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Journal of Child Neurology
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Muscle Glycogen Depletion and Increased Oxidative Phosphorylation Following Status Epilepticus

Marina Michelson-Kerman, MD

Mitochondrial Disease Clinic Metabolic Neurogenetic Service Pediatric Neurology Unit, Wolfson Medical Center, Holon Sackler School of Medicine Tel-Aviv University Tel-Aviv, Israel

Nathan Watemberg, MD

Mitochondrial Disease Clinic Metabolic Neurogenetic Service Pediatric Neurology Unit, Wolfson Medical Center, Holon Sackler School of Medicine Tel-Aviv University Tel-Aviv, Israel

Andreea Nissenkorn, MD

Mitochondrial Disease Clinic Metabolic Neurogenetic Service Pediatric Neurology Unit, Wolfson Medical Center, Holon Sackler School of Medicine Tel-Aviv University Tel-Aviv, Israel

Eli Gilad, MD

Pediatric Intensive Care Unit, Wolfson Medical Center, Holon Sackler School of Medicine Tel-Aviv University, Tel-Aviv Israel

Menachem Sadeh, MD

Neurology Department, Wolfson Medical Center, Holon Saclder School of Medicine Tel-Aviv University Tel-Aviv, Israel

Tally Lerman-Sagie, MD

Mitochondrial Disease Clinic Metabolic Neurogenetic Service Pediatric Neurology Unit Wolfson Medical Center, Holon Sackler School of Medicine Tel-Aviv University Tel-Aviv, Israel

We describe complete glycogen depletion and increased respiratory chain enzyme activity in a muscle biopsy obtained prior to the demise of a patient in multiorgan failure following status epilepticus. These findings validate the theoretical basis of muscle energy turnover during status epilepticus: the increased demand for energy leads to complete depletion of glycogen reserves. The attempt to preserve adenosine triphosphate requirements results in increased activity of respiratory chain enzymes. (J Child Neurol 2003;18: 876-877).

Journal of Child Neurology, Vol. 18, No. 12, 876-878 (2003)
DOI: 10.1177/088307380301801208
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