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0203 Run On A Brain

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Last Updated: 13 December 2020

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General | Latest Info

Do migraines damage the brain? This is an enquiry often received at Migraine Trust, especially following stories appearing in the media that raise questions about whether Migraine can cause harmful changes in the brain, so we ask our medical Trustees for some help in interpreting research. Migraine Research sometimes includes the use of imaging technology, or scans, to examine brain structure and compare the brain of Migraine sufferers with those who are not sufferers. Therefore, trying to understand whether there are differences in the structure of Migraine brain might help in developing new and more effective treatments for Migraine. In the paper by Dr Bashir and others, authors review 19 earlier studies, 13 of which were studies of people who attend Migraine clinics. Compared with non-migraineurs, those with Migraine with aura had a small but statistically significant increase in the appearance of white-matter abnormalities. Infarct-like lesions were statistically more common in people with Migraine with aura than in those who had Migraine without aura. However, reassuringly, these were no more common in either group of migraineurs than in people without Migraine. Research shows that people who have Migraine without aura are not at any important risk for either white-matter abnormalities or infarct-like lesions compared to people without Migraine. In addition, there are no cognitive problems caused by Migraine or by having MRI scan similar to those in studies. Research shows that current recommended treatment for Migraine do not need to be change, and that there is no need for scans for those who have definite diagnosis of Migraine with no unusual symptoms. Unusual symptoms that raise concern and warrant further investigation like MRI scan, are usually picked up when doctors do neurological examination. People with Migraine also had more volume in some parts of their brain, and less volume in other parts of their brain, compared to people without Migraine. Differences in volume that were seen in different parts of the brain seem to be static, that is, not something that appears to be progressive or caused by Migraine attacks. Again, there are no cognitive consequences or implications for treatment of Migraine, based on what is currently know. However, much more research is needed before any further interpretation can be made and these findings may simply mark inheritance of Migraine. Professor Peter Goadsby, Director of NIHR-Wellcome Trust Clinical Research Facility at Kings College Hospital, London, and Trustee of the Migraine Trust, believes that resolving these types of questions is hugely important and will require well-fund, large-scale, population-base imaging study.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Introduction

It is well known that temperature affects dynamics of all physicochemical processes governing neural activity. It is also known that the brain has high levels of metabolic activity, and all energy used for brain metabolism is finally transformed into heat. However, issue of brain temperature As factor reflecting neural activity and affecting various neural functions remains in shadow and is usually ignored by most physiologists and neuroscientists. Data presented in this review demonstrate that brain temperature is not stable, showing relatively large fluctuations within normal physiological and behavioral continuum. I consider mechanisms underlying these fluctuations and discuss Brain thermorecording as an important tool to assess basic changes in neural activity associated with different natural and drug-induce motivated behaviors. I also consider how naturally occurring changes in brain temperature affect neural activity, various homeostatic parameters, and structural integrity of brain cells as well as results of neurochemical evaluations conducted in awake animals. While physiological hyperthermia appears to be adaptive, enhancing the efficiency of neural functions, under specific environmental conditions and following exposure to certain psychoactive drugs, brain temperature could exceed its upper limits, resulting in multiple brain abnormalities and life-threatening health complications. Temperature is traditionally viewed as one of the basic homeostatic parameters of living organisms and its regulation is an essential topic of physiology, which considers mechanisms determining relative stability of core body temperature following highly variable changes in environmental temperatures. Aristotle was probably the first to define temperature as one of five basic biological processes and provided logical account for what we now call temperature regulation. Although it is known that temperature affects neural activity and neural functions, we have limited knowledge of normal and pathological fluctuations of brain temperature and mechanisms underlying Brain thermal homeostasis and its alterations. These issues are usually ignored by thermophysiologists, who examine neural mechanisms underlying stability of body temperature and development of fever, stable increase in body temperature usually associated with viral and bacterial infections. While not clearly stated in most conceptualizations describing body temperature regulation, brain temperature is usually viewed either as a stable, tightly regulated homeostatic parameter or parameter that passively follows body temperature changes. It is well known that the brain plays a crucial role in regulation of body temperature by detecting changes in environmental temperatures, integrating sensory information, and adjusting, via effector mechanisms, heat production and / or heat loss to the external environment. However, brain itself has high levels of metabolic activity, generating a significant amount of heat. Being only a fraction of human body mass, brain accounts for ~20 % of organisms ' total oxygen consumption in resting conditions. Most energy used for neuronal metabolism is expended during restoration of membrane potential after electrical discharges, but significant energy is also used for neural processes not directly related to neuronal electrical activity, particularly for synthesis of macromolecules as well as for functioning of glial, endothelial and epithelial cells, which greatly outnumber amount of neurons.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Patients and methods

