JOURNAL/nrgr/04.03/01300535-202510000-00030/figure1/v/2024-11-26T163120Z/r/image-tiff Sleep disturbances are among the most prevalent neuropsychiatric symptoms in individuals who have recovered from severe acute respiratory syndrome coronavirus 2 infections. Previous studies have demonstrated abnormal brain structures in patients with sleep disturbances who have recovered from coronavirus disease 2019 (COVID-19). However, neuroimaging studies on sleep disturbances caused by COVID-19 are scarce, and existing studies have primarily focused on the long-term effects of the virus, with minimal acute phase data. As a result, little is known about the pathophysiology of sleep disturbances in the acute phase of COVID-19. To address this issue, we designed a longitudinal study to investigate whether alterations in brain structure occur during the acute phase of infection, and verified the results using 3-month follow-up data. A total of 26 COVID-19 patients with sleep disturbances (aged 51.5 ± 13.57 years, 8 women and 18 men), 27 COVID-19 patients without sleep disturbances (aged 47.33 ± 15.98 years, 9 women and 18 men), and 31 age- and gender-matched healthy controls (aged 49.19 ± 17.51 years, 9 women and 22 men) were included in this study. Eleven COVID-19 patients with sleep disturbances were included in a longitudinal analysis. We found that COVID-19 patients with sleep disturbances exhibited brain structural changes in almost all brain lobes. The cortical thicknesses of the left pars opercularis and left precuneus were significantly negatively correlated with Pittsburgh Sleep Quality Index scores. Additionally, we observed changes in the volume of the hippocampus and its subfield regions in COVID-19 patients compared with the healthy controls. The 3-month follow-up data revealed indices of altered cerebral structure (cortical thickness, cortical grey matter volume, and cortical surface area) in the frontal-parietal cortex compared with the baseline in COVID-19 patients with sleep disturbances. Our findings indicate that the sleep disturbances patients had altered morphology in the cortical and hippocampal structures during the acute phase of infection and persistent changes in cortical regions at 3 months post-infection. These data improve our understanding of the pathophysiology of sleep disturbances caused by COVID-19.

The early diagnosis of Alzheimer's disease has faced significant challenges, as the initial patients have hidden symptoms that are difficult to distinguish from conventional symptoms. In view of this, this article designs a collaborative multitasking algorithm framework that implements a positive feedback loop between classification tasks, significantly improving processing accuracy. Specifically, the algorithm consists of three sub networks: the initial segmentation sub network accurately identifies the hippocampus boundary and generates the initial segmentation mask; The classification subnetwork relies on initial segmentation information to effectively distinguish different stages of Alzheimer's disease; Finally, the fine segmentation sub network finely adjusts the contour of the hippocampus based on the classification results. To verify the superiority of this method, this study used 269 MRI sample of Alzheimer's disease patients, including clinical and public datasets. The experimental results demonstrate that the proposed method exhibits superior performance in both hippocampal classification and segmentation tasks. Specifically, in terms of segmentation, the method achieved an average Dice Similarity Coefficient (DSC) of 94.0% and a Jaccard Index (JA) of 80.6%. For classification tasks, the method demonstrated an accuracy (AC) of 98.8%, sensitivity (SEN) of 98.8%, specificity (SP) of 98.6%, and F1 score (F1) of 97.8%, collectively indicating excellent clinical performance.

Language is a sophisticated cognitive skill that relies on the coordinated activity of cerebral cortex. Acquiring a second language creates intricate modifications in brain connectivity. Although considerable studies have evaluated the impact of second language acquisition on brain networks in adulthood, the results regarding the ultimate form of adaptive plasticity remain inconsistent within the adult population. Furthermore, due to the assumption that subcortical regions are not significantly involved in language-related tasks, the thalamus has rarely been analyzed in relation to other language-relevant cortical regions. Given these limitations, we aimed to evaluate the functional connectivity and volume modifications of thalamic subfields using magnetic resonance imaging (MRI) modalities following the acquisition of a second language. Structural MRI and fMRI data from 51 participants were collected from the OpenNeuro database. The participants were divided into three groups: monolingual (ML), early bilingual (EB), and late bilingual (LB). The EB group consisted of individuals proficient in both English and Spanish, with exposure to these languages before the age of 10 years. The LB group consisted of individuals proficient in both English and Spanish, but with exposure to these languages after the age of 14 years. The ML group included participants proficient only in English. Our results revealed that the ML group exhibited increased functional connectivity in all thalamic subfields (anterior, intralaminar-medial, lateral, ventral, and pulvinar) compared with the EB and LB groups. In addition, a significantly decreased volume of the left suprageniculate nucleus was found in the bilingual groups compared with the ML group. This study provides valuable evidence suggesting that acquiring a second language may be protective against dementia, due to its high plasticity potential, which acts synergistically with cognitive functions to slow the degenerative process.

The thalamus is critical for the relay and modulation of visual information. As such, injury to the developing thalamus may result in cerebral visual impairment (CVI). This study investigated quantitative volume reductions of the thalamus in cerebral visual impairment compared to controls and probed the association between thalamic volume and the severity of cerebral visual impairment-related visual dysfunctions. Thalamic volumes were quantified using T1-weighted magnetic resonance imaging (MRI) data from 23 participants with cerebral visual impairment and 42 controls. Nineteen participants with cerebral visual impairment also completed the CVI Questionnaire. Cerebral visual impairment was associated with significant volume reductions of the global thalami, anterior, lateral, and ventral thalamic regions, as well as several nuclei, particularly in those with cerebral visual impairment due to periventricular leukomalacia. Within the cerebral visual impairment group, smaller volumes of the right thalamus and lateral pulvinar were significantly associated with more reported difficulties moving through space. Together, these results provide empirical evidence supporting aberrant thalamic development as a potential mechanism underlying cerebral visual impairment.

Converging evidence from clinical neuroimaging and animal models has strongly implicated dysfunction of thalamocortical circuits in the pathophysiology of schizophrenia. Preclinical models of genetic risk for schizophrenia have shown reduced synaptic transmission from auditory thalamus to primary auditory cortex, which may represent a correlate of auditory disturbances such as hallucinations. Human neuroimaging studies, however, have found a generalized increase in resting state functional connectivity (RSFC) between whole thalamus and sensorimotor cortex in people with schizophrenia (PSZ). We aimed to more directly translate preclinical findings by specifically localizing auditory and visual thalamic nuclei in unmedicated PSZ and measuring RSFC to primary sensory cortices.

