Tag: 2022

Efficacy and safety of Ma’s Bamboo-based medicinal moxibustion therapy for chronic fatigue syndrome

Abstract:

Background: Chronic fatigue syndrome (CFS) is a recurrent functional disease with an unknown pathogenesis. Modern treatment mainly focuses on symptomatic and supportive care, but no specific treatment has emerged. Ma’s Bamboo-based Medicinal Moxibustion therapy is a folk traditional Chinese medicine developed in Jinsha County, Guizhou Province. Over a long period of practice in the primary health care setting, it has been confirmed in folk medicine that the therapy can significantly improve the symptoms of patients with CFS, but there is no sufficient and scientific clinical evidence. Therefore, this randomised controlled pilot study was designed to preliminarily evaluate the efficacy and safety of Ma’s Bamboo-based Medicinal Moxibustion therapy.

Methods/design: This is a parallel, randomized, controlled, and exploratory study. Sixty patients with CFS admitted to the First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine will be randomly assigned to the experimental or control group. The experimental group will receive Ma’s Bamboo-based Medicinal Moxibustion therapy, whereas the control group will undergo conventional acupuncture. Both groups will be treated once daily for 6 consecutive days as a course of treatment, and two courses separated by 1 day will be completed (12 total treatments). All patients will undergo follow-up after the end of treatment. The baseline period is 2 days. The Fatigue Assessment Instrument score as the primary efficacy measure and secondary efficacy measures, including the Clinical Symptom Score and Fatigue Scale-14, will be evaluated at baseline, after one and two courses of treatment, and during follow-up. Serum T lymphocyte subset counts (CD3+, CD4+, CD8+, CD4+/CD8+) and safety measures ((blood routine test, liver and kidney function and electrocardiogram) will be evaluated at baseline and after two courses of treatment. All adverse events occurring between baseline and the end of follow-up will be summarised at the end of the follow-up.

Discussion: The results of this trial will clarify whether Ma’s Bamboo-based Medicinal Moxibustion therapy can improve the symptoms of patients with CFS and provide preliminary evidence for the effectiveness and safety of Ma’s Bamboo-based Medicinal Moxibustion therapy for this indication.

Ethics approval: This study has been approved by the Ethics Review Committee of the First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine (No.K2020–038).

Trial Registration:  Chinese Clinical Trial Registry, ChiCTR2000038860. Registered on 7 October 2020.

Source: Xue, Kaiyang MMa,b; Wang, Xianzhu MMa,b; Quan, Fei MMa,b; Tang, Jiaxuan MMa,b; Wang, Xin MMa; Lan, Lan MMa; Fu, Jing PhDa; Cui, Jin PhDa,∗ Efficacy and safety of Ma’s Bamboo-based medicinal moxibustion therapy for chronic fatigue syndrome, Medicine Case Reports and Study Protocols: January 2022 – Volume 3 – Issue 1 – p e0193
doi: 10.1097/MD9.0000000000000193 https://journals.lww.com/md-cases/Fulltext/2022/01000/Efficacy_and_safety_of_Ma_s_Bamboo_based_medicinal.6.aspx (Full text)

Chronic Fatigue After Thyroidectomy: A Patient-Centered Survey

Abstract:

Background: Fatigue after thyroidectomy is common, but there is a paucity of data regarding its prevalence and duration. We hypothesized that total thyroidectomy (TT) patients would have more long-term fatigue than thyroid lobectomy (TL) patients.

Methods: Statewide survey of thyroidectomy patients (2004-2017) was carried out.

Results: 281 patients completed the survey. 216 respondents (77%) had TT and 65 (23%) had TL. Within one year of surgery, 172 (61%) respondents recalled being troubled by new fatigue all, most, or some of the time. Total thyroidectomy patients were more likely to report new fatigue (69% vs. 44%, aOR 2.72, 95% CI 1.44 to 5.18). Of patients (n = 172) reporting new fatigue, 67 (39%) reported at least moderate improvement. Nineteen (28%) saw improvement within 1 year, 35 (52%) saw improvement in 1-2 years, and 11 (16%) saw improvement after 2 years.

Conclusion: Long-term fatigue after TT can be debilitating, long-lasting, and less prevalent after TL.

