Neurologic complications of coronavirus and other respiratory viral infections

Cavallieri, Francesco; Sellner, Johann; Zedde, Marialuisa; Moro, Elena

doi:10.1016/b978-0-323-91532-8.00004-5

Cited by 22 publications

(24 citation statements)

References 267 publications

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“…The expansion of the lobes due to the air trapping can cause compression on the (not quantified) intra-alveolar blood vessels with a shift of blood flow to the blood vessels with a diameter of 5 mm 2 . It is also known that endothelitis (Cavallieri et al, 2022) in the capilary vessels of the lungs can cause this shift in blood flow to the larger vessels. Alveolar-capillary damage or microvascular pathology might result in a declined DLCO/VA (Hughes & Pride, 2012).…”

Section: Discussionmentioning

confidence: 99%

Unraveling pathophysiologic mechanisms contributing to symptoms in patients with post‐acute sequelae of COVID‐19 (PASC): A retrospective study

Dierckx

Backer

Ides

et al. 2023

Physiological Reports

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Patients with post-acute sequelae of COVID-19 (PASC) present with a decrease in physical fitness. The aim of this paper is to reveal the relations between the remaining symptoms, blood volume distribution, exercise tolerance, static and dynamic lung volumes, and overall functioning. Patients with PASC were retrospectively studied. Pulmonary function tests (PFT), 6-minute walk test (6MWT), and cardiopulmonary exercise test were performed. Chest CT was taken and quantified. Patients were divided into two groups: minor functional limitations (MFL) and severe functional limitations (SFL) based on the completed Post-COVID-19 Functional Status scale (PCFS). Twenty one patients (3 M; 18 FM), mean age 44 (IQR 21) were studied. Eighteen completed the PCFS (8 MFL; 10SFL). VO 2 max was suboptimal in both groups (not significant). 6MWT was significantly higher in MFL-group (p = 0.043). Subjects with SFL, had significant lower TLC (p = 0.029). The MFL-group had more air trapping (p = 0.036). Throughout the sample, air trapping correlated significantly with residual volume (RV) in L (p < 0.001). An increase in air trapping was related to an increase in BV5 (p < 0.001). Mean BV5 was 65% (IQR 5%). BV5% in patients with PASC was higher than in patients with acute COVID-19 infection. This increase in BV5% in patients with PASC is thought to be driven by the air trapping in the lobes. This study reveals that symptoms are more driven by occlusion of the small airways.Patients with more physical complaints have significantly lower TLC. All subjects encounter physical limitations as indicated by suboptimal VO 2 max. Treatment should focus on opening or re-opening of small airways by recruiting alveoli.

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Section: Discussionmentioning

confidence: 99%

Unraveling pathophysiologic mechanisms contributing to symptoms in patients with post‐acute sequelae of COVID‐19 (PASC): A retrospective study

Dierckx

Backer

Ides

et al. 2023

Physiological Reports

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“… 21 Much rarer symptoms include seizures, myelitis, and encephalopathy. 22 , 23 Despite the common neurologic symptoms being nonspecific and possibly multifactorial, there exists a strong biological plausibility of direct neurologic involvement of COVID-19 because SARS-CoV-2 RNA has been found in brain specimens as well as neuropathological abnormalities such as microgliosis, astrogliosis, edema, and hemorrhagic lesions. Whether these findings are due to neuroinvasion or a brain inflammatory lesion with hypoxic/ischemic injury is still currently debated but the latter is more likely.…”

Section: Brief Overview Of Long Covid Syndromementioning

confidence: 99%

Gastrointestinal and Hepatobiliary Symptoms and Disorders with Long (Chronic) COVID Infection

Rizvi

Ziv

Crawford

et al. 2023

Gastroenterology Clinics of North America

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“…The neurobiological underpinnings of long COVID are less well understood, but similar direct viral or indirect effects on the nervous system likely play a role. 69 Given that microglia and macrophages are key to learning and memory systems, dysregulated neural-immune interactions may play a central role in the cognitive impairment often seen with long COVID. 70 Supporting this hypothesis, the extent of cognitive deficits in patients with long COVID correlate with structural neuroimaging abnormalities (e.g., global decrease in brain volume, structural abnormalities in the limbic system and cerebellum, white matter hyperintensities, and changes in diffusivity in many structures), 71 72 which may represent biomarkers of the neuroinflammatory response.…”

Section: Mechanisms Of Neurologic Dysfunction In Long Covidmentioning

confidence: 99%

Neurorecovery after Critical COVID-19 Illness

2023

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With the hundreds of millions of people worldwide who have been, and continue to be, affected by pandemic coronavirus disease (COVID-19) and its chronic sequelae, strategies to improve recovery and rehabilitation from COVID-19 are critical global public health priorities. Neurologic complications have been associated with acute COVID-19 infection, usually in the setting of critical COVID-19 illness. Neurologic complications are also a core feature of the symptom constellation of long COVID and portend poor outcomes. In this article, we review neurologic complications and their mechanisms in critical COVID-19 illness and long COVID. We focus on parallels with neurologic disease associated with non-COVID critical systemic illness. We conclude with a discussion of how recent findings can guide both neurologists working in post-acute neurologic rehabilitation facilities and policy makers who influence neurologic resource allocation.

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Neurologic complications of coronavirus and other respiratory viral infections

Cited by 22 publications

References 267 publications

Unraveling pathophysiologic mechanisms contributing to symptoms in patients with post‐acute sequelae of COVID‐19 (PASC): A retrospective study

Unraveling pathophysiologic mechanisms contributing to symptoms in patients with post‐acute sequelae of COVID‐19 (PASC): A retrospective study

Gastrointestinal and Hepatobiliary Symptoms and Disorders with Long (Chronic) COVID Infection

Neurorecovery after Critical COVID-19 Illness

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