Matter Of Brain Research Articles

Low-grade carotid artery stenosis is associated with progression of brain atrophy and cognitive decline. The SMART-MR study

Asymptomatic low-grade carotid artery stenosis (LGCS) is a common finding in patients with manifest arterial disease, however its relationship with brain MRI changes and cognitive decline is unclear. We included 902 patients (58 ± 10 years; 81% male) enrolled in the Second Manifestations of Arterial Disease – Magnetic Resonance (SMART-MR) study without a history of cerebrovascular disease. LGCS was defined as 1–49% stenosis on baseline carotid ultrasound, whereas no LGCS (reference category) was defined as absence of carotid plaque. Brain and white matter hyperintensity (WMH) volumes and cognitive function were measured at baseline and after 4 (n = 480) and 12 years (n = 222) of follow-up. Using linear mixed-effects models, we investigated associations of LGCS with progression of brain atrophy, WMH, and cognitive decline. LGCS was associated with greater progression of global brain atrophy (estimate −0.03; 95%CI, −0.06 to −0.01; p = 0.002), and a greater decline in executive functioning (estimate −0.02; 95%CI, −0.031 to −0.01; p < 0.001) and memory (estimate −0.012; 95%CI, −0.02 to −0.001; p = 0.032), independent of demographics, cardiovascular risk factors, and incident brain infarcts on MRI. No association was observed between LGCS and progression of WMH. Our results indicate that LGCS may represent an early marker of greater future brain atrophy and cognitive decline.

Predictive models demonstrate age-dependent association of subcortical volumes and cognitive measures.

Whether brain matter volume is correlated with cognitive functioning and higher intelligence is controversial. We explored this relationship by analysis of data collected on 193 healthy young and older adults through the "Leipzig Study for Mind-Body-Emotion Interactions" (LEMON) study. Our analysis involved four cognitive measures: fluid intelligence, crystallized intelligence, cognitive flexibility, and working memory. Brain subregion volumes were determined by magnetic resonance imaging. We normalized each subregion volume to the estimated total intracranial volume and conducted training simulations to compare the predictive power of normalized volumes of large regions of the brain (i.e., gray matter, cortical white matter, and cerebrospinal fluid), normalized subcortical volumes, and combined normalized volumes of large brain regions and normalized subcortical volumes. Statistical tests showed significant differences in the performance accuracy and feature importance of the subregion volumes in predicting cognitive skills for young and older adults. Random forest feature selection analysis showed that cortical white matter was the key feature in predicting fluid intelligence in both young and older adults. In young adults, crystallized intelligence was best predicted by caudate nucleus, thalamus, pallidum, and nucleus accumbens volumes, whereas putamen, amygdala, nucleus accumbens, and hippocampus volumes were selected for older adults. Cognitive flexibility was best predicted by the caudate, nucleus accumbens, and hippocampus in young adults and caudate and amygdala in older adults. Finally, working memory was best predicted by the putamen, pallidum, and nucleus accumbens in the younger group, whereas amygdala and hippocampus volumes were predictive in the older group. Thus, machine learning predictive models demonstrated an age-dependent association between subcortical volumes and cognitive measures. These approaches may be useful in predicting the likelihood of age-related cognitive decline and in testing of approaches for targeted improvement of cognitive functioning in older adults.

“Greasy Thumb”—The Man Who Made the Chicago Mob

“Greasy Thumb”—The Man Who Made the Chicago Mob

Changes in the structure of synaptic intercellular contacts in focal brain lesions

