This study prospectively examined neuropsychological (NP) functioning associated with adolescent substance use and withdrawal. Participants were youths with histories of substance use disorders (n = 47) and demographically comparable youths with no such lifetime histories (n = 26). They were followed with NP testing and substance involvement interviews at 7 time points spanning 8 years, from ages 16 to 24, on average. After controlling for recent use, age, education, practice effects, and baseline NP functioning, substance use over the 8-year follow-up period significantly predicted performances on tests of memory and attention at Year 8. Additionally, withdrawal symptoms during the follow-up predicted visuospatial and attention scores at Year 8. Findings suggest that use and withdrawal may differentially impact neurocognitive functioning during youth, with heavy use leading to learning, retention, and attentional difficulties, and withdrawal leading to problems with visuospatial functioning. (JINS, 2002, 8, 873–883.)

Work on implicit memory in normal subjects has demonstrated the influence of stimulus modality on the retrieval of semantic information. The present study examined the effects of auditory and visual semantic priming on the recognition of visual words using a lexical decision task. Performance was studied in a group of 20 patients with DSM–IV schizophrenia and 26 normal volunteers of similar age and sex. There were two versions of the task: ipsimodal, in which the word or nonword visual target followed 400 ms after the onset of a visual word prime which may or may not be semantically related to the target; and cross-modal, in which the visual target followed 400 ms after the onset of an auditory word prime. Both groups showed significant priming in both modality conditions, although the schizophrenia patients exhibited significantly greater priming in the cross-modal condition. Priming effects in the ipsimodal condition did not differ substantially between patients and controls. The priming effects in the two conditions correlated with each other in the schizophrenia patients only. The results suggest that priming may occur through amodal semantic representations. In schizophrenia, there appears to be increased cross-modal connectivity (reduced modality modularity and informational encapsulation) between lexical representations that could result in impaired language, particularly speech, processing. (JINS, 2002, 8, 884–892.)

Intraindividual variability of physical status and affect/beliefs as well as their relations with cognition were examined in 3 groups of older adults: healthy elderly, individuals with a nonneurological health-related disturbance (arthritis) and people with neurological compromise (dementia). The findings showed that greater inconsistency in physical performance was observed in groups characterized by central nervous system dysfunction. By contrast, fluctuations in affect appeared to reflect other more transient sources, such as pain. In general, increased inconsistency in non-cognitive domains was associated with poorer cognitive function. There were cross-domain links between inconsistency in physical functioning and fluctuations in cognitive performance, although the nature of the links depended largely upon the neurological status of the individuals. Considered together, the result indicated that measures of cognitive as well as physical variability are important behavioral markers of neurological integrity. (JINS, 2002, 8, 893–906.)

Rapid eye movement (REM) sleep behavior disorder (RBD) is a sleep disturbance that commonly occurs in Dementia with Lewy bodies (DLB). Retrospective examination of DLB course has shown that RBD and cognitive decline may precede the onset of parkinsonism and visual hallucinations. Therefore, some patients with DLB may initially present with dementia and RBD, but would not meet current formal criteria for probable DLB at that time. The purpose of this study is to determine whether patients with dementia and RBD, who do not have parkinsonism or visual hallucinations, have cognitive profiles that can be distinguished from autopsy-confirmed definite AD, but not from clinically probable DLB. If so, this would support the hypothesis that the presence of RBD and dementia, as the only presenting symptoms, reflects the early manifestation of DLB. Results show that early dementia in probable DLB and dementia with RBD are neuropsychologically indistinguishable. Both groups differ from definite AD of a similar early stage with significantly worse visual perceptual organization, sequencing and letter fluency but significantly better confrontation naming and verbal memory. In addition, follow-up data from a subset of patients with dementia and RBD reveal the subsequent development of parkinsonism or hallucinations 1 to 6 years later. Results indicate that the presentation of dementia and RBD is suggestive of underlying Lewy body disease and not Alzheimer's disease. This provides further evidence in support of including RBD as one of the core diagnostic features of DLB. (JINS, 2002, 8, 907–914.)

