Permanent Cognitive Impairment Research Articles

Knowledge and utilization of iodized salt among expectant mothers in Harar City's public health facilities: a multicenter study in Eastern Ethiopia.

Insufficient iodine intake during pregnancy can result in abortion, stillbirths, neonatal mortality, cretinism and permanent cognitive impairment. Even although iodized salt is widely accessible in Ethiopia, pregnant women still experience persistent problems related to iodine deficiency disorders. A facility-based cross-sectional study was conducted among randomly selected 573 pregnant women who were attending antenatal care services at public health facilities. Bivariate and multivariable logistic regression models were used, and independent predictors were determined based on adjusted ORs with 95% CIs and p<0.05. Knowledge and practice of pregnant women on iodized utilization were 35.6% (95% CI 31.8 to 39.6%) and 37.7% (95% CI 32.1 to 42.9%), respectively. Living in urban areas (adjusted OR [AOR]=1.976, 95% CI 1.136 to 3.435) and having a higher level of education (AOR=2.018, 95% CI 1.037 to 3.930) were associated with having adequate knowledge. Having a diploma or higher education (AOR=2.684, 95% CI 1.137 to 6.340) and adequate knowledge about iodized salt utilization (AOR=2.095, 95% CI 1.273 to 3.447) were significantly associated with good practice. The current study highlights the level of knowledge and practices of pregnant women on iodized salt. It emphasizes the necessity for targeted programs about the benefits of iodized salt and how to use it correctly, particularly for those with low literacy levels and those living in rural areas.

Memory loss and aberrant neurogenesis in mice exposed to patient anti-N-methyl-d-aspartate receptor antibodies

ObjectiveAnti-N-methyl-d-aspartate receptor (anti-NMDAR) encephalitis results in chronic epilepsy and permanent cognitive impairment. One of the possible causes of cognitive impairment in anti-NMDAR could be aberrant neurogenesis, an established contributor to memory loss in idiopathic drug-resistant epilepsy. We developed a mouse model of anti-NMDAR encephalitis and showed that mice exposed to patient anti-NMDAR antibodies for 2 weeks developed seizures and memory loss. In the present study, we assessed the delayed effects of patient-derived antibodies on cognitive phenotype and examined the corresponding changes in hippocampal neurogenesis. MethodsMonoclonal anti-NMDAR antibodies or control antibodies were continuously infused into the lateral ventricle of male C56BL/6J mice (8–12 weeks) via osmotic minipumps for 2 weeks. The motor and anxiety phenotypes were assessed using the open field paradigm, and hippocampal memory and learning were assessed using the object location, Y maze, and Barnes maze paradigms during weeks 1 and 3–4 of antibody washout. The numbers of newly matured granule neurons (Prox-1+) and immature progenitor cells (DCX+) as well as their spatial distribution within the hippocampus were assessed at these time points. Bromodeoxyuridine (BrdU, 50 mg/kg, i.p., daily) was injected on days 2–12 of the infusion, and proliferating cell immunoreactivity was compared in antibody-treated mice and control mice during week 4 of the washout. ResultsMice infused with anti-NMDAR antibodies demonstrated spatial memory impairment during week 1 of antibody washout (p = 0.02, t-test; n = 9–11). Histological analysis of hippocampal sections from these mice revealed an increased ectopic displacement of Prox-1+ cells in the dentate hilus compared to the control-antibody-treated mice (p = 0.01; t-test). Mice exposed to anti-NMDAR antibodies also had an impairment of spatial memory and learning during weeks 3–4 of antibody washout (object location: p = 0.009; t-test; Y maze: p = 0.006, t-test; Barnes maze: p = 0.008, ANOVA; n = 8–10). These mice showed increased ratios of the low proliferating (bright) to fast proliferating (faint) BrdU+ cell counts and decreased number of DCX+ cells in the hippocampal dentate gyrus (p = 0.006 and p = 0.04, respectively; t-tests) suggesting ectopic migration and delayed cell proliferation. SignificanceThese findings suggest that memory and learning impairments induced by patient anti-NMDAR antibodies are sustained upon removal of antibodies and are accompanied by aberrant hippocampal neurogenesis. Interventions directed at the manipulation of neuronal plasticity in patients with encephalitis and cognitive loss may be protective and therapeutically relevant.

