Stress, the Brain and Depression, by Herman M. van Praag, Ron de Kloet, and Jim van Os. (2004). Cambridge, UK: Cambridge University Press. 293 pp., $110.00, £65.00.

This book addresses one of the fundamental questions in the etiology of depression: Does stress cause depression? Although intuitively one may answer yes to this question, the book presents detailed psychological and neurobiological evidence to show the complexity of the issue. The book focuses on three major themes: (1) pathophysiology of stress in depression; (2) stress-inducible subtypes of depression; and (3) diagnosing depression to understand biological underpinnings of the condition. Although each of the three authors wrote individual chapters (with van Praag writing most chapters), the book is well organized and flows smoothly. The book is well written in an entertaining style, especially the chapters written by van Praag. For example, when discussing the problems with the current DSM-IV diagnostic system, van Praag states, “psychiatric diagnosing is locked up in a nosological straightjacket, and thus immobilized” (p. 8). It is this type of commentary, sprinkled throughout the book, that holds the reader's interest. In addition, the authors provide a fresh perspective on diagnostic issues in depression, stress/negative life events, and the neurobiology of depression. I expect the volume will stimulate research ideas. To get the most out of the book, it should be read in its entirety. Exceptions are the chapters reviewing the psychobiology of stress and depression, which provide very comprehensive summaries of the research literature, and may serve as a good reference. The initial chapters build the theoretical foundation for the presentation of the biological data, and the final chapters integrate the biological data with the initial hypotheses. The authors take issue with diagnostic trends in psychiatry, definitions of stress and life events, and to a lesser extent, neurobiological approaches to psychiatric research. The authors do not rehash old findings, but include the most recent literature. For example, when discussing corticotrophin releasing hormone (CRH) receptors, they present new findings supporting a possible parallel parasympathetic-related system in addition to the traditional sympathetic response. When the data presentation becomes complex, information is summarized in easy-to-read tables.

Essays in Social Neuroscience. John T. Cacioppo and Gary G. Berntson (Eds.). 2004. Cambridge, MA: The MIT Press, 168 pp., $32.00/£20.95.

Essays in Social Neuroscience, edited by John T. Cacioppo and Gary G. Berntson, is a slim collection of highly engaging and—for the overextended neuropsychologist—enjoyably brief essays surveying current research and theory in the emerging field of social neuroscience. Each contributor attests to the variety of examples of research bridging the historic divide between neuroscience and social psychology. For neuropsychologists, this volume offers enlightening demonstrations of the potential for traditional methods in neuroscience to speak to the complex and reciprocal interplay between neural systems and the social world. From Sue Carter's essay “Oxytocin and the Prairie Vole: A Love Story” to Shelley E. Taylor's contribution “The Accidental Neuroscientist: Positive Resources, Stress Responses, and Course of Illness,” these essays speak to such diverse issues as interpersonal attraction, loyalty, emotional reactivity, and environmental contributions to autoimmune disease. Some essays speak more to the potential for bridging the gap than to demonstrated success in this effort, but those essays remain pleasurable, rewarding reads. The large majority of essays, four of which are described in more detail below, beautifully exemplify the fruitfulness of this area of inquiry.

Developmental Motor Disorders: A Neuropsychological Perspective. Deborah Dewey and David E. Tupper (Eds.). (2004). New York: Guilford, 501 pp., $70.00.

This book is thorough, thoughtful, and uniquely useful in the questions it asks and attempts to answer. Included, for example, are discussions of problems associated with the use of traditional neurological “soft signs” to detect and predict long-term motor impairment; patterns of newborn movement that predict childhood cerebral palsy; strengths and weaknesses of tests and observational checklists to assess motor proficiency; how best to diagnose and treat phonological disorders versus verbal apraxia, or dysgraphia versus motor dyspraxia; analysis and treatment of handwriting problems; brain systems that subserve proprioception and how these systems develop or derail; neuroimaging that assists in making the diagnosis of periventricular leukomalacia; and, treatment approaches for children with Developmental Coordination Disorder.

Board of Governors Meeting, February 1, 2005, St. Louis, Missouri.

Minutes From the Thirty-Third Annual International Neuropsychological Society Meeting: St. Louis, Missouri.

Members Present: Erin Bigler, Jason Brandt, Gordon Chelune, H. Branch Coslett, Bruce Crosson, Robert Heaton, Ritva Laaksonen, Ann Marcotte, Morris Moscovitch, H. Gerry Taylor, Daniel Tranel, Eli Vakil, Faraneh Vargha-Khadem, Barbara A. Wilson, Robert Bornstein (ex officio)

Members Absent: Elizabeth Warrington

Academic neuropsychologists are increasingly engaged in (and are part of) cognitive neuroscience. Neuroimaging is currently high on the agenda, neuroplasticity is a very topical field within neuroscience, and a number of neuropsychologists work on animal models of brain injury. Clinical neuropsychologists, particularly those involved in rehabilitation, will usually tell you that their work needs to be guided by theory or else they risk the accusation of being simply pragmatic. The fundamental question for clinical neuropsychologists is which theory or theories are most relevant and useful for the patients and families with whom they work? While it would seem that most clinical neuropsychologists consider cognitive neuroscience to be of direct or at least indirect benefit to clinical neuropsychological practice, it is part of the argument of this paper to suggest that the benefits are less substantial than is sometimes claimed. As I work with both academic and clinical neuropsychologists, I hold the conviction that theory should be relevant to clinical practice while, at the same time, wanting neuropsychological rehabilitation to be respectable in the eyes of the academic community. However, when treating a patient with brain injury it is sometimes a struggle to implement, or even see the relevance of findings from cognitive neuroscience.

