Although pathologically distinct from Alzheimer's disease, LBD usually occurs in combination with the neurofibrillary tangles and plagues of AD, suggesting an etiological connection between these two forms of dementia that has not yet been discovered. Epidemiological characteristics such as the low rate of pure LBD cases, the higher rate of LBD in males than females, and the more rapid course of LBD compared to pure AD, may provide clues into the risk and etiological factors of LBD.
The most widely accepted criteria for LBD (McKeith et al., 1996) are progressive cognitive decline and two of the following: fluctuating cognition with variations in alertness and attention, recurrent well-formed and detailed visual hallucinations, or spontaneous motor symptoms of parkinson-ism. Other criteria symptoms suggestive of LBD are repeated falls, syncope, transient loss of consciousness, neuroleptic sensitivity, systematized delusions, and hallucinations in modalities other than visual. Postmortem studies indicate these criteria are highly specific but not particularly sensitive to identifying true cases of LBD. Missed cases are most often diagnosed either pure AD or VaD. The lack of distinction between LBD and AD is certainly complicated by their frequent co-occurrence and their similarly affected brain regions. On the other hand, misdiagnosed cases of LBD as MD may, in part, reflect clinicians' being less aware of the need to consider LBD as a rule-out dementia diagnosis, particularly in the presence of symptoms such as variations in alertness, visual hallucinations, and motor impairments.
Studies that compare pure LBD to pure AD remind us that the cognitive symptoms of these dementias share far more similarities than differences (Salmon et al., 1996). Several neuropsychology studies have found greater impairment among patients with LBD, compared to AD, in the areas of attention, fluency, visuospatial and constructional abilities, psychomotor speed, and frontal symptoms. However, it must be recognized that a statistically significant difference in average scores across groups does not always lead to accurate classification of individuals. Thus far, the literature suggests that the differential diagnosis of LBD and AD cannot be based on distinct patterns of cognitive deficits in either group. Several factors may be masking their distinction. First, they most often coexist and, even in their pure forms, they affect the same regions of the brain, rendering them less likely to produce distinctive clinical indicators. Second, few studies are prospective comparisons with postmortem confirmation of diagnoses; hence, we must assume that inaccurate clinical diagnoses exaggerate overlapping symptoms. Finally, many of these studies are based on small sizes, and measures used across studies are not standardized. These factors certainly thwart efforts to produce replication across studies.
While LBD and AD appear to share many cognitive impairments, psychiatric and motor disturbances may have greater utility in differentiating LBD from AD. Recurrent, complex, and vivid visual hallucinations are prominent features of LBD, as are delusions. Again, these symptoms are not pathognomonic of LBD because they also are present in other forms of dementia and delirium. Further research should examine the hypothesis that the persistence and predominance of these symptoms, rather than merely their presence, are diagnostic indicators. In addition, more studies are needed to discern if the motor abnormalities such as bradykinesia, rigidity, masked facies, and parkinsonian gait may be helpful in distinguishing LBD from AD patients (Galasko et al., 1996; Hansen et al., 1990).
The importance of accurate diagnosis is perhaps most apparent in consideration of the possible iatrogenic effects of treating patients with LBD with neuroleptics or antiparkinsonian medications. While these treatment strategies may initially seem appropriate, the misdiagnosed LBD patient treated with neuroleptics may face irreversible parkinsonism, impaired consciousness, and autonomic disturbances; or if treated with antiparkin-sonian medication, the patient may face worsening psychotic symptoms. Given the serious limitations on using antipsychotic and antiparkinsonian medications, research on nonpharmacological behavioral treatment strategies is imperative.
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