Aphasia Essay Conclusion

Aphasia Essay Conclusion-25
Following the examination of several others whose damage included the left frontal lobe, Broca (1865) concluded that the third frontal convolution, an area commonly referred to today as Broca's area, is the seat of articulate language.This claim was disputed by many of Broca's contemporaries (e.g., Jackson 1866; Freud 1891; see Lorch 2008 for a more detailed discussion), but perhaps the most fervent challenge was posed by one of Broca's former interns, Pierre Marie.

Following the examination of several others whose damage included the left frontal lobe, Broca (1865) concluded that the third frontal convolution, an area commonly referred to today as Broca's area, is the seat of articulate language.This claim was disputed by many of Broca's contemporaries (e.g., Jackson 1866; Freud 1891; see Lorch 2008 for a more detailed discussion), but perhaps the most fervent challenge was posed by one of Broca's former interns, Pierre Marie.

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Despite being perhaps the most studied form of aphasia, the critical lesion location for Broca's aphasia has long been debated, and in chronic patients, cortical damage often extends far beyond Broca's area.

In a group of 70 patients, we examined brain damage associated with Broca's aphasia using voxel-wise lesion-symptom mapping (VLSM).

Although the type of speech impairment that characterized Paul Broca's most famous case, Leborgne (1861) has been disputed (La Pointe 2012; Code 2013), it seems clear that he did not have what would be considered typical Broca's aphasia.

Leborgne was almost completely mute and mostly spoke only one word, “tan,” the name by which he was later identified.

The idea that Broca's aphasia could not be attributed to localized brain damage was later promoted by proponents of more holistic views of aphasia such as Goldstein (1910) and Head (1926).

A century after Broca's initial description of Leborgne, the localizationist view of aphasia was resurrected, primarily by Geschwind (1965, 1970).Geschwind asserted that Broca's aphasia is caused by damage to Broca's area.As before, this view was challenged on the grounds that (1) damage confined to Broca's area often does not lead to Broca's aphasia and (2) those with Broca's aphasia typically have damage that extends beyond Broca's area and involves structures such as the left insula and regions in the parietal lobe (Mohr et al. This observation was underscored by Dronkers et al.However, since the lesion location that causes Broca's aphasia still eludes us, it is difficult to see what we can assume in this matter or, for example, if the symptoms of Broca's aphasia can be related to contemporary neuroanatomical models of speech processing (Hickok and Poeppel 2007; Hickok 2012).To identify the pattern of cortical damage that gives rise to Broca's aphasia, we examined a group of 70 participants of whom 20 had Broca's aphasia.Our findings suggest that persons with Broca's aphasia have damage to both Broca's and Wernicke's areas, a conclusion that is incongruent with classical neuropsychology, which has rarely considered the effects of damage to both areas.Broca's aphasia is one of the most common and, perhaps, iconic types of aphasia.Lesion overlay maps for all 70 individuals included in the study (top panel), individuals with Broca's aphasia (middle panel), and individuals with forms other than Broca's aphasia (bottom panel).The crosshairs denote the voxel where the highest lesion overlap occurred.Broca's aphasia has received disproportionate attention in the literature compared with other aphasia types over the past few decades, perhaps because individuals with Broca's aphasia have grammatical processing problems that manifest in both speech production and comprehension and display a distinctive non-fluent speech pattern.One reason for this interest may be based on the premise that grammatical problems displayed by such patients can tell us something about the neural architecture that supports syntax (Caramazza and Zurif 1976; Grodzinsky and Friederici 2006).

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