The relative insensitivity of traditional IQ tests to mild cognitive deficits has led investigators to develop a version of the widely used Wechsler intelligence scales that allows quantitative analysis of underlying qualitative responses. This instrument, the Wechsler Adult Intelligence Scale–Revised as a Neuropsychological Instrument (WAIS–R NI) was administered to 16 Parkinson's disease (PD) patients and 30 normal controls (NC). The 2 groups did not differ significantly in mean age or education, or on their mean Mattis Dementia Rating Scale score. Relative to NC participants, PD patients showed decreased visual attention span, longer response latencies, slower visuomotor processing, and more stimulus-bound errors. Many of the WAIS–R NI measures were able to detect cognitive impairment in a greater percentage of patients than the traditional WAIS–R measures, making it easier to identify deficits that could affect quality of life early in the course of the disease. (JINS, 2001, 7, 535–543.)

Word-list verbal learning and memory tests with appropriate normative data can be highly sensitive to cognitive decline, but there are significant limitations of such tests available for use with older Hispanic and non-Hispanic people living in the US. The purpose of this study was to (1) create a new word-list learning and memory test in both English and Spanish and, (2) validate it with respect to sensitivity to cognitive impairment, and (3) develop statistical corrections for the effects of significant demographic variables, including ethnicity, language of administration, age, education, and gender. A community dwelling sample of 801 English- and Spanish-speaking older people was employed. Recall on learning trials and the delayed recall trial of the word-list learning test were strongly related to the Mini-Mental State Examination (MMSE), moderately related to age, and weakly related to gender and education. The relationship of word-list variables and the MMSE did not significantly differ across ethnicity/language groups. Regression coefficients for demographic variables were used in a statistical correction formula to adjust raw word-list scores, and then to develop specific percentile cut-off values. (JINS, 2001, 7, 544–555.)

Visuospatial processing is accomplished in distinct neuroanatomic pathways. One such pathway, known as the where pathway, involves a dorsal route through magnocellular thalamic cells to occipital and parietal cortices and conveys location and motion information. A second pathway, known as the what pathway, involves a ventral route through parvocellular thalamic cells to occipital and temporal cortices and conveys color and form information. The where pathway is thought to be responsible for processing spatial relationships while the what pathway is responsible for object identification. Children with early-treated congenital hypothyroidism (CH) who exhibit selective visuospatial deficits may provide a good model to study the differential development of these pathways. Because children with CH lacked thyroid hormone at a time when needed by developing brain regions such as the parietal cortex, these children may be affected to a greater degree on tasks tapping where but not what pathway processing. We tested this hypothesis via retrospective analysis of their performance on 6 spatial tasks. Compared were 49 adolescents with CH and 49 matched control participants. On the basis of confirmatory factor analysis, tasks were assigned to either where or what pathway groupings. A repeated measures ANOVA showed the CH group was impaired relative to a normal comparison group only on where pathway tasks. Regression analyses indicated that severity of early hypothyroidism was the strongest predictor of where pathway processing but had no effect on what pathway tasks. It is concluded that thyroid hormone is required during late gestation and early life for the normal development of the where aspects of visuospatial processing. (JINS, 2001, 7, 556–562.)

Differential performance on measures of episodic and semantic memory were examined in AD, cortical vascular dementia (CVaD), subcortical vascular dementia (SVaD), and controls. Groups were matched on age, education, and gender; dementia groups also were matched on severity. Recognition/retrieval differences were found only between SVaD and AD groups, not between CVaD and AD. Thus, recognition/retrieval differences are likely secondary to subcortical pathology rather than to vascular etiology per se. Similarly, significant numbers of memory errors were associated with cortical pathology, regardless of etiology. Error rate differences were found only between SVaD and AD groups, not between CVaD and AD. Finally, rapid forgetting was unique to AD; however, since no difference was found between SVaD and AD, rapid forgetting may occur only as AD progresses. No semantic memory measure differentiated AD from either CVaD or SVaD subjects. Results suggest that some previously reported episodic differences may be due to cortical versus white matter subcortical pathology, rather than to AD versus vascular etiology. (JINS, 2001, 7, 563–573.)