Barbara Wilson is a creative and influential clinician–scientist who has dedicated her working life to finding ways to rehabilitate brain-damaged people in all the confusing complexity of their damaged brains and lives. Her behavioral training at the Institute of Psychiatry in London inspired her to apply the powerful methods of applied behavior analysis to shape functionally relevant behaviors in the real-life contexts in which these people have to learn new ways of living. I, on the other hand, have chosen to work with people who have specific cognitive deficits such as unilateral neglect (Robertson et al., 1998), impaired sustained attention (Robertson et al., 1997) or goal-neglect-type executive deficits (e.g., Manly et al., 2002). I have specifically avoided trying to carry out research on people with complex problems, specifically because I tried to understand how these strange interchanges we call rehabilitation actually work (Robertson, 2002; Robertson & Murre, 1999). In my research (not, I hasten to add, in my clinical practice), I try to identify relatively pure processes that can be replicated anywhere in the world—not to solve the pressing problems of a particular, unique and complex life.

Functional Magnetic Resonance Imaging, by Scott A. Huettel, Allen W. Song and Gregory McCarthy. 2004. Sunderland, MA: Sinauer Associates, Inc. 492 pp., $79.95.

Imaging the human brain at work was revolutionized by the discovery of functional magnetic resonance imaging (fMRI) in the early 1990s. Prior to this, functional brain mapping was limited to a handful of medical centers capable of conducting positron emission tomography (PET) scans of regional cerebral blood flow. With the discovery of the endogenous blood oxygen level dependent (BOLD) contrast method in 1992, fMRI “democratized” the field by expanding the number of medical centers capable of functional brain imaging. Today, over a thousand peer-reviewed fMRI articles are published each year, many in high profile scientific journals that receive additional attention by the popular press. This explosion of scientific research is relatively easy to understand: fMRI can be conducted on the majority of the 6,600 MRI scanners installed in the US alone, the technique is completely noninvasive since it does not require injection of MRI contrast agents or radiopharmaceuticals, and, as an added benefit, fMRI provides a unique combination of high spatial and temporal resolution. Not surprisingly, fMRI is the imaging technique of choice for mapping cognitive and emotional systems in the healthy brain. More recently, fMRI has been applied to clinical populations to identify the brain mechanisms governing recovery of function from stroke and head trauma, detect early brain changes in neurodegenerative conditions, and measure the effects of psychoactive medications on neurodevelopmental disorders, as examples. fMRI provides a complementary method for testing neuropsychological models of brain function derived from other methods (lesion, electrophysiology).

Vascular Dementia: Cerebrovascular Mechanisms and Clinical Management. Robert H. Paul, Ronald Cohen, Brian R. Ott, and Stephen Salloway (Eds.). 2004. Totowa, NJ: Humana Press, 356 pp., $145.00, £91.00 (HB).

Interest in how vascular factors contribute to dementia is ascendant, propelled by a number of factors. One is the widespread use of MRI, which is a highly sensitive (if not always specific) test for cerebrovascular lesions. A second is a string of epidemiological reports revealing that Alzheimer's disease shares many of the well established risk factors for cardiovascular and cerebrovascular disease (Skoog & Gustafson, 2003). Recent autopsy studies using cohorts obtained outside of the potentially winnowing influence of the Alzheimer's disease centers have reminded us that vascular lesions are common in patients with dementia (Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study, 2001). The Nun study report suggesting that infarcts create an additive or greater effect on mental function in concert with AD pathology (Snowdon et al., 1997) received particularly wide exposure and helped revive interest in combined effects of AD and ischemic lesions. Finally, the discovery that polymorphisms of the apoE gene, long of interest in cardiovascular disease, strongly modify the risk of AD suggested the possibility of shared pathophysiological mechanisms between AD and vascular dementia (Panza et al., 2004; Strittmatter & Roses, 1995). The volume Vascular Dementia, edited by Paul, Cohen, Ott and Salloway, is thus a timely resource for those interested in the numerous issues surrounding the role of vascular factors in dementia.

Cognitive and Behavioral Rehabilitation: From Neurobiology to Clinical Practice. Jennie Ponsford (Ed.). 2004. New York: Guilford Press. 366 pp., $50.00 (HB).

The World Health Organization estimates that approximately 90 million people, or 1.5% of the world population, are in need of rehabilitation services at any given point in time (WHO, 2003). Many of these individuals are at risk for long-term disability due to brain injury and disease. They range from the young, who increasingly survive early brain insults, to older adults, whose independence and every day functioning may be threatened by the onset of neurologic impairments. As medical advances improve survival rates and longevity, the number of those in need of cognitive and behavioral rehabilitation services to enhance functioning is likely to grow. This situation raises pressing questions, such as, who will get better with what rehabilitation treatment, and why?