How does the infant brain process speech? An fNIRS meta-analysis

Objective To explore the developmental characteristics of white matter volume in autism spectrum disorder (ASD) children longitudinal. Methods From May 2011 to September 2014, 37 ASD children (ASD group) and 27 developmental delays (DD) children (control group) were treated at the Child Mental Health Research Center, Nanjing Brian Hospital Affiliated of Nanjing Medical University, and the children whose age, gender and developmental quotient matched with the ASD children were scanned by structure magnetic resonance imaging (sMRI) at the age of 2-3 years old and 4-5 years old respectively.Region of interest(ROI) technology was adopted to investigate the change of the cerebrum white and the sub-lobes structure white matter volume with time.Then the correlation between clinical symptoms and brain white matter volume changes was analyzed. Results Among the 2-3 years old, compared with the control group, the white matter volume of the total brain[(383 521.84±6 427.57) mm3vs. (364 014.06±6 856.97) mm3], the left cerebral hemisphere [(191 609.35±3 206.60) mm3vs. (181 695.89±3 389.54) mm3], temporal lobe [(41 860.49±816.38) mm3vs. (39 444.18±834.85) mm3] and the right temporal lobe [(21 312.79±414.07) mm3vs. (20 084.22±412.13) mm3] were significantly larger in the ASD group, and the differences were statistically significant (all P 0.05). Among the 4-5 years old, compared with the control group, the white matter volumes of the total brain[(417 651.42±6 443.86) mm3vs. (394 317.27±6 404.86) mm3], left cerebral hemisphere [(208 714.16±3 214.61) mm3vs. (197 192.82±3 262.02) mm3], right cerebral hemisphere [(208 937.26±3 242.09) mm3vs. (7 124.45±3 193.13) mm3], frontal lobe [(107 107.46±1 681.99) mm3vs. (100 326.19±1 883.24) mm3], left frontal lobe [(54 569.63±846.85) mm3vs. (51 177.25±979.09) mm3], right frontal lobe [(52 537.83±841.99) mm3vs. (49 148.94±928.31) mm3], temporal lobe [(45 189.75±833.29) mm3vs.(42 487.73±786.27) mm3], left temporal lobe [(22 204.21±411.77) mm3vs. (20 922.90±418.46) mm3], and right temporal lobe [(22 985.54±426.93) mm3vs. (21 564.83±378.78) mm3] were significantly larger in the ASD group, and the differences were statistically significant (all P 0.05). For longitudinal analysis, there was a significant difference in the white matter volume between the whole brain, left cerebral hemisphere, right cerebral hemisphere, frontal lobe, left frontal lobe, right frontal lobe, temporal lobe, left temporal lobe, right temporal lobe and the differences were statistically significant(F=5.521, 5.533, 5.459, 5.830, 5.800, 5.723, 4.857, 4.418, 5.159, all P<0.05). There was a positive correlation between the changes of the volume of whole brain, the white matter volume in the whole brain, bilateral cerebral hemisphere, frontal lobe, parietal lobe, right parietal lobe and Childhood Autism Rating Scale(r=0.367, 0.343, 0.321, 0.349, 0.296, 0.308, 0.351, all P<0.05). Conclusions Among the 2-3 years old, the white matter volume of the brain regions have been increased significantly in ASD.Among the 4-5 years old, the increase of the white matter volume of the brain regions implicated more widely which mainly concentrated in the frontal and temporal lobe in ASD.The severity of the clinical symptoms of ASD may be associated with the white matter volume of the total brain, bilateral cerebral hemisphere, frontal lobe, parietal lobe and right parietal lobe. Key words: Autism spectrum disorder; White matter; Volume; Magnetic resonance imaging; Longitudinal study

