Corpus Callosum Research Articles

Targeted Transarterial Embolization for Treatment of a Symptomatic Venous Varix in the Draining Vein of an Arteriovenous Malformation: Case Report and Literature Review.

Venous varices in the draining vein of arteriovenous malformations (AVMs) can result in compression symptoms. This condition is extremely rare, and its treatments and long-term outcomes are unresolved. Herein, we describe the treatment of a thrombosed venous varix in a draining vein and review the relevant literature. The patient presented with progressive right-sided hemiparesis and aphasia. Magnetic resonance imaging revealed flow void accumulation from the corpus callosum to the left ventricle and a 30-mm mass in the left putamen. The patient underwent targeted transarterial embolization to reduce the blood flow to the venous varix and relieve the neurologic symptoms. The patient had recovered completely from the right hemiparesis and aphasia 4 years after treatment, with a modified Rankin scale score of 0. Targeted transarterial embolization for symptomatic venous varix is a palliative treatment that may improve long-term functional outcomes.

Spectris™ treatment preserves corpus callosum structure in Alzheimer's disease.

To examine the impact of 40Hz gamma stimulation on the preservation of the corpus callosum, a critical structure for interhemispheric connectivity, in people with mild cognitive impairment or Alzheimer's disease. OVERTURE (NCT03556280) participants were randomized 2:1 (Active:Sham) to receive daily, 1-h, 40Hz gamma sensory stimulation or sham treatment for 6 months. Structural magnetic resonance imaging data were analyzed to assess changes in corpus callosum area (N = 50; 33 for active, 17 for sham). Bayesian linear mixed-effects modeling was used to assess differences in longitudinal changes of corpus callosum area between the two treatment groups. All observed differences in corpus callosum area favored the active treatment group. Differences were observed in the total corpus callosum area (2.28 ± 0.87%, p < 0.02) and its subregions, including genu/rostrum (2.36 ± 0.90%, p < 0.02), anterior-body (2.64 ± 1.26%, p < 0.04), mid-body (2.79 ± 1.18%, p < 0.03), posterior-body (2.87 ± 1.41%, p < 0.05), and splenium (1.58 ± 0.73%, p < 0.04). Total corpus callosum area and some of the sub-regional differences, such as genu/rostrum and splenium, were observed as early as 3 months after commencement of treatment. The structural magnetic resonance imaging results from the OVERTURE Phase 2 study suggest that 6 months of non-invasive 40Hz stimulation reduces the rate of atrophy of the corpus callosum in individuals with Alzheimer's disease. The preservation of structural integrity in the corpus callosum, crucial for interhemispheric communication and cognitive function, may be achievable through this non-invasive approach, potentially providing a promising disease-modifying alternative in Alzheimer's disease management.

Mild Encephalopathy/Encephalitis with Reversible Splenial Lesions after Amphetamine and Opioid Use.

A 47-year-old woman with a history of substance abuse, depression, and insomnia experienced a collapse. Upon arrival at the hospital, the patient displayed low systolic blood pressure, confusion, dehydration, and renal failure. Urine tests confirmed an amphetamine and opioid overdose. Her condition fluctuated with reduced consciousness, myoclonic movements, fever, and suspected psychogenic seizures. Brain magnetic resonance imaging revealed abnormalities in the splenium of the corpus callosum, which later resolved. The patient's condition gradually improved without any specific treatment. This unique case represents the first report of mild encephalopathy/encephalitis with reversible splenial lesions associated with amphetamine and opioid use.

Pirfenidone mitigates demyelination and electrophysiological alterations in multiple sclerosis: Targeting NF-κB, sirt1, and neurotrophic genes.

