Post-acute COVID-19 neuropsychiatric symptoms are not associated with ongoing nervous system injury

A proportion of patients infected with severe acute respiratory syndrome coronavirus 2 experience a range of neuropsychiatric symptoms months after infection, including cognitive deficits, depression and anxiety. The mechanisms underpinning such symptoms remain elusive. Recent research has demonstrated that nervous system injury can occur during COVID-19. Whether ongoing neural injury in the months after COVID-19 accounts for the ongoing or emergent neuropsychiatric symptoms is unclear. Within a large prospective cohort study of adult survivors who were hospitalized for severe acute respiratory syndrome coronavirus 2 infection, we analysed plasma markers of nervous system injury and astrocytic activation, measured 6 months post-infection: neurofilament light, glial fibrillary acidic protein and total tau protein. We assessed whether these markers were associated with the severity of the acute COVID-19 illness and with post-acute neuropsychiatric symptoms (as measured by the Patient Health Questionnaire for depression, the General Anxiety Disorder assessment for anxiety, the Montreal Cognitive Assessment for objective cognitive deficit and the cognitive items of the Patient Symptom Questionnaire for subjective cognitive deficit) at 6 months and 1 year post-hospital discharge from COVID-19. No robust associations were found between markers of nervous system injury and severity of acute COVID-19 (except for an association of small effect size between duration of admission and neurofilament light) nor with post-acute neuropsychiatric symptoms. These results suggest that ongoing neuropsychiatric symptoms are not due to ongoing neural injury

Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease

One in ten severe acute respiratory syndrome coronavirus 2 infections result in prolonged symptoms termed long coronavirus disease (COVID), yet disease phenotypes and mechanisms are poorly understood1. Here we profiled 368 plasma proteins in 657 participants ≥3 months following hospitalization. Of these, 426 had at least one long COVID symptom and 233 had fully recovered. Elevated markers of myeloid inflammation and complement activation were associated with long COVID. IL-1R2, MATN2 and COLEC12 were associated with cardiorespiratory symptoms, fatigue and anxiety/depression; MATN2, CSF3 and C1QA were elevated in gastrointestinal symptoms and C1QA was elevated in cognitive impairment. Additional markers of alterations in nerve tissue repair (SPON-1 and NFASC) were elevated in those with cognitive impairment and SCG3, suggestive of brain–gut axis disturbance, was elevated in gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2-specific immunoglobulin G (IgG) was persistently elevated in some individuals with long COVID, but virus was not detected in sputum. Analysis of inflammatory markers in nasal fluids showed no association with symptoms. Our study aimed to understand inflammatory processes that underlie long COVID and was not designed for biomarker discovery. Our findings suggest that specific inflammatory pathways related to tissue damage are implicated in subtypes of long COVID, which might be targeted in future therapeutic trials

Stuck in the middle with who? the class identity of knowledge workers

The coming of the information age has been associated with widespread social transformation and new, or dissolved, class structures. Central to this claim is the emergence of `knowledge workers' including information technology professionals. While previous discussion has focused on the paradox faced by IT workers as both professionals and employees, this article, using empirical data from five software organizations in Scotland, examines their perceptions of class structure and their own class position. It finds that participants clearly retained varying class models of society but expressed conflict between their own self-rated class identity and that which they awarded to their occupation and profession

Could recidivism in prisoners be linked to traumatic grief? A review of the evidence

© 2008 Informa plcTraumatic grief arises as a result of interpersonal trauma experienced as a betrayal of attachment. The distinct set of symptoms associated with it were first recognized in the 1990s. Losses associated with traumatic grief can be either death or non-death related. A variety of studies have demonstrated that many prisoners have suffered from losses and trauma throughout their lives, and in many instances they have never received any support or interventions to address resultant problems. This paper examines whether there could be a relationship between many of the maladaptive behaviours demonstrated by the prisoners (including substance use), mental illness and traumatic grief. Of particular importance is the exploration of whether the high rates of recidivism seen in many developed countries (and which in Australia have been reported as high as 77%) may be related to traumatic grief. This paper explores new concepts that may be relevant to the development of strategies to reduce recidivism.Raelene M. Leach ; Teresa Burgess ; Chris Holmwoo