Recency discrimination has been conceptualized as an executive ability by some investigators and as an aspect of episodic memory by others. We compared the performance of 261 neurologically healthy adults on a recency discrimination task (RDT) with their performance on measures of executive functioning and explicit memory. Mean z-transformed raw scores were used to construct indices of visual and verbal explicit memory, fluency, and executive functioning. Analyses revealed that RDT performance correlated more closely with visual (r = 0.32; p < 0.001) and verbal memory (r = 0.25; p < 0.001) than with fluency (r = 0.16; p < 0.05) and executive functioning (r = 0.13; p < 0.05). These findings suggest that recency discrimination might be better understood as an aspect of episodic memory that is subserved primarily by hippocampal and medial temporal structures than as an executive function that is subserved primarily by prefrontal cortex. (JINS, 2007, 13, 710–715.)

Previous studies have shown a significant association between reading skills and the performance on visuo-motor tasks. In order to clarify whether reading and writing skills modulate non-linguistic domains, we investigated the performance of two literacy groups on a visuo-motor integration task with non-linguistic stimuli. Twenty-one illiterate participants and twenty matched literate controls were included in the experiment. Subjects were instructed to use the right or the left index finger to point to and touch a randomly presented target on the right or left side of a touch screen. The results showed that the literate subjects were significantly faster in detecting and touching targets on the left compared to the right side of the screen. In contrast, the presentation side did not affect the performance of the illiterate group. These results lend support to the idea that having acquired reading and writing skills, and thus a preferred left-to-right reading direction, influences visual scanning. (JINS, 2007, 13, 359–364.)

Speed of information processing in persons with postconcussion syndrome (PCS) was examined using word fluency tasks. Twenty patients with PCS and twenty controls matched for age, gender, and occupation were given two word fluency tasks, and the speed of word generation was measured. Response latencies were analyzed to determine whether slowed retrieval or degradation of words in semantic memory was responsible for problems with word retrieval after traumatic brain injury. The PCS group recalled fewer words, had significantly longer interresponse times, and took significantly longer to generate their first word than the controls. There was no evidence that either structure loss or slowness in word retrieval from semantic memory could account for the word fluency deficits. Rather, the findings suggest that the primary cause of word retrieval difficulties in patients with PCS is a generalized slowness of cognitive processing (JINS, 2007, 13, 178–182.)The study described was part of Maria Crawford's doctoral thesis. This research was supported by a University of Otago Research Grant awarded to Robert G. Knight and a Ph.D. scholarship awarded to Maria Crawford.

Because MS patients frequently report visual acuity disturbances, neuropsychologists often screen patients for severe visual acuity disturbances and tailor test batteries that minimize the need for intact vision. Less is known about how mild visual acuity disturbances may influence neuropsychological test performance. This study examined the extent to which mild visual acuity disturbances influence performance on visually-based tests of complex attention. Relapsing-remitting and secondary progressive MS patients who reported adequate vision were recruited for this study. A battery was administered that included the oral version of the Symbol Digit Modalities Test (SDMT), the Visual Elevator (VE) subtest from the Test of Everyday Attention, and a reduced near vision eye chart. Results suggested that, in addition to measuring higher order cognitive processes, visual tests of attention are sensitive to mild primary visual disturbances in MS. (JINS, 2007, 13, 544–548.)

A central role for neuropsychological evaluations is the measurement of change in cognitive functioning over time. However, change scores obtained from repeated neuropsychological assessments may be affected by normal variability because of measurement error and practice effects caused by repeated measurements. The current study uses reliable change estimates to establish normative rates of change on the Dementia Rating Scale from baseline to first follow-up testing among 1080 cognitively normal adults aged 65 and older. Results showed that a 6-point decline by European Americans or a 9-point decline by African American adults within a 9–15 month test-retest interval represents reliable change. Within a 16–24-month test-retest interval, a 7-point decline among European Americans or an 8-point decline among African American adults represents reliable change. In addition, preliminary cross-validation was performed in a clinical comparison sample of another 22 older adults. The findings are discussed in the context of potential clinical and research applications. (JINS, 2007, 13, 716–720.)

Minutes from the Thirty-Fifth Annual International Neuropsychological Society Meeting, Portland, Oregon.

