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Background The management of people living with HIV (PLWH) lost to follow-up can be challenging especially due to the possible onset of opportunistic infections. However, sometimes even in these individuals clinical scenarios can be not related to HIV infection but explained by the patient’s medical history or habits.Case presentation We present the case of a 53-year-old man living with HIV since 2013 who was lost to follow-up in 2022 (at his last evaluation, HIV RNA was undetectable and CD4+ count was 586 cells/mm 3). In May 2025 the individual presented to the Emergency Department due to weight loss (approximately 24 kg over three months), impaired hand-eye coordination, ideomotor slowing and lower limb weakness. During hospitalization viroimmunological restaging was performed: HIV RNA was 648,000 copies/mL and CD4+ count was 1 cell/mm3 (ratio CD4+/CD8+ 0).All microbiological and radiological investigations ruled out AIDS-related conditions and other common causes of neurological symptoms. Brain MRI, chest and abdominal CT scan, quantiferonTB, cryptococcal antigen, CMV-DNA and CSF studies were negative, except for CSF HIV-RNA (46 copies/mL). After exclusion of opportunistic diseases, cART with BIC/TAF/FTC was reintroduced.Neuropsychological assessment was performed to investigate ideomotor slowing: tests confirmed impaired cognitive and executive function with marked ideational and ideomotor retardation.During the hospital stay a package containing undefined seeds, imported from Nepal, was found at the individual’s bedside. The person, as part of his customary practices, had been taking this supplement daily for an indeterminate period of time. One tablet was sent to the Toxicologic reference centre to identify its components and a high concentration of manganese was detected (36 μg/g). This supplement was therefore discontinued with progressive significant improvement of neurological symptoms. At discharge HIV-RNA was 1,000 copies/mL and CD4+ count was 23 cells/mm3.At a follow-up visit three months after discontinuation of his daily supplement no new neurological symptoms were reported and slight improvement in the neurocognitive profile was confirmed by neuropsychological testing. The patient had gained 5 kg and VL was undetectable.Discussion and Conclusions Manganese excess is known to cause neurotoxic effects due to its accumulation in the basal ganglia of the brain, a deposition that is not always radiologically detectable. This accumulation may lead to neurological manifestations ranging from slowed reactions and impaired hand–eye coordination to a Parkinsonism-like syndrome. However, similar symptoms may also be caused by opportunistic conditions typically observed in people living with HIV who discontinue antiretroviral therapy. Therefore, a correct evaluation of patient’s habits and medical history, together with tests for opportunistic infections, may be needed to investigate every possible cause of neurologic deterioration.