Vulnerability of Thalamic Nuclei at CSF Interface During the Entire Course of Multiple Sclerosis.

BACKGROUND AND OBJECTIVES: Thalamic atrophy can be used as a proxy for neurodegeneration in multiple sclerosis (MS). Some data point toward thalamic nuclei that could be affected more than others. However, the dynamic of their changes during MS evolution and the mechanisms driving their differential alterations are still uncertain. METHODS: We paired a large cohort of 1,123 patients with MS with the same number of healthy controls, all scanned with conventional 3D-T1 MRI. To highlight the main atrophic regions at the thalamic nuclei level, we validated a segmentation strategy consisting of deep learning-based synthesis of sequences, which were used for automatic multiatlas segmentation. Then, through a lifespan-based approach, we could model the dynamics of the 4 main thalamic nuclei groups. RESULTS: All analyses converged toward a higher rate of atrophy for the posterior and medial groups compared with the anterior and lateral groups. We also demonstrated that focal MS white matter lesions were associated with atrophy of groups of nuclei when specifically located within the associated thalamocortical projections. The volumes of the most affected posterior group, but also of the anterior group, were better associated with clinical disability than the volume of the whole thalamus. DISCUSSION: These findings point toward the thalamic nuclei adjacent to the third ventricle as more susceptible to neurodegeneration during the entire course of MS through potentiation of disconnection effects by regional factors. Because this information can be obtained even from standard T1-weighted MRI, this paves the way toward such an approach for future monitoring of patients with MS.

[A case of Holmes tremor in which 123I-IMP SPECT and MRI findings suggest damage to the cerebellothalamic tract and the dentato-rubro-olivary pathway].

A 75-year-old woman was referred to our department in October 2022 with ataxia and involuntary movements of the right upper and lower limbs. She had experienced a left pontine hemorrhage in March 2021, which was managed conservatively. However, she had residual right-sided hemiplegia. In addition, she had cerebellar ataxia and a 2 |Hz resting tremor of the right upper and lower limbs, which was enhanced while maintaining posture and contemplation. Based on her history, and the findings of MRI and nuclear medicine imaging, we diagnosed the patient with Holmes tremor due to pontine hemorrhage. Holmes tremor is a rare movement disorder secondary to brainstem and thalamic lesions, characterized by a unilateral low-frequency tremor. In this case, 123I-IMP SPECT and MRI shows damage to the cerebellothalamic tract and dentaro-rubro-olivary pathway.

Altered brain morphology and functional connectivity in postmenopausal women: automatic segmentation of whole-brain and thalamic subnuclei and resting-state fMRI.

The transition to menopause is associated with various physiological changes, including alterations in brain structure and function. However, menopause-related structural and functional changes are poorly understood. The purpose of this study was not only to compare the brain volume changes between premenopausal and postmenopausal women, but also to evaluate the functional connectivity between the targeted brain regions associated with structural atrophy in postmenopausal women. Each 21 premenopausal and postmenopausal women underwent magnetic resonance imaging (MRI). T1-weighted MRI and resting-state functional MRI data were used to compare the brain volume and seed-based functional connectivity, respectively. In statistical analysis, multivariate analysis of variance, with age and whole brain volume as covariates, was used to evaluate surface areas and subcortical volumes between the two groups. Postmenopausal women showed significantly smaller cortical surface, especially in the left medial orbitofrontal cortex (mOFC), right superior temporal cortex, and right lateral orbitofrontal cortex, compared to premenopausal women (p < 0.05, Bonferroni-corrected) as well as significantly decreased functional connectivity between the left mOFC and the right thalamus was observed (p < 0.005, Monte-Carlo corrected). Although postmenopausal women did not show volume atrophy in the right thalamus, the volume of the right pulvinar anterior, which is one of the distinguished thalamic subnuclei, was significantly decreased (p < 0.05, Bonferroni-corrected). Taken together, our findings suggest that diminished brain volume and functional connectivity may be linked to menopause-related symptoms caused by the lower sex hormone levels.