Source: Lumpkin ST, Button J, Stratton L, Strassle PD, Kim LT. Chronic Fatigue After Thyroidectomy: A Patient-Centered Survey. Am Surg. 2022 Feb;88(2):260-266. doi: 10.1177/0003134821989054. Epub 2021 Jan 31. PMID: 33517685. https://pubmed.ncbi.nlm.nih.gov/33517685/

Circadian rhythm disruption in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Implications for the post-acute sequelae of COVID-19

Abstract:

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a common and disabling disorder primarily characterized by persistent fatigue and exercise intolerance, with associated sleep disturbances, autonomic dysfunction, and cognitive problems. The causes of ME/CFS are not well understood but may coincide with immune and inflammatory responses following viral infections. During the current SARS-CoV2 coronavirus pandemic, ME/CFS has been increasingly reported to overlap with persistent “long COVID” symptoms, also called the post-acute sequelae of COVID-19 (PASC).

Given the prominence of activity and sleep problems in ME/CFS, circadian rhythm disruption has been examined as a contributing factor in ME/CFS. While these studies of circadian rhythms have been pursued for decades, evidence linking circadian rhythms to ME/CFS remains inconclusive. A major limitation of older chronobiology studies of ME/CFS was the unavailability of modern molecular methods to study circadian rhythms and incomplete understanding of circadian rhythms outside the brain in peripheral organ systems. Major methodological and conceptual advancements in chronobiology have since been made.

Over the same time, biomarker research in ME/CFS has progressed. Together, these new developments may justify renewed interest in circadian rhythm research in ME/CFS. Presently, we review ME/CFS from the perspective of circadian rhythms, covering both older and newer studies that make use of modern molecular methods. We focus on transforming growth factor beta (TGFB), a cytokine that has been previously associated with ME/CFS and has an important role in circadian rhythms, especially in peripheral cells.

We propose that disrupted TGFB signaling in ME/CFS may play a role in disrupting physiological rhythms in sleep, activity, and cognition, leading to the insomnia, energy disturbances, cognition problems, depression, and autonomic dysfunction associated with ME/CFS. Since SARS-like coronavirus infections cause persistent changes in TGFB and previous coronavirus outbreaks have caused ME/CFS-like syndromes, chronobiological considerations may have immediate implications for understanding ME/CFS in the context of the COVID-19 pandemic and possibly suggest new avenues for therapeutic interventions.

Source: Michael J. McCarthy. Circadian rhythm disruption in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Implications for the post-acute sequelae of COVID-19. Brain, Behavior, & Immunity – Health, Volume 20, 2022, 100412, ISSN 2666-3546, https://doi.org/10.1016/j.bbih.2022.100412. (Full text)

“I feel like my body is broken”: Exploring the experiences of people living with long COVID

Abstract:

Background: Long COVID, an illness affecting a subset of individuals after COVID-19, is distressing and poorly understood. Exploring the experiences of people with long COVID could help inform current conceptualizations of the illness, guide supportive care strategies, and validate patients’ perspectives on the condition. Thus, the objective of this study was to better understand and explore individuals’ experiences with long COVID and commonly reported symptoms, using qualitative data collected from open-ended survey responses.

Methods: Data were collected from adults living with long COVID following a confirmed or suspected SARS-CoV-2 infection who participated in a larger observational, online survey. Within the larger survey, participants had the option of answering seven open-ended items. Data from the open-ended items were analyzed following guidelines for reflective thematic analysis.

Results: From the 213 who were included in the online survey, 169 participants who primarily self-identified as women (88.2%), aged 40-49 (33.1%), and who had been experiencing long COVID symptoms for ≥ 6 months (58.6%) responded to the open-ended questions. Four overlapping and interconnected themes were identified: (1) My long COVID symptoms are numerous, hard to describe, and debilitating, (2) All aspects of my day-to-day functioning have been impacted, (3) I can no longer be physically active, and (4) I keep asking for help, but no one is listening, and very little is working.

Conclusion: Findings highlight the complex nature of long COVID and show the ways in which individuals affected by the illness are negatively impacted. Participants recounted struggling and altering their daily activities while managing relapsing-remitting symptoms, an uncertain prognosis, lost pre-COVID identities, and a healthcare system (that does not always offer guidance nor take them seriously). More support and recognition for the condition are needed to help this cohort navigate the process of adapting to long COVID.

