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Current definitions of migraine that are based mainly on clinical characteristics do not account for other patient's features such as those related to an impaired quality of life, due to loss of social life and productivity, and the differences related to the geographical distribution of the disease and cultural misconceptions which tend to underestimate migraine as a psychosocial rather than neurobiological disorder. Global differences definition, care access, and health equity for headache disorders, especially migraine are reported in this paper from a collaborative group of the editorial board members of the Journal of Headache and Pain. Other components that affect patients with migraine, in addition to the impact promoted by the migraine symptoms such as stigma and social determinants, are also reported. [ABSTRACT FROM AUTHOR]

Headache is one of the most prevalent, although often underreported, symptoms of coronavirus disease 2019 (COVID-19). It is generally accepted that this symptom is a form of secondary headache due to systemic viral infection. There are several hypotheses that try to explain its aetiopathogenesis. One of the most compelling is related to innate immune response to viral infection. This rationale is supported by similarities to other viral infections and the temporal overlap between immunological reactions and headache. Moreover, several key factors in innate immunity have been shown to facilitate headache e.g. interferons, interleukin (IL) -1-β, IL-6, and tumour necrosis factor. There is also a possibility that the virus causes headache by the direct activation of afferents through pattern recognition receptors (i.e. Toll-like receptor 7). Moreover, some data on post-COVID-19 headache and after vaccination against SARS-CoV-2 infection suggests a similar cytokine-mediated pathomechanism in these clinical situations. Future research should look for evidence of causality between particular immune response factors and headache. Identifying key molecules responsible for headache during acute viral infection would be an important step towards managing one of the most prevalent secondary headache disorders. [ABSTRACT FROM AUTHOR]

Background-Wuhan, Hubei's capital, reported severe pneumonia in December 2019. China reported the epidemic to the WHO on December 31, 2019, based on respiratory sample aetiology. SARS CoV-2 caused COVID-19. Confusion, depression, anxiety, memory loss, and insomnia are more common in COVID-19 patients. SARS (severe acute respiratory syndrome) infection has been linked to acute psychiatric symptoms, elevated inflammatory markers, and many neurologic manifestations in critically ill COVID-19 patients with comorbidities. Methods: After Institutional Ethics Committee approval, this prospective study was conducted in the Department of Medicine, MGM Medical College and M.Y.H. and Associated Hospitals, Indore. COVID-positive patients aged 18-80 who consented were included. Severity of covid-19 patients divided into two groups and neuropsychiatric manifestations were observed. Demographics, comorbidities, disease severity, neurological/psychiatric symptoms, and diagnoses were compared. Statistical analysis compared the groups. Results: A total of 300 patients were included in the study. The mean age of the patients was 50.8 ±10.2 years, and their mean BMI was 26.04 5.63 kg/m2. The patients fell into the COVID-19 mild 94 (31.30%) and moderate 206 (68.7%) severity categories. The neurological as well as psychiatric manifestation were seen more in moderately severe cases. Conclusion: Neurological/psychiatric symptoms are common in COVID-19 and can evolve over time. COVID-19's neuropsychiatric and neurological symptoms are expected to increase healthcare costs. Thus, treating these patients urgently requires recognition and familiarity with these neurological/psychiatric conditions. [ABSTRACT FROM AUTHOR]

The ongoing global health crisis due to the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has significantly impacted all aspects of life. While the majority of early research following the coronavirus disease caused by SARS-CoV-2 (COVID-19) has focused on the physiological effects of the virus, a substantial body of subsequent studies has shown that the psychological burden of the infection is also considerable. Patients, even without mental illness history, were at increased susceptibility to developing mental health and sleep disturbances during or after the COVID-19 infection. Viral neurotropism and inflammatory storm damaging the blood-brain barrier have been proposed as possible mechanisms for mental health manifestations, along with stressful psychological factors and indirect consequences such as thrombosis and hypoxia. The virus has been found to infect peripheral olfactory neurons and exploit axonal migration pathways, exhibiting metabolic changes in astrocytes that are detrimental to fueling neurons and building neurotransmitters. Patients with COVID-19 present dysregulated and overactive immune responses, resulting in impaired neuronal function and viability, adversely affecting sleep and emotion regulation. Additionally, several risk factors have been associated with the neuropsychiatric sequelae of the infection, such as female sex, age, preexisting neuropathologies, severity of initial disease and sociological status. This review aimed to provide an overview of mental health symptoms and sleep disturbances developed during COVID-19 and to analyze the underlying mechanisms and risk factors of psychological distress and sleep dysfunction. [ABSTRACT FROM AUTHOR]

Background: Coronaviruses are the important pathogens of humans and animals that can cause diseases ranging from the common cold to more severe or even fatal respiratory infections. Regarding nervous system complications, existing literature has revealed increasing reports of neurological manifestations in coronavirus disease 2019 (COVID-19)-positive patients ranging from mild-to-severe manifestations. Aim: In this study, we aimed to determine the prevalence of neurological manifestations in COVID-19-positive patients. Furthermore, we sought to ascertain the most common and most severe manifestations and to find the significant associations with laboratory or clinical findings. Setting and Design: This is a retrospective cross-sectional observational study that was conducted at two centers. Materials and Methods: Patient data were collected in periods from of March 1 to of July 30, 2020 labeled as the first wave, and from December 1, 2021 to January 30, 2022 labeled as the second wave in two tertiary care hospitals, Al-Noor Specialist Hospital and King Abdullah Medical City, situated in Makkah city, Saudi Arabia. The study included patients who were ≥ 18 years of age and were found to have any neurological manifestations and/or complications secondary to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The study was conducted in different periods to assess the different waves of the COVID-19 pandemic and to allow the comparison between them. Results: From a total number of 4751 patients with confirmed SARS-CoV-2 infection eligible during the periods included in our study, we found neurological manifestations in 263 patients, particularly 229 from the first wave and 34 from the second wave. In the first wave patients, 102 (44.5%) were aged between 18 and 39 years of age. The prevalence of neurological manifestations was 6.4% in the first wave and 2.9% in the second wave. Conclusion: Our study showed a large variety of neurological manifestations in COVID-19-positive patients. The most common neurological manifestations were headache and impaired level of consciousness, whereas the most severe conditions were cerebrovascular events, seizure, encephalopathy, and brain death. [ABSTRACT FROM AUTHOR]

Chemosensory scientists have been skeptical that reports of COVID-19 taste loss are genuine, in part because before COVID-19 taste loss was rare and often confused with smell loss. Therefore, to establish the predicted prevalence rate of taste loss in COVID-19 patients, we conducted a systematic review and meta-analysis of 376 papers published in 2020–2021, with 235 meeting all inclusion criteria. Drawing on previous studies and guided by early meta-analyses, we explored how methodological differences (direct vs. self-report measures) may affect these estimates. We hypothesized that direct measures of taste are at least as sensitive as those obtained by self-report and that the preponderance of evidence confirms taste loss is a symptom of COVID-19. The meta-analysis showed that, among 138,015 COVID-19-positive patients, 36.62% reported taste dysfunction (95% confidence interval: 33.02%–40.39%), and the prevalence estimates were slightly but not significantly higher from studies using direct (n = 15) versus self-report (n = 220) methodologies (Q = 1.73, df = 1, P = 0.1889). Generally, males reported lower rates of taste loss than did females, and taste loss was highest among middle-aged adults. Thus, taste loss is likely a bona fide symptom of COVID-19, meriting further research into the most appropriate direct methods to measure it and its underlying mechanisms. [ABSTRACT FROM AUTHOR]

