This study was designed to examine the patterns of apraxic disturbances and the relationships between action knowledge and other measures of semantic knowledge about objects in 10 well-characterized Alzheimer's disease (AD) patients. Five tasks were used to assess components of action knowledge (action–tool relationships, pantomime recognition, and sequential organization of action) and praxis execution (actual use, pantomiming) according to the cognitive model of praxis. Three tasks (verbal comprehension, naming, and a visual semantic matching task) were used to assess verbal–visual semantics. Considering patterns of apraxia first, conceptual apraxia was found in 9 out of the 10 AD patients, suggesting that it is a common feature even in the early stages of AD. Second, we found partly parallel deficits in tests of action-semantic and verbal–visual semantic knowledge in 9 AD patients. Impaired action knowledge was found only in patients with a semantic language deficit. These findings provide no evidence that “action semantics” may be separated from other semantic information. Our results support the view of a unitary semantic system, given that the representations of action-semantic and other semantic knowledge of objects are often simultaneously disrupted in AD. (JINS, 2000, 6, 693–703.)

The Boston Diagnostic Aphasia Examination Battery (BDAE) is one of the most widely used aphasia tests worldwide. Information about general population performance, however, is limited. This paper analyzes the effects of gender, age, socioeconomic status (SES), academic achievement, and occupation on the BDAE Spanish version. The BDAE was administered to a randomized sample of 156 occupationally active 19–60-year-old participants (75 male and 81 female) from two SES groups. Gender and age had a significant effect on some reading and writing subtests. Body-part naming and mechanics of writing scores were significantly decreased in the low SES group. Education had a significant impact over most of the BDAE subtests. A stepwise regression model showed that academic achievement was best able to predict the variance in BDAE scores with a low (<15%) to modest (>17%) but significant capability (F MANOVA p < .01). A factor analysis disclosed 7 factors that explained 67% of the total variance. (JINS, 2000, 6, 802–814.)

The purpose of this study was to examine the independent and interactive effects of HIV-1 serostatus and cocaine on neuropsychological (NP) performance in a sample of 237 gay and bisexual urban-dwelling African American men. Consistent with current evidence, it was expected that the greatest neuropsychological performance deficits would be evident (1) in the symptomatic seropositives (SSPs), especially in domains affected by HIV (i.e., memory and psychomotor speed), and on tests that are sensitive to subtle slowing; (2) in those who are recent and frequent cocaine abusers; and (3) in those who are both HIV seropositive and cocaine abusers. Multivariate analyses controlling for age and alcohol use confirmed expectations, with symptomatic seropositives (SSPs) evidencing significantly poorer psychomotor speed than the seronegatives (SNs), and slower reaction time and poorer nonverbal memory than the asymptomatic seropositives (ASPs). Moderate to heavy recent cocaine use was associated with slower psychomotor speed. However, contrary to expectations, no interaction of serostatus and cocaine was noted for any NP domain, and the expected serostatus and cocaine effects on verbal memory and frontal systems were not obtained. Level of alcohol consumption exacerbated the detrimental effects of HIV-1 on a computerized reaction time test which is especially sensitive to subtle slowing. This study provides one of the first descriptions of the neuropsychological effects of HIV–AIDS in a noninjection drug-using community sample of gay and bisexual African American men. (JINS, 2000, 6, 322–335.)

What we call computational neuroscience involves construction of mathematical and numerical models for understanding cognitive phenomena. This issue is devoted to showing how it can also be used to help in the analysis of cognitive defects. Although the models may seem abstract to clinicians, they are based on the reality of brain anatomy. The theoretical papers presented here are connectionist: They posit a network of cells connected by synapses whose weights are modified during learning. Architecture of connectionist models has progressed and ramified considerably since they were first introduced, and we include some examples of the current state of the art. The final work presented here is concerned with the connection of the constructed models with clinical experience and experiment.

Prospective memory can be defined as the timely execution of a previously formed intention, and is critical in daily life because of its inherent involvement in goal-directed behavior. Cognitive systems involved in prospective memory have been hypothesized as involving the frontal cortex, and in adults, associated with working memory and executive functions. This study introduces a new computerized measure of prospective memory designed for children. In this study prospective memory is examined in a driving game task called the CyberCruiser. In a sample of 80 children ages 6–12 years, variables from this task demonstrated a significant age effect and were significantly correlated with other well known measures of executive function, even after controlling for chronological age. Performance on this task also demonstrated the anticipated pattern of strategic monitoring that has been demonstrated in other studies of prospective memory. (JINS, 2000, 6, 62–70.)

