-term monitoring and preventative strategies for neurologic conditions post COVID recovery that might impair quality of life and increase overall healthcare burden in the U.S.Copyright © 2023
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Bell palsy is caused by impaired functioning of the 7th cranial nerve. A disparity in the stable state of the cytokine regulatory axis and a cytokine storm are observed to occur from the binding of the ACE2 to the COVID, and the subsequent functional alterations in the ACE2/AT2R suggest that COVID-19 may use direct or indirect processes to produce neurological symptoms. Increased cases of Bell palsy were reported during the CoV pandemic, so our study aimed to estimate the incidence rate of Bell palsy among COVID-19 patients in South Bangalore, India. Secondary data of patients with Bell palsy were obtained retrospectively from two multispecialty Hospitals in South Bangalore. COVID positive populations were collected between the period of March 2021 and February 2022, and many Bell palsy cases within 3 months of post-Covid period were included. Confirmatory calls were made for patients with Covid Positive who were not diagnosed to discover the occurrence of Bell palsy. A retrospective analysis of Bell palsy cases found 11 incidences between March 2021 and February 2022, when there were 1577 COVID patients in total. According to descriptive statistical analysis, the prevalence of Bell palsy increased by 0.7% during the COVID-19 pandemic. Bell palsy could be considered one of the neurological complications among COVID-19 patients, and appropriate preventative measures should be taken.Copyright © 2023 International Journal of Nutrition, Pharmacology, Neurological Diseases Published by Wolters Kluwer - Medknow.
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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak is a major challenge for clinicians. SARS-CoV-2 infection results in coronavirus disease 2019 (COVID-19), and it is best known for its respiratory symptoms. It can also result in several extrapulmonary manifestations such as neurological complications potentially experienced during the course of COVID-19. The association of dermatomyositis (DM) with COVID-19 pathogenesis has not been well-studied. This study aimed to present a previously healthy 37-year-old man, a soldier by profession, with symptoms of DM on the 4th day from the onset of COVID-19. The patient presented DM symptoms with both skin and muscle manifestations. The patient suffered from cough, fever, and fatigue to begin with, and reverse-transcription polymerase chain reaction (RT-PCR) reported positive for SARS-CoV-2 infection. The laboratory findings showed, intra alia, elevated muscle enzymes CK 8253 U/l (N: <145 U/l), a positive test for myositis-specific autoantibodies (anti-Mi-2), electrodiagnostic tests exhibited features of myopathy, with the presence of muscle and skin symptoms. The patient improved with corticosteroids and immunosuppressive agent therapy. In summary, the association between COVID-19 and the development of multi-system autoimmune disorders such as DM remains unclear. Nevertheless, viral infections such as SARS-CoV-2 may likely serve as a trigger.
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A patient presented with COVID-19-induced enteritis and colitis associated with a high D-dimer. Serotonin released by activated platelets can lead to inflammation and multiorgan failure in COVID-19 infection. Cyproheptadine blocks serotonin receptors. In light of a prior report that showed that cyproheptadine successfully treated neurologic sequelae in COVID-19, we applied this treatment to this patient. Rapid clinical improvement and reduction of D-dimer occurred after 3 doses of cyproheptadine. This inexpensive, well-Tolerated, oral medication may be applicable to treat hyperinflammatory sequelae of COVID-19 infection.Copyright © 2023 American College of Gastroent. All rights reserved.
