An 80‑year‑old man with hypertension treated with amlodipine presents with visual hallucinations, hypoglycemia, dysphagia, decreased sweating, and preserved memory. What is the most likely diagnosis?

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Lewy Body Dementia

The most likely diagnosis is B. Lewy Body Dementia (DLB), based on the pathognomonic combination of visual hallucinations with preserved memory, autonomic dysfunction (decreased sweating), and dysphagia. 1

Clinical Reasoning

Core Diagnostic Features Present

  • Visual hallucinations with intact memory is the distinguishing feature that separates DLB from Alzheimer's disease, where memory impairment is the hallmark early feature 1, 2, 3

  • Autonomic dysfunction (decreased sweating) is characteristic of Lewy body dementia and represents involvement of the peripheral autonomic nervous system, which is one of the earliest sites affected in Lewy body disease 1, 4

  • Dysphagia is a spontaneous motor feature consistent with the parkinsonian syndrome spectrum that includes DLB 1, 2

  • Preserved memory is critical—this patient's intact memory essentially rules out Alzheimer's disease, which presents with prominent early memory impairment 1, 3

Why Other Diagnoses Are Excluded

Alzheimer's Dementia (Option A) is ruled out because memory impairment is the hallmark early feature of Alzheimer's disease, which this patient does not have 1. Visual hallucinations are uncommon in pure Alzheimer's disease and typically occur only in advanced stages 1.

Multi-Infarct Dementia (Option C) is inconsistent because it typically presents with stepwise cognitive decline, focal neurological deficits, and evidence of multiple strokes—none of which are described in this patient 1. While the patient has hypertension as a vascular risk factor, the clinical presentation lacks the typical vascular pattern of cognitive impairment 1.

Prion Disease (Option D) is ruled out because the clinical picture lacks the characteristic myoclonus, ataxia, and rapidly progressive dementia typical of Creutzfeldt-Jakob disease 1. Prion diseases present with very rapid cognitive decline, which is not consistent with this patient's presentation 1.

Clinical Pathophysiology

The pathological hallmark of DLB involves numerous alpha-synuclein-positive Lewy bodies in the cerebral cortex, particularly neocortical and limbic areas, in addition to nigral Lewy body degeneration 3. The earliest sites of involvement in Lewy body disease are the olfactory bulb, dorsal motor nucleus of the vagal nerve, peripheral autonomic nervous system (including the enteric nervous system), and brainstem 4. This explains why autonomic dysfunction and dysphagia can appear early in the disease course.

Important Clinical Pitfalls

Do not confuse this with Charles Bonnet Syndrome (CBS), which requires pre-existing significant vision loss, insight that hallucinations are not real, and no other neurological signs 1, 5. The presence of neurological signs such as dysphagia and autonomic dysfunction alongside visual hallucinations mandates consideration of Lewy body dementia rather than CBS 1.

The hypoglycemia episode requires prompt evaluation and treatment as it is associated with increased mortality in elderly patients 1, but it does not explain the chronic neurological presentation and should be managed separately.

Fluctuating cognition is another core feature of DLB that should be assessed, characterized by pronounced variations in attention and alertness 2, 3. While not explicitly mentioned in this case, it is commonly present and should be inquired about.

References

Guideline

Diagnosis and Clinical Features of Lewy Body Dementia

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Visual signs and symptoms of dementia with Lewy bodies.

Clinical & experimental optometry, 2012

Research

How to diagnose dementia with Lewy bodies: state of the art.

Movement disorders : official journal of the Movement Disorder Society, 2005

Guideline

Management of Charles Bonnet Syndrome in Elderly Patients

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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