لکنت زبان تالاموس: یک نهاد بالینی متمایز؟
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33475||2003||5 صفحه PDF||سفارش دهید||2655 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Brain and Language, Volume 85, Issue 2, May 2003, Pages 185–189
A 38-year-old right-handed male with no history of speech or language problems presented with neurogenic stuttering following an ischaemic lesion of the left thalamus. He stuttered severely in propositional speech (conversation, monologue, confrontation naming, and word retrieval) but only slightly in non-propositional speech (automatic speech, sound, word and sentence repetition, and reading aloud). It is suggested that thalamic stuttering may constitute a distinct clinical entity.
Although stuttering most often has its onset in childhood, usually somewhere between the ages of two and five (Johnson & Associates, 1959), dysfluent speech may appear also for the first time later in life, beyond the typical childhood period. A dysfluency that originates after the typical childhood period has been called acquired stuttering, or sometimes also late-onset stuttering or adult onset stuttering. Acquired stuttering may have various causes. It can be of psychogenic origin, drug-induced or malingered. Most frequently, however, acquired stuttering is of neurogenic origin, i.e., associated with damage to the central nervous system. In recent years, several cases of neurogenic stuttering have been reported (see Ringo & Dietrich, 1995 and Van Borsel, 1997, for a review). At first sight, it would seem that neurogenic stuttering is not linked to any specific lesion site. The damage that lies at the origin of the dysfluencies in neurogenic stuttering may be bilateral or unilateral, focal or diffuse, cortical or subcortical, situated in the right hemisphere or the left hemisphere. Within one hemisphere the lesion may be localized in the frontal lobe, the temporal lobe, or the parietal lobe. Only in conjunction with damage to the occipital lobe neurogenic stuttering has not been observed. This should not mean, however, that neurogenic stuttering has no localizing significance at all. There is still the possibility that within neurogenic stuttering the symptoms vary according to the lesion site and that different types of neurogenic stuttering can be distinguished accordingly, just like is the case in other neurogenic disorders of speech and language, such as dysarthria and aphasia. A few proposals in that direction with regard to neurogenic stuttering have already been formulated (Ackermann, Hertrich, Ziegler, Bitzer, & Bien, 1996; Koller, 1983). The present paper reports a case of neurogenic stuttering due to a thalamic stroke. An analysis of the dysfluency pattern prompted the suggestion that thalamic stuttering may be a distinct clinical entity.