There are a variety of ways to assess mobility in rehabilitation setting 27 as described elsewhere in this issue. This review focus on endurance capacity and cardiorespiratory fitness. How to best assess physiologic and metabolic aspects of mobility are important considerations. Understanding acute responses and long term adaptations are keys to understanding whether exercise intervention will have a positive effect on overall health. The gold standard for measuring physical fitness is to measure peak VO 2 during maximal grade exercise test in which workload progressively increase. These tests are most often performed on treadmills or cycle ergometers or some other device on which workload can be increased incrementally. Protocols have been designed that are similar to standard cardiac stress tests that measure heart rate, blood pressure and electrocardiogram. Optimally, these tests should include collection of expired gases so the subject's metabolic response can be assess. In addition to peak oxygen uptake, metabolic response provides additional information on carbon dioxide production and pulmonary ventilation. Simple calculations with these variables allow one to estimate cardiac stroke volume and efficiency of breathing during exercise. Since all variables are measured continuously, submaximal responses can be monitored to provide an estimate of efficiency of movement. Movement efficiency is particularly important when one considers the high incidence of neuromusculoskeletal abnormalities in patients with TBI. Because of balance and gait impairments that many patients with TBI demonstrate, cycle ergometer, upright or recumbent, is commonly used for exercise testing. However, patients with TBI elicit higher peak VO 2 when being tested on treadmill versus bicycle ergometer 22 due to localized muscle fatigue. Using test-retest designs, both leg cycle ergometry 17 and treadmill testing 28 have been shown to be reliable in patients recovering from TBI. Besides eliciting higher peak VO 2, treadmill testing is recommend, when feasible and safe, because it is more functional. Body weight support harness systems can be used to provide an added level of security for individual being test. Since testing of peak VO 2 requires expensive equipment and highly trained personnel, alternative submaximal methods of testing have been develop. One can estimate aerobic capacity using a timed walk or run test. First proposed by Cooper, 29 these tests have been used frequently in a variety of patient populations. 30 31 most common is a six minute walk and is a measure of the total distance walked in 6 minutes with a minimal number of turns or changes in direction. It is best to combine with a measure of heart rate so an estimate of energy expenditure can be calculate. The test has been shown to be reliable in subjects with TBI. 32 modified 20 meter shuttle run 33, another variation of walk / run test used to estimate peak oxygen consumption, was also one of the first to be evaluated for reliability in patients with TBI.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Results

This 44-year old, right-hand male sustained concussion while playing soccer. After a head-to-head collision with another player, he loses consciousness for approximately 90 seconds, followed by confusion, and about 1-2 minutes of retrograde and 3-4 minutes of anterograde amnesia. Approximately 20 minutes after the event, his physical and neurological exams were normal, and remain normal 10 days later. For 2 weeks following the accident, he complained of fatigue and poor concentration, memory problems, mild headache and some difficulty sleeping. These symptoms had markedly improved by week 6, although he still complained of mild headaches, slight fatigue, and intermittent memory difficulties. Four weeks later, 10 weeks after concussion, he was completely asymptomatic and had fully resumed normal daily activities. On Immediate Postconcussion Assessment and Cognitive Test, he had total symptom score of 13 at week 2 and 8 at week 6. No daily medications were administered for any of these symptoms, but he was given acetaminophen to be take as needed for headaches. He was not taking any drugs known to alter brain excitability, plasticity, or excitation / inhibition balance. He worked as manager of the multimedia Department, where he continued working after the accident. He had a history of four prior episodes diagnosed as concussions while athlete in college, over 20 years prior to the present episode. In two of these episodes, there was no actual loss of consciousness, but they all been associated with varying degrees of retrograde and anterograde amnesia, mild and transient concentration and memory difficulties, headaches, and dizziness that had completely subsided within 2 months from episode. The last episode was 21 years prior. Past Medical history, Review of system and family history were otherwise negative. He was Test twice, 2 and 6 weeks after the present concussion. His findings were compared to a control group of 12 healthy adults, aged between 19 and 55 years old. We look for control subjects spanning a wide age range to minimize potential ImPACT of age-related effects. The age of patient was included within this age range. Comparison of results in our patient with a subset of control subjects closer to his age does not affect any of the report findings. Control subjects had no psychiatric or neurological conditions, normal neurological and medical exams, no history of concussions or TBI, were not taking any medications, and had no contraindications to receive TMS. All participants tolerate procedures, including TMS, without any side effect or complication. In particular, patients do not have any headaches either just before or at the end of each session. No other adverse events were report. All participants gave write informed consent for participation in the study, which had been approved by the local Institutional Review Board. Brain MRI and DTI studies were obtained using a 3T GE scanner. Anatomical images were acquired using T1-weight, three-dimensional, magnetization-prepared, rapid-acquisition, gradientecho volume acquisition with voxel resolution of 1 mM 3.