Source: Amanda Wurz, S. Nicole Culos-Reed, Kelli Franklin, Jessica DeMars, James G. Wrightson, Rosie Twomey. “I feel like my body is broken”: Exploring the experiences of people living with long COVID. medRxiv 2022.01.20.22269617; doi: https://doi.org/10.1101/2022.01.20.22269617 (Full text)

Multiple Early Factors Anticipate Post-Acute COVID-19 Sequelae

Summary:

Post-acute sequelae of COVID-19 (PASC) represent an emerging global crisis. However, quantifiable risk-factors for PASC and their biological associations are poorly resolved. We executed a deep multi-omic, longitudinal investigation of 309 COVID-19 patients from initial diagnosis to convalescence (2-3 months later), integrated with clinical data, and patient-reported symptoms.
We resolved four PASC-anticipating risk factors at the time of initial COVID-19 diagnosis: type 2 diabetes, SARS-CoV-2 RNAemia, Epstein-Barr virus viremia, and specific autoantibodies. In patients with gastrointestinal PASC, SARS-CoV-2-specific and CMV-specific CD8+ T cells exhibited unique dynamics during recovery from COVID-19. Analysis of symptom-associated immunological signatures revealed coordinated immunity polarization into four endotypes exhibiting divergent acute severity and PASC. We find that immunological associations between PASC factors diminish over time leading to distinct convalescent immune states. Detectability of most PASC factors at COVID-19 diagnosis emphasizes the importance of early disease measurements for understanding emergent chronic conditions and suggests PASC treatment strategies.

Source: : Su, Y., Yuan, D., Chen, D.G., Ng, R.H., Wang, K., Choi, J., Li, S., Hong, S., Zhang, R., Xie, J., Kornilov, S.A., Scherler, K., Pavlovitch-Bedzyk, A.J., Dong, S., Lausted, C., Lee, I., Fallen, S., Dai, C.L., Baloni, P., Smith, B., Duvvuri, V.R., Anderson, K.G., Li, J., Yang, F., Duncombe, C.J., McCulloch, D.J., Rostomily, C., Troisch, P., Zhou, J., Mackay, S., DeGottardi, Q., May, D.H, Taniguchi, R., Gittelman, R.M, Klinger, M., Snyder, T.M, Roper, R., Wojciechowska, G., Murray, K., Edmark, R., Evans, S., Jones, L., Zhou, Y., Rowen, L., Liu, R., Chour, W., Algren, H.A, Berrington, W.R., Wallick, J.A., Cochran, R.A., Micikas, M.E., the ISB-Swedish COVID19 Biobanking Unit, Terri Wrin, Petropoulos, C.J., Cole, H.R., Fischer, T.D., Wei, W., Hoon, D.S.B., Price, N.D., Subramanian, N., Hill, J.A, Hadlock, J., Magis, A.T., Ribas, A., Lanier, L.L., Boyd, S.D., Bluestone, J.A., Chu, H., Hood, L., Gottardo, R., Greenberg, P.D., Davis, M.M., Goldman, J.D., Heath, J.R., Multiple Early Factors Anticipate Post-Acute COVID-19 Sequelae, Cell (2022), doi: https://doi.org/10.1016/j.cell.2022.01.014. (Full text)

Chronic Fatigue and Postexertional Malaise in People Living with Long COVID: An Observational Study

Abstract:

Objectives: People living with long COVID describe a high symptom burden, and a more detailed assessment is needed to inform rehabilitation recommendations. The objectives were to use validated questionnaires to measure the severity of fatigue and compare this with normative data and thresholds for clinical relevance in other diseases; measure and describe the impact of postexertional malaise (PEM); and assess symptoms of dysfunctional breathing, self-reported physical activity, and health-related quality of life.

Methods: This was an observational study with a cross-sectional survey design (data collection from February 2021 to April 2021). Eligible participants were adults experiencing persistent symptoms due to COVID-19 that did not predate the confirmed or suspected infection. Questionnaires included the Functional Assessment of Chronic Illness Therapy-Fatigue Scale (FACIT-F) and the DePaul Symptom Questionnaire-Post-Exertional Malaise.

