Long Covid Land Toolbox
Digital Download: Request for Covid Accommodation in Health Care Facilities
Everyone deserves safe access to health care, but we know many people are facing resistance to simple, reasonable requests for Covid accommodations like respirators and air filters cleaners.
So we’re making it easier for you to request accommodations from your primary care doctor, dentist, specialists, or other health care workers, with a fillable PDF form that clearly lays out your requested accommodations and your legal rights to them.
Download our Request for Accommodation in Health Care Facilities PDF today.
Neurological, psychological, psychosocial complications of long-COVID and their management
Since it first appeared, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has had a significant and lasting negative impact on the health and economies of millions of individuals all over the globe. At the level of individual health too, many patients are not recovering fully and experiencing a long-term condition now commonly termed ‘long-COVID’. Long-COVID is a collection of symptoms which must last more than 12 weeks following initial COVID infection, and which cannot be adequately explained by alternate diagnoses. The neurological and psychosocial impact of long-COVID is itself now a global health crisis and therefore preventing, diagnosing, and managing these patients is of paramount importance. This review focuses primarily on: neurological functioning deficits; mental health impacts; long-term mood problems; and associated psychosocial issues, among patients suffering from long-COVID with an eye towards the neurological basis of these symptoms.
Neurological complications caused by SARS-CoV-2
SARS-CoV-2 can not only cause respiratory symptoms but also lead to neurological complications. Research has shown that more than 30% of SARS-CoV-2 patients present neurologic symptoms during COVID-19 (A. Pezzini and A. Padovani, Nat Rev Neurol 16:636–644, 2020, https://doi.org/10.1038/s41582-020-0398-3). Increasing evidence suggests that SARS-CoV-2 can invade both the central nervous system (CNS) (M.S. Xydakis, M.W. Albers, E.H. Holbrook, et al. Lancet Neurol 20: 753–761, 2021 https://doi.org/10.1016/S1474-4422(21)00182-4 ) and the peripheral nervous system (PNS) (M.N. Soares, M. Eggelbusch, E. Naddaf, et al. J Cachexia Sarcopenia Muscle 13:11–22, 2022, https://doi.org/10.1002/jcsm.12896), resulting in a variety of neurological disorders. This review summarized the CNS complications caused by SARS-CoV-2 infection, including encephalopathy, neurodegenerative diseases, and delirium. Additionally, some PNS disorders such as skeletal muscle damage and inflammation, anosmia, smell or taste impairment, myasthenia gravis, Guillain-Barré syndrome, ICU-acquired weakness, and post-acute sequelae of COVID-19 were described.
Endothelial inflammation in COVID-19
Disrupted endothelial function underlies the multiorgan complications of COVID-19
The vascular endothelium forms a crucial interface between tissues and the blood stream and maintains normal blood flow (1). In its homeostatic state, the endothelium resists blood clotting, vasoconstriction, and inflammation and maintains selective barrier functions. This tightly regulated suite of properties can shift rapidly to unleash a series of functions vital to stanch blood loss from wounds or mobilize innate and adaptive immune defenses to repair injury and fight pathogenic microorganisms. But these defensive actions of endothelial cells can, if overexuberant, aggravate disease. Infection with severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) has highlighted how altered endothelial functions contribute to multiorgan health effects during the acute phase of COVID-19 and potentially to the longer-term consequences associated with Long Covid.
Chronic autonomic symptom burden in long-COVID: a follow-up cohort study
2025 Feb 5
Abstract
Purpose: Autonomic dysfunction is a common and often debilitating feature of long-COVID (LC), however, studies evaluating frequency and severity of chronic autonomic dysfunction in LC are limited. We utilized an established online cohort of participants with LC to assess duration and severity of autonomic dysfunction, impact on quality of life, risk factors of autonomic diagnoses including postural tachycardia syndrome (POTS), and efficacy of common treatments.
Conclusions: Evidence of chronic moderate-to-severe autonomic dysfunction was seen in most participants with LC in our cohort and was significantly associated with reduced quality of life and functional disability. POTS was the most common post-COVID autonomic diagnosis.
The LongCovid Research Consortium is a scientific collaboration to rapidly and comprehensively study LongCovid.
LongCovid is no longer a mystery. New research is revealing key drivers of the condition, including evidence strongly suggesting that patients with LongCovid do not fully clear the SARS-CoV-2 virus. Instead, the virus may persist in tissue where it continues to provoke the immune system. This could drive a wide range of downstream consequences such as blood clotting, neuroinflammation, and neuropathy. The persistence of SARS-CoV-2 in tissue is called a viral reservoir.
The LongCovid Research Consortium has established a comprehensive research program on LongCovid disease mechanisms, with a focus on viral reservoir. The program includes scientists and clinicians from institutions including Harvard Medical School, University of California San Francisco, the J. Craig Venter Institute, Johns Hopkins, University of Pennsylvania, the Icahn School of Medicine at Mount Sinai, Cardiff University and Yale University.
LONG COVID CANADA LINK LIBRARY
The Long Covid Link Library provides a comprehensive and continuously updated repository of the latest research, clinical findings, and scientific developments related to Long COVID. This dynamic resource aggregates peer-reviewed studies, clinical guidelines, and emerging treatment protocols from leading medical institutions worldwide.
The library covers crucial aspects of Long COVID research, including symptom characterization, risk factors, potential mechanisms, and treatment strategies. Content spans multiple disciplines, from immunology and neurology to cardiology and rehabilitation medicine.
Whether you’re a healthcare provider, researcher, patient, or caregiver, staying current with the rapidly evolving landscape of Long COVID research is essential for understanding this complex condition and its management.
Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19
SARS-CoV-2 infection is associated with long-lasting neurological symptoms, although the underlying mechanisms remain unclear. Using optical clearing and imaging, we observed the accumulation of SARS-CoV-2 spike protein in the skull-meninges-brain axis of human COVID-19 patients, persisting long after viral clearance.
Further, biomarkers of neurodegeneration were elevated in the cerebrospinal fluid from long COVID patients, and proteomic analysis of human skull, meninges, and brain samples revealed dysregulated inflammatory pathways and neurodegeneration-associated changes.
Similar distribution patterns of the spike protein were observed in SARS-CoV-2-infected mice. Injection of spike protein alone was sufficient to induce neuroinflammation, proteome changes in the skull-meninges-brain axis, anxiety-like behavior, and exacerbated outcomes in mouse models of stroke and traumatic brain injury.
Vaccination reduced but did not eliminate spike protein accumulation after infection in mice. Our findings suggest persistent spike protein at the brain borders may contribute to lasting neurological sequelae of COVID-19.