A veritable explosion of research in neuropsychology has occurred over the past decade in the search for cognitive and brain changes during a so-called “preclinical” phase of dementia that precedes its overt clinical manifestations. Fueling this explosion, in part, has been the revolution in the genetic bases of disease formulated from the international work of decoding the human genome (International Human Genome Sequencing Consortium, 2001; see also Patenaude et al., 2002, for discussion). The discovery of preclinical cognitive, brain, and genetic markers of dementia is helping to push back the point at which diseases can be reliably identified. Very early detection of dementia is extremely important now that a variety of investigational treatments that might prevent or delay disease progression (e.g., amyloid vaccine, anti-oxidants, nonsteroidal anti-inflammatory agents, cholinesterase inhibitors, estrogens, and others in the case of Alzheimer's disease) are on the horizon.

A triplet repeat (CAG) expansion mutation in the huntingtin gene on chromosome 4 is responsible for Huntington's disease (HD). Presymptomatic genetic testing for this mutation has identified clinically normal persons who are virtually certain to develop this dementing illness if they live a normal lifespan. The present study sought to determine whether these “mutation-positive” persons have impairments in cognitive functioning. Seventy-five mutation-positive persons did not differ from 128 mutation-negative persons on tests selected for their sensitivity to early-stage HD. Interestingly, however, those with the mutation viewed themselves as more likely to develop HD than did those without the mutation. Among mutation-positive subjects, having a longer CAG repeat mutation was likewise not associated with cognitive impairment. However, being closer to estimated disease onset (a product of repeat length and parent's age at onset) was associated with selected cognitive impairments. When viewed in light of previous studies showing atrophy of the caudate nucleus and putamen in mutation-carriers who are close to onset but not those far from onset, these results suggest that subtle changes in brain and behavior may be detected shortly before subjects with the HD mutation develop sufficient signs and symptoms for diagnosis. Conceptual and methodological problems associated with the search for presymptomatic cognitive and behavioral indicators of dementing illness are discussed. (JINS, 2002, 8, 918–924.)

We examined asymmetry of hippocampal volume as well as other temporal lobe structures (temporal lobe, temporal horn of the lateral ventricular system, parahippocampal and fusiform gyri) in 194 subjects from the Cache County, Utah study, with varying disorders [85 with Alzheimer's disease (AD), 59 with some cognitive or neuropsychiatric disorder—referenced as a Mixed Neuropsychiatric group, 30 with mild ambiguous/mild cognitive impairment (MA/MCI) and 20 controls] and APOE genotypes. Asymmetry was determined by subtracting left-side volume from the right corrected by total intracranial volume. No significant asymmetry was observed to be associated with presence of the ε4 allele. Since the AD-ε4 allele risk effect may be expressed early in the course of the disorder, we also examined asymmetry indices in AD, MA/MCI and Mixed Neuropsychiatric subjects early in the course of their disorder (2 years or less) to those with longer duration illness (greater than 2 years). We observed a leftward asymmetry (i.e., left side larger) regardless of APOE genotype in hippocampal volume where both AD and MCI subjects demonstrated a leftward shift in hippocampal size when length of disease (LOD) was less but not more than 2 years. Leftward asymmetry was not associated with LOD in the Mixed Neuropsychiatric group. These findings do not support an association between ε4 and hippocampal asymmetry in dementia. We also examined whether asymmetry influenced neuropsychological performance, but minimal effects were observed. Where significance or strong trends were observed, better neuropsychological performance was associated with larger parenchymal volume of temporal lobe structures. These findings were interpreted as representing cognitive reserve effects where larger volume was protective against impairment. The role of asymmetry research in understanding neuropsychological performance in dementia is discussed. (JINS, 2002, 8, 925–933.)

