Heterogeneity of cerebral atrophic rate in mild cognitive impairment and its interactive association with proteins related to microglia activity on longitudinal cognitive changes.

BACKGROUND: Heterogeneity of cerebral atrophic rate commonly exists in mild cognitive impairment (MCI), which may be associated with microglia-involved neuropathology and have an influence on cognitive outcomes. OBJECTIVE: We aim to explore the heterogeneity of cerebral atrophic rate among MCI and its association with plasma proteins related to microglia activity, with further investigation of their interaction effects on long-term cognition. SUBJECTS: A total of 630 MCI subjects in the ADNI database were included, of which 260 subjects were available with baseline data on plasma proteins. METHODS: Group-based multi-trajectory modeling (GBMT) was used to identify the latent classes with heterogeneous cerebral atrophic rates. Associations between latent classes and plasma proteins related to microglia activity were investigated with generalized linear models. Linear mixed effect models (LME) were implemented to explore the interaction effects between proteins related to microglia activity and identified latent classes on longitudinal cognitive changes. RESULTS: Two latent classes were identified and labeled as the slow-atrophy class and the fast-atrophy class. Associations were found between such heterogeneity of atrophic rates and plasma proteins related to microglia activity, especially AXL receptor tyrosine kinase (AXL), CD40 antigen (CD40), and tumor necrosis factor receptor-like 2 (TNF-R2). Interaction effects on longitudinal cognitive changes showed that higher CD40 was associated with faster cognitive decline in the slow-atrophy class and higher AXL or TNF-R2 was associated with slower cognitive decline in the fast-atrophy class. CONCLUSIONS: Heterogeneity of atrophic rates at the MCI stage is associated with several plasma proteins related to microglia activity, which show either protective or adverse effects on long-term cognition depending on the variability of atrophic rates.

Neuroimaging Abnormalities in Patients with Subacute Sclerosing Panencephalitis : Prospective Follow-up Study.

OBJECTIVE: This study aimed to assess the neuroimaging abnormalities and their progression in patients with Subacute sclerosing panencephalitis (SSPE) and identify clinical predictors of these imaging findings. METHODS: This prospective observational study evaluated clinical and neuroimaging features in patients with SSPE. Patients were categorized using Dyken's criteria, Jabbour's staging system, and the definition of fulminant SSPE. They underwent comprehensive clinical assessments, cerebrospinal fluid examination, Electroencephalogram (EEG), and Magnetic Resonance Imaging (MRI) scans. Treatment involved intrathecal interferon­α and antiepileptic medications. Functional disability was assessed using the modified Barthel index. Follow-ups were performed at 6 months, including reassessment of Modified Barthel Index (MBI) and Jabbour's staging and EEG and MRI scans. RESULTS: The mean age was 13.9 ± 6.7 years, with males comprising 81.5% (44/54) of the cohort. Fulminant SSPE was noted in 33% (18/54) of cases. Disease duration before presentation varied significantly between fulminant and non-fulminant forms (p = 0.001). Neuroimaging abnormalities were more prevalent in JS III stage patients, with diffuse cerebral atrophy being a significant finding (p = 0.011). Basal ganglia involvement correlated with movement disorders. The 6­month follow-up showed increased cerebral atrophy (p = 0.004). Increasing disease duration was an independent predictor of cerebral atrophy. An Intercomplex interval (ICI) of more than 10 minutes correlated with normal neuroimaging, 10 patients died within the study period, 8 of whom had fulminant SSPE. CONCLUSION: Parieto-occipital White matter hyperintensity (WMH) is the most prevalent and sensitive neuroimaging finding for the diagnosis of SSPE. Despite interferon treatment, cerebral atrophy progressed in both aggressive and fulminant SSPE. Increasing disease duration is an independent predictor of cerebral atrophy.

Early-Onset Epileptic Encephalopathy Responsive to Phenytoin: A Diagnostic Clue for Fibroblast Growth Factor 12 Mutation.