In this case-control study, 82 unmedicated PSZ and 55 matched healthy controls (HC) completed RSFC functional magnetic resonance imaging (fMRI). Auditory and visual thalamic nuclei were localized for 55 unmedicated PSZ and 46 HC who additionally completed a sensory thalamic nuclei localizer fMRI task (N = 101). Using localized nuclei as RSFC seeds we assessed group differences in auditory and visual thalamocortical connectivity and associations with positive symptom severity.

Auditory thalamocortical connectivity was not significantly different between PSZ and HC, but hyperconnectivity was associated with greater positive symptom severity in bilateral superior temporal gyrus. Visual thalamocortical connectivity was significantly greater in PSZ relative to HC in secondary and higher-order visual cortex, but not predictive of positive symptom severity.

These results indicate that visual thalamocortical hyperconnectivity is a generalized marker of schizophrenia, while hyperconnectivity in auditory thalamocortical circuits relates more specifically to positive symptom severity.

Brain connectivity can be estimated in many ways, depending on modality and processing strategy. Here, we present the Krakencoder, a joint connectome mapping tool that simultaneously bidirectionally translates between structural and functional connectivity, and between different atlases and processing choices via a common latent representation. These mappings demonstrate exceptional accuracy and individual-level identifiability; the mapping between structural and functional connectivity has identifiability 42-54% higher than existing models. The Krakencoder combines all connectome flavors via a shared low-dimensional latent space. This fusion representation better reflects familial relatedness, preserves age- and sex-relevant information, and enhances cognition-relevant information. The Krakencoder can be applied, without retraining, to new out-of-distribution data while still preserving inter-individual differences in the connectome predictions and familial relationships in the latent representations. The Krakencoder is a notable leap forward in capturing the relationship between multimodal brain connectomes in an individualized, behaviorally and demographically relevant way.

Thalamic stimulation is a promising approach to controlling seizures in patients with intractable epilepsy. It does not, however, provide good control for everyone. A big issue is that the role of the thalamus in seizure organization and propagation is unclear. When using responsive stimulation devices, they must detect seizure activity before sending stimulation. So, it's important to know which parts of the thalamus are involved in different seizures.

To better choose thalamic targets for stimulation, we studied how different seizures spread to each stimulation target. Expert reviews and automated tools were used to identify seizure spread recorded from invasive recordings. We categorized seizures based on how they start and spread, and determined whether seizures reached thalamic areas early or late. We used generalized linear models (GLM) to evaluate which seizure properties are predictive of time of spread to the thalamus, testing effect significance using Wald tests.

We show that seizures with <2 Hz synchronized-spiking patterns do not spread early to the thalamus, while seizures starting with faster activity (<20 Hz) spread early to all thalamic areas. Most importantly, seizures that begin broadly across the brain quickly recruit the centromedian and pulvinar areas, suggesting these may be better stimulation targets in such cases. Alternatively, seizures that start deep in the temporal lobe tend to involve the anterior part of the thalamus, meaning the centromedian might not be the best choice for those seizures.

Our results suggest that by analyzing electrical activity during seizures, we can better predict which parts of the thalamus are involved. This could lead to more effective stimulation treatments for people with epilepsy.

The striatum is divided into two interdigitated tissue compartments, the striosome and matrix. These compartments exhibit distinct anatomical, neurochemical, and pharmacological characteristics and have separable roles in motor and mood functions. Little is known about the functions of these compartments in humans. While compartment-specific roles in neuropsychiatric diseases have been hypothesized, they have yet to be directly tested. Investigating compartment-specific functions is crucial for understanding the symptoms produced by striatal injury, and to elucidating the roles of each compartment in healthy human skills and behaviors. We mapped the functional networks of striosome-like and matrix-like voxels in humans in-vivo. We utilized a diverse cohort of 674 healthy adults, derived from the Human Connectome Project, including all subjects with complete diffusion and functional MRI data and excluding subjects with substance use disorders. We identified striatal voxels with striosome-like and matrix-like structural connectivity using probabilistic diffusion tractography. We then investigated resting-state functional connectivity (rsFC) using these compartment-like voxels as seeds. We found widespread differences in rsFC between striosome-like and matrix-like seeds (p < 0.05, family wise error corrected for multiple comparisons), suggesting that striosome and matrix occupy distinct functional networks. Slightly shifting seed voxel locations (<4 mm) eliminated these rsFC differences, underscoring the anatomic precision of these networks. Striosome-seeded networks exhibited ipsilateral dominance; matrix-seeded networks had contralateral dominance. Next, we assessed compartment-specific engagement with the triple-network model (default mode, salience, and frontoparietal networks). Striosome-like voxels dominated rsFC with the default mode network bilaterally. The anterior insula (a primary node in the salience network) had higher rsFC with striosome-like voxels. The inferior and middle frontal cortices (primary nodes, frontoparietal network) had stronger rsFC with matrix-like voxels on the left, and striosome-like voxels on the right. Since striosome-like and matrix-like voxels occupy highly segregated rsFC networks, striosome-selective injury may produce different motor, cognitive, and behavioral symptoms than matrix-selective injury. Moreover, compartment-specific rsFC abnormalities may be identifiable before disease-related structural injuries are evident. Localizing rsFC differences provides an anatomic substrate for understanding how the tissue-level organization of the striatum underpins complex brain networks, and how compartment-specific injury may contribute to the symptoms of specific neuropsychiatric disorders.

Modafinil promotes wakefulness and enhances cognitive function through mechanisms and neural effects that are still partially unknown. Several studies have shown that the compound alters the functional cortical architecture. In contrast, its influence on subcortical regions and thalamocortical connections, which are crucial for modulating neocortical connectivity, remains unexplored. The acute modulation of thalamo-cortical connectivity was assessed in two groups of participants who received either a single 100 mg dose of modafinil (N = 25) or a placebo (N = 25). Magnetic Resonance Imaging (MRI) was used to parcel the thalamus into its constituent nuclei, which served as seeds for voxel-wise resting state functional connectivity analyses. Additionally, maps of nuclei-specific functional reorganization were compared to those of receptor/transporter expression to assess their spatial overlaps. Modafinil, but not placebo, altered the connectivity of three thalamic nuclei. Specifically, the medial pulvinar nuclei showed increased connectivity with cortical regions of the Sensorimotor and Salience/Ventral Attention (SVAN) Networks. These functional changes spatially overlapped with the distribution of the norepinephrine transporter (NET). Additionally, the anterior and inferior pulvinar complex exhibited enhanced connectivity with the insular and supramarginal regions of the SVAN and superior frontal area of the Default Mode Network (DMN). However, unlike the medial pulvinar, these effects were not spatially linked to the expression of any specific receptor or transporter. Finally, the ventro-lateral anterior complex exhibited increased connectivity with the posterior region of the DMN and the Fronto-Parietal Control Network, along with decreased connectivity to the premotor cortex. The topography of these functional modifications mainly overlaps with the distribution of glutamatergic and serotonergic receptors. In summary, our findings highlight modafinil's influence on thalamocortical circuits, emphasizing the role of higher-order pulvinar nuclei and ventro-lateral anterior complex.

