Posterior Corpus Research Articles

Differences in Brain Volume and Thickness between Shammah (Smokeless Tobacco) Users and Non-Users: A Cross-Sectional Study.

Aims/Background Previous research has shown that smoking tobacco is associated with changes or differences in brain volume and cortical thickness, resulting in a smaller brain volume and decreased cortical thickness in smokers compared with non-smokers. However, the effects of smokeless tobacco on brain volume and cortical thickness remain unclear. This study aimed to investigate whether the use of shammah, a nicotine-containing smokeless tobacco popular in Middle Eastern countries, is associated with differences in brain volume and thickness compared with non-users and to assess the influence of shammah quantity and type on these effects. Methods Male shammah users (aged 20 to 47 years, n = 30) and non-users (n = 39) underwent 1.5T magnetic resonance imaging (MRI) scans, and cortical brain volumes and thicknesses were measured using FreeSurfer. Results Significant differences were found in the volume of the right pallidum (p = 0.02), total pallidum (p = 0.02), total ventricle (p = 0.02), middle posterior corpus callosum (p = 0.04), and brainstem (p = 0.02) between shammah users and non-users. Furthermore, yellow shammah users exhibited smaller volumes in the right lateral ventricle (p = 0.02), total lateral ventricle (p = 0.03), and right putamen (p = 0.02) compared with users of other types of shammah. Regarding cortical thickness, significant differences were observed in the right medial orbito-frontal thickness (p = 0.03), left rostral middle frontal thickness (p = 0.03), and right rostral anterior cingulate thickness (p = 0.04). Conclusion These findings shed light on the potential neurobiological effects of shammah use, particularly the yellow shammah, and highlighting the need for further research to fully understand its implications for brain structure and function.

Longitudinal Imaging Biomarkers Correlate with Progressive Motor Deficit in the Mouse Model of Charlevoix-Saguenay Ataxia.

In autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) disease, severity and age of onset vary greatly, hindering to objectively measure and predict clinical progression. Thickening of the retinal nerve fiber layer is distinctive of ARSACS patients, as assessed by optical coherence tomography, whereas conventional brain magnetic resonance imaging findings include both supratentorial and infratentorial changes. Because longitudinal imaging studies in ARSACS patients are not available to define these changes as biomarkers of disease progression, we aimed to address this issue in the ARSACS mouse model. We performed longitudinal retinal OCT and brain MRI in the Sacs-/- ARSACS mouse model, alongside motor and coordination assessment in the beam walking test. We also investigated visual function and the molecular mechanisms underlying RNFL increased thickness by histology and immunofluorescence. We demonstrated that RNFL thickening by OCT gradually increases in the early stages of pathology in the Sacs-/- mouse model, reflecting the progression of motor impairment, and later reaches a plateau when thinning of the posterior corpus callosum becomes detectable by MRI. Mechanistically, we unveiled that RNFL thickening is associated with aberrant accumulation of non-phosphorylated neurofilament H and glial fibrillary acidic protein. We also uncovered mild signs of myelin pathology coherent with increased latency of visual evoked potentials, and altered retinal activation by photopic electroretinography. We show that both RNFL thickening and MRI changes may represent biomarkers of disease progression in the Sacs-/- mouse model. Our data gathers knowledge instrumental to clinical studies, holding potential as readout for treatment efficacy. ANN NEUROL 2024.

Corpus callosum structure and auditory interhemispheric transfer in spina bifida myelomeningocele.

Maldevelopment of the posterior corpus callosum is common in spina bifida myelomeningocele (SBM) due to hydrocephalus-related hypoplasia and congenital partial hypogenesis. This study examined the relations of macro- and microstructural integrity of the interhemispheric temporal tract in SBM and auditory interhemispheric transfer using consonant-vowel dichotic listening. We collected T₁-weighted and diffusion tensor imaging data from 46 individuals with SBM and 15 typically developing individuals. Probabilistic tractography was used to isolate the interhemispheric white matter connecting auditory processing regions in both hemispheres. Interhemispheric transfer was assessed with a dichotic listening task. Although the typically developing group and the group with SBM showed the normative right-ear advantage, fewer participants showed a right-ear advantage in the group with SBM. The absence of the right-ear advantage was largely in the subgroup with hypogenesis of the splenium or severe posterior hypoplasia. Sex, anterior commissure cross-sectional area, and number of shunt pathways visible on magnetic resonance imaging predicted right-ear superiority. Interhemispheric transfer is disrupted in individuals with SBM and hypogenesis or severe hypoplasia of the posterior corpus callosum. Preservation of interhemispheric transfer is related to expected connections through the posterior corpus callosum and possibly compensatory pathways in the anterior commissure. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Effect of gestational age on cerebral lesions in neonatal encephalopathy

ObjectiveTo determine the risk on brain lesions according to gestational age (GA) in neonates with neonatal encephalopathy.DesignSecondary analysis of the prospective national French population-based cohort, Long-Term Outcome of NeonataL EncePhALopathy.SettingFrench...