Headache is among the most frequently reported symptoms after resolution of COVID-19. We assessed structural brain changes using T1- and diffusion-weighted MRI processed data from 167 subjects: 40 patients who recovered from COVID-19 but suffered from persistent headache without prior history of headache (COV), 41 healthy controls, 43 patients with episodic migraine and 43 patients with chronic migraine. To evaluate gray matter and white matter changes, morphometry parameters and diffusion tensor imaging-based measures were employed, respectively. COV patients showed significant lower cortical gray matter volume and cortical thickness than healthy subjects (p < 0.05, false discovery rate corrected) in the inferior frontal and the fusiform cortex. Lower fractional anisotropy and higher radial diffusivity (p < 0.05, family-wise error corrected) were observed in COV patients compared to controls, mainly in the corpus callosum and left hemisphere. COV patients showed higher cortical volume and thickness than migraine patients in the cingulate and frontal gyri, paracentral lobule and superior temporal sulcus, lower volume in subcortical regions and lower curvature in the precuneus and cuneus. Lower diffusion metric values in COV patients compared to migraine were identified prominently in the right hemisphere. COV patients present diverse changes in the white matter and gray matter structure. White matter changes seem to be associated with impairment of fiber bundles. Besides, the gray matter changes and other white matter modifications such as axonal integrity loss seemed subtle and less pronounced than those detected in migraine, showing that persistent headache after COVID-19 resolution could be an intermediate state between normality and migraine. [ABSTRACT FROM AUTHOR]

COVID‐19 caused by SARS‐CoV‐2 infection affects humans not only during the acute phase of the infection, but also several weeks to 2 years after the recovery. SARS‐CoV‐2 infects a variety of cells in the human body, including lung cells, intestinal cells, vascular endothelial cells, olfactory epithelial cells, etc. The damages caused by the infections of these cells and enduring immune response are the basis of long COVID. Notably, the changes in gene expression caused by viral infection can also indirectly contribute to long COVID. We summarized the occurrences of both common and uncommon long COVID, including damages to lung and respiratory system, olfactory and taste deficiency, damages to myocardial, renal, muscle, and enduring inflammation. Moreover, we provided potential treatments for long COVID symptoms manifested in different organs and systems, which were based on the pathogenesis and the associations between symptoms in different organs. Importantly, we compared the differences in symptoms and frequency of long COVID caused by breakthrough infection after vaccination and infection with different variants of concern, in order to provide a comprehensive understanding of the characteristics of long COVID and propose improvement for tackling COVID‐19. [ABSTRACT FROM AUTHOR]

Objective: The COVID‐19 pandemic impacted the care of people with epilepsy (PWE). Several online surveys were conducted but there is limited data regarding the impact on low‐income PWE from lower‐middle income countries (LMICs) who have no access or ability to answer online surveys. The purpose of this interview was to understand the challenges faced by low‐income PWE during the lockdown phase of the pandemic. Method: PWE visiting the epilepsy specialty outpatient department of a tertiary referral government hospital to avail of subsidized services were interviewed. In the interview, they discussed challenges in obtaining medical care, the impact on wellbeing, employment, and vaccination status during the lockdown phase of the pandemic. Results: Out of the 214 PWE interviewed, 20.6% had increased seizure frequency, 28.9% did not have access to medication mainly due to travel restrictions, 30.5% reported lack of availability of medication and 50% were not able to afford the medication mainly due to loss of income. 51% were unable to have follow‐up consultations. 36% reported worsening of mood and some reported impact on other aspects of wellbeing. The impact on wellbeing was significantly associated with an increase in seizure frequency (P <.05). The study revealed hesitation related to vaccines in the majority and expectations of financial support by the government and assistance for procuring medication. There was a lack of awareness about telemedicine services and the same was not adequately offered by government hospitals. Significance: The study underscores the need to learn lessons from the challenging experiences of low‐income PWE and create an action plan for the future to address the issues of lack of affordability of medical care and access to telemedicine. It is critical that the care of the marginalized, underrepresented PWE from lower‐middle income countries is not neglected during a pandemic. [ABSTRACT FROM AUTHOR]

Objectives: As part of the COVID‐19 and Epilepsy (COV‐E) global study, we aimed to understand the impact of COVID‐19 on the medical care and well‐being of people with epilepsy (PWE) in the United States, based on their perspectives and those of their caregivers. Methods: Separate surveys designed for PWE and their caregivers were circulated from April 2020 to July 2021; modifications in March 2021 included a question about COVID‐19 vaccination status. Results: We received 788 responses, 71% from PWE (n = 559) and 29% (n = 229) from caregivers of persons with epilepsy. A third (n = 308) of respondents reported a change in their health or in the health of the person they care for. Twenty‐seven percent (n = 210) reported issues related to worsening mental health. Of respondents taking ASMs (n = 769), 10% (n = 78) reported difficulty taking medications on time, mostly due to stress causing forgetfulness. Less than half of respondents received counseling on mental health and stress. Less than half of the PWE reported having discussions with their healthcare providers about sleep, ASMs, and potential side effects, while a larger proportion of caregivers (81%) reported having had discussions with their healthcare providers on the same topics. More PWE and caregivers reported that COVID‐19‐related measures caused adverse impact on their health in the post‐vaccine period than during the pre‐vaccine period, citing mental health issues as the primary reason. Significance: Our findings indicate that the impact of the COVID‐19 pandemic in the US on PWE is multifaceted. Apart from the increased risk of poor COVID‐19 outcomes, the pandemic has also had negative effects on mental health and self‐management. Healthcare providers must be vigilant for increased emotional distress in PWE during the pandemic and consider the importance of effective counseling to diminish risks related to exacerbated treatment gaps. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic has led to a radical lifestyle change, which may unintendedly change physical activity levels. We aimed to perform a systematic review to investigate the physical activity changes in people with neurological diseases, and to examine the relationship between physical activity and disease symptoms, and psychosocial factors. The review was performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. A systematic search of the literature across five databases (PubMed, CINAHL, Web of Science, SCOPUS, and Cochrane Library) was carried out using the keywords relating to COVID-19, physical activity, sedentary behaviour, exercise, and the name of the neurological diseases. The systematic search was updated on 4 February 2021 with the same keywords. Fourteen studies (n = 7662 persons with neurological diseases, n = 1663 healthy controls) were eligible for this review. The study populations were Parkinson disease (n = 7), dementia (n = 1), multiple sclerosis (n = 1), spinal cord injury (n = 1), hereditary spastic paraplegia (n = 1), neuromuscular diseases (n = 1), Charcot-Marie-Tooth neuropathy (n = 1), and epilepsy (n = 1). Thirteen studies reported a decreased physical activity level, one study reported a high interruption rate of physiotherapy/rehabilitation. Furthermore, the physical activity reduction was associated with worse disease symptoms, depression, perceived health, and mental and physical components of quality of life. The COVID-19 pandemic has a negative impact on the physical activity levels of people with neurological diseases, and this change was related to the worsening of disease symptoms and psychosocial factors. Registration number A protocol of the review was registered with the PROSPERO database (CRD42020207676). [ABSTRACT FROM AUTHOR]

