C Leiva-Santana1, M Alvarez-Saúco. 1. Servico de Neurología, Hospital General Universitario de Alicante, 03010 Alicante, Espana. leiva_car@gva.es
Abstract
AIMS: Most of the patients with Parkinson's disease evaluated in formal neuropsychological studies are found to have cognitive disorders similar to those of patients with lesions in the prefrontal cortex. A large number of anatomical, physiological, pharmacological and clinical data indicate that dopamine transmission plays an important role in frontal cortical functions. We review the main types of cognitive impairment in Parkinson's disease and their response to treatment with levodopa. DEVELOPMENT: In studies involving the acute administration of levodopa, the results obtained with regard to the cognitive functions have been heterogeneous, since improvements, exacerbations and the absence of any changes have all been observed. This heterogeneity is affected by methodological problems deriving from the disease itself, the treatment administered and the way evaluation is carried out. Longitudinal studies show a pattern of initial improvement, followed by stability, or maintenance, over a period of 2 or 3 years and then renewed exacerbation with no response to levodopa. On occasions, patients may only respond after a certain period of continued treatment. Generally speaking, the more severe the cognitive impairment is, the poorer the response to levodopa will be. CONCLUSIONS: Therapy with levodopa modifies, in one sense or another, the cognitive disorders in Parkinson's disease, which indicates that the dopaminergic deficit unquestionably plays a role in these disorders. The absence of response in some patients or in some cognitive functions or the fact that it 'wears off' in most patients suggests that the dopaminergic deficit is only one of the factors in the aetiopathogenesis of the cognitive dysfunction found in Parkinson's disease.
AIMS: Most of the patients with Parkinson's disease evaluated in formal neuropsychological studies are found to have cognitive disorders similar to those of patients with lesions in the prefrontal cortex. A large number of anatomical, physiological, pharmacological and clinical data indicate that dopamine transmission plays an important role in frontal cortical functions. We review the main types of cognitive impairment in Parkinson's disease and their response to treatment with levodopa. DEVELOPMENT: In studies involving the acute administration of levodopa, the results obtained with regard to the cognitive functions have been heterogeneous, since improvements, exacerbations and the absence of any changes have all been observed. This heterogeneity is affected by methodological problems deriving from the disease itself, the treatment administered and the way evaluation is carried out. Longitudinal studies show a pattern of initial improvement, followed by stability, or maintenance, over a period of 2 or 3 years and then renewed exacerbation with no response to levodopa. On occasions, patients may only respond after a certain period of continued treatment. Generally speaking, the more severe the cognitive impairment is, the poorer the response to levodopa will be. CONCLUSIONS: Therapy with levodopa modifies, in one sense or another, the cognitive disorders in Parkinson's disease, which indicates that the dopaminergic deficit unquestionably plays a role in these disorders. The absence of response in some patients or in some cognitive functions or the fact that it 'wears off' in most patients suggests that the dopaminergic deficit is only one of the factors in the aetiopathogenesis of the cognitive dysfunction found in Parkinson's disease.