Neurologia (Barcelona, Spain) · 2003
[Aphasias for verbal and sign languages are due to lesions of nearly localised but not identical brain regions of the left hemisphere].
Клинический случайАннотация на английскомСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Gallego E, Quiñones D, de Yébenes J G
Аннотация
OBJECTIVES: To study the characteristics of verbal and sign language aphasia in a patient fluent in both languages, who had had a recent left hemisphere stroke as well as to localise the site responsible for Spanish sign language aphasia.
PATIENT AND METHODS: 56 years old male, with risk factors for stroke, who presented an episode of sudden onset aphasia and right hemiplegia that partially recovered in a few hours. The residual deficit of language was explored with a detailed protocol that included comprehension, denomination, oral and phonetic praxis, propositional and automatic spontaneous language, reading and writing tasks. The examination of verbal and sign language was video-recorded. The lesion was localised by magnetic resonance imaging 24 days after the stroke.
RESULTS: The patient, whose infarction involved the superior temporal gyrus and sylvian operculum, presented similar abnormalities for comprehension of complex sentences, many phonemic paraphasias and no trouble to repeat single words. Oral language was not fluent, but sign language was quite fluent with a rich vocabulary, but with semantic paraphasias, agrammatism and without self-criticism for his own mistakes.
CONCLUSIONS: The pattern of oral and sign language alterations is partially different, more for expressive than perceptive discourse, although both types of aphasias are caused by lesions of the left hemisphere. The regions responsible for these abnormalities of both symbolic languages are localised close to each other, but not in the same place.
PATIENT AND METHODS: 56 years old male, with risk factors for stroke, who presented an episode of sudden onset aphasia and right hemiplegia that partially recovered in a few hours. The residual deficit of language was explored with a detailed protocol that included comprehension, denomination, oral and phonetic praxis, propositional and automatic spontaneous language, reading and writing tasks. The examination of verbal and sign language was video-recorded. The lesion was localised by magnetic resonance imaging 24 days after the stroke.
RESULTS: The patient, whose infarction involved the superior temporal gyrus and sylvian operculum, presented similar abnormalities for comprehension of complex sentences, many phonemic paraphasias and no trouble to repeat single words. Oral language was not fluent, but sign language was quite fluent with a rich vocabulary, but with semantic paraphasias, agrammatism and without self-criticism for his own mistakes.
CONCLUSIONS: The pattern of oral and sign language alterations is partially different, more for expressive than perceptive discourse, although both types of aphasias are caused by lesions of the left hemisphere. The regions responsible for these abnormalities of both symbolic languages are localised close to each other, but not in the same place.