In addition to the typical respiratory manifestations, various disorders including involvement of the nerve system have been detected in COVID-19 ranging from 22 to 36%. Although growing records are focusing on neurological aspects of COVID-19, the pathophysiological mechanisms and related therapeutic methods remain obscure. Considering the increased concerns of SARS-CoV-2 potential for more serious neuroinvasion conditions, the present review attempts to focus on the neuroprotective effects of natural compounds as the principle source of therapeutics inhibiting multiple steps of the SARS-CoV-2 infection cycle. The great majority of the natural products with anti-SARS-CoV-2 activity mainly inhibit the attachment, entry and gene expression rather than the replication, assembly, or release. Although microbial-derived natural products comprise 38.5% of the known natural products with neuroprotective effects following viral infection, the neuroprotective potential of the majority of microorganisms is still undiscovered. Among natural products, chrysin, huperzine A, ginsenoside Rg1, pterostilbene, and terrein have shown potent in vitro neuroprotective activity and can be promising for new or repurpose drugs for neurological complications of SARS-CoV-2. [ABSTRACT FROM AUTHOR]

Objective: This article describes the clinical features, etiology, differential diagnosis, management, and prognosis of new daily persistent headache., Latest Developments: New daily persistent headache has attracted renewed attention as it may arise in the setting of a COVID-19 infection. Spontaneous intracranial hypotension, particularly from CSF-venous fistulas, remains an important secondary headache disorder to consider before diagnosing new daily persistent headache. Symptomatic treatment for new daily persistent headache may include acute and preventive therapies used for migraine and tension-type headache, such as triptans, oral preventive agents, onabotulinumtoxinA, and agents that target calcitonin gene-related peptide., Essential Points: New daily persistent headache is a daily headache syndrome that starts acutely and can only be diagnosed after 3 months have elapsed and other secondary and primary headache diagnoses have been excluded. The clinical manifestations largely resemble either chronic migraine or chronic tension-type headache. The underlying cause is unknown, but it is plausible that multiple etiologies exist and that it is not a single disease entity. The prognosis is variable but often poor, and the treatment approach is largely extrapolated from the management of chronic migraine and chronic tension-type headache., (Copyright © 2024 American Academy of Neurology.)

SARS-CoV-2 is a new coronavirus that has affected the world since 2019. Interstitial pneumonia is the most common clinical presentation, but additional symptoms have been reported, including neurological manifestations. Severe forms of infection, especially in elderly patients, present as an excessive inflammatory response called "cytokine storm", which can lead to acute respiratory distress syndrome (ARDS), multiorgan failure and death. Little is known about the relationship between symptoms and clinical outcomes or the characteristics of virus–host interactions. The aim of this narrative review is to highlight possible links between neurological involvement and respiratory damage mediated by pathological inflammatory pathways in SARS-CoV-2 infection. We will focus on neuro–immune interactions and age-related immunity decline and discuss some pathological mechanisms that contribute to negative outcomes in COVID-19 patients. Furthermore, we will describe available therapeutic strategies and their effects on COVID-19 neurological symptoms. [ABSTRACT FROM AUTHOR]

After healing from COVID-19, patients often experience a slew of symptoms known as post COVID-19 sequelae. Despite the fact that the SARS-CoV-2 pandemic is still ongoing, post-Covid-19 syndrome is already a difficult problem to address: long-term multiorgan sequelae, while frequently described, have yet to be systematized. As a result, post-Covid-19 syndrome can have a major influence on surviving patients' working capacity as well as their personal lives. The clinical spectrum and long-term course of this clinical entity must be better understood. Post-Covid syndrome affects a wide spectrum of individuals (16–87%), with pneumological and cognitive symptoms being the most common. Pulmonary fibrosis was the most common organic consequence seen in post-Covid patients. In conclusion, post-Covid-19 syndrome can have a major impact on the health of survivors. Working-age patients should seek rehabilitation and follow-up in interdisciplinary rehabilitation programmes. Given the pandemic's global extent, it's obvious that COVID-19-related healthcare demands will continue to climb for the foreseeable future. For COVID-19 survivors' long-term mental and physical health, present outpatient infrastructure will be utilised, scalable healthcare models will be built, and cross-disciplinary collaboration will be required. [ABSTRACT FROM AUTHOR]

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Background: Headache is one of the most frequently reported symptoms in post-COVID patients. The clinical phenotype of COVID-19 headache combines phenotypic features of both tension-type headache (TTH) and migraine. We aimed to assess the effectiveness, side effects and predictors of amitriptyline (AMT) response in a real-world study setting. Methods: We performed an observational multicentric study with a retrospective cohort. All consecutive patients with confirmed COVID-19 infection who received AMT for post-COVID headache from March 2020 to May 2021 were included. Response was evaluated by the reduction in the number of headache days per month (HDM) between weeks 8 and 12, compared with the baseline. We explored which variables were associated with a higher probability of response to AMT. Results: Forty-eight patients were eligible for the study, 40/48 (83.3%) females, aged 46.85 (SD: 13.59) years. Patients had history of migraine 15/48 (31.3%) or TTH 5/48 (10.4%). The mean reduction of HDM was 9.6 (SD: 10.9; 95% CI 6.5, 12.7) days. Only 2/48 (5%) of patients discontinued AMT due to poor tolerability. History of TTH (10.9, 95% CI 1.3, 20.6) and nausea (− 8.5, 95% CI − 14.6, − 2.5) were associated with AMT response. Conclusions: This study provides real-world evidence of the potential benefit of AMT in patients with post-COVID-19 headache, especially in patients with history of TTH and without concomitant nausea. [ABSTRACT FROM AUTHOR]

Background: COVID-19 is known to be associated to potentially fatal neurological complications; therefore, it is essential to understand the risk factors for its development and the impact they have on the outcome of COVID-19 patients. Aims: To determine the risk factors for developing fatal neurological complications and their outcome in hospitalized COVID-19 patients. Material and methods: Case control study based on hospitalized patients was conducted from July 15th 2021 to December 15th 2021. Cases and controls were COVID-19 confirmed patients with and without severe neurological manifestations. Age, comorbid conditions, vaccination status, Blood Sugar Random (BSR), D-dimers levels, anticoagulation type and dosage were taken as predictors (exposure variables) for developing neurological complications. In the case-only (subgroup) analysis, 28-day mortality were analyzed using the same predictors including admission hypoxemia. Chi square test and regression model were built to calculate OR with 95%CI. Results: Among 383 patients (median age, 56 years [IQR, 24–110]; 49.9% men); 95 had neurological complications (cases) and 288 did not (controls). Development of neurological complications among COVID-19 related hospitalizations was significantly associated with old age >71 yrs. (cases, 23.2%; controls, 13.5%; OR, 3.31; 95% CI, 1.28–8.55), presence of diabetes mellitus (37.9% vs. 24%; OR, 1.9; 95% CI, 1.2–3.1), admission hyperglycemia (BSR 351–600 mg/dl), (29.5% vs. 7.6%; OR, 3.11; 95%CI, 1.54–6.33), raised D-dimer levels 5000–10,000 ng/ml (41% vs. 11.8%; OR, 5.2; 95% CI, 3.02–8.9), prophylactic dose anticoagulation (43.2% vs. 28.1%; OR, 1.9; 95%CI, 1.2–3.1), and unvaccinated status of COVID-19 patients (90.5% vs. 75.6%; OR, 3.01; 95% CI, 1.44–6.25). Neurological complications with COVID-19 were associated with increased likelihood of death or invasive mechanical ventilation by day 28 (86.3% vs. 45.1%; OR, 7.66; 95% CI, 4.08–14.4). In case-only analysis (median age, 56 years [IQR, 27,110]; 50.5% women), 67 (70.5%) had CVE, 21 (22.1%) had Encephalitis, and 7 (7.4%) had GBS as neurological manifestations. 28-day mortality among these patients was strongly associated with a lower likelihood of vaccination. (6.1% cases vs. 30.8% controls; OR,.146; 95%CI,.033-.64), being younger 17–45 yrs. (12.2% vs. 46.2%; OR,.162; 95%CI,.045-.58), having no comorbid condition (19.5% vs. 61.5%; OR,.151; 95%CI,.044-.525), having cerebrovascular events and GBS as type of neurological manifestation (76.8% vs.30.8%; OR, 7.46; 95%CI, 2.06–26.96), (2.4% vs. 38.4%; OR,.04; 95%CI,.007- 0.24) respectively, and presence of hypoxemia at admission (91.5% vs. 15.4%; OR, 58.92; 95%CI, 10.83–320.67). Conclusion: Old age, presence of Diabetes Mellitus, unvaccinated status of patients, high BSR at admission, high D-dimers, and prophylactic dose anticoagulation were identifies as increased risk factors for developing serious neurological complications among COVID-19 patients. Neurological problems in COVID-19 patients raised death risk 7.6-fold. The most common neurological complication was cerebrovascular events, followed by encephalitis and GBS. Unvaccinated status, cerebrovascular events, and admission hypoxemia are associated with an increased likelihood of 28-day mortality among these patients. [ABSTRACT FROM AUTHOR]