Ultra-High Contrast MRI: The Whiteout Sign Shown with Divided Subtracted Inversion Recovery (dSIR) Sequences in Post-Insult Leukoencephalopathy Syndromes (PILS).

Ultra-high contrast (UHC) MRI describes forms of MRI in which little or no contrast is seen on conventional MRI images but very high contrast is seen with UHC techniques. One of these techniques uses the divided subtracted inversion recovery (dSIR) sequence, which, in modelling studies, can produce ten times the contrast of conventional inversion recovery (IR) sequences. When used in cases of mild traumatic brain injury (mTBI), the dSIR sequence frequently shows extensive abnormalities in white matter that appears normal when imaged with conventional T2-fluid-attenuated IR (T2-FLAIR) sequences. The changes are bilateral and symmetrical in white matter of the cerebral and cerebellar hemispheres. They partially spare the anterior and posterior central corpus callosum and peripheral white matter of the cerebral hemispheres and are described as the whiteout sign. In addition to mTBI, the whiteout sign has also been seen in methamphetamine use disorder and Grinker's myelinopathy (delayed post-hypoxic leukoencephalopathy) in the absence of abnormalities on T2-FLAIR images, and is a central component of post-insult leukoencephalopathy syndromes. This paper describes the concept of ultra-high contrast MRI, the whiteout sign, the theory underlying the use of dSIR sequences and post-insult leukoencephalopathy syndromes.

Mri findings, looking behaviour and affect recognition in very preterm children: A pilot study

Children born very preterm often exhibit atypical gaze behaviors, affect recognition difficulties and are at risk for cerebral white matter damage. This study explored links between these sequalae. In 24 12-year-old children born very preterm, ventricle size using Evans and posterior ventricle indices, and corpus callosum area were used to measure white matter thickness. The findings revealed a correlation between less attention towards the eyes and larger ventricle size. Ventricle and posterior corpus callosum sizes were correlated to affect-recognition proficiency. Findings suggest a link between white matter damage, gaze behavior, and affect recognition accuracy, emphasizing a relation with social perception.

Lesion Frequency Distribution Maps of Traumatic Axonal Injury on Early Magnetic Resonance Imaging After Moderate and Severe Traumatic Brain Injury and Associations to 12 Months Outcome.

Traumatic axonal injury (TAI) is a common finding on magnetic resonance imaging (MRI) in patients with moderate-severe traumatic brain injury (TBI), and the burden of TAI is associated with outcome in this patient group. Lesion mapping offers a way to combine imaging findings from numerous individual patients into common lesion maps where the findings from a whole patient cohort can be assessed. The aim of this study was to evaluate the spatial distribution of TAI lesions on different MRI sequences and its associations to outcome with use of lesion mapping. Included prospectively were 269 patients (8-70 years) with moderate or severe TBI and MRI within six weeks after injury. The TAI lesions were evaluated and manually segmented on fluid-attenuated inversed recovery (FLAIR), diffusion weighted imaging (DWI), and either T2* gradient echo (T2*GRE) or susceptibility weighted imaging (SWI). The segmentations were registered to the Montreal Neurological Institute space and combined to lesion frequency distribution maps. Outcome was assessed with Glasgow Outcome Scale Extended (GOSE) score at 12 months. The frequency and distribution of TAI was assessed qualitatively by visual reading. Univariable associations to outcome were assessed qualitatively by visual reading and also quantitatively with use of voxel-based lesion-symptom mapping (VLSM). The highest frequency of TAI was found in the posterior half of corpus callosum. The frequency of TAI was higher in the frontal and temporal lobes than in the parietal and occipital lobes, and in the upper parts of the brainstem than in the lower. At the group level, all voxels in mesencephalon had TAI on FLAIR. The patients with poorest outcome (GOSE scores ≤4) had higher frequencies of TAI. On VLSM, poor outcome was associated with TAI lesions bilaterally in the splenium, the right side of tectum, tegmental mesencephalon, and pons. In conclusion, we found higher frequency of TAI in posterior corpus callosum, and TAI in splenium, mesencephalon, and pons were associated with poor outcome. If lesion frequency distribution maps containing outcome information based on imaging findings from numerous patients in the future can be compared with the imaging findings from individual patients, it would offer a new tool in the clinical workup and outcome prediction of the patient with TBI.