Multiple sclerosis (MS) is a demyelinating disease affecting thecentral nervous system associated with progressive neurodegeneration. Pirfenidone (Pir) is a well-known antifibrotic agent; however, Pir's function in MS is little explored. We evaluated the neuroprotective effects of Pir in MS and its possible underlying mechanisms. Forty male Swiss mice were divided equally into control, cuprizone (CPZ), Pir, and CPZ + Pir groups. Assessment of motor function was conducted using neurobehavioral tests, EMG, and nerve conduction velocity (NCV). Mice's brains were extracted to measure oxidative stress, neuroinflammatory markers, and the expression of neurotrophic genes. The corpus callosum and the sciatic nerve were subjected to histopathological and immunohistochemical studies. The CPZ group was associated with significant reductions in muscle power, frequency of contraction, sciatic NCV, SOD, IL-10, SIRT1, NGF, and neuregulin-1. Significant increases in MDA, TNF-α, INF-γ, IL-17, TGF-β, and NF-κB were also detected. Multiple areas of partially demyelinated nerve fibers in the corpus callosum, the loss of oligodendrocyte nuclei, and increased microglia and astrocytes were also observed. The sciatic nerve revealed partial demyelination with significantly reduced myelin basic protein (MBP) expression. Pir significantly restored motor function, demyelination, and neurodegenerative changes induced by CPZ. Besides the antifibrotic action of Pir, we concluded that it improves motor function in MS by alleviating the demyelinating process and neurodegeneration. Its potential anti-inflammatory, antioxidant, and antifibrotic properties could be contributing factors. These effects could be mediated by modulating the NF-κB, SIRT1, NGF, and neuregulin-1 pathways. Pir is a promising agent for treating MS.

Isolated intracranial myeloid sarcoma as an acute myeloid leukemia relapse: A case report

Abstract Introduction/Objective Adequate assessment during intraoperative consultation on a patient with a brain mass is imperative to provide critical information that will direct the therapeutic approach during surgery. Methods/Case Report The patient is a 67-year-old female with acute myeloid leukemia (AML) on maintenance therapy and in remission for the past 2 years that developed altered mental status and seizures. Imaging revealed a diffuse intra-axial mass within the corpus callosum and right hypothalamic region. A brain stereotactic biopsy was performed. Blood work showed mild leukopenia (3.63x109/L), thrombocytopenia (platelet count of 82x109/L), and an essential normal hemoglobin level of 11.9 g/dL. A frozen section assessment during intraoperative consultation revealed an infiltration of small blue cells, suggesting a hematolymphoid process. Further histological assessment showed small to intermediate-sized monomorphic cells in sheets and around the vessels with open fine chromatin, prominent nuclei, and scant cytoplasm admixed with tingible body macrophages. Differential diagnoses included high- grade B-cell lymphoma, Burkitt lymphoma, mantle cell lymphoma blastoid variant, lymphoblastic lymphoma, and myeloid sarcoma (MS). The tumor cells were positive for CD34, CD43, and MPO (subset) and negative for CD20, PAX5, TdT, CD3, and AE1/AE3 by immunohistochemical staining, consistent with MS. Concurrent bone marrow biopsy with flow cytometric evaluation showed progressive trilineage hematopoiesis without evidence of residual leukemia. Results (if a Case Study enter NA) NA Conclusion Intracranial MS is extremely rare, and literature reviews are limited to primarily case reports. MS can occur before, during, or after the initial presentation of AML. Interestingly, this patient had an isolated intracranial myeloid sarcoma as an AML relapse without bone marrow involvement. We aim to increase the awareness of isolated recurrence of AML in the form of an intracranial MS; this disease warrants consideration in patients with a history of a myeloid neoplasm who present with neurological symptoms despite the absence of peripheral disease.

Neuroradiologic, clinic and genetic characterization of cerebellar heterotopia: a pediatric multicentric study.