Amnestic mild cognitive impairment (aMCI) is associated with neuropathological changes in medial-temporal and frontal-system structures. By definition, retrospective memory is mildly impaired in aMCI. We examined whether prospective memory (PM) is also impaired, in particular time-based PM, which requires considerable self-initiation and inhibition. We administered time- and event-based PM tasks to 42 healthy older adults, 45 individuals with aMCI, and 24 individuals with Alzheimer's disease (AD). The healthy group performed better than the aMCI group, and the aMCI group performed better than the AD group on both PM tasks. Importantly, the aMCI group performed more poorly on the time- than event-based task, whereas the other groups performed comparably on both tasks. Findings suggest that PM, particularly time-based PM, is sensitive to the earliest cognitive changes associated with aMCI, possibly reflecting decreased self-initiation, attention switching, and/or inhibition on memory tasks because of early involvement of the frontal system. (JINS, 2007, 13, 365–369.)

Human Hand Function, by Lynette A. Jones and Susan J. Lederman. 2006. New York: Oxford University Press. 270 pp., $65.00 (HB).

Our hands are more than just convenient appendages for supporting our morning cup of coffee and bagel. They are highly evolved effectors capable of performing a vast array of complex tasks and the rapid decoding of multi-sensory information from the environment. Human Hand Function synthesizes the empirical evidence on nearly all aspects of hand function. The book is thoughtfully organized. Following the overview in which the authors introduce a conceptual framework of understanding hand function, there is the obligatory chapter on evolutionary development of hand anatomy. This chapter is more than just a review of phylogeny, as the authors link anatomical capacity with functional success and failures throughout the evolutionary ladder. Chapter 2 ends with a brief overview of biomechanical models that left this reviewer wanting more. It would have been nice to see more tables that synthesize complex concepts into a useful format. For example, following the discussion of biomechanical models in Chapter 2, it would have been helpful to see a table that translates various forces the hand is capable of generating into familiar operational behaviors, such as those we engage in daily.

Human immunodeficiency virus (HIV)-infected adults frequently evidence both neurocognitive and psychiatric dysfunction. It was hypothesized that apathy and irritability, but not anxiety and depression, are related to HIV effects on frontal–subcortical systems. This hypothesis was evaluated by determining the degree to which these psychiatric features are associated with neurocognitive functioning that is dependent upon frontal–subcortical circuitry and, therefore, thought to be sensitive to the central nervous system effects of HIV. Rating scales assessing irritability, apathy, depression, and anxiety and a dual-task paradigm were administered to 189 HIV-seropositive (HIV+) and 53 HIV-seronegative participants. Deficits in dual-task performance and greater anxiety, depression, apathy, and irritability were observed in HIV+ participants. Simultaneous multivariate regression and communality analyses revealed that only apathy and irritability were associated with dual-task performance in HIV+ participants. Thus, these findings suggest that apathy and irritability, but not depression and anxiety, are likely associated with the effects of HIV on frontal–subcortical circuitry. (JINS, 2007, 13, 549–554.)

Cognitive Reserve: Theory and Applications. Yaakov Stern (Ed.). 2007. New York: Taylor and Francis, 344 pp., $99.00 (HB).

Successful aging has been on my mind more and more these days. Time flows forward and I am now reasonably certain that I'm not getting any younger. Thankfully, cognitive reserve (CR) gives me a reason to be hopeful: although I never made it to the Boston Symphony Orchestra or the Olympic medals platform, perhaps all those French horn lessons and 6 am swim-team practices will ultimately pay off.

Bowers et al. (2006) cite my 1984 review of the neuropsychology of facial expression (Rinn, 1984) as “the underlying impetus” for their recent investigation of facial expression in Parkinson's disease (PD). In that paper, I noted that impaired basal ganglia function in PD results in diminished spontaneous expressive facial movements, yet it produces no true paralysis for volitionally induced facial movements. Bowers et al. take my statements a step further: “According to Rinn (1984), patients with Parkinson's disease (PD) have little difficulty posing facial emotions when explicitly told to do so. They just fail to do so spontaneously.” They also quote me as describing Parkinson's disease as “the ‘model system’ for subcortical, basal ganglia influences on facial expression.” Bowers then goes on to demonstrate that the facial expression deficiencies of PD patients are not confined to a lack of spontaneous emotional movements (the masked face), and that volitionally posed facial expressions in PD are also aberrant [i.e., slow (bradykinesic) and of diminished amplitude].

