Ingestion of gasoline in a suicide attempt: an uncommon cause of bilateral basal ganglia T1 hyperintensities

Abstract

A 70-year-old man with a 27-year history of psychosis and hypertension was brought comatose to our Emergency Room following a suicide attempt with oral unleaded gasoline ingestion that was witnessed and described by his neighbors. His neurological examination disclosed a Glasgow Coma Scale Score of 8 (eye opening response 2 points, verbal response 2 points, motor response 2 points), with normal brainstem reflexes and spontaneous breathing. The subject was treated with a gastric lavage (gastric content, almost 2 l of gasoline) and activated charcoal. A baseline brain CT was unremarkable, while his liver function tests were normal. His neurological status did not improve and was transferred to the Intensive Care Unit of our institution where severe aspiration pneumonia was diagnosed. A brain MRI was performed at 16 days following his suicide attempt. Bilateral hyperintensities affecting the globus pallidus and the caudate nucleus were shown on axial T1, T2 and FLAIR sequences (Fig. 1). The patient expired 3 weeks later because of his aspiration pneumonia. Lesions with high signal intensity on spin-echo Tl-weighted MR images are unusual and are associated with relatively few entities, including lipids, calcification, high protein count, laminar necrosis in cerebral infarction, neoplasms and paramagnetic substances such as methemoglobin, melanin, copper and manganese [1]. Manganese, in particular, is considered a neurotoxic agent causing movement and psychological disorders characterized by rigidity, tremor and hypokinesia in workers involved in the alloy industry (miners, welders, smelters), in patients receiving long-term total parenteral nutrition and in hepatic encephalopathy patients with portal liver shunts [1–3]. Since the introduction of MRI in clinical practice, bilateral symmetric high signal intensities at the globus pallidus and substantia nigra have been well described in patients with manganese neurotoxicity. The most plausible explanation for the increased T1 signal intensity is a rise in manganese concentration that has paramagnetic properties in the central nervous system (CNS), with preferential deposition in the globus pallidus. Methylcyclopentadienyl manganese tricarbonyl (MMT) is an octane-improving additive to unleaded gasoline, which has recently attracted attention with regard to the prospect of worldwide manganese exposure as increases in environmental manganese concentrations have been recorded relative to traffic density [4]. We postulate that in the present case oral ingestion of large quantities of gasoline resulted in MMT absorption, which in turn resulted in increased CNS manganese concentrations leading to bilateral T1 basal ganglia hyperintensities. However, it should be noted that manganese concentrations were not measured in blood, while we have no neuropathological confirmation of manganese deposition in globus pallidus. In conclusion, the present case highlights bilateral T1 basal ganglia hyperintensities related to oral ingestion of gasoline in a suicide case and underscores manganese neurotoxicity as the potential underlying cause of this uncommon neuroimaging presentation. G. Tsivgoulis (&) I. Heliopoulos K. Vadikolias C. Piperidou Department of Neurology, Democritus University of Thrace, University Hospital of Alexandroupolis, Kapodistriou 3, Nea Xili, 68100 Alexandroupolis, Greece e-mail: tsivgoulisgiorg@yahoo.gr