Abstract:Scientific evidence concerning the subacute and long-term effects of coronavirus disease 2019 (COVID-19) is on the rise. It has been established that infection by serious acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a systemic process that involves multiple organs. The complications and long-term consequences of COVID-19 are diverse and patients need a multidisciplinary treatment approach in the acute and post-acute stages of the disease. A significant proportion of COVID-19 patients experience neu… Show more
“…1 ). ( Rudroff et al, 2021 ). Figure 1 Role of PET scan in the early assessment of cognitive impairment or dementia in PDPACS.…”
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confidence: 99%
“…MRI analysis showed that 41 of 57 patients (71%) had perfusion abnormalities and ischemic and hemorrhagic lesions in white matter ( Lambrecq et al, 2021 ). In contrast, PET scans allow the observation of the earliest abnormalities like hypometabolism in amygdala, and hippocampus, and the spread towards the thalamus, pons, medulla, and bilateral cerebellum, correlated with patients abnormalities such as hyposmia/anosmia, memory loss, and cognitive complaints of significant clinical relevance in PDPACS ( Rudroff et al, 2021 ). PET advantages over MRI are due to the use of [18F] fluorodeoxyglucose (18F-FDG) radiotracer as a glucose consumption biomarker, which can help target metabolic changes in the brain before structural abnormalities mainly observed by MRIs ( Rudroff et al, 2021 ).…”
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confidence: 99%
“…By using PET, they observed a reduction in the 18F-FDG uptake in the parietal, temporal, and prefrontal lobes. They found a mild to moderate AD (93% sensitivity and specificity) and very mild AD (i.e., mini-mental status examination (MMSE ≥ 4) (with 84% sensitivity and 93% specificity) ( Rudroff et al, 2021 ). AD and PET scans of post-COVID-19 share similar pathological changes associated with cellular metabolic stress as an early marker of dementia.…”
“…1 ). ( Rudroff et al, 2021 ). Figure 1 Role of PET scan in the early assessment of cognitive impairment or dementia in PDPACS.…”
mentioning
confidence: 99%
“…MRI analysis showed that 41 of 57 patients (71%) had perfusion abnormalities and ischemic and hemorrhagic lesions in white matter ( Lambrecq et al, 2021 ). In contrast, PET scans allow the observation of the earliest abnormalities like hypometabolism in amygdala, and hippocampus, and the spread towards the thalamus, pons, medulla, and bilateral cerebellum, correlated with patients abnormalities such as hyposmia/anosmia, memory loss, and cognitive complaints of significant clinical relevance in PDPACS ( Rudroff et al, 2021 ). PET advantages over MRI are due to the use of [18F] fluorodeoxyglucose (18F-FDG) radiotracer as a glucose consumption biomarker, which can help target metabolic changes in the brain before structural abnormalities mainly observed by MRIs ( Rudroff et al, 2021 ).…”
mentioning
confidence: 99%
“…By using PET, they observed a reduction in the 18F-FDG uptake in the parietal, temporal, and prefrontal lobes. They found a mild to moderate AD (93% sensitivity and specificity) and very mild AD (i.e., mini-mental status examination (MMSE ≥ 4) (with 84% sensitivity and 93% specificity) ( Rudroff et al, 2021 ). AD and PET scans of post-COVID-19 share similar pathological changes associated with cellular metabolic stress as an early marker of dementia.…”
“…Although the most significant cluster was of a negative correlation, located in the right dorsal anterior cingulate gyrus, we also found clusters of significant positive correlation, involving the left inferior temporal gyrus and the left inferior occipital gyrus. Changes in brain metabolism have been documented in COVID-19 patients, although its pattern is more inconsistent, and may be affected by the severity of disease, patients age and comorbidities [123]. Hosp and colleagues analyzed the pattern o covariance of PET-FDG brain images between COVID-19 patients and controls and reported several regions of cortical hypometabolism in the frontal and parietal lobes, as well as the caudate nuclei, and hypermetabolism in the white matter, cerebellum, brainstem and the mesial temporal lobe, and this pattern was predictive of cognitive deficits [23].…”
People recovered from COVID-19 may still present complications including respiratory and neurological sequelae. In other viral infections, cognitive impairment occurs due to brain damage or dysfunction caused by vascular lesions and inflammatory processes. Persistent cognitive impairment compromises daily activities and psychosocial adaptation. Some level of neurological and psychiatric consequences were expected and described in severe cases of COVID-19. However, it is debatable whether neuropsychiatric complications are related to COVID-19 or to unfoldings from a severe infection. Nevertheless, the majority of cases recorded worldwide were mild to moderate self-limited illness in non-hospitalized people. Thus, it is important to understand what are the implications of mild COVID-19, which is the largest and understudied pool of COVID-19 cases. We aimed to investigate adults at least four months after recovering from mild COVID-19, which were assessed by neuropsychological, ocular and neurological tests, immune markers assay, and by structural MRI and 18FDG-PET neuroimaging to shed light on putative brain changes and clinical correlations. In approximately one-quarter of mild-COVID-19 individuals, we detected a specific visuoconstructive deficit, which was associated with changes in molecular and structural brain imaging, and correlated with upregulation of peripheral immune markers. Our findings provide evidence of neuroinflammatory burden causing cognitive deficit, in an already large and growing fraction of the world population. While living with a multitude of mild COVID-19 cases, action is required for a more comprehensive assessment and follow-up of the cognitive impairment, allowing to better understand symptom persistence and the necessity of rehabilitation of the affected individuals.
“…As the usual suspects have been excluded, this includes looking for answers outside the chest. Brain imaging studies have found clues in areas with hypometabolism in relation to patients’ symptoms [ 14 ]; a completely different hypothesis regarding the persistent pulmonary symptoms is thus the possibility of persistent, low-grade brainstem dysfunction affecting the respiratory neurone circuits [ 15 ]. In addition, post-viral, ongoing immunological aberrations could be the cause of long-term complaints [ 16 ].…”
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