The thalamus is the brain's central communication hub, playing a key role in processing and relaying sensorimotor and cognitive information between the cerebral cortex and other brain regions. It consists of specific and non-specific nuclei, each with a different role. Specific thalamic nuclei relay sensory and motor information to specific cortical and subcortical regions to ensure precise communication. In contrast, non-specific thalamic nuclei are involved in general functions such as attention or consciousness through broader and less targeted connections. In the present study, we aimed to investigate the functional connectivity patterns of the thalamic nuclei identified in our previous study as being involved in motor (finger-tapping) and sensory (finger-touch) tasks. The results of this study show that thalamic nuclei are not static hubs with a predefined role in neural signal processing, as they show different task-specific functional connectivity patterns in the anterior, middle, lateral, and posterior thalamic nuclei. Instead, they are all functional hubs that can flexibly change their connections to other brain regions in response to task demands. This work has important implications for understanding task-dependent functional connectivity between thalamic nuclei and different brain regions using task-based fMRI at 9.4 Tesla.

Cognitive decline in Parkinson's disease (PD) significantly impacts patients' quality of life, yet early detection remains challenging. While structural brain abnormalities in cortical regions have been widely documented using magnetic resonance imaging (MRI), subcortical regions have received less analytical attention despite their potential role as early biomarkers. This study investigated changes in specific subregions of the amygdala, thalamus, and hypothalamus in patients with PD before cognitive decline development. We analyzed MRI data from 163 participants (97 healthy controls [HC] and 66 patients with PD) from the Parkinson's Progression Markers Initiative database. The patients with PD were classified based on cognitive status during a four-year follow-up: 21 who developed cognitive impairment (PDCI) and 45 who maintained normal cognition (PDNC). Cognitive function was assessed using the Montreal Cognitive Assessment and domain-specific tests. The PDCI group showed significantly lower corrected brain volumes in specific subregions of the amygdala (left basal nucleus), thalamus (bilateral lateral geniculate nuclei, right medial dorsal nucleus, and right anterior pulvinar nucleus), and hypothalamus (bilateral anterior-superior and left superior tubular parts) compared to that of HC. A significant difference between the PDCI and PDNC groups was observed only in the left lateral geniculate nucleus. In contrast, widespread structural changes were observed in cortical regions in the PDCI group, which showed stronger correlations with memory, attention, executive function, and visuospatial abilities. Hazard ratio analysis confirmed that structural changes in multiple cortical regions were significant predictors of cognitive decline. Although structural alterations were observed in subcortical regions, cortical changes demonstrated stronger associations with cognitive decline. These findings suggest that structural abnormalities may appear in the cerebral cortex before the stage proposed by conventional α-synuclein propagation models, potentially involving multiple mechanisms beyond α-synuclein, including global neural circuit dysfunction, disruption of neurotransmitter systems, breakdown of compensatory mechanisms, and coexisting pathologies (beta-amyloid and tau proteins). This study provides insights into early brain changes in PD and emphasizes the need for a comprehensive approach considering multiple mechanisms in early diagnosis and intervention strategies for PD-related cognitive impairment.

Deep brain stimulation of the dentate nucleus (DN-DBS) is an emerging therapy to improve upper extremity (UE) motor function after stroke. This study sought to investigate the physiologic mechanisms of acute DN-DBS in chronic stroke survivors enrolled in a phase I trial for DN-DBS.

Twelve chronic stroke participants with moderate-to-severe UE impairment received (acute) single sessions (≥45 min) of active DBS and sham DBS in a sham-controlled, double-blind, cross-over experiment (order randomized). Transcranial magnetic stimulation (TMS) was used to evaluate corticomotor physiology. We also characterized the relationship between acute DBS effects on physiology and baseline clinical and neuroimaging measures, and chronic DBS effects on motor function.

Acute active DBS led to an increase in ipsilesional corticomotor excitability evident as a 5.2 % maximal stimulator output (MSO) reduction in active motor threshold (p = 0.017, d = 0.28), but there was no effect of acute sham DBS. Increases in corticomotor excitability observed with acute DBS were associated with higher microstructural integrity of ipsilesional corticospinal tract (r > 0.70, p < 0.017) and dentato-thalamo-cortical pathways (ρ > 0.69, p < 0.022). Gains in corticomotor excitability with acute DBS were associated with higher dexterity gains made with chronic DBS plus rehabilitation (r > 0.65, p < 0.028).

Acute DN-DBS leads to heightened ipsilesional corticomotor excitability in moderate-to-severe chronic stroke survivors. Effects of acute DN-DBS on physiology are contingent upon structural preservation of key white matter tracts and associated with motor gains made with chronic DN-DBS. Findings provide mechanistic support of DN-DBS as a potential therapy for post-stroke motor recovery and potential of TMS to monitor responses.

