Neuropsychiatric symptoms (NPS) such as apathy, agitation, anxiety, depression, delusions, or hallucinations frequently accompany cognitive symptoms in dementias. They often constitute a diagnostic challenge in cognitively impaired patients. Single symptoms or combinations of NPS also contribute to patient and caregiver distress, increase caregiver burden and health care costs. Various instruments such as the BEHAVE-AD and the Neuropsychiatric Inventory (NPI) have been validated and allow clinicians to recognize and score NPS. In Alzheimer's disease (AD), although NPS are not part of the diagnostic criteria, they clearly accompany the cognitive symptoms, evolve over time in a specific pattern and respond to acetylcholinesterase inhibitors. Functional neuroimaging and neuropathological data show that they probably derive from progression of the pathology to defined cortical regions. In Dementia with Lewy Bodies (DLB) visual hallucinations are one of the core diagnostic criteria. Delusions frequently occur. Nevertheless Parkinson’s disease (PD) and Parkinson’s disease with dementia (PDD) also present with these NPS and respond to acetylcholinesterase inhibitors explaining why the boundaries between these diseases appear less distinct than anticipated. The influence of levodopa on visual hallucinations and psychosis in PD and PDD is undebated but more and more data point to the fact that dementia is an important predictor in the expression of these NPS. Accumulation of Lewy Bodies in visual associative and limbic areas may explain visual hallucinations. Interestingly in progressive supranuclear palsy (PSP), although cholinergic deficits participate in the neuropathology of the disease and presumably in the pathogenesis of apathy, the first trial of acetycholinesterase inhibitors failed to show significant changes in the behavior of the patients. In frontotemporal dementia (FTD), NPS are more difficult to apprehend. Loss of emotions and insight, selfishness, gluttony and sweet food preference, wandering were more characteristics of FTD and differentiated the most FTD from AD in a recent study. Another group found that the early presence of socially undesirable behaviors such as criminal behaviors, aggression, loss of job, alienation from friends or relatives, financial recklessness, sexually deviant behavior, abnormal response to marital crisis significantly occurred in right-sided FTD. To conclude, NPS are not only secondary reactions to the disease. They are linked to specific neuronal networks in the brain as demonstrated with functional neuroimaging and are explained by involvement of the pathology in specific brain regions. They respond to treatment such as acetycholinesterease inhibitors, antidepressants, atypical antipsychotics. Future directions include behavioral neurogenetics and functional neuroimaging. Genetic polymorphism may predispose individuals to express specific NPS. Probes measuring neuropathological markers (neurofibrillary tangles, senile plaques or microglia) will permit in vivo correlations with NPS. A multidisciplinary approach combining clinical data, neuroimaging, neuropharmacology and behavioral neurogenetics will not only improve understanding of the biological basis of NPS but will enhance quality of care for all patients with dementias.
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