Brain development during early life in healthy individuals is rapid and dynamic, indicating that this period plays a very important role in neural and functional development. The frontal and temporal lobes are known to play a particularly important role in cognition. The study of healthy frontal and temporal lobe development in children is therefore of considerable importance. A better understanding of how these brain regions develop could also aid in the diagnosis and treatment of neurodevelopmental disorders. Some devel-opmental studies have used magnetic resonance imaging (MRI) to examine infant brains, but it remains the case that relatively little is known about cortical brain development in the first few years of life. In the present study we examined whole brain, temporal lobe and frontal lobe developmental trajectories from infancy to early adulthood in healthy individuals, considering gender and brain hemisphere differences. We performed a cross-sectional, longitudinal morphometric MRI study of 114 healthy individuals (54 females and 60 males) aged 1 month to 25 years old (mean age ± SD 8.8 ± 6.9). We measured whole brain, temporal and frontal lobe gray matter (GM)/white matter (WM) volumes, following previously used protocols. There were significant non-linear age-related volume changes in all regions. Peak ages of whole brain, temporal lobe and frontal lobe development occurred around pre-adolescence (9-12 years old). GM volumes for all regions increased significantly as a function of age. Peak age was nevertheless lobe specific, with a pattern of earlier peak ages for females in both temporal and frontal lobes. Growth change in whole brain GM volume was larger in males than in females. However, GM volume growth changes for the temporal and frontal lobes showed a somewhat different pattern. GM volume for both temporal and frontal lobes showed a greater increase in females until around 5-6 years old, at which point this tendency reversed (GM volume changes in males became greater), with male GM volume increasing for a longer time than that of females. WM volume growth changes were similar across regions, all increasing rapidly until early childhood but slowing down thereafter. All regions displayed significant rightward volumetric asymmetry regardless of sex. Furthermore, the right temporal and frontal lobes showed a greater volumetric increase than the left for the first several years, with this tendency reversing at around 6 years of age. In addition, the left frontal and temporal lobes increased in volume for a longer period of time. Taken together, these findings indicated that brain developmental trajectories differ depending on brain region, sex and brain hemisphere. Gender-related factors such as sex hormones and functional laterality may affect brain development.

Objective To measure the electroconvulsive threshold in different parts of rat cerebral cortex and observe the pathophysiological changes after the convulsive threshold is stable. Methods Healthy female SD rats weighing 180-220 g were randomly divided into a study group and a control group. Electrodes were placed in the frontal lobe, temporal lobe, and cerebellar cortex of all rats. Direct current stimulation was applied twice daily in the study group, but not in the control group. After stable convulsive threshold was achieved in the study group, the SNK-q test was used to compare the convulsive threshold in different subgroups. The rats were then sacrificed to observe the changes of hippocampal neuron damage by Nissl's staining. The number of neurons in the hippocampus of rats in each group was counted and then compared using the SNK-q test. Results At the first and second days, the convulsive threshold in the three stimulation subgroups was high, which was ~1100 μA in the frontal lobe, ~1200 μA in the temporal lobe, and ~2100 μA in the cerebellar cortex. With the increase in the duration of stimulation, the threshold of the three groups continued to decrease, eventually reaching a stable level. The mean stable threshold was (511.00±10.97) μA in the frontal lobe, (440±12.46) μA in the temporal lobe, and (1300±53.63) μA in the cerebellar cortex. Although the mean stable threshold did not differ significantly between the frontal lobe and temporal lobe (P>0.05), there was a significant difference between the cerebellum and frontal lobe and between the cerebellum and temporal lobe (P<0.05). With the extension of stimulation time, compared with the control group, hippocampal CA3 area in rats of the study group exhibited varying degrees of changes, such as disordered neuron arrangement and neuron loss. The average number of neurons was 36 in the control group, 22 in the frontal lobe subgroup, 17 in the temporal lobe subgroup, and 26 in the cerebellum subgroup. Compared with the control group, the number of neurons in the study group decreased significantly (P<0.05). There was also a significant difference in the neuron number among the three subgroups (P<0.05). The symptoms of rats after electrical stimulation in the cerebellar cortex subgroup were different from those in the frontal and temporal lobe subgroups. The frontal and temporal lobe groups showed typical epileptiform convulsion, such as nodding, limb convulsion, and tonic-clonic seizures; however, the cerebellum group was characterized by systemic tetanic convulsion of limbs and trunk, running, and jumping. Conclusions At the same intensity of electrical stimulation, the temporal lobe and frontal lobe are more sensitive than cerebellar cortex and are easier to develop pathological changes, and the susceptibility to electrical stimulation is comparable between the temporal lobe and frontal lobe. Electrical stimulation can cause pathological changes in the hippocampus, and the hippocampal damage in the temporal lobe subgroup is the most serious. Cerebellar cortex stimulation has the minimum effect on the hippocampus. Key words: Epilepsy; Cortex convulsive threshold; Neuron damage; Electrical kindling model; Rats