Effects of gene dosage and development on subcortical nuclei volumes in individuals with 22q11.2 copy number variations.

The 22q11.2 locus contains genes critical for brain development. Reciprocal Copy Number Variations (CNVs) at this locus impact risk for neurodevelopmental and psychiatric disorders. Both 22q11.2 deletions (22qDel) and duplications (22qDup) are associated with autism, but 22qDel uniquely elevates schizophrenia risk. Understanding brain phenotypes associated with these highly penetrant CNVs can provide insights into genetic pathways underlying neuropsychiatric disorders. Human neuroimaging and animal models indicate subcortical brain alterations in 22qDel, yet little is known about developmental differences across specific nuclei between reciprocal 22q11.2 CNV carriers and typically developing (TD) controls. We conducted a longitudinal MRI study in a total of 385 scans from 22qDel (n = 96, scans = 191, 53.1% female), 22qDup (n = 37, scans = 64, 45.9% female), and TD controls (n = 80, scans = 130, 51.2% female), across a wide age range (5.5-49.5 years). Volumes of the thalamus, hippocampus, amygdala, and anatomical subregions were estimated using FreeSurfer, and the linear effects of 22q11.2 gene dosage and non-linear effects of age were characterized with generalized additive mixed models (GAMMs). Positive gene dosage effects (volume increasing with copy number) were observed for total intracranial and whole hippocampus volumes, but not whole thalamus or amygdala volumes. Several amygdala subregions exhibited similar positive effects, with bi-directional effects found across thalamic nuclei. Distinct age-related trajectories were observed across the three groups. Notably, both 22qDel and 22qDup carriers exhibited flattened development of hippocampal CA2/3 subfields relative to TD controls. This study provides novel insights into the impact of 22q11.2 CNVs on subcortical brain structures and their developmental trajectories.

Bilateral thalamic high-grade astrocytomas in an early-adolescent child: A case report.

An early-adolescent girl presented with incoordination, headache, vomiting and dysphonia. MRI brain demonstrated diffuse increased T2 and FLAIR signal in bilateral thalami, consistent with anaplastic astrocytomas. A stereotactic burr-hole biopsy provided frozen tissues sections demonstrating an IDH-1 wildtype astrocytoma (anaplastic grade III according to prior WHO classification 2016-21). Chemoradiotherapy was commenced. Bilateral thalamic high-grade astrocytomas are very rare in the paediatric population and require timely diagnosis and interdisciplinary management. CT and MR imaging help point towards this diagnosis in the correct clinical context.

Functional connectome hierarchy of thalamus impacts fatigue in acute stroke patients.

This study aimed to explore the topographic features of thalamic subregions, functional connectomes and hierarchical organizations between thalamus and cortex in poststroke fatigue patients. We consecutively recruited 121 acute ischemic stroke patients (mean age: 59 years) and 46 healthy controls matched for age, sex, and educational level. The mean age was 59 years (range 19-80) and 38% of acute stroke patients were females. Resting-state functional and structural magnetic resonance imaging were conducted on all participants. The fatigue symptoms were measured using the Fatigue Severity Scale. The thalamic functional subdivisions corresponding to the canonical functional network were defined using the winner-take-all parcellation method. Thalamic functional gradients were derived using the diffusion embedding analysis. The results suggested abnormal functional connectivity of thalamic subregions primarily located in the temporal lobe, posterior cingulate gyrus, parietal lobe, and precuneus. The thalamus showed a gradual increase from the medial to the lateral in all groups, but the right thalamus shifted more laterally in poststroke fatigue patients than in non- poststroke fatigue patients. Poststroke fatigue patients also had higher gradient scores in the somatomotor network and the right medial prefrontal and premotor thalamic regions, but lower values in the right lateral prefrontal thalamus. The findings suggested that poststroke fatigue patients had altered functional connectivity and thalamocortical hierarchical organizations, providing new insights into the neural mechanisms of the thalamus.

