Other studies suggest that disconnection may not be the only mechanism of conduction aphasia. Some cases of conduction aphasia were caused by lesions that clearly spared the arcuate fasciculus (Marshall, Lazar, Mohr, Van Heer-tum, & Mast, 1996; Mendez & Benson, 1985). Similarly, lesions confined to the arcuate fasciculus have not always resulted in conduction aphasia (Shuren et al., 1995).
Physiologic data provided by positron emission tomography (PET) imaging does not clearly support the disconnection theory. In one study of stroke and conduction aphasia, cerebral metabolic patterns had no clear correlation to clinical findings (Kempler et al., 1988), suggesting that functional disconnection is not necessary to produce conduction aphasia.
PET studies are correlated by two independent reports of cortical mapping using electrical stimulation of implanted electrodes. In these cases, impaired repetition, with other features of conduction aphasia, was transiently elicited by stimulations of the posterior superior temporal gyrus (Anderson et al., 1999; Quigg & Fountain, 1999). The selective and reversible impairment of a specific region of cortex suggests that conduction aphasia is mediated by regions of specialized cortex.
Although the classic Wernicke model is insufficient to account for all cases of conduction aphasia, it remains a clinically useful means by which to organize deficits in language.
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