Clinical Toxicology, 44:89–90, 2006 Copyright © Taylor & Francis LLC ISSN: 0731-3810 print / 1097-9875 online DOI: 10.1080 IMAGES IN CLINICAL TOXICOLOGY LCLT Methanol Neurotoxicity Matthew Salzman, M.D. METHANOL NEUROTOXICITY Clinical Toxicology Downloaded from informahealthcare.com by Dalhousie University on 12/30/14 For personal use only. Drexel University College of Medicine, Philadelphia, Pennsylvania, USA glycol ingestion was initiated, including intravenous fomepizole, thiamine, folic acid, and, eventually, hemodialysis. Approximately 6 hours after presentation, the serum methanol level was reported as 570 mg/dL. Over the next 36 hours, the patient had intermittent generalized seizure activity and, despite aggressive care, had no improvement in mental status. A repeat head CT obtained 36 hours after presentation, demonstrated bilateral putamen infarcts as well as subcortical white matter destruction (see image). Necrosis of the putamen is the typical neuropathological finding in methanol poisoning, that may be demonstrated with neuroimaging. (1) Formic acid, the toxic metabolite of methanol, inhibits cytochrome oxidase and oxidative metabolism, leading to Na+/K+ ATPase pump failure, cerebral edema and cell death. The putamen appears to be more susceptible to this A 46-year-old male without significant past medical history presented to our Emergency Department in an unconscious state with bilateral ocular leftward deviation. The patient was afebrile with stable vital signs and SpO2 of 98% on room air. A fingerstick blood sugar was 112. Intravenous access was established and the patient was intubated. An emergent head CT was normal. Post-intubation arterial blood gas revealed a pH of 6.93, pCO2 of 30 and PAO2 of 654. An anion gap of 36 and an osmolar gap of 138 was ascertained. An ethanol level was zero and salicylates were 5.6 mg/dL. A toxic alcohol panel was sent, and aggressive treatment for methanol and ethylene Address correspondence to Matthew Salzman, M.D., Drexel University College of Medicine, Emergency Medicine Control, Philadelphia, PA, USA; E-mail: matthew.s.salzman@drexel.edu 89 Clinical Toxicology Downloaded from informahealthcare.com by Dalhousie University on 12/30/14 For personal use only. 90 M. G. SALZMAN histotoxic hypoxia than other regions in the brain, although it is unclear as to why. One theory suggests that breakdown of the blood brain barrier results in higher levels of formic acid diffusion into the putamen. (2) Other theories postulate that a combination of high local concentrations of formic acid plus poor venous drainage result in increased histiotoxic hypoxia. In addition, the putamen may manifest higher oxygen and glucose consumption as compared with other areas of the brain thereby making this tissue more susceptible to histiotoxic hypoxia.(3) Putamen infarcts, while suggestive of, are not pathognomonic for methanol toxicity. The differential diagnosis for this neuroradiologic finding includes Leigh’s disease, Wilson’s disease, Kearns-Sayre syndrome, Leber’s optic atrophy, carbon monoxide poisoning as well as hypoxic and ischemic injuries. (4,5) Our patient, however, had no known episodes of hypoxia, no exposure to carbon monoxide and a significant methanol intoxication. The brain imaging study presented correlates with a severe methanol poisoning. REFERENCES 1. Anderson C, et al. MRI enhancing brain lesions in methanol intoxication. Journal of Computer Assisted Tomography. Sept/Oct 1997; Vol 21(5):834–836. 2. Onder F, et al. Acute blindness and putamenal necrosis in methanol intoxication. International Opthalmology, 1999; 22:81–84. 3. Barceloux DG, et al. American academy of clinical toxicology practice guidelines on the treatment of methanol poisoning. Clinical Toxicology, 2002; 40(4):415–446. 4. Kuteifan K, et al. Necrosis and haemorrhage of the putamen in methanol poisoning shown on MRI. Neuroradiology, 1998; 40:158–160. 5. Penney Gaul H, et al. MR findings in methanol intoxication. AJNR: American Journal of Neuroradiology, Oct. 1995; 16(9):1783–6. Prospective authors should send questions and submissions for the “Images in Clinical Toxicology” section to Michael Greenberg (mgreenbe@drexelmed.edu). Submissions should be high quality, high resolution images that illustrate interesting, novel or instructive elements of the science and practice of medical, occupational or environmental clinical toxicology. Each submission should be a single image and be accompanied by a written narrative that describes the image and discusses the salient clinical features that the image depicts. The narrative should be no more that 500 words and should include no more that three references. The specifics of image and text submissions should be consistent with those described in the general instructions for authors for the Journal. All submissions are subject to editorial review.