Criminal behavior in alcohol-related dementia and Wernicke-Korsakoff syndrome: a Nationwide Register Study.

Chronic heavy alcohol use may lead to permanent brain damage, cognitive impairment, and dementia. While the link between alcohol use and crime is strong, virtually no research exists on the criminal behavior of patients with the alcohol-related neurocognitive disorders of Wernicke-Korsakoff syndrome (WKS) and alcohol-related dementia (ARD). The study population included all persons diagnosed with WKS (n = 1149) or ARD (n = 2432) in Finland in 1998-2015. Data on diagnoses, mortality, and crime were obtained from Finnish nationwide registers. Crime incidences were calculated 4 years before and after diagnosis. Crime types, incidences, and mortality were compared between disorders and with the general population. Altogether 35.6% of WKS patients and 23.6% of ARD patients had committed crimes in the 4 years preceding diagnosis, most commonly property and traffic crimes, followed by violent crimes. The incidence of criminal behavior decreased significantly after diagnosis; in WKS patients, the standardized criminality ratio (SCR), the ratio of observed to expected number of crimes (95% CI), was 3.91 (3.72-4.10) in 4 years before and 2.80 (2.61-3.00) in 4 years after diagnosis. Likewise, in ARD patients, the SCRs were 2.63 (2.51-2.75) before and 0.84 (0.75-0.92) after diagnosis. No significant difference emerged in mortality between persons with and without a criminal history. Persons with alcohol-related neurocognitive disorders frequently engage in criminal behavior prior to diagnosis, especially multiple offending. In the 4 years before and after diagnosis, crime rates declined in a linear fashion, with a marked reduction after diagnosis.

Therapy preferences of patients with cancer.

e24205 Background: Clear understanding of patient (pt) preferences is crucial for creating a treatment (tx) plan that aligns with pt's goals and expectations. We developed "Therapy Preference Scale" (TPS), a self-reported questionnaire, to measure tx preferences of pts with cancer. TPS includes 30 questions: 19 questions on pt preferences on safety, efficacy, and other aspects of therapy (on scale of 0-10), 8 questions on importance of different aspects of tx (on 4-item Likert scale with choices of 'strongly disagree,' 'disagree,' 'agree,' and 'strongly agree.'), and 3 questions on intent of therapy, expenses, and life expectancy gain. This report presents results of the 8 questions rated on the 4-item Likert scale from a prospective study using TPS. Methods: 300 pts &gt; 18 yrs with a cancer diagnosis completed TPS. We divided pts into 4 groups: Male &lt; 60 yrs (M &lt; 60), Male ≥60 yrs (M ≥60), Female &lt; 60 yrs (F &lt; 60), and Female ≥60 yrs (F ≥60). We compared responses between M &lt; 60 and M≥60 and between F &lt; 60 and F≥60. The responses were categorized into 2 groups: "disagree" (combining "strongly disagree" and "disagree") and "agree" (combining "strongly agree" and "agree"). Results: Median age was 61 yrs (range 19-89). 62% had solid tumors. 57% indicated cure as their tx goal versus gain in life expectancy without cure (35%) or symptom relief (8%). 4 groups were 20% M &lt; 60, 32% M ≥60, 19% F &lt; 60, and 29% F ≥60. M &lt; 60 were more likely to accept tx with side effects and financial burden, while M ≥60 prioritized avoiding poor quality of life (QoL). F &lt; 60 were more likely to undergo tx causing significant pain, while F ≥60 would avoid permanent cognitive impairment. Table 1 shows percentage of pts who agreed with the 8 questions. Conclusions: Despite similar preferences for a cure, age and gender play role in prioritizing tx options, including those with potential side effects such as life-threatening infection, poor QoL, financial burden, severe pain, and permanent cognitive impairment. TPS can improve the precision medicine approach and aid in choosing the right tx for each pt. [Table: see text]