Structural neuroimaging studies of patients with Juvenile Myoclonic Epilepsy (JME) typically present two findings: 1-volume reduction of subcortical gray matter structures, and 2-abnormalities of cortical thickness. The general trend has been to observe increased cortical thickness primarily in medial frontal regions, but heterogeneity across studies is common, including reports of decreased cortical thickness. These differences have not been explained. The cohort of patients investigated here originates from the Juvenile Myoclonic Epilepsy Connectome Project, which included comprehensive neuropsychological testing, 3 T MRI, and high-density 256-channel EEG. 64 JME patients aged 12-25 and 41 age and sex-matched healthy controls were included. Data-driven approaches were used to compare cortical thickness and subcortical volumes between the JME and control participants. After differences were identified, supervised machine learning was used to confirm their classification power. K-means clustering was used to generate imaging endophenotypes, which were then correlated with cognition, EEG frequency band lagged coherence from resting state high-density EEG, and white and grey matter based spatial statistics from diffusion imaging. The volumes of subcortical gray matter structures, particularly the thalamus and the motor-associated thalamic nuclei (ventral anterior), were found to be smaller in JME. In addition, the right hemisphere (primarily) sulcal pre-motor cortex was abnormally thicker in an age-dependent manner in JME with an asymmetry in the pre-motor cortical findings. These results suggested that for some patients JME may be an asymmetric disease, at least at the cortical level. Cluster analysis revealed three discrete imaging endophenotypes (left, right, symmetric). Clinically, the groups were not substantially different except for cognition, where left hemisphere disease was linked with a lower performance on a general cognitive factor ("g"). HD-EEG demonstrated statistically significant differences between imaging endophenotypes. Tract-based spatial statistics showed significant changes between endophenotypes as well. The left dominant disease group exhibited diffuse white matter changes. JME patients present with heterogeneity in underlying imaging endophenotypes that are defined by the presence and laterality of asymmetric abnormality at the level of the pre-motor sulcal cortex; these endophenotypes are linked to orderly relationships with cognition, EEG, and white matter pathology. The relationship of JME's adolescent onset, age-dependent cortical thickness loss, and seizure upon awakening all suggest that synaptic pruning may be a key element in the pathogenesis of JME. Individualized treatment approaches for neuromodulation are needed to target the most relevant cortical and subcortical structures as well as develop disease-modifying and neuroprotective strategies.

To investigate high-frequency activities (HFA) associated with thalamic sleep spindles.

We studied a cohort of ten pediatric patients with medication resistant epilepsy who were identified as potential candidates for thalamic neuromodulation. These patients had thalamic sampling as well as presumed epileptogenic zones, using stereotactic EEG (SEEG) with a sampling frequency of 2,000 Hz. We quantified the summated high-frequency activity (HFA) in the fast ripple band associated with sleep spindles using 20-minute scalp EEG and SEEG recordings during non-REM sleep and analyzed its correlation with spindle characteristics.

HFA, with a median peak frequency of 330 Hz, was distinctively observed in the thalamus and temporally correlated with thalamic sleep spindles. Such HFA demonstrated significant coupling with the sleep spindle range of 11-16 Hz. The duration of HFA positively correlated with higher density and longer duration of accompanying thalamic spindles. Thalamic HFA's duration negatively correlated with the presence of cortical interictal epileptiform discharges. Thalamic spindles generated in channels with HFA often coincided with sleep spindles in various brain regions.

Fast ripple band HFA associated with sleep spindles was observed exclusively in the thalamus.

Thalamic HFA associated with thalamic spindles may represent a thalamus-specific physiological phenomenon.

Responsive Neurostimulation (RNS) is a closed-loop neuromodulation therapy approved for treating drug resistant epilepsy (DRE) with 1 or 2 seizure foci, but its potential utility for treating complex seizure networks, such as in focal cortical dysplasia (FCD), remains uncertain. This review and commentary discuss the current practice of RNS use in focal cortical dysplasia-related drug-resistant epilepsy(FCD-DRE), and the potential of individualized approaches.

Our scoping review followed a search to identify relevant studies on epilepsy and RNS across MEDLINE, Embase, and Web of Science, yielding 674, 1,255, and 579 results, respectively followed by abstract and full text review to include FCD-DRE. Data on history, imaging, intracranial EEG, RNS implantation and programming strategies were recorded.

78 patients with FCD-DRE across 25 studies were included. The most common lead configuration was two depth electrodes in 53 % (19/36). The median seizure reduction was 85 % [IQR = 66, 96] with a median follow up of 17 months., including 6 patients (7.6 %) achieving seizure freedom for a median 15 months. In 17 patients with resections and RNS implantation, median seizure frequency reduction was 87 % (N = 15), not significantly different from the group with RNS only. 8 patients with cortical and thalamic leads had median seizure frequency reduction of 87 % [IQR = 51, 92]. RNS was effective when used in refractory status epilepticus associated with FCDs.

RNS is a flexible therapy that effectively reduces seizures in FCD-DRE. Electrographic and imaging signatures can potentially be leveraged. Hybrid resection with RNS approaches and the role in refractory status epilepticus associated with FCD is highlighted. Future studies are necessary to optimize RNS therapy in FCD-DRE.

Childhood maltreatment is a significant risk factor for schizophrenia, and there are correlations between these adversities and thalamic gray matter density. The thalamus, a subcortical structure with various nuclei with specific connections, relays sensory information and participates in higher cognitive processes. Thalamic alterations are evident in psychotic disorders, and early-life adversities may affect its development, potentially contributing to psychosis. However, no evidence exists of volumetric alterations in thalamic nuclei in first-episode psychosis (FEP) patients related to early traumatic events. This study recruited 70 FEP patients and 68 age-matched healthy controls, who underwent 3 T structural MRI and clinical scales, including the Childhood Trauma Questionnaire (CTQ). The thalamus was analyzed for shape and segmented into nuclei to assess volume. Additionally, peripheral blood was analyzed for the expression of VCAN, CSGALNACT1, ST8SIA4, NRGN, SP4, and TOX genes, which are related to neuronal plasticity in the thalamus and psychosis. Results showed volumetric reductions in the whole thalamus and specific nuclei (lateral posterior, lateral geniculate, medial geniculate, ventrolateral, centromedian, anteroventral, mediodorsal, and pulvinar). The thalamus did not show shape alterations. A significant association was observed between physical neglect during childhood and the volume of the left thalamus and its anteroventral nucleus. Reduced expression of ST8SIA4 and SP4 genes was detected in FEP patients compared to healthy controls, with correlations between thalamic nuclei volumes and gene expression differing between groups. In conclusion, this study links thalamic nuclei volume with childhood adversities in FEP and highlights changes in ST8SIA4 and SP4 expression, correlating with thalamic nuclei volumes.

The thalamic ventral posterior (VP) nuclear complex includes several subnuclei, including the VPM, VPL, VPI, and VMb, each with distinct inputs, axonal trajectories, and staining properties. Understanding the three-dimensional organization of neuronal fiber structures of the VP complex is crucial for understanding intra-thalamic and thalamocortical connections related to somatosensory processing. In this study, an ex vivo block of the human brain was scanned using mesoscopic Diffusion Tensor Imaging (DTI), and the four VP subnuclei were identified using existing histological atlases as references. The VP subnuclei were characterized using a mean diffusivity (MeanD) map, orientation-coded fractional anisotropy (FA) map, and tractography obtained from DTI. The results demonstrated differential patterns in MeanD and orientation-coded FA maps among the four subnuclei, underscoring the potential of mesoscale imaging to identify and differentiate these subnuclei. The tractography identified patterns of afferent and efferent fibers unique to each nucleus, offering insights into their functional roles in sensory processing. The findings highlighted the advantages of DTI in visualizing the direction of fibrous structures and conducting three-dimensional tractography, offering a foundation for further investigations into in vivo imaging applications and the neural mechanisms of somatosensory disorders, including central pain syndrome.