Purpose: to evaluate changes in the structure of synaptic contacts in various types of focal brain pathology. Materials and methods. The results of treatment of 40 cases of supratentorial focal lesions of the brain (FLB) were retrospectively evaluated. The cases are divided into groups: 30 gliomas of various degrees of malignancy and 5 consequences of TBI, 5 epilepsy. All patients underwent surgical interventions. The synaptic plasticity of axo-dendritic and axo-spiny asymmetric synapses of neurons of the VI-VII layers of the frontotemporal cortex was studied by electron microscopy. Morphometric analysis was carried out on a computer image analyzer САИ-01АВН using the software "Kappa opto-electronics GmbH" using the STATISTICA 7 program package. The results. It was established that the density of synapses decreased in glioblastomas (GB) and craniocerebral injury (ССІ). Qualitative changes demonstrate the plasticity of architectonics of synapse, in particular due to the increase in the number of perforated synaptic contacts. Maximum thickening and diffuse stratification of the postsynaptic seal indicates a violation of the functional capacity of the postsynaptic component of the contacts. A decrease in the number of synaptic vesicles was revealed in ССІ and GB, with their rearrangement, which is probably a manifestation of synaptic dysfunction. The latter proves the irreversibility of destructive local changes and is unfavorable criterion. The risk of the formation of destructive-degenerative changes in the synaptic apparatus is 7.64 times higher in DA, 3.17 times higher in GB, and 17.31 times higher in ССІ compared to cases of epilepsy, with GB significantly increases by 13.5 times compared to DA. Therefore, the assessment of the structural features of neuroplasticity should take into account the morphogenesis of the BM in comparison with clinical data Conclusions. In the zones of invasive growth of gliomas of various degrees of malignancy and in ССІ and epilepsy, the indicators of synaptic plasticity differ statistically significantly. The density of placement of synapses is lower in GB and ССІ. The probability of non-reversibility of destructive-degenerative changes of synapses according to the number of SVs in FLB correlates with the degree of glioma differentiation with a sensitivity of 81.0% and a specificity of 76.0%. According to the structural changes of synaptic connections in tumors, probable differences between the variants have been proven: GB and DA, the sensitivity of the discriminant model is 85.0%, the specificity is 74.0%, which is an indirect evidence of the growth rate of the tumor mass and its destructive effect on the surrounding brain matter. The obtained results are important in assessing the prognosis of the further course of the disease.

Association of liver fibrosis with cognitive test performance and brain imaging parameters in the UK Biobank study.

We hypothesized that liver fibrosis is associated with worse cognitive performance and corresponding brain imaging changes. We examined the association of liver fibrosis with cognition and brain imaging parameters in the UK Biobank study. Liver fibrosis was assessed using the Fibrosis-4 (FIB-4) score. The primary cognitive outcome was the digit symbol substitution test (DSST); secondary outcomes were additional executive function/processing speed and memory tests. Imaging outcomes were hippocampal, total brain, and white matter hyperintensity (WMH) volumes. We included 105,313 participants with cognitive test data, and 41,982 with magnetic resonance imaging (MRI). In adjusted models, liver fibrosis was associated with worse performance on the DSST and tests of executive function but not memory. Liver fibrosis was associated with lower hippocampal and total brain volumes, without compelling association with WMH volume. Liver fibrosis is associated with worse performance on select cognitive tests and lower hippocampal and total brain volumes. It is increasingly recognized that chronic liver conditions impact brain health. We performed an analysis of data from the UK Biobank prospective cohort study. Liver fibrosis was associated with worse performance on executive function tests. Liver fibrosis was not associated with memory impairment. Liver fibrosis was associated with lower hippocampal and total brain volumes.

Galactosylceramidase deficiency and pathological abnormalities in cerebral white matter of Krabbe disease

Krabbe Disease (KD) is an autosomal recessive disorder that results from loss-of-function mutations in the GALC gene, which encodes lysosomal enzyme galactosylceramidase (GALC). Functional deficiency of GALC is toxic to myelin-producing cells, which leads to progressive demyelination in both the central and peripheral nervous systems. It is hypothesized that accumulation of psychosine, which can only be degraded by GALC, is a primary initiator of pathologic cascades. Despite the central role of GALC in KD pathomechanism, investigations of GALC deficiency at a protein level are largely absent, due in part, to the lack of sensitive antibodies in the field. Leveraging two custom antibodies that can detect GALC at endogenous levels, we demonstrated that GALC protein is predominantly localized to oligodendrocytes in cerebral white matter of an infant brain, consistent with its functional role in myelination. Mature GALC could also be quantitatively detected as a 26 kDa band by western blotting and correlated to enzyme activity in brain tissues. The p.Ile562Thr polymorphic variant, which is over-represented in the KD population, was associated with reduced mature GALC protein and activity. In three infantile KD cases, homozygous null mutations in GALC lead to deficiency in total GALC protein and activity. Interestingly, although GALC activity was absent, normal levels of total GALC protein were detected by a sandwich ELISA using our custom antibodies in a later-onset KD brain, which suggests that the assay has the potential to differentiate infantile- and later-onset KD cases. Among the infantile KD cases, we quantified a 5-fold increase in psychosine levels, and observed increased levels of acid ceramidase, a key enzyme for psychosine production, and hyperglycosylated lysosomal-associated membrane protein 1, a marker for lysosomal activation, in periventricular white matter, a major pathological brain region, when compared with age-matched normal controls. While near complete demyelination was observed in these cases, we quantified that an early-infantile case (age of death at 10 months) had about 3-fold increases in both globoid cells, a pathological hallmark for KD, and CD8-positive T lymphocytes, a pathological marker for multiple sclerosis, in the white matter when compared with a slower progressing infantile case (age of death at 21 months), which suggests a positive correlation between clinical severity and neuropathology. Taken together, our findings have advanced the understanding of GALC protein biology in the context of normal and KD brain white matter. We also revealed new neuropathological changes that may provide insights to understand KD pathogenesis.