We present a case of a three-year-old girl with a rare genetic epilepsy with developmental delay. She was born to a non-consanguineous parentage and required resuscitation soon after delivery via cesarean section. The patient had her first seizure within 36 hours of life, which progressed into refractory epilepsy. She required multiple hospital admissions due to prolonged seizures. Despite being tried on multiple drug combinations over the years, she responded only to phenytoin. Basic imaging and other investigations, including genetic analysis, revealed a fibroblast growth factor 12 (FGF12) mutation. Mutations in these genes cause refractory early-onset seizures associated with severe developmental delay. Due to early and appropriate intervention with phenytoin, she had good seizure control which probably resulted in a better developmental outcome.

Neuropsychiatric and Cognitive Symptoms: Two Sides of the Same Coin?

Neuropsychiatric symptoms (NPS) are increasingly being recognized as clinical markers for incipient dementia in Alzheimer's disease (AD dementia). NPS may reinforce cognitive impairment or decline and vice versa. Although NPS are frequent already in mild cognitive impairment, their mechanisms are poorly understood. It is unclear if they share biological mechanisms with cognitive symptoms and how they are associated to structural brain changes, but evidence suggests associations of NPS to cerebral atrophy. An additional NPS dimension in AD dementia concepts might add valuable information to detect patients at risk for AD dementia.

Late Presentation of ß-Thalassemia Major Patient With Left Hemiparesis: A Case Report.

Thalassemia is a hereditary autosomal recessive disorder that is distinguished by a diminished rate of hemoglobin (Hb) synthesis arising from an anomaly in the synthesis of α or ß globin chains. Classical symptoms of ß-thalassemia are frequently observed in patients who present late for blood transfusion (BT), which is typical among South Asian countries in light of their limited resources. This case report is an uncommon instance of a typical occurrence that has been infrequently reported in the South Asian region. The reporting of this case will assist healthcare workers in managing cases appropriately. We present a 12-year-old female child diagnosed with ß-thalassemia major with a late presentation than usual accompanied by an unusual finding of left hemiparesis at a young age of five years. The patient had been lost to follow-up, presented with easy fatiguability, poor weight gain, and growth restriction, all of which are classic symptoms of ß-thalassemia. The patient was treated with a BT and continued to be monitored for transfusion and iron overload management.

The effect of patient age on the degree of midline shift caused by chronic subdural hematomas: a volumetric analysis.

OBJECTIVE: Chronic subdural hematomas (CSDHs) are the among the most common conditions treated by neurosurgeons. Midline shift (MLS) is used as a radiological marker of CSDH severity and the potential need for urgent surgical evacuation. However, a patient's age may affect the degree of MLS for a given hematoma volume. This study aimed to investigate the correlation between the patient's age and the MLS caused by CSDH. METHODS: The database of patients treated for CSDH was reviewed in a single institution. Patients with unilateral CSDH were included. To measure CSDH volume, the preprocedural head CT scans underwent 3D volumetric reconstruction using the TeraRecon software. The effect of age on MLS after adjusting for CSDH volume was investigated using linear regression analysis. RESULTS: Sixty-nine hematomas in 69 patients were included. The age of patients ranged from 25 to 94 years (mean 71.6 years). Hematoma volume and MLS ranged from 27.8 to 215 mL (mean 99.3 mL) and 0-17 mm (mean 6.5 mm), respectively. On multivariate regression analysis, MLS showed a significant independent negative correlation with age after adjusting for CSDH volume (OR -0.11, 95% CI -0.16 to -0.06; p < 0.001), meaning that for a fixed CSDH volume, with each 10-year increase in age the MLS will reduce by 1.1 mm. Moreover, MLS-to-volume ratio showed a significant negative linear correlation with age (r2 = 0.32; p < 0.001). Ten-milliliter increments in CSDH volume resulted in a 1.09-mm increase in MLS in patients younger than 60 years, which is 2.4-fold higher compared to the 0.46-mm increase in those older than 75 years (p < 0.001). CONCLUSIONS: For a fixed CSDH volume, older age correlates with significantly lower MLS. This could be explained by higher parenchymal compliance in older individuals due to increased brain atrophy, and a larger subdural space. Clinical use of MLS to estimate severity of CSDH and gauge treatment decisions should take the patient's age into account.

Autologous olfactory mucosa mesenchymal stem cells treatment improves the neural network in chronic refractory epilepsy.

