When compared to a control group, people those who tested positive for COVID-19 had more brain shrinkage, grey matter shrinkage, and tissue damage. The damage occurs predominantly in areas of the brain that are associated with odour, ambiguity, strokes, reduced attention, headaches, sensory abnormalities, depression, and mental abilities for few months after the first infection.
The COVID-19 individuals investigated herein were often unable to produce a proper copy of Rey’s figure, and had difficulties in memory. Immediate and delayed recall seems to be secondary to the copy impairment. The lack of ability to assemble or organize parts into a whole object or figure is considered constructional apraxia, a neuropsychological syndrome which results in inability to accurately reproduce two-dimensional or three-dimensional visual models.
Participants were mostly female (83%), with a mean age of 45 ± 11 years. The median time of evaluation was 9 months after COVID-19 (range 3–12 months), and most (11/12, 92%) had a history of only a mild infection. The most common neuro-PASC symptoms were cognitive difficulties and fatigue, and there was evidence for mild cognitive impairment in half of the patients (MoCA score <26). The majority (83%) had a very disabling disease, with Karnofsky Performance Status ≤80.
Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can lead to neuropsychiatric effects during acute COVID-19, including confusion, stroke, and neuromuscular disorders. These may arise from neuroinflammation, coagulopathy, neuronal injury, and possibly viral infection in the central nervous system. Causes of Long Covid symptoms affecting the nervous system may result from the emergence and persistence of these mechanisms.
This is to our knowledge the first longitudinal imaging study of SARS-CoV-2 in which the participants were initially scanned before any of them had been infected. Our longitudinal analyses revealed a significant, deleterious impact associated with SARS-CoV-2. This effect could be seen mainly in the limbic and olfactory cortical system, for example, with a change in diffusion measures—proxies for tissue damage—in regions that are functionally connected to the piriform cortex, olfactory tubercle and anterior olfactory nucleus, as well as a more pronounced reduction of grey matter thickness and contrast in the participants infected with SARS-CoV-2 in the left parahippocampal gyrus and lateral orbitofrontal cortex. Although the greater atrophy for the participants who tested positive for SARS-CoV-2 was localised to a few, mainly limbic, regions, the increase in CSF volume and decrease in whole-brain volume suggests an additional diffuse loss of grey matter superimposed onto the more regional effects observed in the olfactory-related areas.
People who had recovered from COVID-19, including those no longer reporting symptoms, exhibited significant cognitive deficits versus controls when controlling for age, gender, education level, income, racial-ethnic group, pre-existing medical disorders, tiredness, depression and anxiety. The deficits were of substantial effect size for people who had been hospitalised (N = 192), but also for non-hospitalised cases who had biological confirmation of COVID-19 infection (N = 326).
Research presented at the Alzheimer’s Association International Conference suggests even mild cases of COVID-19 may be associated with cognitive deficits months after recovery.
Up to one-third of patients with COVID-19 analyzed in this review experienced at least 1 neurologic manifestation. One in 50 patients experienced stroke. In those >60 years of age, more than one-third had acute confusion/delirium; the presence of neurologic manifestations in this group was associated with nearly a doubling of mortality.
Coronavirus disease 2019 (COVID-19) can damage cerebral small vessels and cause neurological symptoms. Here we describe structural changes in cerebral small vessels of patients with COVID-19 and elucidate potential mechanisms underlying the vascular pathology.
Our observations of SARS-CoV-2 in the brainstem, which comprises the primary respiratory and cardiovascular control center, it is possible that SARS-CoV-2 infection, at least in some instances, might aggravate respiratory or cardiac insufficiency—or even cause failure—in a CNS-mediated manner.