26 An arbitrary “1-year rule” is frequently used to “separate” them by proposing that onset, of dementia within 12 months of parkinsonism qualifies as DLB and more than 12 months of parkinsonism before dementia qualifies as Parkinson’s disease dementia (PDD).This is certainly helpful

in individual clinical case diagnosis and management, but is increasingly hard to justify from a neurobiological point of view. There do not seem to be major neuropathological differences between DLB and PDD, and it is not. possible to make a confident retrospective clinical diagnosis based on autopsy findings alone. A Task Force of the Movement. Inhibitors,research,lifescience,medical Disorders Society is presently addressing the issues of PD dementia, and its recommendations should help to clarify this complex and currently problematic

area. Clinical criteria for DLB The core clinical features of DLB, as check details defined by consensus criteria (Table II.);27 are fluctuating cognitive Inhibitors,research,lifescience,medical impairment, recurrent, visual hallucinations, and parkinsonism. The specificity of a clinical diagnosis of “probable DLB” (two or more core features present) is high at >80%,but sensitivity is generally limited to around 50%. 28 The use of the more lenient, “possible DLB” criteria, which require the presence of only one core feature, increases case detection rates Inhibitors,research,lifescience,medical at the cost of reduced diagnostic accuracy and may be useful in Inhibitors,research,lifescience,medical clinical practice for screening purposes.29 Table II. Consensus guidelines for the clinical diagnosis of probable

and possible dementia with Lewy bodies (DLB).27 Clinical presentation and course of DLB In general terms, the onset of DLB tends to be insidious, although reports of a period of increased confusion, the onset of hallucinations, or a significant fall may give the impression of a sudden onset. The main differential diagnoses of DLB are AD, vascular Inhibitors,research,lifescience,medical dementia, PDD, atypical parkinsonian syndromes, such as progressive supranuclear palsy (PSP), multiple system atrophy (MSA), and corticobasal degeneration (CBD), and also Creutzfeld-Jakob disease (CJD).27 The course of DLB is progressive, with cognitive test scores declining about. 10% per annum, similar to AD.30 Cognitive fluctuations may contribute to large variability in because repeated test scores, eg, five Mini-Mental State Examination (MMSE) points difference over the course of a few days or weeks,31 making it difficult, to be sure of the severity of cognitive impairment by single examination. Survival times from onset, until death are similar to AD,32 although a minority of DLB patients have a very rapid disease course.33,34 The clinical diagnosis of DLB rests on obtaining a detailed history of symptoms from the patient and an informant, mental state examination, appropriate cognitive testing, and neurological examination. Systemic and pharmacological causes of delirium need to be excluded.