Rehabilitación neuropsicológica de un caso con sintomatología de afasia de conducción y anómica por evento isquémico / Neuropsychological rehabilitation in a case of conduction and anomic aphasia symptomatology by ischemic event

El tema de la rehabilitación de las afasias es explorado con frecuencia en la literatura de las últimas décadas, debido a que es una de las secuelas más comunes del daño cerebral y de las que más presenta variaciones dependiendo del caso, por lo cual los profesionales a cargo de los pacientes que sufren de esta condición se ven en la necesidad de buscar métodos eficaces para tratarlos. El objetivo de esta investigación es mostrar el diseño de un único caso con sintomatología de afasia de conducción y anomia pura. Se trata de un paciente masculino de 62 años de edad, con nivel académico de doctorado, diagnóstico de afasia de conducción y anomia a causa de un evento isquémico con 18 meses de evolución. Recibió tratamiento neuropsicológico en base a modelos histórico-culturales y neurocognitivos en dos periodos diferentes, una hora por semana. Se llevó a cabo una evaluación neuropsicológica antes y después del programa de rehabilitación, además se hizo uso de líneas bases en ambos periodos y se tomó en cuenta la perspectiva del paciente y su esposa. El rendimiento en la primera y segunda evaluación muestra un mejor desempeño en algunas áreas del lenguaje, mientras que en las líneas bases y en la apreciación del paciente y su esposa se observaron cambios importantes, concluyendo que el programa tuvo efectos favorables en la comunicación del paciente en el hogar.

The subject of aphasia rehabilitation is frequently explored in recent literature since it is one of the most common forms of brain damage and presents an assortment of variations depending on the specific case, making it so that professionals who are in charge of patients with this condition find themselves in need of effective treatment methods. This article aims to present the design for the single case study rehabilitation of a patient with conduction aphasia and pure anomia. The patient in question is a 62-year-old male with a P.h.D. level education, diagnosed with conduction aphasia and anomia caused by an ischemic event with an 18-month evolution, he received neuropsychological treatment following the historic-cultural and neurocognitive models, spanning two different treatment periods, one hour a week. A neuropsychological evaluation was made before and after the rehabilitation program, as well as using a baseline for both periods and taking into account the perspective of both the patient and his wife. Patient performance in the first and second evaluations shows improvement in some language areas, while the baselines, as well as the patient and his wife's assessment speak of important changes, concluding that the program had favorable effects on the patient's communication at home

Afasia de conducción como consecuencia de un astrocitoma anaplásico parieto–temporo–occipital izquierdo: estudio de caso / Conduction aphasia as a result of left parietal-temporal-occipital anaplastic astrocytoma: a case study

La afasia de conducción es un trastorno caracterizado por un lenguaje espontáneo relativamente fluido, buena comprensión, pero dificultades en la repetición asociadas con parafasias fonológicas. Se ha atribuido a lesiones del fascículo arqueado por desconexión entre el lóbulo temporal posterior y el frontal, sin embargo se ha debatido esta postura, planteando que la integridad y funcionamiento del fascículo arqueado no es indispensable en la repetición verbal. Se presenta un caso de un sujeto varón de 23 años que, como consecuencia de un astrocitoma anaplásico recidivante que abarca áreas parietales y temporo-occipitales, presenta una afasia de conducción. Se plantea una reconceptualización de esta afasia, analizándola en términos clínicos, neuropsicológicos y en las redes neuronales existentes entre áreas cerebrales posteriores ipsilaterales y contralaterales.

Conduction aphasia is a language disorder characterized by an impaired ability to repeat verbal material associated with phonological paraphasias but a relatively fluent spontaneous speech and preserved comprehension. It has been attributed to lesions of the arcuate fasciculus by disconnection between posterior temporal lobe and frontal lobe, however, this idea has been debated, because the integrity and function of the arcuate fasciculus does not seem to be essential in verbal repetition. We report a case of a 23 year old male, with conduction aphasia as a result of a recurrent anaplastic astrocytoma in parietal and temporo-occipital areas. We propose a reconceptualization of the aphasia, analyzing it in terms of clinical neuropsychological and neural networks between ipsilateral and contralateral posterior brain areas.

Pathogenesis Investigation of Broca-like and Wernicke-like Conduction Aphasia Using Image Methods / 中国康复理论与实践

@#To investigate the pathogenesis of Broca-like and Wernicke-like conduction aphasia. Methods 7 cases with Broca-like aphasia (Group A), 7 cases with Wernicke-like aphasia (Group B) and 10 healthy volunteers (Group C) participated in the study. Broca'sarea, Wernicke's area, and the arcuate fasciculus were analyzed by diffusion tensor imaging, and their fractional anisotropy (FA) weremeasured and compared; The fiber construction of Broca's and Wernicke's areas were also compared by diffusion tensor imaging-fibre tractography.Results In Group C, All of the FA was higher in the left hemisphere than in the right hemisphere (P<0.05); In Group A, the FA ofthe Broca's area and anterior segment of the arcuate fasciculus were less in the left than in the right hemisphere (P<0.05)； In Group B, theFA of the Wernicke's area and posterior segment of the arcuate fasciculus were less in the left than in the right (P<0.05). Conclusion Conductionaphasia results not only from arcuate fasciculus destruction, but also from disruption of the associated cortical area. A lesion involvingBroca's area and the anterior segments of the arcuate fasciculus would lead to Broca-like conduction aphasia, whereas a lesion involvedWernicke's area and posterior segments of the arcuate fasciculus would lead to Wernicke-like conduction aphasia.

Brain Lesions in Conduction Aphasia

OBJECTIVE: To investigate the neuroanatomical correlation of conduction aphasia by analyzing neuroimage data of patients who were diagnosed as conduction aphasia after stroke. METHOD: Nine patients with conduction aphasia after stroke were retrospectively reviewed with their medical records. Language functions of patients were assessed by Korean-version Western Aphasia Battery (K-WAB). Stroke lesions were assessed by brain computed tomography or magnetic resonance images taken within 1 month after onset of stroke. RESULTS: The stroke subtypes were cerebral infarction in 5 patients and intracranial hemorrhage in 4 patients. The lesions were located in left hemisphere in 8 subjects and right hemisphere in 1 subject. The left hemispheric lesion were located in the insula and superior temporal lobe in 3, the inferior parietal lobe in 2, the corona radiate in 1, the basal ganglia in 1 patient and both corona radiata and basal ganglia in 1. The right hemispheric lesion was located in the inferior parietal and superior temporal lobe. CONCLUSION: 6 of 9 patients with conduction aphasia had brain lesions in the path of arcuate fasciculus in the left hemisphere, however, 3 of 9 patients showed other brain lesions. These findings suggested that conduction aphasia could be caused by heterogeneous brain lesions. The characteristic features of conduction aphasia according to diverse brain lesions may need further investigation.

A Case of the Fluent Form of Primary Progressive Aphasia Presenting as Conduction Aphasia

Primary progressive aphasia(PPA) can be classified into nonfluent and fluent types. The fluent PPA usually manifests as Wernicke's or transcortical sensory aphasia. We report a 61-year-old right-handed woman who presented with a fluent PPA. An aphasia test revealed fluent speech and intact comprehension but decreased repetition and naming, consistent with conduction aphasia. Other cognitive functions and activities of daily living were preserved. Brain MRI and SPECT respectively showed a focal atrophy and a hypoperfusion in the left temporal lobe.