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A Case Study Evaluating the Impact of Chelation Therapy on the Progression of Dementia

      Introduction

      There is a growing body of evidence that supports the fact that heavy metal exposure can cause neurological sequelae like dementia. Chelation therapy has been shown to improve symptoms in some dementia patients. We describe in our case report Mr. TN, a 66 year old Caucasian male who worked as a welder in shipyards and power plants over several decades. He was admitted to our psychiatric in-patient unit for dementia with behavioral disturbances. He needed assistance with his ADLs and was mostly mute. His medical history was significant for hyperlipidemia and had no other significant past psychiatric history. According to his wife, TN suffered from mild memory deficits since 2004 and difficulties with calculation since 2008. In 2010 was when he first saw a neurologist as he had some vision changes and there was a concern that it could be amaurosis fugax. The neurologist ordered hair toxicology studies given TN's occupational history. Results showed significant levels of uranium, cadmium, aluminum, arsenic, and mercury. Cadmium level was at the 95th percentile.

      Methods

      TN began weekly chelation therapy with EDTA in the fall of 2010. Approximately 7 months later the patient ended EDTA treatment and began receiving DMPS. Within two months of beginning DMPS the patient had begun to experience markedly increased irritability, agitation, paranoia, worsening of cognitive deficits, and steep decline in functioning. Chelation therapy was discontinued in October 2011. Cognitive decline and personality changes did not improve after cessation of therapy, and within the next three months the patient began to become aggressive and was subsequently diagnosed with dementia in March 2012.

      Results

      The progression of the patient's personality changes and memory deficits occurred in the absence of infection, major medical problems, stress or cerebrovascular accident, which are the common precipitators of rapid cognitive decline in dementia. By January 2012 TN had developed a marked change in his speech and was experiencing outbursts of anger which resulted in property destruction. He was hospitalized at that time, treated for UTI and improved on Risperdal, Aricept, and Flomax. He was discharged to a skilled nursing facility. He could no longer be managed by his family. It was at this skilled nursing facility where he became aggressive and the symptoms prompted his current admission.

      Conclusions

      Because of this unusual presentation, we did a literature search about chelation therapies and dementia. Our search did not yield any studies positively associating chelation therapy with rapid cognitive decline in dementia patients; to the contrary, chelation therapy has previously been shown to improve symptoms in some dementia patients. However, this case suggests that we need more randomized double blind studies to justify the use of chelating agents in chronic neurodegenerative illnesses.