Kannayiram Alagiakrishnan, MD, MPH, FRCP(C), Associate Professor, Division of Geriatric Medicine, Department of Medicine, University of Alberta, Edmonton, AB.
Cheryl A. Sadowski, BSc(Pharm), PharmD, Associate Professor, Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB.

Cholinergic deficits are seen in the brains of individuals with non-Alzheimer’s dementia. Antidementia drugs such as cholinesterase inhibitors and memantine have showed some cognitive and behavioural benefits in non-Alzheimer’s dementia trials, but more evidence is needed to define their role.
Key words: mixed dementia, cholinesterase inhibitors, Lewy body dementia, Parkinson disease dementia, vascular dementia.

Karl Farcnik, BSc, MD, FRCPC
Michelle Perskyo, Psy.D, C.Psych
Psychiatrist,
Division of Geriatric Psychiatry,
University Toronto
Part-time staff,
Toronto Western Hospital

Introduction
In 1912, Frederic H. Lewy first described a disease associated with the formation of lesions, which are now known to be intracytoplasmic inclusions, in the brains of affected individuals. Evidence now suggests that this disease, Lewy body Dementia (DLB), may be the second most common cause of dementia after Alzheimer's disease (AD).¹

In 1980, K. Kosaka described the first clinical case of DLB. However, since a number of different entities associated with Lewy bodies have been described, clinical diagnosis of DLB remains challenging. These entities include diffuse Lewy body disease, cortical Lewy body disease, senile dementia of Lewy type, and a Lewy body variant of Alzheimer's Disease. For this reason, efforts have been made to standardize a single set of criteria to make a diagnosis of DLB. In addition, over the past ten years there has been a concerted effort to better characterize this condition, as well as to focus on aspects of its treatment. This article will review the pathophysiology, diagnostic features, and treatment of DLB.