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Purpose of study COVID-19 primarily affects the respiratory system from flu-like syndrome to acute hypoxic respiratory failure. Neurological manifestations are uncommon and can result in serious complications. We report a unique case of sudden onset of rapidly progressive encephalopathy in the setting of COVID-19. Methods used Reviewed the manifestations, clinical course, and outcome for a patient presenting with altered mental status secondary to COVID-19. Summary of results A 48-year-old with no significant past medical history presented to the emergency department complaining of severe headache for four days. His vital signs on presentation showed a blood pressure of 154/90, pulse of 114 bpm, temperature of 99.6 degreeF, and oxygen saturation of 97% on room air. Physical exam was unremarkable. Lab work showed elevated D-dimer 8,500 ng/L, Elevated ESR:42, LDH:340 and Ferritin:692. White blood count: 7.59 uL, Platelets 50 x 103 uL. Computer tomography angiography (CTA) of the chest showed bilateral multifocal pneumonia. CT Head was performed and was negative for an acute hemorrhage, hydrocephalus or territorial infarcts. Patient spiked a fever shortly after admission 103degreeF. Patient was started on Ceftriaxone and Azithromycin. Blood and urine cultures were positive for Klebsiella pneumonia. Patient was re-evaluated in the morning and was found altered with associated neck stiffness. Antibiotics were switched to cover for suspected meningitis. Neurology was consulted and recommended lumbar puncture. Within a few hours, the patient's mental status deteriorated and was found to be hypertensive with a blood pressure of 220/110. Repeat CT Head was negative. The patient was tested and found to be positive for COVID-19. Patient further decompensated within a few hours and became unresponsive, pulseless. ACLS was performed and the patient was transferred to the intensive care unit. Conclusions This case report highlights the heterogenous presentation in patients with COVID-19 and the importance of recognizing a new onset, severe headache as the only initial presentation. Headaches in some cases may precede the respiratory symptoms or may be the only manifestations in COVID-19 patients and it is crucial to be aware of the neurological complications and the rapid decompensation these patients may undergo if not recognized early.
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A 55-year-old woman was admitted to our hospital because of gait disturbance and urinary retention that acutely emerged 1 week after severe acute respiratory syndrome coronavirus 2 infection. Acute inflammatory myelopathy was clinically suspected, based on bilateral lower-limb weakness with an extensor plantar response and an elevated immunoglobulin G level in the cerebrospinal fluid. Whole-spine magnetic resonance imaging findings were normal. The central conduction time was extended, based on somatosensory evoked potentials. Her lower-limb weakness was partially ameliorated with immunosuppressive therapy. Postinfectious myelopathy is a rare neurological complication of coronavirus disease 2019 and can develop with normal radiological findings.
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Introduction: Articles published in the literature report neurological manifestations or "complications" of SARS-CoV-2 infection and conclude that the different neurological manifestations are relatively similar, but with different frequencies. This study aimed to determine the frequency of neurological manifestations of COVID-19 and to identify which are associated with mortality. Method(s): We performed a retrospective study of all patients diagnosed with SARS-CoV-2 infection by RT-PCR at Hospital 1degree de Octubre, in Mexico, from the beginning of the pandemic to 22 December 2020. A total of 561 patients were identified, 370 of whom presented neurological manifestations. Result(s): The global mortality rate was 37.8% (140/370), increasing to 92.4% among intubated patients (135/146). Of the 370 patients included, approximately 20% of neurological symptoms (headache, neurological impairment, anosmia, ageusia) accounted for 80% of cases of neurological manifestations. Conclusion(s): At our hospital, 80% of the patients with neurological manifestations of COVID-19 presented headache, neurological impairment, ageusia, and/or anosmia. Neurological impairment at admission or before arriving at hospital was identified as a risk factor for mortality.Copyright © 2021 Sociedad Espanola de Neurologia
