Temporo-parietal Cortical Regions Research Articles

Factors predicting long-term recovery from post-stroke aphasia

ABSTRACT Background It remains widely accepted that spontaneous recovery from aphasia is largely limited to the first related factors. This has direct implications for acute and chronic interventions for aphasia. few months following stroke. A few recent studies challenge this view, revealing that some individuals’ language abilities improve even during the chronic stage. Aims To identify prognostic indicators of long-term aphasia recovery. Methods & Procedures Eighteen people with aphasia initially evaluated in the chronic stage were retested at least one year later. The Western Aphasia Battery-Revised (WAB-R) Aphasia Quotient (AQ) was used to quantify changes in language impairment. Prognostic factors included those related to the patient (demographic, psychosocial), stroke (lesion volume and location), and treatment (medical, rehabilitative). Outcomes & Results Twelve participants improved and 6 remained stable or declined. Linear regression analysis revealed that lesion volume predicted long-term language gains, with smaller lesions yielding greater improvements. Individuals who did not improve were more likely to have lesions encompassing critical frontal and temporoparietal cortical regions and interconnecting white matter pathways. Exploratory regression analysis of psychosocial and treatment-related factors revealed a positive relationship between improvement and satisfaction with life participation, and a negative relationship between improvement and perceived impairment severity. Critically, psychosocial and treatment-related factors significantly improved model fit over lesion volume, suggesting that these factors add predictive value to determining long-term aphasia prognosis. Conclusions Long-term aphasia recovery is multidetermined by a combination of stroke-, psychosocial-, and treatment-related factors. This has direct implications for acute and chronic interventions for aphasia.

Faces in the mirror, from the neuroscience of mimicry to the emergence of mentalizing.

In the current opinion paper, we provide a comparative perspective on specific aspects of primate empathic abilities, with particular emphasis on the mirror neuron system associated with mouth/face actions and expression. Mouth and faces can be very salient communicative classes of stimuli that allow an observer access to the emotional and physiological content of other individuals. We thus describe patterns of activations of neural populations related to observation and execution of specific mouth actions and emotional facial expressions in some species of monkeys and in humans. Particular attention is given to dynamics of face-to-face interactions in the early phases of development and to the differences in the anatomy of facial muscles among different species of primates. We hypothesize that increased complexity in social environments and patterns of social development have promoted specializations of facial musculature, behavioral repertoires related to production and recognition of facial emotional expression, and their neural correlates. In several primates, mirror circuits involving parietal-frontal regions, insular regions, cingulate cortices, and amygdala seem to support automatic forms of embodied empathy, which probably contribute to facial mimicry and behavioural synchrony. In humans these circuits interact with specific prefrontal and temporo-parietal cortical regions, which facilitates higher order cognitive functions such as cognitive empathy and mental state attribution. Our analysis thus suggests that the evolution of higher forms of empathy, such as mentalizing, is also linked to the coupling between the perceptual and motor system related to face processing, which may have undergone a process of exaptation during primate phylogeny.

Cortical and subcortical contributions to state- and strength-based perceptual judgments

Perceptual judgments can be made on the basis of different kinds of information: state-based access to specific details that differentiate two similar images, or strength-based assessments of relational match/mismatch. We explored state- and strength-based perception in eleven right-hemisphere stroke patients, and examined lesion overlap images to gain insight into the neural underpinnings of these different kinds of perceptual judgments. Patients and healthy controls were presented with pairs of scenes that were either identical or differed in that one scene was slightly expanded or contracted relative to the other. Same/different confidence judgments were used to plot receiver-operating characteristics and estimate the contributions of state- and strength-based perception. The patient group showed a significant and selective impairment of strength-based, but not state-based, perception. This finding was not an artifact of reduced levels of overall performance, because matching perceptual discriminability levels between controls and patients revealed a double dissociation, with higher state-based, and lower strength-based, perception in patients vs. controls. We then conducted exploratory follow-up analyses on the patient group, based on the observation of substantial individual differences in state-based perception — differences that were masked in analyses based on the group mean. Patients who were relatively spared in state-based perception (but impaired in strength-based perception) had damage that was primarily in temporo-parietal cortical regions. Patients who were relatively impaired in both state- and strength-based perception had overlapping damage in the thalamus, putamen, and adjacent white matter. These patient groups were not different in any other measure, e.g., presence of spatial neglect symptoms, age, education, lesion volume, or time since stroke. These findings shed light on the different roles of right hemisphere regions in high-level perception, suggesting that the thalamus and basal ganglia play a critical role in state- and strength-based perception, whereas temporo-parietal cortical regions are important for intact strength-based perception.

