Methanol intoxication: pathological changes of central nervous system (17 cases)

• Published in: The American journal of forensic medicine and pathology Vol. 31; no. 1; pp. 34 - 36
• Main Authors: Karayel, Ferah, Turan, Arzu A, Sav, Aydin, Pakis, Isil, Akyildiz, Elif U, Ersoy, Gokhan
• Format: Journal Article
• Language: English
• Published: United States 01-03-2010
• Subjects: Accidents; Adult; Alcohol Drinking; Brain - pathology; Brain Edema - pathology; Brain Ischemia - pathology; Encephalocele - pathology; Female; Forensic Pathology; Forensic Toxicology; Formates - blood; Humans; Intracranial Hemorrhages - pathology; Male; Methanol - administration & dosage; Methanol - poisoning; Middle Aged; Solvents - administration & dosage; Solvents - poisoning
• ISSN: 0195-7910; 1533-404X
• DOI: 10.1097/PAF.0b013e3181c160d9

The nervous system has increased susceptibility for methanol intoxication. The aim of this study is to investigate various central nervous system lesions of methanol intoxication in 17 cases autopsied in the mortuary department of the Council of Forensic Medicine in Istanbul, Turkey. The reasons of methanol intoxication in the cases was likely the unwitting ingestion of methanol while drinking illegal alcohol. Survival times ranged from several hours to days. In 8 cases (47%), cerebral edema and in 9 cases (53%) at occipital, temporal and parietal cortex, basal ganglia and pons, petechial bleeding was observed. In addition to these findings, hemorrhagic necrosis were observed in thalamus, putamen, and globus pallidus in 5 cases (29.4%) and, in cerebral cortex in another 3 cases (17.6%). In 3 of the cases (17.6%) in which cerebral edema was found, herniation findings accompanied to the situation and in 2 cases (11.7%), pons bleeding was observed. Around the basal ganglia, in 2 of the cases with hemorrhagic necrosis, the situation ended with a ventricular compression. In 7 cases (41%), the associated findings of chronic ischemic changes in cortical neurons, lacunae formation, degeneration of granular cell layer of the cerebellum, and reactive gliosis were considered as the results of chronic alcoholism.