Objective: The impact of the coronavirus disease 2019 (COVID‐19) pandemic on epilepsy care across Japan was investigated by conducting a multicenter retrospective cohort study. Methods: This study included monthly data on the frequency of (1) visits by outpatients with epilepsy, (2) outpatient electroencephalography (EEG) studies, (3) telemedicine for epilepsy, (4) admissions for epilepsy, (5) EEG monitoring, and (6) epilepsy surgery in epilepsy centers and clinics across Japan between January 2019 and December 2020. We defined the primary outcome as epilepsy center‐specific monthly data divided by the 12‐month average in 2019 for each facility. We determined whether the COVID‐19 pandemic‐related factors (such as year [2019 or 2020], COVID‐19 cases in each prefecture in the previous month, and a state of emergency) were independently associated with these outcomes. Results: In 2020, the frequency of outpatient EEG studies (−10.7%, P <.001) and cases with telemedicine (+2608%, P =.031) were affected. The number of COVID‐19 cases was an independent associated factor for epilepsy admission (−3.75 × 10−3% per case, P <.001) and EEG monitoring (−3.81 × 10−3% per case, P =.004). Furthermore, a state of emergency was an independent factor associated with outpatient with epilepsy (−11.9%, P <.001), outpatient EEG (−32.3%, P <.001), telemedicine for epilepsy (+12,915%, P <.001), epilepsy admissions (−35.3%; P <.001), EEG monitoring (−24.7%: P <.001), and epilepsy surgery (−50.3%, P <.001). Significance: We demonstrated the significant impact that the COVID‐19 pandemic had on epilepsy care. These results support those of previous studies and clarify the effect size of each pandemic‐related factor on epilepsy care. [ABSTRACT FROM AUTHOR]

Introduction: The emergence of the global COVID-19 pandemic caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2) has created a substantial burden on healthcare systems worldwide resulting in over 4 million deaths. The systemic impacts of COVID-19 infection are severe and broad in their implications, and the cardiovascular system is no exception. The SARS-CoV-2 binds the angiotensin-converting enzyme-2 (ACE2) receptor to infect host cells, with ACE2 representing a critical regulator of blood pressure homeostasis and proper cardiovascular functioning. Discussion: Patients with a history of cardiovascular disease are at an increased risk for hospitalization and mortality, and COVID-19 infection has now been demonstrated to initiate acute, but serious, episodes of cardiovascular events such as stroke or myocardial infarction (MI). As cases continue to rise around the world, understanding the interplay between COVID-19 infection and the cardiovascular system will be important for healthcare systems to adequately respond to the pandemic and prepare for future challenges. Conclusion: Evidence suggests that COVID-19 infection can spur the onset of various cardiovascular pathologies, including thrombosis, stroke, arrhythmia, and MI, and these complications contribute to poorer patient outcomes. Patients presenting with symptoms of cardiovascular disease may also be foregoing medical treatment out of fear that is brought on by the pandemic or due to strain on healthcare systems preventing access to care. The direct physiological and indirect social consequences of COVID-19 will undoubtedly lead to further challenges for healthcare systems now and in the future. Relevance: This paper discusses the deleterious cardiovascular consequences induced by the global COVID-19 pandemic. [ABSTRACT FROM AUTHOR]

Infection of the CNS with the SARS-CoV-2 can occur via different routes and results in para- or post-infectious manifestations with a variety of neurological symptoms. In patients with neurodegenerative diseases, SARS-CoV-2 is often associated with a higher fatality rate, which is a relevant problem in increasingly older populations. Apart from the direct consequences of an infection in patients with neurodegenerative diseases, indirect consequences of the pandemic such as limited access to care facilities and treatment have negative effects on the course of these chronic disorders. The occurrence of long-lasting neurological symptoms after infection with SARS-CoV-2 indicates a prolonged impact on the CNS. However, while it is known that SARS-CoV-2 affects neuronal populations that are relevant in the pathogenesis of neurodegenerative diseases, it is yet unclear whether an infection with SARS-CoV-2 is sufficient to trigger neurodegeneration. Reflecting on the impact of SARS-CoV-2 on neurodegeneration, we provide a concise overview on the current knowledge of SARS-CoV-2-induced pathology in the CNS and discuss yet open questions in the field. [ABSTRACT FROM AUTHOR]

Introduction: Coronavirus Disease-19 (COVID-19) is an ongoing pandemic caused by highly contagious virus severe acute respiratory syndrome coronavirus-2 (SARS-COV-2) that has infected millions of people across the world. Most of the countries have seen two wave patterns of the pandemic. The second wave is potentially more challenging due to high influx of cases, differing properties of the emerging mutants, and other dynamics of the evolving pandemic. Neurological manifestations are common among COVID-19 positive patients. In this context, the present study attempts to compare the neurological manifestation in the first and second waves of COVID-19. Methodology: A single-center retrospective observational study was undertaken to compare neurological manifestations in the first and second waves of COVID-19. A sample of 1500 patients in the second wave admitted with COVID-19 were included in this study and the findings were compared with 1700 patients in the first wave (data derived from a former study in the same center). A detailed questionnaire addressing co-morbidities, admission details, and clinical features was employed to collect data from the hospital records. Results: Out of 1500 COVID-19 patients in the second wave of COVID-19, 355 (23.7%) of them had one or more neurological manifestations during their in-patient stay. The most common neurological symptom in the 2nd wave of COVID-19 was headache reported in 216 (14.4%) of patients followed by fatigue in 130 (8.7%), myalgia in 120 (8.0%), smell and taste disorders (STD) in 90 (6.0%), altered sensorium in 40 (2.7%), dizziness in 24 (1.6%), seizures in 34 (2.3%), encephalopathy in 26 (1.7%), strokes in 13 (0.9%), etc., Compared to the first wave of COVID-19, dizziness (P < 0.001), myalgia (P = 0.001), headache (P < 0.001) and meningoencephalitis (P = 0.01) were more common while cerebrovascular syndromes (P = 0.001) were less common in the second wave. The mortality in the 2nd wave neurological subgroup was higher [66 (18.6%)] than 1st wave neurological subgroup [23 (10%)]. Conclusion: Meningoencephalitis, headache, and seizures were found to be more common in second wave as compared to first wave. The severity and mortality rate were higher in the second wave. [ABSTRACT FROM AUTHOR]