3. Discussion

The brain undergoes a series of maturational processes during childhood and adolescence that is thought to drive enhanced cognitive function in adulthood. To gain better understanding of these developmental factors at circuit level, we use histological and electrophysiological approaches to test for changes in axonal myelination and neurotransmission speed in developing mPFC of male rats. Between two and six weeks of age, large numbers of axons are being myelinated in this anterior region of the brain, and addition of myelin segments along axon appear to move anterogradely from corpus callosum out toward axonal terminals in Layer V of the adjacent cortex. These data complement previous studies investigating white matter changes in the developing brain of rodents, and provide new evidence suggesting that the increase in prefrontal white matter could be partially due to de novo myelination of axons rather than thickening of myelin sheaths on previously-myelinated axons. Correspondent with myelination of prefrontal axons, was a significant increase in the speed at which electrical signals travel down these axons. By isolating monosynaptic projections, we gain insight into how electrical information travels from anterior branches of corpus callosum to mPFC. Robust morphologic changes and improvements in transmission speed in individual prefrontal axons that were observed in the present study provide means by which cognitive processing could improve between childhood and adolescence. Myelination of prefrontal axons appears to be a key factor underlying developmental increases in neural processing. There was a significant increase in the number of myelinated axons in CC FM and Cg1 and the change in size of CC FM in older animals is presumably due to de novo myelination of axons rather than thickening of myelin sheaths on previously-myelinated axons. Consistent with this interpretation, we do not find an age-dependent increase in relative thickness of myelin. In older animals, electrical signals travel twice as fast along axonal projections from CC FM to neurons in Layer V of Cg1. Two different mechanisms could account for increased transmission speed: larger diameter of axons or myelination of axons. As there was no age difference in mean diameter or range of diameters in myelinated axons, we can rule out increased diameter as a mechanism for increased axonal speed. Instead, myelination appears to be responsible for the developmental increase in axonal signal transmission speed. To the best of our knowledge, this is the first demonstration of increased conduction velocity in this specific fiber population, providing insight into one mechanism by which neural processing is enhanced during development. Perhaps similar increases in conduction velocity are occurring in axons within posterior branches of corpus callosum and other regions that are being myelinated during this time. Data herein allows us to make inferences about how the myelination process takes place in the juvenile prefrontal cortex.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Discussion

The first known hemispherectomy was performed on dogs in 1888 by German physiologist Friedrich Goltz. In humans, neurosurgeon Walter Dandy pioneered an operation at Johns Hopkins University in 1923 on brain tumor patient. The procedure is among the most drastic kinds of brain surgery. You can't take more than half. If you take the whole thing, you've got a problem, Johns Hopkins neurologist John Freeman quips. One side effect Canadian neurosurgeon Kenneth McKenzie reported in 1938 after hemispherectomy on a 16-year-old girl who suffered a stroke was that her seizures stop. Nowadays, surgery is performed on patients who suffer dozens of seizures every day that resist all medication, and which ARE due to conditions that mostly afflict one hemisphere. These disorders ARE often progressive and damage the rest of the brain if not treat, University of California, Los Angeles, neurosurgeon Gary Mathern say. Freeman concurs: hemispherectomy is something that one only do when alternatives ARE worse. Anatomical hemispherectomies involve removal of the entire hemisphere, whereas functional hemispherectomies only take out parts of the hemisphere, AS well AS severing corpus callosum, fiber bundle that connects two halves of the brain. Evacuated cavity is left empty, filling with cerebrospinal fluid in day or SO. The strength of anatomical hemispherectomies, specialty of Hopkins, lies in the fact that leaving even a little bit of brain behind can lead to seizures return, Freeman say. On the other hand, functional hemispherectomies, which UCLA surgeons usually perform, lead to less blood loss. Our patients ARE usually under two years of age, SO they have less blood to lose, Mathern say. Most Hopkins hemispherectomy patients ARE five to 10 years old. Neurosurgeons have performed operations on children AS young AS three months old. Astonishingly, memory and personality develop normally. A recent study found that 86 percent of 111 children who underwent hemispherectomy at Hopkins between 1975 and 2001 ARE either seizure-Free or have nondisabling seizures that do not require medication. Patients who still suffer seizures usually have congenital defects or developmental abnormalities, where brain damage is often not confined to just one hemisphere, Freeman explain. Another study found that children that underwent hemispherectomies often improve academically once their seizures stop. One was the champion bowler of her class, one was the chess champion of his state, and others ARE in college doing very nicely, Freeman say. Of course, operation has its downside: you can walk, runsome dance or skipbut you lose use of hand opposite of hemisphere that was remove. You have little function in that arm and vision on that side is lose, Freeman say. Remarkably, few other impacts ARE see. If the left side of the brain is taken out, most people have problems with their speech, But it used to be think that if you take that side out after age two, you'd never talk again, and we've proven that untrue, Freeman say. The younger person is when they undergo hemispherectomy, less disability you have in talking.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Cite

