Thursday, 19 July 2018
Positron emission tomography (PET) scans provide two- and three-dimensional pictures of brain activity by measuring radioactive isotopes that are injected into the bloodstream. PET scans of the brain are used to detect or highlight tumors and diseased tissue, measure cellular and/or tissue metabolism, show blood flow, evaluate patients who have seizure disorders that do not respond to medical therapy and patients with certain memory disorders, and determine brain changes following injury or drug abuse, among other uses.
PET may be ordered as a follow-up to a CT or MRI scan to give the physician a greater understanding of specific areas of the brain that may be involved with certain problems. Scans are conducted in a hospital or at a testing facility, on an outpatient basis. A low-level radioactive isotope, which binds to chemicals that flow to the brain, is injected into the bloodstream and can be traced as the brain performs different functions.
The patient lies still while overhead sensors detect gamma rays in the body’s tissues. A computer processes the information and displays it on a video monitor or on film. Using different compounds, more than one brain function can be traced simultaneously.
PET is painless and relatively risk-free. Length of test time depends on the part of the body to be scanned. PET scans are performed by skilled technicians at highly sophisticated medical facilities.
The French investigators performed F-18 fluoro-L-dopa (FDOPA) positron emission tomography (PET) in patients with temporal lobe epilepsy (TLE) and compared the findings to those with fluorodeoxyglucose (FDG) PET This study was motivated by a prior observation that F-18 FDOPA uptake in basal ganglia is decreased in patients with refractory TLE. A correlation was observed between the localization of seizure focus hypometabolism and decreased FDOPA uptake in both the basal ganglia and the substantia nigra, suggesting that there is a dopamine involvement in TLE. In another study the impact of TLE duration on brain FDG PET pattern was investigated. A negative correlation was demonstrated between epilepsy duration and ipsilateral glucose metabolism and a positive correlation with the contralateral glucose metabolism. This observation suggested that duration of TLE correlates with asymmetric glucose metabolism in the temporal lobes possibly reflecting the compensatory increased metabolism in the more normal temporal lobe over time.
The Brazilian researchers compared the FDG PET brain glucose metabolism with Tc-99m ethylcysteinate dimer (ECD) single-photon emission computed tomography (SPECT) brain regional cortical blood flow in patients with Alzheimer dementia. This study showed that similar functional cerebral regions are involved on PET and SPECT in Alzheimer's disease, although PET seemed to be more powerful in depicting the extent and severity of the functional impairments.
The impact of FDG PET on the diagnosis and clinical management of patients with dementia was reported by the investigators from the Kettering Medical Center in Kettering, Ohio. FDG PET scans were performed on 96 patients with suspected dementia or mild cognitive impairment. Referring physicians were also surveyed to report on whether and how results of the PET scan influenced patient management. The survey response rate was 76%. The survey indicated that PET changed the initial diagnosis to Alzheimer dementia in 26% and disease management in 27% of patients leading to initiation of anticholinergic drug therapy.
There has also been a growing interest in imaging beta-amyloid deposits directly with PET in Alzheimer dementia. An Australian study evaluated the relationship between amyloid burden as assessed by Pittsburgh Compound-B (PIB) PET and cognitive decline in predominantly normal elderly population (age 73 ± 6 years). These investigators observed that subjects with declining cognition were more likely to show cortical PIB retention than in stable subjects, suggesting that amyloid deposition is not a part of normal aging and likely represents preclinical Alzheimer's disease (described as those up to 30% of otherwise normal persons who are over 75 years but show amyloid deposition at autopsy). The researchers from the University of Pennsylvania compared the amyloid imaging agents [F-18]3'-F-PIB and [C-11]PIB in patients with Alzheimer's disease and in healthy subjects. The F-18-labeled compound showed uptake and retention characteristics similar to those of C-11-labeled compound in the more important cortical brain regions with SUV in the range of 3.1 to 4.5. Another similar study corroborated this finding and concluded that the F-18-labeled PET ligand might permit wide application of the compound due to longer half life and more ease of distribution in comparison to the C-11-labeled compound.
The potential benefit of contrast-enhanced PET-CT was compared to non-enhanced PET-CT for differentiation of brain tumor recurrence from radiation necrosis. In this study, 29% of recurrent tumors were missed on non-enhanced PET-CT and were identified correctly on the enhanced scan. Additionally contrast enhancement revealed enhancing lesions in the other areas of brain away from the immediate region of interest. However, the clinical significance of these findings was unclear. The authors concluded that contrast-enhanced PET-CT is more suited in this clinical setting than the more common current procedure of using non-enhance scans.
The Belgian researchers evaluated the diagnostic utility of PET with F-18 fluorotyrosine (FTYR), as a marker of amino acid transport, for detection of skull base meningioma. All tumours showed high FTYR uptake with an average tumor to cortex ratio of 2.53 ± .35. The metabolic abnormality on PET extended beyond the magnetic resonance imaging (MRI) abnormality in 38% and was smaller in 8% of cases. The authors concluded that FTYR PET was useful for the detection of residual meningiomas of the skull base with almost in half of the cases the tumor extent as depicted on PET differing from that on MRI, clinical significance of which is currently undetermined.
