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S Kempton

Publications and source records attributed to S Kempton.

2 recordsLinked to original sources

Executive function and attention deficit hyperactivity disorder: stimulant medication and better executive function performance in children.

BACKGROUND: Executive function deficits have been reported repeatedly in children with Attention Deficit Hyperactivity Disorder (ADHD). Stimulant medication has been shown to be effective in improving cognitive performance on most executive function tasks, but neuropsychological tests of executive function in this population have yielded inconsistent results. Methodological limitations may explain these inconsistencies. This study aimed to measure executive function in medicated and non-medicated children with ADHD by using a computerized battery, the Cambridge Neuropsychological Test Automated Battery (CANTAB), which is sensitive to executive function deficits in older patients with frontostriatal neurological impairments. METHODS: Executive function was assessed in 30 children with ADHD: 15 were stimulant medication naive and 15 were treated with stimulant medication. These two groups were compared to 15 age, sex and IQ matched controls. RESULTS: The unmedicated children with ADHD displayed specific cognitive impairments on executive function tasks of spatial short-term memory, spatial working memory, set-shifting ability and planning ability. Impairments were also seen on spatial recognition memory and delayed matching to sample, while pattern recognition memory remained intact. The medicated children with ADHD were not impaired on any of the above executive function tasks except for deficits in spatial recognition memory. CONCLUSIONS: ADHD is associated with deficits in executive function. Stimulant medication is associated with better executive function performance. Prospective follow-up studies are required to examine these effects.

Adolescent↗

Both ethanol toxicity and thiamine deficiency are necessary to produce long-term memory deficits in the young chick.

This series of studies revealed that a 2.5-mg dose of oxythiamine administered over 2 days yielded memory deficits from 10 min following passive avoidance learning. This result existed in association with slowing of righting reflex. Administration of thiamine reversed the memory deficit and the slowing of the righting reflex. A combination of oxythiamine and peripheral alcohol administration also resulted in memory deficits appearing from 10 min after training; however, in contrast to the effect of thiamine deficiency alone, the deficits induced by thiamine deficiency in association with acute administration of alcohol could not be reversed by thiamine resupplementation. The combination of alcohol and oxythiamine also slowed the righting reflex, but higher doses of thiamine also were unable to ameliorate the memory deficit caused by a combination of oxythiamine and alcohol; however, the slowing of righting reflex was reversed. The results suggest that preexistent thiamine deficiency may make the subject susceptible to the neurotoxicological effects of alcohol on memory function.

Animals↗