RESUMO
The term "extrapyramidal" originally described a collection of tegmentospinal pathways that conveyed the propagation of cortically-induced seizures to the spinal cord of dogs with bilateral transection of the pyramidal tracts. The extrapyramidal concept developed into unwarranted avenues to include forebrain structures involved in motor control, such as the basal ganglia, or as a broad synonym of clinical syndromes characterized by nonparalytic abnormal involuntary movements and postures. Clinicians and pathologists assumed that, similarly to mammals in general, the human extrapyramidal system was also organized in parallel with the pyramidal tracts. Several inconsistencies of this model, as applied to humans, were overlooked despite compelling clinicoanatomic evidence showing that (i) bilateral damage to the pyramidal tracts at any level from the pontomedullary transition to the motor cortex produces the locked-in syndrome and (ii) the extrapyramidal tracts are sparse in man. In the present essay I advance the hypothesis that the human extrapyramidal system is fundamentally different from its mammalian counterparts both anatomically and functionally. To test this hypothesis, a systematic analysis of the residual motor patterns observed on a natural model of a bilateral section of the human pyramidal tracts, the locked-in syndrome, is provided. This analysis reveals that the human extrapyramidal system underpins the organization of the following categories of motor synergies: (i) oculofacial and oculocephalic, (ii) faciorespiratory, (iii) axial-appendicular, and (iv) plurisegmental. Anatomically, these functional repertoires of motor integration are mediated by six collections of axons defined by their brainstem nuclei of origin and spinal cord destinations: reticulospinal (medial and lateral), vestibulospinal (medial and lateral), rubrospinal (lateral only), and tectospinal (medial only) fiber systems. I conclude that the extrapyramidal concept can reliably be extended to humans, albeit its physiological and anatomical scope is considerably narrower than traditionally assumed.
Assuntos
Tratos Extrapiramidais/fisiologia , Sistema Nervoso Central/fisiologia , Humanos , Modelos TeóricosRESUMO
The concept of the extrapyramidal system comprises an amalgam of disparate and often conflicting ideas with a tortuous history. To the theoretical neuroscientist or practicing clinician, it promptly evokes semantic associations that are hardly reminiscent of its original meaning. The purpose of this article is to revisit the sources of the extrapyramidal concept and to examine the transformations that it went through from its inception, in the late 1890s, up to the neuroimaging revolution of the 1980s. Our review shows that the use of "extrapyramidal" as a surrogate for the basal ganglia, disorders of movement, or certain manifestations of spastic hemiplegia does not apply to humans; rather, it represents the historical product of the unwarranted translation of results of animal experimentation into the interpretation of clinical findings on human patients, misguided clinico-anatomic deductions, and fanciful phylogenetic notions. We conclude that the extrapyramidal concept is a valid and robust anatomic concept as long as it strictly refers to the collection of descending fibers originating in a few discrete brainstem tegmental motor nuclei that project to the spinal cord.
Assuntos
Doenças dos Gânglios da Base/história , Neurologia/história , Gânglios da Base/anatomia & histologia , Doenças dos Gânglios da Base/fisiopatologia , Tratos Extrapiramidais/anatomia & histologia , Tratos Extrapiramidais/fisiologia , Hemiplegia/história , Hemiplegia/fisiopatologia , História do Século XIX , História do Século XX , Humanos , Reflexo de Babinski/históriaRESUMO
Following a brief review of the concept of extrapyramidal system, clinical and anatomic evidence is presented against its relative prominence in man. It is proposed that the greatest part of those structures traditionally labeled as extrapyramidal effects its respective functional activities by way of the pyramidal tracts themselves. Such structures, centered around the basal nuclei, the cerebellum and possibly, the limbic areas of the prosencephalon are, according to the present suggestion, indeed, pre pyramidal. This model is based upon the clinical analysis of patients and agrees with more than one century of anatomic verifications in human brains, favoring the notion of the singularity of the human brain.