The Study of Sectional Anatomy of Sheep and Human Brain by Various Staining Methods

Five different staining methods were done on the sheep brain compared and the best method was employed to stain the human brain, Alstons staining method is found to be the best among the five staining method, which shows excellent differentiation of grey and white matter. Alston’s method has low shrinkage percentage and the time taken for this procedure is around 8 hrs 30 min. When compared with the unstained section with the stained section show pronounced grey matter. Learning neuroanatomy with wet brain section is difficult in unstained brain specimens, with the induction of staining method in the nueroanatomical structures will be helpful in differentiating the grey and white matter of brain. With the coronal and axial sections in this study various macroscopic neuroanatomical structures can be studied easily.

P01.19.A The temporo-parieto-occipital junction in the non-dominant hemisphere as a challenging hub for glioma surgery: functional and oncological outcomes

Abstract Background The temporo-parieto-occipital junction (TPOJ) in the non-dominant hemisphere is a complex region intersected by multiple white matter bundles (Optic radiations, Inferior-fronto-occipital tract, inferior-longitudinalis-tract, superior-longitudinalis-tract, vertical-occipital-tract, medial-dorsal-longitudinal-tract, parietal-aslant-tract), subserving several high-level neurological functions such as spatial recognition, visual agnosia, visual field, attention and working memory. Few data are available on the optimum brain mapping strategy to be adopted for resecting tumors involving this area. Ideally it should allow surgeon to effectively identify several tracts and safely preserve all functions. Material and Methods We developed a proper protocol to approach this complex area integrating, in awake condition, intraoperative visual test (iVT) to mapping visual field, semantic association test (SRAT) to prevent visual agnosia and preserve working memory, hand manipulation task (hMT) to preserve spatial abilities. We reviewed its efficacy in a series of 38 patients with tumors involving non-dominant TPOJ, looking to functional (neurologic-neuropsychological) and oncological (EOR) outcomes. we perform a lesion symptom map and a disconnectome analysis to evaluate what region predict a decline in neuropsychological function and which tract of white brain matter are correlated in the decline of performance. Results Feasibility was high and all patients were able to perform and complete the protocol, which lasted, on the average11 min cortically and 25 min subcortically. Specificity was &amp;gt;95%. Immediate post-operative deficits were documented in 87.4% of patients, permanent in 3.9% (visual field, visual spatial abilities). Attentive and emotional domains were those mostly affected in the neuropsychological evaluation. Lesion symptom mapping and disconnectomic analysis showed that the postoperative decrease in neuropsychological performance was associated with resection of a cluster of voxels corresponding to the anterior portion of the temporo-parietal junction. The white matter tracts mainly involved were the anterior and posterior segment of the middle longitudinal fasciculus (aMdLF and pMdLF) and the parietal aslant tract (PAT). Conclusion Effective and safe resection of tumors involving non-dominant TPOJ is feasible. The adoption of a specific brain mapping protocol in awake setting is recommended to achieve a full functional preservation and extend tumor resection. Further analysis should be performed to assess the role of this subcortical tracts.

Tau and amyloid biomarkers modify the degree to which cognitive reserve and brain reserve predict cognitive decline.

