In neurosurgeon Dr. Russell Blaylock's book "Exitoxins: The Taste That Kills," he writes that aspartame causes major neurological changes, and in heavy users, may even precipitate lupus and methanol toxicity, which at first appears to be multiple sclerosis. ___________________________ FROM MEDLINE REGARDING METHANOL TOXICITY Arq Neuropsiquiatr 1994 Mar;52(1):93-5 [Computed tomography in methanol intoxication]. [Article in Portugese] Carrete Junior H, Nogueira RG, Abdala N, Nalli DR Departamento de Diagnostico por Imagem (DDI), Escola Paulista de Medicina (EPM), Sao Paulo, Brasil. We had the opportunity to follow a methanol intoxication case with CT scans, at the 1st and 6th day after admission. Symmetrical putaminal and white matter lesions were seen on the last CT examination, and occurred with the worsening of neurological manifestations, despite the appropriated treatment. The CT demonstration of brains lesions disclosed the toxic effect of the methanol and could be a guideline to the neurological prognosis. PMID: 8002818, UI: 94271020 ------------------------------------------------------------------------ AJNR Am J Neuroradiol 1995 Aug;16(7):1492-4 Methanol intoxication with putaminal and white matter necrosis: MR and CT findings. Rubinstein D, Escott E, Kelly JP Department of Radiology, University of Colorado Health Sciences, Denver 80262, USA. We report a case of methanol intoxication in which the initial CT scans appeared normal. MR at 4 days showed the typical putaminal lesions of methanol intoxication and, in addition, peripheral white matter lesions that spared a thin rim of subcortical white matter. A CT scan at 17 days showed the putaminal and white matter lesions. The white matter lesions correspond well to lesions previously described in pathologic specimens. PMID: 7484638, UI: 96029917 ------------------------------------------------------------------------ J Comput Assist Tomogr 1997 Sep-Oct;21(5):834-6 MRI enhancement of brain lesions in methanol intoxication. Anderson CA, Rubinstein D, Filley CM, Stears JC Department of Neurology, University of Colorado Health Sciences Center, Denver 80262, USA. Methanol intoxication can cause necrosis of the putamen and subcortical white matter that is evident on neuroimaging. We report a 47-year-old man with significant methanol intoxication who had enhancing lesions in the caudate nuclei, putamina, hypothalamus, and subcortical white matter by MRI. This case demonstrates that contrast enhancement of brain lesions can be observed after methanol poisoning. PMID: 9294585, UI: 97440278 ------------------------------------------------------------------------ Neuroradiology 1998 Mar;40(3):158-60 Necrosis and haemorrhage of the putamen in methanol poisoning shown on MRI. Kuteifan K, Oesterle H, Tajahmady T, Gutbub AM, Laplatte G Service de Reanimation Medicale, Centre hospitalier Louis Pasteur, Colmar, France. Methanol, a highly toxic substance, is used as an industrial solvent and in automobile antifreeze. Acute methanol poisoning produces severe metabolic acidosis and serious neurologic sequelae. We describe a 50-year-old woman with accidental methanol intoxication. MRI showed haemorrhagic necrosis of the putamina and lesions in the deep white matter. PMID: 9561519, UI: 98222303 ------------------------------------------------------------------------ Chung Hua I Hsueh Tsa Chih (Taipei) 1992 Apr;49(4):283-8 Bilateral putaminal necrosis caused by methanol poisoning: a case report. Hsieh FY, Leu TM, Chia LG Division of Neurology, Taichung Veterans General Hospital, Taiwan, R.O.C. Abnormalities of the cerebrospinal fluid included an initial pressure of 240 mmH2 O, RBC 286/mm3, WBC 8/mm3, and protein 179 mg/dl. Peritoneal dialysis was performed on the 2nd day after drinking. A blood test for methanol was not performed until the 5th day, and its results was negative. However, computed tomography (CT) on the 3rd day showed necrosis and hemorrhage of bilateral putamina and the cerebral cortex, and post-contrast enhancement of meninges. On the 22nd day, a CT revealed further changes: necrosis of bilateral subcortical white matter, and post-contrast gyral enhancement at the otherwise normal-looking areas of the cerebral cortex. We suggest that, in certain situations, the characteristic CT findings are helpful in the diagnosis of methanol poisoning. PMID: 1318154, UI: 92288776 ------------------------------------------------------------------------ Methanol optic neuropathy: a histopathological study. Sharpe JA, Hostovsky M, Bilbao JM, Rewcastle NB The histopathologic effects of methanol on the optic nerve were studied in four patients. Circumscribed myelin damage occurred behind the lamina cribrosa in each nerve. Axons were preserved. Demyelination also occurred in cerebral hemispheric white matter in one patient. This selective myelinoclastic effect of methanol metabolism is probably caused by histotoxic anoxia in watershed areas of the cerebral and distal optic nerve circulations. Juxtabulbar demyelination may cause optic disk edema in methanol poisoning by compressive obstruction of orthograde axoplasmic flow. Visual loss may be due to disruption of saltatory conduction. Retrolaminar demyelinating optic neuropathy is an early morphologic correlate of visual loss in meCircumscribed myelin PMID: 6889696, UI: 83013425 ------------------------------------------------------------------------ Ann Neurol 1980 Aug;8(2):161-7 Methanol poisoning: a clinical and pathological study. McLean DR, Jacobs H, Mielke BW Computed tomographic scans in both patients demonstrated bilateral symmetrical infarction of the frontocentral white matter and putamen. Electromyography in 1 patient showed extensive denervation, mainly involving the legs, but normal motor conduction velocities. L-Dopa administered to the more severely affected patient had no effect. Autopsy revealed cystic resorption of the putamen and the frontocentral subcortical white matter in additon to widespread neuronal damage PMID: 7425569, UI: 81037897