Cerebrovascular Disease, Cognitive Impairment and Dementia is the second edition of Cerebrovascular Disease and Dementia (2000). The new edition is over 160 pages longer than the earlier version, with several new chapters devoted to the pathophysiology of cerebrovascular disease [including provocative chapters on neurotransmitter changes in vascular dementia (VaD), the contributions of homocysteine and low vitamin B to VaD, and a good overview of hereditary forms of VaD], vascular mild cognitive impairment, noncognitive symptoms, and an expanded discussion of prevention and treatment. It is written for both clinical and scientific audiences. As in the first edition, there is a laudable comparative emphasis, with epidemiologic studies of vascular dementia in Europe, North America, Japan, and China. Indeed, the editors hail from the U.K, Australia, Sweden, and the U.S, and this affords the volume a useful global perspective. With five editors and 22 additional contributors, however, this book suffers a bit from the “too many cooks” syndrome. There is a good bit of redundancy. After the fifth or sixth description of classification criteria for vascular dementia, the reader begins to feel on the receiving end of some repetitive rehearsal therapy for her own dementia.

Perhaps most validating for those of us in clinical positions is the scientific confirmation that VaD and Alzheimer's disease (AD) are not necessarily the totally discrete entities described in textbooks. While historically we have been taught to rule out VaD in making a diagnosis of probable AD, evidence from the Nun Study (Snowdon et al., 1997) and the Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (2001) showed that the two are often entwined. Holmes et al. (1999) suggested that AD and VaD occur together more commonly than VaD alone. Amyloid angiopathy is commonly associated with both AD and VaD. The apolipoprotein-E genotype is associated with the onset of both atherosclerosis and AD. Hypertension and vascular events are key in developing AD, and other biological markers for AD, such as increased tau protein levels, are also found in VaD. Similarly, where VaD was once characterized exclusively as having an abrupt onset with stepwise progression, we now know that such a syndrome is just one form of the disorder. Growing evidence suggests a large percentage of VaD cases are typified by microvascular changes that can lead to an insidious onset and gradual progression, as is typical of AD, further blurring the presentation of the two disorders.

Gustafson and Passant, in their chapter on clinical pathological correlates, describe the confluence of multiple factors in the expression of dementing disorders as follows: “Stroke may not only give rise to circumscribed, delineated neurological and psychological impairments but also global changes of mentation and behavior. These symptoms, however, may not only be the result of the vascular brain lesion but also of other concomitant brain disease and somatic disorders some of which, such as cardiac disease, blood pressure pathology and diabetes, are well known risk factors for cerebrovascular disease. Previous mental and physical health, medication, alcohol consumption, and socioeconomic conditions may also play an important role” (p. 197).

While it is increasingly clear that multiple systems are in play for the expression of all dementias, there is still value in understanding the specific forms of cerebrovascular disorders. The pathophysiological classification of VaD includes large vessel dementia, which can involve multiple lesions or a single, strategic infarct; small vessel dementia, in the subcortex or throughout the brain; hypoperfusive, hypoxic-ischemic dementia; venous infarct dementia; hemorrhagic dementia; and hereditary forms of VaD, such as cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL syndrome). A preclinical stage of these disorders, akin to mild cognitive impairment (MCI) as a precursor to AD, is now described as vascular cognitive impairment (VCI).

Hachinski and Bowler (1993) first described VCI as being all-encompassing of cognitive decline from the earliest stage through the most profound, late-stage dementia. More recently, the term refers to subtle cognitive changes resulting from cerebrovascular disease that signal a decline but \.do not meet full criteria for dementia. Unlike MCI, memory might not be impaired in VCI. Depending on the lesion load and location, attention and/or executive changes might appear in the absence of memory impairment. As in MCI, early intervention in VCI often produces the best outcome.

While the authors are comprehensive in their descriptions of the current state-of-the-art in classification and diagnosis of VaD, focusing on imaging, biological markers, and clinical observation techniques, they also provide six chapters on the management of these disorders. In this final section of the book, as in the beginning, it becomes clear that there are more similarities than differences in the treatment and management of different dementias.

It turns out that the best prevention strategies for VaD are also salient for the prevention of AD. Controlling blood pressure appears to be crucially important in the prevention of both types of dementia. Additionally, controlling blood glucose levels, smoking cessation, cholesterol control, and limiting alcohol are targeted for primary prevention of VaD. Following stroke, secondary prevention measures such as anticoagulation therapy, carotid endarterectomy, and cerebrovascular angioplasty may interrupt further cerebrovascular disease and concomitant cognitive decline.

Until fairly recently, cholinesterase inhibitors were prescribed only for AD. These drugs (e.g., donepezil and galantamine) do not treat the underlying cause of AD. Rather, they treat the cholinergic deficit that causes some of the symptoms of dementia. In his chapter on treatment of cognitive impairment in VaD, Wilkinson indicates that the data now show that cholinesterase inhibitors have a significant impact on cognitive functioning in patients with VaD. The positive effects of NMDA antagonists (e.g., memantine) and neuroprotective agents (e.g., propentofylline) on VaD are less clearly established to date but are also under investigation. While more beneficial drug therapies are likely to emerge in the near future, it seems clear that cholinesterase inhibitors should now be considered in the management of mild to moderate VaD, just as they are now routinely used for AD and dementia with Lewy bodies (DLB).

The final two chapters of the book discuss family and long-term care issues in VaD. These are clearly universal issues that transcend specific dementia etiology. As we all know, once dementing disorders reach late stage, they all look pretty much the same, and the burdens on families and society are indistinguishable. The authors argue persuasively for keeping patients at home for as long as possible and for employing multiple in-home supportive services to care for the patient and to ease the burden on families.

In conclusion, Cerebrovascular Disease, Cognitive Impairment and Dementia is a broad-based review of cerebrovascular disorders that offers new insights into their underlying causes, expressions, diagnosis, and management. It is definitely not written solely for an audience of neuropsychologists. In fact, several of the assessment-oriented chapters seem to gloss over the usefulness of comprehensive neuropsychological testing. Only one chapter specifically focuses on neuropsychological assessment.

Despite such a parochial concern, this book is a useful reference tool, and the section on pathophysiology of cerebrovascular disease is particularly strong. It is a good text for trainees, once they've made it through Lezak and Heilman & Valenstein. It is somewhat ironic that a nearly 400-page book focused on vascular dementia makes such persuasive arguments against the compartmentalization of dementing disorders, but this pan-diagnostic view of dementia is one of the book's primary strengths. This is a valuable addition to my bookshelf, and I'm sure I'll refer to it often in the future. While I believe that the volume would have benefited from more aggressive editing, the redundancy is really more of an annoyance than a problem. Better to have too much information than not enough.