CVLT and WMS–R Digit Span variables were used to calculate indexes of seven specific short- and long-term memory processes: working memory span and central executive functions, and long-term memory encoding, consolidation, retention, retrieval, control abilities. Scores on these indexes were then cluster-analyzed to determine whether subtypes of memory performance exist that correspond to deficits in these theoretical memory constructs. Parallel analyses were conducted with two large samples (N = 150 and N = 151) of individuals who had sustained a traumatic brain injury (TBI). Findings showed that TBI results in subgroups of memory disorders with specific deficits in consolidation, retention, and retrieval processes. Control problems (keeping track of list versus non-list items) only appeared in conjunction with retrieval deficits. Working memory span and central executive functioning (i.e., the ability to manipulate information in working memory) do not appear to be deficits characteristic of TBI as no such clusters emerged in the analyses. By using specific indexes of memory processes, and in contrast to previous studies, patterns of memory dysfunction were found that correspond to deficits in theoretically meaningful memory constructs. (JINS, 2001, 7, 574–585.)

The ability to generate items belonging to categories in verbal fluency tasks has been attributed to frontal cortex. Nonverbal fluency (e.g., design fluency) has been assessed separately and found to rely on the right hemisphere or right frontal cortex. The current study assessed both verbal and nonverbal fluency in a single group of patients with focal, frontal lobe lesions and age- and education-matched control participants. In the verbal fluency task, participants generated items belonging to both letter cues (F, A, and S) and category cues (animals and boys' names). In the design fluency task, participants generated novel designs by connecting dot arrays with 4 straight lines. A switching condition was included in both verbal and design fluency tasks and required participants to switch back and forth between different sets (e.g., between naming fruits and furniture). As a group, patients with frontal lobe lesions were impaired, compared to control participants, on both verbal and design fluency tasks. Patients with left frontal lesions performed worse than patients with right frontal lesions on the verbal fluency task, but the 2 groups performed comparably on the design fluency task. Both patients and control participants were impacted similarly by the switching conditions. These results suggest that verbal fluency is more dependent on left frontal cortex, while nonverbal fluency tasks, such as design fluency, recruit both right and left frontal processes. (JINS, 2001, 7, 586–596.)

The interpretation of neurobehavioral change over time requires knowledge of the test–retest characteristics of the measures. Without this information it is not possible to distinguish a true change (i.e., one reflecting the occurrence or resolution of an intervening process) from that occurring on the basis of chance or systematic bias. We tested a group of 72 healthy young to middle aged adults twice over a 12-to-16-week interval in order to observe the change in scores over time when there was no known intervention. The test battery consisted of seven commonly used cognitive measures and the Profile of Mood States (POMS). Test–retest regression equations were calculated for each measure using initial performance, age, education, and a measure of general intellectual function (Wonderlic Personnel Test) as regressors. Test–retest correlations ranged from .39 (POMS Fatigue) to .89 (Digit Symbol). Cognitive measures generally yielded higher correlations than did the POMS. Univariate regressions based only on initial performance adequately predicted retest performance for the majority of measures. Age and education had a relatively minor influence. Practice effects and regression to the mean were common. These test–retest regression equations can be used to predict retest scores when there has been no known intervention. They can also be used to generate statistical statements regarding the significance of change in an individual's performance over a 12-to-16-week interval. (JINS, 2001, 7, 597–605.)