Human high-order thalamic nuclei activity is known to closely correlate with conscious states. However, it is not clear how those thalamic nuclei and thalamocortical interactions directly contribute to the transient process of human conscious perception. We simultaneously recorded stereoelectroencephalography data from the thalamic nuclei and prefrontal cortex (PFC), while patients with implanted electrodes performed a visual consciousness task. Compared with the ventral nuclei and PFC, the intralaminar and medial nuclei presented earlier and stronger consciousness-related activity. Transient thalamofrontal neural synchrony and cross-frequency coupling were both driven by the θ phase of the intralaminar and medial nuclei during conscious perception. The intralaminar and medial thalamic nuclei thus play a gate role to drive the activity of the PFC during the emergence of conscious perception.

Despite perinatal damage to the cerebellum being one of the highest risk factors for later being diagnosed with autism spectrum disorder (ASD), it is not yet clear how the cerebellum might influence the development of cerebral cortex and whether this co-developmental process is distinct between neurotypical and ASD children. Leveraging a large structural brain MRI dataset of neurotypical children and those diagnosed with ASD, we examined whether structural variation in cerebellar tissue across individuals was correlated with neocortical variation during development, including the thalamus as a coupling factor. We found that the thalamus plays a distinct role in moderating cerebro-cerebellar structural coordination in ASD. Notably, structural coupling between cerebellum, thalamus, and neocortex was strongest in younger childhood and waned by early adolescence, mirroring a previously undescribed trajectory of behavioral development between ASD and neurotypical children. Complementary functional connectivity analyses likewise revealed atypical connectivity between cerebellum and neocortex in ASD. This relationship was particularly prominent in a model of cerebellar structure predicting functional connectivity, where ASD and neurotypical children showed divergent patterns. Interestingly, these functional-structural relationships became more prominent with age, while structural effects were most prominent earlier in childhood, and showed significant lateralization. This pattern may suggest a developmental sequence where early uncoordinated structural growth amongst regions is followed by increasingly atypical functional synchronization. These findings provide multimodal evidence in the living brain for a cerebellar diaschisis model of autism, where both increased cerebellar-cerebral structural coupling and altered functional connectivity in cerebro-cerebellar pathways contribute to the ontogeny of this neurodevelopmental disorder.

To investigate structural alterations in the thalamus in patients with primary trigeminal neuralgia and provide a detailed perspective on thalamic remodeling in response to chronic pain at the level of individual thalamic nuclei.  METHODS: We analyzed a sample of 62 patients with primary trigeminal neuralgia who underwent surgical treatment, along with 28 healthy participants. Magnetic resonance imaging (MRI) data were acquired using a 3T system equipped with a 16-channel receiver head coil. Segmentation of the thalamic nuclei was performed using FreeSurfer 7.2.0. We divided the group of patients with trigeminal neuralgia into two subgroups: those with right-sided pain and those with left-sided pain. Each subgroup was compared to a control group by means of one-way ANOVA. Associations between morphometric and clinical variables were assessed with Spearman correlation coefficient.

Our results revealed significant gray matter volume changes in thalamic nuclei among patients with trigeminal neuralgia. Notably, the intralaminar nuclei (centromedian/parafascicular) and nuclei associated with visual and auditory signal processing (lateral and medial geniculate bodies) exhibited significant alterations, contrasting with the ventral group nuclei involved in nociceptive processing. Additionally, we found no substantial volume increase in any of the studied nuclei following successful surgical intervention 6 months later. The volumes of thalamic nuclei were negatively correlated with pain intensity and disease duration.

The results of this study, although preliminary, hold promise for clinical applications as they reveal previously unknown structural alterations in the thalamus that occur in patients with chronic trigeminal neuralgia.

The pulvinar nucleus of the thalamus has extensive cortical connections with the temporal, parietal, and occipital lobes. Deep brain stimulation (DBS) targeting the pulvinar nucleus, therefore, carries the potential for therapeutic benefit in patients with drug-resistant posterior quadrant epilepsy (PQE) and neocortical temporal lobe epilepsy (TLE). Here, we present a single-center experience of patients managed via bilateral DBS of the pulvinar nucleus.

A single-institution retrospective review of five patients who underwent bilateral pulvinar DBS for drug-resistant TLE or PQE was performed. Stimulation parameters were adjusted monthly as needed, and side effects were monitored. The primary outcome was the percentage reduction in patient-reported seizure frequency in comparison to the preimplant baseline. The location of the active electrode contacts in relation to pulvinar thalami that produced the best seizure outcome was identified. Chronic sensing of the pulvinar local field potentials (LFPs) and circadian pattern of modulation of the LFP amplitudes were analyzed.

Four patients (80%) experienced a >70% reduction in seizure frequency, whereas one patient had >50% reduction in seizure. Mean seizure reduction was 79% at a median follow-up of 13 months (range = 9-21 months). No significant side effects were noted. Of all the pulvinar subnuclei, stimulation of the medial pulvinar nucleus (MPN) produced the best seizure outcome in all patients except for two, in whom active contacts in the MPN but also in more lateral and inferior locations resulted in the most significant reduction in seizures. Chronic timeline data identified changes in LFP amplitude associated with stimulation and seizure occurrences.

In this first ever report on a series of patients undergoing bilateral pulvinar DBS for drug-resistant epilepsy, we demonstrate that stimulation of the pulvinar and in particular the MPN is a safe and viable option for patients with nonlesional PQE or TLE. The optimal target for stimulation and relative merits of open versus closed loop stimulation should be delineated in future studies.

To determine if reading development between ages 6 and 8 years related to changes in fractional anisotropy (FA) in the optic radiations (OR), and if these associations were similar in children born full term (FT) and preterm (PT) and in language tracts.

FT (n = 34) and PT (n = 34) children completed the Word Identification subtest of the Woodcock Reading Mastery Test at 6, 7, and 8 years. Diffusion MRI (96-directions, b=2500 sec/mm2) was acquired at 6 and 8 years. Probabilistic tractography identified bilateral OR and three left-hemisphere language tracts: inferior longitudinal fasciculus (ILF), superior longitudinal fasciculus (SLF), and arcuate fasciculus (AF). Linear mixed models determined if FA changes in these tracts were associated with reading growth.

