The exact cause of Lewy body dementia is largely unknown. Attempts to correlate the degree of neurologic impairment with density or distribution of Lewy bodies themselves have been largely inconclusive. Genetics, environment, and normal aging are believed to play a role.
Decreased levels of cholinergic neurons in the CNS are seen in patients with Lewy body dementia. This is coupled with decreased levels of choline acetyltransferase (ChAT). An inverse relationship between ChAT levels and hallucinations has been observed in these patients.
α-Synuclein is the main component of eosinophilic cytoplasmic inclusions, which are found in Lewy bodies. These are identified histologically in brain tissue. This molecule is mostly located on presynaptic terminals and is believed to play a role in neurotransmitter release
Lewy bodies are eosinophilic cytoplasmic inclusions within nerve cells. They are composed of aggregates of alpha-synuclein. While these inclusions are found in abundance in patients with Lewy body dementia, their role in disease has not been entirely established.
Visual hallucinations are extremely common in patients with Lewy body dementia and are considered a hallmark of the disease. These are present in roughly two-thirds of patients with this disease. This can be used to aid in distinguishing this disease from Alzheimer’s, where visual hallucinations are much less common
Lewy body dementia is characterized by early loss in cognitive function. This can manifest as impaired activities of daily living, poor job performance, or impaired attention.
Patients with Lewy body dementia often exhibit episodes of fluctuating cognition. These episodes may last anywhere from a few seconds to days at a time. Episodes can be mild such as to interfere slightly with activities of daily living or severe enough to warrant evaluation for stroke or seizure.
Patients with Lewy body dementia often exhibit severe REM parasomnias. Patients may sleep talk or mime complex actions. Patients will physically “act out” their dreams as they sleep. This is believed to be due to brainstem dysfunction.
Parkinsonian symptoms are seen in up to 90% of patients with Lewy body dementia. These symptoms include tremor, bradykinesia, limb rigidity and/or gait disturbances.
Cholinesterase inhibitors such as rivastigmine and donepezil have been shown to ameliorate cognitive, psychological, and parkinsonian symptoms of disease. Patients should be monitored closely, however, as some patients report worsening of their symptoms upon starting treatment.
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