توهم شنوایی کلامی و اختلال در عملکرد بسترهای عصبی گفتار
|کد مقاله||سال انتشار||تعداد صفحات مقاله انگلیسی||ترجمه فارسی|
|34783||2001||15 صفحه PDF||سفارش دهید|
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Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Schizophrenia Research, Volume 50, Issues 1–2, 30 May 2001, Pages 61–78
Objective: to evaluate the neural substrate of auditory verbal hallucinations (AVH), the correlation between AVH and subvocal speech (hereafter SVS), and the relationship between speech and AVH. Method: we reviewed the papers found by an electronic literature search on hallucinations and speech. The review was extended to the papers cited in these publications and to classical works. Results: there is no conclusive evidence of structural abnormality of the speech perception area in hallucinating schizophrenic patients. However there is evidence of electrophysiological abnormalities of the auditory and speech perception cortices. Functional imaging data are inconsistent, yet point to the left superior temporal gyrus as one of the neural substrates for AVH. There is also evidence that SVS could accompany the experience of AVH. Conclusion: there is evidence that dysfunction of brain areas responsible for speech generation is a fundamental mechanism for generating AVH in schizophrenia. It results in a secondary activation of Wernicke's area (speech perception) and Broca's area (speech expression). The first leading to the experience of hallucinations, and the second, eventually, gives rise to a variable degree of vocal muscle activity detectable by EMG, and/or faint vocalizations detectable by sensitive microphones placed at proximity of the larynx. Direct stimulation or disease of Wernicke's area produces AVH without SVS.
Auditory verbal hallucinations (AVH) refer to the experience of perceiving speech in the auditory modality without corresponding external stimuli. Up to 70% of schizophrenic and a variety of psychiatric and neurological patients suffer from AVH. Understanding the neural correlates of AVH is important for the clarification of the pathophysiology of schizophrenia and related illnesses and an important insight into brain function. Some advocate that AVH reflect an auditory dysfunction (Mckay et al., 2000), but most relate this type of hallucination to a speech disorder (Frith and Done, 1988 and Hoffman, 1986). Accumulating evidence from lesion and functional imaging studies indicate that speech generation is supported by a distributed neural network involving areas such as the supplementary motor area (SMA), left premotor area, left dorsal prefrontal area, thalamus, Broca's and Wernicke's areas (Sadato et al., 1998), and left inferior frontal gyrus, left superior and posterior middle temporal gyri (Herholz et al., 1996). The roles of each of these brain regions are not clear but it is established that Broca's and Wernicke's areas subserve speech motor execution and perception, respectively. In this study we examine the evidence correlating AVH with the abnormality of the speech perception area and with the motor component of speech or subvocal speech (SVS). Contrary to the theory suggesting that hallucinating patients are virtually hearing their SVS, which is activating the auditory system just as external speech (Gould, 1950, Beck and Kinsbourne, 1987 and Frith and Done, 1988), we suggest that both the motor (SVS) and perceptive (AVH) components are related to a central process, most likely speech generation. This hypothesis is consistent with current neuropsychiatric theories implicating inner speech in the pathogenesis of hallucinations and draws support from multiple methodologies.
نتیجه گیری انگلیسی
The reviewed data indicate the following points: 1. Functional correlation between the AVH in different illnesses and with different characteristics and the perceptive speech area. 2. There is no conclusive evidence about structural abnormality of the speech perception area in hallucinating schizophrenic patients. 3. Lesions of the speech perception area sometimes but not invariably cause AVH. 4. AVH are associated with SVS. 5. SVS blocking maneuvers fail to abort AVH. 6. Multiplicity of brain areas implicated in AVH as indicated by functional imaging and stimulation studies. Many of these areas are implicated in speech generation. 7. Inner and external speech have the same developmental origin and both have perceptive and motor components. In our view, the following hypothesis accounts adequately for the above points. Speech generation pathology is a fundamental mechanism for AVH in schizophrenia. It results in an abnormal activation of speech perception (Wernicke) and production (Broca) areas. The activation of the former underlies the experience of AVH and the activation of the latter induces variable degrees of speech muscle activity that may be detectable. AVH, possibly without SVS, could take place by direct stimulation or disorder of Wernicke's area. According to this hypothesis, maneuvers like mouth opening only block SVS without affecting the hallucinatory experience, while maneuvers such as listening to speech could block AVH.