Long COVID syndrome‐associated brain fog

Asadi‐Pooya, Ali A.; Akbari, Ali; Emami, Amir; Lotfi, Mehrzad; Rostamihosseinkhani, Mahtab; Nemati, Hamid; Barzegar, Zohreh; Kabiri, Maryam; Zeraatpisheh, Zahra; Farjoud-Kouhanjani, Mohsen; Jafari, Anahita; Sasannia, Fateme; Ashrafi, Shayan; Nazeri, Masoume; Nasiri, Sara; Shahisavandi, Mina

doi:10.1002/jmv.27404

Cited by 139 publications

(133 citation statements)

References 26 publications

(48 reference statements)

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“…Improvements in t-MoCA scores over time should generate a degree of optimism regarding recovery from long-COVID, particularly since "brain fog", confusion and dysexecutive function appear to be common protracted post-acute sequelae [29][30][31] . While the pathogenesis of post-acute cognitive dysfunction is likely multifactorial, possibilities include post-hypoxic brain injury, blood brain barrier disruption with ongoing inflammation, autoimmune mechanisms or even neurodegenerative disease 32 .…”

Section: Discussionmentioning

confidence: 99%

Trajectories of Neurological Recovery 12 Months after Hospitalization for COVID-19: A Prospective Longitudinal Study

Frontera

Yang

medircherla

et al. 2022

Preprint

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Background/Objectives: Little is known about trajectories of recovery 12-months after hospitalization for severe COVID. Methods: We conducted a prospective, longitudinal cohort study of patients with and without neurological complications during index hospitalization for COVID-19 from March 10, 2020-May 20, 2020. Phone follow-up batteries were performed at 6- and 12-months post-COVID symptom onset. The primary 12-month outcome was the modified Rankin Scale (mRS) comparing patients with or without neurological complications using multivariable ordinal analysis. Secondary outcomes included: activities of daily living (Barthel Index), telephone Montreal Cognitive Assessment (t-MoCA) and Neuro-QoL batteries for anxiety, depression, fatigue and sleep. Changes in outcome scores from 6 to 12-months were compared using non-parametric paired-samples sign test. Results: Twelve-month follow-up was completed in N=242 patients (median age 65, 64% male, 34% intubated during hospitalization) and N=174 completed both 6- and 12-month follow-up. At 12-months 197/227 (87%) had ≥1 abnormal metric: mRS>0 (75%), Barthel<100 (64%), t-MoCA≤18 (50%), high anxiety (7%), depression (4%), fatigue (9%) and poor sleep (10%). 12-month mRS scores did not differ significantly among those with (N=113) or without (N=129) neurological complications during hospitalization after adjusting for age, sex, race, pre-COVID mRS and intubation status (adjusted OR 1.4, 95% CI0.8-2.5), though those with neurological complications had higher fatigue scores (T-score 47 vs 44, P=0.037). Significant improvements in outcome trajectories from 6- to 12-months were observed in t-MoCA scores (56% improved, median difference 1 point, P=0.002), and Neuro-QoL anxiety scores (45% improved, P=0.003). Non-significant improvements occurred in fatigue, sleep and depression scores in 48%, 48% and 38% of patients, respectively. Barthel and mRS scores remained unchanged between 6 and 12-months in >50% of patients. Discussion: At 12-months post-hospitalization for severe COVID, 87% of patients had ongoing abnormalities in functional, cognitive or Neuro-QoL metrics and abnormal cognition persisted in 50% of patients without a prior history of dementia/cognitive abnormality. Only fatigue severity differed significantly between patients with or without neurological complications during index hospitalization. However, significant improvements in cognitive (t-MoCA) and anxiety (Neuro-QoL) scores occurred in 56% and 45% of patients, respectively, between 6- to 12-months. These results may not be generalizable to those with mild/moderate COVID.

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Section: Discussionmentioning

confidence: 99%

Trajectories of Neurological Recovery 12 Months after Hospitalization for COVID-19: A Prospective Longitudinal Study

Frontera

Yang

medircherla

et al. 2022

Preprint

View full text Add to dashboard Cite

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“…Finally, the mechanism associated with the alteration of cognition and induction of “brain fog” is not clear; however, it could be due to the high viral load in patients with COVID-19 that involves the CNS, which causes the compromise of neurons with high-level energy metabolism, causing selective mitochondrial neuronal targeting in SARS-CoV-2 infection, leading to neuroinflammation, rupture of the blood–brain barrier, microvasculitis and hypoxia, which could give rise to the symptoms of brain fog [ 20 , 21 , 22 ]. Therefore, the pathogenesis of these sequelae in COVID-19 survivors is unknown and there are many pending questions to investigate.…”

Section: Discussionmentioning

confidence: 99%

Post-Coronavirus Disease 2019 Triggers the Appearance of Mixed Polyneuropathy and Brain Fog: A Case Report