Engineered Mesenchymal Stem Cells Over-Expressing BDNF Protect the Brain from Traumatic Brain Injury-Induced Neuronal Death, Neurological Deficits, and Cognitive Impairments.

Traumatic brain injury (TBI) causes transitory or permanent neurological and cognitive impairments, which can intensify over time due to secondary neuronal death. However, no therapy currently exists that can effectively treat brain injury following TBI. Here, we evaluate the therapeutic potential of irradiated engineered human mesenchymal stem cells over-expressing brain-derived neurotrophic factor (BDNF), which we denote by BDNF-eMSCs, in protecting the brain against neuronal death, neurological deficits, and cognitive impairment in TBI rats. BDNF-eMSCs were administered directly into the left lateral ventricle of the brain in rats that received TBI damage. A single administration of BDNF-eMSCs reduced TBI-induced neuronal death and glial activation in the hippocampus, while repeated administration of BDNF-eMSCs reduced not only glial activation and delayed neuronal loss but also enhanced hippocampal neurogenesis in TBI rats. In addition, BDNF-eMSCs reduced the lesion area in the damaged brain of the rats. Behaviorally, BDNF-eMSC treatment improved the neurological and cognitive functions of the TBI rats. The results presented in this study demonstrate that BDNF-eMSCs can attenuate TBI-induced brain damage through the suppression of neuronal death and increased neurogenesis, thus enhancing functional recovery after TBI, indicating the significant therapeutic potential of BDNF-eMSCs in the treatment of TBI.

Transient cognitive impairment in the acute phase of stroke – prevalence, risk factors and influence on long-term prognosis in population of patients with stroke (research study – part of the PROPOLIS study)

BackgroundCognitive impairment is a common complication of the acute phase of stroke, which can be transient and resolve while still in the hospital. This study evaluated the prevalence and risk factors for transient cognitive impairment and their impact on long-term prognosis in a population of acute-phase stroke patients.MethodsConsecutive patients admitted to a stroke unit with acute stroke or transient ischemic attack were screened twice for cognitive impairment using the parallel version of Montreal Cognitive Assessment: the first time between the first and third day and the second time between the fourth and seventh day of hospitalization. If the second test score increased by two or more points, transient cognitive impairment was diagnosed. Patients were scheduled for follow-up visits three and 12 months after stroke. Outcome assessment included place of discharge, current functional status, dementia, or death.ResultsFour hundred forty-seven patients were included in the study, 234 (52.35%) were diagnosed with transient cognitive impairment. Delirium was the only independent risk factor for transient cognitive impairment (OR 2.417, 95%CI 1.096–5.333, p = 0.029). In the analysis of effects on three- and twelve-month prognosis, patients with transient cognitive impairment had a lower risk of hospital or institution stay 3 months after stroke compared with patients with permanent cognitive impairment (OR 0.396, 95%CI 0.217–0.723, p = 0.003). There was no significant effect on mortality, disability or risk of dementia.ConclusionsTransient cognitive impairment, which often occurs in the acute phase of stroke, does not increase the risk of long-term complications.