Hypothetical pathway for exercise-mediate effects on brain functions: both endurance and resistance exercise, even IF with different kinetics and properties, allow muscle synthesis, and release myokines, AS well AS of metabolites into circulation; These molecules can cross the blood-Brain barrier at the level of brain capillaries and affect functions of both neurons and glial cells, thus modifying neurotransmission in different regions of Brain. AS explained in the text, neurotransmission can then activate pathways leading to modifications of gene expression. AS: astrocytes; BC: Brain capillaries; Neu: neurons; OL: oligodendrocytes.


Discussion

There is a growing body of preclinical data that suggest eCB system may be involved in ASD pathophysiology. Specifically, AEA signaling has been shown to exert a modulatory role in rodent behaviors that are relevant to ASD symptomatology and to pharmacologically rescue social deficits observed in ASD rodent models. The present study is the first to translate these preclinical data to patients, by optimizing the LC-MS / MS method to quantitatively analyze AEA concentrations in small volumes of banked plasma with short sample preparation time and high sample repeatability. Two significant findings were observe: plasma AEA concentrations significantly differentiated ASD cases from controls, such that children with lower AEA concentrations were more likely to have ASD, and AEA concentrations were significantly lower in ASD compared to control children. These results, although preliminary, corroborate preclinical evidence that AEA signaling may be impaired in patients with ASD. Detection of biomarkers in plasma is highly advantageous for brain disorders due to relatively non-invasive procedures required to collect blood. Circulating eCB concentrations are thought to be in equilibrium with brain-related eCB concentrations, suggesting that plasma eCB concentrations may be a viable proxy for behavioral effects generated by bioactive, brain-related AEA. Therefore, although plasma AEA concentrations do not perfectly classify idiopathic ASD and control participants, AEA signaling impairments nevertheless may characterize specific subset of ASD patients or be useful for inclusion in multidimensional biomarker panel employ to detect idiopathic ASD. Present findings are preliminary and warrant subsequent replication by an independent study cohort. These findings must also be considered in the context of several limitations. First, our study was not power to assess potential sex differences and relationships between behavioral symptomology and AEA concentrations within heterogeneous ASD population. Second, our ASD participants were taking a variety of prescription medications in contrast to the control participants, who were medication free. Thus, it is possible that our findings were driven by medication status, particularly as inclusion criteria only required medication to be stable for 1 week prior to blood collection. We think this is unlikely in light of the aforementioned preclinical AEA data; Nevertheless, future research is required to evaluate the impact of commonly prescribed ASD medications on plasma AEA concentrations and other eCBs. Finally, we measure single eCB analyte using extrapolate AEA concentrations. Further optimization of the present LC-MS / MS methodology would allow for more precise AEA quantitation as well as concomitant study of additional eCBs, such as 2-arachidonoylglycerol, which has also been implicated in preclinical ASD models with respect to pathophysiology and behavioral features. AEA concentrations have been studied in other brain disorders and have been reported to be lower in patients with temporal lobe epilepsy and post-traumatic stress disorder. Whether lower plasma AEA concentrations observed in ASD patients in the present study are related to common, associated features, or core symptoms, remains to be determine.


Introduction

Metabolic disorders, particularly aberrations in lipid homeostasis, such as obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease, and hypertriglyceridemia, often manifest together as metabolic syndrome. Despite major advances in our understanding of pathogenesis of these disorders, prevalence of MetS continues to rise. Since MetS constitutes increased risk to cardiovascular morbidity and mortality, more detailed understanding of common causes, and integration between these disorders of energy homeostasis, is necessary to identify novel therapeutic targets and interventions that may halt development of severe metabolic disease. It is becoming increasingly apparent that the central nervous system is a major contributor to regulation of systemic metabolism and lipid balance. In CNS, nutritional status of the body is constantly being surveyed and assessed by key energy-sensing regions of the brain, such as the hypothalamus. Key nuclei within the hypothalamus, such as the ventromedial nucleus, arcuate nucleus, dorsomedial hypothalamic nucleus, and paraventricular nucleus, integrate signals to elicit peripheral responses, such as changes in feeding behavior, fuel mobilization, energy utilization, and energy storage. These nuclei detect both nutrients and nutritionally regulated endocrine factors, such as insulin, ghrelin, melanocortin, and leptin, in order to regulate feeding and energy balance. Here, in this review, we will focus on mechanisms involved in lipid sensing in the brain and its emerging influence on systemic metabolism.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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