Lewy Body Dementia
The most likely diagnosis for this patient is Lewy body dementia (LBD), based on the presence of all four core clinical features: progressive cognitive decline with prominent visuospatial dysfunction, recurrent visual hallucinations, spontaneous parkinsonism (rigidity, bradykinesia, resting tremor), and objective evidence of reduced dopamine transporter uptake on DAT scan. 1, 2
Diagnostic Reasoning
Core Clinical Features Present
This patient demonstrates all the hallmark features that distinguish LBD from other dementias:
- Visual hallucinations: She sees people in her home who are not there—these are the well-formed, detailed visual hallucinations characteristic of LBD 1, 2
- Parkinsonism: The presence of rigidity, bradykinesia (slow movements), resting tremor, and shuffling gait with freezing episodes represents spontaneous extrapyramidal motor features 1, 2
- Cognitive impairment: Progressive decline over 3 years with prominent visuospatial difficulties (getting lost in familiar places, low MoCA visuospatial scores) 1
- DAT scan confirmation: Reduced dopamine uptake in the basal ganglia provides objective biomarker support for LBD 1
Why Not Alzheimer's Disease
The National Institute on Aging-Alzheimer's Association guidelines explicitly state that probable AD dementia should NOT be applied when there is evidence of core features of Dementia with Lewy bodies other than dementia itself. 3 This patient has three core LBD features (visual hallucinations, parkinsonism, and likely cognitive fluctuations based on the EEG findings), which excludes a primary AD diagnosis despite the positive amyloid biomarkers 3
The presence of AD pathology (positive amyloid PET, elevated tau in CSF, hippocampal atrophy) represents common mixed pathology—LBD frequently coexists with AD pathology, but the clinical syndrome is driven by the Lewy body disease when core features are present 3, 1, 4
Why Not Vascular Dementia
The vascular changes are explicitly described as "mild periventricular white matter hyperintensities" that are "not significant enough to confirm vascular dementia" [@case presentation]. Vascular dementia does not explain the constellation of visual hallucinations, parkinsonism, and REM sleep-related symptoms that characterize this presentation [@5@]
The elevated blood pressure (158/92 mmHg) represents a vascular risk factor but does not override the dominant LBD clinical picture [@2@]
Clinical Implications for Management
Treatment Considerations
- Cholinesterase inhibitors are first-line treatment for both cognitive symptoms and visual hallucinations in LBD [@6@, @8@, 5,6]
- Traditional antipsychotics must be absolutely avoided due to severe neuroleptic sensitivity that significantly increases morbidity and mortality [@5@, 2,7]
- Levodopa should be used cautiously for motor symptoms, as dopaminergic agents carry risk of inducing or worsening psychotic symptoms [@10@]
Diagnostic Certainty
The DAT scan provides Level A evidence supporting the LBD diagnosis by demonstrating reduced striatal dopamine transporter binding [@5@, @10@]. The EEG showing occipital slowing further supports LBD over pure AD [@case presentation, 8]
This represents a classic case of LBD with mixed AD pathology—a common scenario where the clinical syndrome and biomarker profile (DAT scan) clearly indicate LBD as the primary driver of the dementia syndrome, despite coexisting Alzheimer pathology. 3, 4