Book contents
- Frontmatter
- Contents
- Contributors
- Foreword
- Acknowledgements
- Biographical note on F. H. Lewy
- Abbreviations
- Group photograph
- Introduction
- Part one Clinical issues
- Part two Pathological issues
- Part three Treatment issues
- 28 Psychopharmacology of cognitive impairment in Parkinson's disease
- 29 Management of the noncognitive symptoms of Lewy body dementia
- 30 Altered consciousness and transmitter signalling in Lewy body dementia
- 31 Cholinergic therapy and Lewy body dementia
- 32 Clinical heterogeneity in dementia: responders to cholinergic therapy
- 33 Tacrine and symptomatic treatment in Lewy body dementia
- 34 Neurochemical correlates of pathological and iatrogenic extrapyramidal symptoms
- 35 Neurotrophins and the cholinergic system in dementia
- 36 Relevance of Lewy bodies to alterations in oxidative stress in Lewy body dementia and Parkinson's disease
- Résumé of treatment workshop sessions
- Appendices
- Index
- Plate section
33 - Tacrine and symptomatic treatment in Lewy body dementia
from Part three - Treatment issues
Published online by Cambridge University Press: 06 July 2010
- Frontmatter
- Contents
- Contributors
- Foreword
- Acknowledgements
- Biographical note on F. H. Lewy
- Abbreviations
- Group photograph
- Introduction
- Part one Clinical issues
- Part two Pathological issues
- Part three Treatment issues
- 28 Psychopharmacology of cognitive impairment in Parkinson's disease
- 29 Management of the noncognitive symptoms of Lewy body dementia
- 30 Altered consciousness and transmitter signalling in Lewy body dementia
- 31 Cholinergic therapy and Lewy body dementia
- 32 Clinical heterogeneity in dementia: responders to cholinergic therapy
- 33 Tacrine and symptomatic treatment in Lewy body dementia
- 34 Neurochemical correlates of pathological and iatrogenic extrapyramidal symptoms
- 35 Neurotrophins and the cholinergic system in dementia
- 36 Relevance of Lewy bodies to alterations in oxidative stress in Lewy body dementia and Parkinson's disease
- Résumé of treatment workshop sessions
- Appendices
- Index
- Plate section
Summary
Summary
Two characteristics of senile dementia of the Lewy body type (SDLT) compared with Alzheimer's disease (AD) are relevant to treatment management: relative hypocholinergic activities and behavioural disturbances such as psychotic manifestations with neuroleptic hypersensitivity. A better tacrine responsiveness of SDLT patients has been proposed. An open trial with tacrine (120mg/day) prescribed in 22 probable AD patients (meeting NINCDS–ADRDA criteria) resulted in no memory improvement in the four patients meeting SDLT criteria. The potential of GABAergic agents, particularly carbamazepine, in the management of delirium and psychotic symptoms in SDLT is discussed.
Introduction
In recent years there has been an increasing interest in behavioural disorders in dementia since psychiatric disturbance is considered to be one of the most troublesome aspects of the disease by many relatives of demented patients. They are an important risk factor for institutionalization. On the other hand, behavioural abnormalities are not usually considered in the diagnosis of degenerative dementia although psychotic symptoms and mood disorders may be the earliest signs of frontal lobe dementia or Lewy body disease. Episodic confusion, depressive and psychotic symptoms are frequently observed in senile dementia of Lewy body type (SDLT). Hallucinations are more often reported in SLDT than in dementia of Alzheimer type (AD) (Ballard et al., 1995). Dopamine hyperactivity is a putative neurochemical basis for psychosis and cholinergic/dopaminergic imbalance with relative dopamine excess linked to hallucinations in different neurological diseases such as Parkinson's disease. Moreover, physostigmine reduced delusions in two AD patients (Cummings et al., 1993). In SLDT, in which hallucinations are frequent, cholinergic hypometabolism (e.g. choline acetyltransferase decrease) has been reported (Perry et al., 1993).
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- Dementia with Lewy BodiesClinical, Pathological, and Treatment Issues, pp. 439 - 448Publisher: Cambridge University PressPrint publication year: 1996
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