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Lewy Body Dementia

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Lewy Body Dementia

NINDS Dementia With Lewy Bodies Information Page

"Dementia with Lewy bodies (DLB) is one of the most common types of progressive dementia. The central feature of DLB is progressive cognitive decline, combined with three additional defining features: (1) pronounced “fluctuations” in alertness and attention, such as frequent drowsiness, lethargy, lengthy periods of time spent staring into space, or disorganized speech; (2) recurrent visual hallucinations, and (3) parkinsonian motor symptoms, such as rigidity and the loss of spontaneous movement. People may also suffer from depression. The symptoms of DLB are caused by the build-up of Lewy bodies – accumulated bits of alpha-synuclein protein -- inside the nuclei of neurons in areas of the brain that control particular aspects of memory and motor control. … The similarity of symptoms between DLB and Parkinson’s disease, and between DLB and Alzheimer’s disease, can often make it difficult for a doctor to make a definitive diagnosis. In addition, Lewy bodies are often also found in the brains of people with Parkinson's and Alzheimer’s diseases. These findings suggest that either DLB is related to these other causes of dementia or that an individual can have both diseases at the same time. DLB usually occurs sporadically, in people with no known family history of the disease."

Highlighted Article

Dementia with lewy bodies. (Semin Neurol. 2007)

"The presentation of DLB is typically one of cortical and subcortical cognitive impairments, with worse visuospatial and executive dysfunction than Alzheimer's disease. There may be relative sparing of memory especially in the early stages. Core clinical features of DLB include fluctuating attention, recurrent visual hallucinations, and parkinsonism. Suggestive features include REM sleep behavior disorder, severe neuroleptic sensitivity, and low dopamine transporter uptake in the basal ganglia on functional neuroimaging. Additional supportive features that commonly occur in DLB, but with lower specificity, include repeated falls and syncope, transient, unexplained loss of consciousness, severe autonomic dysfunction, hallucinations in other modalities, systematized delusions, depression, relative preservation of medial temporal lobe structures on structural neuroimaging, reduced occipital activity on functional neuroimaging, prominent slow wave activity on electroencephalogram, and low uptake myocardial scintigraphy."

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Lewy Body Dementia

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Evidence that incidental Lewy body disease is pre-symptomatic Parkinson's disease. (Acta Neuropathol. 2008)

Incidental Lewy Body Disease and Preclinical Parkinson Disease (Arch Neurol 2008)

Lewy body dementia and Parkinson's disease with dementia. (J Neurol. 2008) “Parkinson's disease (PD) is characterized by its motor impairment. However, non-motor symptoms such as psychiatric disorders, autonomic disturbances and sleep disorders frequently complicate the course of the disease. In particular, psychiatric disturbances including cognitive impairment, depression and psychosis impact these patients considerably. Approximately 31 % of PD patients suffer from cognitive impairment and dementia. Currently, two different clinical presentations are distinguished in PD patients, who present with dementia: Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB), which are two different presentations of a single underlying disease process leading to the deposition of alpha-synuclein.”

Lower urinary tract symptoms in dementia with Lewy bodies, Parkinson disease, and Alzheimer disease (NEUROLOGY 2008) “Conclusions: Urgency and urge incontinence suggest detrusor overactivity, which was more prevalent in dementia with Lewy bodies than in Parkinson disease and Alzheimer disease, whereas mean voided volume, free flow, cystometric bladder capacity, and detrusor pressor were similar in the groups. Frequency of micturition could not be reliably assessed in patients with dementia.”

Prevalence and impact of vascular and Alzheimer pathologies in Lewy body disease. (Acta Neuropathol. 2008)

 

 

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