“When Resilience is Not Enough: Finding Our Way to Age-Friendly Hospitals”

This discussion features a multidisciplinary panel of providers from two different Arizona hospital systems. Each group will describe what they have done to create innovative approaches to preventing and mitigating hospital-acquired delirium. Drs. Agarwal and Hendrie from Banner University Medical Center, Phoenix, will present their EMR-based delirium detection tool and the Hospital Geriatrician Team response to those patients in their daily rounds. Anna Bourguet and Stephanie Lee from Southern Arizona VA Health Care System in Tucson will describe the creation and use of a Delirium Risk Assessment and Treatment computer-based tool for providers.Delirium, often referred to as toxic-metabolic encephalopathy, is the most common neuropsychiatric syndrome that occurs in the general hospital setting. Incidence can range from 10-30% in general hospital wards, up to 87% in ICU settings, up to 46% in surgical wards. Older adults are at higher risk for delirium than other age groups, and in 10-35% delirium is already present at hospital admission. Patients who meet criteria for “frail elderly” may have up to 60% incidence of delirium, regardless of their medical condition.Delirium vastly increases hospital costs ($152 billion annually has been reported), length of stay, and other medical morbidities. Post-delirium, risk of death is increased at time of discharge and even one year later. Risk of post-delirium institutionalization is increased. Another complication is less well known is permanent cognitive impairment. There is a reciprocal relation between delirium and dementia: dementia does lower the threshold for developing delirium, and after delirium there is an acceleration of cognitive decline. Treatment of delirium is largely via nonpharmacologic mitigation approaches, there are no FDA approved medications to treat this condition. The moderator of the session will describe the clinical syndrome of delirium, its prevalence and outcomes. In addition, the Hospital Elder Life program as well as ICU treatment strategies will be presented. We will describe the concept of Age-Friendly Hospitals and how they are used around the world.

Review of Neurofilaments as Biomarkers in Sepsis-Associated Encephalopathy.

Sepsis is a common and fatal disease, especially in critically ill patients. Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction with acute altered consciousness, permanent cognitive impairment, and even coma, accompanied by sepsis, without direct central nervous system infection. When managing SAE, early identification and quantification of axonal damage facilitate faster and more accurate diagnosis and prognosis. Although no specific markers for SAE have been identified, several biomarkers have been proposed. Neurofilament light chain (NFL) is a highly expressed cytoskeletal component of neurofilament (NF) proteins that can be found in blood and cerebrospinal fluid (CSF) after exposure to axonal injury. NFs can be used as diagnostic and prognostic biomarkers for sepsis-related brain injury. Phosphorylation of NFs contributes to the maturation and stabilization of cytoskeletal structures, especially axons, and facilitates axonal transport, including mitochondrial transport and energy transport. The stability of NF proteins can be assessed by monitoring the expression of NF genes. Furthermore, phosphorylation levels of NFs can be monitored to determine mitochondrial axonal transport associated with cellular energy metabolism at distal axons to assess progression during SAE treatment. This paper provides new insights into the biological characteristics, detection techniques, and scientific achievements of NFs, and discusses the underlying mechanisms and future research directions of NFs in SAE.

Alzheimer' disease prediction and classification using CT images through machine learning.

Numerous surveys using different techniques have been conducted in recent years to accurately classify Alzheimer's disease (AD). This research emphasized the identification of AD through neuroimaging data. However, it is important to identify symptoms as soon as possible when the disease-modifying medications function best during infection before a permanent cognitive impairment develops. The use of automated algorithms to detect the early symptom of AD to this information was very important. Machine Learning (ML) has been proposed for the evaluation of various image segmentation and database techniques. In addition, Visual Geometry Group (VGG)-16 et Improved Faster Recurrent Convolutional Neural Network (IFRCNN) method developed for the ImageNet database utilizing the mathematical model based on action recognition as a feature extractor for categorization work. Experiments are being conducted on the Alzheimer's Neuroimaging Initiative (ADNI) dataset, and the proposed system achieves the 98.32 % accuracy level (Tab. 6, Fig. 4, Ref. 34). Text in PDF www.elis.sk. Keywords: mild cognitive impairment, deep learning, Alzheimer's disease, expected risk.

Frontal aslant tract in the non-dominant hemisphere: A systematic review of anatomy, functions, and surgical applications.