Brain reserve, cognitive reserve, and education are thought to protect against late-life cognitive decline, but these variables have not been directly compared to one another in the same model, using future cognitive and functional decline as outcomes. We sought to determine whether the influence of these protective factors on executive function (EF) and daily function decline was dependent upon Alzheimer's disease (AD) pathology severity, as measured by the total tau to beta-amyloid (T-τ/Aβ1-42) ratio in cerebrospinal fluid (CSF). Participants were 1201 older adult volunteers in the Alzheimer's Disease Neuroimaging Initiative (ADNI) study. Brain reserve was defined using a composite index of structural brain volumes (total brain matter, hippocampus, and white matter hyperintensity). Cognitive reserve was defined as the variance in episodic memory performance not explained by brain integrity and demographics. At higher levels of T-τ/Aβ1-42, brain and cognitive reserve predicted slower decline in EF. Only brain reserve attenuated decline at lower levels of T-τ/Aβ1-42. Education had no independent association with cognitive decline. These results point to a hierarchy of protection against aging- and disease-associated cognitive decline. When pathology is low, only structural brain integrity predicts rate of future EF decline. The ability of cognitive reserve to predict future EF decline becomes stronger as CSF biomarker evidence of AD increases. Although education is typically thought of as a proxy for cognitive reserve, it did not show any protective effects on cognition after accounting for brain integrity and the residual cognitive reserve index.

It takes two to tango: Widening our understanding of the onset of schizophrenia from a neuro-angiogenic perspective.

Schizophrenia is a chronic debilitating mental disorder characterized by perturbations in thinking, perception, and behavior, along with brain connectivity deficiencies, neurotransmitter dysfunctions, and loss of gray brain matter. To date, schizophrenia has no cure and pharmacological treatments are only partially efficacious, with about 30% of patients describing little to no improvement after treatment. As in most neurological disorders, the main descriptions of schizophrenia physiopathology have been focused on neural network deficiencies. However, to sustain proper neural activity in the brain, another, no less important network is operating: the vast, complex and fascinating vascular network. Increasing research has characterized schizophrenia as a systemic disease where vascular involvement is important. Several neuro-angiogenic pathway disturbances have been related to schizophrenia. Alterations, ranging from genetic polymorphisms, mRNA, and protein alterations to microRNA and abnormal metabolite processing, have been evaluated in plasma, post-mortem brain, animal models, and patient-derived induced pluripotent stem cell (hiPSC) models. During embryonic brain development, the coordinated formation of blood vessels parallels neuro/gliogenesis and results in the structuration of the neurovascular niche, which brings together physical and molecular signals from both systems conforming to the Blood-Brain barrier. In this review, we offer an upfront perspective on distinctive angiogenic and neurogenic signaling pathways that might be involved in the biological causality of schizophrenia. We analyze the role of pivotal angiogenic-related pathways such as Vascular Endothelial Growth Factor and HIF signaling related to hypoxia and oxidative stress events; classic developmental pathways such as the NOTCH pathway, metabolic pathways such as the mTOR/AKT cascade; emerging neuroinflammation, and neurodegenerative processes such as UPR, and also discuss non-canonic angiogenic/axonal guidance factor signaling. Considering that all of the mentioned above pathways converge at the Blood-Brain barrier, reported neurovascular alterations could have deleterious repercussions on overall brain functioning in schizophrenia.

Association of liver disease with brain volume loss, cognitive decline, and plasma neurodegenerative disease biomarkers

Although liver dysfunction has been implicated in Alzheimer's disease (AD), it remains unknown how liver disease may influence the trajectory of brain and cognitive changes in older adults. We related self-reported liver disease to longitudinal measures of brain structure and cognition, as well as baseline measures of plasma AD/neurodegeneration biomarkers in the Baltimore Longitudinal Study of Aging. Liver disease was identified using ICD-9 classification codes. Brain volume and cognition were assessed serially using 3T-MRI and a cognitive battery. 1008, 2157, and 780 participants were included in the MRI, cognitive, and plasma biomarker analysis, respectively. After adjustment for confounders, liver disease was associated with accelerated decline in total brain and white matter volume, but not total gray matter or AD signature region volume. Although liver disease showed no relationship with domain-specific cognitive decline or plasma biomarkers, participants with a history of hepatitis demonstrated accelerated decline in verbal fluency and elevated neurofilament light. Results suggest all-cause liver disease may accelerate brain volume loss but does not appear to promote AD-specific neurocognitive changes.