In this journal, Anstey et al. (2006) reported the results of a potentially important clinical study on the effect of cataract removal on the cognitive performance of older adults. Unfortunately, because of inappropriate data analyses, some reported results are meaningless. Consequently, the conclusions drawn by the authors regarding the impact of the cataract surgery cannot be considered valid.

Given the largely prefrontostriatal neuropathogenesis of HIV-associated neurobehavioral deficits, it is often presumed that HIV infection leads to greater impairment on letter versus category fluency. A meta-analysis of the HIV verbal fluency literature was conducted (k = 37, n = 7110) to assess this hypothesis and revealed generally small effect sizes for both letter and category fluency, which increased in magnitude with advancing HIV disease severity. Across all studies, the mean effect size of category fluency was slightly larger than that of letter fluency. However, the discrepancy between category and letter fluency dissipated in a more conservative analysis of only those studies that included both tests. Thus, HIV-associated impairments in letter and category fluency are of similar magnitude, suggesting that mild word generation deficits are evident in HIV, regardless of whether traditional letter or semantic cues are used to guide the word search and retrieval process (JINS, 2007, 13, 183–189.)

Gilmore (2007) argues that the use of ANCOVA in Anstey et al. (2006) is invalid. Based on quotes in Winer (1971), he claims that covariates cannot be used to adjust interaction terms involving within-subject variables. Because the within-subject variable in Anstey et al. (2006) is time, he concludes that the results involving Time × Group interaction coefficient are invalid and consequently all analyses need to be re-done.

Mild Cognitive Impairment: International Perspectives. Holly A. Tuokko and David F. Hultsch (Eds.). 2006. New York: Taylor & Francis, 319 pp., $99.00 (HB).

As neuropsychologists, it is our job to differentiate normal from abnormal. We act as arbiters of behavior, defining “impairments” and using normative data and estimates of premorbid functioning to delineate post-injury or post-disease decline. Although one is obviously inclined to steer the diagnostic process in such a way as to comply with the prevailing taxonomy, because of the categorical nature of our classification system, this task is most difficult at the border zones, those areas that lie somewhere between “normal” and “abnormal.” The categories applicable to “abnormal ageing” have varied greatly over the years and are still evolving. Mild cognitive impairment or MCI is one such border zone category, which is believed to be a precursor to dementia in some patients. As with most border zone diagnostic entities, those patients at the cusp of the border will always be most difficult to classify. There will be certain low functioning “normal” people who score marginally low on our tests. Likewise, there will be certain high functioning “abnormal” people who score similarly. Even when the line is drawn with confidence and the MCI diagnosis is rendered, what does one impart to the patient about prognosis given the lack of clear relationship between the diagnosis and conversion to dementia, as well as the lack of clear relationship between the diagnosis and underlying brain pathology? It is a difficult and uncomfortable label because we know that a certain percentage we assign this moniker will “get better” (or is it regression to the mean?), become demented (or do they have less cognitive reserve?), or stay the same (or do they have more cognitive reserve?). The research literature behind abnormal ageing is incredibly diverse with regard to populations studied, methods of assessment, cut-offs utilized, nature and number of cognitive domains considered, and the extent to which subjective patient complaints are considered. As the heterogeneity in this construct becomes more apparent, there is need to increase the number of available labels as evidenced by evolving concepts like “amnestic MCI.” Thus, from a historical and clinical perspective, applying the term “MCI” is a bit like throwing a rock at a moving target.

Autism: A Neurological Disorder of Early Brain Development. Roberto Tuchman and Isabelle Rapin (Eds.). 2006. London, England: Mac Keith Press for the International Child Neurology Association, 354 pp., $115.00/£65.00.

Historically, the need or drive to connect to other humans is absent from the instincts that Freud considered fundamental to all humans, and from the work of Charles Darwin (1965), who heavily influenced Freud. Despite the fact that Darwin's last major publication focused on the expression of emotion in humans and animals, neither major theorist, both critical to the development of psychology, gave a place in their theories to the desire to connect to others. Yet new research consistently points to a desire for social connection in all of us and in our closest relatives on the evolutionary chain. When social relatedness is impaired, the results are devastating, and nowhere is this devastation more apparent than in a child with autism, the subject of this multi-authored volume.

Fluent Aphasia, by Susan Edwards. 2006. New York: Cambridge University Press. 230 pp., $75.00 (HB).