Reduced regional volumes associated with total psychopathy scores in an adult population with childhood lead exposure

BackgroundReduced cerebral blood flow (CBF) is a risk factor for white matter damage. Apolipoprotein E (APOE) e4, a genetic risk factor for Alzheimer’s disease and vascular health modifier, is associated with lower CBF. However, it remains unknown if lower CBF is associated with more severe white matter damage among APOE‐e4 carriers. We examine whether associations among regional CBF, cerebrovascular reactivity (CVR), and white matter integrity are modified by APOE‐e4 status in older adults.MethodVanderbilt Memory and Aging Project participants (n = 313, 73±7 years) underwent 3T brain MRI. Resting grey matter CBF and CVR (CBF response to hypercapnic stimulus, ΔCBF/100*ΔCO2) were quantified in regions of interest from pseudo‐continuous arterial spin labeling (ASL). Fractional anisotropy (FA) was quantified from diffusion tensor imaging in tracts of interest derived from tractography templates. Linear regressions related regional CBF and CVR to tract‐specific FA, adjusting for demographic and vascular variables, regional tissue volume, cognitive status, and APOE‐e4 status. Follow‐up models tested an APOE‐ε4 status x ASL variable interaction term.ResultIn main models, lower temporal lobe CBF was associated with lower FA in the occipital lobe, suggesting compromised white matter integrity (p = 0.02). Lower CBF and higher CVR in the occipital lobe were associated with compromised lower FA in all lobes (all p‐values&lt;0.04). Temporal lobe CBF and CVR interacted with APOE‐e4 status, such that lower temporal lobe CBF related to lower FA in the frontal lobe (p = 0.01) and higher temporal lobe CVR related to lower FA in the frontal (p = 0.001) and temporal (p = 0.007) lobes among APOE‐e4 carriers only. Frontal lobe CVR interacted with APOE‐e4 status, such that higher CVR related to lower FA in the frontal (p&lt;0.001) and temporal lobes (p = 0.008) in APOE‐e4 carriers only.ConclusionAmong older adults, APOE‐e4 modifies associations between cerebral hemodynamics and white matter integrity, such that reduced CBF and greater CVR in the temporal lobe are associated with greater white matter damage in APOE‐e4 carriers. APOE‐e4 carriers may be more susceptible to changes in temporal lobe hemodynamics, and vascular changes in the temporal lobe may have a stronger impact on brain health outcomes for carriers compared to non‐carriers.

