Some reports have emerged describing the occurrence of Guillain-Barré syndrome and polyneuropathy related to vitamin B(12) deficiency in some patients with Parkinson's disease (PD) treated with continuous duodenal levodopa infusion. We describe five PD patients who developed axonal polyneuropathy and vitamin B(12) deficiency while on treatment with duodenal levodopa infusion, review other cases reported in the literature, discuss potential etiologic factors, and suggest a possible algorithm for the management and prevention of this complication. One case of Guillain-Barré syndrome and at least 12 cases of polyneuropathy related to vitamin B(12) deficiency have been reported in PD patients treated with duodenal levodopa infusion. Levodopa gel infusion may induce a decrease in vitamin B(12) levels, leading to peripheral neuropathy. Additional pathogenetic mechanisms include alterations related to the metabolism of L: -dopa, abnormal L: -dopa absorption, and direct neurotoxicity of L: -dopa at high doses. Vitamin B(12) supplementation may need to be considered in PD patients on duodenal levodopa infusion therapy. Vitamin B(12) deficiency in patients on duodenal levodopa infusion therapy may be more frequent than the published data suggest. We must be alert.
Mancozeb is a ethylene-bis-dithiocarbamate (EBDC) fungicide that contains zinc and manganese. 1 In humans, chronic EBDC inhalation has been associated with neurocognitive impairment and parkinsonism 2 while acute intoxication elicit reversible headache, dizziness, and seizures in a few cases, all of which were rapidly reversible. 3 We report a case of severe and reversible parkinsonism in a man after the accidental oral ingestion of mancozeb.A 55-year-old man with history of alcohol abuse was admitted with a 4 days alcohol withdrawal. At examination, he was found to be alert, oriented, and showed postural tremor and diaphoresis. Treatment with tiapride (300 mg/day during 4 days) and thiamine was started. On the fourth day of hospitalization, he was diagnosed of acute cholecystitis and was surgically treated. Seven days later, he was found to be confused. At physical examination, the patient was alert, slow minded, and disoriented. He had a masked facies (video, segment 2) dysarthria and hypophonia resulting in his speech being unintelligible. He was noted to have poverty and slowness of movements (video, segment 2) and generalized cogwheel rigidity (video, segment 1), particularly in the jaw. His posture was stooped and he was unable to walk without assistance (video, segment 3). Bilateral resting tremor and isolated reflex myoclonus were observed. Startle reflex was pathologic. All deep tendon reflexes were brisk. He recognized having intake accidentally 5 g of a vegetable fungicide containing mancozeb.Laboratory test showed normal concentrations of blood glucose, creatinine, alkaline phosphatise, total bilirrubin, aspartate aminotransferase, and alanine aminotransferase level. c-Glutamyl transferase was 112 U/L (normal range 6-38). Hepatitis B and C serologies were negative. Serum ammonium was within normal range but serum or urine manganese was not assessed. Cerebral magnetic resonance (MR) showed moderate generalized atrophy. Electroencephalogram was normal. SPECT examination using [ 123 I]FP-CIT showed a normal dopamine transporter (DAT) uptake in both putamen. Levodopa-carbidopa therapy was initiated with no motor improvement and was interrupted few weeks later. During the following 8 months, the neurological symptoms spontaneously remitted and 16 months later, he was still abstinent and without signs of parkinsonism.
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