Recovery of orthographic processing after stroke: A longitudinal fMRI study.

An intact orthographic processing system is critical for normal reading and spelling. Here we investigate the neural changes associated with impairment and subsequent recovery of the orthographic lexical processing system in an individual with an ischemic left posterior cerebral artery (PCA) stroke. This work describes a longitudinal case study of a patient, whose initials are MMY, with impairments in orthographic lexical processing for reading and spelling at stroke onset, and who recovered these skills within 1 year post stroke. We tested the hypothesis that this acute impairment to reading and spelling would be associated with a selective loss of neural activation in the left fusiform gyrus (FG), and that subsequent recovery would be associated with a gain of neural activation in this region. MMY's case provided a unique opportunity to assess the selectivity of neural changes because she demonstrated a behavioral recovery of naming as well; i.e., if there is neural recovery for reading and spelling, but not naming, then these neural changes are selective to the recovery of orthographic processing. To test our hypothesis, we examined longitudinal behavioral and functional magnetic resonance imaging (fMRI) data of reading, spelling, and visual object naming acquired acutely, 3 weeks, 5 months, and one year post stroke. In confirmation of our hypothesis, the loss and subsequent gain of orthographic lexical processing was associated with up-regulation of neural activation in areas previously associated with orthographic lexical processing: i.e., the left mid-FG and inferior frontal junction (IFJ). Furthermore, these neural changes were found to be selective to orthographic processing, as they were observed for reading and spelling, but not for visual object naming within the left mid-FG. This work shows that left PCA stroke can temporarily and selectively disrupt the orthographic lexical processing system, not only in the posterior region adjacent to the stroke, but also in relatively distant frontal orthographic processing regions.

Imaging network level language recovery after left PCA stroke.

PURPOSE: The neural mechanisms that support aphasia recovery are not yet fully understood. Our goal was to evaluate longitudinal changes in naming recovery in participants with posterior cerebral artery (PCA) stroke using a case-by-case analysis. METHODS: Using task based and resting state functional magnetic resonance imaging (fMRI) and detailed language testing, we longitudinally studied the recovery of the naming network in four participants with PCA stroke with naming deficits at the acute (0 week), sub acute (3-5 weeks), and chronic time point (5-7 months) post stroke. Behavioral and imaging analyses (task related and resting state functional connectivity) were carried out to elucidate longitudinal changes in naming recovery. RESULTS: Behavioral and imaging analysis revealed that an improvement in naming accuracy from the acute to the chronic stage was reflected by increased connectivity within and between left and right hemisphere "language" regions. One participant who had persistent moderate naming deficit showed weak and decreasing connectivity longitudinally within and between left and right hemisphere language regions. CONCLUSIONS: These findings emphasize a network view of aphasia recovery, and show that the degree of inter- and intra- hemispheric balance between the language-specific regions is necessary for optimal recovery of naming, at least in participants with PCA stroke.

The association of insular stroke with lesion volume.

The insula has been implicated in many sequelae of stroke. It is the area most commonly infarcted in people with post-stroke arrhythmias, loss of thermal sensation, hospital acquired pneumonia, and apraxia of speech. We hypothesized that some of these results reflect the fact that: (1) ischemic strokes that involve the insula are larger than strokes that exclude the insula (and therefore are associated with more common and persistent deficits); and (2) insular involvement is a marker of middle cerebral artery (MCA) occlusion. We analyzed MRI scans of 861 patients with acute ischemic hemispheric strokes unselected for functional deficits, and compared infarcts involving the insula to infarcts not involving the insula using t-tests for continuous variables and chi square tests for dichotomous variables. Mean infarct volume was larger for infarcts including the insula (n = 232) versus excluding the insula (n = 629): 65.8 ± 78.8 versus 10.2 ± 15.9 cm(3) (p < 0.00001). Even when we removed lacunar infarcts, mean volume of non-lacunar infarcts that included insula (n = 775) were larger than non-lacunar infarcts (n = 227) that excluded insula: 67.0 cm(3) ± 79.2 versus 11.5 cm(3) ± 16.7 (p < 0.00001). Of infarcts in the 90th percentile for volume, 87% included the insula (χ(2) = 181.8; p < 0.00001). Furthermore, 79.0% infarcts due to MCA occlusion included the insula; 78.5% of infarcts without MCA occlusion excluded the insula (χ(2) = 93.1; p < 0.0001). The association between insular damage and acute or chronic sequelae likely often reflects the fact that insular infarct is a marker of large infarcts caused by occlusion of the MCA more than a specific role of the insula in a range of functions. Particularly in acute stroke, some deficits may also be due to ischemia of the MCA or ICA territory caused by large vessel occlusion.

Acute Ischemic Lesions Associated with Impairments in Expression and Recognition of Affective Prosody.

PURPOSE: We aimed to: (a) review existing data on the neural basis of affective prosody;(b) test the hypothesis that there are double dissociations in impairments of expression and recognition of affective prosody; and (c) identify areas of infarct associated with impaired expression and/or recognition of affective prosody after acute right hemisphere (RH) ischemic stroke. METHODS: Participants were tested on recognition of emotional prosody in content-neutral sentences. Expression was evaluated by measuring variability in fundamental frequency. Voxel-based symptom mapping was used to identify areas associated with severity of expressive deficits. RESULTS: We found that 9/23 patients had expressive prosody impairments; 5/9 of these patients also had impaired recognition of affective prosody; 2/9 had selective deficits in expressive prosody; recognition was not tested in 2/9. Another 6/23 patients had selective impairment in recognition of affective prosody. Severity of expressive deficits was associated with lesions in right temporal pole; patients with temporal pole lesions had deficits in expression and recognition. CONCLUSIONS: Expression and recognition of prosody can be selectively impaired. Damage to right anterior temporal pole is associated with impairment of both, indicating a role of this structure in a mechanism shared by expression and production of affective prosody.