Dementia with Lewy Bodies
Dementia with Lewy Bodies (DLB) is a progressive neurodegenerative condition that is construed on a spectrum between Alzheimer's disease and Parkinson's disease. Core symptoms of LBD are gradual cognitive decline, fluctuation in alertness, visual hallucinations, and parkinsonism (motor symptoms such as rigidity, gait changes, or bradykinesia). Pathophysiology of DLB consists of the build-up of Lewy bodies, which are composed of α-synuclein protein. Treatment and management usually includes acetylcholinesterase inhibitors, such as donepezil and rivastigmine, for cognitive symptoms and occasionally levodopa for parkinsonian features.
ABSTRACT:
Dementia with Lewy Bodies
The advent of new immunostains have improved our ability to detect limbic and cortical Lewy bodies, and it is now evident that Dementa with Lewy bodies (DLB) is the second most common neurodegenerative dementia, after Alzheimer’s disease (AD). Distinguishing DLB from AD has important implications for treatment, in terms of substances that may worsen symptoms (i.e., anticholinergic and certain neuroleptic medications) and those that may improve them (i.e., cholinesterase inhibitors, carbidopa-levodopa). Neurocognitive patterns, psychiatric features, extrapyramidal signs and sleep disturbance are helpful in differentiating DLB from AD early in the disease course. Differences in the severity of cholinergic depletion as well as type and distribution of neuropathology contribute to these clinical differences, though DLB patients with a high density of co-occuring AD pathology are less clinical distinguishable from AD. [Ferman, T. J. & Boeve, B. F. (2007), Neurologic Clinic, 25 (3), 741-760]
ABSTRACT:
Neuropsychological Characteristics of Dementia with Lewy Bodies and Parkinson’s Disease with Dementia: Differentiation, Early Detection, and Implications for “Mild Cognitive Impairment” and Biomarkers
Parkinson’s disease with dementia (PDD) and dementia with Lewy bodies (DLB) are neurodegenerative conditions sharing a disorder of α-synuclein metabolism. Temporal differences in the emergence of symptoms and clinical features warrant the continued clinical distinction between DLB and PDD. While DLB and PDD groups’ neuropsychological profiles often differ from those in Alzheimer’s disease (AD), the diagnostic sensitivity, specificity, and predictive values of these profiles remain largely unknown. PDD and DLB neuropsychological profiles share sufficient similarity to resist accurate and reliable differentiation. Although heterogeneous cognitive changes (predominantly in memory and executive function) may manifest earlier and more frequently than previously appreciated in Parkinson’s disease (PD), and executive deficits may be harbingers of dementia, the enthusiasm to uncritically extend the concept of mild cognitive impairment (MCI) to PD should be tempered. Instead, future research might strive to identify the precise neuropsychological characteristics of the prodromal stages of PD, PDD, and DLB which, in conjunction with other potential biomarkers, facilitate early and accurate diagnosis, and the definition of neuroprotective, neurorestorative, and symptomatic treatment endpoints. [Tröster, A. (2008), Neuropsychology Review, 18, 103–119]
FURTHER READING:
ABSTRACT:
Dementia with Lewy Bodies
The advent of new immunostains have improved our ability to detect limbic and cortical Lewy bodies, and it is now evident that Dementa with Lewy bodies (DLB) is the second most common neurodegenerative dementia, after Alzheimer’s disease (AD). Distinguishing DLB from AD has important implications for treatment, in terms of substances that may worsen symptoms (i.e., anticholinergic and certain neuroleptic medications) and those that may improve them (i.e., cholinesterase inhibitors, carbidopa-levodopa). Neurocognitive patterns, psychiatric features, extrapyramidal signs and sleep disturbance are helpful in differentiating DLB from AD early in the disease course. Differences in the severity of cholinergic depletion as well as type and distribution of neuropathology contribute to these clinical differences, though DLB patients with a high density of co-occuring AD pathology are less clinical distinguishable from AD. [Ferman, T. J. & Boeve, B. F. (2007), Neurologic Clinic, 25 (3), 741-760]
ABSTRACT:
Neuropsychological Characteristics of Dementia with Lewy Bodies and Parkinson’s Disease with Dementia: Differentiation, Early Detection, and Implications for “Mild Cognitive Impairment” and Biomarkers
Parkinson’s disease with dementia (PDD) and dementia with Lewy bodies (DLB) are neurodegenerative conditions sharing a disorder of α-synuclein metabolism. Temporal differences in the emergence of symptoms and clinical features warrant the continued clinical distinction between DLB and PDD. While DLB and PDD groups’ neuropsychological profiles often differ from those in Alzheimer’s disease (AD), the diagnostic sensitivity, specificity, and predictive values of these profiles remain largely unknown. PDD and DLB neuropsychological profiles share sufficient similarity to resist accurate and reliable differentiation. Although heterogeneous cognitive changes (predominantly in memory and executive function) may manifest earlier and more frequently than previously appreciated in Parkinson’s disease (PD), and executive deficits may be harbingers of dementia, the enthusiasm to uncritically extend the concept of mild cognitive impairment (MCI) to PD should be tempered. Instead, future research might strive to identify the precise neuropsychological characteristics of the prodromal stages of PD, PDD, and DLB which, in conjunction with other potential biomarkers, facilitate early and accurate diagnosis, and the definition of neuroprotective, neurorestorative, and symptomatic treatment endpoints. [Tröster, A. (2008), Neuropsychology Review, 18, 103–119]
FURTHER READING:
- Mild cognitive impairment associated with underlying Alzheimer’s disease versus Lewy body disease [Boeve, B.F. (2012),Parkinsonism and Related Disorders, 18S1, S41–S44]
- Amyloid PET Imaging in Lewy Body Disorders. [Donaghy P, Thomas AJ, O'Brien JT. (2013),American Journal of Geriatric Psychiatry,doi: 10.1016/j.jagp.2013.03.001. [Epub ahead of print]
- Dementia with Lewy bodies. Review of diagnosis and pharmacologic management. [Frank C. (2003),Canadian Family Physician, 49, 1304-1311]
About the Contributor:
Surabhi Patwardhan, Ph. D. is a post-doctoral resident in clinical neuropsychology at the Arizona Psychology Training Consortium.
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