Activation of the Prefrontal Cortex Is Associated with Exertional Dyspnea in Chronic Obstructive Pulmonary Disease

Background: Exertional dyspnea is the primary symptom that limits exercise in patients with chronic obstructive pulmonary disease (COPD). It is unknown which activated brain area is associated with this symptom in COPD patients. Objectives: To investigate the activation of cortical areas associated with dyspnea during exercise in COPD patients. Methods: COPD patients (n = 10) and age-matched controls (n = 10) performed mild-intensity constant work rate cycle exercise (40% of their symptom-limited peak work rates) for 10 min, while cerebral hemodynamics and oxygenation were measured by near-infrared spectroscopy (NIRS). Ventilatory responses (breathing pattern and pulmonary gas exchange) and Borg scale ratings of dyspnea and leg fatigue were measured during exercise. Three NIRS probes were placed over the prefrontal and temporoparietal cortical regions of the subjects’ heads. Changes in cortical oxyhemoglobin (oxy-Hb), deoxyhemoglobin (deoxy-Hb), and total hemoglobin (total Hb) concentrations from baseline recordings were measured. Increased oxy-Hb (oxygenation) was assumed to reflect cortical activation. Results: Oxy-Hb concentration was significantly increased in the prefrontal region during exercise in both groups but not in the temporoparietal regions. The change in prefrontal oxy-Hb concentration of COPD patients was not different from that of controls. Dyspnea scores were positively correlated with changes in oxy-Hb concentrations of the prefrontal regions in both groups. Multivariate analysis showed that oxy-Hb concentration in the prefrontal region was the best predictor of dyspnea in both groups. Conclusions: Exertional dyspnea was related to activation (oxygenation) of the prefrontal cortex in COPD patients and control subjects.

Neuroanatomical substrate of visuospatial and visuoperceptual impairment in Parkinson's disease

To determine magnetic resonance imaging patterns of gray matter (GM) atrophy underlying visuospatial and visuoperceptual impairment in Parkinson's disease (PD), we applied voxel-based morphometry to 36 nondemented PD patients and correlated their whole brain GM density with performance on three visuospatial and visuoperceptual tests. In addition, group comparisons between patients and 20 healthy controls were also performed. Correlations between visuospatial performance and GM density were found in the superior parietal lobules and the superior occipital gyrus of PD patients. Poor performance on visuoperceptual tests was also found to be significantly associated with GM decreases in the fusiform, the parahippocampus, and the middle occipital gyrus. Finally, group comparisons between controls and patients showed widespread GM cortical reductions in PD, involving posterior temporal and parietal regions. Taken together, these findings suggest that visuospatial and visuoperceptual dysfunctions reflect structural GM changes in temporo-parietal cortical regions of PD patients.

Cognitive reserve hypothesis: Pittsburgh Compound B and fluorodeoxyglucose positron emission tomography in relation to education in mild Alzheimer's disease

The reduced risk for Alzheimer's disease (AD) in high-educated individuals has been proposed to reflect brain cognitive reserve, which would provide more efficient compensatory mechanisms against the underlying pathology, and thus delayed clinical expression. Our aim was to find possible differences in brain amyloid ligand 11C-labeled Pittsburgh Compound B ([11C]PIB) uptake and glucose metabolism in high- and low-educated patients with mild AD. Twelve high-educated and 13 low-educated patients with the same degree of cognitive deterioration were studied with PET using [11C]PIB and 18F-fluorodeoxyglucose as ligands. The between-group differences were analyzed with voxel-based statistical method, and quantitative data were obtained with automated region-of-interest analysis. High-educated patients showed increased [11C]PIB uptake in the lateral frontal cortex compared with low-educated patients. Moreover, high-educated patients had significantly lower glucose metabolic rate in the temporoparietal cortical regions compared with low-educated patients. Our results suggesting more advanced pathological and functional brain changes in high-educated patients with mild AD are in accordance with the brain cognitive reserve hypothesis and point out the importance of development of reliable markers of underlying AD pathology for early AD diagnostics.

Brain 1H magnetic resonance spectroscopic differences in myotonic dystrophy type 2 and type 1

To evaluate cerebral metabolism and intergroup differences in closely matched patients with myotonic dystrophy type 2 (DM2, n = 15) and type 1 (DM1, n = 14), we performed (1)H magnetic resonance spectroscopic (MRS) analyses of the occipital and temporoparietal cortical regions as well as of subcortical frontal white matter. Relative to healthy subjects, the concentration of N-acetylaspartate was significantly reduced in all tested brain regions in both disease groups. In the DM1 patients we also observed a concomitant depletion of creatine and choline levels, particularly in the frontal white matter. A discriminant analysis based on the (1)H-MRS data distinguished between the DM2, DM1, and control groups with an overall accuracy of 88%. (1)H-MRS indicates that neurochemical alterations involving gray and white matter occur in patients with DM2 and DM1. Although structural abnormalities (cerebral atrophy, white matter lesions) are similar in DM2 and DM1, changes in cerebral metabolites can differentiate these disease groups, suggesting that the diseases differ in their neurocellular pathology.

Cognitive impairment in Alzheimer's disease correlates with ventricular width and atrophy-corrected cortical glucose metabolism

We compared the correlation of PET and MRI with neuropsychological tests in 26 patients with probable Alzheimer's disease (AD). The width of the temporal horns and the third ventricle, regional metabolic rates of glucose (rCMRGlu) and the proportion of cerebrospinal fluid space in mesial temporal and temporoparietal cortical regions were measured with three-dimensionally coregistered PET and MRI in two planes perpendicular to the Sylvian fissure. Highly significant correlations between rCMRGlu and neuropsychological tests were found mainly in the temporoparietal cortex, with and without correction for atrophy. Correlations of similar magnitude were seen also between most tests and the width of the temporal horns and third ventricle. Changes in the third ventricle and mesial temporal lobe were best seen with MRI, whereas PET most clearly depicted alterations in neocortical association areas. These two aspects of the disease correlated with the severity of dementia to a similar degree.