Since the first-reported case of Severe Acute Respiratory Distress Syndrome-Coronavirus 2 in December 2019, COVID-19 has caused a global pandemic associated with significant morbidity and mortality. After a year of advances in vaccine research and development, three vaccines for the prevention of COVID-19 (manufactured by Pfizer, Moderna and Johnson & Johnson's Janssen Biotech) are approved for use in the USA. We report the first case of Guillain-Barre Syndrome after receiving the second dose of the Pfizer COVID-19 vaccine, in a 42-year-old woman presenting with progressive ascending weakness and paresthesias. Diagnostic workup demonstrated cytoalbuminologic dissociation on cerebrospinal fluid analysis with confirmatory evidence of early demyelinating electrodiagnostic features on nerve conduction study and an extensive serological workup being negative for other viral or autoimmune disease triggers. Management included administration of intravenous immunoglobulin (total of 2 gm/kg), with frequent monitoring of forced vital capacity and negative inspiratory force. A longitudinal risk profile of neurologic complications caused from COVID-19 vaccines remains limited, and prompt recognition of potential neurological complications from the COVID-19 vaccine is of interest to public health.

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HIV-sensory neuropathy (HIV-SN) is a debilitating complication in HIV patients with or without anti-retroviral treatment (ART). Common symptoms of HIV-SN include pain, decreased sensation, paresthesias and dysesthesias in a symmetric stocking-glove distribution. While HIV-1 protein such as gp120 is implicated in HIV-SN (e.g. impaired large-diameter fiber), ART itself was recently shown to contribute to HIV-SN in HIV patients and impair thin fiber. Multiple host mechanisms may play roles during the pathogenesis of HIV-SN, including neuron-glia interactions in the spinal dorsal horn (SDH), inflammation, mitochondrial dysfunction and endoplasmic reticulum stress. Concurrent infections, such as tuberculosis, also carry a higher likelihood of HIV-SN as well as environmental or genetic predisposition. Pro-inflammatory cytokines such as IL-1, IL2 receptor-alpha and tumor necrosis factor (TNF) along with abnormal lactate levels have been identified as potential players within the complex pathophysiology of this condition. In this paper, we review the pathophysiology of HIV neuropathy, focusing on the various treatment options available or under investigation. Although several treatment options are available e.g., the capsaicin patch and spinal cord stimulation, symptomatic control of HIV-SN are often challenging. Alternative approaches such as self-hypnosis, resistance exercise, cannabinoids, and acupuncture have all shown promising results, but need further investigation.

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