Asymmetry of thalamic hypometabolism on FDG-PET/CT in neurofibromatosis type 1: Association with peripheral tumor burden.

BACKGROUND AND PURPOSE: Thalamic hypometabolism is a consistent finding in brain PET with F-18 fluorodeoxyglucose (FDG) in patients with neurofibromatosis type 1 (NF1). However, the pathophysiology of this metabolic alteration is unknown. We hypothesized that it might be secondary to disturbance of peripheral input to the thalamus by NF1-characteristic peripheral nerve sheath tumors (PNSTs). To test this hypothesis, we investigated the relationship between thalamic FDG uptake and the number, volume, and localization of PNSTs. METHODS: This retrospective study included 22 adult NF1 patients (41% women, 36.2 ± 13.0 years) referred to whole-body FDG-PET/contrast-enhanced CT for suspected malignant transformation of PNSTs and 22 sex- and age-matched controls. Brain FDG uptake was scaled voxelwise to the individual median uptake in cerebellar gray matter. Bilateral mean and left-right asymmetry of thalamic FDG uptake were determined using a left-right symmetric anatomical thalamus mask. PNSTs were manually segmented in contrast-enhanced CT. RESULTS: Thalamic FDG uptake was reduced in NF1 patients by 2.0 standard deviations (p < .0005) compared to controls. Left-right asymmetry was increased by 1.3 standard deviations (p = .013). Thalamic hypometabolism was higher in NF1 patients with ≥3 PNSTs than in patients with ≤2 PNSTs (2.6 vs. 1.6 standard deviations, p = .032). The impact of the occurrence of paraspinal/paravertebral PNSTs and of the mean PNST volume on thalamic FDG uptake did not reach statistical significance (p = .098 and p = .189). Left-right asymmetry of thalamic FDG uptake was not associated with left-right asymmetry of PNST burden (p = .658). CONCLUSIONS: This study provides first evidence of left-right asymmetry of thalamic hypometabolism in NF1 and that it might be mediated by NF1-associated peripheral tumors.

Volumetric magnetic resonance imaging differences between complex febrile seizure and recurrent simple febrile seizure.

PURPOSE: We investigated the volumetric differences in cortical and subcortical structures between patients with complex febrile seizure (FS) and recurrent simple FS. We aimed to identify the brain morphological patterns of children with complex FS. METHODS: Twenty-five patients with complex FS and age- and sex-matched 25 patients with recurrent simple FS with structural magnetic resonance imaging (MRI) scans were studied. Cortical volumetric analysis was performed using a voxel-based morphometry method with the CAT12 toolbox within SPM12. FSL-FIRST was used to obtain volume measures of subcortical deep grey matter structures (amygdala, caudate nucleus, thalamus, nucleus accumbens, putamen, globus pallidus, and hippocampus). The volumetric asymmetry index (AI) and laterality index (LI) were calculated for each subcortical structure. RESULTS: Compared with recurrent simple FS, complex FS demonstrated lower volume in the left putamen (p = .003) and right nucleus accumbens (p = .001). Additionally, patients with complex FS presented a higher magnitude of AI of the nucleus accumbens (p < .001) compared with recurrent simple FS. CONCLUSIONS: The findings indicate that volumetric analysis may be a useful marker for the detection of FS-induced changes that reflect microstructural alterations. This study is the first to report on alterations in the putamen and nucleus accumbens in FS.

Thalamic connectivity topography in newborns with spina bifida: association with neurological functional level but not developmental outcome at 2 years.

