
Psychosomatics 43:84-86, February 2002
© 2002 The Academy of Psychosomatic Medicine
Probable Lewy Body Dementia Presenting as "Delirium"
Michael J. Robinson, MD, FRCPC, Queen's University, Kingston, ON, Canada
Key Words: Dementias (general) Delirium
TO THE EDITOR: Dementia with Lewy bodies (DLB) is the second most common form of degenerative dementia in old age. Consensus criteria for the clinical diagnosis of DLB report core features of progressive cognitive decline, fluctuating cognition, recurrent visual hallucinations, and spontaneous motor symptoms of parkinsonism. There may be other associated features, such as repeated falls, syncope, transient loss of consciousness, neuroleptic sensitivity, systematized delusions, and hallucinations in other modalities. Symptoms of prominent or persistent memory impairment are not always present early in the course of DLB. Rather, early cognitive impairment is often marked by prominent attentional deficits and visuospatial dysfunction. Fluctuation in cognitive function is common in DLB. This includes variations in attention and alertness, excessive daytime drowsiness, and transient confusional states. The fluctuations may be observed within a day or from day to day.1,2 Additional features for consideration include rapid eye movement sleep behavior disorder and depressive symptoms.15
These clinical features of DLB look similar to the clinical presentation of delirium, which is defined as a disturbance in consciousness, with reduced ability to focus, sustain, or shift attention; and a change in cognition, or the development of a perceptual disturbance.6 I report a case of probable DLB in which the patient presented with an admitting diagnosis of "delirium."
Case Report
Ms. A. is an 80-year-old woman who presented with a 3- to 4-week history of progressively worsening inappropriate behavior, confusion, inability to perform routine tasks such as dressing, suspicious behavior, periods of "blanking out," repeated falls, inability to speak and walk at times, visual hallucinations of faces, auditory hallucinations, and agitation with disinhibition. Ms. A. appeared to have brief periods in which she seemed to be improved and "back to herself," and the above symptoms had fluctuated in severity over the last 46 weeks. She saw her family doctor, who performed a Folstein Mini-Mental State Exam; Ms. A. reportedly scored 27 of 30, with "no problems identified."
Because of ongoing confusion, she was later brought to the emergency room for investigation. On admission to the hospital, her medications included vitamin E, vitamin D, calcium supplement, latanoprost (Xalatan), ophthalmic solution, and Arthrotec (one tablet tid), and there had been no recent changes. Her admission diagnosis was "delirium" and she received a medical and neurologic workup. Laboratory investigations included complete blood count, electrolytes, blood glucose, calcium, phosphorus, magnesium, aspartate aminotransferase, alanine aminotransferase, gammaglutamyltransferase, alkaline phosphatase, amylase, total bilirubin, albumin, thyroid-stimulating hormone, vitamin B12, morning cortisol, blood and urine cultures, and a syphilis screen. All tests were normal. Computed tomography (CT) of the head was reported to show cerebral and cerebellar atrophy and a right cerebellar pontine-angle mass most compatible with a meningioma, with no mass effect. Magnetic resonance imaging did not reveal anything different from the CT scan. An electroencephalogram was essentially normal, with some drowsiness and medication effect. A lumbar puncture was attempted but after one failed attempt, the family refused consent for a repeat attempt.
During her admission to the general hospital, Ms. A. received three doses of haloperidol (2 mg im) for agitation and developed significant cogwheel rigidity, bradykinesia, and impaired gait. The opinion upon neurologic consultation was "Parkinson disease worsened by neuroleptics." Psychiatric examination found significant visuospatial (e.g., 10-point clock-drawing test)7 and attention cognitive impairments and bradykinesia. She also continued to report visual and auditory hallucinations with delusions of persecution. Initial psychiatric consultation opinion was probable DLB, based on the established criteria listed above. Upon psychogeriatric consultation, the initial opinion was "delirium," with DLB high on the differential diagnosis, and the recommended initial management of her psychotic symptoms was low-dose quetiapine (12.5 mg po bid). She was transferred to a psychogeriatric service for ongoing care. Quetiapine treatment did not significantly alter her perceptual disturbances, and she experienced continued fluctuation in her cognitive symptoms. After further observation and treatment trials, it was concluded that Ms. A.'s clinical presentation was consistent with a probable diagnosis of DLB.
Discussion
This case illustrates the complex and difficult diagnostic picture that can be associated with the clinical presentation of DLB. The presentation of fluctuation in cognition, visual hallucinations, and cognitive impairment may closely resemble the clinical presentation of delirium. Because of the prominent symptoms, patients with DLB may present to many different clinicians, which may include geriatricians, internists, neurologists, and psychiatrists. In particular, the psychiatrist for the medically ill should remember DLB as a potential possibility in the differential diagnosis of "delirium presentations," especially in the elderly. This is an important consideration because neuroleptics, which are frequently used in the treatment of delirium, may exacerbate the parkinsonian symptoms that often accompany DLB.
REFERENCES
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Manos PJ: The utility of the ten-point clock test as a screen for cognitive impairment in general hospital patients. Gen Hosp Psychiatry 1997; 19:439-444[CrossRef][Medline]
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