Objective: Characterization of rural elderly patients from farming communities in the coastal plains of Southwest Georgia, United States with cognitive impairment, mood disturbance, gait disturbance, bone demineralization and manganese (Mn) elevations in plasma. Design: Case series Materials & Methods: LabCorp (Birmingham, Alabama) measured manganese and other heavy metal levels in whole blood, plasma, and urine using inductively coupled plasma-mass spectrometry. Results: Six African-American patients, 2 males, 4 females, mean age 63.5 ± 16.5 with postgraduate education displayed: depressed mood; irritability; migraine with aura; exaggerated startle responses; poor concentration; acalculia, visual-spatial impairment; phonemic errors; right-left confusion in some cases; dysgraphia or agraphia; complex partial seizures; weakness of proximal muscles in shoulder and hip girdles; bradykinesia; retropulsion; impaired tandem walking; bruxism, sleep automatisms, sleep myoclonus, and periodic limb movements. Bone demineralization in weight bearing bones, e.g. pelvis, required hip replacement in some. Mean ± SE plasma Mnp = 6.7 ± 0.7 (reference norm < 2.5 mg/L); urine Mnp = 5.4 ± 2.6 (reference norm < 2.5 mg/L); urine Mn/urine Cr ratio = 4.75 ± 0.5 (reference norm < 3.0). Whole blood MnB was 13.5 ± 2.7 mg/L (reference norm < 18.7 mg/L) elevated in only 2 of 6. Manganese is excreted in the bile and stool, yet renal fractional excretion of Mn was 65.0 ± 11.1 %. (These data excluded a 92 year old outlier: MnB = 10.8 mg/L; Mnp = 5.3 mg/L; Mnu = 16.1 mg/L; Mnu /Cru ratio = 33.5; fractional excretion = 696 %). Conclusions: Manganese causes parkinsonism that does not respond to dopamine agonists. T1 weighted MRI of the brain detects Mn deposits in the basal ganglia. Visuospatial impairment and other features of parietal lobe dysfunction not generally associated with manganism but characteristic of Gerstmann syndrome (finger agnosia, agraphia, acalculia, right-left confusion) without finger agnosia may be unique. Oral exposure to Mn causes rickets by binding to phosphorous in the intestines; demineralization of bone is an unusual finding in airborne occupational manganism raising consideration for oral exposure. Plasma Mn elevations might be artifact, but, other metals assayed by inductively coupled plasma-mass spectrometry (e.g., nickel, cadmium, mercury) as well as lead and arsenic were not detected. Furthermore, these findings were consistent when submitted to ARUP (Salt Lake City, Utah). Yet, the laboratory findings do not reconcile with classical manganism since whole blood Mn was not elevated. Recent studies link exposure to elevated serum Mn levels and demonstrate neuropsychological impairment at MnB ³ 7 mg/L (i.e., within present reference ranges emphasizing a need for functional norms). There is a need for epidemiological research to adjust for confounding factors (e.g., heterogeneity of clinical stage; cumulative exposure; unknown point source of exposure; exposure to herbicides, fungicides, insecticides, and fertlizers) to substantiate Mn as a unifying etiology. Elevated plasma Mn may possibly reflect efflux or displacement by an unidentified element competing for the divalent metal transporter DMT1.
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