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Arquivos de Neuro-Psiquiatria

Print version ISSN 0004-282X

Arq. Neuro-Psiquiatr. vol.20 no.3 São Paulo Sept. 1962

http://dx.doi.org/10.1590/S0004-282X1962000300001 

Fisiopatologia do sistema extrapiramidal. Novos conceitos decorrentes dos resultados experimentais e cirúrgicos

 

The pathological physiology of the extrapyramidal system. New concepts based on experimental and post-operative results

 

 

Horácio M. Canelas

Assistente-Docente de Clínica Neurológica (Prof. Adherbal Tolosa) da Faculdade de Medicina da Universidade de São Paulo

 

 


RESUMO

O autor revê o histórico do tratamento cirúrgico das afecções extrapiramidais, desde Horsley (1890) até Buey e Buchanan (1931) e outros adeptos das intervenções sôbre o sistema "piramidal", e depois, a partir de Meyers (1940), as agressões sôbre os núcleos da base. Os efeitos favoráveis da palidectomia e da talamectomia sôbre o tremor e a rigidez parkinsonianos forçaram a reformulação dos conceitos sôbre a fisiopatologia do sistema extrapiramidal.
O autor discute a localização da lesão responsável pela sintomatologia parkinsoniana, aceitando a opinião dos que consideram a destruição da substância negra como a base dos distúrbios hipercinéticos e tônicos, da mesma forma que a lesão do núcleo subtalâmico origina o hemibalismo. É feita a crítica do conceito clássico da sede preponderantemente palidal da lesão e da errônea interpretação jacksoniana dos fenômenos.
É destacada a contribuição experimental e cirúrgica para o conhecimento da patofisiologia do pálido medial e dos núcleos ventrolaterais do tálamo.
O tremor parkinsoniano pode ser considerado como resultante da hiperatividade da formação reticular pontomesencefálica (Jenkner e Ward), condicionada pela perda da ação inibidora do locus niger, associada à persistência da facilitação palidotalâmica. Na periferia, os estímulos reticulos-pinais "tremorogênicos" seguem a rota α.
A rigidez parkinsoniana decorreria dos mesmos processos patológicos encefálicos, porém sua fisiopatogenia periférica é controvertida. Para alguns, resulta de hiperatividade γ, associada à hipersensibilidade das vias inibidoras dos motoneurônios (sistema δ de Hufschmidt). Outros pesquisadores, entretanto, aduziram dados experimentais em favor de uma paralisia parcial do sistema γ, com hiperatividade α.
Finalmente, são referidas algumas teorias que tentam explicar o mecanismo básico do processo fisiopatológico nas afecções extrapiramidais, particularmente no parkinsonismo: descargas anormais de neurônios em degeneração (Cooper), hipersensibilidade de núcleos desaferentizados (Jenkner e Ward), desequilíbrio entre as estruturas lesadas e as indenes (Alberts e colaboradores).


ABSTRACT

The author gives the historical background of the surgical therapy of the extrapyramidal diseases, from Horsley (1890) to Bucy and Buchanan (1931) and other neurosurgeons who adopted the attack on the "pyramidal" tract, and, afterwards, beginning with Meyers (1940), the operations at the level of the basal ganglia. The good results of pallidectomy and thalamectomy on the parkinsonian tremor and rigidity imposed a reformulation of concepts on the physiopathology of the extrapyramidal system.
The author discusses the site of the lesion responsible for the parkinsonian symptomatology, accepting the view that the dyskinesia and the rigidity are caused by a lesion of the substantia nigra, in the same way as lesions of the subthalamic nucleus are responsible for the hemiballism. The author criticizes the classificai concept of the prevailing pallidal site of the lesion and the erroneous jacksonian interpretation of the phenomena.
The experimental and surgical contributions to the study of the pathological physiology of the medial pallidum and the ventrolateral nuclei of the thalamus are emphasized.
The parkinsonian tremor can be regarded as the result of hyperactivity of the pontomesencephalic reticular formation (Jenkner and Ward), owing to the loss of the inhibitory drive of the locus niger, associated to the sparing of the pallidothalamic facilitation. In the periphery the tremorogenic reticulospinal impulses follow the
α route.
The parkinsonian rigidity would depend on the same encephalic pathologic processes, but its peripheral physiopathogenesis is controversial. Some authors believe that it results from
γ hyperactivity, associated to oversensibility of the inhibitory pathways of the motoneurons (HufSchmidt's 5 system). Other investigators, however, have brought to light experimental data pointing to the partial paralisys of the γ sytem, associated to hyperactivity of the α drive.
Finally, the author refers to some theories which try to explain the basic mechanism of the physiopathologic process in the extrapyramidal diseases, especially in parkinsonism: abnormal discharges of degenerating neurons (Cooper), oversensibility of the deafferented nuclei (Jenkner and Ward), imbalance between damaged and preserved neural structures (Alberts et al.).


 

 

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Clínica Neurológica - Hospital das Clinicas, Faculdade de Medicina, Universidade de São Paulo - Caixa Postal SU61 - São Paulo, Brasil.
Trabalho apresentado no Departamento de Neurologia da Associação Paulista de Medicina em 5 abril 1952.

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