Background and purpose:Cerebellar heterotopia (CH) is a neuroradiological abnormality poorly reported and investigated in the literature. It can be observed as an isolated finding, but it has been mainly reported in the context of cerebellar dysgenesis and in syndromic conditions. The aim of this study is to provide a comprehensive neuroradiological, clinical, and genetic characterization of a cohort of pediatric patients with cerebellar heterotopia.Materials and methods:Patients with a diagnosis of CH were systematically selected from the neuroimaging databases of the four Italian Centers participating in this retrospective study. For each patient, information regarding demographic, clinical, genetic and neuroradiological data were collected.Results:Thirty-two pediatric patients were recruited and subdivided into two groups: patients with isolated CH and/or cerebellar malformations (n= 18) and patients with CH associated with cerebral malformations (n=14). Isolated CH consistently showed a peripheral subcortical localization in the inferior portion of cerebellar hemispheres, with either unilateral or bilateral distribution. Ten patients belonging to the second group had a diagnosis of CHARGE syndrome, and their nodules of CH were mainly but not exclusively bilateral, symmetric, located in the peripheral subcortical zone and in the inferior portion of the cerebellar hemispheres; the remaining 4 patients of the second group, showed either bilateral or unilateral CH, located in both peripheral cortex and deep white matter and in the superior and inferior portions of cerebellum. Patients with isolated CH showed high prevalence of language development delay; neurodevelopmental disorders were the most represented clinical diagnoses. Recurring features were behavioral problems and motor difficulties. A conclusive genetic diagnosis was found in 18/32 patients.Conclusions:We found distinctive neuroradiological patterns of CH. Genetic results raise the possibility of a correlation between cerebellar morphological and functional developmental disruption, underscoring the importance of CH detection and reporting to orient the diagnostic path.Abbreviations CH Cerebellar heterotopia; MRI Magnetic resonance imaging; CC Corpus callosum; ASD autism spectrum disorder; IVH inferior vermian hypoplasia.

NEURONAL INJURY DRIVES GLIOBLASTOMA INITIATION

Abstract AIMS Glioblastoma (GBM), the most common primary brain malignancy in adults, remains incurable. Pervasive heterogeneity and plasticity underpin therapy resistance and lethal recurrence, suggesting that prevention or earlier intervention may be required. Improved understanding of GBM initiation is a prerequisite for achieving this goal. GBM frequently originates from neural stem cells (NSCs) of the subventricular zone, which, upon acquisition of mutations, migrate away from their niche and form tumours at distal sites through unknown mechanisms. Here, we explored GBM initiation and its microenvironment. METHOD We combined a murine somatic GBM model which faithfully recapitulates the human disease with PDX models and patient tissue datasets. We used immunohistochemistry, scRNA-sequencing, immuno-phenotyping, behavioural and survival studies and in vivo gain- and loss-of-function experiments in Sarm1-/- lines. RESULTS Time-course analysis of tumour development identified neuronal degeneration as an early event in GBM tumourigenesis, occurring preferentially in white matter, where we find mutated NSCs are immediately rerouted. Axonal loss was accompanied by a robust inflammatory response, marked by microglial and astrocytic activation. Neuronal degeneration played a causative role, in that transection injury of corpus callosum axons accelerated tumourigenesis and, conversely, GBM development was delayed in Sarm1-/- mice with impaired Wallerian degeneration, a major mode of neuronal death following injury. Consistently, terminal Sarm1-/- tumours were more diffuse, contained more immature tumour cells and were less immune-infiltrated than their WT counterparts. Strikingly, behavioural studies revealed that Sarm1-/- tumour-bearing mice also retained improved motor performance compared to WT mice, even at terminal disease stages. CONCLUSION Our work provides important insights into GBM development, identifying white matter injury as a key initiating event, elicited by early tumour cells and orchestrated by neuronal degeneration. It identifies Wallerian degeneration, a druggable pathway already in clinical trials for neurodegenerative diseases, as a therapeutic target for GBM, with the potential to extend survival and ameliorate cognition.

Neuropathologic Findings and Electrolyte Abnormalities in a Case of Lennox-Gastaut Syndrome (SCN2a- related) Encountered at Autopsy

