Abstract

BACKGROUND: Craniopharyngiomas occur in the suprasellar region of the brain, an area associated with psychiatric disease. In addition, cranial irradiation may damage the hippocampus and white matter tracts of the developing frontal lobe, areas involved in development and behavior. We hypothesize that children with craniopharyngioma will have a high risk of psychiatric disorders. METHODS: Patients were identified from the Lucile Packard Children's Hospital (LPCH) Pediatric Brain Tumor Database and were included if they were aged birth to 30 years at the time of diagnosis between 1/1/1997 - 6/1/2013. Demographic, treatment, and psychiatric information was abstracted from eligible patients' charts. Descriptive statistics were performed using 2-tailed student's t-test and Fisher's exact test where appropriate. RESULTS: Craniopharyngioma cases were identified in 28 patients, seven of whom had psychiatric symptoms (25%), including psychosis (1) and mood/anxiety disorders (6). Median time to psychiatric symptoms was 4.2 years. There was not a significant difference in age at diagnosis, gender, use of radiation therapy, or use of an Ommaya reservoir between cases and controls. Compared with data reported previously on patients with germ cell tumor (GCT), children with craniopharyngioma were younger at diagnosis (p = 0.03). Although the rate of psychosis appeared less in children with craniopharyngioma (3.6%) compared with GCT (14.3%), the difference was not statistically significant (p = 0.35). There was no difference in time to develop psychiatric symptoms. CONCLUSIONS: Psychiatric sequelae of pediatric brain tumors are under-recognized and poorly understood. We note that pediatric patients with craniopharyngiomas have a high risk for late psychiatric symptoms, particularly mood disorders, although we have not yet elucidated risk factors. Similar rates of psychosis and mood disorders within pediatric patients with craniopharyngioma and GCT suggest psychiatric illness relates to tumor location, and subsequent possible disruption of neural circuitry involving the basal ganglia, hypothalamus, and frontal lobes.

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