To compare neural responses to high and low-energy food images in patients with Anorexia Nervosa (AN) and an age-matched Healthy Control (HC) group. 25 adolescents with AN and 21 HCs completed a diagnostic interview, self-report questionnaires and fMRI, during which they viewed food images evoking responses of disgust, happiness, or fear. Following whole brain analyses, neural responses in six regions of interest were examined in a series of between-group contrasts, across the three emotive categories. Compared to the HCs, people in the AN group showed increased responsivity to high-energy (1) disgust images in temporal lobe, frontal lobe, insula, and cerebellum anterior lobe; (2) fear images in occipital lobe, temporal, and frontal lobes and (3) happy images in frontal lobe, cerebellum anterior lobe, sub-lobar, and cuneus. More activity was observed in response to low-energy (1) disgust food images in the temporal lobe, frontal lobe, insula, cerebellum anterior and posterior lobes, parietal lobe, occipital lobe, and limbic lobe; (2) and happy food images in frontal lobes. Few correlations were found with levels of eating disorder symptoms. The findings highlight the emotional impact of diverse high and low-energy foods for people with AN. People without AN may have a better capacity to filter salient from non-salient information relating to the current task when viewing high energy foods. In summary, for those with AN, it would seem their ability to efficiently ‘sort-out’ information (especially information pertaining to disorder-relevant stimuli such as food images) to complete the task at hand, may be diminished.

ObjectiveBulimia nervosa (BN) and binge eating disorder (BED) are eating disorders (EDs) characterized by recurrent binge eating (BE) episodes. Overlap exists between ED diagnostic groups, with BE episodes presenting one clinical feature that occurs transdiagnostically. Neuroimaging of the responses of those with BN and BED to disorder-specific stimuli, such as food, is not extensively investigated. Furthermore, to our knowledge, there have been no previous published studies examining the neural response of individuals currently experiencing binge eating, to low energy foods. Our objective was to examine the neural responses to both low energy and high energy food images in three emotive categories (disgust; fear; and happy) in BN and BED participants.MethodsNineteen females with BN (n = 14) or BED (n = 5), comprising the binge eating group (BEG; N = 19), and 19 age-matched healthy control (HC)’s completed thorough clinical assessment prior to functional MRI (fMRI). Neural response to low energy and high energy foods and non-food images was compared between groups using whole-brain exploratory analyses, from which six regions of interest (ROI) were then selected: frontal, occipital, temporal, and parietal lobes; insula and cingulate.ResultsIn response to low energy food images, the BEG demonstrated differential neural responses to all three low energy foods categories (disgust; fear; and happy) compared to HCs. Correlational analyses found a significant association between frequency of binge episodes and diminished temporal lobe and greater occipital lobe response. In response to high energy food images, compared to HC’s, the BEG demonstrated significantly decreased neural activity in response to all high energy food images. The HC’s had significantly greater neural activity in the limbic system, occipital lobe, temporal lobe, frontal lobe, and limbic system in response to high energy food images.ConclusionResults in the low energy food condition indicate that binge frequency may be related to increased aberrant neural responding. Furthermore, differences were found between groups in all ROI’s except the insula. The neural response seen in the BEG to disgust food images may indicate disengagement with this particular stimuli. In the high energy food condition, results demonstrate that neural activity in BN and BED patients may decrease in response to high energy foods, suggesting disengagement with foods that may be more consistent with those consumed during a binge eating episode.

The intralaminar distribution of choline acetyltransferase, galactocerebrosides, gangliosides and proteins were determined in frontal (Brodmann's area 9) and temporal (Brodmann's area 22) cortices from subjects with autopsy-proven Alzheimer's disease and controls matched for sex, age and postmortem delay. In normal brain choline acetyltransferase (CAT) activity was higher in the II and IV layers in the temporal cortex, while in frontal cortex CAT activity was relatively high in the II-III layer, appearing as a single peak. The intracortical distribution of galactocerebrosides normally shows a trend to a higher activity from the pial surface to white matter either in frontal or temporal cortices. Higher concentrations of gangliosides were associated with the cell body layers in either frontal or temporal cortices. In either frontal and temporal cortices from 5 patients with Alzheimer's disease the pattern of intralaminar distribution of CAT activity was completely disrupted and it was significantly lower than in all cortical layers of the controls. Galactocerebrosides concentration was significantly decreased in the lower layers (IV, V and VI) in both frontal and temporal cortices and ganglioside sialic acid concentration was also decreased in the Alzheimer brain consistently in the lower (III-IV) layers of the frontal and temporal cortices. These observations indicate a widespread involvement of cholinergic activities through all cortical layers. However, the selective decrease in galactocerebroside concentration in the lower layers (IV-VI) suggests a selective loss of ascending fibers from subcortical nuclei. The decreased concentration of ganglioside sialic acid in lower layers suggests a selective axodendritic degeneration in these laminae of frontal association and temporal cortex in Alzheimer's disease.

