I! Jr @ Lt Editorial Lewy Body Dementia - Diagnosis and Treatment IAN G. McKEITH,DOUGLASGALASKO,GORDONK. WILCOCKand E. JANE BYRNE British Journal of Psychiatry (1995), 167, 709—717 In the foreword to a volume entitled Recent Advances in Psychogeriatrics published in 1992, Tom Arie remarked upon the sudden appearance of Lewy body dementia (LBD) on the clinical scene. A diagnosis not previously found in the long list of causes of dementia was apparently being proclaimed as possibly the second most common cause of dementia in the elderly. There has followed considerable debate as to how this new concept should be handled. Points of uncertainty or disagreement include whether or not precise neuropathological criteria of LBD have been established, and, if so, whether such patients have a distinguishable clinical syndrome. If LBD is identifiable ante-mortem, how should patients and their relatives be advised and what implications are there for management? At least part of the heterogeneity of opinion about LBD probably derives from the fact that patients may present in approximately equal numbers to old age psychiatry services (cognitive impairment, psychosis and behavioural disturbance), geriatric medicine (acute confusional states, syncope and falls), or neurological services (Parkinsonism). An authority from each of these specialities was therefore asked to write a brief review of the topic from their own particular perspective. The neurologist Neocortical Lewy bodies (LB), after escaping detection for years, are now in sharp focus as major contributors to dementia and psychiatric symptoms in the elderly. In severalautopsy seriesof demented patients, LB rank as the second most common type of degenerative pathology, occurring in 15-25% of cases, exceeded only by the senile plaques (SP) and neurofibrillary tangles (NFF) of Alzheimer's disease (AD). This brief review, coloured by the experience of a research centre conducting longitudinal studies in dementia, willhighlightthe overlap betweenLBD and AD, as well as those features attributable to LB. A burgeoning nomenclature has been used to describe patients with LBD, reflecting the diversity of clinical and pathological findings. The term ‘¿diffuse Lewy body disease' (DLBD) was originally coined for demented patients whose brains showed widespreadLB, found in the hippocampus,temporal lobe, cingulate and neocortex, in addition to their classic sites in the substantia mgra and other subcortical regions. It was assumed that the diffusely distributed LB accounted for dementia and distinguished DLBD from idiopathic Parkinson's disease (PD), in which LBD were thought to be restricted to subcortical areas. However, recent studies have shown that virtually every PD patient has at least some cortical LB. What then differentiates LBD patients from non demented PD patients? One factor is the number of LB, particularly in the cortex, as there is a direct correlation between the density of cortical LB and the severity of dementia assessed close to the time of death. Alternatively, the presence of additional pathology, such as that of AD, may add to the LB burden to produce dementia. To clarify the relationship between LB and cognitive or psychiatric symptoms, more information is needed about the physiologicalfunction and anatomical connections of the cortical neurons that are vulnerable to LB formation. Many patients with cortical LB also show SP and NFF. In the hippocampus, the AD pathology may be fairly severe, accounting for memory dysfunction. However, NFT counts usually are much lower in neocortical areas in LBD than in AD, and some patients with LBD have minimal AD pathology. AD lesions and LB are both associated with old age, and their coincidence may be due to chance alone. It is interesting that LB and NFT share several features: both are cytoskeletal derangements containing neurofilaments or related proteins, which undergo phosphorylation and ubiquitination. These events may occur late in lesion formation, and stronger evidence is required to make a case that similar mechanisms lead to the formation of LB and NFT. Just as cortical LB may evade casual inspection, so can the clinical picture of LBD be overlooked. Since patients with LBD commonly have AD lesions, clinical features usually overlap with those characteristic of AD, and include the gradual onset of forgetfulness, followed by difficulty with word fmding, calculation and other cognitive skills. The age of onset of LBD is similar to that of AD, although 709