Knowledge of both the spatial organization and functions of white-matter fiber tracts is steadily increasing. We report here the anatomy and functions of the frontal aslant tract (FAT) in the non-dominant hemisphere (usually the right hemisphere). Despite the structural symmetry between the right and left FAT, these two tracts seem to display functional asymmetry, with several brain functions in common, but others, such as visuospatial and social cognition, music processing, shifting attention or working memory, more exclusively associated with the right FAT. Further studies are required to determine whether damage to the right FAT causes permanent cognitive impairment. Such studies will constitute the best means of testing whether this tract is a critical pathway that must be taken into account during neurosurgical procedures and the essential tasks to be incorporated into intraoperative monitoring during awake craniotomy.

Undifferentiated non-hepatic hyperammonemia in the ICU: Diagnosis and management.

Hyperammonemia occurs frequently in the critically ill but is largely confined to patients with hepatic dysfunction or failure. Non-hepatic hyperammonemia (NHHA) is far less common but can be a harbinger of life-threatening diagnoses that warrant timely identification and, sometimes, empiric therapy to prevent seizures, status epilepticus, cerebral edema, coma and death; in children, permanent cognitive impairment can result. Subsets of patients are at particular risk for developing NHHA, including the organ transplant recipient. Unique etiologies include rare infections, such as with Ureaplasma species, and unmasked inborn errors of metabolism, like urea cycle disorders, must be considered in the critically ill. Early recognition and empiric therapy, including directed therapies towards these rare etiologies, is crucial to prevent catastrophic demise. We review the etiologies of NHHA and highlight the first presentation of it associated with a concurrent Ureaplasma urealyticum and Mycoplasma hominis infection in a previously healthy individual with polytrauma. Based on this clinical review, a diagnostic and treatment algorithm to identify and manage NHHA is proposed.

Tracking the Effect of Therapy With Single-Trial Based Classification After Stroke.

Stroke is a debilitating disease that leads, in the 50% of cases, to permanent motor or cognitive impairments. The effectiveness of therapies that promote recovery after stroke depends on indicators of the disease state that can measure the degree of recovery or predict treatment response or both. Here, we propose to use single-trial classification of task dependent neural activity to assess the disease state and track recovery after stroke. We tested this idea on calcium imaging data of the dorsal cortex of healthy, spontaneously recovered and rehabilitated mice while performing a forelimb retraction task. Results show that, at a single-trial level for the three experimental groups, neural activation during the reward pull can be detected with high accuracy with respect to the background activity in all cortical areas of the field of view and this activation is quite stable across trials and subjects of the same group. Moreover, single-trial responses during the reward pull can be used to discriminate between healthy and stroke subjects with areas closer to the injury site displaying higher discrimination capability than areas closer to this site. Finally, a classifier built to discriminate between controls and stroke at the single-trial level can be used to generate an index of the disease state, the therapeutic score, which is validated on the group of rehabilitated mice. In conclusion, task-related neural activity can be used as an indicator of disease state and track recovery without selecting a peculiar feature of the neural responses. This novel method can be used in both the development and assessment of different therapeutic strategies.

Advance Care Planning-further development of the patient advance directive : What the specialist in internal medicine must know