The 21st-century aphasiologist may be surprised to find a new book with such a title as Fluent Aphasia. Three decades of cognitive neuropsychology advances would seem sufficient to relegate a fuzzy concept like “fluent aphasia” as a relic of the past, or, at best, restrict it to the realm of shorthand descriptions meant to facilitate daily communication among clinicians. Even among those accustomed to strict collaboration, a concept like “fluent aphasia” may cause misunderstanding. I personally learned about aphasia directly from the Boston school. Yet, when I speak with my Italian colleagues from Milan, whom I have known for most of my professional life, and with whom I have written quite a few papers on aphasia, I am often unsure about what they mean when they label an aphasic patient as “fluent.” I still remember Harold Goodglass telling me, in almost the same words Susan Edwards quotes from him, how “fluency is best rated in terms of the longest occasional uninterrupted strings of words that are produced.” My own understanding of his teaching included the concept that the presence of phonetic problems and/or abnormal articulation effort was not so essential in drawing the fluency-non fluency distinction: according to his rule of thumb, fluent aphasia should be diagnosed when a patient can produce at least five connected words. This rule derived from observations made in Goodglass, Quadfasel, and Timberlake's (1964) study on phrase length and type of aphasia, whereby it was shown that aphasics can be dichotomized on the basis of the number of words that they can typically utter as an uninterrupted string. Edwards reports that other people entertain different beliefs about what is fluent aphasia. Surely several, heterogeneous criteria such as phrase length, verbal agility, melodic line, amount of articulation effort, and grammatical form are differently weighted by different aphasiologists as they consider their diagnosis.

Learning Disabilities: From Identification to Intervention. Jack M. Fletcher, G. Reid Lyon, Lynn S. Fuchs, and Marcia A. Barnes. 2007. New York: The Guilford Press, 324 pp, $38.00 (HB).

Four senior leaders in the fields of neuropsychology, cognitive neuroscience, and special education tackle the complex issue of learning disabilities in Learning Disabilities: From Identification to Intervention. They summarize research conducted over the past 30 years that has contributed to our understanding of how to assess, identify, and treat learning disabilities. Determining the presence of a learning disability is different from measuring the manifestations of brain damage caused by brain injury or disease states that neuropsychologists typically evaluate. Fletcher et al. point out that the construct of a learning disability is a latent variable. It is not observable directly and is consequently difficult to operationally define, identify, and measure. They also show that characteristics associated with a learning disability are dimensional and occur along a continuum. Adding to the intricacy is the difficulty keeping abreast with education policy and knowledge of how federal law drives clinical practice.

Mental Retardation and Developmental Delay: Genetic and Epigenetic Factors, by Moyra Smith. 2006. New York: Oxford University Press, 344 pp., $49.95 (HB).

Most of us have had the experience of evaluating a child who looks just like other children, whose MRI scan is read as normal, and whose test performance results in a diagnosis of mental retardation. Such children cause us to ponder the question, “How can a brain look so normal, yet work so abnormally?” As the results are presented, parents ponder a different question. They want to know why this has happened to their child. What makes the question a hard one to respond to is that we ask ourselves the same question but often do not have an answer. The neuropsychological conceptualization of mental retardation starts with skill patterns and works backwards through neural networks looking for cause. Mental Retardation and Developmental Delay: Genetic and Epigenetic Factors begins with the inner workings of the cell, examining genes, gene products, and cell metabolism as the basis for the observed disruption of learning and memory.

Brain and Culture: Neurobiology, Ideology, and Social Change, by Bruce E. Wexler. 2006. Cambridge, Massachusetts: The MIT Press, 307 pp., $34.00 (HB).

In Brain and Culture: Neurobiology, Ideology, and Social Change, Bruce Wexler takes on the age old debate of “nature versus nurture.” His premise is that neurological and psychological functions are intrinsically tied to one another, that each one drives the development of the other, making it impossible to differentiate the two. In order to make his case, Dr. Wexler adeptly covers an impressive breadth of research from a diverse array of disciplines. He includes seminal works from cognitive psychology, developmental psychology, psychoanalysis, experimental psychology, sociology, anthropology, and of course, neuropsychology. Although Dr. Wexler does not present any new research in this book, by juxtaposing information from many disciplines, a new spin on the old debate clearly emerges.