A structural equation modeling approach using behavioral and neuroimaging markers in major depressive disorder

Major depressive disorder (MDD) has consistently proven to be a multifactorial and highly comorbid disease. Despite recent depression-related research demonstrating causalities between MDD-related factors and a small number of variables, including brain structural changes, a high-statistical power analysis of the various factors is yet to be conducted. We retrospectively analyzed data from 155 participants (84 healthy controls and 71 patients with MDD). We used magnetic resonance imaging and diffusion tensor imaging data, scales assessing childhood trauma, depression severity, cognitive dysfunction, impulsivity, and suicidal ideation. To simultaneously evaluate the causalities between multivariable, we implemented two types of MDD-specified structural equation models (SEM), the behavioral and neurobehavioral models. Behavioral SEM showed significant results in the MDD group: Comparative Fit Index [CFI] = 1.000, Root Mean Square Error of Approximation [RMSEA]) = 0.000), with a strong correlation in the scales for childhood trauma, depression severity, suicidal ideation, impulsivity, and cognitive dysfunction. Based on behavioral SEM, we established neurobehavioral models showing the best-fit in MDD, especially including the right cingulate cortex, central to the posterior corpus callosum, right putamen, pallidum, whole brainstem, and ventral diencephalon, including the thalamus (CFI >0.96, RMSEA <0.05). Our MDD-specific model revealed that the limbic-associated regions are strongly connected with childhood trauma rather than depression severity, and that they independently affect suicidal ideation and cognitive dysfunction. Furthermore, cognitive dysfunction could affect impulsivity.

Metronidazole: A culprit to balance and speech

In a country like India, oral metronidazole is the commonly prescribed drug of choice for entities such as amebiasis and visceral abscesses. Oral such cases, it is usually well tolerated and safe but can cause serious neurological adverse events. Peripheral neuropathy commonly encounters in practice but central nervous system toxicity is also well documented as it crosses the blood–brain barrier easily. Neurological toxicity of metronidazole may be due to prolonged administration, high doses, or high cumulative doses. Magnetic resonance imaging (MRI) of brain is the modality of choice to evaluate brain involvement. In the brain, the splenium of the corpus callosum, dentate nucleus of the cerebellum, and posterior pons involvement are commonly seen and diagnostic. Here, we have an interesting case report of a patient who was on oral metronidazole treatment for his large liver abscess, presenting with a complaint of neurological symptoms of unsteady gait, vertigo, dysdiadochokinesia, and difficulty in speech. Moreover, thus suspected as metronidazole drug toxicity and further investigated for the same, and MRI typically shows cerebellar and posterior corpus callosal involvement.

Smaller total and subregional cerebellar volumes in posttraumatic stress disorder: a mega-analysis by the ENIGMA-PGC PTSD workgroup

Although the cerebellum contributes to higher-order cognitive and emotional functions relevant to posttraumatic stress disorder (PTSD), prior research on cerebellar volume in PTSD is scant, particularly when considering subregions that differentially map on to motor, cognitive, and affective functions. In a sample of 4215 adults (PTSD n = 1642; Control n = 2573) across 40 sites from the ENIGMA-PGC PTSD working group, we employed a new state-of-the-art deep-learning based approach for automatic cerebellar parcellation to obtain volumetric estimates for the total cerebellum and 28 subregions. Linear mixed effects models controlling for age, gender, intracranial volume, and site were used to compare cerebellum volumes in PTSD compared to healthy controls (88% trauma-exposed). PTSD was associated with significant grey and white matter reductions of the cerebellum. Compared to controls, people with PTSD demonstrated smaller total cerebellum volume, as well as reduced volume in subregions primarily within the posterior lobe (lobule VIIB, crus II), vermis (VI, VIII), flocculonodular lobe (lobule X), and corpus medullare (all p-FDR < 0.05). Effects of PTSD on volume were consistent, and generally more robust, when examining symptom severity rather than diagnostic status. These findings implicate regionally specific cerebellar volumetric differences in the pathophysiology of PTSD. The cerebellum appears to play an important role in higher-order cognitive and emotional processes, far beyond its historical association with vestibulomotor function. Further examination of the cerebellum in trauma-related psychopathology will help to clarify how cerebellar structure and function may disrupt cognitive and affective processes at the center of translational models for PTSD.

