Evidence-Based Review of Therapeutic Approaches in Dementia with Lewy Bodies

Ouf, Aya; Szigeti, Kinga

doi:10.4172/2161-0460.1000406

Cited by 1 publication

(2 citation statements)

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“…The use of antipsychotics should be avoided given the risk of serious reactions in DLB [13], while atypical antipsychotic agents like quetiapine and clozapine less likely may exacerbate parkinsonism. Levodopa was generally well tolerated, but produced less motor response in DLB than in PDD [132] and may increase the risk of psychosis [128]. Bilateral deep brain stimulation of the nucleus basalis of Meynert for PDD showed no improvement in primary cognitive outcomes [133].…”

Section: Neuropathological Featuresmentioning

confidence: 99%

“…Currently, no disease-modifying therapies of LB dementias are available. Clinical management of both disorders include cholinesterase inhibitors (ChEIs) to treat cognitive and psychiatric symptoms [128,129]. Although the effects of ChEIs were relatively small [130], effort is necessary to differentiate them more clearly and to clarify the underlying pathogenic mechanisms to enable effective treatment, while, currently, no diseasemodifying therapies are available.…”

Section: Managementmentioning

confidence: 99%

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Dementia with Lewy Bodies and Parkinson's Disease-Dementia: Current Perspectives

A¹

2018

Int J Neurol Neurother

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Dementia with Lewy bodies (DLB) and Parkinson's disease-dementia (PDD) are two closely related major neurocognitive disorders with Lewy bodies of unknown etiology, showing notable overlap in their clinical presentation, pathological features, biochemistry, and genetic risk factors. According to international consensus, their diagnosis is based on an arbitrary distinction between the time of onset of motor and cognitive symptoms: dementia preceding parkinsonism in DLB, while it develops after onset of parkinsonism in PDD (the one-year rule). Clinically, both syndromes show cognitive impairment with severe deficits in executive function, visuo-spatial processing, fluctuating attention and parkinsonism, with higher prevalence of Alzheimer-type lesions in DLB that may account for earlier onset and severity of cognitive deficits. These are also associated with multiple neurotransmitter deficits indicating that cognitive impairment in Lewy body disesses is multifactorial. Recent intra vitam neuroimaging, clinico-pathological studies and animal models suggest that DLB and PDD represent closely related but different, heterogenic subtypes of an α-synuclein-associated disease spectrum (Lewy body diseases) or parts of a continuum with PDD at the mild end of the spectrum, DLB in the middle, and DLB+AD at the more severe end. In view of the controversies about the nosology of both disorders, continuous effort is necessary to differentiate them more clearly and to clarify the underlying pathogenic mechanisms in order to enable effective mechanistic-based treatment, while, currently, no disease-modifying therapies are available.

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