SLE is a multisystem autoimmune disorder and can result in end-organ damage. MNM is a type of painful and asymmetric mixed sensory and motor peripheral neuropathy. It is defined as lesions affecting two or more nerves that cannot be explained by a single root or plexus injury. MNM is a complication of the vasculitic process affecting the small and medium sized vasculature through autoantibody deposition and cell infiltration.

The pathophysiology of SLE involves environmental triggers in genetically predisposed individuals resulting in autoimmune activation. In SLE, T cells show abnormal gene expression, driving defective T-cell activity and activating autoreactive B cells. This leads to autoantibody production, immune complex deposition, complement activation, and widespread tissue damage, including to the neurovascular unit. Although this patient was adherent to hydroxychloroquine, low dose daily prednisone, and anifrolumab-fnia infusions, she ultimately developed disease progression to include MNM and required targeted therapy.

This case underscores the neurological manifestations of SLE, with particular focus on its impact to the peripheral nervous system. The development of progressive, asymmetric neuropathy in the context of active lupus should raise clinical suspicion for MNM. Early initiation of immunosuppressive therapy is critical in preventing irreversible neurological damage and mitigating potentially life-threatening complications.