Introduction: Coronavirus disease 2019 (COVID-19), the disease linked to severe acute respiratory syndrome coronavirus-2, is a widespread infectious disease. Coronaviruses cause multiple systemic infections, but neurological involvement has been reported very rarely. Materials and Methods: The present study is a single-centre prospective study conducted during the COVID-19 pandemic from November 2020 to April 2021, at Mogamedicity Superspeciality Hospital, Punjab, India. All COVID-19 patients with de novo neurologic manifestations were eligible to take part in the study. A total of 810 confirmed COVID-19 patients were enrolled for the study. Demographic features and initial clinical manifestations were noted, and patients were followed up during the hospital stay for the development of any new neurological signs and symptoms. For analytical purposes, neurological presentations were grouped into the central nervous system, peripheral nervous system and musculoskeletal system manifestations. Appropriate laboratory testing was employed as required on a case-to-case basis. Results: In this study, the mean age of the patients was 46.6 ± 15.5 years. Five hundred and fifty two (66.9%) patients were male, while 268 (33.1%) were female. Neurological illness was a primary manifestation in 48 (6%) cases. These included encephalopathy (n = 30), ischaemic stroke (n = 4), Guillain–Barre syndrome, (n = 2), facial nerve palsy (n = 4) and encephalitis (n = 1). The most common neurological symptoms were headache (284 [35%]) and hyposmia (78 [9.6%]), followed by encephalopathy (68 [8.3%]). More serious complications such as seizures (14 [0.7%]) and stroke (18 [2.2%]) were also seen. Conclusion: COVID-19 can present with a neurological illness, and we should remain vigilant to the possibility of neurological presentation of COVID-19 that can be thrombo-embolic, inflammatory or immune-mediated. [ABSTRACT FROM AUTHOR]

Seizures have been increasingly identified as a neurologic manifestation of coronavirus disease 2019 (COVID-19) infection. They may be symptomatic due to systemic infections, as a result of direct central nervous system (CNS) invasion, or occur in response to inflammatory reactions to the virus. It is possible that proinflammatory molecules released in response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to hyperexcitability and epileptogenesis, similar to infections caused by other neurotrophic viruses. Cerebral spinal fluid (CSF) in patients with COVID-19 and seizures is negative for SARS-CoV-2 (PCR) in the majority of patients, but has been found to be positive for proinflammatory molecules like IL-6, IL-8, and anti-neuronal autoantibodies. Electroencephalogram (EEG) in COVID-19 patients are nonspecific. However, in the encephalopathic and critically ill subpopulation, EEG is essential in detecting nonconvulsive seizures and status epilepticus which is associated with increased overall mortality in COVID-19 patients. Thus, as encephalopathy is often the only CNS symptom evidenced in patients with nonconvulsive seizures, more judicious use of continuous EEG in encephalopathic COVID-19 patients should be considered. This would facilitate earlier detection and treatment of seizures in this population, which would ultimately improve outcomes. Further research into the onset and potential for development of seizures and epilepsy in patients with COVID-19 is needed. [ABSTRACT FROM AUTHOR]

Background: The burden of post-coronavirus disease (COVID)-19 symptoms has been increasing and is of great concern in patients with pre-existing chronic medical conditions.This study aimed to delineate the post-COVID-19 neuropsychiatric symptoms among migraine patients compared to the non-migraine control group. Methods: Two groups, each of 204 COVID-19 survivors, were enrolled in the study after 3 months of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, one group fulfilling the episodic migraine criteria and the other serving as a matching control group. Subjects were evaluated through an in-person interview for post-COVID-19 neuropsychiatric symptoms, including detailed headache patterns and severity, using the visual analogue scale. Results: The Frequency of headache during the acute phase of COVID-19 was more frequent in migraine patients (OR = 1.60, 95%CI = 1.04–2.45, P-value = 0.031). The reported significant post-COVID-19 neuropsychiatric symptoms in migraine patients compared to controls were fatigue (OR = 1.662, 95%CI = 1.064–2.596, P-value = 0.025), anosmia/hyposmia (OR = 2.06, 95%CI = 1.164- 3.645, P-value = 0.012), cacosmia (OR = 2.663, 95%CI = 1.145–6.195, P-value = 0.019), depression (OR = 2.259, 95%CI = 1.284- 3.975, P-value = 0.004), anxiety (OR = 3.267, 95%CI = 1.747- 6.108, P-value ≤ 0.001), insomnia (OR = 2.203, 95%CI = 1.298- 3.739, P-value = 0.003), and headache (OR = 3.148, 95%CI = 1.616–6.136, P-value = ≤ 0.001).While there was no statistically significant difference between migraine patients and controls regarding the post-COVID-19 functional status score (P-value = 0.102). The pattern of post-COVID-19 headache was reported as chronic headache transformation in 17.6% of the migraine group, with the median intensity rate being 5.5 and IQR (3–7). In the control group, 14% experienced chronic headache attributed to systemic viral infection with a median intensity rate of 2 and IQR (2–5), while 12% experienced a new daily persistent headache with a median intensity of 5 and IQR (1–6). Conclusion: The study highlighted the importance of follow-up migraine patients upon recovery from COVID-19 infection, being more vulnerable to post-COVID-19 symptoms. [ABSTRACT FROM AUTHOR]

Guillain-Barré syndrome (GBS) has been reported as one of the neurological manifestations linked to COVID-19, a severe acute respiratory syndrome caused by coronavirus 2. We present the case of a 72-year-old male patient attending a tertiary care hospital in Muscat, Oman, in 2020 with a history of progressive bilateral limb weakness and numbness. The current diagnosis was in line with a rare complication of COVID-19. After exclusion of other possible causes, a diagnosis of GBS induced by COVID-19 was made. The patient received 0.4g/kg of intravenous immunoglobulin (IVIG) per day for five days. This case report highlights the characteristics and course of GBS following COVID-19 infection. Further studies are needed to characterize the manifestations and course of various neuromuscular disorders in relation to COVID-19 infection. [ABSTRACT FROM AUTHOR]

Introduction: Evidence is emerging about an extra-pulmonary involvement of SARS-CoV-2, including the nervous system. Autonomic dysfunction in patients recovering from acute coronavirus disease 2019 (COVID-19) has been recently described. Dysautonomic symptoms have been reported in the acute phase of the disease, but clear evidence is lacking, especially in the non-critical forms of the infection. Objective: The aim of this study is to assess the prevalence of dysautonomia in acute, non-critically ill COVID-19 patients. Methods: In this observational, cross-sectional study, we compared 38 non-critically ill patients with acute COVID-19 (COVID + group) to 38 healthy volunteers (COVID − group) in order to assess the prevalence of signs and symptoms of dysautonomia through the administration of the composite autonomic symptom score 31 (COMPASS-31) and an active standing test. Comparisons between groups were performed by means of both univariate and multivariate analyses. Results: The prevalence of orthostatic hypotension was significantly higher in the COVID + group. Higher total scores of COMPASS-31 were observed in the COVID + group than controls. Significant differences between groups emerged in the secretomotor, orthostatic intolerance, and gastrointestinal COMPASS-31 domains. All these results maintained the statistical significance after the adjustment for concomitant drugs with a known effect on the autonomic nervous system assumed by the study participants, except for the differences in the gastrointestinal domain of COMPASS-31. Conclusion: Our results suggest that an autonomic dysfunction could be an early manifestation of COVID-19, even in the contest of mild forms of the infection. [ABSTRACT FROM AUTHOR]

