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Updated: Mar 26, 2026
Functional Neuroimaging Using Ultrasonic Blood-brain Barrier Disruption and Manganese-enhanced MRI
Published on: July 12, 2012
MRI pallidal signal in children exposed to manganese in drinking water
Laurie-Anne Dion1, Maryse F Bouchard2, Sébastien Sauvé3
1Department of Psychology, Université du Québec à Montréal, Québec, Canada; Sainte-Justine University Hospital Research Center, Montréal, Québec, Canada.
Background:
Manganese (Mn) can have neurotoxic effects upon overexposure. We previously reported poorer cognitive and motor development in children exposed to Mn through drinking water, suggesting possible neurotoxic effects from Mn in water. Hyperintensity in the globus pallidus (GP) on T1-weighted magnetic resonance imaging (MRI) indicates excessive brain Mn accumulation. Previous studies have reported GP hyperintensity related to Mn exposure in occupationally exposed individuals. However, no study has used MRI in children exposed to Mn in drinking water and who show no sign of overt intoxication.
Objective:
To examine MRI signal intensity in the GP in children exposed to contrasted levels of Mn in drinking water.
Methods:
We enrolled 13 children exposed to low Mn concentration in water and 10 children (ages 9-15 years) with high concentration (median of 1 and 145μg/L, respectively). We calculated three MRI T1 indexes: (i) standard pallidal index (PI) using frontal white matter as reference; (ii) PI using pericranial muscles as reference; and (iii) T1 relaxation time. Each MRI index was compared between exposure groups, and with respect to the estimated Mn intake from water consumption.
Results:
The standard PI did not differ between Mn-exposure groups. However, children in the group with high water-Mn concentration had significantly lower pericranial muscles PI than those with lower exposure and, accordingly, higher T1 relaxation time. Mn intake from water consumption was not correlated with the standard PI, but was significantly related to the pericranial muscles PI and T1 relaxation time. Motor performance was significantly lower in the high-exposure group.
Conclusion:
We observed lower signal intensity in the GP of children with higher exposure to Mn from drinking water. This result stands in contrast to previous MRI reports showing GP hyperintensity with greater Mn exposure. Differences in exposure pathways are discussed as a potential explanation for this discrepancy.
Insights
Children exposed to higher manganese (Mn) levels in drinking water showed lower globus pallidus (GP) signal intensity on MRI scans. This contrasts with previous findings and may be linked to different exposure routes, impacting motor performance.
Area of Science:
- Neuroscience
- Environmental Health
- Radiology
Background:
- Manganese (Mn) overexposure can cause neurotoxicity.
- Previous studies linked Mn in drinking water to developmental issues in children.
- Globus pallidus (GP) T1-weighted MRI hyperintensity suggests brain Mn accumulation, but studies in children with low-level water exposure are lacking.
Purpose of the Study:
- To investigate MRI signal intensity in the GP of children with varying manganese (Mn) exposure levels from drinking water.
Main Methods:
- Enrolled children (ages 9-15) into low (1 μg/L) and high (145 μg/L) Mn water exposure groups.
- Calculated three MRI T1 indexes: standard pallidal index (PI), PI using pericranial muscles, and T1 relaxation time.
- Compared MRI indexes between groups and correlated them with estimated Mn intake from water.
Main Results:
- Standard PI did not differ between exposure groups.
- High-Mn group showed significantly lower pericranial muscles PI and higher T1 relaxation time.
- Mn intake correlated with pericranial muscles PI and T1 relaxation time, but not standard PI. Motor performance was lower in the high-Mn group.
Conclusions:
- Higher manganese exposure via drinking water was associated with lower globus pallidus signal intensity in children.
- This finding contrasts with prior studies showing GP hyperintensity with increased Mn exposure.
- Differences in exposure pathways may explain the observed discrepancy and impact on neurodevelopment.