Results: After data cleaning, 213 participants were included in the analysis. The total FACIT-F score was 18 (SD = 10) (where the score can range from 0 to 52 and a lower score indicates more severe fatigue), and 71.4% were experiencing chronic fatigue. Postexertional symptom exacerbation affected most participants, and 58.7% met the PEM scoring thresholds used in people living with myalgic encephalomyelitis/chronic fatigue syndrome.

Conclusion: Long COVID is characterized by chronic fatigue that is clinically relevant and at least as severe as fatigue in several other clinical conditions. PEM is a significant challenge for this patient group. Because of the potential for setbacks and deteriorated function following overexertion, fatigue and postexertional symptom exacerbation must be monitored and reported in clinical practice and in studies involving interventions for people with long COVID.

Impact: Physical therapists working with people with long COVID should measure and validate the patient’s experience. Postexertional symptom exacerbation must be considered, and rehabilitation needs to be carefully designed based on individual presentation. Beneficial interventions might first ensure symptom stabilization via pacing, a self-management strategy for the activity that helps minimize postexertional malaise.

Source: Twomey R, DeMars J, Franklin K, Culos-Reed SN, Weatherald J, Wrightson JG. Chronic Fatigue and Postexertional Malaise in People Living with Long COVID: An Observational Study. Phys Ther. 2022 Jan 13:pzac005. doi: 10.1093/ptj/pzac005. Epub ahead of print. PMID: 35079817. https://pubmed.ncbi.nlm.nih.gov/35079817/

Decreased NO production in endothelial cells exposed to plasma from ME/CFS patients

Abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disease characterized by severe and persistent fatigue. Along with clinical studies showing endothelial dysfunction (ED) in a subset of ME/CFS patients, we have recently reported altered ED-related microRNAs in plasma from affected individuals. Inadequate nitric oxide (NO), mainly produced by the endothelial isoform of nitric oxide synthase (eNOS) in endothelial cells (ECs), is a major cause of ED. In this study, we hypothesized that plasma from that cohort of ME/CFS patients induces eNOS-related ED in vitro.

To test this, we cultured human umbilical vein endothelial cells (HUVECs) in the presence of either plasma from ME/CFS patients (ME/CFS-plasma, n = 11) or healthy controls (HC-plasma, n = 12). Then, we measured the NO production in the absence or presence of tyrosine kinase and G protein-coupled receptors agonists (TKRs and GPCRs, respectively), well-known to activate eNOS in ECs.

Our data show that HUVECs incubated with ME/CFS-plasma produced less NO either in the absence or presence of eNOS activators compared to ones in presence of HC-plasma. Also, the NO production elicited by bradykinin, histamine, and acetylcholine (GPCRs agonists) was more affected than the one triggered by insulin (TKR agonist). Finally, inhibitory eNOS phosphorylation at Thr495 was higher in HUVECs treated with ME/CFS-plasma compared to the same treatment with HC-plasma. In conclusion, this study in vitro shows a decreased NO production in HUVECs exposed to plasma from ME/CFS patients, suggesting an unreported role of eNOS in the pathophysiology of this disease

Source: Bertinat R, Villalobos-Labra R, Hofmann L, Blauensteiner J, Sepúlveda N, Westermeier F. Decreased NO production in endothelial cells exposed to plasma from ME/CFS patients. Vascul Pharmacol. 2022 Jan 21:106953. doi: 10.1016/j.vph.2022.106953. Epub ahead of print. PMID: 35074481. https://pubmed.ncbi.nlm.nih.gov/35074481/

Letter: Could endothelial dysfunction and vascular damage contribute to pain, inflammation and post-exertional malaise in individuals with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)?

To the Editor,

In their hypothesis paper, Wirth, Scheibenbogen, and Paul describe how endothelial dysfunction could produce a wide range of neurological symptoms in people with ME/CFS [1]. As they and others work to refine their understanding of ME/CFS and the related Long COVID syndrome, I would encourage consideration of the possibility that endothelial dysfunction and vascular damage could also explain other symptoms, including widespread pain and inflammation and post-exertional malaise.