Imaging of Eating Disorders: Multiple Techniques to Demonstrate the Dynamic Brain

Objective To investigate the phenotypes and genetics of an early-onset familial Alzheimer′s disease (EO-FAD) family. Methods The clinical manifestations, brain MRI results and neuropathological findings of the proband and pedigree members of the EO-FAD family were evaluated. Autopsy was performed in the proband. Results Fifteen members of this family had a presenilin 1 (PSEN1) p. G378E mutation and nine of them had clinical manifestations or the MRI changes of EO-FAD. Neuropathological findings from autopsy of the proband disclosed moderate cortical atrophy throughout the brain, especially in frontal lobe and temporal lobe. Neuronal loss with gliosis was observed in the cortices of the frontal, temporal and occipital lobes, as well as in parahippocampal gyrus. Numerous senile plaques and neurofibrillary tangles were present in the cerebral cortex. The proband′s younger sister showed similar clinical presentations and MRI changes, and other members of this family demonstrated progressive memory loss. Conclusion A p. G378E mutation in the PSENl gene was identified in a Chinese EO-FAD pedigree. Key words: Alzheimer disease, familial; PSEN1 gene; Gene mutation

Aim In order to study the mechanism of post-stroke depression (PSD), we used diffusion kurtosis imaging (DKI) to describe the changes in white matter (WM) microstructure in PSD patients, to investigate the association between WM damage in limbic-cortical-striatal-pallidal-thalamic (LCSPT) circuit and PSD, and the utility of DKI in the diagnosis of PSD. Methods Fifty-eight participants were divided into different groups: control group (n=20), stroke patients without depression (Non-PSD, n=21) and PSD group (n=17). All were taken DKI scans. The WM of bilateral superior frontal gyrus, middle frontal gyrus, inferior frontal gyrus, temporal lobe, parietal lobe, occipital lobe, the anterior and posterior limb of internal capsule, the genu and splenium of corpus callosum were selected as the regions of interest (ROI) and selected mean kurtosis (MK), radial kurtosis (RK), axial kurtosis (AK) as the DKI parameters. Results Compared with control and Non-PSD, MK of PSD group in bilateral superior frontal gyrus, middle frontal gyrus, temporal lobe and the genu of corpus callosum were decreased significantly, as well as the RK in left superior frontal gyrus, bilateral middle frontal gyrus and temporal lobe. But there was no significant difference in AK. Besides, the decrease in MK and RK in frontal and temporal lobe was negatively associated with the severity of PSD. Conclusion Our research indicated that the damage to WM microstructure in the frontal lobe, temporal lobe and the genu of corpus callosum may be related toPSD. DKI explores the microstructural changes of WM in PSD patients and may be an auxiliary diagnostic method for PSD.