The recent development of an isometric instrument for the precise quantification of hand force persistence has created a novel opportunity for the evaluation of potential motor asymmetries in schizophrenia and their response to treatment. A study of asymmetries in the unmedicated state may provide insight into the pathogenesis of schizophrenia, whereas alterations of asymmetries in response to antipsychotic medication could assist the delineation of a cerebral mechanism for the effects of pharmacotherapy. The hand force persistence of 21 unmedicated patients with schizophrenia was compared to 21 age, gender, and handedness matched normal controls. The effect of neuroleptic treatment on hand force persistence was then evaluated on a subset of 10 patients after at least 30 days of treatment. The anticipated asymmetry was evident in the unmedicated sample that showed impaired right hand force persistence compared to the normal control sample. The prospective comparison showed an alleviation of the asymmetry resulting from an improvement of right hand force persistence with treatment. In addition to providing further support to a primary left hemisphere cerebral involvement in schizophrenia, the present results suggest that prior investigations of motor asymmetry may have been compromised by the study of medicated patients. The apparently paradoxical improvement of motor skill may relate to the substantial number of patients treated with 2nd generation neuroleptic medications which may implicate an improvement in left hemisphere physiology in the cognitive advantages of the novel treatments. (JINS, 2001, 7, 606–614.)

This study used a semantic-category visual search task to investigate skill acquisition and automatic process development in a severe closed-head injured (CHI) population. Eighteen severe CHI participants (> 1 year post injury) and 18 matched controls completed over 3600 trials of training in both consistent mapping (CM) and varied mapping (VM) training situations. Transfer conditions were also used to test for development of an automatic attention response (AAR) that was independent of general, task-related learning. For both the severe CHI and control group, CM training, where individuals always responded in the same way to a specific class of stimuli, resulted in dramatic performance improvements and the development of an AAR. In the VM training condition, where individuals could not respond in the same way to a class of stimuli from one stimulus exposure to the next, there was little performance improvement and continued reliance on controlled processes. The visual search rates of the CHI participants also remained slower than those of controls following extended VM but not extended CM practice. These results indicate that skill acquisition training guidelines can be used to teach severe CHI patients to develop a new automatic skill. (JINS, 2001, 7, 615–630.)

Normals (N = 42) and patients with mild memory difficulty (N = 123) were given a neuropsychological test battery, and then followed annually for 3 years to determine which individuals developed sufficient functional change that they met clinical criteria for AD. Twenty-three of the 123 participants with mild memory difficulty converted to a diagnosis of probable Alzheimer's disease (AD) within 3 years of follow-up. Four of the 20 neuropsychological measures obtained at baseline, were useful in discriminating the groups on the basis of their status 3 years after the tests were given. The 4 discriminating tests pertained to assessments of memory and executive function. When the controls were compared to the individuals with memory impairments who ultimately developed AD (the converters), the accuracy of discrimination was 89%, based on the neuropsychological measures at baseline. The discrimination of the controls from the individuals with mild memory problems who did not progress to the point where they met clinical criteria for probable AD over the 3 years of follow-up (the Questionables) was 74% and the discrimination of the questionables from the converters was 80%. The specific tests that contributed to these discriminations, in conjunction with recent neuropathological and neuroimaging data from preclinical cases, have implications for which brain regions may be affected during the prodromal phase of AD. (JINS, 2001, 7, 631–639.)

Magnetic resonance (MR) images and neuropsychological testing data of 69 carbon monoxide (CO) poisoned patients were prospectively obtained within 1 day of CO poisoning, two weeks and six months. CO patients' Day 1 cross-sectional fornix surface area measurements, corrected for head size by using a fornix-to-brain ratio (FBR), were compared to normal age and gender-matched controls. Additionally, a within-subjects analysis was performed comparing the mean areas between CO patients' Day 1, 2 weeks and 6-month FBR. The FBR was correlated with patients' neuropsychological data. There were no significant differences between CO patients' Day 1 fornix measurements compared to normal control subjects. However, significant atrophic changes in the fornix of CO poisoned patients occurred at two weeks with no progressive atrophy at 6 months. By 6 months, CO patients showed significant decline on tests of verbal memory (when practice effects were taken into account), whereas visual memory, processing speed and attention/concentration did not decline. This study indicates that CO results in brain damage and cognitive impairments in the absence of lesions and other neuroanatomic markers. (JINS, 2001, 7, 640–646.)