Superimposing Pre-Cranioplasty on Pre-Craniectomy Images to Gauge Feasibility of Early Cranioplasty: A Proof of Concept.

Cranioplasty to reconstruct a skull defect after a decompressive craniectomy (DC) is a common neurosurgical procedure. However, cranioplasty is associated with relatively high complication rates, with optimal timing from craniectomy to cranioplasty remaining a controversial matter. Recent studies demonstrated early cranioplasty with appropriate risk mitigation to be a viable option with many clinical advantages, propelling the advocacy for cranioplasty as soon as brain swelling resolves. We report on a 33-year-old male with traumatic brain injury who received an early cranioplasty, 18 days post-DC. The extent of adequate brain swelling resolution was determined by superimposing selected pre-cranioplasty computed tomography (CT) images onto corresponding pre-craniectomy CT images. By ensuring all brain matter lies within the outer table of the skull in superimposed brain images, the extent of brain swelling resolution could be determined reliably and the feasibility of cranioplasty can be assessed objectively.

Resveratrol reduces inflammatory response and detrimental effects in chronic cerebral hypoperfusion by down-regulating stimulator of interferon genes/TANK-binding kinase 1/interferon regulatory factor 3 signaling.

Inflammatory responses induced by chronic cerebral hypoperfusion (CCH) play a critical role in the progression of vascular dementia. Stimulator of interferon genes (STING) signaling function as a key mediator of inflammation and immunological responses in the central nervous system (CNS), and resveratrol (RES) exerts potent anti-inflammatory effects. However, the role of STING signaling and the relationship between RES and STING signaling in persistent hypoperfusion-induced cerebral inflammation remain unclear. In this study, Sprague–Dawley rats were subjected to either Sham or bilateral common carotid artery occlusion (2VO) surgery and received RES or vehicle daily by intraperitoneal injection for 4 or 8 weeks. Morris’s water maze was used for the analysis of cognitive function. The neuroinflammatory responses in white matter and hippocampus of the rat brain were assessed by Western blot, Immunofluorescence staining, and qRT-PCR analyses. Myelin integrity, neutrophil infiltration, and microglia proliferation were assessed by Immunohistochemistry and histologic analysis. We demonstrated that after CCH, neurons, microglia, and astrocyte under endoplasmic reticulum (ER) stress upregulated the expression of STING, TANK-binding kinase 1 (TBK1), and the transcription factor interferon regulatory factor 3 (IRF3), as well as translocation of IRF3 into the nucleus. These were accompanied by infiltration of neutrophils, activation of microglia, and overproduction of proinflammatory mediators. Improvements in cognitive deficits were related to reduced hippocampal neuronal cell death and increased myelin integrity in RES-treated rats. The neuroprotective effects of RES were associated with suppression of the expression of tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecule 1 (ICAM-1), VCAM-1, interferon-β (IFN-β), and IL-1β, likely through mitigation of the STING/TBK1/IRF3 pathway. These inhibitory effects exerted by RES also inhibited the levels of myeloperoxidase, reduced excess expression of reactive astrocytes, and activated microglia. In conclusion, the STING/TBK1/IRF3 axis may be critical for proinflammatory responses in cerebral tissue with persistent hypoperfusion, and RES exerts its anti-inflammatory effects by suppressing STING/TBK1/IRF3 signaling.

The potential role of DNA methylation as preventive treatment target of epileptogenesis.

Pharmacological therapy of epilepsy has so far been limited to symptomatic treatment aimed at neuronal targets, with the result of an unchanged high proportion of patients lacking seizure control. The dissection of the intricate pathological mechanisms that transform normal brain matter to a focus for epileptic seizures—the process of epileptogenesis—could yield targets for novel treatment strategies preventing the development or progression of epilepsy. While many pathological features of epileptogenesis have been identified, obvious shortcomings in drug development are now believed to be based on the lack of knowledge of molecular upstream mechanisms, such as DNA methylation (DNAm), and as well as a failure to recognize glial cell involvement in epileptogenesis. This article highlights the potential role of DNAm and related gene expression (GE) as a treatment target in epileptogenesis.