White matter disconnection impacts proprioception post-stroke.

Proprioceptive impairments occur in approximately 50-64% of people following stroke. While much is known about the grey matter structures underlying proprioception, our understanding of the white matter correlates of proprioceptive impairments is less well developed. It is recognised that behavioural impairments post-stroke are often the result of disconnection between wide-scale brain networks, however the disconnectome associated with proprioception post-stroke is unknown. In the current study, white matter disconnection was assessed in relation to performance on a robotic arm position matching (APM) task. Neuroimaging and robotic assessments of proprioception were collected for 203 stroke survivors, approximately 2-weeks post-stroke. The robotic assessment was performed in a KINARM Exoskeleton robotic device and consisted of a nine-target APM task. First, the relationship between white matter tract lesion load and performance on the APM task was assessed. Next, differences in the disconnectome between participants with and without impairments on the APM task were examined. Greater lesion load to the superior longitudinal fasciculus (SLF II and III), arcuate fasciculus (all segments) and fronto-insular tracts were associated with worse APM task performance. In those with APM task impairments, there was, additionally, disconnection of the posterior corpus callosum, inferior fronto-occipital fasciculus, inferior longitudinal fasciculus and optic radiations. This study highlights an important perisylvian white matter network supporting proprioceptive processing in the human brain. It also identifies white matter tracts, important for relaying proprioceptive information from parietal and frontal brain regions, that are not traditionally considered proprioceptive in nature.

RADT-50. EVIDENCE-BASED MULTIVARIATE NORMAL TISSUE COMPLICATION PROBABILITY (NTCP) STUDY OF DOMAIN-SPECIFIC COGNITIVE DECLINE AFTER PARTIAL BRAIN RADIATION (RT)

Abstract Beyond the hippocampus, there are no evidence-based dose constraints for eloquent brain structures which subserve cognitive domains. We performed a multivariate NTCP analysis of post-RT neurocognitive decline, examining dosimetric predictors of eloquent brain regions in a prospective longitudinal clinical trial. 83 patients with primary brain tumors receiving fractionated RT completed comprehensive neurocognitive evaluation and high-resolution volumetric and diffusion MRI at baseline and 6 months post-RT. Image processing using robust, validated automated segmentation parcellated individual white matter (WM) tracts, cortical regions, and hippocampi. Well-validated neurocognitive tests evaluating multiple cognitive domains were assessed with negative reliable change indices adjusted for practice effects between timepoints scored as decline. Univariate logistic regression and multivariate model building were performed examining dose to eloquent structures and clinical variables. Univariate analysis showed mean dose to the bilateral caudal anterior cingulate cortex and WM were correlated with decline in executive function. Attention/processing speed decline was correlated with mean/max dose to the posterior corpus callosum (CC), volume getting &amp;gt;20 Gy in the combined CC, as well as anti-epileptic use and chemotherapy. On multivariate analysis for attention automated bootstrapped logistic regression performance at nested cross-validation by AUC was 0.59 (0.54-0.65); LASSO model performance by AUC was 0.60 (0.54-0.66) with mean dose to combined CC being the most frequent variable in both. The top three most important variables in Random Forest by mean decrease in Gini coefficient were max dose to posterior and combined CC and mean dose to anterior CC. Model performance by AUC was 0.70 (0.64-0.75). Here we present the first, to our knowledge, NTCP model for decline in attention/processing speed, along with dosimetric predictors of executive function decline. We found that after partial brain RT, dose to several ROIs significantly correlated with post-RT impairment. These data can guide future cognitive-sparing strategies for brain RT.