Schizophrenia probably has a developmental origin. This review refers to three of our published series of studies related to this hypothesis: loss of dendritic spines on cerebral neocortical pyramidal neurons, decreased numerical density of glutamatergic neurons, and microgliosis. First, brains of schizophrenic patients and non-schizophrenic controls were obtained post mortem and blocks of multiple cortical areas impregnated with a Rapid Golgi method. Spines were counted on the dendrites of pyramidal neurons of which the soma was in layer III (which takes part in corticocortical connectivity) and which met strict criteria for impregnation quality. Data were obtained blind: diagnoses were only revealed by a third party after measurements were completed. The mean spine count in all cortical areas studied in the control series was 243 mm(-1) of dendrite and in the schizophrenics 108. Measurements in frontal and temporal association cortex showed the greatest reduction in spine number in schizophrenia (299 in control frontal cortex and 101 in schizophrenics, and 276 mm(-1) in control temporal cortex and 125 in schizophrenics). There was no correlation of spine loss with age at death. Our results support the concept of a neurodevelopmental defect in the neuropil affecting glutamatergic neurons in schizophrenia and may help to explain loss of cortical volume without loss of neurons. In a second part of our study we used an antibody to the kainate receptor subunit GluR 5/6/7 and showed a decrease in numerical density of presumed glutamatergic neurons in schizophrenic orbitofrontal cortex. Finally, as glia play a major role in the developing nervous system, we investigated whether schizophrenia was associated with glial changes in frontal and temporal cortex. Astroglia and microglia were identified in schizophrenic and control brains, using antibodies to glial fibrillary acidic protein (GFAP) and class II human leucocyte antigen (HLA-DR), respectively. Significant increases were found in microglial numerical density in schizophrenics compared with controls: 28% in frontal area 9 (115 cells mm(-2) compared with 89), and a 57% increase in temporal area 22 (139 cells mm(-2) compared with 88). For both areas, astroglia showed no significant differences between schizophrenics and controls. No significant differences were found in cortical thickness or total neuronal numerical density between the two groups. This specific increase in numerical density of microglia in temporal and frontal cortex of chronic schizophrenics, not related to aging, could be related to possible changes in cortical neuropil architecture as revealed by loss of dendritic spines.

To determine whether the blood flow abnormalities frequently associated with arteriovenous malformations (AVMs) can alter functional magnetic resonance (MR) imaging evaluation of language lateralization and whether reorganization of language function occurs in patients with brain AVMs. Eleven patients with left-hemisphere brain AVMs and 10 age-matched control subjects were examined with 1.5-T blood oxygen level-dependent (BOLD) functional MR imaging. Verbal fluency, sentence repetition, and story listening tasks were performed. The functional MR imaging laterality index in the frontal and temporal lobes was defined as the (L - R)/(L + R) ratio, where L and R are the numbers of activated pixels in the left and right hemispheres, respectively. Statistical analyses were performed with Wilcoxon signed rank, Fisher exact, and Kruskal-Wallis tests. Control subjects had left-sided language dominance, although symmetric pixel counts were observed in the frontal lobes in two subjects and in the temporal lobes in one subject. Six patients had left-sided language dominance similar to that observed in control subjects. Five of these patients had AVMs outside frontal or temporal language areas, without flow abnormalities. Five patients had abnormally right-sided asymmetric indexes (below mean control subject value - 2 SDs), which suggested language reorganization (P <.05). Results of Wada examination and/or postembolization functional MR imaging performed in two of these patients showed that the abnormal laterality indexes were at least partly due to severe flow abnormalities that impaired detection of BOLD MR imaging signal intensity. These data suggest that flow abnormalities may interfere with language lateralization assessment with functional MR imaging.

The clinical significance of intracerebral hematoma (ICH) following rupture of a middle cerebral artery (MCA) aneurysm was studied in 31 surgical patients having a mean age of 52 years. Sixteen patients were not included in this study, because of massive intraventricular bleeding (2), postoperative complications (7), operation trouble (5), and symptomatic vasospasm (2). One patient died in postoperative period. The remaining 30 patients were followed for a mean of 3.7 years postoperatively. Sixteen patients almost fully recovered, nine were self-sufficient with some deficits, two were partially dependent, one was fully dependent, and three died. The locations of the ICH were as follows: temporal lobe in 18 cases; frontal lobe in five; frontal and temporal lobes in three; temporal and parietal lobes in four; and temporal lobe and internal capsule in one. Fourteen patients had permanent neurological deficits. Left homonymous hemianopsia occurred in one patient who had a large hematoma in the right temporal lobe but became self-sufficient. Motor disturbances were mild in 11 cases, and severe in three (hemiplegia in two and tetraparesis in one). Six of the 11 patients with dominant hemispheric ICH experienced motor dominant aphasia and one had global aphasia. Although there was no definite correlation between hemisphere and outcome, patients with medium to large ICH in the dominant hemisphere tended to develop motor dominant aphasia. In terms of motor disturbance and aphasia due to ICH following MCA aneurysm rupture, the prognosis appears fairly good because these ICH are originally subcortical.