Abstract Introduction/Objective Lennox-Gastaut syndrome is a severe form of childhood epilepsy which may be due to several conditions, including sodium channelopathies which alter neuronal firing patterns. We present a case of a 6-year-old female with Lennox-Gastaut syndrome (SCN2A-related) complicated by developmental delay, spastic quadriplegia, and gastrojejunostomy tube dependence who was referred for medicolegal autopsy due to death subsequent to becoming unresponsive during a supervised bath. Methods/Case Report A complete autopsy was performed, including gross and microscopic examination of all primary organ systems, formal neuropathologic examination, and postmortem microbiology, toxicology, and vitreous electrolyte studies. The decedent showed evidence of developmental delay and flexion contractures of the extremities. No significant traumatic injuries were identified. A postmortem nasopharyngeal swab was positive for Rhinovirus/Enterovirus and Influenza A H3. A postmortem vitreous electrolyte panel demonstrated a dehydration pattern, including markedly elevated sodium and chloride and elevated urea nitrogen. Gross examination of the brain showed a thin corpus callosum, small hippocampi, as well as abnormal cerebellar dentate and inferior olivary nuclei. Microscopic examination of the brain tissue supported the gross findings, including dentato-olivary dysplasia. The cause of death was certified as dehydration complicating Lennox-Gastaut syndrome (SCN2a-related). Rhinovirus/Enterovirus and Influenza A H3 infections were considered contributory to death. The manner of death remained undetermined, since it was unknown if the decedent’s natural diseases, issues following a scheduled gastrojejunostomy feeding regimen, neglect, or some combination thereof caused the dehydration. Results (if a Case Study enter NA) NA Conclusion This case highlights unique and rarely documented neuropathologic findings and electrolyte abnormalities that may be seen in Lennox-Gastaut syndrome associated with an SCN2A mutation in addition to demonstrating the challenges of cause and manner death certification in cases of severe developmental disorders of childhood related to sodium channelopathies.

Clinical analysis of Marchiafava-Bignami disease

BackgroundMarchiafava-Bignami disease (MBD) is an exceptionally rare condition, a fact that should pique the professional curiosity of medical practitioners. In recent years, case reports of this disease have been infrequent, and no comprehensive analysis or summary of the characteristics of the published cases has been conducted.MethodsWe collected the medical records of three patients treated at our hospital from March 2022 to March 2023. Furthermore, we searched PubMed for “case reports” from January 2017 to March 2023 and included 30 cases. By retrospectively analyzing these 33 cases, we summarized the characteristics of the disease.ResultsBased on our analysis, we found that MBD primarily affects middle-aged men and typically has an acute or subacute onset, with the primary clinical manifestations being disturbances of consciousness, speech disorders, cognitive impairment, and psychiatric or behavioral abnormalities, often leading to misdiagnosis of psychiatric disorders. Most patients have a history of alcohol consumption or malnutrition. Head CT or MRI revealed symmetric lesions in the corpus callosum, with the splenium being the most commonly affected area. Lesions might also involve white matter outside the corpus callosum, and a wider range of lesions suggested a poor prognosis. However, the prognosis is generally favorable with timely and adequate administration of B vitamins, providing reassurance to medical professionals and patients alike.ConclusionThe early recognition and treatment of Marchiafava-Bignami disease are paramount, as they can significantly improve the prognosis. This underscores the critical need for prompt clinical intervention in the early stages of the disease, instilling a sense of urgency and significance in the work of medical professionals.

A Systematic Review of EEG and MRI Features for Predicting Long-Term Neurological Outcomes in Cooled Neonates With Hypoxic-Ischemic Encephalopathy (HIE).

Neonatal hypoxic-ischemic encephalopathy (HIE) represents a significant global disease burden, but more importantly, it leaves a lasting impact of disability on individual children and their families.HIE outcome prognostication is important for guiding clinical interventions and counseling families. The objective of this study was to systematically review early electroencephalogram (EEG) and magnetic resonance imaging (MRI) features associated with long-term neurological outcomes in infants after perinatal HIE. Articles were extracted from PubMed, CINAHL, and Scopus. Twenty studies were included that assessed EEG and/or MRI patterns in neonates who underwent therapeutic hypothermia and were followed to determine long-term outcomes. Articles that did not meet the inclusion criteria were excluded. Covidence review manager (Melbourne, Australia: Covidence) was used to extract, evaluate, and synthesize review results. Of the articles included, eight focused on EEG features, eight on MRI features, and four on assessments using both EEG and MRI. Abnormal EEG background and burst suppression severity were associated with poor outcomes. Higher MRI injury scores in the basal ganglia and thalamus were also correlated with poor outcomes. Finally, studies also revealed restricted diffusion and greater lesion size in the subcortical gray matter correlated with poor outcomes. We also identified limitations in the included studies which primarily involved sample size, potential for MRI pseudonormalization, and the potential tradeoff between retention of infants able to receive long-term follow-up and attrition of those lost to follow-up. We conclude that EEG background patterns, MRI scoring, subcortical lesion burden, and MRI diffusivity are sensitive metrics for predicting outcomes. Both early EEG and MRI features may serve as high-fidelity biomarkers for secondary energy failure and for counseling families of neonates at high risk for devastating neurologic outcomes. Additionally, there is a paucity of information on the impact of HIE on brain areas outside of the standard clinical basal-ganglia and watershed patterns, especially in locations like the corpus callosum. Finally, MRI pseudonormalization may underestimate the extent of injury in these studies.