Trotz der zur Verfügung stehenden Vorsorgeinstrumente Patientenverfügung, Vorsorgevollmacht und Betreuungsverfügung ist der Behandlungswille des Patienten in der konkreten Situation oft nicht in handlungsleitender Weise bekannt. Ziele des systemisch angelegten Konzepts „Behandlung im Voraus Planen“ – advance care planning, sind die Ermittlung, Dokumentation und Umsetzung des Behandlungswillens des Patienten für den Fall, dass er selbst nicht (mehr) rechtsverbindlich über seine Behandlung entscheiden kann. Auf der individuellen Ebene unterstützt ein speziell geschulter Gesprächsbegleiter zunächst bei der Formulierung der Einstellungen zu Leben, schwerer Erkrankung und Sterben. Darauf aufbauend können die Behandlungswünsche für verschiedene medizinische Situationen besprochen und z. B. in einer Patientenverfügung dokumentiert werden. Hierzu gehören der Notfall, die Situation im Krankenhaus bei unklarer Dauer der Einwilligungsunfähigkeit und die Situation bei dauerhaftem Verlust der Einwilligungsfähigkeit. Durch achtsame, nichtdirektive Gesprächsführung im Sinne einer gemeinsamen Entscheidungsfindung („shared decision making“) wird der Vorausplanende befähigt, gut informiert und reflektiert zu entscheiden („informed consent“). Die an den zukünftigen Behandlungsentscheidungen beteiligten Personen, insbesondere der zukünftige Vertreter, werden möglichst frühzeitig einbezogen. Die institutionelle und regionale Implementierung des Konzepts fördert die Umsetzung des auf diese Weise ermittelten und wirksam dokumentierten Patientenwillens in der gesamten Versorgungskette. Durch den neuen § 132 g SGB V, der den Einrichtungen der stationären Altenhilfe und der Eingliederungshilfe ermöglicht, Behandlung im Voraus Planen zulasten der GKV anzubieten, ist eine zunehmende Verbreitung des Konzepts zu erwarten.Zusatzmaterial onlineDie Online-Version dieses Beitrags (10.1007/s00108-022-01333-9) enthält die Muster-Patientenverfügungen der DiV-BVP „Einstellung zu Leben, schwere Krankheit und Sterben“ und „Ärztliche Anordnung für den Notfall“ (© Deutsche interprofessionelle Vereinigung Behandlung im Voraus Planen e.V. (DiV-BVP), Frankfurt am Main, www.div-bvp.de).

Newborn Screening in Pediatric Endocrine Disorders

Two endocrine disorders, congenital hypothyroidism (CH) and congenital adrenal hyperplasia (CAH), when untreated, can have devastating, irreversible and fatal outcomes. Permanent cognitive impairment, growth failure and dysmorphic appearance are seen in congenital hypothyroidism (CH) and early infant death in males with salt wasting CAH (as most females are discovered by presence of atypical genital appearance, while males appeared normal). Newborn screening (NBS) for CH was developed with broader engagement of centers, and was more rapidly adopted throughout the US and other large or developed countries, while NBS for CAH was pioneered by relatively few and was not fully adopted in the US until the initiation of Universal Expanded Newborn Screening Panel in 2005. Advances in genetic understanding of CH and CAH continue with NBS. Cost–benefit analysis, showing CH NBS as more successful than CAH NBS, may not fully recognize the cost of a life saved with CAH NBS. Early treatment of CH is much simpler with taking a pill a day unlike CAH requiring multiple medication doses, and possibly surgery apart from enteral and parenteral stress doses during adrenal crisis. CAH management outcomes with gender identity matters in persons with atypical genital appearance and androgen effects are still being studied.

Delayed presentation to hospital care is associated with sequelae but not mortality in children with cerebral malaria in Malawi