Localization of Silent Cerebral Infarcts in Children with Sickle Cell Disease Impacts Structural Disconnection

Silent cerebral infarcts (SCIs) occur in 40% of children with sickle cell disease (SCD) by 18 years of age and are associated with cognitive dysfunction. SCIs localize to the border zone of the brain, but the significance of this localization is unclear. In adults with stroke, an infarct's disruption of white matter (WM) tracts, or structural disconnection, is more strongly associated with the functional impact of the infarct than the size of the lesion. We aim to define the WM tracts disconnected by SCIs and the relationship between structural disconnection and functional connectivity (FC) in SCD. Simulated and real-world data were used to test the hypothesis that specific WM tracts are vulnerable to disconnection if an infarct occurs in the region at highest risk for SCIs, and that FC will decrease with increased structural disconnection in SCD. Utilizing data from the Silent Infarct Transfusion (SITT) trial, the regions at greatest risk for SCIs were defined (risk region, PMID 30061156). A simulated dataset comprised of 1000 infarcts within the risk region and 1000 infarcts within the white matter outside of the risk region was created. The real-world dataset was comprised of 44 participants with SCD and SCIs (median age 13.0 [11.0, 15.8] years, 29 female/15 male). The Human Connectome Project (HCP) 842 atlas contains thousands of streamlines comprising 28 WM tracts (excluding brainstem and cerebellar tracts). The Lesion Connectivity Toolbox defined streamlines within the HCP 842 atlas that intersected with each individual lesion, permitting quantification of two measures of structural disconnection: tract-wise disconnection (the percentage of streamlines within each tract that intersect a lesion) and global disconnection (the average percentage of streamlines connecting each pair of gray matter (GM) parcels in the FC parcellation (PMID 25316338)). Tract density images (TDi) illustrate the number of streamlines impacted by a lesion within each voxel of the brain permitting computation of total lesion impact as the volume of the TDi image associated with each lesion. Resting state functional connectivity MRI was obtained in 27 of the real-world participants for computation of whole brain modularity as a metric of global FC. The WM tracts with the highest mean tract-wise disconnection due to lesions within the risk region were the posterior and mid-anterior corpus callosum, superior longitudinal fasciculus, frontal aslant tract, and middle longitudinal fasciculus while the inferior frontal occipital fasciclus, anterior commissure, inferior longitudinal fasciculus, posterior corpus callosum, and arculate fasciculus were most impacted by lesions outside of the risk region. Numerous tracts showed a significant difference in tract-wise disconnection resulting from lesions in the risk region vs. lesions outside the risk region. The tracts impacted due to real-world lesions were similar to tracts impacted from lesions within the risk region (Table 1). Despite lesioned volume being equivalent (p = 0.31) for simulated data within and outside the risk region, the average volume of lesion impact as measured by volume of the TDi image was significantly larger for lesions occurring inside the risk region (p &amp;lt; 0.001; Fig 1). In the real-world dataset, whole brain modularity, a metric of global FC, decreased as global structural disconnection increased (r = -0.49, p =0.009) Using simulated data that was validated with a real-world dataset, specific WM tracts vulnerable to SCIs were identified. Previous work on cerebral hemodynamics in SCD elucidated the mechanism of injury in the border zone, and these results demonstrate the significance of the localization of this injury to the border zone. SCIs have a far-reaching effect as lesions in the risk region within the border zone were associated with a greater volume of structural disconnection compared to lesions of the same size distributed outside the risk region. These results suggest that the regions in which the SCIs localize represent “high impact” areas of the brain, where a lesion of a given volume may intersect a large number of streamlines. Further, given the correlation between global structural disconnection and whole brain modularity, these data link structural disconnection with function of the brain, suggesting these “high impact” regions may also play a key role in mediating communication between functionally connected GM regions.

Abstract 088: Treatment of a Ruptured AVM with Inflow Aneurysms: Mixed approach using coil and liquid embolization

