The Stroop revisited: a meta-analysis of interference control in AD/HD

Background: An inhibition deficit, including poor interference control, has been implicated as one of the core deficits in AD/HD. Interference control is clinically measured by the Stroop Colour-Word Task. The aim of this meta-analysis was to investigate the strength of an interference deficit in AD/HD as measured by the Stroop Colour-Word Task and to assess the role of moderating variables that could explain the results. These moderating variables included: methods of calculating the interference score, comorbid reading and psychiatric disorders, AD/HD-subtypes, gender, age, intellectual functioning, medication, and sample size. Methods: Seventeen independent studies were located including 1395 children, adolescents, and young adults, in the age range of 6-27 years. A meta-analysis was conducted to assess the effect sizes for the scores on the word and the colour card as well as the interference score. Results: Children with AD/HD performed more poorly on all three dependent variables. The effect sizes for word reading (d = .49) and colour naming (d = .58) were larger and more homogeneous than the effect size for the interference score (d = .35). The method used to calculate the interference score strongly influenced the findings for this measure. When interference control was calculated as the difference between the score on the colour card minus the score on the colour-word card, no differences were found between AD/HD groups and normal control groups. Discussion: The Stroop Colour-Word Task, in standard form, does not provide strong evidence for a deficit in interference control in AD/HD. However, the Stroop Colour-Word Task may not be a valid measure of interference control in AD/HD and alternative methodologies may be needed to test this aspect of the inhibitory deficit model in AD/HD. © Association for Child Psychology Psychiatry, 2004

Differential effects and rates of normal aging in cerebellum and hippocampus

Cognitive functions show many alternative outcomes and great individual variation during normal aging. We examined learning over the adult life span in CBA mice, along with morphological and electrophysiological substrates. Our aim was to compare cerebellum-dependent delay eyeblink classical conditioning and hippocampus-dependent contextual fear conditioning in the same animals using the same conditioned and unconditioned stimuli for eyeblink and fear conditioning. In a subset of the behaviorally tested mice, we used unbiased stereology to estimate the total number of Purkinje neurons in cerebellar cortex and pyramidal neurons in the hippocampus. Several forms of synaptic plasticity were assessed at different ages in CBA mice: long-term depression (LTD) in both cerebellum and hippocampus and NMDA-mediated long-term potentiation (LTP) and voltage-dependent calcium channel LTP in hippocampus. Forty-four CBA mice tested at one of five ages (4, 8, 12, 18, or 24 months) demonstrated statistically significant age differences in cerebellum-dependent delay eyeblink conditioning, with 24-month mice showing impairment in comparison with younger mice. These same CBA mice showed no significant differences in contextual or cued fear conditioning. Stereology indicated significant loss of Purkinje neurons in the 18- and 24-month groups, whereas pyramidal neuron numbers were stable across age. Slice electrophysiology recorded from an additional 48 CBA mice indicated significant deficits in LTD appearing in cerebellum between 4 and 8 months, whereas 4- to 12-month mice demonstrated similar hippocampal LTD and LTP values. Our results demonstrate that processes of aging impact brain structures and associated behaviors differentially, with cerebellum showing earlier senescence than hippocampus