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Background: Aim: Study of lung damage syndromes and extra-respiratory complications in children with CoV-2 infection. Method(s): The study included 53children with CoV-2 infection and were evaluated clinically to identify the evolutionary consequences of these diseases. Laboratory tests, pulmonary CT, brain CT, EcoCG were performed. Diagnostic tests to confirm CoV-2: RT PCR-test and/or serological tests for IgM, IgG Ab to CoV-2. Result(s): COVID-19 infection was confirmed by RT PCR test in 79.2%(CI51.7%-78.5%) children, and in 20.8%(CI 10.8%-34.1%) cases by IgM and IgG Ab to SARS-CoV- 2 virus. The mean age of the patients -6.03+/- 5.68. Respiratory manifestations at the COVID-19 stage had of 81.5% children (bronchitis -14.8%, pneumonia -62.9%), and the evolutionary stages were detected pulmonary fibrosis (30.5%), atelectasis (30.5%), bronchiectasis (11.11%). COVID-19- associated neurological syndromes were found in 39.6% of children-migraine headache (9.4%), toxic encephalopathy (7.5%), psychotic disorders (3.8%), neurotic anorexia (1.9%), but also severe neurological complications -multifocal leukoencephalitis(5.7%), acute cerebellitis (3.8%), polyradiculoneuropathy (3.8%), epilepsy (1.9%). Signs of cardiovascular damage were reported in 21.2% of cases:bouts of tachycardia (7.7%), toxic heart disease (5.7%). Children with CHDs (7.7%) had severe heart failure in the post-Covid- 19 stages. Conclusion(s): Clinical manifestations in the evolutionary stages of Covid-19 in children are dominated by impaired respiratory system with signs of pulmonary fibrosis, atelectasis, which are often associated with neurological complications and sometimes with cardiovascular signs.
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Introduction We present a case of myelin-oligodendrocyte glycoprotein antibody disease (MOGAD) requiring long-term immunosuppression triggered by a dose of the AstraZeneca COVID-19 vaccination. Relapsing MOGAD is thus far an unknown complication of COVID-19 vaccination. Case Description: A 58-year-old lady developed headache, nausea, dizziness, facial numbness, ataxia and slurred speech 8 days after the COVID-19 AstraZeneca vaccination. Her imaging showed acute disseminated encephalomyelitis (ADEM) with a white matter lesion in the left cerebellum and bilateral smaller lesions. Her cerebrospinal fluid showed 38 white cells and elevated protein. She initially responded well to steroids, however relapsed with optic neuritis 7 months later, requiring long-term immunosuppres- sion with mycophenolate mofetil. Discussion Although there have been some case reports of MOGAD following COVID-19 infection, to our knowledge this is only the second reported case of MOGAD following vaccination against COVID-19, and the first such case to require long-term immunosuppression. The other reported case also occurred following the COVID-19 AstraZeneca vaccine, and also presented with ADEM. This is in contrast to reported cases of MOGAD following COVID-19 infection, where adults mostly presented with optic neuritis. We wanted to highlight the possibility of this vaccine-related neurological complication occurring, particularly in the context of potentially frequent ongoing COVID-19 booster vaccinations.
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Background: Delayed post-hypoxic leukoencephalopathy (DPHL) with associated microbleeds is a clinical entity presenting with cognitive impairment days or weeks after an episode of acute hypoxic brain injury. Case report: We describe a 68-year-old male with SARS-CoV2 infection who had cardiac arrest, required sedation and mechanical ventilation for 17 days, and after sedation was discontinued, he became unresponsive. Brain MRI showed diffuse confluent hyperintense signals in the subcortical white matter and multiple subcortical white matter microhemorrhages. EEG revealed diffuse attenuation of brain electrical activity with isolated polymorphic delta waves in the frontal region without epileptiform activity. Conclusion(s): Clinicians need to be aware that patients with Covid-19 can develop delayed post-hypoxic leukoencephalopathy.Copyright © 2022 The Authors
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Different neurological manifestations of COVID-19 in adults and children and their impact have not been well characterized. We aimed to determine the prevalence of neurological manifestations and in-hospital complications among hospitalized COVID-19 patients and ascertain differences between adults and children. We conducted a prospective multicenter observational study using the International Severe Acute Respiratory and emerging Infection Consortium cohort across 1507 sites worldwide from January/30th/2020 to May/25th/2021. Analyses of neurological manifestations and neurological complications considered unadjusted prevalence estimates for predefined patient subgroups, and adjusted estimates as a function of patient age and time of hospitalization using generalized linear models. Overall, 161,239 patients (158,267 adults; 2,972 children) hospitalized