Introduction Arteriovenous malformations(AVMs) are high‐flow vascular abnormalities characterized by direct communications between arteries and veins of various complexities. Cerebral AVMs may manifest with new‐onset seizures or intraparenchymal (IPH) or subarachnoid hemorrhages (SAH). Life‐threatening bleeds may occur from the AVM nidus or associated aneurysms. We report a patient with hemorrhage from a complex AVM that included a prominent nidus and large inflow aneurysms requiring several endovascular techniques for treatment. Methods N/A Results A 35 year old male patient newly arrived from the Philippines with a history of hypertension presented to the hospital after being found unresponsive at home with frothing from the mouth and incontinence. The patient regained consciousness in the ER, complaining of a posterior headache which he had been experiencing for a week. NIHSS of 0 was noted with no neurological deficits. CT‐head revealed extensive SAH in interhemispheric falx anterior to and outlining the entire corpus callosum with intraventricular extension. CT‐ angiogram demonstrated a prominent AVM with a well‐developed nidus situated to the left of midline about the posterior corpus callosum. Two large inflow aneurysms, felt to be the rupture site, projecting from the proximal left pericallosal artery were also demonstrated. An incidental ACA aneurysm was also noted. Cerebral angiography redemonstrated these findings as well as the drainage of the AVM primarily through the straight sinus. Graded as Spetzler Martin 4. Common femoral approach was used. An access catheter was passed into the left ICA. The pericallosal artery was accessed with a detachable tip microcatheter which was further advanced past the inflow aneurysms into the main pedicle feeding the AVM nidus. The inflow aneurysms were accessed and embolized with coils using a second microcatheter prior to AVM embolization. This sealed off access to the aneurysms and parent vessel against liquid agent backflow. Onyx‐18 was then injected into the main AVM pedicle under a blank roadmap. Extensive but partial filling of the AVM was noted anteriorly but full embolization of the posterior aspect of the nidus was not achieved. Finally coiling of the ACA aneurysm was performed after accessing the right ICA. An MRI with and without contrast was performed and an expected acute infarction in the left ACA territory was observed. A repeat angiogram was performed a week later revealing posterior cerebral artery and posterior choroidal branches feeding the posterior 1/3 of the AVM. Embolization of three posterior feeding pedicles was subsequently performed utilizing dilute NBCA. Because of coil impaction the proximal pericallosal inflow aneurysm required re‐treatment with further coil placement 8 months after initial treatment. The patient has regular angiograms to monitor the AVM, which appears stable without significant residual shunting. Conclusion Ruptured AVMs are fatal events requiring careful treatment to prevent further bleeding while preserving viable brain tissue. AVMs are fragile formations of vessels which can receive collaterals from multiple targets and often have associated high risk features like inflow aneurysms. Accordingly endovascular treatment may require a mixture of techniques to ensure adequate and safe embolization. Regular monitoring of these structures and adjacent vessels is required to prevent any poor outcomes.

1 Sluggish Cognitive Tempo in Children and Adolescents with Fetal Alcohol Spectrum Disorders: Associations with Executive Function and Subcortical Volumes

Objective:Fetal alcohol spectrum disorder (FASD) is a common neurodevelopmental condition associated with deficits in cognitive functioning (executive functioning [EF], attention, working memory, etc.), behavioral impairments, and abnormalities in brain structure including cortical and subcortical volumes. Rates of comorbid attention-deficit/hyperactivity disorder (ADHD) are high in children with FASD and contribute to significant functional impairments. Sluggish cognitive tempo (SCT) includes a cluster of symptoms (e.g. underactive/slow-moving, confusion, fogginess, daydreaming) found to be related to but distinct from ADHD, and previous research suggests that it may be common in FASD. We explored SCT by examining the relationship between SCT and both brain volumes (corpus callosum, caudate, and hippocampus) and objective EF measures in children with FASD vs. typically developing controls.Participants and Methods:This is a secondary analysis of a larger longitudinal CIFASD study that consisted of 35 children with prenatal alcohol exposure (PAE) and 30 controls between the ages of 9 to 18 at follow-up. Children completed a set of cognitive assessments (WISC-IV, DKEFS, &amp; NIH Toolbox) and an MRI scan, while parents completed the Child Behavior Checklist (CBCL), which includes a SCT scale. We examined group differences between PAE and controls in relation to SCT symptoms, EF scores, and subcortical volumes. Then, we performed within-and between-group comparisons with and without controlling for total intracranial volume, age, attention problems, and ADHD problems between SCT and subcortical brain volumes. Finally, we performed correlations between SCT and EF measures for both groups.Results:Compared to controls, participants with PAE showed significantly more SCT symptoms on the CBCL (t [57] = 3.66, p = 0.0006), more parent-rated attention problems and ADHD symptoms, lower scores across several EF measures (DKEFS Trail-Making and Verbal Fluency; WISC-IV Digit Span, Symbol Search, and Coding; effect sizes ranging from 0.44 to 1.16), and smaller regional volumes in the caudate, hippocampus, and posterior areas of the corpus callosum. In the PAE group, a smaller hippocampus was associated with more SCT symptoms (controlling for parent-rated attention problems and ADHD problems, age, and intracranial volume). However, in the control group, a larger mid posterior and posterior corpus callosum were significantly associated with more SCT symptoms (controlling for parent-rated attention problems, intracranial volume, and age; r [24] = 0.499, p = 0.009; r [24] = 0.517, p = 0.007). In terms of executive functioning, children in the PAE group with more SCT symptoms performed worse on letter sequencing of the Trail-Making subtest (controlling attention problems &amp; ADHD symptoms). In comparison, those in the control group with more SCT symptoms performed better on letter sequencing and combined number letter sequencing of the Trail-Making subtest (controlling attention problems).Conclusions:Findings suggest that children with FASD experience elevated SCT symptoms compared to typically developing controls, which may be associated with worse performance on EF tasks and smaller subcortical volumes (hippocampus) when taking attention difficulties and ADHD symptoms into account. Additional research into the underlying causes and correlates of SCT in FASD could result in improved tailoring of interventions for this population.

