BMC neurology · 2025
Delayed emergence of parkinson's disease after reversible manganese-induced parkinsonism: a case report.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Shin Hae-Won
Аннотация
BACKGROUND: Chronic manganese (Mn) exposure, particularly in occupational settings such as welding, can lead to Mn-induced parkinsonism, a condition typically considered reversible and distinct from idiopathic Parkinson's disease (PD). However, the neurotoxic effects of Mn may contribute to or accelerate dopaminergic degeneration in susceptible individuals.
CASE PRESENTATION: We report the case of a 53-year-old male welder who initially presented with symmetrical parkinsonism and characteristic T1 hyperintensities in the globus pallidus in Brain MRI, consistent with Mn-induced parkinsonism. Symptoms and Brain MRI abnormalities fully resolved one year after cessation of Mn exposure. Three years later, the patient developed new, progressive, and asymmetric parkinsonian symptoms, including a unilateral resting tremor and bradykinesia. 18- fluoropropyl-2β-carbomethoxy-3β-4-iodophenyl nortropane positron emission tomography imaging demonstrated a marked reduction in striatal dopamine transporter uptake, and the patient responded well to levodopa, confirming the diagnosis of idiopathic PD.
CONCLUSIONS: This case illustrates a rare longitudinal transition from reversible Mn-induced parkinsonism to idiopathic PD, suggesting that prior Mn exposure may act as a precipitating or accelerating factor for PD pathogenesis. Functional neuroimaging is critical for differentiating between these two syndromes. This report underscores the importance of long-term neurological follow-up in patients with occupational Mn exposure and supports the hypothesis that environmental toxins can contribute to neurodegenerative processes.
CASE PRESENTATION: We report the case of a 53-year-old male welder who initially presented with symmetrical parkinsonism and characteristic T1 hyperintensities in the globus pallidus in Brain MRI, consistent with Mn-induced parkinsonism. Symptoms and Brain MRI abnormalities fully resolved one year after cessation of Mn exposure. Three years later, the patient developed new, progressive, and asymmetric parkinsonian symptoms, including a unilateral resting tremor and bradykinesia. 18- fluoropropyl-2β-carbomethoxy-3β-4-iodophenyl nortropane positron emission tomography imaging demonstrated a marked reduction in striatal dopamine transporter uptake, and the patient responded well to levodopa, confirming the diagnosis of idiopathic PD.
CONCLUSIONS: This case illustrates a rare longitudinal transition from reversible Mn-induced parkinsonism to idiopathic PD, suggesting that prior Mn exposure may act as a precipitating or accelerating factor for PD pathogenesis. Functional neuroimaging is critical for differentiating between these two syndromes. This report underscores the importance of long-term neurological follow-up in patients with occupational Mn exposure and supports the hypothesis that environmental toxins can contribute to neurodegenerative processes.