This isn't meant to denigrate what's happened to Bruce Willis; rather this post is intended to bring to light some other possible complications from Covid-19. Article represents preliminary work to identify whether or not there is a link to aphasia and Covid-19.
There are now growing reports with evidence of neurological and dysexecutive syndromes subsequent to interference of brain functions in acute patients with COVID-19, leading to variable aphasia-like symptoms. COVID-19 affected chronic PWA more in terms of disrupted communication and daily routines, …
BTW, I haven't been able to find any articles which reveal whether or not Bruce Willis had gotten Covid-19, or whether he had been vaccinated.
It isn't. Many things can cause it. But covid is also one of the many things shown to cause it.
This is the stuff that's not being covered too. Know 3 very bright attorneys who have quit practicing law from long covid. None ever saw a hospital with it either. Mild cases. They're in their 40s and 50s. It goes way back to the original Sars. Think 50,000 people or so got that. 40% of survivors had diagnosed neurological and mental conditions even 9 years later.
Seeing articles like the one below makes me think there is a greater connection than we know. This article suspiciously leaves covid out when it's a distinct possibility not mentioned.
The pandemic brain: Neuroinflammation in non-infected individuals during the COVID-19 pandemic
Abstract
While COVID-19 research has seen an explosion in the literature, the impact of pandemic-related societal and lifestyle disruptions on brain health among the uninfected remains underexplored. However, a global increase in the prevalence of fatigue, brain fog, depression and other “sickness behavior”-like symptoms implicates a possible dysregulation in neuroimmune mechanisms even among those never infected by the virus.
We compared fifty-seven ‘Pre-Pandemic’ and fifteen ‘Pandemic’ datasets from individuals originally enrolled as control subjects for various completed, or ongoing, research studies available in our records, with a confirmed negative test for SARS-CoV-2 antibodies. We used a combination of multimodal molecular brain imaging (simultaneous positron emission tomography / magnetic resonance spectroscopy), behavioral measurements, imaging transcriptomics and serum testing to uncover links between pandemic-related stressors and neuroinflammation.
Healthy individuals examined after the enforcement of 2020 lockdown/stay-at-home measures demonstrated elevated brain levels of two independent neuroinflammatory markers (the 18 kDa translocator protein, TSPO, and myoinositol) compared to pre-lockdown subjects. The serum levels of two inflammatory markers (interleukin-16 and monocyte chemoattractant protein-1) were also elevated, although these effects did not reach statistical significance after correcting for multiple comparisons. Subjects endorsing higher symptom burden showed higher TSPO signal in the hippocampus (mood alteration, mental fatigue), intraparietal sulcus and precuneus (physical fatigue), compared to those reporting little/no symptoms. Post-lockdown TSPO signal changes were spatially aligned with the constitutive expression of several genes involved in immune/neuroimmune functions.