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Discordance Between Cerebral Oxygen and Glucose Metabolism, and Hemodynamics in a Mitochondrial Encephalomyopathy, Lactic Acidosis, and Strokelike Episode Patient
Author(s) -
Nariai Tadashi,
Ohno Kikuo,
Ohta Yoshihisa,
Hirakawa Kimiyoshi,
Ishii Kenji,
Senda Michio
Publication year - 2001
Publication title -
journal of neuroimaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.822
H-Index - 64
eISSN - 1552-6569
pISSN - 1051-2284
DOI - 10.1111/j.1552-6569.2001.tb00057.x
Subject(s) - mitochondrial encephalomyopathy , lactic acidosis , medicine , cerebral blood flow , positron emission tomography , lesion , acidosis , oxygenation , cardiology , pathology , nuclear medicine , mitochondrial dna , biochemistry , chemistry , gene
A patient with mitochondrial encephalomyopathy, lactic acidosis, and strokelike episode (MELAS) syndrome underwent serial measurement of cerebral blood flow with xenon computed tomography (Xe‐CBF) while presenting with strokelike episodes accompanied by a cerebral lesion. He underwent positron emission tomography (PET) measurement of the regional cerebral blood flow (PET‐CBF), metabolic rate of oxygen (CMRO 2 ), and glucose (CMRGlu) after his symptoms and lesion disappeared. During the symptomatic period, Xe‐CBF and the Xe‐CBF response to acetazolamide loading were well preserved both in and outside the low‐density lesion. In the PET study, decreased CMRO 2 and increased PET‐CBF and CMRGlu were noted in the entire brain. The strokelike episodes of patients with MELAS are more likely attributed to the failure of oxygen metabolism than to a vascular accident.