Chronic Fatigue, Depression and Anxiety Symptoms in Long COVID Are Strongly Predicted by Neuroimmune and Neuro- Oxidative Pathways Which Are Caused by the Inflammation during Acute Infection

HK Al-Hakeim et al in Michael Maes’ lab report in J. Clinical Medicine (2023) on very important findings about immune and oxidative changes in long COVID with “physio- somatic (chronic fatigue syndrome and somatic symptoms) and affective (depression and anxiety) symptoms. The severity of the long COVID physio-affective phenome is largely predicted by increased peak body temperature (BT) and lowered oxygen saturation (SpO2) during the acute infectious phase…..  We recruited 86 patients with long COVID (3–4 months after the acute phase) and 39 healthy controls and assessed serum C-reactive protein (CRP), caspase 1, interleukin (IL) 1?, IL-18, IL-10, myeloperoxidase (MPO), advanced oxidation protein products (AOPPs), total antioxidant capacity (TAC), and calcium (Ca), as well as peak BT and SpO2 during the acute phase. Results: Cluster analysis revealed that a significant part (34.9%) of long COVID patients (n = 30) show a highly elevated NT (neurotoxicity) index as computed based on IL-1?, IL-18, caspase 1, CRP, MPO, and AOPPs. Partial least squares analysis showed that 61.6% of the variance in the physio-affective phenome of long COVID could be explained by the NT index, lowered Ca, and peak BT/SpO2 in the acute phase and prior vaccinations with AstraZeneca or Pfizer. The most important predictors of the physio-affective phenome are Ca, CRP, IL-1?, AOPPs, and MPO. Conclusion: The infection–immune–inflammatory core of acute COVID-19 strongly predicts the development of physio-affective symptoms 3–4 months later, and these effects are partly mediated by neuro-immune and neuro-oxidative pathways.”

Editors Note:  These finding are important as they may lead to new treatment interventions.  BNN readers are reminded of a previous BNN article by investigators from Yale (written by by Isabella Backman on Dec. 13, 2022) that in a new case study, they found that guanfacine plus N-acetylcysteine (which is an anti-inflammatory, anti-oxidant, and glutathione precursor) “mitigated and sometimes eliminated the cognitive impairment known as “brain fog” that often accompanies long COVID.

Following Collisions, High School Football Players with No Signs of Concussion May Still Have Neurological Impairment

August 23, 2017 · Posted in Risk Factors · Comment 

brain injury in football

In a small 2014 study in the Journal of Neurotrauma, researcher Thomas M. Talavaga and colleagues reported that repeated head trauma that did not produce concussion symptoms was still associated with neurocognitive and neurophysiological changes to the brain in high school football players.

The longitudinal study tracked ‘collision events’ experienced by 11 teens who played football at the same high school. The young men also completed neurocognitive testing and magnetic resonance imaging (MRI) scans of their brains over time.

The researchers expected to see the participants fall into two categories: those who had no concussions and normal neurological function, and those who had at least one concussion and subsequent neurological changes. They ended up observing a third group: young men who had not exhibited concussion symptoms, but nonetheless had measurable changes to their neurological functioning, including impairments to visual working memory and altered activation of the dorsolateral prefrontal cortex. Young men in this last group had had more collisions that impacted the top front of the head, directly above the dorsolateral prefrontal cortex.

The authors suggest that the discovery of this third category mean that some neurological injuries are going undetected in high school football players. The players who are injured in this way are not likely to seek treatment, and may continue playing football, risking more neurological brain injury or brain damage with subsequent collisions.