This paper is a literature review on assessment of fitness to drive in older drivers with cognitive impairment. Early studies on dementia and driving generally failed to distinguish between safe and unsafe drivers on the basis of cognitive test performance. Predictive studies demonstrated that cognitively impaired persons as a group perform significantly worse than controls on both neuropsychological and driving measures. A high prevalence of cognitive impairment was found in groups of older drivers involved in traffic accidents and crashes. However, a large range in neuropsychological test scores has been found. Low to moderate correlations could be established between neuropsychological test results and on-road driving performance, making it difficult to discriminate between cognitively impaired subjects who are fit or unfit to drive. The review concludes with a discussion of methodological difficulties in the field of dementia and driving, including participant selection, the choice of neuropsychological tests, and the operationalization of driving performance. (JINS, 2000, 6, 480–490.)

This article suggests how brain mechanisms of learning, attention, and volition may give rise to hallucinations during schizophrenia and other mental disorders. The article suggests that normal learning and memory are stabilized through the use of learned top-down expectations. These expectations learn prototypes that are capable of focusing attention upon the combinations of features that comprise conscious perceptual experiences. When top-down expectations are active in a priming situation, they can modulate or sensitize their target cells to respond more effectively to matched bottom-up information. They cannot, however, fully activate these target cells. These matching properties are shown to be essential towards stabilizing the memory of learned representations. The modulatory property of top-down expectations is achieved through a balance between top-down excitation and inhibition. The learned prototype is the excitatory on-center in this top-down network. Phasic volitional signals can shift the balance between excitation and inhibition to favor net excitatory activation. Such a volitionally mediated shift enables top-down expectations, in the absence of supportive bottom-up inputs, to cause conscious experiences of imagery and inner speech and thereby to enable fantasy and planning activities to occur. If these volitional signals become tonically hyperactive during a mental disorder, the top-down expectations can give rise to conscious experiences in the absence of bottom-up inputs and volition. These events are compared with data about hallucinations. The article predicts where these top-down expectations and volitional signals may act in the laminar circuits of visual cortex and, by extension, in other sensory and cognitive neocortical areas, and how the level of abstractness of learned prototypes may covary with the abstractness of hallucinatory content. A similar breakdown of volition may lead to delusions of control in the motor system. (JINS, 2000, 6, 583–592.)

A history of the early years (1965–1985) of the International Neuropsychological Society (INS) is presented. Themes than run through these years—such as the need for an organizational structure, attempts to make the Society truly international, and the involvement of the membership, especially, the “younger” members, in governance—are clearly evident. After a somewhat shaky start, the Society came of age toward the end of this formative 20-year period. (JINS, 2000, 6, 491–509.)

Prominent apathy and/or irritability are frequently observed among individuals infected with the human immunodeficiency virus (HIV). Although these symptoms often occur as part of a mood disorder, compelling evidence suggests that they may occur independently of depression in neurologic disease/disorder. The current study examined the prevalence of both apathy and irritability among a sample of HIV-infected individuals and explored the degree to which these neuropsychiatric (NP) phenomena were associated with performance on neurocognitive measures thought to be sensitive to the potential CNS effects of HIV-1. Clinician-administered rating scales assessing apathy and irritability were administered to 65 HIV-seropositive (HIV+) and 21 HIV-seronegative (HIV−) participants who also completed a dual-task reaction time paradigm and the Stroop task. NP disturbance was significantly more prevalent among HIV+ participants compared with HIV− controls and was associated with specific neurocognitive deficits suggestive of executive dysfunction. Relative to both HIV− controls and to neuropsychiatrically intact HIV+ participants, those HIV+ individuals with evidence of prominent apathy and/or irritability showed deficits in dual-task, but not single-task, performance and on the interference condition of the Stroop. Unexpectedly, NP disturbance did not show a robust relationship with HIV disease stage. These results suggest that the presence of prominent apathy and/or irritability among HIV+ individuals may signify greater HIV-associated CNS involvement. In HIV/AIDS, the disruption of frontal–subcortical circuits may be a common mechanism causing both executive dysfunction and NP disturbance. (JINS, 2000, 6, 336–347.)