Characterization of Glial Populations in the Aging and Remyelinating Mouse Corpus Callosum.

Cells in the white matter of the adult brain have a characteristic distribution pattern in which several cells are contiguously connected to each other, making a linear array (LA) resembling pearls-on-a-string parallel to the axon axis. We have been interested in how this pattern of cell distribution changes during aging and remyelination after demyelination. In the present study, with a multiplex staining method, semi-quantitative analysis of the localization of oligodendrocyte lineage cells (oligodendrocyte progenitors, premyelinating oligodendrocytes, and mature oligodendrocytes), astrocytes, and microglia in 8-week-old (young adult) and 32-week-old (aged) corpus callosum showed that young adult cells still include immature oligodendrocytes and that LAs contain a higher proportion of microglia than isolated cells. In aged mice, premyelinating oligodendrocytes were decreased, but microglia continued to be present in the LAs. These results suggest that the presence of microglia is important for the characteristic cell localization pattern of LAs. In a cuprizone-induced demyelination model, we observed re-formation of LAs after completion of cuprizone treatment, concurrent with remyelination. These re-formed LAs again contained more microglia than the isolated cells. This finding supports the hypothesis that microglia contribute to the formation and maintenance of LAs. In addition, regardless of the distribution of cells (LAs or isolated cells), astrocytes were found to be more abundant than in the normal corpus callosum at 24weeks after cuprizone treatment when remyelination is completed. This suggests that astrocytes are involved in maintaining the functions of remyelinated white matter.

Disrupted Brain Structural Network Connection in de novo Parkinson's Disease With Rapid Eye Movement Sleep Behavior Disorder.

ObjectiveTo explore alterations in white matter network topology in de novo Parkinson's disease (PD) patients with rapid eye movement sleep behavior disorder (RBD).Materials and MethodsThis study included 171 de novo PD patients and 73 healthy controls (HC) recruited from the Parkinson's Progression Markers Initiative (PPMI) database. The patients were divided into two groups, PD with probable RBD (PD-pRBD, n = 74) and PD without probable RBD (PD-npRBD, N = 97), according to the RBD screening questionnaire (RBDSQ). Individual structural network of brain was constructed based on deterministic fiber tracking and analyses were performed using graph theory. Differences in global and nodal topological properties were analyzed among the three groups. After that, post hoc analyses were performed to explore further differences. Finally, correlations between significant different properties and RBDSQ scores were analyzed in PD-pRBD group.ResultsAll three groups presented small-world organization. PD-pRBD patients exhibited diminished global efficiency and increased shortest path length compared with PD-npRBD patients and HCs. In nodal property analyses, compared with HCs, the brain regions of the PD-pRBD group with changed nodal efficiency (Ne) were widely distributed mainly in neocortical and paralimbic regions. While compared with PD-npRBD group, only increased Ne in right insula, left middle frontal gyrus, and decreased Ne in left temporal pole were discovered. In addition, significant correlations between Ne in related brain regions and RDBSQ scores were detected in PD-pRBD patients.ConclusionsPD-pRBD patients showed disrupted topological organization of white matter in the whole brain. The altered Ne of right insula, left temporal pole and left middle frontal gyrus may play a key role in the pathogenesis of PD-RBD.

Imaging pathologies of the corpus callosum

The corpus callosum is the largest fiber bundle in the cerebral white matter in the human brain. Amultitude of disorders including congenital malformations, acute and chronic traumatic lesions, ischemia, neoplasms, secondary manifestations of metabolic, toxic or degenerative diseases as well as chronic inflammatory and demyelinating diseases can primarily or secondarily affect the corpus callosum. This article presents magnetic resonance imaging (MRI) characteristics of the most relevant diseases affecting the corpus callosum.

Microstructure in patients with visual snow syndrome: an ultra-high field morphological and quantitative MRI study.