Rates of reading growth were similar in both groups. For the OR, FA change from 6 to 8 years was negatively associated with reading growth in both groups. A similar pattern was observed in the left ILF but not in the SLF or AF.

Individual differences in reading development were associated with FA change of the OR and left ILF in FT and PT children. Negative associations implicate increasing axonal diameter and/or complexity in fiber structure as drivers of faster reading development.

Major depressive disorder (MDD) is a significant contributor to global disease burden, with somatic symptoms frequently complicating its diagnosis and treatment. Recent advances in neuroimaging have provided insights into the neurobiological underpinnings of MDD, yet the role of the glymphatic system remains largely unexplored. This study aimed to assess glymphatic function in drug-naïve somatic depression (SMD) patients using the diffusion tensor image analysis along the perivascular space (DTI-ALPS) index. A total of 272 participants, including somatic depression patients (SMD), pure depression (PMD), and healthy controls (HC), were enrolled. We collected T1-weighted (T1w) and DTI (diffusion tensor image) scans and clinical data of all participants. The DTI-ALPS indices were calculated and compared among three groups. Gray matter regions associated with the DTI-ALPS index were identified by voxel-based morphometry analysis (VBM), revealing a cluster located in the thalamus. Then, we performed partial correlation analyses to further investigate the relationships between the DTI-ALPS index, thalamic volume, and clinical data. The DTI-ALPS index was significantly higher in the MDD group compared to the HC group, particularly in the SMD group. Furthermore, a significant positive correlation was observed between the DTI-ALPS index and thalamic volume, with lower DTI-ALPS values associated with reduced thalamic volumes, especially in the SMD group. Our findings suggest heightened glymphatic activity in MDD patients, especially SMD patients, and a potential link between glymphatic function and thalamic vulnerability. Therefore, the thalamus' vulnerability to glymphatic system function may play a role in the pathophysiology of depression, particularly somatic depression, suggesting that both the glymphatic system and the thalamus could serve as potential therapeutic or intervention targets for future treatments.

BackgroundParkinson's disease (PD)-related anxiety occurs frequently and may be associated with imbalance between anxiety-related circuits. While the thalamus is a shared region of these circuits, its role in PD-related anxiety has not been explored so far.ObjectiveTo identify changes in volume of the thalamus and its subnuclei in patients with PD-related anxiety.MethodsCognitively intact PD patients (n = 105) were divided into two groups based on their score on the Parkinson anxiety scale (PAS): 31 PD patients had anxiety (Anx-PD) and 74 did not have anxiety (non-Anx-PD). Forty-five healthy control subjects were included. Participants underwent 7-Tesla MRI scanning. Using automatic segmentation, the volumes of the thalamus and its subnuclei were measured, compared between the groups and regressed on the PAS.ResultsThe volumes of the thalamus and its subnuclei did not significantly differ between the groups. However, in anxious PD patients, more severe anxiety was strongly associated with a smaller volume of the right medial thalamic subregion, specifically the right mediodorsal magnocellular nucleus and the right mediodorsal parvocellular nucleus (R = 0.63, ßPAS = -0.546, p-valuemodel = 0.007 and R = 0.60, ßPAS = -0.547, p-valuemodel = 0.016, respectively), and of the left anteroventral thalamus (R = 0.73, FDR p-valuemodel = 0.002, ßPAS = -0.407, p-valuePAS = 0.01).ConclusionsA reduced volume of the mediodorsal and anteroventral thalamus, overlapping structures between the anxiety related circuits, are associated with more severe PD-related anxiety and may explain its high prevalence in the disease.

Exposure to childhood maltreatment can contribute to multiple behavioral and clinical manifestations, including the development of psychotic illnesses and pain-related abnormalities. Aberrant pain perception in individuals with psychosis may be associated with the worsening psychiatric symptoms, including an increase in mood episodes and a higher risk for suicidality. Despite the multiple connections between psychosis, pain, and childhood maltreatment, the combined investigation of these three domains remains limited.

In this study, patients with schizophrenia (SZ, n = 20) or bipolar I disorder (BD, n = 24) and healthy controls (HC, n = 24) underwent a comprehensive clinical evaluation followed by quantitative sensory testing (QST), where behavioral sensitivity to thermal stimuli was quantified. Central pain circuitry was probed using a combination of functional and structural magnetic resonance imaging. Neuroimaging analyses focused on thermal stimulation fMRI responses, resting-state connectivity, and gray matter morphological properties.

fMRI demonstrated diminished sensorimotor activation during an evoked pain state for both SZ and BD patients, where reduced activity in thalamic subdivisions (i.e., pulvinar nucleus) in BD patients negatively correlates with the severity of childhood maltreatment. Resting-state connectivity analyses revealed altered connectivity of various cortical regions with the postcentral gyri and thalamic nuclei, suggesting potential altered neural mechanisms underlying pain perception in patients with SZ and BD. Morphological analysis identified reduced gray matter thickness in the postcentral sulcus of BD patients, which correlated with the severity of childhood maltreatment.

These findings provide insight into the multidimensional nature of clinical presentations in SZ and BD and contribute to our understanding of the complex relationship between childhood maltreatment and central pain processing in patients with psychotic illnesses.

Predictive coding is a theoretical framework that integrates models of brain dysconnectivity and psychopathology in psychosis. Thalamocortical dysconnectivity as well as reduced thalamic volumes have been reported in psychotic disorders. However, the role of the thalamus in predictive coding is not clear. We examined the relationship between magnetic resonance imaging (MRI)- based thalamic nuclei volumes and mismatch negativity (MMN), a purported index of prediction error signaling known to be impaired in psychosis.

We obtained MRI and MMN using a roving paradigm from individuals with SCZ spectrum disorder (SSD, n = 60) or bipolar disorder (BD, n = 69) and HC (n = 252). We segmented volumes of 25 thalamic nuclei bilaterally and tested their associations with MMN amplitude using linear models while covarying for age, sex, diagnosis, and intracranial volumes (ICV).

We did not find group differences in thalamic volumes that could account for differences in MMN, neither did we find significant volume × diagnosis interactions on MMN for any of the 25 nuclei examined. Across the whole sample, significant positive associations were found between MMN amplitude and the volumes of several higher-order thalamic nuclei, including the mediodorsal medial and lateral nuclei, anterior and medial pulvinar, nucleus reuniens, as well as the lateral geniculate nucleus.