A Mouse Model of Temporal Lobe Contusion.

Trauma to the brain can induce a contusion characterized by a discrete intracerebral or diffuse interstitial hemorrhage. In humans, "computed tomography-positive," that is, hemorrhagic, temporal lobe contusions (tlCont) have unique sequelae. TlCont confers significantly increased odds for moderate or worse disability and the inability to return to baseline work capacity compared to intra-axial injuries in other locations. Patients with tlCont are at elevated risks of memory dysfunction, anxiety, and post-traumatic epilepsy due to involvement of neuroanatomical structures unique to the temporal lobe including the amygdala, hippocampus, and ento-/perirhinal cortex. Because of the relative inaccessibility of the temporal lobe in rodents, no preclinical model of tlCont has been described, impeding progress in elucidating the specific pathophysiology unique to tlCont. Here, we present a minimally invasive mouse model of tlCont with the contusion characterized by a traumatic interstitial hemorrhage. Mortality was low and sensorimotor deficits (beam walk, accelerating rotarod) resolved completely within 3-5 days. However, significant deficits in memory (novel object recognition, Morris water maze) and anxiety (elevated plus maze) persisted at 14-35 days and nonconvulsive electroencephalographic seizures and spiking were significantly increased in the hippocampus at 7-21 days. Immunohistochemistry showed widespread astrogliosis and microgliosis, bilateral hippocampal sclerosis, bilateral loss of hippocampal and cortical inhibitory parvalbumin neurons, and evidence of interhemispheric connectional diaschisis involving the fiber bundle in the ventral corpus callosum that connects temporal lobe structures. This model may be useful to advance our understanding of the unique features of tlCont in humans.

Comparisons of MR and EM inferred tissue microstructure properties using a human autopsy corpus callosum sample

Degeneration of white matter (WM) microstructure in the central nervous system is characteristic of many neurodegenerative conditions. Previous research indicates that axonal degeneration visible in ex vivo electron microscopy (EM) photomicrographs precede the onset of clinical symptoms. Measuring WM microstructural features, such as axon diameter and packing fraction, currently require these highly invasive methods of analysis and it is therefore of great importance to develop methods for in vivo measurements. Diffusion weighted Magnetic Resonance Imaging (MRI) is a non-invasive method which can be used in conjunction with temporal diffusion spectroscopy (TDS) and an oscillating gradient spin echo (OGSE) pulse sequence to probe micron-scale structures within neural tissue. The current experiment aims to compare axon diameter measurements, mean effective axon diameter (AxD¯), and packing fractions calculated from EM histopathological analysis and inferred values from MR images. Mathematical models of axon diameters used for analysis include the ActiveAx Frequency-Dependent Extra-Axonal Diffusion (AAD) model and the AxCaliber Frequency-Dependent Extra-Axonal Diffusion (ACD) model using ROI (Region of Interest) based analysis (RBA) and voxel-based analysis (VBA), respectively. Overall, it was observed that MRI inferred WM microstructural parameters overestimate those calculated from EM. This may be attributable to tissue shrinkage during EM dehydration, the sensitivity of MR pulse sequences to larger diameter axons, and/or inaccurate model assumptions. The results of the current study provide a means to characterize the precision and accuracy of RBA-ACD and VBA-AAD OGSE-TDS and highlight the need for further research investigating the relationship between ex vivo MRI and EM, with the goal of reaching in vivo MRI.