Spina bifida affects spinal cord and cerebral development, leading to motor and cognitive delay. We investigated whether there are associations between thalamocortical connectivity topography, neurological function, and developmental outcomes in open spina bifida. Diffusion tensor MRI was used to assess thalamocortical connectivity in 44 newborns with open spina bifida who underwent prenatal surgical repair. We quantified the volume of clusters formed based on the strongest probabilistic connectivity to the frontal, parietal, and temporal cortex. Developmental outcomes were assessed using the Bayley III Scales, while the functional level of the lesion was assessed by neurological examination at 2 years of age. Higher functional level was associated with smaller thalamo-parietal, while lower functional level was associated with smaller thalamo-temporal connectivity clusters (Bonferroni-corrected P < 0.05). Lower functional levels were associated with weaker thalamic temporal connectivity, particularly in the ventrolateral and ventral anterior nuclei. No associations were found between thalamocortical connectivity and developmental outcomes. Our findings suggest that altered thalamocortical circuitry development in open spina bifida may contribute to impaired lower extremity function, impacting motor function and independent ambulation. We hypothesize that the neurologic function might not merely be caused by the spinal cord lesion, but further impacted by the disruption of cerebral neuronal circuitry.

Quantification of Thalamic Atrophy in MS: From the Multicenter Italian Neuroimaging Network Initiative Data Set to Clinical Application.

BACKGROUND AND PURPOSE: Thalamic atrophy occurs from the earliest phases of MS; however, this measure is not included in clinical practice. Our purpose was to obtain a reliable segmentation of the thalamus in MS by comparing existing automatic methods cross-sectionally and longitudinally. MATERIALS AND METHODS: MR images of 141 patients with relapsing-remitting MS (mean age, 38 years; range, 19-58 years; 95 women) and 69 healthy controls (mean age, 36 years; range, 22-69 years; 47 women) were retrieved from the Italian Neuroimaging Network Initiative repository: T1WI, T2WI, and DWI at baseline and after 1 year (136 patients, 31 healthy controls). Three segmentation software programs (FSL-FIRST, FSL-MIST, FreeSurfer) were compared. At baseline, agreement among pipelines, correlations with age, disease duration, clinical score, and T2-hyperintense lesion volume were evaluated. Effect sizes in differentiating patients and controls were assessed cross-sectionally and longitudinally. Variability of longitudinal changes in controls and sample sizes were assessed. False discovery rate-adjusted P < .05 was considered significant. RESULTS: At baseline, FSL-FIRST and FSL-MIST showed the highest agreement in the results of thalamic volume (R = 0.87, P < .001), with the highest effect size for FSL-MIST (Cohen d = 1.11); correlations with demographic and clinical variables were comparable for all software. Longitudinally, FSL-MIST showed the lowest variability in estimating thalamic volume changes for healthy controls (SD = 1.07%), the highest effect size (Cohen d = 0.44), and the smallest sample size at 80% power level (15 subjects per group). CONCLUSIONS: Multimodal segmentation by FSL-MIST increased the robustness of the results with better capability to detect small variations in thalamic volumes.

Interthalamic Adhesion: Can it be used to Diagnose Idiopathic Intracranial Hypertension?

OBJECTIVE: This retrospective study aimed at determining the dimension of the interthalamic adhesion (ITA) in patients with the idiopathic intracranial hypertension (IIH) for assisting in preoperative radiologic diagnosis. METHODS: The study universe consisted of magnetic resonance images of 20 patients with IIH (age: 22.70 ± 4.04 years, sex: 14 females and 6 males) and 20 normal subjects (age 22.30± 2.94 years, sex: 14 females and 6 males). To determine the morphology of ITA, its height (vertical diameter) and width (horizontal diameter) were measured on the coronal and axial planes, respectively. RESULTS: The height and width of ITA in IIH were measured as 2.58 ± 0.71 mm (range: 1.40-4.20 mm) and 2.73 ± 0.77 mm (range: 1.70-4.40 mm), respectively. Its height and width in controls were measured as 4.99 ± 1.04 mm (range: 2.70-6.30 mm) and 4.92 ± 1.11 mm (range: 2.60-6.50 mm), respectively. ITA height and width in IIH was significantly smaller compared with controls (P < 0.001). For an arbitrary cutoff of 3.85 mm, the sensitivity of the height of ITA was 85% with 95% specificity. For an arbitrary cutoff of 4.45 mm, the sensitivity of the width of ITA was 75% with 100% specificity. CONCLUSIONS: The height and width of ITA are approximately 50% smaller in IIH than controls; therefore alterations in the dimension of ITA may be a valuable radiologic sign for the diagnosis of IIH.