Visual snow syndrome is a neurological condition characterized by continuous visual disturbance and a range of non-visual symptoms, including tinnitus and migraine. Little is known about the pathological mechanisms underlying visual snow syndrome. Here, we assessed brain morphometry and microstructure in visual snow syndrome patients using high-resolution structural and quantitative MRI. Forty visual snow syndrome patients (22 with migraine) and 43 controls underwent 7-Tesla MRI (MP2RAGE, 0.75 mm isotropic resolution). Volumetric and quantitative T1 values were extracted for white and grey matter regions and compared between groups. Where regions were significantly different between groups (false discovery rate corrected for multiple comparisons), post hoc comparisons were examined between patients with and without migraine. For visual snow syndrome patients, significant MRI variables were correlated with clinical severity (number of visual symptoms, perceived visual snow intensity, disruptiveness, fatigue and quality of life) and psychiatric symptoms prevalent in visual snow syndrome (depression, anxiety and depersonalization). Finally, cortical regions and individual thalamic nuclei were studied. Compared with controls, visual snow syndrome patients demonstrated a trend towards larger brain and white matter volumes and significantly lower T1 values for the entire cortex (P < 0.001), thalamus (P = 0.001) and pallidum (P = 0.001). For the patient group, thalamic T1 correlated with number of visual symptoms (P = 0.019, r = 0.390) and perceived disruptiveness of visual snow (P = 0.010, r = 0.424). These correlations did not survive multiple comparison corrections. As for specificity in visual snow syndrome group, T1 changes were most evident in caudal regions (occipital cortices) followed by parietal, temporal and prefrontal cortices. T1 values differed between groups for most individual thalamic nuclei. No differences were revealed between patients with and without migraine. In visual snow syndrome patients, we observed no changes in morphometry, instead widespread changes in grey matter microstructure, which followed a caudal-rostral pattern and affected the occipital cortices most profoundly. Migraine did not appear to independently affect these changes. Lower T1 values may potentially result from higher neurite density, myelination or increased iron levels in the visual snow syndrome brain. Further investigation of these changes may enhance our understanding of the pathogenesis of visual snow syndrome, ultimately leading to new treatment strategies.

Brain structural abnormalities in six major psychiatric disorders: shared variation and network perspectives.

Common brain abnormalities are a possible explanation for comorbidities in psychiatric disorders. Challenges in understanding these conditions are likely due to the paucity of studies able to analyze the extent and regional distribution of shared morphometric abnormalities between disorders. Recently, Opeal et al. presented an elegant rationale to investigate shared and specific morphometric measures of cortical thickness and subcortical gray matter volume between healthy individuals and subjects across six major psychiatric disorders. Although their approach has the potential to systematically portray shared brain alterations, the chosen principal component analysis solution may not address the central question of the observed shared versus specific brain alterations due to misspecification of the number of components. Given how this misspecification can lead to different conclusions, we reanalyzed Opel et al. data to thoroughly determine the number of factors to be considered, explore the alternative solution, and visualize the patterns of shared brain matter correlations using network analysis. Our approach suggests that a unidimensional solution was appropriate in this situation. The unidimensional solution indicated that brain alterations in autism spectrum disorder (ASD) had a significant negative component loading, suggesting that brain abnormalities found in ASD covaried with major depressive disorder (MDD), bipolar disorder (BD), schizophrenia (SCZ), and obsessive-compulsive disorder (OCD), a finding not demonstrated by the original work. Network analysis indicated that SCZ had the highest strength, BD the highest closeness, and BD and MDD had the highest betweenness in the network. This work highlights how different component solutions can lead to different conclusions, with important implications for the understanding of overlapped patterns of symptoms among six major psychiatric diseases. The network approach is complementary in indicating central markers of specific psychopathology domains. Investigations using shared-variation and network perspectives are promising for the study of pathophysiological patterns of common brain alterations.

The role of the venous system in the maintenance of cerebral perfusion pressure in acute ischemic stroke

The article analyzes the state of cerebral venous hemodynamics in the acute period of ischemic stroke based on the results of clinical neurological, Dopplerographic, neuroimaging and cerebrospinal fluid examination of patients with different amounts of brain matter damage. Factors for predicting the development of moderate or severe cerebral venous dyscirculation have been identified. Attention is paid to the importance of a comprehensive examination of patients with assessment of cerebral venous blood flow in the acute period of ischemic stroke.