Clinical Geriatrics

Introduction
Dementia with Lewy bodies (DLB) is either the second or third most common cause for dementia in the economically developed world,¹ yet it is frequently not recognized. While it is often mistaken for Alzheimer’s disease (AD) early in the course because the parkinsonian features frequently develop after the dementia has begun, making the correct diagnosis leads to better management. The development of parkinsonism in a person with dementia not taking neuroleptics or on very low doses should always raise this consideration,² but other signs and symptoms often point to the correct diagnosis.

Case Presentation
A 78-year-old, right-handed man was referred to a movement disorders clinic for evaluation of parkinsonism. The patient had been having memory problems for approximately five years. Three years after his memory problems first began, he was diagnosed with AD and was started on donepezil with mild benefit. Approximately 18 months before this evaluation, he began developing slowly progressive walking problems, with short steps and slowness. As his gait worsened, the patient developed a walking problem that propelled him, sometimes causing him to run or walk on the balls of his feet despite using a cane. His wife noted that he had difficulty judging distances and would often nearly miss a chair when sitting down. Approximately six months ago, he began having visual hallucinations of deceased family members. For an unknown period of time, he has had severely impaired smell and taste, and has had multiple episodes of becoming unresponsive, lasting up to 10 minutes, without focal deficits or seizure activity noted, occurring when seated. He did not have behaviors suggestive of rapid eye movement sleep behavior disorder (RBD). His wife noted that his level of confusion varies during the day. At times, the patient cannot identify family members or his best friend, whereas at other times, he has only minor memory problems.

The patient had been evaluated for his unresponsive episodes, and a heart pacemaker was implanted for a presumed bradycardic explanation, but it was unhelpful. He denied feeling lightheaded on standing, but had been treated with fludrocortisone, without reduction in unresponsive spells. Although electroencephalograms revealed no epileptic activity, the patient was placed on lamotrigine, with uncertain benefit. His wife had stopped calling emergency services when the patient became unresponsive, choosing to let him recover at home. Following each spell, he slept much of the day but recovered to baseline.

There was no history of alcohol or substance abuse or any recent use of nonprescribed drugs. His history was positive for hypertension, hypercholesterolemia, and orthostatic hypotension. He had a brain magnetic resonance imaging (MRI) scan five years prior that reportedly showed “mini-strokes,” and he was reported to have had transient ischemic attacks, but details were not available. There was no family history of Parkinson’s disease (PD), AD, or other neurological disorders.

His medications included solifenacin 5 mg daily, simvastatin 40 mg daily, clopidogrel 75 mg daily, memantine 10 mg twice per day, metoprolol 25 mg daily, lisinopril 10 mg daily, hydrochlorothiazide 12.5 mg daily, lamotrigine 200 mg daily, fludrocortisone 0.15 mg daily, and donepezil 10 mg daily. He had not been on dopamine receptor-blocking drugs.

On examination, the patient was a thin, athletic-appearing man who knew his age but not the month, season, or year. Although he had watched a ball game the previous night, he could not recall the visiting team. His naming was impaired, although his speech was fluent, without paraphasias or pauses for word-finding. Cranial nerves were normal.