doi:10.1016/j.jemermed.2009.08.010 Visual Diagnosis in Emergency Medicine TYPICAL BILATERAL PUTAMINAL LESIONS OF METHANOL INTOXICATION Hossein Sanaei-Zadeh, MD Department of Forensic Medicine and Toxicology, Tehran University of Medical Sciences, Hazrat Rasoul Akram Hospital, Tehran, Iran Reprint Address: Hossein Sanaei-Zadeh, MD, Department of Forensic Medicine and Toxicology, Hazrat Rasoul Akram Hospital, Niayesh Street, Sattar-Khan Ave., Tehran 1445613131, Iran CASE REPORT A comatose 36-year-old man presented to the emergency department with mild mydriasis and bilaterally unreac- tive pupils. He had a severe metabolic acidosis. No methanol was detected in his serum. The computed to- mography (CT) scan showed cerebral edema and bilat- eral symmetrical putaminal lesions (Figure 1). DISCUSSION Methanol toxicity affects primarily the central nervous system (CNS) and the eye. Formic acid (an end product of methanol metabolism) is primarily responsible for the toxicity in methanol poisoning. More severely exposed patients who present late may have coma, seizure, blind- ness, gastrointestinal hemorrhage, and pancreatitis (1). Findings on fundoscopy range from hyperemic optic disks to papilledema, retinal hemorrhages, and fixed mydriasis (2). A CT scan or magnetic resonance imaging study of the brain may show bilateral hemorrhage and necrosis of the putaminal areas, diffuse white matter necrosis, cerebral herniation, and subarachnoid hemorrhage, findings seen in severe cases or late in the course of methanol poisoning (3). The toxic effect on the basal ganglia may not be evident in the acute stage because it is concealed by pronounced CNS depression (4). Direct toxicity of formic acid, ischemic injury, and acidosis are postulated mechanisms of putami- nal injury. The brain in general and the neurons in caudate nucleus, putamen, globus pallidus, and cerebral white mat- ter, in particular, are susceptible to hypoxic injury. These changes may occur simultaneously and early or sequentially and late (5). In absence of an exposure history, methanol poison- ing is difficult to diagnosis, therefore, methanol poison- ing should be considered in every patient with a meta- RECEIVED: 12 June 2009; FINAL SUBMISSION RECEIVED: 9 July 2009; ACCEPTED: 10 August 2009 Figure 1. Non-contrast computed tomography scan at the level of the basal ganglia obtained at hospital admission shows cerebral edema, and bilateral symmetrical, low- density lesions in the putaminal region. The Journal of Emergency Medicine, Vol. 42, No. 2, pp. 178 –179, 2012 Copyright © 2012 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$–see front matter 178