The overall rate of ACVE was 7.951% ( I n i = 164/2050, 95% CI 7.602-8.299) for patients with severe COVID-19 and 2.69% ( I n i = 265/9836, 95% CI 2.136-3.251) for those with nonsevere COVID-19. Laboratory-confirmed COVID-19 From the 4769 patients with laboratory-confirmed COVID-19, 143 patients developed ACVE (2.998%, 95% CI 2.739-3.257). Keywords: COVID-19; hemorrhagic stroke; ischemic stroke; sinus venous thrombosis; stroke; transitory ischemic attack EN COVID-19 hemorrhagic stroke ischemic stroke sinus venous thrombosis stroke transitory ischemic attack 631 639 9 08/09/22 20220801 NES 220801 Introduction Since the beginning of the pandemic, patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have presented diverse neurological manifestations, being acute cerebrovascular events (ACVE) among the most important because of their related mortality and impairment of the quality of life ([4]; [15]; [17]; [18]; [23]). However, we decided to make a subanalysis of the studies that evaluated only patients with laboratory-confirmed COVID-19 and of the studies that analyzed the cohort of patients with COVID-19 and other neurological manifestations. [Extracted from the article]

Medication overuse headache (MOH), new daily persistent headache (NDPH), and persistent refractory headache attributed to severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection represent a significant burden in terms of disability and quality of life, and a challenge in terms of definition, pathophysiology, and treatment. Regarding MOH, prevention without withdrawal is not inferior to prevention with withdrawal. Preventive medications like topiramate, onabotulinumtoxinA, and calcitonin gene-related peptide (CGRP) monoclonal antibodies improve chronic migraine with MOH regardless of withdrawal. The differential diagnosis of NDPH is broad and should be carefully examined. There are no guidelines for the treatment of NDPH, but options include a short course of steroids, nerve blocks, topiramate, nortriptyline, gabapentin, CGRP monoclonal antibodies, and onabotulinumtoxinA. The persistence of headache 3 months after SARS-CoV2 infection is a predictor of poor prognosis. [ABSTRACT FROM AUTHOR]

Headache is one of the most common diagnoses in neurology. A thorough understanding of the clinical presentation of secondary headache, which can be life-threatening, is critical. This review provides an overview of the diagnostic approach to a patient with headache, including discussion of "red," "orange," and "green" flags. We emphasize particular scenarios to help tailor the clinical workup to individual circumstances such as in pregnant women, when particular attention must be paid to the effects of blood pressure and hypercoagulability, as well as in older adults, where there is a need for higher suspicion for an intracranial mass lesion or giant cell arteritis. Patients with risk factors for headache secondary to alterations in intracranial pressure, whether elevated (e.g., idiopathic intracranial hypertension) or decreased (e.g., cerebrospinal fluid leak), may require more specific diagnostic testing and treatment. Finally, headache in patients with COVID-19 or long COVID-19 is increasingly recognized and may have multiple etiologies. [ABSTRACT FROM AUTHOR]

Headache is among the most frequent symptoms persisting or newly developing after coronavirus disease 2019 (COVID-19) as part of the so-called long COVID syndrome. The knowledge on long COVID headache is still limited, however growing evidence is defining the features of this novel condition, in particular regarding clinical characteristics, some pathophysiological mechanisms and first treatment recommendations. Long COVID headache can present in the form of worsening of a preexisting primary headache, or, more specifically, in the form of a new (intermittent or daily) headache starting during the acute infection or after a delay. It often presents together with other long COVID symptoms, most frequently with hyposmia. It can manifest with a migrainous or, more frequently, with a tension-type-like phenotype. Persistent activation of the immune system and trigeminovascular activation are thought to play a role. As there are virtually no treatment studies, treatment currently is largely guided by the existing guidelines for primary headaches with the corresponding phenotype. The present report, a collaborative work of the international group of the Junior Editorial Board of The Journal of Headache and Pain aims to summarize the most recent evidence about long COVID headache and suggests approaches to the diagnosis and treatment of this disorder. [ABSTRACT FROM AUTHOR]

Background: Nearly 55 percent of patients are said to be affected by the neurological effects of COVID-19. COVID-19 was shown to be related with stroke in 0.9 to 5% of people. It's critical to assess the impact of COVID-19 on the outcomes of acute ischemic stroke. The goal of this study was to look at the outcomes and characteristics of patients who had an acute ischemic stroke due to covid-19 infection. Results: The participants in this study were 399 people who had had a stroke. COVID-19 positivity was confirmed in 77 cases, while COVID-19 negativity was confirmed in 322. In the COVID-19 and control groups, the average age of the patients was 65.4 ± 10.2 and 65.3 ± 11.8, respectively. The Covid-19 and control groups had a mean stroke onset of 5.2 ± 2.1 and 5.7 ± 3.8 h, respectively (P = 0.12). There was a high in-hospital mortality rate among patients with COVID-19 with a rate of 11.7% compared to 4.04% among the control group (P = 0.02). At discharge, the number of patients with mRS > 2 was higher (P = 0.001) among the COVID-19. There was a correlation between the mean levels of D-Dimer (r = 0.668, P < 0.001), the severity of COVID-19 (r = 0.802, P < 0.001), and mRS > 2. Conclusion: Despite receiving equal acute care as non-COVID-19 patients, COVID-19 patients had more severe strokes and had worse outcomes. This includes a high chance of death while in the hospital as well as a significant level of disability. Neurologists should use timely and effective therapies, particularly for patients who are at a higher risk of having a stroke. This includes elderly patients, patients with severe COVID-19, patients with high levels of D-Dimer, and those with high NIHSS. [ABSTRACT FROM AUTHOR]

The novel coronavirus SARS-CoV-2 emerged in late 2019, rapidly reached pandemic status, and has maintained global ubiquity through the emergence of variants of concern. Efforts to develop animal models have mostly fallen short of recapitulating severe disease, diminishing their utility for research focusing on severe disease pathogenesis and life-saving medical countermeasures. We tested whether route of experimental infection substantially changes COVID-19 disease characteristics in two species of nonhuman primates (Macaca mulatta; rhesus macaques; RM, Chlorocebus atheiops; African green monkeys; AGM). Species-specific cohorts were experimentally infected with SARS-CoV-2 by either direct mucosal (intratracheal + intranasal) instillation or small particle aerosol in route-discrete subcohorts. Both species demonstrated analogous viral loads in all compartments by either exposure route although the magnitude and duration of viral loading was marginally greater in AGMs than RMs. Clinical onset was nearly immediate (+1dpi) in the mucosal exposure cohort whereas clinical signs and cytokine responses in aerosol exposure animals began +7dpi. Pathologies conserved in both species and both exposure modalities include pulmonary myeloid cell influx, development of pleuritis, and extended lack of regenerative capacity in the pulmonary compartment. Demonstration of conserved pulmonary pathology regardless of species and exposure route expands our understanding of how SARS-CoV-2 infection may lead to ARDS and/or functional lung damage and demonstrates the near clinical response of the nonhuman primate model for anti-fibrotic therapeutic evaluation studies. Author summary: The advent of COVID-19's quick emergence as a human disease necessitated near immediate development of animal models that would recapitulate the viral syndrome to facilitate study of spread, health effects, and evaluation of medications that could either treat or prevent disease. In this study, we compared the health effects of viral infection in two species of nonhuman primates, using two distinct routes of infection which were aerosol or instillation into the nose and upper lung. The results showed that although not effecting overall response in either species of animal, the route by which the experimental infection was performed effected the movement of infectious virus in the animal's body once infected. These results have implications of what is known about the potential route of transmission of this emerging viral disease. [ABSTRACT FROM AUTHOR]