with COVID-19 and assessed for neurological manifestations and complications were included. In adults and children, the most frequent neurological manifestations at admission were fatigue (adults: 37.4%; children: 20.4%), altered consciousness (20.9%; 6.8%), myalgia (16.9%; 7.6%), dysgeusia (7.4%; 1.9%), anosmia (6.0%; 2.2%), and seizure (1.1%; 5.2%). In adults, the most frequent in-hospital neurological complications were stroke (1.5%), seizure (1%), and central nervous system (CNS) infection (0.2%). Each occurred more frequently in ICU than in non-ICU patients. In children, seizure was the only neurological complication to occur more frequently in ICU vs. non-ICU (7.1% vs. 2.3%, P < .001). Stroke prevalence increased with increasing age, while CNS infection and seizure steadily decreased with age. There was a dramatic decrease in stroke over time during the pandemic. Hypertension, chronic neurological disease, and the use of extracorporeal membrane oxygenation were associated with increased risk of stroke. Altered consciousness was associated with CNS infection, seizure, and stroke. All in-hospital neurological complications were associated with increased odds of death. The likelihood of death rose with increasing age, especially after 25 years of age. In conclusion, adults and children have different neurological manifestations and in-hospital complications associated with COVID-19. Stroke risk increased with increasing age, while CNS infection and seizure risk decreased with age.
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Introduction: Anosmia and ageusia were observed as frequent neurological complications of SARS-CoV-2 infections. the aim of the study was to elaborate methods for detection of pathological proteins in nerve endings and to evaluate the frequency and intensity of pathological proteins expression in patients with persistent anosmia. Material(s) and Method(s): the study included 249 patients (181 females and 68 males) aged 47 +/-14 years from NeuroCOViD Polyclinic in Poznan observed from April 2021 untill now. the mucosal biopsy was performed using endoscopy from anterior ethmoid cells. the expression of alpha-synuclein was evaluated using immunofuorescence, and amyloid, tau and tDP43 proteins-using immunohistochemistry. Result(s): Anosmia was observed in 42% of patients and cacosmia-in 6%. Ageusia/dysgeusia was observed in 31% cases. in patients with mild clinical course of COViD19-not hospitalized anosmia (45%) and dys-geusia were more frequent (33%), and cacosmia was observed only in this group. in hospitalized patients anosmia was found in 22% of cases, dysgeusia in 13%, and cacosmia was not observed at all. the expression of alpha-synuclein, amyloid, tau and tDP43 proteins was found in nerve bundles, epithelial cells and in surrounding (nerve endings) of gland cells. Conclusion(s): SARS-CoV-2 infection may induce the expression of pathological proteins in olfactory mucosa of post-COViD patients with anosmia.
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Title: To estimate oxidative stress and DNA damage in Post COVID patients. Background There are a subset of COVID-19 patients who develop sequelae to the disease and oxidative stress is a less studied factor in the development of the sequelae. Aims and Objectives: We have estimated levels of lipid peroxidation (LPO) via malondialdehyde assay kit and DNA damage via alkaline comet assay in hospitalized post-COVID patients symptomatic 4 weeks after testing RT-PCR positive and studied their clinical radiological correlation as a means of estimating the oxidative stress in them. Method(s): It was a single-center, hospital-based comparative case-control pilot study in which 40 post-COVID-19 patients and 40 healthy controls were enrolled. The residual symptoms and baseline clinical and radiological profile of the subjects were also assessed and lipid peroxidation and DNA comet analysis were performed in the blood samples of patients and controls. Result(s): Mean value of LPO was increased (1155.9 +/- 204.82 nmol/ml) in post COVID subjects as compared to controls (715.5 +/- 85.51nmole/ml (P=0.0405). Values were directly proportional to the Severity of COVID (P=0.0317) and X-ray severity score(P=0.009) and were found higher in patients with comorbidities (P=0.0320) and multisystem involvement specifically in those developing a neurological sequela (P=0.0083). Damaged DNA tails and the tailing is directly proportional to DNA damage. The comet parameters measured in our study were Tail length, Tail DNA (%), and Olive tail moment. All these comet parameters were found elevated in Post COVID subjects as compared with healthy controls. Conclusion(s): Oxidative stress and DNA damage, has a role in the development of post-COVID sequelae as seen by high levels of LPO and tail DNA in these subjects.
