Abnormal cerebral glucose metabolism in long-term survivors of childhood acute lymphocytic leukemia

✍ Scribed by Dr Peter C. Phillips; James R. Moeller; John J. Sidtis; Vijay Dhawan; Peter G. Steinherz; Steven C. Strother; James Z. Ginos; David A. Rottenberg

• Publisher: John Wiley and Sons
• Year: 1991
• Tongue: English
• Weight: 916 KB
• Volume: 29
• Category: Article
• ISSN: 0364-5134
• DOI: 10.1002/ana.410290306

✦ Synopsis

Abstract

Chemotherapy and radiation treatment of the central nervous system may cause delayed neurotoxicity in children with acute lymphocytic leukemia. We evaluated 12 long‐term survivors of childhood leukemia using [^18^F]fluorodeoxyglucose positron emission tomography, computed tomography scans, clinical neurological examinations, and neuropsychological tests. Regional cerebral metabolic rate for glucose (rCMRGIc) values for white matter were lower in the older long‐term survivors (> 18 years old) treated with cranial radiation and intrathecal chemotherapy than in normal control subjects or survivors who had been treated with intrathecal chemotherapy alone. The ratio of white matter: cortex rCMRGlc values was lower than control values in the long‐term survivors treated with cranial radiation and intrathecal chemotherapy, regardless of age, but not in those treated with intrathecal chemotherapy alone. By contrast, thalamic rCMRGlc values were lower than control values in older survivors regardless of treatment, and the ratio for thalamus: cortex rCMRGIc values was lower in all the treatment groups than in control subjects. The highest rCMRGIc values were found in the youngest children, indicating an important effect of age on cerebral glucose metabolism. No neuropsychological deficits were identified in patients treated only with intrathecal chemotherapy; however, lower IQ scores were found in the long‐term survivors who had been treated with cranial radiation and intrathecal chemotherapy. Treatment of the central nervous system with cranial radiation and intrathecal chemotherapy may cause prolonged alterations in white‐matter and thalamic rCMRGIc, which may permit the identification and assessment of neurotoxicity in long‐term survivors of acute lymphocytic leukemia by [^18^F]fluorodeoxyglucose positron emission tomography.