BACKGROUND AND AIMS: Refractory epilepsy is also known as drug-resistant epilepsy with limited clinical treatment. Benefitting from its safety and easy availability, olfactory mucosa mesenchymal stem cells (OM-MSCs) are considered a preferable MSC source for clinical application. This study aims to investigate whether OM-MSCs are a promising alternative source for treating refractory epilepsy clinically and uncover the mechanism by OM-MSCs administration on an epileptic mouse model. METHODS: OM-MSCs were isolated from turbinal and characterized by flow cytometry. Autologous human OM-MSCs treatment on a patient was carried out using intrathecal administration. Epileptic mouse model was established by 1 mg/kg scopolamine and 300 mg/kg pilocarpine treatment (intraperitoneal). Stereotaxic microinjection was employed to deliver the mouse OM-MSCs. Mouse electroencephalograph recording was used to investigate the seizures. Brain structure was evaluated by magnetic resonance imaging (MRI). Immunohistochemical and immunofluorescent staining of GFAP, IBA1, MAP2, TUBB3, OLIG2, CD4, CD25, and FOXP3 was carried out to investigate the neural cells and Treg cells. QRT-PCR and ELISA were performed to determine the cytokines (Il1b, Il6, Tnf, Il10) on mRNA and protein level. Y-maze, the object location test, and novel object recognition test were performed to measure the cognitive function. Footprint test, rotarod test, balance beam test, and grip strength test were conducted to evaluate the locomotive function. Von Frey testing was carried out to assess the mechanical allodynia. RESULTS: Many beneficial effects of the OM-MSC treatment on disease status, including seizure type, frequency, severity, duration, and cognitive function, and no apparent adverse effects were observed at the 8-year follow-up case. Brain MRI indicated that autologous OM-MSC treatment alleviated brain atrophy in epilepsy patients. A study in an epileptic mouse model revealed that OM-MSC treatment recruited Treg cells to the brain, inhibited inflammation, rebuilt the neural network, and improved the cognitive, locomotive, and perceptive functions of epileptic mice. CONCLUSIONS: Autologous OM-MSC treatment is efficacious for improving chronic refractory epilepsy, suggesting a future therapeutic candidate for epilepsy. TRIAL REGISTRATION: The study was registered with Chinese Clinical Trial Registry (ChiCTR2200055357).

Arteriolosclerosis CSVD: a common cause of dementia and stroke and its association with cognitive function and total MRI burden.

Objective: Arteriolosclerosis cerebral small vessel disease (CSVD) is a common type of CSVD. This study aimed to explore the factors associated with cognitive function and total MRI burden related to the disease. Methods: The demographic characteristics, clinical manifestations, cognitive function score, Barthel Index (BI), blood test index, and follow-up results of arteriolosclerosis CSVD patients treated for the first time in our hospital from January 2014 to August 2022 were collected. White matter hyperintensity (WMH) Fazekas score, total MRI burden, and cerebral atrophy grade were evaluated according to brain MRI findings. Factors associated with CSVD cognitive function were analyzed by binary logistic regression. The correlative factors related to the total MRI burden of CSVD were analyzed by ordered multiple logistic regression. Results: A total of 146 patients were included in this study, of which 132 cases (90.4%) had hypertension. There were 108 patients (74.0%) with cognitive dysfunction, 97 patients (66.4%) with balance and gait disorders, and 83 patients (56.8%) with moderate-to-severe dependence in daily life (BI ≤ 60 points). Of 146 patients, 79 (54.1%) completed clinical and imaging follow-ups for a median of 3 years. The number of patients with cognitive impairment and BI ≤ 60 points after follow-up significantly increased compared with the first admission (P < 0.001). There were also significant differences in total MRI burden (P = 0.001), WMH Fazekas score, and cerebral atrophy grade (P < 0.001). Mean age (P = 0.012), median deep WMH Fazekas score (P = 0.028), and median deep (P < 0.001) and superficial (P =0.002) cerebral atrophy grade of patients with cognitive impairment at first admission were all higher than those with non-cognitive impairment. Multivariate analysis showed that deep cerebral atrophy was independently and significantly associated with cognitive impairment of CSVD (P = 0.024), and hypertension was significantly and independently associated with total MRI burden (P = 0.001). Conclusion: The disease course of arteriolosclerosis CSVD may be related to cognitive function and total MRI burden. Deep cerebral atrophy was an independent risk factor for cognitive dysfunction in arteriolosclerosis CSVD, and hypertension was an independent risk factor for total MRI burden.

