The accredited CME learning activity based on this article is offered under the auspices of the CE department of the University of Toronto. Participating physicians are entitled to one (1) MAINPRO-M1 credit by completing this program, found online at www.geriatricsandaging.ca/cme

Lonn Myronuk, MD, FRCPC, Member of the Canadian Academy of Geriatric Psychiatry; President, GeriPsych Medical Services, Inc., Parksville, BC.

Progress in basic neuroscience has brought disparate clinical phenotypes of dementia together in categories based on common pathophysiological processes. Degenerative dementias are all proteinopathies featuring abnormal processing and CNS accumulation of different proteins in different neuroanatomic distributions dictating patterns of presentation of clinical symptoms and potential responsiveness to treatment. Alzheimer’s disease (AD) is an amyloidopathy. Dementia with Lewy bodies (DLB), Parkinson’s disease (PD) and multiple system atrophy (MSA) are synucleinopathies. Frontotemporal lobar degeneration (FTLD), progressive supranuclear palsy, and corticobasal degeneration are tauopathies. Vascular dementia (VaD) has been considered a distinct pathophysiologic process yet may exist on a continuum with AD. Currently available dementia treatments are not specific for a single disorder, yet not all dementias are treatment responsive. Exclusion of otherwise treatable depressive disorders and metabolic derangements as well as surveillance for deleterious cognitive effects of medication remain central to the assessment and treatment of the older adult with cognitive complaints. Identification of those syndromes for which certain medications may be contraindicated, as well as those that may be selectively responsive to particular compounds, will continue to increase in importance as our range of therapeutic options widens over the coming years.
Key Words: Alzheimer’s disease, Lewy body, frontotemporal lobar degeneration, vascular dementia, differential diagnosis.

Chris MacKnight, MD, MSc, FRCPC, Assistant Professor, Division of Geriatric Medicine, Dalhousie University, Halifax, NS.

Introduction
Lewy body disease is one of the many conditions causing dementia. As it is relatively common, and has an effective management distinct from that of Alzheimer disease,¹ all physicians who see older adults should have some familiarity with Lewy body disease.

Diagnosis
Lewy body disease is underdiagnosed.² It should be suspected in an older adult who presents with cognitive impairment (even if quite mild) in addition to hallucinations or parkinsonism. Clinical criteria are presented in Table 1.^3,4 The criteria of fluctuation have proven difficult to apply at the bedside, but clinical tools are now available.⁵ The parkinsonism is often mild and subtle, and is more often rigidity than tremor. An important feature is neuroleptic sensitivity. Up to 80% of these patients can, even with low doses, develop reactions to neuroleptics or atypical agents, which are often severe.⁶ Extrapyramidal symptoms and cognitive decline are the most common manifestations. The decline can be permanent, and neuroleptic malignant syndrome can occur. This likelihood of reaction to neuroleptics is one of the chief reasons to be familiar with the disorder and to have a low threshold to at least suspect its presence.

It can sometimes be difficult to distinguish Lewy body disease from Alzheimer disease, Parkinson's disease or delirium.