<bold>Objective</bold>To explore the cortical control mechanisms of auditory comprehension and verbal expression deficits in post-stroke aphasia (PSA) patients based on a naturalistic paradigm that closely mimics real-world scenarios. <bold>Methods</bold> A total of 26 PSA patients (PSA group) treated in the Second Rehabilitation Hospital of Shanghai from March 2024 and February 2025 were enrolled, along with 21 gender-, age-, and education-matched healthy controls (control group). All participants completed an auditory comprehension-verbal expression task under functional near-infrared spectroscopy (fNIRS) monitoring. A block-task paradigm was designed based on a natural question-answer language model, consisting three phases, including listening to questions embedded in short narratives, thinking, and responding, with the entire paradigm repeated six times. fNIRS monitoring encompassed bilateral temporal, parietal, and prefrontal lobes. The Western Aphasia Battery (WAB) and the Boston Diagnostic Aphasia Examination (BDAE) were used to evaluate language function. The fNIRS system was used to assess cortical activation levels in various channels and brain regions, including the superior temporal gyrus (STG), middle temporal gyrus (MTG), supramarginal gyrus (SMG), fusiform gyrus (FG), angular gyrus (AG), somatosensory association cortex (SAC), primary somatosensory cortex (PSC), primary motor cortex (PMC), pre-motor and supplementary motor cortex (PMSC), pars triangularis of Broca's area (PT), pars opercularis (PO), dorsolateral prefrontal cortex (DLPFC), and frontal eye fields (FEF), during auditory comprehension and verbal expression tasks. To analyze the correlations between WAB auditory comprehension/verbal expression scores, WAB-AQ scores, BDAE scores, and cortical activation levels in the PSA group during auditory comprehension and verbal expression tasks.<bold>Results</bold>In the auditory comprehension task, the control group showed significant bilateral brain activation, with higher activation levels in the right hemisphere than the left, including the superior temporal gyrus (STG) (P=0.041), middle temporal gyrus (MTG) (P=0.002), and supramarginal gyrus (SMG) (P=0.028). In contrast, the PSA group primarily relied on the right-hemisphere homologue of Wernicke's area, including the STG (P=0.030) and MTG (P=0.024), with significantly reduced activation in the left hemisphere (P&lt;0.05). During the verbal expression task, the control group showed pronounced activation in the left Broca's area and related regions, including the PT (P=0.036), PO (P=0.001), and PMC (P=0.002), with symmetrical activation in the right hemisphere. The PSA group demonstrated compensatory activation in the right hemisphere, including the PT (P=0.035), PO (P=0.002), and PMC (P=0.017), while activation in the left hemisphere(particularly Broca's area) decreased significantly(P&lt;0.05). WAB auditory comprehension scores in patients with PSA correlated with the degree of activation in the bilateral DLPFC (r=-0.401, P=0.047), PMSC (r =-0.417, P=0.038), and PMC (r=-0.414, P=0.040). WAB spontaneous speech scores correlated with activation in the left DLPFC (r =-0.423, P=0.035), PMC (r =-0.400, P = 0.048), and PSC (r =-0.481, P = 0.015), as well as with activation in the right STG (r=-0.404, P = 0.045). <bold>Conclusion</bold> The degree of cortical activation during auditory comprehension and verbal expression tasks in PSA patients is significantly correlated with language function impairment scores, emphasizing the crucial role of the right hemisphere in PSA recovery.