Visual impairment following aluminum phosphide poisoning: A rare case.

Key Clinical Message: Aluminum phosphide poisoning may cause rare visual impairment. In a case, a 31-year-old female, visual loss was linked to shock-induced hypoperfusion, causing oxygen lack and cerebral atrophy, emphasizing the need for identifying atypical symptoms. Abstract: This case report describes the multidisciplinary evaluation of a 31-year-old female patient who suffered from visual impairment as a result of aluminum phosphide (AlP) poisoning. Phosphine, which is formed in the body when AlP reacts with water, cannot cross the blood-brain barrier; therefore, visual impairment seems unlikely to be the direct result of phosphine. To our knowledge, it is the first documented report of such impairment due to AlP.

Burden of dilated perivascular spaces in patients with moyamoya disease and moyamoya syndrome is related to middle cerebral artery stenosis.

Background and objective: The correlation between intracranial large artery disease and cerebral small vessel disease (CSVD) has become a noteworthy issue. Dilated perivascular spaces (dPVS) are an important marker of CSVD, of which cerebral atrophy has been regarded as one of the pathological mechanisms. DPVS has been found to be associated with vascular stenosis in patients with moyamoya disease (MMD), but the underlying mechanism remains unclear. The purpose of our study was to explore the correlation between the middle cerebral artery (MCA) stenosis and dPVS in the centrum semiovale (CSO-dPVS) in patients with MMD/moyamoya syndrome (MMS) and to determine whether brain atrophy plays a mediating role in this relationship. Methods: A total of 177 patients were enrolled in a single-center MMD/MMS cohort. Images of their 354 cerebral hemispheres were divided into three groups according to dPVS burden: mild (dPVS 0-10), moderate (dPVS 11-20), and severe (dPVS > 20). The correlations among cerebral hemisphere volume, MCA stenosis, and CSO-dPVS were analyzed, adjusting for the confounding factors of age, gender, and hypertension. Results: After adjustment for age, gender, and hypertension, the degree of MCA stenosis was independently and positively associated with ipsilateral CSO-dPVS burden (standardized coefficient: ß = 0.247, P < 0.001). A stratified analysis found that the subgroup with a severe CSO-dPVS burden exhibited a significantly higher risk of severe stenosis of the MCA [p < 0.001, OR = 6.258, 95% CI (2.347, 16.685)]. No significant correlation between CSO-dPVS and ipsilateral hemisphere volume was found (p = 0.055). Conclusion: In our MMD/MMS cohort, there was a clear correlation between MCA stenosis and CSO-dPVS burden, which may be a direct effect of large vessel stenosis, without a mediating role of brain atrophy.

Novel compound heterozygous mutations in the AFG3L2 gene in a Chinese child with microcephaly, early-onset seizures, and cerebral atrophy.

Background: The most common disease caused by biallelic AFG3L2 mutations is spastic ataxia type 5 (SPAX5). Identification of complex phenotypes resulting from biallelic AFG3L2 mutations has been increasing in recent years. Methods: A retrospective analysis was performed on a child with microcephaly and recurrent seizures. The child underwent physical and neurological examinations, laboratory tests, electroencephalography (EEG), and brain magnetic resonance imaging (MRI). Trio-whole-exome sequencing (trio-WES) was performed to identify possible causative mutations. Results: We described a child who exhibited early-onset and intractable epilepsy, developmental regression, microcephaly, and premature death. Neuroimaging revealed global cerebral atrophy (GCA) involving the cerebrum, cerebellum, corpus callosum, brainstem, cerebellar vermis, and basal ganglia. On trio-WES, two novel compound heterozygous mutations, c.1834G > T (p.E612*) and c.2176-6T > A in the AFG3L2 gene, were identified in this patient. Conclusions: Our findings have expanded the mutation spectrum of the AFG3L2 gene and identified a severe neurodegenerative phenotype of global cerebral atrophy caused by biallelic AFG3L2 mutations.