White matter alterations associated with chronic cannabis use disorder: a structural network and fixel-based analysis

Cannabis use disorder (CUD) is associated with adverse mental health effects, as well as social and cognitive impairment. Given prevalence rates of CUD are increasing, there is considerable efforts, and need, to identify prognostic markers which may aid in minimising any harm associated with this condition. Previous neuroimaging studies have revealed changes in white matter (WM) organization in people with CUD, though, the findings are mixed. In this study, we applied MRI-based analysis techniques that offer complimentary mechanistic insights, i.e., a connectome approach and fixel-based analysis (FBA) to investigate properties of individual WM fibre populations and their microstructure across the entire brain, providing a highly sensitive approach to detect subtle changes and overcome limitations of previous diffusion models. We compared 56 individuals with CUD (median age 25 years) to a sample of 38 healthy individuals (median age 31.5 years). Compared to controls, those with CUD had significantly increased structural connectivity strength (FDR corrected) across 9 edges between the right parietal cortex and several cortical and subcortical regions, including left orbitofrontal, left temporal pole, and left hippocampus and putamen. Utilizing FBA, WM density was significantly higher in those with CUD (FWE-corrected) across the splenium of the corpus callosum, and lower in the bilateral cingulum and right cerebellum. We observed significant correlation between cannabis use over the past month and connectivity strength of the frontoparietal edge, and between age of regular use and WM density of the bilateral cingulum and right cerebellum. Our findings enhance the understanding of WM architecture alterations associated with CUD.

A history of traumatic brain injury is associated with poorer cognition and imaging evidence of altered white matter tract integrity in UK Biobank (n = 50 376)

Abstract Traumatic brain injury (TBI) is a risk factor for neurodegenerative disease. We currently have no means to identify patients most at risk of neurodegenerative disease following injury and, resultantly, no means to target risk mitigation interventions. To address this, we explored the association between history of traumatic brain injury with cognitive performance and imaging measures of white matter integrity. From the UK Biobank imaging sub-study (n = 50 376), participants were identified with either self-reported (n = 177) or health record coded broad- (injury codes; n = 1096) or narrow-band (TBI specific codes; n = 274) TBI, or as controls with no such documented history (n = 49 280). Cognitive scores and imaging measures of corpus callosum white matter integrity were compared between injury participants (versus no injury), corrected for age, sex, socioeconomic status and medications. TBI was associated with poorer cognitive and imaging phenotypes. The strongest deleterious associations were for narrow-band injury (β difference 0.2–0.3; P &amp;lt; 0.01). All cognitive and imaging phenotypes were strongly inter-correlated (P &amp;lt; 0.001). This study provides insight into possible early biomarkers predating neurodegenerative disease following brain injury. Measures of cognition and white matter following injury may provide means to identify individuals most at risk of neurodegenerative disease, to which mitigation strategies might be targeted.

Pituitary gland duplication syndrome - An international imaging analysis.

Duplication of the pituitary gland is a rare developmental anomaly. Multiple associated craniofacial malformations have previously been reported with the largest series to date consisting of five patients. In this multi-institutional series of ten patients, we present a detailed review of the imaging features and discuss a possible overarching pathogenesis that would explain most of the detected malformations. Inclusion criteria for this retrospective imaging review were the presence of a pituitary stalk and gland duplication and the characteristic appearance of the hypothalamic ventral midline. In addition to the clinical presentation, we recorded the imaging findings of ten patients (9 female) through onsite and online reviews. Genetic analysis was available for six patients. The duplicated pituitary stalk and gland showed normal imaging appearances in all patients. Mammillary bodies were clearly identified lateral to the characteristic prominence of the hypothalamic ventral midline. Strands of tissue extending to the anterior dura ("limited ventral myeloschisis") were noted at the medulla oblongata in 10, and at the cervical spinal cord in 7 patients. The medulla oblongata showed a "butterfly" appearance on axial images in 9 patients. Ten patients had cervical segmentation anomalies ("zipper"-like), 9 anterior-posterior brainstem patterning defects (small pons, elongated medulla), and corpus callosum measurements were abnormal in all patients. Three patients each presented with diencephalic-mesencephalic junction abnormalities and 4 with an anterior mesencephalic "cap". An oropharyngeal teratoma was present in four patients. Genetics was normal in three of the six patients studied; the remainder were found to have mutations in EFNB1 and a gene variant of GIT1, two copies of 7. And 8. exon of SMN1 gene, and 2.126 megabase duplication at bands q11.1 and q11.2 of one chromosome 15, respectively. Duplication of the pituitary gland presents as well-defined craniofacial and cervical spine malformation phenotype. Axial mesoderm duplication generating an excess of Sonic Hedgehog may be the primary embryological driver leading to this condition. CFNS＝ Craniofrontonasal Syndrome; DPG＝ Duplication of the Pituitary Gland; SHH＝ Sonic Hedgehog.

