Background <p>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.</p> Case presentation <p>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.</p> Conclusions <p>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.</p>

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Delayed emergence of parkinson’s disease after reversible manganese-induced parkinsonism: a case report

  • Hae-Won Shin

摘要

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.