Dyke-Davidoff-Masson Syndrome: A Classic Case Report.

Dyke-Davidoff-Masson syndrome (DDMS) is a rare neurological disorder found in children as well as adults. It is characterized by hemi cerebral atrophy. To date, very few cases of this disorder have been reported. Radiological imaging including magnetic resonance imaging (MRI) and computed tomography (CT) are accurate tools for the diagnosis of DDMS. We present a case of a 13-year-old female child who came with complaints of multiple episodes of generalized tonic-clonic seizures. In our case, clinical history and imaging with CT and MRI were accurate enough to diagnose DDMS.

Regular physical activity moderates the adverse impact of type 2 diabetes on brain atrophy independently from HbA1c.

Objective: Brain atrophy has been consistently associated with type 2 diabetes, beginning in early stages of dysglycemia, independently from micro and macrovascular complications. On the contrary, physical activity relates with larger brain volumes. Our aim is to assess the influence of regular physical activity on brain volumes in people with type 2 diabetes. Methods: A cross-sectional multimodal evaluation with 3T MRI was performed on 170 individuals: 85 individuals with type 2 diabetes and 85 controls. They underwent clinical examination, blood sampling and 3T MRI. Brain volumes (mm3) were estimated using FreeSurfer 7. Physical activity duration was self-reported by the participants as the number of hours of physical activity per week for at least the previous 6 months. Statistical analysis was performed with IBM SPSS 27. Results: People with type 2 diabetes had significantly lower cortical and subcortical volumes, adjusted for age and individual intracranial volume, comparing to controls. Regression analysis showed that within type 2 diabetes group, lower gray matter volumes were associated with lesser physical activity duration (hours/week), independently from HbA1c. Moreover, there were significant moderate positive correlations between regular physical activity duration and gray matter volumes of cortical and subcortical subregions, specifically in the diabetes group. Conclusions: This study reveals a putative beneficial effect of regular physical activity independently of glycemic control, as assessed by HbA1c, which might contribute to reduce the negative impact of type 2 diabetes in the brain.

Interrater reliability of modified visual mri rating scale assessing atrophy and white matter changes.

Background and purpose:

Cortical atrophy and white matter changes are common findings on magnetic resonance imaging among elderly. Several visual scales have been proposed to evaluate these changes using neuroimaging. We have recently proposed a scale (Modified Visual Magnetic Resonance Rating Scale) recently which allows us to evaluate atrophy, white matter hyperintensities, basal ganglia and infratentorial infarcts together. Our aim in this study was to evaluate the interrater reliability of magnetic resonance visual assessment using this scale between two neurologists and a radiologist. 

Randomly selected 30 patients in different ages who underwent brain magnetic resonance imaging between January 2014 and March 2015 were included. Axial T1, coronal T2, and axial FLAIR sequences were visually scored by two neurologists and one radiologist separately. Sulcal, ventricular and medial temporal lobe atrophy, periventricular and subcortical white matter hyperintensities, basal ganglia and infratentorial infarcts were graded according to our scale. The interrater reliability and internal consistency analysis were evaluated by using intraclass correlation coefficient and Cronbach’s alpha tests. 

The interrater agreements vary between good to excellent. The interrater correlations are moderate to excellent. Interrater correlations were excellent between two neurologists, especially on ventricular atrophy, medial temporal atrophy, basal ganglia infarcts, infratentorial infarcts. When assessing ventricular atrophy, interrater correlations between individual raters were higher than sulcal atrophy. We found good correlations between neurologists and radiologist, and excellent correlations between the two neurologists for medial temporal atrophy. We found excellent interrater correlations between neurologists and radiologist for white matter hyperintensities.

Our scale is a reliable tool assessing both atrophy and white matter hyperintensities with a good interrater reliability. Ventricular atrophy seems to be a more reliable marker than sulcal atrophy when assessing the atrophy on neuroimaging of a patient with memory decline. We think that the total score of the scale will also guide us in clinical practice.

A Biallelic Truncating Variant in the TPR Domain of GEMIN5 Associated with Intellectual Disability and Cerebral Atrophy.