History, theories, methods and findings are characteristic of all disciplines. Also characteristic is the tendency to keep within a discipline much of what is known from discovery by scholars in other fields. While unintentional for the most part, the scant knowledge sharing across disciplines arises from deficits or uncertainties in understanding the definitions of terms, references to key constructs and features, variations in methodologies, and in interpretations of findings. Yet, as the chapters of this book reveal, much is known across several disciplines that converge on many of the same developmental disorders that are (and have been for decades) the focus of considerable research activity. The extensive interest in the study of developmental disorders exists both to understand their natures and causes as well as to reveal differences and similarities in development across normal and abnormal populations.

All you ever wanted to know about the human frontal lobes seems to be contained in this multiauthored text, at least up to 1996 or 1997. The editors, Miller and Cummings, are acknowledged experts on the topic of human disorders of the frontal lobes. They have done a monumental job of collecting 53 authors and 34 chapters. The book is divided into five sections, frontal lobe neuroanatomy, frontal lobe neurochemistry and neurophysiology, frontal lobe neuropsychology, neurological diseases involving the frontal lobes, and psychiatric diseases involving the frontal lobes.

The primary focus of this volume is on the impact of alcohol on brain development. It is a perfect example of how research on both animals and humans can interact to produce very important findings. In the case of prenatal alcohol exposure, dialogue between animal and human researchers has proved to be very profitable for both lines of research. Initial observations by human researchers identified a syndrome of facial stigmata, physical malformations, and early behavioral disturbances that was related to maternal alcohol abuse during pregnancy. They gave this syndrome the name Fetal Alcohol Syndrome. However, human researchers were unable to state unequivocally that prenatal alcohol exposure was teratogenic to the fetus. Thus, they turned to animal researchers who were able to model Fetal Alcohol Syndrome in a variety of animals and to confirm the teratogenicity of alcohol on the developing fetus. The quarter century of studies of the damage caused by prenatal alcohol exposure is replete with such interactions between these two groups of researchers. Without the input and pioneering studies of animal researchers on the effects of prenatal alcohol exposure, human researchers would have much less understanding of the damage caused by alcohol exposure in utero or insights into possible treatment or remediation strategies for those damaged by alcohol exposure.

A few years ago, at the end of a lecture on handedness, a neuropsychology graduate student asked, “Why should I care about handedness? Left-handedness is not a disease.” She had missed the main point of the lecture, namely that left-handedness is an exciting experiment of nature. In the left-hander we find the opportunity to study a healthy brain that is organized differently from other healthy brains. Here is a chance to study the effects of neural diversity without the vagaries of pathology. The study of handedness differences is not just about handedness.

This volume is an introductory text summarizing much of the brain–behavior literature emphasizing the neuroanatomical underpinnings of psychiatric disorders. Because it has been written by a neuroanatomist and a neuropsychiatrist, much of the material in the book is typically not covered in the more orthodox texts written from a behavioral neurology or neuropsychological perspective. As such, this volume will be a valuable resource for students and practitioners of clinical psychology and psychiatry.

The title Bender Gestalt: Screening for Brain Dysfunction (2nd ed.) indicates that the primary utility of the Bender Gestalt Test (BGT) is one of screening for the presence of brain impairment. The author, Patricia Lacks, quickly dispels this notion in the preface to her book where she states, “My book is not about how to use the BGT as a single test of ‘organicity’, a long outdated practice. Instead, the focus is on neuropsychological assessment as a continuum” (p. vii). Indeed, Lacks advocates, throughout her book, the more general use of the BGT as an important part of any standard neuropsychological test battery. She writes, “Even though the BGT has been shown to be useful for identifying persons with a wide range of cognitive impairment, it primarily assesses disordered perceptual-motor and executive functions” (p. 27). Unfortunately, Lacks does not provide the reader with any data to support her above statement regarding what the BGT actually measures. Before taking the latter point any further, allow me to briefly describe the BGT and its history.