Assuntos
Tratos Extrapiramidais/fisiopatologia , Hemiplegia/fisiopatologia , Movimento , Quadriplegia/fisiopatologia , Tratos Extrapiramidais/fisiologia , HumanosRESUMO
Após revisäo sumária do conceito de sistema extrapiramidal, säo apresentadas evidências clínicas e anatômicas contra sua importância relativa no homem. Propöe-se que as estruturas tradicionalmente agrupadas sob o rótulo extrapiramidal efetuem a maior parte de suas atividades funcionais, respectivamente, por intermédio dos próprios feixes piramidais. Tais estruturas - centradas no núcleos da base dos hemisférios cerebrais, no cerebelo e, possivelmente, também, na áreas límbicas do prosencéfalo -, de acordo com nossa proposiçäo säo, na verdade pre-piramidais. Esse modelo se baseia na análise clínica de pacientes, está de acordo com mais de um século de verificaçöes anatômicas em cérebros humanos e depöe a favor da noçäo de singularidade do cérebro humano
Assuntos
Humanos , Tratos Extrapiramidais/fisiopatologia , Hemiplegia/fisiopatologia , Movimento , Quadriplegia/fisiopatologia , Tratos Extrapiramidais/fisiologiaRESUMO
La observación de signos y sintomas similares a la activación extrapiramidal, y la hipotésis que el Clorhidrato de Ketamina podría tener efectos semejantes a los neurolépticos en los núcleos de la base, nos indujo a realizar el presente trabajo, observando los efectos de la Ketamina en ratas sometidas a tratamiento previo con L-Dopa. Se realizaron dos grupos de experimentos. En el primero se administró L-Dopa durante 15 dias, y en el segundo, una dosis única de L-Dopa 24 horas antes del comienzo del experimento. Posteriormente se administró Clorhidrato de Ketamina, comparando los resultados de los grupos pretratados con L-Dopa con los grupos controles. Se observaron los siguientes resultados: el pretratamiento con L-Dopa durante 15 días evitó la aparición de signos motores colaterales indeseables provocados por la Ketamina en las ratas. Estos signos, sin embargo, no desaparecen en el grupo pretratado con una sola dosis. Además en ambos grupos de experimentos se observó que el tiempo de inducción anestésica disminuye, el tiempo de sueño se prolonga y el tiempo de recuperación se acorta. Las diferencias de los resultados de los grupos pretratados con L-Dopa y los grupos controles son estadísticamente significativas. Por último, el pretratamiento con L-Dopa no altera las frecuencias cardiaca y respiratoria en animales anestesiados con Ketamina
Assuntos
Ketamina/farmacologia , Levodopa/farmacologia , Anestesia , Anestesia/estatística & dados numéricos , Anestésicos Dissociativos , Dopamina/fisiologia , Frequência Cardíaca , Levodopa/administração & dosagem , Pesquisa , Respiração , Sono , Sono/fisiologia , Tratos Extrapiramidais , Tratos Extrapiramidais/fisiologiaRESUMO
La observación de signos y sintomas similares a la activación extrapiramidal, y la hipotésis que el Clorhidrato de Ketamina podría tener efectos semejantes a los neurolépticos en los núcleos de la base, nos indujo a realizar el presente trabajo, observando los efectos de la Ketamina en ratas sometidas a tratamiento previo con L-Dopa. Se realizaron dos grupos de experimentos. En el primero se administró L-Dopa durante 15 dias, y en el segundo, una dosis única de L-Dopa 24 horas antes del comienzo del experimento. Posteriormente se administró Clorhidrato de Ketamina, comparando los resultados de los grupos pretratados con L-Dopa con los grupos controles. Se observaron los siguientes resultados: el pretratamiento con L-Dopa durante 15 días evitó la aparición de signos motores colaterales indeseables provocados por la Ketamina en las ratas. Estos signos, sin embargo, no desaparecen en el grupo pretratado con una sola dosis. Además en ambos grupos de experimentos se observó que el tiempo de inducción anestésica disminuye, el tiempo de sueño se prolonga y el tiempo de recuperación se acorta. Las diferencias de los resultados de los grupos pretratados con L-Dopa y los grupos controles son estadísticamente significativas. Por último, el pretratamiento con L-Dopa no altera las frecuencias cardiaca y respiratoria en animales anestesiados con Ketamina