Diffusion Restriction in Bilateral Thalami: Beyond Artery of Percheron Infarct.

Background: Bilateral thalamic infarction, especially the medial thalamus, has been characteristically described in the artery of Percheron (AOP) affection. However, bilateral thalamic restriction has been described in many entities beyond the AOP infarction. Objective: Here we describe a case series (three cases) with infection as an etiology for bilateral thalamic lesions in the topographic distribution of the AOP from a tertiary care center in tropical India. Materials and Methods: : Case series during a 1-year period collecting cases with bilateral thalamic diffusion restriction on MRI who did not have thalamic infarcts and their outcomes. Results: : Bilateral thalamic lesion can occur in both bacterial and viral infections such as tuberculosis, dengue, and SARS-COV-2. Thus, we intend to add infections as one of the etiologies in the ever-expanding list of conditions that produce bilateral thalamic restriction. Conclusions: All the acute symmetric thalamic lesions are not always secondary to vascular insult. Accurate assessment and prompt diagnosis can prevent unnecessary delays in treatment. To our knowledge, this is the first case series in the literature that throws light on the bilateral thalamic lesions in the topographic distribution of the AOP secondary to infections in a tropical country like India.

Suppression of beta oscillations by delayed feedback in a cortex-basal ganglia-thalamus-pedunculopontine nucleus neural loop model.

Excessive neural synchronization of neural populations in the beta (ß) frequency range (12-35 Hz) is intimately related to the symptoms of hypokinesia in Parkinson's disease (PD). Studies have shown that delayed feedback stimulation strategies can interrupt excessive neural synchronization and effectively alleviate symptoms associated with PD dyskinesia. Work on optimizing delayed feedback algorithms continues to progress, yet it remains challenging to further improve the inhibitory effect with reduced energy expenditure. Therefore, we first established a neural mass model of the cortex-basal ganglia-thalamus-pedunculopontine nucleus (CBGTh-PPN) closed-loop system, which can reflect the internal properties of cortical and basal ganglia neurons and their intrinsic connections with thalamic and pedunculopontine nucleus neurons. Second, the inhibitory effects of three delayed feedback schemes based on the external globus pallidum (GPe) on ß oscillations were investigated separately and compared with those based on the subthalamic nucleus (STN) only. Our results show that all four delayed feedback schemes achieve effective suppression of pathological ß oscillations when using the linear delayed feedback algorithm. The comparison revealed that the three GPe-based delayed feedback stimulation strategies were able to have a greater range of oscillation suppression with reduced energy consumption, thus improving control performance effectively, suggesting that they may be more effective for the relief of Parkinson's motor symptoms in practical applications.

Thalamic nuclei volumes in schizophrenia and bipolar spectrum disorders - Associations with diagnosis and clinical characteristics.

BACKGROUND: The thalamus is central to brain functions ranging from primary sensory processing to higher-order cognition. Structural deficits in thalamic association nuclei such as the pulvinar and mediodorsal nuclei have previously been reported in schizophrenia. However, the specificity with regards to clinical presentation, and whether or not bipolar disorder (BD) is associated with similar alterations is unclear. METHODS: We investigated thalamic nuclei volumes in 334 patients with schizophrenia spectrum disorders (SSD) (median age 29 years, 59 % male), 322 patients with BD (30 years, 40 % male), and 826 healthy controls (HC) (34 years, 54 % male). Volumes of 25 thalamic nuclei were extracted from T1-weighted magnetic resonance imaging using an automated Bayesian segmentation method and compared between groups. Furthermore, we explored associations with clinical characteristics across diagnostic groups, including psychotic and mood symptoms and medication use, as well as diagnostic subtype in BD. RESULTS: Significantly smaller volumes were found in the mediodorsal, pulvinar, and lateral and medial geniculate thalamic nuclei in SSD. Similarly, smaller volumes were found in BD in the same four regions, but mediodorsal nucleus volume alterations were limited to its lateral part and pulvinar alterations to its anterior region. Smaller volumes in BD compared to HC were seen only in BD type I, not BD type II. Across diagnoses, having more negative symptoms was associated with smaller pulvinar volumes. CONCLUSIONS: Structural alterations were found in both SSD and BD, mainly in the thalamic association nuclei. Structural deficits in the pulvinar may be of relevance for negative symptoms.