The results demonstrate a positive association between MMN amplitude and volumes of thalamic association nuclei in patients with psychotic disorders and HC. These findings may suggest a modulatory role of the thalamus in prediction error signaling.

We prospectively studied asymptomatic C9orf72 mutation carriers, identifying those developing amyotrophic lateral sclerosis (ALS) or frontotemporal dementia (FTD).

We enrolled 56 asymptomatic family members (AFM) with a C9orf72 mutation (AFM C9+), 132 non-carriers (AFM C9-), and 359 population-based controls. Using 3 T magnetic resonance imaging, we measured cortical thickness, gyrification, and subcortical volumes longitudinally. Linear mixed-effects models on non-converting AFM C9+ scans (n = 107) created a reference for these measurements, establishing individual atrophy patterns. Atrophy patterns from presymptomatic phenoconverters (n = 10 scans) served as a template for group comparisons and similarity assessments. Similarity with phenoconverters was quantified using Dice similarity coefficient (DSC) for cortical and Kullback-Leibler similarity (KLS) for subcortical measures. Using longitudinal similarity assessments, we predicted when participants would reach the average similarity level of phenoconverters at their first post-onset scan.

Five AFM C9+ converted to ALS or ALS-FTD. Up to 6 years before symptoms, these phenoconverters exhibited significant atrophy in frontal, temporal, parietal, and cingulate cortex, along with smaller thalamus, hippocampus, and amygdala compared to other AFM C9+. Some non-converted AFM C9+ had high DSC and KLS, approaching values of phenoconverters, whereas others, along with AFM C9- and controls, had lower values. At age 80, we predicted 27.9% (95% confidence interval, 13.2-40.1%) of AFM C9+ and no AFM C9- would reach the same DSC as phenoconverters.

Distinctive atrophy patterns are visible years before symptom onset on presymptomatic scans of phenoconverters. Combining baseline and follow-up similarity measures may serve as a promising imaging biomarker for identifying those at risk of ALS or ALS-FTD. ANN NEUROL 2025;97:281-295.

Essential tremor (ET) is a neurological disorder primarily characterized by upper limb action tremor. It is widely recognized that the thalamus is implicated in ET pathophysiology, playing a central role in treatment approaches. This study aimed to explore thalamic morphology, assessing macrostructural changes and intrinsic thalamic networks in ET patients.

A total of 109 ET (41 with and 68 without resting tremor) and 81 healthy controls (HC) were enrolled in the study. An automatic probabilistic segmentation of thalamic nuclei was employed on T1-weighted MRI images using FreeSurfer 7.4. Subsequently, volumetric data were extracted, and graph theoretical analysis was applied on the cortical-thalamic nuclei network, assessing global and local network properties.

No significant differences were observed in the volume of thalamic nuclei between ET patients and HC. ET patients exhibited significant alterations in the global thalamic network, suggesting a less efficient brain network in comparison with HC. ET patients also showed local alterations of thalamic network such as lower eccentricity and path length in the ventral nuclei and reduced efficiency in the pulvinar, indicating a less interconnected network. No significant differences were observed between ET patients with and without rest tremor.

Our study demonstrates reduced global and local efficiency of brain networks in ET patients, suggesting impaired communication and interconnection between brain regions. These findings confirm the involvement of the ventral lateral and pulvinar nuclei as key regions in tremor pathophysiology in ET patients, supporting the targeting of these regions for therapeutic approaches.

The thalamus serves as a central relay station within the brain, and thalamic connectional anomalies are increasingly thought to be present in major depressive disorder (MDD). However, the use of conventional MRI scanners and acquisition techniques has prevented a thorough examination of the thalamus and its subnuclear connectional profile. We combined ultra-high field diffusion MRI acquired at 7.0 Tesla to map the white matter connectivity of thalamic subnuclei.

Fifty-three MDD patients and 12 healthy controls (HCs) were involved in the final analysis. FreeSurfer was used to segment the thalamic subnuclei, and MRtrix was used to perform the preprocessing and tractography. Fractional anisotropy, axial diffusivity, mean diffusivity, radial diffusivity, and streamline count of thalamic subnuclear tracts were measured as proxies of white matter microstructure. Bayesian multilevel model was used to assess group differences in white matter metrics for each thalamic subnuclear tract and the association between these white matter metrics and clinical features in MDD.

Evidence was found for reduced whiter matter metrics of the tracts spanning from all thalamic subnuclei among MDD versus HC participants. Moreover, evidence was found that white matter in various thalamic subnuclear tracts is related to medication status, age of onset and recurrence in MDD.

Structural connectivity was generally reduced in thalamic subnuclei in MDD participants. Several clinical characteristics are related to perturbed subnuclear thalamic connectivity with cortical and subcortical circuits that govern sensory processing, emotional function, and goal-directed behavior.

Alzheimer's disease is a disabling neurodegenerative disorder for which no effective treatment currently exists. To predict the diagnosis of Alzheimer's disease could be crucial for patients' outcome, but current Alzheimer's disease biomarkers are invasive, time consuming or expensive. Thus, developing MRI-based computational methods for Alzheimer's disease early diagnosis would be essential to narrow down the phenotypic measures predictive of cognitive decline. Amnestic mild cognitive impairment (aMCI) is associated with higher risk for Alzheimer's disease, and here, we aimed to identify MRI-based quantitative rules to predict aMCI to possible Alzheimer's disease conversion, applying different machine learning algorithms sequentially. At baseline, T1-weighted brain images were collected for 104 aMCI patients and processed to obtain 146 volumetric measures of cerebral grey matter regions [regions of interest (ROIs)]. One year later, patients were classified as converters (aMCI-c = 32) or non-converters, i.e. clinically and neuropsychologically stable (aMCI-s = 72) based on cognitive performance. Feature selection was performed by random forest (RF), and the identified seven ROIs volumetric data were used to implement support vector machine (SVM) and decision tree (DT) classification algorithms. Both SVM and DT reached an average accuracy of 86% in identifying aMCI-c and aMCI-s. DT found a critical threshold volume of the right entorhinal cortex (EC-r) as the first feature for differentiating aMCI-c/aMCI-s. Almost all aMCI-c had an EC-r volume <1286 mm3, while more than half of the aMCI-s patients had a volume above the identified threshold for this structure. Other key regions for the classification between aMCI-c/aMCI-s were the left lateral occipital (LOC-l), the middle temporal gyrus and the temporal pole cortices. Our study reinforces previous evidence suggesting that the morphometry of the EC-r and LOC-l best predicts aMCI to Alzheimer's disease conversion. Further investigations are needed prior to deeming our findings as a broadly applicable predictive framework. However, here, a first indication was derived for volumetric thresholds that, being easy to obtain, may assist in early identification of Alzheimer's disease in clinical practice, thus contributing to establishing MRI as a useful non-invasive prognostic instrument for dementia onset.