BackgroundCerebral malaria is still a major cause of death in children in sub-Saharan Africa. Among survivors, debilitating neurological sequelae can leave children with permanent cognitive impairments and societal stigma, resulting in taxing repercussions for their families. This study investigated the effect of delay in presentation to medical care on outcome in children with cerebral malaria in Malawi.MethodsThis retrospective study included participants enrolled in a longstanding study of cerebral malaria between 2001 and 2021 and considered coma duration prior to arrival at hospital (with or without anti-malarial treatment), HIV status, blood lactate levels at admission and age as factors that could affect clinical outcome. Outcomes were categorized as full recovery, sequelae at the time of discharge, or death. A multinomial regression was fit and run controlling for coma duration, HIV status, lactate levels and age, to determine the association between each explanatory variable and outcome.ResultsA total of 1663 children with cerebral malaria, aged 6 months to 14 years were included. Longer coma duration (in hours) was associated with greater odds of developing sequelae (OR = 1.023, 95% CI 1.007–1.039, p = 0.006) but not death (OR = 1.00, 95% CI 0.986–1.015, p = 0.961). Younger age (in months) was also correlated with higher rates of sequelae, (OR = 0.990, 95% CI 0.983–0.997, p = 0.004) but not with increased mortality (OR = 0.998, 95% CI 0.993–1.003, p = 0.335). Blood lactate levels on admission were correlated with mortality (OR = 1.125, 95% CI 1.090–1.161, p < 0.001) but not associated with increased rates of sequelae (OR = 1.016, 95% CI 0.973–1.060, p = 0.475). Positive HIV status and treatment with an anti-malarial (artemisinin or non-artemisinin-based) prior to arrival at the hospital were not significantly associated with either adverse outcome.ConclusionsIn Malawian children with cerebral malaria, higher rates of sequelae were significantly associated with extended coma duration prior to admission and younger age. Mortality rates were correlated with increased lactate levels on admission. The differential effects of variables on clinical outcomes suggest that there may be different pathogenic pathways leading to sequelae and death. Actions taken by parents and health care professionals are critical in defining when patients arrive at hospital and determining their ultimate outcome.

Delirium-an interdisciplinary challenge

Delirium is acommon and potentially life-threatening disease that often poses major problems for hospitals in terms of care. It mainly affects older patients and is multifactorial, especially in older people. Permanent functional and cognitive impairments after delirium are not uncommon in geriatric patients. Often, delirious syndromes are not recognized or are misinterpreted. This is especially the case with the hypoactive form of delirium. Various screening and test procedures are available for the detection of delirium, the routine use of which is essential. In many cases, delirium can be avoided with suitable preventive measures. Above all, nondrug prevention strategies and multidimensional approaches play an important role here. For the drug treatment of delirium in geriatric patients, low-potency, classic and atypical neuroleptics, as well as dexmedetomidine for severe courses are recommended.

HSI-LFS-BERT: Novel Hybrid Swarm Intelligence Based Linguistics Feature Selection and Computational Intelligent Model for Alzheimer’s Prediction Using Audio Transcript

Alzheimer’s dementia (AD) affects memory, language, and cognition which worsens over time. It is critical to develop a reliable early detection method before permanent brain atrophy and cognitive impairment. This study uses clinical transcripts, a text-based adaptation of the original audio recordings of Alzheimer’s patients. This audio transcript data is taken from DementiaBank which is the largest public dataset of AD transcripts. The study aims to show how transfer learning-based models and swarm intelligence optimization techniques can be used to predict Alzheimer’s disease. To enhance the prediction performance for Alzheimer’s disease, a hybrid swarm intelligence linguistic feature selection (HSI-LFS) approach is proposed that extracts a combined feature set using Particle Swarm Optimization (PSO), Dragonfly Optimization (DO), and Grey Wolf Optimization (GWO) algorithms. In addition, a transfer learning-based model called HSI-LFS-BERT, a combination of the HSI-LFS feature selection method and Bidirectional Encoder Representations from Transformer (BERT) algorithm is proposed. The proposed model is compared using two feature sets: first set consists of the initial feature set and the second set contains hybrid feature set that has been extracted using the suggested HSI-LFS method. The BERT embedding with HSI-LFS outperformed the conventional feature set providing the most accurate modeling parameters while reducing the computations by 27.19%. The proposed HSI-LFS-BERT model excelled state-of-the-art models achieving 98.24% accuracy, 91.56% precision, and 98.78% recall.

Examining the association between traumatic brain injury and headache.

