Recent neuropathologic autopsy studies found that 15 to 25% of elderly demented patients have Lewy bodies (LB) in their brainstem and cortex, and in hospital series this may constitute the most common pathologic subgroup after pure Alzheimer's disease (AD). The Consortium on Dementia with Lewy bodies met to establish consensus guidelines for the clinical diagnosis of dementia with Lewy bodies (DLB) and to establish a common framework for the assessment and characterization of pathologic lesions at autopsy. The importance of accurate antemortem diagnosis of DLB includes a characteristic and often rapidly progressive clinical syndrome, a need for particular caution with neuroleptic medication, and the possibility that DLB patients may be particularly responsive to cholinesterase inhibitors. We identified progressive disabling mental impairment progressing to dementia as the central feature of DLB. Attentional impairments and disproportionate problem solving and visuospatial difficulties are often early and prominent. Fluctuation in cognitive function, persistent well-formed visual hallucinations, and spontaneous motor features of parkinsonism are core features with diagnostic significance in discriminating DLB from AD and other dementias. Appropriate clinical methods for eliciting these key symptoms are described. Brainstem or cortical LB are the only features considered essential for a pathologic diagnosis of DLB, although Lewy-related neurites, Alzheimer pathology, and spongiform change may also be seen. We identified optimal staining methods for each of these and devised a protocol for the evaluation of cortical LB frequency based on a brain sampling procedure consistent with CERAD. This allows cases to be classified into brainstem predominant, limbic (transitional), and neocortical subtypes, using a simple scoring system based on the relative distribution of semiquantitative LB counts. Alzheimer pathology is also frequently present in DLB, usually as diffuse or neuritic plaques, neocortical neurofibrillary tangles being much less common. The precise nosological relationship between DLB and AD remains uncertain, as does that between DLB and patients with Parkinson's disease who subsequently develop neuropsychiatric features. Finally, we recommend procedures for the selective sampling and storage of frozen tissue for a variety of neurochemical assays, which together with developments in molecular genetics, should assist future refinements of diagnosis and classification.

Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB) Report of the consortium on DLB international workshop

Dementia with Lewy bodies (DLB) was considered to be an uncommon cause of dementia until improved neuropathological staining methods for ubiquitin were developed in the late 1980's. Subsequent recognition that 10-15% of dementia cases in older people were associated with Lewy body pathology led to the publication in 1996 of Consensus clinical and pathological diagnostic criteria for the disorder. These have greatly raised global awareness of DLB and helped to generate a body of knowledge which informs modern clinical management of this pharmacologically sensitive group of patients. They have also enabled important issues surrounding the relationships of DLB with Alzheimer's disease and Parkinson's disease to be addressed and partially resolved. A recent re-evaluation of the Consensus criteria has confirmed many aspects of the original recommendations, supplementing these with suggestions for improved pathological characterisation, clinical detection and management. Virtu-ally unrecognised 20 years ago, DLB could within this decade be one of the best characterised and potentially treatable neurodegenerative disorders of late life.

Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the Consortium on DLB International Workshop

Objective: To assess the importance of vascular cognitive impairment and its three subgroups (cognitive impairment, no dementia; vascular dementia; and AD with a vascular component) to the prevalence and burden of cognitive impairment in elderly people. Background: Vascular lesions may produce a spectrum of cognitive changes. Omitting elderly patients whose cognitive impairment falls short of dementia (vascular cognitive impairment, no dementia) may give a falsely low indication of the prevalence and burden of disease. To test this proposition, we compared the rates of adverse outcomes for patients with no cognitive impairment, vascular cognitive impairment (and its subgroups), and probable AD. Methods: The Canadian Study of Health and Aging is a prospective cohort study of 10,253 randomly selected community-dwelling and institution-dwelling respondents aged 65 years or older. In the community, all participants (n = 9,008) were screened for cognitive impairment; those who screened positive and a sample of those who screened negative received a clinical assessment (n = 1,659). All patients living in institutions received a clinical assessment (n = 1,255). Participants were reassessed 5 years after the original survey. Results: Vascular cognitive impairment without dementia was the most prevalent form of vascular cognitive impairment among those aged 65 to 84 years. Rates of institutionalization and mortality for those with vascular cognitive impairment were significantly higher than those of people who had no cognitive impairment, and the mortality rate for patients with vascular cognitive impairment was similar to that of patients with AD. Conclusions: Failure to consider vascular cognitive impairment without dementia underestimates the prevalence of impairment and the risk for adverse outcomes associated with vascular cognitive impairment.

Prevalence and outcomes of vascular cognitive impairment

Dementia with Lewy bodies. Clinical diagnostic criteria for dementia with Lewy bodies. Progressive disabling mental impairment is a mandatory requirement for the diagnosis of DLB. Core features. Fluctuation. Visual hallucinations. Motor parkinsonism. Supportive features. Repeated falls, syncope, and transient losses of consciousness. Neuroleptic sensitivity. Systematized delusions and hallucinations in other modalities. Exclusion features. Clinical methods.

Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the consortium on DLB international workshop

Dementia with Lewy bodies is relatively common cause of degenerative dementia in older people. This debilitating disorder is comprised of core features including dementia, fluctuating cognition, motor parkinsonism, and visual hallucinations, as well as other symptoms such as rapid eye movement sleep behavior disorder, olfactory dysfunction, autonomic dysfunction, sensitivity to neuroleptics, anxiety, depression, and delusions. Pharmacotherapy, so far exclusively symptomatic, should be implemented with caution and only when symptoms are disturbing and after non-pharmacological interventions fail. Treatment with acetylcholinesterase inhibitors (AChEi), such as donepezil and rivastimine, is considered a first line therapy. There is substantial evidence that AChEi address cognitive as well as behavioral symptoms without substantially increasing parkinsonism. Dopaminergic treatment for motor symptoms requires balancing risk of worsened psychosis and is consider only moderately beneficial.

https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-4422(03)00619-7.pdf

Dementia With Lewy Bodies

We measured the concentrations of the monoamines, their precursors, and their metabolites, and the activity of choline acetyltransferase (ChAT) in basal ganglia and cortical regions of postmortem brains from cases with histologically verified pure Alzheimer's disease (AD), AD with diffusely distributed Lewy bodies (Lewy body variant [LBV]), and normal controls. Dopamine and homovanillic acid (HVA) were severely depleted in basal ganglia of the LBV cases but were not significantly altered in pure AD cases; tyrosine hydroxylase levels in putamen were also significantly reduced in LBV but not AD cases. These reductions in basal ganglia dopamine and HVA suggest that LBV cases have a level of dopamine depletion similar to Parkinson's disease (PD). Additionally, ChAT activity in caudate and norepinephrine concentration in putamen were significantly reduced in the LBV group, which may have contributed to the absence of resting tremor and the milder presentation of parkinsonian features in this group compared with classic PD. In frontal, parietal, and temporal cortex, activity of ChAT in the LBV group was significantly reduced compared with controls and lower than in pure AD.

Neurotransmitters in basal ganglia and cortex of Alzheimer's disease with and without Lewy bodies

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Neurotransmitters in basal ganglia and cortex of Alzheimer's disease with and without Lewy bodies