<p>Long COVID (LC) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are serious multisystemic conditions that may develop post-infection. These medical conditions are associated with enormous strain and inability to work in those affected. Risk factors for developing these conditions include female sex, younger age, and previous viral infections in ME/CFS. Vaccination against SARS-CoV‑2 has a&#xa0;protective effect. The most widely used diagnostic frameworks are the World Health Organization’s diagnostic definition for LC and the Canadian Consensus Criteria for ME/CFS. No definitive biomarkers are currently available to confirm the diagnosis of either condition. The most frequent neuropsychiatric symptoms include post-exertional malaise, persistent fatigue, cognitive impairment, sleep disturbances, depressive symptoms, and anxiety. There is substantial symptom overlap between LC and ME/CFS. In addition, there are significant overlaps with depressive and anxiety disorders. Similar patterns have also been described in imaging and biomarker studies. Published works on neurobiological changes in LC report, among other things, evidence of neuroinflammation, changes in neuroplastic processes, cerebrovascular dysfunction, and neurotransmitter imbalances. These findings are discussed as possible pathophysiological correlates of neuropsychiatric LC symptoms and provide starting points for potential therapeutic targets. Against this background, substances are already being used off-label in clinical practice, including selected phytotherapeutics (e.g., Silexan, Ginkgo biloba), antidepressants (selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, as well as, for example, bupropion, vortioxetine, mirtazapine, tianeptine), and augmentation strategies (e.g., aripiprazole, daridorexant, and (es)ketamine). Owing to their plausible mechanisms of action and the first promising preliminary clinical case reports, these approaches should be systematically evaluated in controlled studies to define their significance in the treatment of neuropsychiatric symptoms in LC and, potentially, ME/CFS.</p>

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Psychopharmakologisches Repurposing bei postviralen Erschöpfungssyndromen: Von der neurobiologischen Rationale zur klinischen Anwendung

  • Noam Hartman,
  • Dominik Ivkic,
  • Marie Celine Dorczok,
  • Ina Bozic,
  • Lutz Reinfried,
  • Anna-Christina Moser,
  • Gernot Fugger,
  • Birgit Ludwig,
  • Florian Buchmayer,
  • Marie Spies,
  • Ana Weidenauer,
  • Lucie Bartova

摘要

Long COVID (LC) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are serious multisystemic conditions that may develop post-infection. These medical conditions are associated with enormous strain and inability to work in those affected. Risk factors for developing these conditions include female sex, younger age, and previous viral infections in ME/CFS. Vaccination against SARS-CoV‑2 has a protective effect. The most widely used diagnostic frameworks are the World Health Organization’s diagnostic definition for LC and the Canadian Consensus Criteria for ME/CFS. No definitive biomarkers are currently available to confirm the diagnosis of either condition. The most frequent neuropsychiatric symptoms include post-exertional malaise, persistent fatigue, cognitive impairment, sleep disturbances, depressive symptoms, and anxiety. There is substantial symptom overlap between LC and ME/CFS. In addition, there are significant overlaps with depressive and anxiety disorders. Similar patterns have also been described in imaging and biomarker studies. Published works on neurobiological changes in LC report, among other things, evidence of neuroinflammation, changes in neuroplastic processes, cerebrovascular dysfunction, and neurotransmitter imbalances. These findings are discussed as possible pathophysiological correlates of neuropsychiatric LC symptoms and provide starting points for potential therapeutic targets. Against this background, substances are already being used off-label in clinical practice, including selected phytotherapeutics (e.g., Silexan, Ginkgo biloba), antidepressants (selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, as well as, for example, bupropion, vortioxetine, mirtazapine, tianeptine), and augmentation strategies (e.g., aripiprazole, daridorexant, and (es)ketamine). Owing to their plausible mechanisms of action and the first promising preliminary clinical case reports, these approaches should be systematically evaluated in controlled studies to define their significance in the treatment of neuropsychiatric symptoms in LC and, potentially, ME/CFS.