Suárez-Sánchez

Vega-Cabrera

Fernández-Moya

et al. 2022

Clinics and Practice

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Coronavirus disease 2019 (COVID-19) can directly or indirectly affect the central and peripheral nervous systems, resulting in cognitive impairment, memory problems, and a wide range of neuromuscular involvement, including neuropathies. However, the long-term neurological complications of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection are not clear. The aim this study was to analyze a case report the presence of neurological sequelae due to post-Coronavirus disease 19 in a patient without apparent previous neurological symptoms. Clinical case: A 46-year-old patient, with no relevant history for the described condition, who, after severe COVID-19 infection, started a mixed neuropathy and mental fog syndrome as the main sequel. Multiple laboratory and imaging studies were performed during and after his hospital stay, and it was corroborated by an electromyography that it occurred from a neuropathy triggered by COVID-19 infection. Conclusions: This case provides additional evidence that mixed neuropathy and brain fog syndrome are potential complications of post-coronavirus disease 2019 syndrome. The neurological sequelae that manifest after a COVID-19 episode can be rapidly enhanced as a consequence of another alteration in some systems of the organism. However, future studies are necessary to elucidate the incidence of these neurological complications, their pathophysiological mechanisms and their therapeutic options.

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“…Recent studies have reported the presence of neurological symptoms 4 months after the acute phase; this was also seen in patients who did not required hospitalisation [64]. The term 'brain fog' has been used to describe a nonspecific cognitive disorder reported in 7.2% of patients with post-COVID-19 sequelae and in 81% of patients who specifically reported neurological symptoms that persisted after the acute phase [64,65]. A possible mechanism that could explain the development of brain fog is the presence of a high viral load affecting the central nervous system and, specifically, the neuronal mitochondria in patients with COVID-19 [66].…”

Section: Neurocognitive Alterationsmentioning

confidence: 99%

Post-COVID-19 sequelae

Gramegna¹,

Mantero²,

Amati³

et al. 2021

Covid-19

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Characterisation of the underlying mechanisms of long-term COVID-19 sequelae is still ground for ongoing research; sequelae may result from irreversible organ damage during the acute infection phase, or may reflect the manifestations secondary to a persistent hyperinflammatory state or ongoing viral activity with poor host antibody response. This chapter presents a summary of the evidence available as at October 2021 regarding the different manifestations and severity of post-COVID-19 sequelae in adult patients. Recurrence, relapse and readmission after recoveryRecurrence and relapse of COVID-19Re-infection with SARS-CoV-2 has emerged as a possible outcome after full recovery from COVID-19. Several authors have reported that patients might present with a new positive respiratory sample after previous negative results. TO et al. [7] reported a real case of COVID-19 recurrence; they documented re-infection by a different strain of SARS-CoV-2 with IgG seroconversion. Conversely, KANG et al. [8] analysed 292 re-positive cases from South Korea; patients were asymptomatic or reported minor symptoms and the authors concluded that new positive samples were probably due to previous false-negative laboratory tests or persistent viral shedding rather than real re-infection.A systematic review of published evidence identified 1350 similar cases [9]. The re-positivity occurred mainly in asymptomatic patients; interestingly, only 5.6% of patients were pyrexial mean±SD 34.5±18.7 days after the initial onset of symptoms. Fortunately, the outcome was favourable in the majority of cases (96.7%) and only 2.1% died. GIDARI et al.[9] evaluated a total of nine re-positive patients and inoculated six new positive respiratory samples in Vero-E6 cells showing no growth and negative PCR results. This suggests an absence of live virus in re-positive patients who, therefore, should be considered not contagious. The authors hypothesised that this phenomenon was due to prolonged RNA persistence in the upper respiratory tract [9]. A meta-analysis of potential COVID-19 recurrence included >30,000 publications and analysed patient data for age, sex, time of re-occurrence or relapse of symptoms, and a persistent SARS-CoV-2 PCR test [10]. Relapse occurred after a mean±SD of 34±10.5 days of recovery. This group reported persistent positive SARS-CoV-2 results 39±9 days after the initial positive testing. Relapse predominantly occurred in older individuals with an anergic immune response. There were no reports of any clinical re-infections after a 70-day period following initial infection. Readmission and death in post-COVID-19Readmission and death after hospital discharge contribute to the burden of the disease. An observational study based in a large multihospital system in Michigan (USA) included 2179 hospitalised patients and reported readmission and death within 60 days of discharge in 19.9% and 9.1% of patients, respectively [11]. The most common reasons for readmission were COVID-19 (30.2%), sepsis (8.5%), pneumonia (3.1%) and heart failure ...

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Long COVID syndrome‐associated brain fog

Cited by 139 publications

References 26 publications

Trajectories of Neurological Recovery 12 Months after Hospitalization for COVID-19: A Prospective Longitudinal Study

Trajectories of Neurological Recovery 12 Months after Hospitalization for COVID-19: A Prospective Longitudinal Study

Post-Coronavirus Disease 2019 Triggers the Appearance of Mixed Polyneuropathy and Brain Fog: A Case Report

Post-COVID-19 sequelae

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