For the past four years, my wife and I have been caregivers for our teenage daughter, who has ME/CFS, hypermobile Ehlers-Danlos syndrome, craniocervical instability, Chiari malformation and several other comorbid conditions. Through observation and trial and error, I have developed a number of hypotheses on these matters that I offer here in the hope they might prompt formal research into how to effectively treat these conditions [2].

Widespread pain and inflammation

Discussion of endothelial dysfunction and vascular damage in ME/CFS and Long COVID generally focuses on how leakages from dysfunctional blood vessels lead to reduced blood flow, which has many consequences, including reduced oxygenation of muscles and reduced cerebral brain flow. As researchers study this phenomenon, I would encourage consideration of the additional possibility that the leaking fluid causes independent damage. Lipedema researchers have found that leakages from microangiopathic blood vessels cause an excess of interstitial fluid that stimulates the formation of subcutaneous adipose tissue [3], which generates hypoxic conditions and becomes fibrotic, contributing to pain and inflammation [4].

I hypothesize that a similar process happens when fluid leaks from faulty blood vessels in ME/CFS, possibly exacerbated by endothelial dysfunction in lymphatic vessels that inhibit the fluid’s removal, causing widespread pain and inflammation. This mechanism appears most pronounced among people with hypermobility or other connective tissue disorders, a common trait among people with both ME/CFS and lipedema.

My daughter experiences pain from fibrotic adipose tissue as well as what appears to be nerve compression from accumulated interstitial / lymphatic fluid. Manual lymphatic drainage, the squeezing of affected tissue, and the manual break-up of fibrotic adipose tissue have helped to ameliorate these symptoms.

In my daughter, I have also observed impaired drainage of fluid from the glymphatic system, both at the cribriform plate and down her spine. Could this be related to damaged lymphatic vessels or blockages from fibrotic adipose tissue?

Post-exertional malaise

Like many people with moderate or severe ME/CFS, my daughter struggles to recover from even small amounts of physical exertion. In addition to mitigating her pain, manual lymphatic drainage and the squeezing of affected tissue greatly accelerates this recovery process. We have observed a direct dose–response relationship: the more exercise, the more fluid is present in her tissues, and the more manual draining / squeezing is necessary for her to recover.

Based on this experience, I hypothesize that excess interstitial fluid resulting from dysfunctional blood and lymphatic vessels contributes to the experience of post-exertional malaise, with fluid literally drowning affected tissue, leading to hypoxic conditions and inflammation. Possible explanations for the increased interstitial fluid are increases in blood pressure during physical exertion, hypermobile joints going out of place, prompting localized increases in interstitial fluid, and increases in cortisol that generate an increase in fluid and blood volume. Increases in fluid leakage due to elevated cortisol levels may also explain why some people with ME/CFS feel worse when stressed or anxious. The role of cortisol (or another mediator with fluid retaining properties) may explain why cognitive exertion can also generate post-exertional malaise. When present, elevated estrogen levels may exacerbate leakage by increasing fluid volume.

I am not sure why there is typically a delay between physical exertion and the experience of the most acute symptoms of post-exertional malaise. One possibility is that it takes time for the tissue inundated with fluid to feel the full effects of the hypoxic conditions. Another possibility is that a biphasic reaction triggered during physical exertion leads to the release of a mediator that causes heightened endothelial dysfunction and fluid release.

Further research is needed into the causes of endothelial dysfunction and damage (in addition to initial infection and inflammatory overreaction, consider major “crashes,” mast cell activations, surgeries and microclots as additional contributors) and appropriate treatment.

References

1. Wirth KJ, Scheibenbogen C, Paul F. An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. J Transl Med. 2021;19:471. https://doi.org/10.1186/s12967-021-03143-3.

Article PubMed PubMed Central Google Scholar

2. For background, see Lubell, J. To speed progress in treating chronic conditions, engage patients and caregivers as research partners. 2021 Sept.20 In: BMJ Opinion. https://blogs.bmj.com/bmj/2021/09/20/to-speed-progress-in-treating-chronic-conditions-engage-patients-and-caregivers-as-research-partners/

3. Allen M, Schwartz M, Herbst KL. Interstitial Fluid in Lipedema and Control Skin. Womens Health Rep (New Rochelle). 2020;1(1):480–7. https://doi.org/10.1089/whr.2020.0086.PMID:33786515;PMCID:PMC7784769.

