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).Tags: A Change In Your Life Narrative EssayPre Written Expository EssaysOutsourcing Advantages And Disadvantages EssayPro Choice Research PaperResearch Paper Works CitedEssay On Technology In The ClassroomThe Best American Essays Sixth College EditionBook Reviews For Sale
(2007) who used high-resolution MRI to re-examine Leborgne's brain and found that his cortical lesion extended far beyond inferior frontal gyrus and included structures such as the insula and the inferior parietal lobe.
In some cases, the damage that causes Broca's aphasia actually spares Broca's area (e.g., Fridriksson et al. Although the debates about the region(s) causing Broca's aphasia have continued for well over a century, the current consensus is that the damage probably includes parts of Broca's area and some other adjacent structures (Dejerine 1906a,b; Geschwind 1970; Mohr et al. It remains unknown, however, what exactly those other adjacent structures are.
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.
Six persons with global aphasia were excluded from the study as these patients have severe speech and language deficits in both production and comprehension.
Aphasia types were classified according to the Western Aphasia Battery (WAB; Kertesz 1982).A lesion map that included all participants revealed the greatest lesion overlap in the white matter underlying the left superior, anterior insula (MNI: −30,2,18), where 48 participants had damage.The greatest lesion overlap for individuals with Broca's aphasia was in the anterior insula (MNI: −42,0,15) and in the white matter deep to the temporal–parietal junction for participants who had other types of aphasia (MNI: −38,−40,24).Each of the 70 participants underwent clinical examination as well as high-resolution MRI.Voxel-wise lesion-symptom mapping (VLSM) was utilized to compare patients with Broca's aphasia with patients with aphasia of other kinds.Marie suggested that aphasia required damage to Wernicke's area and that “Broca's aphasia” was a combination of aphasia, caused by damage to Wernicke's area, and anarthria, a motor speech problem caused by damage to what he referred to as the “lenticular zone,” a collection of subcortical structures such as the putamen and pallidum (Marie 1906a).Jules Dejerine, a prominent academic neurologist and a rival of Marie, defended Broca's original position, arguing that damage to Broca's area was necessary for Broca's aphasia, although he acknowledged the important contribution of other brain structures such as the insula, parietal regions, and underlying white matter (Dejerine 1906a,b, 1914, as discussed in Paciaroni and Bogousslavsky 2011; Krestel et al. However, Marie countered that Dejerine (and others) failed to observe a consistent relationship between damage to the third frontal convolution and Broca's aphasia: that is, some individuals presented with symptoms of Broca's aphasia and yet had the third frontal convolution completely intact, while other patients who had damage to the third frontal convolution did not have the speech symptoms of Broca's aphasia (Marie 1906b,d).We found that damage to the posterior portion of Broca's area, the damage, we found that patients with Broca's aphasia had greater damage in the left superior temporal gyrus (STG; roughly Wernicke's area) than those with other aphasia types.Using discriminant function analysis and logistic regression, based on proportional damage to the and Wernicke's area, to predict whether individuals had Broca's or another types of aphasia, over 95% were classified correctly.The study sample was selected from a database that includes 76 patients with chronic left hemispheric stroke.All patients were at least 6 months post-stroke and the mean time since stroke onset was 36.7 months (SD = 45.51; range = 6–276).