The present study examined neuropsychological (NP) functioning and associated medical, neurological, brain magnetic resonance imaging (MRI), and psychiatric findings in 389 nondemented males infected with Human Immunodeficiency Virus-Type 1 (HIV-1), and in 111 uninfected controls. Using a comprehensive NP test battery, we found increased rates of impairment at each successive stage of HIV infection. HIV-related NP impairment was generally mild, especially in the medically asymptomatic stage of infection, and most often affected attention, speed of information processing, and learning efficiency; this pattern is consistent with earliest involvement of subcortical or frontostriatal brain systems. NP impairment could not be explained on the bases of mood disturbance, recreational drug or alcohol use, or constitutional symptoms; by contrast, impairment in HIV-infected subjects was related to central brain atrophy on MRI, as well as to evidence of cellular immune activation and neurological abnormalities linked to the central nervous system. (JINS, 1995, 1, 231–251.)

The ability to detect dementia of the Alzheimer type (DAT) in a community-dwelling sample of elderly individuals on the basis of neuropsychological test performance was examined. Three hundred sixty community-dwelling individuals were identified by neurological examination as having probable or possible Alzheimer’s disease, being at risk for Alzheimer’s disease, or having no cognitive impairment. A logistic model comprised of tests of verbal and nonverbal memory, mental flexibility, and confrontation naming correctly classified 82% of DAT subjects and 98% of normal elderly subjects. The logistic model classified 77% of subjects who were diagnosed as at risk for Alzheimer's disease as being cognitively normal. A cross-validation with a clinically based sample of subjects correctly classified 89% of DAT patients and 100% of normal control subjects. The results suggest that psychometric discrimination of dementia may be less accurate in community-dwelling populations than in clinically based samples. (JINS, 1995, I, 252–260.)

The study aimed at investigating lateralization effects and signs of transfer and crowding in children with congenital lateralized brain damage with the aid of a dichotic listening test, a chimeric test, and verbal and nonverbal neuropsychological tests. Thirty-three children with spastic hemiplegia and 86 control children (age 5.0–12.0 yr) were assessed. Children with left-hemisphere damage (n = 17) were found to have a pathological left-ear advantage for verbal material, and children with right-hemisphere damage (n = 16) were found to have a pathological right visual half-field advantage for visual material. Children with left-hemisphere damage and a left-ear advantage on the dichotic test were also found to have a right visual half-field advantage on the chimeric test, which was regarded as a sign of reversed dominance. No verbal or nonverbal differences emerged between the left-hemisphere and the right-hemisphere damage groups, nor did differences emerge when the children were reclassified by considering children with left-hemisphere damage and signs of reversed dominance as having damage to the nondominant hemisphere. It was concluded that although lateralized brain damage may alter the dominance for verbal and visual functions, there is still considerable inter-individual variability with respect to inter- and intrahemispheric neural adjustment to damage. The dichotic and the chimeric tests did not indicate the presence of brain damage accurately, but they indicated the lateralization of damage in children with stated abnormality with a high degree (91.3%) of accuracy. (JINS, 1995, I, 261–270.)

This experiment investigated the effects of verbal labels on recognition memory for ambiguous visual figures in patients with Alzheimer's disease (AD), patients with Huntington's disease (HD), and matched normal control subjects. The study employed ambiguous figures that could be interpreted in two different ways. During the study phase each figure was presented together with a verbal label that corresponded to one interpretation of the figure. After a 30-min retention interval a recognition memory test was given during which the study figures and distractor figures were presented one at a time without verbal labels. For each study figure two distractor figures were employed, each corresponding to a different interpretation of the study figure. The patients' overall recognition memory performance was severely impaired compared to control subjects. However, all subject groups tended to produce responses and response latencies to distractor items that were consistent with the verbal labels presented during the study phase. This bias effect occurred in the AD patients despite the fact that their recognition memory performance was at chance level. Indeed, there was no significant difference in the bias evidenced by the AD and HD patients and their respective matched control subjects. The bias effects were obtained in an explicit memory task, and the findings are discussed in terms of unconscious influences on explicit memory processes. (JINS, 1995, I, 271–280.)

Neuropathology in Huntington's disease (HD) known to project to areas that process olfactory information raises the questions of which olfactory function, if any, is most affected in HD, and how to explain such dysfunction in terms of olfactory sensitivity and cognition. These questions were studied by comparing HD patients and controls (matched for age, gender, and education) on absolute detection, intensity discrimination, quality discrimination, short-term recognition memory, and lexical- and picture-based identification for odor. Taste or vision were used as comparison modalities. The results suggest that whereas odor-recognition memory is not affected in patients with HD, these patients have impaired olfactory functioning with respect to absolute detection, intensity discrimination, quality discrimination, and identification. The three latter impairments were significantly explained by poor detection sensitivity. Odor identification was the function most affected. (JINS, 1995, I, 281–290.)

We administered the Multiscale Depression Inventory (MDI) and the Beck Depression Inventory (BDI) to 84 multiple sclerosis (MS) patients, 101 patients diagnosed with major depression and 87 nonmedical, nonpsychiatric controls. The MDI consists of three separate depression scales measuring mood, vegetative, and evaluative symptoms. We found that: (a) MS patients did not significantly differ from the controls in mood symptoms, (b) the depression prevalence rate in MS patients was significantly lower when measured by the mood scale (17·7%) than by the BDI (30·5%) or MDI total score (26·6%), and (c) MS patients showed significantly less mood disturbance than a non-MS comparison group matched on BDI measured depression severity. We suggest that the inclusion of nonmood symptoms in self-report depression scales may artificially raise both prevalence rates and severity ratings of MS related depression and that the most valid measure of depression in MS is mood disturbance. (JINS, 1995, I, 291–296.)

The present study examined the relationship between rate of cognitive decline in patients with Alzheimer's disease (AD) and the integrity of the network of associations that comprise their semantic knowledge. The integrity of the semantic network of 12 AD patients was determined by comparing their networks to a standard normal control network derived with Pathfinder analysis, a multidimensional graphic analysis technique. A simple linear regression analysis, comparing the degree of semantic network deterioration with rate of cognitive decline as measured by the difference between the Dementia Rating Scale (DRS) scores obtained at the time of the testing of semantic knowledge (Year 1) and one year later (Year 2), was highly significant (r2 = .84; p < .001). These results suggest that a sensitive measure of the structural deterioration of semantic knowledge may be useful for predicting the rate of progression of cognitive changes in patients with AD. (JINS, 1995, I, 297–303.)

The current review was conducted to address the ongoing debate regarding the presence or absence of neuropsychological impairment in asymptomatic HIV-Type 1 (HIV-1) seropositive individuals. Results were summarized from 57 studies that compared the performances of seropositive asymptomatic and seronegative individuals. Overall, the differences observed between median rates of impairment for asymptomatic (35%) and seronegative (12%) groups provided the clearest indication of deficits in asymptomatics. In addition, five variables were examined as possible contributors to inconsistencies found in the literature: mode of infection, test battery type, test battery size, sample size, and method of data analysis. Of these variables, only mode of infection and test battery size appeared to substantially influence the outcome of the studies reviewed with regard to identifying neuropsychological impairment in asymptomatics. (JINS, 1995, I, 304–315.)