Slight and hidden hearing loss in young rats is associated with impaired recognition memory and reduced myelination in the corpus callosum.

Slight and hidden hearing loss in children have been linked to cognitive and social difficulties, and yet the neurobiological mechanisms behind these issues remain poorly understood. Most animal models focus on severe hearing loss, leaving the effects of hidden or slight hearing loss largely unexplored. To uncover the neural mechanisms connecting slight/hidden hearing loss to cognitive and social challenges, we induced hearing loss in young (4-week-old) Wistar rats through noise exposure. We then examined cognitive function (object recognition test) and social behavior (juvenile play behavior and social interaction). Changes in brain anatomy were assessed using cortical thickness and hippocampal size measurements, while (immuno)histochemical staining investigated neuronal circuitry maturation (myelin basic protein, parvalbumin, and perineuronal nets) and neurogenesis (doublecortin). Noise-exposed rats displayed slight high-frequency hearing loss (around 20 dB) and hidden hearing loss at other tested frequencies. This slight/hidden hearing loss was associated with impaired object recognition but did not alter social behavior. Slight/hidden hearing loss was associated with reduced myelin basic protein expression in the corpus callosum but no other alterations in cortical thickness, hippocampal size, or other markers of maturation and neurogenesis were found. These findings show that even slight/hidden hearing loss can lead to subtle brain alterations tied to cognitive deficits. This study emphasizes the need for further research to fully understand the brain changes associated with slight/hidden hearing loss and to pinpoint the mechanisms connecting these changes to behavioral deficits. This information is crucial to develop interventions to prevent the cognitive and social consequences of hearing loss. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

The value of amide proton transfer imaging in assessing brain damage in patients with obstructive sleep apnea

ObjectiveTo investigate the application value of amide proton transfer (APT) magnetic resonance imaging in evaluating brain damage in patients with obstructive sleep apnea (OSA). Materials and methods49 OSA patients and 25 healthy individuals matched for age and sex were included as case and control groups. All study participants underwent conventional 3D T1WI and APT imaging of the head. The APT values were measured in each of the brain regions of interest (ROI). To compare the differences in APT values of each brain region between the case and control groups, to compare the differences in the efficacy of APT values of each brain region in diagnosing OSA, and to investigate the correlation between APT values of each brain region and Apnea Hypopnea Index (AHI) and minimum blood oxygen saturation. ResultsCompared to the control group, patients with OSA had elevated APT values in several brain regions (P < 0.05), and the diagnostic efficacy of the combined diagnosis of OSA by multiple brain regions is better than that by each brain region alone.Left frontal APT values were positively correlated with AHI in the case group (r = 0.33, P = 0.020).In the case group, the APT values of bilateral frontal lobe, parietal lobe, occipital lobe, left temporal lobe, right thalamus, left internal capsule, left lenticular nucleus, right cerebellar hemisphere and splenium of corpus callosum were negatively correlated with the minimum blood oxygen saturation, and the APT values for each of the above ROIs were positively correlated. ConclusionAPT imaging has a certain value in evaluating brain damage in OSA patients, which may provide a new objective imaging basis for the clinical diagnosis of OSA.

The therapeutic potential of reduced graphene oxide in attenuating cuprizone-induced demyelination in mice.

