Related Experiment Video
Updated: Jul 5, 2026

14:21
Creating Dynamic Images of Short-lived Dopamine Fluctuations with lp-ntPET: Dopamine Movies of Cigarette Smoking
Published on: August 6, 2013
Methanol intoxication-induced nigrostriatal dysfunction detected using 6-[18F]fluoro-L-dopa PET
Laura Airas1, Teemu Paavilainen, Reijo J Marttila
1Department of Neurology, University of Turku, Turku, Finland. laura.airas@utu.fi
Neurotoxicology
|May 17, 2008
Summary
A man suffered severe methanol poisoning from windshield washer liquid, leading to blindness and movement disorders. Positron emission tomography (PET) scanning revealed impaired dopamine activity in his brain.
Area of Science:
- Neuroscience
- Toxicology
- Radiochemistry
Background:
- Methanol poisoning can cause severe neurological deficits, including visual impairment and movement disorders.
- The precise neurochemical underpinnings of these deficits, particularly dopaminergic system involvement, require further elucidation.
Observation:
- A 49-year-old male presented with acute severe methanol intoxication after ingesting windshield washer fluid.
- Clinical manifestations included optic atrophy with blindness and an extrapyramidal syndrome.
- Brain MRI revealed putaminal injury and subcortical white matter hyperintensity.
Findings:
- Positron emission tomography (PET) scanning using 6-[18F]fluoro-L-dopa demonstrated symmetrical, impaired presynaptic dopaminergic activity in the striatum.
- Functional impairment of dopaminergic nigrostriatal neurons was indicated, with more severe reduction in the putamina (40% of controls) than caudate nuclei (60% of controls).
- This represents the first reported 18F-dopa PET scan findings in acute methanol poisoning.
Implications:
- 18F-dopa PET scanning can detect functional dopaminergic deficits in methanol intoxication.
- Findings suggest nigrostriatal dopaminergic pathway damage contributes to the extrapyramidal syndrome in methanol poisoning.
- This imaging technique may aid in understanding and potentially monitoring neurological sequelae of toxic exposures.