We aimed to evaluate the admissions to the Pediatric Emergency Department (PED) due to seizures one year before and one year after the first COVID-19 case in Turkey. We divided the admission time into two: The prelockdown period (March 2019-February 2020) and the lockdown period (March 2020 - February 2021). We divided the seizures into six parts: First simple febrile convulsion (FK), first complex FK, recurrent simple FK, recurrent complex FK, first non-febrile seizure, and recurrent non-febrile seizure. We compared the prelockdown and lockdown periods in terms of demographic and clinical characteristics and monthly admission of patients. The total number of patients admitted to PED was 37.323 and 10.191 during the prelockdown and lockdown period, respectively. While seizure-related PED accesses were 918 during the prelockdown period, 508 patients were admitted to PED during the lockdown period. Monthly average admissions decreased in all seizure types during the lockdown period. The ratio of first simple febrile seizures to total seizures decreased from 22.4% (206/918) to 16.3% (83/508), while the ratio of first afebrile seizures to total seizures increased from 29.6% (272/918) to 36.8% (186/508). While the rate of first febrile seizures decreased, we observed a significant increase in the rate of first afebrile seizures. The findings suggested that risk factors such as depression/anxiety or screen exposure may have caused seizures in patients with a predisposition to seizures. [ABSTRACT FROM AUTHOR]

A few cases of parkinsonism linked to COVID-19 infection have been reported so far, raising the possibility of a post-viral parkinsonian syndrome. The objective of this review is to summarize the clinical, biological, and neuroimaging features of published cases describing COVID-19-related parkinsonism and to discuss the possible pathophysiological mechanisms. A comprehensive literature search was performed using NCBI's PubMed database and standardized search terms. Thirteen cases of COVID-19-related parkinsonism were included (7 males; mean age: 51 years ± 14.51, range 31–73). Patients were classified based on the possible mechanisms of post-COVID-19 parkinsonism: extensive inflammation or hypoxic brain injury within the context of encephalopathy (n = 5); unmasking of underlying still non-symptomatic Parkinson's Disease (PD) (n = 5), and structural and functional basal ganglia damage (n = 3). The various clinical scenarios show different outcomes and responses to dopaminergic treatment. Different mechanisms may play a role, including vascular damage, neuroinflammation, SARS-CoV-2 neuroinvasive potential, and the impact of SARS-CoV-2 on α-synuclein. Our results confirm that the appearance of parkinsonism during or immediately after COVID-19 infection represents a very rare event. Future long-term observational studies are needed to evaluate the possible role of SARS-CoV-2 infection as a trigger for the development of PD in the long term. [ABSTRACT FROM AUTHOR]

The presence of neurological symptoms within the clinical range of COVID-19 disease infection has increased. This paper presents the situation of a 45-year-old man having the medical antecedent diabetes mellitus, who presented to the emergency department with fever, headache, and respiratory symptoms, nine days following vaccination with the Ad26.COV2-S COVID-19 vaccine. The patient tested positive for SARS-CoV-2 based on nasal polymerase chain reaction (RT-PCR). Two weeks after the presentation, he developed Tolosa–Hunt Syndrome, an autoimmune phenomenon, with painful left ophthalmoplegia. Significant improvement was seen in terms of his discomfort; however, ptosis and ocular mobility improved only moderately after treatment with intravenous methylprednisolone, and the patient was discharged on a new insulin regimen. The patient returned after four weeks and the neurological exam results showed significant signs of right hemiparesis, mixed aphasia, incomplete left ophthalmoplegia, severe headache, and agitation; after a few days, the patient experienced a depressed level of consciousness and coma. The patient's clinical condition worsened and, unfortunately, he died. MRI brain images revealed multiple ischemic strokes, meningitis, infectious vasculitis, and hemorrhagic encephalitis, which are all serious complications of COVID-19. [ABSTRACT FROM AUTHOR]

Background: Headache can be a prominent feature of Post‐Acute Sequelae of SARS‐Cov2 infection (PASC) and previous studies have centered around PASC headaches that have resolved within a month of infection. Methods: We performed a retrospective chart review of 31 adults evaluated at the Stanford Headache Clinic between September 2020 and January 2022 who developed new or worsening headaches after COVID‐19 infection that were unresolved at time of evaluation for demographics, medical history, and headache diagnosis. Results: Headache had been present for a mean duration of 7.4±4.8 months after infection. Notably, 25/31 (81%) had a previous history of headache. The specific features of the headache varied considerably, but 23/31 (74%) met International Classification of Headache Disorders, Third Edition (ICHD‐3) criteria for migraine, with 20/31 (65%) meeting ICHD‐3 criteria for chronic migraine, while only 5/31 (16%) met these criteria before COVID infection. Additionally, full‐time employment decreased from 25/31 (81%) to 17/31 (55%). Prior to establishing care at our clinic, 13/18 (72%) of the patients who were started on preventive medications currently indicated for migraine management, reported a decrease in frequency and/or severity of headaches. Conclusions: Our study presents a group of patients with protracted headache after COVID‐19 infection that includes both patients with a previously lower headache burden who largely exhibited chronification from episodic to chronic migraine, as well as patients with no previous history of headache who meet ICHD‐3 criteria for headache attributed to a systemic viral illness, mostly with a migrainous phenotype. [ABSTRACT FROM AUTHOR]

Growing evidence demonstrates the association of encephalitis, meningoencephalitis or encephalomyelitis, with SARS-CoV-2 infection. This study aims to determine the profile and possible mechanisms behind CNS inflammatory diseases in the context of Covid-19. We conducted a systematic review of case reports on Covid-19-related encephalitis, meningoencephalitis, acute necrotizing encephalitis, and acute disseminated encephalomyelitis in adults, published before January 2021. A total of 182 cases (encephalitis = 109, meningoencephalitis = 26, acute disseminated encephalomyelitis = 35, acute necrotizing (hemorrhagic) encephalitis = 12) were included. While cerebrospinal fluid (CSF) pleocytosis and increased protein level was present in less than 50%, magnetic resonance imaging (MRI) and electroencephalogram (EEG) were abnormal in 78 and 93.2% of all cases, respectively. Viral particles were detected in cerebrospinal fluid of only 13 patients and autoantibodies were present in seven patients. All patients presented with altered mental status, either in the form of impaired consciousness or psychological/cognitive decline. Seizure, cranial nerve signs, motor, and reflex abnormalities were among associated symptoms. Covid-19-associated encephalitis presents with a distinctive profile requiring thorough diagnosis and thereby a comprehensive knowledge of the disease. The clinical profile of brain inflammation in Covid-19 exhibits majority of abnormal imaging and electroencephalography findings with mild/moderate pleocytosis or proteinorrhachia as prevalent as normal cerebrospinal fluid (CSF). Oligoclonal bands and autoantibody assessments are useful in further evaluating neuro-covid patients, as supported by our pooled evidence. Despite the possibility that direct viral invasion cannot be easily estimated, it is still more likely that immune-mediated or autoimmune reactions play a more important role in SARS-CoV-2 neuroinflammation. [ABSTRACT FROM AUTHOR]

Stroke is a fatal morbidity that needs emergency medical admission and immediate medical attention. COVID-19 ischemic brain damage is closely associated with common neurological symptoms, which are extremely difficult to treat medically, and risk factors. We performed literature research about COVID-19 and ischemia in PubMed, MEDLINE, and Scopus for this current narrative review. We discovered parallel manifestations of SARS-CoV-19 infection and brain ischemia risk factors. In published papers, we discovered a similar but complex pathophysiology of SARS-CoV-2 infection and stroke pathology. A patient with other systemic co-morbidities, such as diabetes, hypertension, or any respiratory disease, has a fatal combination in intensive care management when infected with SARS-CoV-19. Furthermore, due to their shared risk factors, COVID-19 and stroke are a lethal combination for medical management to treat. In this review, we discuss shared pathophysiology, adjuvant risk factors, challenges, and advancements in stroke-associated COVID-19 therapeutics. [ABSTRACT FROM AUTHOR]

