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Manganese Neurotoxicity as a Complication of Chronic Total Parenteral Nutrition
Alisha Khan1, Jonathan Hingre2, Amit S Dhamoon1
1Department of Medicine, SUNY Upstate Medical University, Syracuse, NY, USA.
Abstract:
Manganese accumulation in the central nervous system creates clinical symptoms of cognitive dysfunction, behavioral changes, and movement disorders resembling Parkinson's disease. Radiographic features of this rare clinical entity include symmetric T1 hyperintensities in the bilateral globus pallidi, with corresponding hypointensities on T2-weighted images. Total parenteral nutrition (TPN) is an increasingly used potentially lifesaving therapy for patients who cannot tolerate enteral nutrition. However, when used over a period of several weeks to months, its associated risks and complications carry significant morbidity and mortality. One of the more rare complications of TPN use is manganese toxicity. We provided care for a 38-year-old female on chronic TPN who presented to the hospital with Parkinsonian features, confusion, falls, and lethargy. MRI brain showed T1 hyperintensities in the bilateral globus pallidi, which were attributed to manganese toxicity from chronic TPN use. Supporting evidence for this rare entity included decreased signal intensity in the bilateral globus pallidi on T2-weighted images and T1 hyperintensities in the substantia nigra. With antifungal treatment and permanent cessation of TPN, her mentation and neurological symptoms began to improve within a week. Repeat MRI brain performed one month after discontinuation of TPN revealed improvement of the T1 hyperintensities in the bilateral globus pallidi. Our objective in presenting this case is to highlight manganese neurotoxicity as a rare complication of TPN in a patient without known hepatic dysfunction and to emphasize the importance of routinely monitoring patients for the possible adverse effects of chronic TPN. Our case is among the handful of published cases in which a patient without known liver dysfunction, which is the primary organ responsible for manganese elimination from the body, developed manganese neurotoxicity.
Insights
Manganese toxicity from long-term total parenteral nutrition (TPN) can cause Parkinsonian symptoms and cognitive changes. Early detection and TPN cessation can lead to symptom improvement, even without liver dysfunction.
Area of Science:
- Neurology
- Toxicology
- Radiology
Background:
- Total parenteral nutrition (TPN) is a life-saving therapy for patients unable to use enteral nutrition.
- Chronic TPN use, especially for weeks to months, carries risks including rare manganese toxicity.
- Manganese accumulation in the central nervous system can mimic Parkinson's disease symptoms.
Observation:
- A 38-year-old female on chronic TPN presented with Parkinsonian features, confusion, falls, and lethargy.
- Brain MRI revealed T1 hyperintensities in the globus pallidi and substantia nigra, with T2 hypointensities in the globus pallidi.
- These radiographic findings were consistent with manganese neurotoxicity.
Findings:
- The patient's symptoms improved within a week after antifungal treatment and permanent cessation of TPN.
- Follow-up MRI showed resolution of T1 hyperintensities in the globus pallidi one month after TPN discontinuation.
- This case highlights manganese neurotoxicity in a patient without known hepatic dysfunction, the primary organ for manganese elimination.
Implications:
- Manganese neurotoxicity is a rare but serious complication of chronic TPN.
- Routine monitoring for TPN adverse effects is crucial, particularly in patients without liver dysfunction.
- This case underscores the importance of considering manganese toxicity in patients with unexplained neurological symptoms while on TPN.
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