GEMIN5 is a multifunctional RNA-binding protein required for the assembly of survival motor neurons. Several bi-allelic truncating and missense variants in this gene are reported to cause a neurodevelopmental disorder characterized by cerebellar atrophy, intellectual disability (ID), and motor dysfunction. Whole exome sequencing of a Pakistani consanguineous family with three brothers affected by ID, cerebral atrophy, mobility, and speech impairment revealed a novel homozygous 3bp-deletion NM_015465.5:c.3162_3164del that leads to the loss of NM_015465.5 (NP_056280.2):p. (Asp1054_Ala1055delinsGlu) amino acid in one of the α-helixes of the tetratricopeptide repeats of GEMIN5. In silico 3D representations of the GEMIN5 dimerization domain show that this variant likely affects the orientation of the downstream sidechains out of the helix axis, which would affect the packing with neighboring helices. The phenotype of all affected siblings overlaps well with previously reported patients, suggesting that NM_015465.5: c.3162_3164del (NP_056280.2):p. (Asp1054_Ala1055delinsGlu) is a novel GEMIN5 pathogenic variant. Overall, our data expands the molecular and clinical phenotype of the recently described neurodevelopmental disorder with cerebellar atrophy and motor dysfunction (NEDCAM) syndrome.

La atrofia cerebral como hallazgo o factor predictor del deterioro cognitivo en el envejecimiento normal / Cerebral Atrophy as a Finding of Predictive Factor for Cognitive Impairment in Normal Aging

Introducción: En el curso del envejecimiento es conocida la existencia de un patrón complejo de cambios estructurales cerebrales, conductuales y cognitivos, en ocasiones relacionados con enfermedades neurológicas y psiquiátricas. Objetivo: Determinar la posible relación de causalidad de la atrofia cerebral en la aparición del deterioro cognitivo en el curso del envejecimiento normal. Métodos: Se desarrolló un estudio retrospectivo, transversal, descriptivo y observacional. El universo estuvo conformado por el total de los pacientes de ambos sexos con edades comprendidas entre 35-74 años de edad, con indicaciones previas de tomografía computarizada de cráneo y cuyos resultados fueron informados con signos de atrofia cerebral, cuya cifra ascendió a 733. Resultados: El grupo de edad que predomino fue el de 45-54 años (35,3 por ciento), así como las pacientes del sexo femenino (66,3 por ciento). El 27,7 por ciento tenía como nivel de escolaridad el técnico medio superior y 36,2 por ciento fueron pacientes amas de casa. El 99,7 por ciento fueron diestros. Un total de 368 voluntarios presentaron deterioro cognitivo y 365 sujetos no evidenciaron declive en las funciones exploradas. Las funciones de atención y cálculo y retención verbal a corto plazo fueron las que se vieron más afectadas, seguidas de orientación espacial y memoria verbal de fijación. Conclusiones: No se logró establecer una relación de causalidad significativa entre el diagnóstico radiológico de atrofia cerebral y la presencia de deterioro cognitivo(AU)

Introduction: In the course of aging, the existence of a complex pattern of behavioral, cognitive and cerebral structural changes is known, sometimes related to neurological and psychiatric diseases. Objective: To determine the possible causal relationship of cerebral atrophy with the onset of cognitive impairment in the course of normal aging. Methods: A retrospective, cross-sectional, descriptive and observational study was carried out. The study universe consisted of all patients of both sexes aged 35-74 years, with previous indications for cranial computed tomography and whose results were reported with signs of cerebral atrophy, which numbered 733. Results: The predominant age group was 45-54 years old (35.3percent), as well as female patients (66.3percent). The educational level of 27.7percent of the patients was technical high school and 36.2percent were housewife patients. A total of 99.7percent were right-handed. A total of 368 volunteers showed cognitive impairment and 365 subjects showed no decline in the tested functions. The functions of attention and calculation, as well as short-term verbal retention, were the most affected, followed by spatial orientation and speech retention memory. Conclusions: No significant causal relationship was established between the radiological diagnosis of cerebral atrophy and the presence of cognitive impairment(AU)

Dialysis adequacy and hemoglobin levels predict cerebral atrophy in maintenance-hemodialysis patients.