A neuropsychiatric case of delayed post-hypoxic leukoencephalopathy from opioid intoxication resulting in Anton-Babinski syndrome and quadriplegia

ABSTRACT This is the case of a 26-year-old male who developed Anton Babinski syndrome (ABS), quadriplegia, and delayed post-hypoxic leukoencephalopathy (DPHL) after an opioid overdose. He exhibited cortical blindness, visual anosognosia, and confabulation upon awakening. Several days later, he experienced acute psychosis and agitation. T2-FSE MRI revealed extensive supratentorial leukoencephalopathy involving both cerebral hemispheres, extending to the posterior corpus callosum due to cerebral anoxia. This case report will discuss different types of encephalopathy from opioid abuse, ABS, visual anosognosia, and confabulation’s pathogenic mechanisms. It underscores the necessity of researching substance-induced neuropsychiatric disorders and their pathogenic mechanisms for effective treatments.

Longitudinal Changes in Regional Brain Volumes and Cognition of Professional Fighters With Traumatic Encephalopathy Syndrome.

Due to current limitations in diagnosing chronic traumatic encephalopathy (CTE) clinically, traumatic encephalopathy syndrome (TES) has been proposed as the clinical presentation of suspected CTE. This study aimed to determine whether there was an association between a clinical diagnosis of TES and subsequent temporal decline in cognitive or MRI volumetric measures. This was a secondary analysis of the Professional Athletes Brain Health Study (PABHS), inclusive of active and retired professional fighters older than 34 years. All athletes were adjudicated as TES positive (TES+) or TES negative (TES-) based on the 2021 clinical criteria. General linear mixed models were used to compare MRI regional brain volumes and cognitive performance between groups. A total of 130 fighters met inclusion criteria for consensus conference. Of them, 52 fighters (40%) were adjudicated as TES+. Athletes with a TES+ diagnosis were older and had significantly lower education. Statistically significant interactions and between-group total mean differences were found in all MRI volumetric measurements among the TES+ group compared with those among the TES- group. The rate of volumetric change indicated a significantly greater increase for lateral (estimate = 5,196.65; 95% CI = 2642.65, 7750.66) and inferior lateral ventricles (estimate = 354.28; 95% CI = 159.90, 548.66) and a decrease for the hippocampus (estimate = -385.04, 95% CI = -580.47, -189.62), subcortical gray matter (estimate = -4,641.08; 95% CI = -6783.98, -2498.18), total gray matter (estimate = -26492.00; 95% CI = -50402.00, -2582.32), and posterior corpus callosum (estimate = -147.98; 95% CI = -222.33, -73.62). Likewise, the rate of cognitive decline was significantly greater for reaction time (estimate = 56.31; 95% CI = 26.17, 86.45) and other standardized cognitive scores in the TES+ group. The 2021 TES criteria clearly distinguishes group differences in the longitudinal presentation of volumetric loss in select brain regions and cognitive decline among professional fighters 35 years and older. This study suggests that a TES diagnosis may be useful in professional sports beyond football, such as boxing and mixed martial arts. These findings further suggest that the application of TES criteria may be valuable clinically in predicting cognitive decline.

Clinical Features, Brain-Structure Changes, and Cognitive Impairment in Basal Ganglia Infarcts: A Pilot Study.