The aim of this study was to examine the associations of apolipoprotein E (APOE) genotype, metabolic changes in the posterior cingulate detected by 1H magnetic resonance spectroscopy (MRS), and neuropsychologic measures of memory and cognition both in normally aging elderly, and in patients with mild cognitive impairment (MCI) and AD. We studied 67 controls, 18 MCI and 33 AD patients. We used the Dementia Rating Scale total score (DRSTOT) as a measure of general cognitive function and the total learning from the Auditory Verbal Learning Test (AVTOT) as a measure of memory performance. No differences were noted on 1H-MRS metabolite ratios or cognitive measures across APOE genotype within control and patient groups. In controls, age was a significant predictor of both cognitive test scores, and NAA/Cr was a univariate associate of DRSTOT. All 3 1H-MRS metabolite ratios, N-acetylaspartate (NAA)/creatine (Cr), myoinositol (MI)/Cr, and NAA/MI, were univariate associates of AVTOT and DRSTOT scores in the combined MCI and AD group. In stepwise regression analyses in the combined patient group only NAA/MI entered the models. These data suggest NAA/Cr could be a modest predictor of general cognitive function in both healthy elderly and impaired patients, while MI/Cr is a more specific marker for neuropsychologic dysfunction associated with neurodegenerative disease. Among 1H-MRS measurements, the NAA/MI ratio maybe the most efficient predictor of memory and cognitive function in patients with MCI and AD. (JINS, 2002, 8, 934–942.)

A subtle decline in episodic memory often occurs prior to the emergence of the full dementia syndrome in nondemented older adults who develop Alzheimer's disease (AD). The APOE-ε4 genotype may engender a more virulent form of AD that hastens this decline. To examine this possibility, we compared the rate of decline in episodic memory during the preclinical phase of AD in individuals with or without at least one APOE ε4 allele. Nondemented normal control (NC; n = 84) participants, nondemented older adults who subsequently developed dementia within 1 or 2 years (i.e., preclinical AD; n = 20), and patients with mild AD (n = 53) were examined with 2 commonly employed tests of episodic memory, the Logical Memory subtest of the Wechsler Memory Scale–Revised and the California Verbal Learning Test. Results revealed a precipitous decline in verbal memory abilities 1 to 2 years prior to the onset of the dementia syndrome, but there was little effect of APOE genotype on the rate of this memory decline. The presence of an APOE-ε4 allele, however, did have a differential effect on the sensitivity of the 2 types of memory tests for tracking progression and made an independent contribution to the prediction of conversion to AD. (JINS, 2002, 8, 943–955.)

Although some studies have reported a category specific naming deficit in Alzheimer's patients (invariably for living things), others have failed to replicate this finding (Laws et al., in press). Inconsistencies may partly stem from the fact that category effects are hidden in group analyses because individual Alzheimer's patients show category deficits in opposing directions, namely, some living and some nonliving (Gonnerman et al., 1997). Additionally, category effects may depend upon the specific composition of living things, such as the ratio of animals to fruits and vegetables, though this has never been explicitly examined. To examine this, we conducted a more detailed fractionation of living and nonliving categories for individual patients.

Patients with apraxia are more impaired when performing transitive pantomimes than intransitive gestures. This dissociation might be related to the differences in movement complexity. Alternatively, the programs for intransitive gestures might be better defined, more widely distributed, or easier to activate than are those for transitive pantomimes. The purpose of this study was to test the complexity versus representational hypotheses. Twenty right-handed normal subjects both performed and discriminated correct from incorrect transitive pantomimes and intransitive gestures. The discrimination was performed by having subjects point at illustrations of hand postures. The subjects performed better when discriminating postures than when performing gestures or pantomimes. On both the production and discrimination tests, subjects performed better with intransitive gestures than transitive pantomimes. Although the finding that even normal subjects had more difficulty performing transitive pantomimes than intransitive gestures might appear to support the complexity hypothesis, that subjects also had more difficulty discriminating transitive than intransitive postures supports the representational activation hypothesis. (JINS, 2002, 8, 958–963.)

In the first chapter the author states “this book is about disabilities affecting children that are due to some malfunction in the brain or nervous system.” The author intends this book as an introduction to the study of developmental disorders, particularly from a neuropsychological perspective. By the author's writing, the text is intended for advanced undergraduate courses in psychology and special education, or for use with beginning graduate courses, particularly in the area of clinical psychology. From my own read of Professor Freides' book, I believe it is most appropriate for advanced undergraduate courses. I found the text to be reasonably comprehensive regarding its stated aims, readable, informative, and there was a clear effort to reference both older, more “classic” studies, and also to insure current research references from relevant literature.