The pathogenesis of cerebral atrophy (CA) is not clear. Previous studies show a high incidence of preterm CA in hemodialysis patients. This study aims to investigate the factors influencing CA and to derive a CA prediction nomogram in maintenance-hemodialysis patients. First, brain volumes of hemodialysis patients (≤55 years) were compared against age- and sex-matched healthy controls, and differences were revealed in bilateral insular cisterns width, maximum cerebral sulci width, Evans index, ventricular-brain ratio, frontal atrophy index, and temporal lobe ratio. Then, the patients were divided equally into "no or mild" or "severe" CA groups. Potential factors influencing CA were screened. Kt/V (urea removal index) and hemoglobin levels negatively correlated with CA degree, and were used to establish a nomogram within randomly assigned training and validation patient groups. The areas under the receiver operating characteristic curves (AUROC) for training and validation groups were 0.703 and 0.744, respectively. When potassium and calcium were added to the nomogram, the AUROC for training/validation group increased to 0.748/0.806. The nomogram had optimal AUROC for training (0.759) and validation (0.804) groups when albumin was also included. Hemodialysis patients showed reduced anterior brain volumes and the nomogram established herein may have predictive value for developing CA.

Diagnostic determination by diffusion tensor imaging of neural axon injury between the 2 hemispheres following traumatic brain injury.

Traumatic brain injury (TBI) is caused by an external mechanical force to the head resulting in alteration of brain function. However, the injury to neural tracts and the connections between them is difficult to diagnose using traditional imaging techniques. A 54-year-old woman visited our clinic because of insufficient coordination of her body. Her personal history included severe TBI with a 10-day coma medically treated 10 years previously. She presented with memory impairment and insufficient coordination of her body, suggesting post-concussion syndrome. Her Glasgow Coma Scale score was 15 and the strength testing result was 5/5 for both sides; however, she could not walk. She had been examined at many medical centers, but without a diagnosis of her condition. She was scanned using morphometric magnetic resonance imaging (MRI), which detected a significant reduction in the corpus callosum. MRI-diffusion tensor imaging (DTI) revealed decreased fractional anisotropy (FA) in the white matter of the right temporal lobe and the corpus callosum. FA reflects the degree of anisotropy of water molecules. The decrease in FA in the corpus callosum indicated loss of connection between the 2 hemispheres. MRI tractography was used to describe the number of neural tracts in the corpus callosum. MRI-DTI and MRI tractography served as powerful diagnostic tools, providing imaging results that offered an explanation for our patient's clinical picture.

Brain atrophy in acute ischaemic stroke patients treated with reperfusion therapy: a systematic review.

BACKGROUND: Brain atrophy (BA) may have a role in acute ischemic stroke (AIS) in mediating outcomes after reperfusion therapy. The extent of this association is not well understood. PURPOSE: : To examine the impact of pre-existing BA on functional outcome, survival, symptomatic intracerebral hemorrhage (sICH), and early neurological change in patients with AIS treated with intravenous thrombolysis (IVT) and/or endovascular thrombectomy (EVT). MATERIAL AND METHODS: PubMed, EMBASE, and the Cochrane library were searched for studies on BA in AIS receiving reperfusion therapy. Studies were included if: (i) patients were aged ≥18 years; (ii) patients had been diagnosed with AIS; (iii) patients received IVT and/or EVT; (iv) studies reported on BA; (v) studies reported on post-reperfusion outcomes; and (vi) studies had a sample size of >25 patients. RESULTS: A total of 4444 patients from eight studies were included. Four out of seven studies reporting on 90-day functional outcome found pre-existing BA to be significantly associated with poor functional outcome. Moreover, two out of four studies found BA to be a significant predictor of 90-day mortality. None of the included studies reported a significant association of BA with sICH or early neurological deterioration. CONCLUSION: This systematic review indicates a potential prognostic role of BA in AIS. Quantitative analysis of association of BA with outcomes in AIS is not possible given the heterogeneity in BA assessment and reporting across studies. Future studies using standardized BA assessment are warranted to clarify its association with clinical and safety outcomes in AIS.