Introduction, not abstract
Countless LC patients have turned to social media forming large peer communities where lived experiences are shared in real time. A recurring patient-reported observation emerging from these communities is the onset or worsening of attention deficit (hyperactivity) disorder (AD(H)D), or AD(H)D-like symptoms, following COVID-19 infection—despite no prior diagnosis. Both adults and children have described cognitive, behavioral, and sensory changes consistent with AD(H)D traits. This mirrors observations in ME/CFS and among neurodivergent youth with high levels of disabling fatigue (Sáez-Francàs et al., 2012, Quadt et al., 2024). Common patient-reported features include brain fog,1 mental exhaustion, impaired attention/concentration, sleep disturbances, impatience, hypersensitivity, conversational difficulties, feeling “different” and, secondarily, feelings of anxiety and depression.
Increasingly recognized by LC healthcare providers, these overlaps suggest a bidirectional relationship between LC and AD(H)D, both involving neuroinflammation and shared neurocognitive symptoms (Braga et al., 2023). Although case series and epidemiological data report AD(H)D as a risk factor for LC and note its higher incidence among LC sufferers (Merzon et al., 2022, Ferrara et al., 2023, Gimbach et al., 2024)—both conditions share hypermobility spectrum disorders as a risk factor—, not all studies support this association (Zemer et al., 2024). This inconsistency underscores the need for deeper investigation into shared phenomenology, symptomatology, prevalence, and potential overlapping pathomechanisms.
Introduction
Few medical conditions in recent memory have generated as intense a research focus in merely five years as Long Covid (LC)—a post-acute infection syndrome. Major investigations have explored etiologies, candidate biomarkers and physiological mechanisms such as viral persistence (Proal et al., 2025), yet definitive therapeutic strategy remains elusive. LC’s current symptom-based definition reflects this early phase of research: its biomedical complexity, heterogeneity, and systemic nature align poorly with current diagnostic standards, resulting in inconsistent clinical profiles. One manifestation, however, is ubiquitous: profound exhaustion and cognitive dysfunction, widely termed “brain fog”, which in turn can present under the umbrella of post-exertional malaise (PEM), the hallmark of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).Countless LC patients have turned to social media forming large peer communities where lived experiences are shared in real time. A recurring patient-reported observation emerging from these communities is the onset or worsening of attention deficit (hyperactivity) disorder (AD(H)D), or AD(H)D-like symptoms, following COVID-19 infection—despite no prior diagnosis. Both adults and children have described cognitive, behavioral, and sensory changes consistent with AD(H)D traits. This mirrors observations in ME/CFS and among neurodivergent youth with high levels of disabling fatigue (Sáez-Francàs et al., 2012, Quadt et al., 2024). Common patient-reported features include brain fog,1 mental exhaustion, impaired attention/concentration, sleep disturbances, impatience, hypersensitivity, conversational difficulties, feeling “different” and, secondarily, feelings of anxiety and depression.
Increasingly recognized by LC healthcare providers, these overlaps suggest a bidirectional relationship between LC and AD(H)D, both involving neuroinflammation and shared neurocognitive symptoms (Braga et al., 2023). Although case series and epidemiological data report AD(H)D as a risk factor for LC and note its higher incidence among LC sufferers (Merzon et al., 2022, Ferrara et al., 2023, Gimbach et al., 2024)—both conditions share hypermobility spectrum disorders as a risk factor—, not all studies support this association (Zemer et al., 2024). This inconsistency underscores the need for deeper investigation into shared phenomenology, symptomatology, prevalence, and potential overlapping pathomechanisms.
