The neuropsychological assets and deficits of several types of pediatric neurological disease, disorder, and dysfunction are described. These are examined from the perspective of the syndrome of nonverbal learning disabilities (NLD) and the "white matter model" designed to explain its complex manifestations. It is concluded that children with some of these diseases exhibit the NLD phenotype, whereas others do not. For the most part, the diseases in which the NLD phenotype is particularly evident are those wherein it has been demonstrated that perturbations of white matter (long myelinated fibers) are particularly prominent.
The earliest neuroanatomical changes in amnestic mild cognitive impairment (aMCI) involve the hippocampus and entorhinal cortex, structures implicated in the integration and learning of associative information. The authors hypothesized that individuals with aMCI would have impairments in associative memory above and beyond the known impairments in item memory. A group of 29 individuals with aMCI and 30 matched control participants were administered standardized tests of object-location recall and symbol-symbol recall, from which both item and associative recall scores were derived. As expected, item recall was impaired in the aMCI group relative to controls. Associative recall in the aMCI group was even more impaired than was item recall. The best group discriminators were measures of associative recall, with which the sensitivity and specificity for detecting aMCI were 76% and 90% for symbol-symbol recall and were 86% and 97% for object-location recall. Associative recall may be particularly sensitive to early cognitive change in aMCI, because this ability relies heavily on the medial temporal lobe structures that are affected earliest in aMCI. Incorporating measures of associative recall into clinical evaluations of individuals with memory change may be useful for detecting aMCI.
Unilateral HS patients with earlier seizure onset and longer duration of epilepsy have more severe HS and greater hippocampal volume asymmetry. This suggests that HS may be a progressive disorder with risk for cognitive dysfunction.
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