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Background: The large proportion of coronavirus disease 2019 (COVID-19) patients has been associated with a large number of neu-ropsychiatric manifestations. Despite the high prevalence of COVID-19, few studies have examined such manifestations, especially in children and adolescents. Objective(s): This study investigated neuropsychiatric manifestations in hospitalized children and adolescents admitted for COVID-19 infection in Iran. Method(s): This prospective observational study included admitted children and adolescents (4-18 years old) diagnosed with COVID-19 infection, pediatric neurologists, child and adolescent psychiatrists, and infectious disease specialists, and assessed 375 infected patients during August and December 2021. Result(s): Of the 375 patients, 176 (47%) were female, with a mean age of 9.0 +/- 3.39 years. Psychiatric and neurological manifestations were reported in 58 (15.5%) and 58 (15.5%) patients, respectively. The most prevalent psychiatric disorders were separation anxiety disorder (SAD) (5.1%), major depressive disorder (MDD) (3.5%), generalized anxiety disorder (GAD) (2.7%), insomnia (2.4%), and op-positional defiant disorder (ODD) (2.4%). Regarding neurological complications, seizures were the most prevalent (13.1%), followed by encephalitis (1.9%), transverse myelitis (0.3%), acute ischemic stroke (0.3%), and Guillain-Barre syndrome (0.3%). There was no significant relationship between the duration of COVID-19 infection (P = 0.54) and ICU admission (P = 0.44) with the emergence of psychiatric symptoms. Conclusion(s): The most prevalent neurologic and psychiatric complications among children and adolescents with COVID-19 infection were seizures and the symptoms of anxiety/mood disorders, respectively.Copyright © 2023, Author(s).
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The 2021 Conference on Retroviruses and Opportunistic Infections (CROI) featured a timely review of the neurologic complications of COVID-19 as well as new research findings on mechanisms by which SARS-CoV-2 may affect the brain. CROI included new and important findings about the neurologic complications of HIV-1, human polyomavirus 2 (also known as JC Virus), and cryptococcus. New long-term analyses of cognition in people with HIV-1 identified that cognitive decline over time is associated with multimorbidity, particularly diabetes, chronic lung disease, and vascular disease risk conditions. These conditions are associated with aging, and the question of whether people with HIV are at risk for premature aging was addressed by several reports. New findings from large analyses of resting state networks also provided valuable information on the structural and functional networks that are affected by HIV-1 infection and cognitive impairment. Several reports addressed changes after initiating or switching antiretroviral therapy (ART). Findings that will improve understanding of the biologic mechanisms of brain injury in people with HIV were also presented and included evidence that host (eg, myeloid activation, inflammation, and endothelial activation) and viral (eg, transcriptional activity and compartmentalization) factors adversely affect brain health. Other research focused on adjunctive therapies to treat HIV-1 and its complications in the central nervous system. This summary will review these and other findings in greater detail and identify key gaps and opportunities for researchers and clinicians.Copyright © 2021, IAS-USA. All rights reserved.
