Revista de neurologia · 2001
[Dopaminomimetic psychosis in Parkinson's disease: first symptom of early dementia?].
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Catalan-Alonso M J, Del Val J
Аннотация
INTRODUCTION: Parkinson s disease (PD) is caused by an abnormal degeneration of the dopamine producing cells in the substantia nigra and ventral tegmental area. When PD advances, degeneration of the nigroestriatal tracts may expand and involve other pathways (mesolimbic and frontal), and also serotonergic and cholinergic systems. This degeneration leads to a multitude of motor and non motor behavioral disturbances.
DEVELOPMENT: On the background of progressive degeneration, chronic levodopa and dopaminergic agonist administration may cause pulsatile non physiologic overstimulation of dopaminergic receptors. This may induce perturbations in limbic and frontal cortex structures and overstimulation of serotonergic, cholinergic and other neurotransmitter systems. These events are the basis of parkinsonian psychosis, perhaps in the setting of early dementia. The treatment of this psychosis is difficult. The reduction or withdrawal of dopaminomimetic agents may improve psychosis with worsening of parkinsonian disability. The recommended order to discontinue antiparkinsonian drugs, when is required, is anticholinergic, selegiline, amantadine and dopamine agonist. Levodopa should be reduced to a tolerable minimum to compensate the motor disturbances. At this point, it may be necessary to add an atypical neuroleptic such as clozapine, quetirapine or olanzapine to improve the symptomatology.
CONCLUSIONS: More studies are needed to asses the relationship between parkinsonian psychosis and early dementia. Additional, the development of new drugs could be helpful to control these psychotic symptoms in PD without serious secondary effects.
DEVELOPMENT: On the background of progressive degeneration, chronic levodopa and dopaminergic agonist administration may cause pulsatile non physiologic overstimulation of dopaminergic receptors. This may induce perturbations in limbic and frontal cortex structures and overstimulation of serotonergic, cholinergic and other neurotransmitter systems. These events are the basis of parkinsonian psychosis, perhaps in the setting of early dementia. The treatment of this psychosis is difficult. The reduction or withdrawal of dopaminomimetic agents may improve psychosis with worsening of parkinsonian disability. The recommended order to discontinue antiparkinsonian drugs, when is required, is anticholinergic, selegiline, amantadine and dopamine agonist. Levodopa should be reduced to a tolerable minimum to compensate the motor disturbances. At this point, it may be necessary to add an atypical neuroleptic such as clozapine, quetirapine or olanzapine to improve the symptomatology.
CONCLUSIONS: More studies are needed to asses the relationship between parkinsonian psychosis and early dementia. Additional, the development of new drugs could be helpful to control these psychotic symptoms in PD without serious secondary effects.