Use of Thalamus L-Sign to Differentiate Periventricular Leukomalacia From Neurometabolic Disorders.

PURPOSE: To assess the diagnostic value of the thalamus L-sign on magnetic resonance imaging (MRI) in distinguishing between periventricular leukomalacia and neurometabolic disorders in pediatric patients. METHODS: In this retrospective study, clinical and imaging information was collected from 50 children with periventricular leukomalacia and 52 children with neurometabolic disorders. MRI was used to evaluate the L-sign of the thalamus (ie, injury to the posterolateral thalamus) and the lobar distribution of signal intensity changes. Age, sex, gestational age, and level of Gross Motor Function Classification System (only for periventricular leukomalacia) constituted the clinical parameters. Statistical evaluation of group differences for imaging and clinical variables were conducted using univariable statistical methods. The intra- and inter-observer agreement was evaluated using Cohen's kappa. Univariable or multivariable logistic regression was employed for selection of variables, determining independent predictors, and modeling. RESULTS: The thalamus L-sign was observed in 70% (35/50) of patients in the periventricular leukomalacia group, but in none of the patients with neurometabolic disorder (P < .001). The gestational age between groups varied significantly (P < .001). Involvement of frontal, parietal, and occipital lobes differed significantly between groups (P < .001). In the logistic regression, the best model included negative thalamus L-sign and gestational age, yielding an area under the curve, accuracy, sensitivity, specificity, and precision values of 0.995, 96.1%, 96%, 96.2%, and 96%, respectively. Both the lack of thalamus L-sign and gestational age were independent predictors (P < .001). CONCLUSIONS: The thalamus L-sign and gestational age may be useful in distinguishing between periventricular leukomalacia and neurometabolic disorders.

Research Progress on the Mechanisms of Central Post-Stroke Pain: A Review.

Central Post-Stroke Pain (CPSP) is a primary sequelae of stroke that can develop in the body part corresponding to the cerebrovascular lesion after stroke, most typically after ischemic stroke but also after hemorrhagic stroke. The pathogenesis of CPSP is currently unknown, and research into its mechanism is ongoing. To summarize current research on the CPSP mechanism and provide guidance for future studies. Use "central post-stroke pain," "stroke AND thalamic pain," "stroke AND neuropathic pain," "post-stroke thalamic pain" as the search term. The search was conducted in the PubMed and China National Knowledge Infrastructure databases, summarizing and classifying the retrieved mechanism studies. The mechanistic studies on CPSP are extensive, and we categorized the included mechanistic studies and summarized them in terms of relevant pathway studies, relevant signals and receptors, relevant neural tissues, and described endoplasmic reticulum stress and other relevant studies, as well as summarized the mechanisms of acupuncture treatment. Studies have shown that the pathogenesis of CPSP involves the entire spinal-thalamo-cortical pathway and that multiple substances in the nervous system are involved in the formation and development of CPSP. Among them, the relevant receptors and signals are the hotspot of research, and the discovery and exploration of different receptors and signals have provided a wide range of therapeutic ideas for CPSP. As a very effective treatment, acupuncture is less studied regarding the analgesic mechanism of CPSP, and further experimental studies are still needed.

Bilateral anterior thalamic symmetrical infarction: a case study.

