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Dementia with Lewy bodies (DLB) is the second most common form of neurodegenerative dementia in older adults.
To be diagnosed, patients will present with dementia in addition to at least two of the following core symptoms: fluctuating cognition, recurrent visual hallucinations, REM sleep behavior disorder, and/or parkinsonism.
Recommended treatment strategies focus on providing symptomatic relief; there is no FDA-approved medication to treat DLB. Pharmacists can help prevent hospitalizations and resultant morbidity by ensuring that patients do not take medications known to exacerbate fall risk and worsen cognitive deficits.
Broadly defined, neurodegenerative dementia is a progressive cognitive decline that adversely and markedly impairs the patient’s overall functionality.1 Dementia with Lewy bodies (DLB) accounts for only 10% to 20% of total dementia diagnoses, but its economic and societal costs are nonetheless burdensome.
Patients with DLB incur higher healthcare costs, have longer hospitalizations, report lower quality of life, and have caregivers with higher levels of distress when compared with patients with Alzheimer disease (AD).
There is no FDA-approved medication to halt the progression of cognitive decline in DLB, which may progress more rapidly than in other dementias.4 Current treatment strategies that focus on symptomatic control provide modest benefit.
Lewy body disease (LBD) is characterized by the presence of Lewy bodies (LBs) and Lewy neurites and comprises a diagnostic spectrum that includes Parkinson’s disease (PD), PD with dementia, and dementia with LBs.
LBs and Lewy neurites are insoluble aggregates composed mainly of phosphorylated α‐synuclein and can be widely distributed throughout the central and peripheral nervous systems.
The distribution of LBs may determine the LBD phenotype. Braak hypothesized that Lewy pathology progresses ascendingly from the peripheral nervous system to the olfactory bulbs and brainstem and then to other brain regions. Braak’s PD staging suggests that LBD is a prion‐like disease. Most typical PD cases fit with Braak’s PD staging, but the scheme fails in some cases.
Alzheimer’s disease, progressive supranuclear palsy, corticobasal syndrome, multiple system atrophy, frontotemporal lobar degeneration, Creutzfeldt–Jakob disease, cerebrovascular diseases, and essential tremor are common misdiagnoses for pathologically confirmed LBD. LBD exhibits considerable heterogeneity in both clinical and pathological settings, which makes clinical diagnosis challenging.
In 1817, Parkinson described the clinical features of six cases of the disease named after him.1 In 1980, Kosaka et al. proposed the term Lewy body disease (LBD).2 In 1996, the first consensus guideline on dementia with Lewy bodies was published.
LBD is a disease concept characterized by the presence of Lewy bodies (LBs) and Lewy neurites and includes Parkinson’s disease (PD), Parkinson’s disease with dementia (PDD), and dementia with Lewy bodies (DLB).
The phenotypes of PD and DLB emphasize motor abnormalities and dementia, respectively (Fig. 1). The clinical phenotype of LBD may be determined by the anatomical distribution of LBs rather than by the severity of Lewy pathology.
The major component of LBs and Lewy neurites is phosphorylated α‐synuclein, LBDs are classified as α‐synucleinopathies.