Stroke has been considered to raise the risk of dementia in several studies, but the relationship between brain structural changes and poststroke cognitive impairment (PSCI) is unclear. In this study, 23 PSCI patients with basal ganglia infarcts after 2 weeks and 29 age-matched controls underwent magnetic resonance imaging measuring cortical thickness and volume changes, as well as neuropsychological tests. CI was derived from a performance score <1.5 standard deviations for normally distributed scores. We compared Z scores in different cognitive domains and cortical thickness and volumes in two groups. Multiple linear regressions were used to investigate the relationship between cortical thickness and volumes and neuropsychological tests. A majority of PSCI patients were in their 50s (55.19±8.52 years). PSCI patients exhibited significantly decreased Z scores in multiple domains, such as memory, language, visuomotor speed, and attention/executive function. The volumes of the middle posterior corpus callosum, middle anterior corpus callosum, and hippocampus in PSCI patients were markedly lower than controls. The thickness of the right inferior temporal cortex and insula were significantly smaller than controls. It found that the reduced right hippocampus was related to executive dysfunction. Hippocampus dysfunction may be involved in language impairment (p<0.05) in PSCI patients with basal ganglia infarcts. These findings demonstrated that brain structure changed after ischemic stroke, and different gray-matter structural changes could lead to specific cognitive decline in PSCI patients with basal ganglia infarcts. Atrophy of the right hippocampus potentially serves as an imaging marker of early executive function of PSCI.

Dynamic cortical and tractography atlases of proactive and reactive alpha and high-gamma activities.

Alpha waves-posterior dominant rhythms at 8-12 Hz reactive to eye opening and closure-are among the most fundamental EEG findings in clinical practice and research since Hans Berger first documented them in the early 20th century. Yet, the exact network dynamics of alpha waves in regard to eye movements remains unknown. High-gamma activity at 70-110 Hz is also reactive to eye movements and a summary measure of local cortical activation supporting sensorimotor or cognitive function. We aimed to build the first-ever brain atlases directly visualizing the network dynamics of eye movement-related alpha and high-gamma modulations, at cortical and white matter levels. We studied 28 patients (age: 5-20 years) who underwent intracranial EEG and electro-oculography recordings. We measured alpha and high-gamma modulations at 2167 electrode sites outside the seizure onset zone, interictal spike-generating areas and MRI-visible structural lesions. Dynamic tractography animated white matter streamlines modulated significantly and simultaneously beyond chance, on a millisecond scale. Before eye-closure onset, significant alpha augmentation occurred at the occipital and frontal cortices. After eye-closure onset, alpha-based functional connectivity was strengthened, while high gamma-based connectivity was weakened extensively in both intra-hemispheric and inter-hemispheric pathways involving the central visual areas. The inferior fronto-occipital fasciculus supported the strengthened alpha co-augmentation-based functional connectivity between occipital and frontal lobe regions, whereas the posterior corpus callosum supported the inter-hemispheric functional connectivity between the occipital lobes. After eye-opening offset, significant high-gamma augmentation and alpha attenuation occurred at occipital, fusiform and inferior parietal cortices. High gamma co-augmentation-based functional connectivity was strengthened, whereas alpha-based connectivity was weakened in the posterior inter-hemispheric and intra-hemispheric white matter pathways involving central and peripheral visual areas. Our results do not support the notion that eye closure-related alpha augmentation uniformly reflects feedforward or feedback rhythms propagating from lower to higher order visual cortex, or vice versa. Rather, proactive and reactive alpha waves involve extensive, distinct white matter networks that include the frontal lobe cortices, along with low- and high-order visual areas. High-gamma co-attenuation coupled to alpha co-augmentation in shared brain circuitry after eye closure supports the notion of an idling role for alpha waves during eye closure. These normative dynamic tractography atlases may improve understanding of the significance of EEG alpha waves in assessing the functional integrity of brain networks in clinical practice; they also may help elucidate the effects of eye movements on task-related brain network measures observed in cognitive neuroscience research.

Generalized Tonic-Clonic Seizures Cause Lumbar Spine Fracture

A 28-year-old man presented to the emergency department after a witnessed GTC seizure. The patient had a history of systemic lupus erythematosus, previous subarachnoid hemorrhage, and pulmonary embolism. He was on regular methylprednisolone 16 mg, enoxaparin 60 mg once daily, and levetiracetam (LEV) 500 mg twice daily. The patient had recently stopped taking LEV. There was no trauma in the history. Neurological examination was normal. He had severe lower back pain that failed to subside despite treatment with analgesics and opioids; therefore, this patient had an indication for radiological imaging. Urgent non-contrast computerized tomography (CT) scan of the lumbar spine revealed a burst fracture of L1. Non-contrast lumbar magnetic resonance imaging (MRI) revealed a bursal fracture in the L1 vertebral corpus that caused approximately 50% height loss, and there was compression of the posterior corpus of the vertebra on the thecal sac; however, no stenosis of the spinal canal was detected. At this level, there was bone marrow edema in the vertebral corpus (Figure 1,2). He was transferred to the neurosurgery department. Written informed consent was obtained from the patient for the publication of this case.