Neurologic manifestations in welders with pallidal MRI T1 hyperintensity

Abstract

Abstract-Background: Neurologic symptoms have been attributed to manganese fumes generated during welding. Increased T1 MRI signal in the basal ganglia is a biologic marker of manganese accumulation. Recent studies have associated welding and parkinsonism, but generally without MRI corroboration. Objective: To characterize the clinical and neuropsychological features of patients with MRI basal ganglia T1 hyperintensity, who were ultimately diagnosed with neurotoxicity from welding fumes. Methods: The medical records of welders referred to the Department of Neurology with neurologic problems and basal ganglia T1 hyperintensity were reviewed. Results: All eight patients were male career welders with increased T1 basal ganglia signal on MRI of the brain. Several different clinical syndromes were recognized: a parkinsonian syndrome (three patients), a syndrome of multifocal myoclonus and limited cognitive impairment (two patients), a mixed syndrome with vestibular-auditory dysfunction (two patients), and minor subjective cognitive impairment, anxiety, and sleep apnea (one patient). Neuropsychometric testing suggested subcortical or frontal involvement. Inadequate ventilation or lack of personal respiratory protection during welding was a common theme. Conclusions: Welding without proper protection was associated with syndromes of parkinsonism, multifocal myoclonus, mild cognitive impairment, and vestibular-auditory dysfunction. The MRI T1 hyperintensity in the basal ganglia suggests that these may have been caused by manganese neurotoxicity. NEUROLOGY 2005;64:2033-2039 Welding utilizes an electric arc to melt and bond metals. Fumes with high concentrations of aerosolized metals generated by welding may cause systemic as well as neurologic problems.1-4 Although many elemental metals are released in welding plumes, the neurotoxicity is presumed to be primarily mediated by manganese. [5][6][7][8][9] Manganese neurotoxicity presents commonly as a parkinsonian syndrome 7,8,10,11 and has been reported to be associated with welding. 5,12 A biologic marker of manganese accumulation within the CNS is bilaterally increased T1 MRI signal within the basal ganglia, especially the globus pallidus, but also the striatum.1,13-18 Although T1 signal changes in these nuclei may be seen in several other conditions (e.g., nonketotic hyperglycemic episodes, hypoxia, neurofibromatosis, and other paramagnetic ions), it is an uncommon pattern. When the T1 hyperintensity is confined to the lentiform nuclei, and in the appropriate clinical setting, it has relative specificity for brain manganese. This MRI appearance suggests that the ambient fume intensity has been sufficient to affect the brain. Although an association between welding and parkinsonism has been postulated in two recent clinical series, the MRI scans in these patients were either normal or not reported. 5,12We report eight patients referred for neurologic evaluation and diagnosed with neurotoxicity from welding fumes. All had chronic and intense exposure to ambient welding fum...

Brain magnetic resonance imaging and manganese concentrations in red blood cells of smelting workers: Search for biomarkers of manganese exposure

“…Most studies prior to this work on MRI and Mn exposure were conducted on exposed welders (Josephs et al, 2005;Kim et al, 1999c;Nelson et al, 1993;Ono et al, 2002). Since the welding fumes generated during the welding process possesses at least 13 metals (Li et al, 2004), the exposure to multiple metals, notably iron (Fe), may complicate the exposure scenario for accurate assessment of Mn exposure.…”

Quantitative magnetic resonance imaging in patients with cirrhosis: a cross-sectional study

“…Thus, increases in manganese concentrations have been observed in whole blood and CSF in these patients (Katsuragi et al, 1999; Kreiger et al, 1995;Spahr et al, 1996) and in pallidal tissue obtained at post-mortem (Krieger et al, 1995; PomierLayrargues et al, 1995; Rose et al, 1999). In addition, strong collateral evidence is provided by observations in individuals with chronic manganese toxicity, resulting from industrial exposure (Nelson et al, 1993;Josephs et al, 2005) or long-term parenteral nutrition (Mirowitz et al, 1991), who show similar cerebral T1 signal abnormalities w h i c h reverse with specific therapy or cessation of long-term nutritional support (Mirowitz et al, 1991;Mirowitz & Westrich 1992;Nelson et al, 1993;Nagatomo et al, 1999). …”

“…The observation that the reduction in MTR rapidly improves after liver transplantation (Cordoba et al 2001) may be supportive of the manganese deposition hypothesis, as cholestasis, which is also associated with pallidal manganese deposition, improves post-transplantation. However, the observation that in occupational manganese exposure the resolution in cerebral pallidal T1 hyperintensity is much slower (Josephs et al 2005) suggests that this is a more complex issue.Low grade cerebral/cellular oedema is often cited as the explanation for reduced MTRs in patients with cirrhosis (Balata et al 2003; Cordoba et al 2001;Miese et al 2006; Poveda et al, 2010;Rovira et al 2001). This is supported by the finding of reduced intracellular levels of the cerebral osmolyte myo-inositol (mI), reported in 1 H MRS studies (Häussinger et al 2000).…”

Protective effects of dietary fibre against manganese-induced neurobehavioral aberrations in rats

“…Excessive chronic exposure to Mn can cause progressive and persistent neurodegenerative damage associated with numerous psychiatric and motor disturbances, resembling the idiopathic Parkinson's disease. The syndrome includes tremor, postural instability, bradykinesia, gait disturbance, rigidity, ataxia, and even cognitive defi cits (1,4). Among these symptoms, cognitive defi cits such as spatial working memory, reference memory, and learning capacity disorders have received less attention than motor function disorders.…”

“…Among these symptoms, cognitive defi cits such as spatial working memory, reference memory, and learning capacity disorders have received less attention than motor function disorders. Josephs et al (4) reported reduced learning capacity in occupationally Mn-exposed welders, and Schneider et al (5) found that monkeys developed subtle defi cits in spatial working memory after exposure to MnSO 4 .…”