COVID-19, which is caused by the SARS-CoV-2, has ravaged the world for the past 2 years. Here, we review the current state of research into the disease with focus on its history, human genetics and genomics and the transition from the pandemic to the endemic phase. We are particularly concerned by the lack of solid information from the initial phases of the pandemic that highlighted the necessity for better preparation to face similar future threats. On the other hand, we are gratified by the progress into human genetic susceptibility investigations and we believe now is the time to explore the transition from the pandemic to the endemic phase. The latter will require worldwide vigilance and cooperation, especially in emerging countries. In the transition to the endemic phase, vaccination rates have lagged and developed countries should assist, as warranted, in bolstering vaccination rates worldwide. We also discuss the current status of vaccines and the outlook for COVID-19. [ABSTRACT FROM AUTHOR]

Objective: To review data regarding the epidemiology, pathophysiology, characteristics, and management of COVID‐19–associated headache. The persistence of headache after the acute phase of COVID‐19 was also reviewed. Background: Headache is a frequent symptom of COVID‐19, and understanding its management is important for health‐care professionals involved in treating the disease. Method: This is a narrative review. A literature review was conducted in the PubMed database with the following terms: "headache" and "COVID‐19." All articles written in English that were considered relevant were included. Results: Half of the patients who have COVID‐19 present with headache, which occurs more frequently in younger patients; in those with previous primary headache or with previous migraine; and in those who have concomitantly presented with anosmia, ageusia, and myalgia. The headache usually begins early in the symptomatic phase, is bilateral, moderate to severe, and has a similar pattern to tension‐type headache. All studies found the migraine pattern and the tension‐type headache pattern to be frequent patterns. The possible pathophysiological mechanisms include direct viral injury, the inflammatory process, hypoxemia, coagulopathy, and endothelial involvement. Common analgesics and nonsteroidal anti‐inflammatory drugs are the most commonly used drugs for headache in the acute phase of COVID‐19. The headache may persist beyond the acute phase, and in such cases, there is an improvement over time. However, not all patients' headaches improve. It seems to be a greater proportion of patients whose headache improves in the first 3 months after the acute phase of the disease than after this period. COVID‐19 may trigger new daily persistent headache. Conclusions: Headache is a clinically significant symptom of COVID‐19. Although its characteristics in the acute phase of the disease are already well known, there is a need for studies on its management and persistence. [ABSTRACT FROM AUTHOR]

Important physiological changes are observed in patients with obesity, such as intestinal permeability, gastric emptying, cardiac output, and hepatic and renal function. These differences can determine variations in the pharmacokinetics of different drugs and can generate different concentrations at the site of action, which can lead to sub therapeutic or toxic concentrations. Understanding the physiological and immunological processes that lead to the clinical manifestations of COVID-19 is essential to correlate obesity as a risk factor for increasing the prevalence, severity, and lethality of the disease. Several drugs have been suggested to control COVID- 19 like Lopinavir, Ritonavir, Ribavirin, Sofosbuvir, Remdesivir, Oseltamivir, Oseltamivir phosphate, Oseltamivir carboxylate, Hydroxychloroquine, Chloroquine, Azithromycin, Teicoplanin, Tocilizumab, Anakinra, Methylprednisolone, Prednisolone, Ciclesonide and Ivermectin. Similarly, these differences between healthy people and obese people can be correlated to mechanical factors, such as insufficient doses of the vaccine for high body mass, impairing the absorption and distribution of the vaccine that will be lower than desired or can be linked to the inflammatory state in obese patients, which can influence the humoral immune response. Additionally, different aspects make the obese population more prone to persistent symptoms of the disease (long COVID), which makes understanding these mechanisms fundamental to addressing the implications of the disease. Thus, this review provides an overview of the relationship between COVID-19 and obesity, considering aspects related to pharmacokinetics, immunosuppression, immunization, and possible implications of long COVID in these individuals., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Introduction: On March 11, 2020, the World Health Organization sounded the COVID-19 pandemic alarm. While efforts in the first few months focused on reducing the mortality of infected patients, there is increasing data on the effects of long-term infection (Post-COVID-19 condition). Among the different symptoms described after acute infection, those derived from autonomic dysfunction are especially frequent and limiting. Objective: To conduct a narrative review synthesizing current evidence of the signs and symptoms of dysautonomia in patients diagnosed with COVID-19, together with a compilation of available treatment guidelines. Results: Autonomic dysfunction associated with SARS-CoV-2 infection occurs at different temporal stages. Some of the proposed pathophysiological mechanisms include direct tissue damage, immune dysregulation, hormonal disturbances, elevated cytokine levels, and persistent low-grade infection. Acute autonomic dysfunction has a direct impact on the mortality risk, given its repercussions on the respiratory, cardiovascular, and neurological systems. Iatrogenic autonomic dysfunction is a side effect caused by the drugs used and/or admission to the intensive care unit. Finally, late dysautonomia occurs in 2.5% of patients with Post-COVID-19 condition. While orthostatic hypotension and neurally-mediated syncope should be considered, postural orthostatic tachycardia syndrome (POTS) appears to be the most common autonomic phenotype among these patients. A review of diagnostic and treatment guidelines focused on each type of dysautonomic condition was done. Conclusion: Symptoms deriving from autonomic dysfunction involvement are common in those affected by COVID-19. These symptoms have a great impact on the quality of life both in the short and medium to long term. A better understanding of the pathophysiological mechanisms of Post-COVID manifestations that affect the autonomic nervous system, and targeted therapeutic management could help reduce the sequelae of COVID-19, especially if we act in the earliest phases of the disease. [ABSTRACT FROM AUTHOR]

Since the first case of Guillain-Barré syndrome (GBS)-associated SARS-CoV-2 (COVID-19) infection reported in 2020, a series of cases have been published in some countries. In this case report, we present a young patient with GBS, whose clinical and laboratory data were appropriate for the diagnosis of GBS due to COVID-19 infection. Neurological examination revealed the muscular weakness of lower limbs with Medical Research Council (MRC) scale of 2/5 associated with diminished reflexes. Laboratory studies showed the positive nasal swab RT-PCR test for COVID-19, leukopenia, increased ferritin and LDH levels, normal electrolyte and liver and kidney function, and normal chest X-ray. The result of cerebrospinal fluid showed the albuminocytologic dissociation. The patient was treated with remdesivir, dexamethasone, anticoagulation, and therapeutic plasma exchange (TPE). Patient's muscle weakness was significantly improved after 1 week of admission. He was discharged at 23rd days of hospitalization and followed-up in the out-patients department. [ABSTRACT FROM AUTHOR]

Evidence suggests that SARS-CoV-2 entry into the central nervous system can result in neurological and/or neurodegenerative diseases. In this review, routes of SARS-Cov-2 entry into the brain via neuroinvasive pathways such as transcribrial, ocular surface or hematogenous system are discussed. It is argued that SARS-Cov-2-induced cytokine storm, neuroinflammation and oxidative stress increase the risk of developing neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Further studies on the effects of SARS-CoV-2 and its variants on protein aggregation, glia or microglia activation, and blood-brain barrier are warranted. [ABSTRACT FROM AUTHOR]