BACKGROUND: Bilateral anterior thalamic symmetrical infarction is very rarely observed in clinical practice and has rarely been reported in the literature. In this paper we introduce a patient with bilateral anterior thalamic symmetrical infarction and discuss his symptoms, treatment process, and follow-up visit results, as well as the potential pathological mechanisms of the disease. CASE PRESENTATION: A 71-year-old male had a sudden cognitive decline four days prior to medical consultation. The patient's brain MRI showed symmetrical high signals in the anterior part of both sides of the thalamus. The patient's head MRV and immunological tests were normal, and we considered that this patient had a rare case of bilateral anterior thalamic infarction. After 10 days of anti-platelet aggregation that lowered blood lipids and improved circulation, the patient's symptoms significantly abated. Two years later, we found through telephone follow-up that the patient's symptoms had not relapsed substantially and that he was able to perform self-care, having only continued to suffer a slight decline in short-term memory. CONCLUSION: For patients with bilateral prethalamic lesions who have only acute cognitive impairment, if the lesions conform to the blood supply area of both thalamic nodular arteries and DWI shows a high signal, the diagnosis of acute cerebral infarction should be considered, and the standard treatment plan for cerebral infarction should be given as soon as possible.

Photochemically induced thalamus infarction impairs cognition in a mouse model.

BACKGROUND: Small subcortical infarcts account for up to 25% of ischaemic strokes. Thalamus is one of the subcortical structures that commonly manifest with lacunar infarcts on MRI of the brain. Studies have shown that thalamus infarction is associated with cognitive decline. However, due to the lack of proper animal models, little is known about the mechanism. We aimed to establish a focal thalamus infarction model, characterise the infarct lesion and assess functional effects. METHODS: Male C57BL/6J mice were anaesthetised, and Rose Bengal dye was injected through the tail vein. The right thalamus was illuminated with green laser light by stereotactic implantation of optic fibre. Characteristics of the infarct and lesion evolution were evaluated by histological analysis and 7T MRI at various times. The cognitive and neurological functions were assessed by behavioural tests. Retrograde tracing was performed to analyse neural connections. RESULTS: An ischaemic lesion with small vessel occlusion was observed in the thalamus. It became a small circumscribed infarct with reactive astrocytes accumulated in the infarct periphery on day 21. The mice with thalamic infarction demonstrated impaired learning and memory without significant neurological deficits. Retrogradely labelled neurons in the retrosplenial granular cortex were reduced. CONCLUSION: This study established a mouse model of thalamic lacunar infarction that exhibits cognitive impairment. Neural connection dysfunctions may play a potential role in post-stroke cognitive impairment. This model helps to clarify the pathophysiology of post-stroke cognitive impairment and to develop potential therapies.

Altered thalamic volume in patients with mild autonomous cortisol secretion: a structural brain MRI study.

PURPOSE: To compare thalamic volume and cognitive functions of patients with mild autonomous cortisol secretion (MACS) with control subjects and patients with overt Cushing's syndrome (CS). METHODS: In this cross-sectional study, volumes of regions of interest were assessed using 3 T magnetic resonance imaging and a voxel-based morphometry approach in 23 patients with MACS, 21 patients with active CS, 27 patients with CS in remission, and 21 control subjects. Cognitive functions were assessed using validated questionnaires. RESULTS: Patients with MACS had smaller left thalamic (F = 3.8, p = 0.023), left posterior thalamic (F = 4.9, p = 0.01), left medial thalamic (F = 4.7, p = 0.028), and right lateral thalamic (F = 4.1, p = 0.025) volumes than control subjects. Patients with active CS also had smaller left thalamic (F = 3.8, p = 0.044), left posterior thalamic (F = 4.9, p = 0.007), left medial thalamic (F = 4.7, p = 0.006), and right lateral thalamic (F = 4.1, p = 0.042) volumes compared to controls. Patients with CS in remission had smaller left medial (F = 4.7, p = 0.030) and right lateral thalamic (F = 4.1, p = 0.028) volumes than controls. Neuropsychological tests showed no difference between the groups. CONCLUSION: MACS may decrease thalamic volume.