Abstract

INTRODUCTION: Manganese (Mn) is an essential element for human health found in nuts, grains, and legumes. Toxic levels can result in parkinsonian features, due to damage to the dopaminergic neurons of the basal ganglia and gliosis. Common causes for toxicity include occupational hazards such as welding, steel industry and ingestion of contaminated water. CASE DESCRIPTION/METHODS: A 55 year old woman with a history of decompensated alcohol related cirrhosis, presented to the ER with a three week history of worsening neck pain and generalized weakness. Physical examination revealed bradykinesia, dysarthria, and dystonia of the neck. She had severe motor weakness and was unable to feed herself or ambulate independently. She denied any hematemesis, hematochezia or melena. The patient had been started by her PCP on Levodopa-Carbidopa 2 weeks prior to admission for these Parkinson like symptoms. Her labs showed anemia with hemoglobin of 7.4 g/dL, ferritin was 5 ng/mL and 20% transferrin saturation. Folate, thiamine and vitamin B12 levels were normal. MRI of the brain revealed T1-weighted signal hyperintensity of the globus pallidus bilaterally. EGD showed small varices and mild PHG, colonoscopy showed internal hemorrhoids and 2 small polyps, no active GI bleeding was seen. Multiple heavy metal levels were checked and blood Mn was elevated to 24.1 ug/L (normal 4.2-16.5). The patient’s symptoms improved following the two week course of Levodopa-Carbidopa prior to discharge. DISCUSSION: Pallidal signal hyperintensity on T1-weighted MRI has been well described in patients with Parkinson’s disease and in patients with Mn toxicity. Increased Mn levels have been reported in patients with cirrhosis and may result from decreased uptake by the liver and increased portosystemic shunting. Although hepatic encephalopathy can present with a large array of neurologic symptoms, the severity of our patient’s neck pain that brought her to the ED and her profound weakness had prompted more thorough workup. Furthermore, Mn and iron share similar mechanisms of absorption and transport, which allows for Mn to influence iron homeostasis and vice versa. Some studies have shown that iron deficiency can lead to accumulation of Mn in the blood and reduce enzymatic protective effect from Mn-induced oxidative stress. It is possible that the concurrent iron deficiency anemia in our patient has led to increased levels of Mn. Early recognition of these findings especially in presence of iron deficiency may warrant evaluation for Mn toxicity.Figure 1.: Hyperintense globi pallidi on T1-weighted magnetic resonance imaging.

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