Article Google Scholar

4. Herbst KL. Subcutaneous Adipose Tissue Diseases: Dercum Disease, Lipedema, Familial Multiple Lipomatosis, and Madelung Disease. [Updated 2019 Dec 14]. In: Feingold KR, Anawalt B, Boyce A, et al., editors. South Dartmouth (MA).

Source: Lubell J. Letter: Could endothelial dysfunction and vascular damage contribute to pain, inflammation and post-exertional malaise in individuals with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)? J Transl Med. 2022 Jan 24;20(1):40. doi: 10.1186/s12967-022-03244-7. PMID: 35073915. https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-022-03244-7

Nervous system consequences of COVID-19

Although severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is considered a respiratory pathogen, myriad neurologic complications—including confusion, stroke, and neuromuscular disorders—manifest during acute COVID-19. Furthermore, maladies such as impaired concentration, headache, sensory disturbances, depression, and even psychosis may persist for months after infection, as part of a constellation of symptoms now called Long Covid. Even young people with mild initial disease can develop acute COVID-19 and Long Covid neuropsychiatric syndromes. The pathophysiological mechanisms are not well understood, although evidence primarily implicates immune dysfunction, including nonspecific neuroinflammation and antineural autoimmune dysregulation. It is uncertain whether unforeseen neurological consequences may develop years after initial infection. With millions of individuals affected, nervous system complications pose public health challenges for rehabilitation and recovery and for disruptions in the workforce due to loss of functional capacity. There is an urgent need to understand the pathophysiology of these disorders and develop disease-modifying therapies.

Read the rest of this article HERE.

Source: Serena Spudich and Avindra Nath. Nervous system consequences of COVID-19. Science, Volume 375 | Issue 6578, 21 January 2022.

Researchers highlight COVID-19 neurological symptoms and need for rigorous studies

Press Release, NINDS/NIH, Jan 20, 2022:

SARS-CoV-2 was initially identified as a respiratory virus, but it can affect the entire body, including the nervous system. In a new Viewpoint published in Science, Avindra Nath, M.D., clinical director of the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS), and Serena Spudich, M.D., Yale School of Medicine, New Haven, Connecticut, highlight what is currently known about the effects of SARS-CoV-2 on the brain, the importance of increased research into the underlying causes of Long Covid and possible ways to treat its symptoms.

Neurological symptoms that have been reported with acute COVID-19 include loss of taste and smell, headaches, stroke, delirium, and brain inflammation. There does not seem to be extensive infection of brain cells by the virus, but the neurological effects may be caused by immune activation, neuroinflammation, and damage to brain blood vessels.

Acute COVID-19 infection can sometimes lead to long-lasting effects, that have collectively been termed “Long Covid,” and can include a wide variety of symptoms in the brain and nervous system that range from a loss of taste and smell, impaired concentration, fatigue, pain, sleep disorders, autonomic disorders and/or headache to psychological effects such as depression or psychosis.

Drs. Nath and Spudich outline the current scientific understanding of the potential body responses to acute COVID-19 infection and how those responses could lead to Long Covid symptoms. They also draw parallels between the symptoms experienced by individuals with Long Covid to those living with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) or post-Lyme disease, which suggests there could be common risk factors involved.

Finally, owing to the significant variability in symptoms from person to person and the fact that many individuals with Long Covid were healthy prior to a relatively mild COVID-19 infection, the authors highlight the urgent need for significant research efforts into identifying the full extent of Long Covid complications and their causes. This kind of research, which would include the careful study of individuals with Long Covid categorized by their specific symptoms, is crucial to the development of diagnostic and therapeutic tools to identify and treat what is becoming an ever-increasing public health concern. The NIH RECOVER COVID initiative is an ambitious research program to reach these goals.

WHO:

Avindra Nath, M.D., clinical director, NINDS. To arrange an interview, please contact NINDSPressTeam@ninds.nih.gov.

ARTICLE:

Spudich S. and Nath A. “Nervous system consequences of COVID-19” Science. January 21, 2022. DOI: 10.1126/science.abm2052.