Posts by:
Gabriella True

Young adults’ experiences of living with paediatric acute-onset neuropsychiatric syndrome. An interview study

Ulla-KarinSchön (2023) Young adults’ experiences of living with paediatric acute-onset neuropsychiatric syndrome. An interview study, International Journal of Qualitative Studies on Health and Well-being, 18:1, DOI: 10.1080/17482631.2023.2267268

This article explores experiential knowledge of living with paediatric acute-onset neuropsychiatric syndrome (PANS), and the factors that are associated with perceived good care.

  • Young adults living fairly isolated lives, dependent on care from relatives.
  • The illness was a tangible presence.
  • They perceived a lack of knowledge among healthcare staff on PANS in healthcare, and negative consequences linked to this. Their experience-based knowledge of their own illness is devalued in healthcare encounters.
  • A feeling of being pushed around in healthcare, without anyone taking responsibility for the treatment
  • Emphasized the need for increased knowledge among staff to identify PANS and be able to offer effective treatment.
Evaluation of Brain-Body Health in Individuals With Common Neuropsychiatric Disorders

Tian YE, Di Biase MA, Mosley PE, et al. Evaluation of Brain-Body Health in Individuals With Common Neuropsychiatric Disorders. JAMA Psychiatry. 2023;80(6):567–576. doi:10.1001/jamapsychiatry.2023.0791

“This multicenter population-based cohort study including 85 748 adults with neuropsychiatric disorders and 87 420 healthy control individuals found that poor body health, particularly of the metabolic, hepatic, and immune systems, was a more marked manifestation of mental illness than brain changes.”

 

Cytokine Effects on the Basal Ganglia and Dopamine Function: the Subcortical Source of Inflammatory Malaise

Felger JC, Miller AH. Cytokine effects on the basal ganglia and dopamine function: the subcortical source of inflammatory malaise. Front Neuroendocrinol. 2012 Aug;33(3):315-27. doi: 10.1016/j.yfrne.2012.09.003. Epub 2012 Sep 21. PMID: 23000204; PMCID: PMC3484236.

  • Cytokines released during inflammation target the basal ganglia and dopamine
  • Cytokines can disrupt dopamine function by effects on synthesis, packaging, release, and reuptake
  • Cytokine effects on basal ganglia dopamine may cause anhedonia, fatigue, and psychomotor slowing
  • Cytokines may contribute to behavioral disorders associated with chronic inflammation
PANDAS/PANS in the COVID-19 Age: Autoimmunity and Epstein–Barr Virus Reactivation as Trigger Agents?
Pallanti S, Di Ponzio M. PANDAS/PANS in the COVID-19 Age: Autoimmunity and Epstein-Barr Virus Reactivation as Trigger Agents? Children (Basel). 2023 Mar 30;10(4):648. doi: 10.3390/children10040648. PMID: 37189896; PMCID: PMC10136983.
  • COVID-19 infection and pandemic-related stressors were associated with worsening neuropsychiatric symptoms in children and adolescents with PANS
  • Obsessions, tics, anxiety, mood symptoms, and overall wellbeing were most commonly affected
  • New symptoms and new-onset PANS cases were reported following SARS-CoV-2 infection
  • Case series of five adolescents showed symptom exacerbation after COVID-19 infection
  • Authors hypothesize roles for neuroinflammation, immune activation, viral reactivation (e.g., EBV), and social isolation–related inflammatory effects
  • PANS is presented as a model for understanding immune-mediated neuropsychiatric post-acute COVID syndromes (PACS)
Persistent SARS-CoV-2 Infection, EBV, HHV-6 and Other Factors May Contribute to Inflammation and Autoimmunity in Long COVID
Vojdani A, Vojdani E, Saidara E, Maes M. Persistent SARS-CoV-2 Infection, EBV, HHV-6 and Other Factors May Contribute to Inflammation and Autoimmunity in Long COVID. Viruses. 2023 Jan 31;15(2):400. doi: 10.3390/v15020400. PMID: 36851614; PMCID: PMC9967513.
“Based on our review of the literature, in both past and recent studies, we have found clues to these mechanisms that might drive this long COVID, with the goal of identifying host or virus factors that can be intervened upon to prevent or reverse this condition. A better understanding of these immunological mechanisms in patients with severe long COVID holds great promise for designing treatment strategies to minimize viral persistence, control the reactivation of latent viruses, and to modulate a dysregulated immune system and host microbiota, which together are involved in the virus-induced inflammation and autoimmunity that are observed in patients with long COVID.”