In a previous study, we demonstrated that unilateral cerebral lesions produce hypometric limb movements of the contralateral arm and hemispatial (i.e., directional) hypometria for movements towards contralateral hemispace. In the present study, we investigated 10 patients with right cerebral lesions and 25 healthy controls using a task to uncouple deficits in sensory perceptual systems and motor-action output systems on directional hypometria. This task required participants, with their eyes closed, to reproduce lateral and medial horizontal displacements (15–27 cm) with each arm. Each participant was seated at a waist high table and had their hand placed at an origin point aligned with the axillary fold on the same side. Their hand was moved by the investigator from the origin point to a target point and brought back to the point of origin (input displacement). The participant was then asked to return their hand to either the same target point or to an equidistant target point in the opposite direction. Healthy dextral participants were significantly more hypometric with their right arm, but patients with right cerebral lesions exhibited an opposite pattern with overall left arm hypometria. In addition, patients were significantly more hypometric for movements when output displacements were toward left hemispace. No effect was found for direction of sensory input. The results suggest that the directional hypometria is predominantly produced by hemispatial output deficits. (JINS, 2000, 6, 71–75.)

Psychotic symptoms are common in Alzheimer's disease (AD) and clinicoanatomical and neuropsychological evidence indicate an association between these symptoms and frontal lobe dysfunction. Neurobehaviors associated with frontal dysfunction were assessed in Alzheimer's disease (AD) patients with (n = 20) and without psychotic symptoms (n = 21) matched for mean age, education, gender, and dementia severity. The Frontal Lobe Personality Scale (FLOPs) was completed by patient caregivers to measure behaviors typically associated with frontal dysfunction. Findings indicated that AD patients with psychotic symptoms exhibited significantly greater neurobehavioral dysfunction (FLOPs M = 130.69, SD = 24.70) than AD patients without psychotic symptoms (FLOPs M = 111.10, SD = 25.83). Subscale analyses indicated that psychotic AD patients were more disinhibited (M = 28.28, SD = 7.54) than patients without psychotic symptoms (M = 20.92, SD = 4.9). Findings are consistent with and contribute to previous neuropsychological and clinicoanatomical research suggesting increased frontal dysfunction in AD with psychotic symptoms and lend additional empirical support to subtyping AD based on the presence of psychotic symptoms. Furthermore, findings provide preliminary evidence indicating which specific type of neurobehavioral abnormalities are related to the presence of distressing psychotic symptoms. (JINS, 2000, 6, 815–820.)

Although a U.S. Presidential Proclamation designated the 1990s “The Decade of the Brain,” not all cerebral constituents shared equally in the limelight. By anyone's accounting, the prefrontal cortex was the darling of clinicians and neuroscientists throughout the '90s, with everything from schizophrenia and anorexia nervosa to pathological gambling and the emergence of artistic skill attributed to “frontal lobe dysfunction” (David, 1992; Miller et al., 1998; Rugle & Melamed, 1993). It should come as no surprise, then, that that most universal of cognitive afflictions, aging, should be linked to changes in frontal cortex.

Age-related declines in executive abilities have been widely reported and are thought to result from neuropathological changes in the prefrontal cortex. Some investigators have suggested that age-related changes in cognition may be the result of slowed information processing speed rather than declines in specific cognitive abilities. We examined the relationships among age, executive abilities, and psychomotor speed in 40 older adults and 46 young adults. Both verbal and nonverbal tasks were administered that measured 2 aspects of executive ability: set formation and set shifting. Executive and psychomotor speed tasks were paired based on similarities in basic task demands. Our results revealed that poorer executive performance was associated with increasing age. Further, although psychomotor speed attenuated the relationship, age accounted for a unique and significant proportion of variance in executive performance after controlling for psychomotor speed. These results suggest that age has an effect on prefrontally mediated executive abilities that cannot be explained solely in terms of psychomotor slowing. (JINS, 2000, 6, 76–82.)

The performance of cognitive behaviors requires an activated, aroused cerebral cortex. Although studies have shown that there are decrements of cognitive functions in the elderly, changes in arousal with aging have not been fully studied. Our objective was to learn if there are attention–arousal changes associated with aging. Visual stimuli were presented to induce orienting responses or arousal reactions. Because changes in pupil size reflect changes in arousal, we recorded and compared pupillary responses of young and older normal participants using infared pupillography. During the 1 s that we recorded pupillary changes, we found major phases: a brief initial constriction (C1), then a maximal dilation (D1)—an arousal response, followed by constriction (C2), a habituation response. Although amplitude of these 3 phases was not different between the 2 groups, the interval between the D1 and C2 response was prolonged in the older group. Although the arousal response is not dramatically altered with aging, habituation appears to be delayed. (JINS, 2000, 6, 348–350.)