Traumatic brain injury is a common and major cause of disability and death that might require emergency neurological and neurosurgical interventions. Traumatic brain injury can result in temporary or permanent physical, cognitive and psychological impairments. One of the most common complications associated with traumatic brain injury is post-traumatic headache, associated with significant disability and reduced quality of life. Post-traumatic headache is a public health concern that can affect the long-term outcome of traumatic brain injury patients. Clinical symptoms of post-traumatic headache significantly overlap with common primary headaches such as migraine and tension-type headaches. Beyond neurobiological factors, psychological factors can play crucial roles in the initiation and sustainment of post-traumatic headache. While neurological mechanisms underlying post-traumatic headache remains unknown, different studies suggest various mechanisms such as physical damages to the cranial nerves and neck structure, hyper-sensitization of the pain modulatory pathway, and inflammation as underlying causes for the neurobiology of headache. I explore the hypothesis that traumatic brain injury is associated with headaches. In particular, I provide an overview of the neurobiology of post-traumatic headache, its diagnosis, presenting recent findings on the etiology, explaining similarities and differences between with primary headaches such as migraine and tension-type headache, discuss pharmacological and non-pharmacological interventions for the treatments, as well as emphasising on the psychological importance of post-traumatic headache.

The frontal aslant tract and its role in executive functions: a quantitative tractography study in glioma patients

Focal white matter lesions can cause cognitive impairments due to disconnections within or between networks. There is some preliminary evidence that there are specific hubs and fiber pathways that should be spared during surgery to retain cognitive performance. A tract potentially involved in important higher-level cognitive processes is the frontal aslant tract. It roughly connects the posterior parts of the inferior frontal gyrus and the superior frontal gyrus. Functionally, the left frontal aslant tract has been associated with speech and the right tract with executive functions. However, there currently is insufficient knowledge about the right frontal aslant tract’s exact functional importance. The aim of this study was to investigate the role of the right frontal aslant tract in executive functions via a lesion-symptom approach. We retrospectively examined 72 patients with frontal glial tumors and correlated measures from tractography (distance between tract and tumor, and structural integrity of the tract) with cognitive test performances. The results indicated involvement of the right frontal aslant tract in shifting attention and letter fluency. This involvement was not found for the left tract. Although this study was exploratory, these converging findings contribute to a better understanding of the functional frontal subcortical anatomy. Shifting attention and letter fluency are important for healthy cognitive functioning, and when impaired they may greatly influence a patient’s wellbeing. Further research is needed to assess whether or not damage to the right frontal aslant tract causes permanent cognitive impairments, and consequently identifies this tract as a critical pathway that should be taken into account during neurosurgical procedures.

Type 2 diabetes mellitus and risk of Alzheimer's disease

The evidences like biological and epidemiological support a link between type 2 diabetes mellitus (DM2) and Alzheimer's disease (AD). Persons with diabetes have a higher rate of cognitive decline and an increased risk of developing dementia of all types. Cognitive deficits in diabetic people get mainly affect the psychomotor efficiency areas like attention, learning and memory, mental ability, flexibility and speed, and executive function. The concrete epidemiological association has suggested the existence of a pathophysiological link. The factors of increased cognitive decline in DM2, however, are less clear. Increased atrophy of cortical and subcortical areas had clearly shows after controlling for diabetic vascular disease and inadequate circulation in cerebral areas.Most recent studies have focused on the role of insulin and insulin resistance as possible links between diabetes and AD. Disturbances in brain insulin signaling mechanisms may contribute to the molecular, biochemical, and histopathological lesions in AD. Hyperglycemia itself is a risk factor for cognitive dysfunction and dementia. Hypoglycemia may also have deleterious effects on cognitive function. Recurrent symptomatic and asymptomatic hypoglycemic episodes have been suggested to cause sub-clinical brain damage, and permanent cognitive impairment. Future trials are required to clarify the mechanistic link, to address the question whether cognitive decline may be prevented by an adequate metabolic control, and to elucidate the role of drugs that may cause hypoglycemic episodes.