P-034 - (Poster #34) An Exploration of Painful Neuropathy in the Context of Long Covid: Mechanisms, Manifestations, and Management

Long Covid, the prolonged sequelae of SARS-CoV-2 infection, has been associated with a myriad of symptoms, including neurological manifestations such as painful neuropathy. This paper reviews the current understanding of painful neuropathy in Long Covid patients, exploring the potential mechanisms, clinical presentations, and therapeutic strategies. We discuss the implications of these findings for both clinical practice and future research.

Purpose/Objectives:

The global spread of SARS-CoV-2 has led to an unprecedented health crisis, with Long Covid emerging as a significant concern. Among the myriad symptoms, painful neuropathy has been reported with increasing frequency, suggesting a direct or indirect neuropathological effect of the virus or its aftermath. This review aims to shed light on this aspect of Long Covid.

Methods:

A comprehensive literature search was conducted using PubMed, Google Scholar, and Scopus databases with keywords including "Long Covid," "painful neuropathy," "neuropathic pain," "SARS-CoV-2," and "neurological complications." Only peer-reviewed articles published in English were considered. Additionally, we included three case studies featured in various journals to highlight different patient experiences and outcomes related to neuropathy in Long Covid.

Results:

The advent of the global SARS-CoV-2 pandemic has brought with it a host of new medical challenges, one of which is Long Covid, characterized by prolonged symptoms long after the initial infection. Among these symptoms, neuropathy or nerve damage has become increasingly recognized, posing significant quality-of-life issues for affected individuals.

Long Covid, or post-acute sequelae of SARS-CoV-2 infection (PASC), encompasses a wide array of symptoms persisting or appearing after the initial infection has resolved. Neurological symptoms, including neuropathy, have been reported in 8.8% to 76.6% of Long Covid cases according to various studies (Nalbandian et al., 2021). The mechanisms behind these effects are multifaceted. Evidence suggests that SARS-CoV-2 might directly infect neural tissue, leading to inflammation or direct nerve damage (Dixon et al., 2021).

Post-infectious immune dysregulation might trigger autoimmune responses against neural tissues (Bohmwald et al., 2022). The virus's affinity for ACE2 receptors in endothelial cells could lead to microvascular dysfunction, impacting nerve health (Varga et al., 2020). Systemic inflammation or cytokine storms may contribute to nerve damage or increased sensitivity (Taquet et al., 2021).

Anticonvulsants, namely gabapentin or pregabalin, antidepressants such as amitriptyline, and multiple topical agents have been used with varying success. Physical therapy, cognitive-behavioral therapy for pain management, and lifestyle modifications are suggested. Research into immunomodulatory drugs or treatments targeting specific pathways of nerve damage or pain signaling potentially offers future relief.

There is evidence suggesting that SARS-CoV-2 could directly infect peripheral nerves, leading to axonal damage or inflammation. Post-infectious immune dysregulation might lead to autoimmune reactions against neural tissues. Endothelial dysfunction and resultant microvascular damage could impair nerve nutrition and function. Systemic inflammation or specific cytokine storms might contribute to nerve damage or increased sensitivity.

There are multiple diagnostic challenges. Symptoms of neuropathy in Long Covid can mimic those from diabetes, vitamin deficiencies, or other post-viral syndromes. Current diagnostics rely heavily on clinical symptoms and exclusion of other causes rather than specific markers for Long Covid- induced neuropathy.

Conclusions/Implications for future research and/or clinical care:

Painful neuropathy as part of Long Covid presents a significant challenge to healthcare systems worldwide. While current treatments focus on symptomatic relief, understanding the underlying mechanisms could lead to more targeted therapies. Future research should aim at defining biomarkers for diagnosis, predicting who is at risk, and exploring novel therapeutic approaches.