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SARS-CoV-2 virus was first identified in 2019 in Wuhan (China) and is responsible for the ongoing COVID-19 pandemic. Although the virus causes mild, transient symptoms of an upper respiratory tract infection in most cases, it can also lead to severe pneumonia, respiratory failure and/or death. Approximately 85% of patients experience central and peripheral neurological symptoms. In the acute phase of the disease, ischaemic strokes, intracranial haemorrhages, meningitis and encephalitis, acute demyelinating diseases and acute inflammatory polyneuropathies may occur. However, mild neurological symptoms that can persist for months and significantly affect daily functioning are much more common. These include headache and dizziness, olfactory and gustatory dysfunction, mild cognitive disturbances, as well as depressive, anxiety, and sleep disorders. Some of them are encompassed by popular terms "post-covid syndrome" and "brain fog." The pathogenesis of neurological complications of SARS-CoV-2 infection is still not fully understood;overproduction of cytokines induced by viral infection may be of great importance. There is no causal treatment, while symptomatic treatment is of limited effectiveness. Primary prevention in the form of SARS-CoV-2 vaccinations is of great importance. In the following review, we would like to present the current knowledge on epidemiology, pathology, pathogenesis and treatment of neurological complications after SARS-CoV-2 infection. Further multi-centre, large-scale clinical studies are necessary to identify the exact pathogenetic mechanismsCopyright © 2022 Sawicka et al.
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The development of long-term symptoms of coronavirus disease 2019 (COVID-19) more than four weeks after primary infection, termed "long COVID" or post-acute sequela of COVID-19 (PASC), can implicate persistent neurological complications in up to one third of patients and present as fatigue, "brain fog", headaches, cognitive impairment, dysautonomia, neuropsychiatric symptoms, anosmia, hypogeusia, and peripheral neuropathy. Pathogenic mechanisms of these symptoms of long COVID remain largely unclear; however, several hypotheses implicate both nervous system and systemic pathogenic mechanisms such as SARS-CoV2 viral persistence and neuroinvasion, abnormal immunological response, autoimmunity, coagulopathies, and endotheliopathy. Outside of the CNS, SARS-CoV-2 can invade the support and stem cells of the olfactory epithelium leading to persistent alterations to olfactory function. SARS-CoV-2 infection may induce abnormalities in innate and adaptive immunity including monocyte expansion, T-cell exhaustion, and prolonged cytokine release, which may cause neuroinflammatory responses and microglia activation, white matter abnormalities, and microvascular changes. Additionally, microvascular clot formation can occlude capillaries and endotheliopathy, due to SARS-CoV-2 protease activity and complement activation, can contribute to hypoxic neuronal injury and blood-brain barrier dysfunction, respectively. Current therapeutics target pathological mechanisms by employing antivirals, decreasing inflammation, and promoting olfactory epithelium regeneration. Thus, from laboratory evidence and clinical trials in the literature, we sought to synthesize the pathophysiological pathways underlying neurological symptoms of long COVID and potential therapeutics.
Subject(s)
COVID-19 , Nervous System Diseases , Humans , COVID-19/complications , SARS-CoV-2 , RNA, Viral , Nervous System Diseases/etiology , Inflammation/complications , Post-Acute COVID-19 SyndromeABSTRACT
Objective: In this study, a systematic review of the literature was performed to study the frequency of neurological symptoms and diseases in adult patients with COVID-19 that may be late consequences of SARS-CoV-2 infection. Methods: Relevant studies were identified through electronic explorations of Scopus, PubMed, and Google Scholar. We followed PRISMA guidelines. Data were collected from studies where the diagnosis of COVID-19 was confirmed and its late neurological consequences occurred at least 4 weeks after initial SARS-CoV-2 infection. Review articles were excluded from the study. Neurological manifestations were stratified based on frequency (above 5, 10, and 20%), where the number of studies and sample size were significant. Results: A total of 497 articles were identified for eligible content. This article provides relevant information from 45 studies involving 9,746 patients. Fatigue, cognitive problems, and smell and taste dysfunctions were the most frequently reported long-term neurological symptoms in patients with COVID-19. Other common neurological issues were paresthesia, headache, and dizziness. Conclusion: On a global scale of patients affected with COVID-19, prolonged neurological problems have become increasingly recognized and concerning. Our review might be an additional source of knowledge about potential long-term neurological impacts.