Reduced Graphene Oxide (rGO) has unique physicochemical properties that make it suitable for therapeutic applications in neurodegenerative scenarios. This study investigates the therapeutic potential of rGO in a cuprizone-induced demyelination model in mice through histomorphological techniques and analysis of biochemical parameters. We demonstrate that daily intraperitoneal administration of rGO (1 mg/ml) for 21 days tends to reduce demyelination in the Corpus callosum by decreasing glial cell recruitment during the repair mechanism. Additionally, rGO interferes with oxidative stress markers in the brain and liver indicating potential neuroprotective effects in the central nervous system (CNS). No significant damage to vital organs was observed, suggesting that multiple doses could be used safely. However, further long-term investigations are needed to understand rGO distribution, metabolism, routes of action and associated challenges in central neurodegenerative therapies. Overall, these findings contribute to the comprehension of rGO effects in vivo, paving the way for possible future clinical research.

Conservation of structural brain connectivity in people with multiple sclerosis

ABSTRACT Multiple sclerosis (MS) is a neurodegenerative disease that affects the central nervous system. Structures affected in MS include the corpus callosum, connecting the hemispheres. Studies have shown that in mammalian brains, structural connectivity is organized according to a conservation principle, an inverse relationship between intra- and interhemispheric connectivity. The aim of this study was to replicate this conservation principle in subjects with MS and to explore how the disease interacts with it. A multicentric dataset has been analyzed including 513 people with MS and 208 healthy controls from seven different centers. Structural connectivity was quantified through various connectivity measures, and graph analysis was used to study the behavior of intra- and interhemispheric connectivity. The association between the intra- and the interhemispheric connectivity showed a similar strength for healthy controls (r = 0.38, p &amp;lt; 0.001) and people with MS (r = 0.35, p &amp;lt; 0.001). Intrahemispheric connectivity was associated with white matter fraction (r = 0.48, p &amp;lt; 0.0001), lesion volume (r = −0.44, p &amp;lt; 0.0001), and the Symbol Digit Modalities Test (r = 0.25, p &amp;lt; 0.0001). Results show that this conservation principle seems to hold for people with MS. These findings support the hypothesis that interhemispheric connectivity decreases at higher cognitive decline and disability levels, while intrahemispheric connectivity increases to maintain the balance.

Rocky Mountain Spotted Fever Encephalitis and "Starry Sky" Pattern on MRI: A Case Report.

Rocky Mountain Spotted Fever (RMSF) is a tick-borne disease caused by Rickettsia rickettsii (R. rickettsii). RMSF presents after a tick bite with fever, rash, and headache but can also cause more serious neurological manifestations. We report a case of RMSF encephalitis presenting with altered sensorium and rapid progression to coma, fever, and petechial rash, and an magnetic resonance imaging (MRI) brain notable for a "starry sky" pattern. A 61-year-old woman presented with confusion and fever and was diagnosed with a urinary tract infection. Two days later, she became comatose. MRI brain revealed lacunar infarcts in the right centrum semiovale and splenium of the corpus callosum. Lumbar puncture was notable for neutrophilic pleocytosis and elevated protein with negative bacterial and viral cultures. Empiric meningitis therapy was initiated, and she was transferred to our institution. On transfer, she was febrile, comatose, and had a diffuse petechial rash. Repeat MRI brain demonstrated diffuse, innumerable punctate foci of diffusion restriction with susceptibility-weighted signal attenuation throughout cerebral hemispheres in a "starry sky" pattern. Skin biopsy revealed perivascular lymphocytic infiltrates. Serologic RSMF antibody titers were obtained, and doxycycline was initiated for presumed RMSF encephalitis. The family opted to pursue palliative measures, given no clinical improvement. RSMF titers and postmortem PCR from brain tissue were positive for R. rickettsii. This case report highlights the clinical presentation of RMSF encephalitis. RMSF encephalitis should be suspected in a patient presenting with encephalopathy, fever, petechial rash, and MRI brain findings of diffuse punctate foci of diffusion restriction and susceptibility-weighted signal attenuation in a "starry-sky" pattern.