Studies of cognitive functioning in patients with systemic lupus erythematosus (SLE) have found deficits even in patients without other evidence of neurologic involvement. The present study used scores on the 11 items of the Mini-Mental State Exam (MMSE) to classify the cognitive impairment of 93 SLE patients as suggestive of “cortical” or “subcortical” dysfunction using a validated statistical algorithm. Ninety-five percent of patients were categorized as having “subcortical” deficits, and 5% were categorized as having “cortical” deficits. When the analysis was limited to only those with total MMSE scores ≤ 24, 81% were classified as “subcortical” and 19% as “cortical.” These results suggest that SLE patients can have psychomotor and mental tracking deficits of a type seen in patients with subcortical brain disease, even in the absence of gross neurologic involvement. (JINS, 2000, 6, 821–825.)

I will confess to a lingering knee-jerk reaction when human cognitive processes are diagramed with boxes and arrows in a way never intended to correspond to identifiable neural pathways. In college and graduate school, such exercises seemed to me a waste of time, when I could be learning how the brain “really” works in mediating memory functions, language, and so forth.

That the human frontal lobes are particularly vulnerable to age-related deterioration has been frequently invoked as an explanation of functional decline in aging. This “frontal aging hypothesis” is evaluated in this review by examining evidence of selectively reduced frontal lobe function in aging. The frontal aging hypothesis predicts that functions largely dependent on frontal regions would decline in aging, while functions largely independent of frontal lobes would remain relatively spared. The hypothesis further predicts that age-related brain change would selectively impact frontal regions. The literatures on working memory, visuospatial attention, face recognition, and implicit memory were reviewed as exemplars of functions dependent on prefrontal, parietal, temporal and occipitotemporal cortices, respectively, with a view to establishing mediating structures and effects of aging. Age sensitivity was seen both in functions dependent on frontal integrity as well as in functions apparently independent of frontal integrity. Further, although prefrontal areas exhibit age-related decreases in regional volume, blood flow and metabolism, nonfrontal cortical regions undergo similar declines. It is concluded that while the frontal lobes are subject to age-related changes reflected in both behavior and pathology, there is only weak and conflicting evidence that frontal regions are selectively and differentially affected by aging. It is argued that a network-based theory of cognitive aging has advantages over the localizationist approach inherent in the frontal aging hypothesis. (JINS, 2000, 6, 705–726.)

Amnesia in its various forms is characterized by defects in one or more components of a complex system. Implantation of short-term memory occurs in the hippocampus, while long-term memory is essentially located in the neocortex; these regions are interconnected through complex synaptic structures. In the hippocampus, physiological data show that, as predicted by Hebb, excitatory synapses between nearby excitatory cells become strengthened by simultaneous activation. In contrast with this local process, the preponderance of clinical and experimental evidence indicates that cortical recall of a “memory” is the reconstruction of fragments stored in different synaptically distant brain regions. A mathematical model of memory must reconcile this apparent contradiction as well as explain how many different memories and “ideas” can be assembled within a given anatomical area. Continuum theory, which treats an ensemble of “cell assemblies” or neural networks, offers a step in this direction. Linear analysis using this approach shows that it is the nature of the neural continuum to generate activity waves of wavelength greater than synaptic connection ranges. These waves grow under certain circumstances, and their wavelength is controlled by the synaptic parameters. Both hippocampal and cortical tissue are subject to such wave growth. In the hippocampus, the local Hebbian strengthening controls the global wave growth, making the difference between wave decay and growth. The cortical wave structure can become very complex, so that reproducible memory recall as well as “creative thought” can be accommodated in the theory. Deficits in the functioning of the system may also be evaluated potentially by means of “goodness-of-fit” of the clinical and spatially resolved data with the model. (JINS, 2000, 6, 593–607.)

Since its first publication in 1978, and even more since having the second edition (1987), this prodigious compilation of clinically relevant information about the spectrum of neuropsychiatric entities and issues has been one of my most used reference books. Among its many virtues are its clarity of presentation, useful documentation, and coverage of just about all neurologic disorders that have behavioral (i.e., psychological and/or psychiatric) implications. I would not have wanted to practice or write without the current edition of Lishman at hand.

This is a reprint of one issue in the Cambridge University Press journal Behavioral and Brain Sciences, originally based on the symposium Controversies in neuroscience IV: Motor learning and synaptic plasticity in the cerebellum, held in Portland Oregon on August 24 to 26, 1993. These symposia were organized by the Robert S. Dow Neurological Sciences Institute and supported by NIH, NSF, and the Good Samaritan Foundation. The subjects of the symposium were the role of the cerebellum in motor learning and the connection between motor learning and synaptic plasticity.