Alzheimer's disease may be associated with early dopamine dysfunction. However, its effects on neurofunctional alterations in the neurotransmission pathways remain elusive. In this study, positron emission tomography atlases and functional MRI data for 86 older adults with mild cognitive impairment Alzheimer's disease (MCI), 58 with mild Alzheimer's disease-dementia and 76 cognitively unimpaired were combined to investigate connectivity alterations associated with the dopaminergic and cholinergic systems. A cross-sectional design was used to compare neurotransmitter-related functional connectivity across groups and associations between functional connectivity and cognitive performance. The findings show that the Alzheimer's disease dementia group showed a decline in mesocorticolimbic dopamine-related connectivity in the precuneus but heightened connectivity in the thalamus, whereas the Alzheimer's disease-MCI group showed a decline in nigrostriatal connectivity in the left temporal areas. Acetylcholine-related connectivity decline was observed in both Alzheimer's disease-MCI and Alzheimer's disease-dementia primarily in the temporo-parietal areas. Episodic memory scores correlated positively with acetylcholine- and dopamine-related connectivity in the temporo-parietal cortex and negatively with dopamine-related functional connectivity in the fronto-thalamic areas. This study shows that connectivity alterations in acetylcholine and dopamine functional pathways parallel cognitive decline in Alzheimer's disease and might be a clinically relevant marker in early Alzheimer's disease.

Tinnitus is a condition in which individuals perceive sounds, such as ringing or buzzing, without any external source. Although the exact cause is not fully understood, recent studies have indicated the involvement of nonauditory brain structures, including the limbic system. We aimed to compare the volumes of specific brain structures between patients with tinnitus and controls.

Voxel-based morphometry and subfield volumetry were applied to analyze the brain structures of 53 patients with tinnitus and 52 age- and sex-matched controls. The volumes of the amygdala, hippocampus, and thalamus were measured and compared between the groups.

Patients with tinnitus had larger volumes in the whole amygdala, basal nucleus, right lateral nucleus, and left paralaminar nucleus compared with controls. In addition, the subiculum head, left fimbria, and left presubiculum head in the hippocampus were larger in patients with tinnitus. No differences were found in the total thalamic volume or thalamic subnuclei between groups. The gray matter volumes in the thalamus, amygdala, and hippocampus were significantly high in the tinnitus group. The cortical thicknesses of both of the marginal branches of the cingulate sulcus, the left superior parietal lobule, and the left subparietal sulcus were also high in the tinnitus group.

These findings indicate the involvement of the limbic system in tinnitus, and enhance our understanding of the condition. The subfield volumetry technique used in this study may aid in identifying the structural differences associated with specific neurological and psychiatric conditions.

Temporal lobe epilepsy (TLE) can lead to structural brain abnormalities, with thalamus atrophy being the most common extratemporal alteration. This study used probabilistic tractography to investigate the structural connectivity between individual thalamic nuclei and the hippocampus in TLE.

Thirty-six TLE patients who underwent pre-surgical 3 Tesla magnetic resonance imaging (MRI) and 18 healthy controls were enrolled in this study. Patients were subdivided into TLE with HS (TLE-HS) and MRI-negative TLE (TLE-MRneg). Tractography and whole brain segmentation, including thalamus parcellation, were performed to determine the number of streamlines per mm3 between the thalamic nuclei and hippocampus. Connectivity strength and volume of regions were correlated with clinical data.

The volume of the entire thalamus ipsilateral to seizure onset was significantly decreased in TLE-HS compared to controls (Mann-Whitney-U test: pFDR < 0.01) with the anterior thalamic nuclei (ANT) as important contributor. Furthermore, decreased ipsilateral connectivity strength between the hippocampus and ANT was detected in TLE-HS (pFDR < 0.01) compared to TLE-MRneg and controls which correlated negatively with the duration of epilepsy (ρ = -0.512, p = 0.025) and positively with seizure frequency (ρ = 0.603, p = 0.006). Moreover, ANT volume correlated negatively with epilepsy duration in TLE-HS (ρ = -0.471, p = 0.042).

ANT showed atrophy and decreased connectivity in TLE-HS, which correlated with epilepsy duration and seizure frequency. Understanding the dynamics of epileptogenic networks has the potential to shed light on surgery-resistant epilepsy and refine the selection process for ideal neurosurgical candidates, consequently enhancing post-surgical outcomes.

Converging evidence from clinical neuroimaging and animal models has strongly implicated dysfunction of thalamocortical circuits in the pathophysiology of schizophrenia. Preclinical models of genetic risk for schizophrenia have shown reduced synaptic transmission from auditory thalamus to primary auditory cortex, which may represent a correlate of auditory disturbances such as hallucinations. Human neuroimaging studies, however, have found a generalized increase in resting state functional connectivity (RSFC) between whole thalamus and sensorimotor cortex in people with schizophrenia (PSZ). We aimed to more directly translate preclinical findings by specifically localizing auditory and visual thalamic nuclei in unmedicated PSZ and measuring RSFC to primary sensory cortices.

In this case-control study, 82 unmedicated PSZ and 55 matched healthy controls (HC) completed RSFC functional magnetic resonance imaging (fMRI). Auditory and visual thalamic nuclei were localized for 55 unmedicated PSZ and 46 HC who additionally completed a sensory thalamic nuclei localizer fMRI task (N = 101). Using localized nuclei as RSFC seeds we assessed group differences in auditory and visual thalamocortical connectivity and associations with positive symptom severity.

Auditory thalamocortical connectivity was not significantly different between PSZ and HC, but hyperconnectivity was associated with greater positive symptom severity in bilateral superior temporal gyrus. Visual thalamocortical connectivity was significantly greater in PSZ relative to HC in secondary and higher-order visual cortex, but not predictive of positive symptom severity.

These results indicate that visual thalamocortical hyperconnectivity is a generalized marker of schizophrenia, while hyperconnectivity in auditory thalamocortical circuits relates more specifically to positive symptom severity.