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ABSTRACT: Radiotherapy is associated with an increased survival rate in children with brain tumors, but also with cognitive decline. This study examined the time-dependent effects of radiation treatment on adaptive functioning in children with brain tumors. The potentially mediating effects of attention span (Trial 1 of the Rey Auditory Verbal Learning Test [RAVLT]) assessed within 7 years of diagnosis were explored.
Twenty-two children treated with cranial radiation for third ventricle or cerebellar tumors were included in this archival study. The mean age at diagnosis was 7.62 years (SD = 4.78) and 10.16 years (SD = 3.83) at evaluation. We examined the extent to which auditory attention span was able to mediate the relationship between time elapsed since the initiation of radiation treatment (M = 2.43 years; SD = 2.37) and adaptive functioning (Vineland Adaptive Behavior Scales [VABS]).
Attention span was found to mediate the relationship between time since the initiation of radiation and daily living skills. These findings were shown to be specific to attention and not a reflection of generalized neuropsychological decline, nor were they a result of increasing time since diagnosis in and of itself.
The results of this study suggest that time since radiation may directly decrease attention and poor attention in turn may be associated with lower adaptive functioning on tasks of daily living.
Pediatric Blood & Cancer 07/2008; 50(6):1253-7. · 1.89 Impact Factor
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ABSTRACT: This archival study sought to determine if the relationship between cognitive and adaptive abilities varied according to brain tumor location. Participants were 36 children treated for brain tumors. The best cognitive predictors of adaptive functioning were hypothesized to be attention span within the cerebellar group and verbal memory within the third ventricle group. Auditory attention span significantly predicted communication skills for the cerebellar group, whereas verbal memory significantly predicted socialization skills for the third ventricle group. These findings suggest that cognitive predictors vary according to tumor location, and highlight the need for more research examining adaptive functioning and its correlates.
Developmental Neuropsychology 02/2008; 33(4):505-20. · 2.56 Impact Factor
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Marla Gearing,
Jorge L Juncos,
Vincent Procaccio,
Claire-Anne Gutekunst,
Elaine M Marino-Rodriguez,
Kymberly A Gyure,
Shoichiro Ono,
Robert Santoianni, Nicolas S Krawiecki,
Douglas C Wallace,
Bruce H Wainer
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ABSTRACT: The neuropathology of the primary dystonias is not well understood. We examined brains from identical twins with DYT1-negative, dopa-unresponsive dystonia. The twins exhibited mild developmental delays until age 12 years when they began developing rapidly progressive generalized dystonia. Genetic, metabolic, and imaging studies ruled out known causes of dystonia. Cognition was subnormal but stable until the last few years. Death occurred at ages 21 and 22 years. The brains were macroscopically unremarkable. Microscopic examination showed unusual glial fibrillary acidic protein-immunoreactive astrocytes in multiple regions and iron accumulation in pallidal and nigral neurons. However, the most striking findings were 1) eosinophilic, rod-like cytoplasmic inclusions in neocortical and thalamic neurons that were actin depolymerizing factor/cofilin-immunoreactive but only rarely actin-positive; and 2) abundant eosinophilic spherical structures in the striatum that were strongly actin- and actin depolymerizing factor/cofilin-positive. Electron microscopy suggested that these structures represent degenerating neurons and processes; the accumulating filaments had the same dimensions as actin microfilaments. To our knowledge, aggregation of actin has not been reported previously as the predominant feature in any neurodegenerative disease. Thus, our findings may shed light on a novel neuropathological change associated with dystonia that may represent a new degenerative mechanism involving actin, a ubiquitous constituent of the cytoskeletal system.
Annals of Neurology 11/2002; 52(4):465-76. · 11.09 Impact Factor