Non-FDG-based PET was highlighted in several presentations. The UCLA group evaluated PET with F-18 fluorothymidine (FLT), as a marker of cell proliferation, in a group of patients with brain tumor who were treated with anti-angiogenic agents such as bevacizumab.] A 25% reduction in tumor FLT uptake was considered as metabolic response which was then compared to MRI and survival data. A multivariate analysis showed that FLT response was the most powerful predictor of survival with a lack of reduction of FLT uptake at 6 weeks after treatment initiation increasing the hazard ratio of death by 5-fold. In another corollary study with FLT, the same group of investigators employed a 3-comparment, 2-tissue kinetic model with metabolite and partial volume corrections to estimate the rate constants during treatment in patients with high grade brain tumors. Changes in the influx rate K and the SUV were linked to treatment response which in turn was correlated to patient outcome.
The Japanese investigators compared C-11 acetate, C-11 methionine (MET), and FDG PET in 16 patients with primary and recurrent brain gliomas (5 low grade, 11 high grade). The sensitivities for low-grade and high-grade gliomas were, respectively, 60% and 100% for MET, 40% and 91% for acetate, and 0% and 40% for FDG. The mean SUV for low grade and high grade tumors were, respectively, 1.4 ± 0.4 and 3.1 ± 1.6 for acetate and 4.2 ± 0.2 and 8.3 ± 3.9 for FDG. There was no significant difference in the MET uptake between the low-grade and high-grade tumors. The authors concluded that although MET might not be able to differentiate the histologic grades, it is more sensitive than both FDG and acetate for tumor detection. Therefore this study suggested that multi-tracer PET may be helpful for a more comprehensive evaluation of patients with brain glioma, although the very low rate of FDG localization in the high-grade tumors in this study is atypical.
Wednesday, 18 July 2018
New research concludes that humans’ ability to identify and categorize what they see is kept up-to-date by reactivating lessons learned and allowing them to become stable over time.
A new study shows that updating visual perceptual skills — which humans rely on to recognize what they see, including potential threats, and ignore unimportant background — is an active process with many similarities to the way they stabilize memories.
Published in Nature Human Behavior, the study led by Brown University researchers tested whether memory reconsolidation, observed in animals, occurs in humans and whether it impacts skill learning.
In animals, when a new memory is formed, that memory is fragile until time passes and the memory is consolidated. When memories are recalled or reactivated, they become temporarily unstable and vulnerable to change until they become stable again, shortly afterward.
Using behavioral techniques and new brain imaging tools, the study provides evidence that memory reconsolidation takes place in humans and that it underlies an important skill — visual perceptual learning.
“This may explain why practice makes your skill and memory better, if you consider practice as a series of reactivations, increasing the level of plasticity again and again.”
“We performed this study because it is controversial whether reactivation makes already consolidated memory fragile again and whether this occurs in humans,” said Yuka Sasaki, a professor of cognitive, linguistic and psychological science at Brown. “If such reactivation and reconsolidation are true functions of the brain, they should also occur in human vision.”
Sasaki and her colleagues, including Takeo Watanabe, a professor of cognitive and linguistic science at Brown, trained study participants to recognize a blurred-stripe image, called a Gabor stimulus, as distinct from random dots. The next day, subjects were briefly tested to recall the skill they learned. They were then trained to find a new Gabor stimulus whose position was the same as the original one but whose orientation was different,immediately afterwards or 3.5 hours later. On the third day, subjects were asked to practice finding the original Gabor stimulus.
They found that the subjects who learned the altered Gabor stimulus immediately after looking at the original Gabor stimulus had significant trouble finding the original blurred stripe, suggesting that the reactivated memory was vulnerable to interference from new learning.
But the subjects who had an interval of 3.5 hours between practicing the original test and the altered Gabor stimuli performed much better. This suggests that the subjects who had more time for their memories to reconsolidate were better able to cement their visual perceptual learning.
These results reveal two important findings, the researchers said: Visual perceptual learning can undergo reconsolidation. And the reconsolidation window closes sometime before 3.5 hours after the initial recall. The results also suggest that consolidation and reconsolidation have similar influences on behavior.
Sasaki and her colleagues also wanted to discover whether reconsolidation is underpinned by the same changes in brain activity. They used magnetic resonance spectroscopy (MRS) to measure concentrations in the excitatory neurotransmitter glutamate and in the inhibitory neurotransmitter GABA during consolidation and reconsolidation.
A different group of participants again practiced the visual perception task or a control task that would not result in new learning. The next day, MRS was used to measure the visual area’s excitatory/inhibitory ratio both before and after the recall test as well as 3.5 hours afterwards.
Immediately after memory reactivation, when the memory was unstable and changeable, there was a significant increase in the excitatory/inhibitory ratio (a decrease of inhibition compared to excitation). Importantly, once the reconsolidation window had closed and the memory was re-stabilized, the amount of excitation/inhibition returned to baseline levels. This suggests that the changeability of the old memory was driven by a decrease in inhibition, similar to the excitation/inhibition ratio for consolidation.
The researchers also investigated whether the consolidation and reconsolidation of learned skills takes place according to similar timelines. They trained participants in a visual perception learning task and re-tested their memory either 3.5 hours after learning (consolidation group) or 3.5 hours after a recall test the next day (reconsolidation group). They found that both groups showed similar accuracy in the task 3.5 hours following learning or reactivation. This led them to conclude that both consolidation and reconsolidation occur over a similar amount of time.
“This may explain why practice makes your skill and memory better, if you consider practice as a series of reactivations, increasing the level of plasticity again and again,” Sasaki said.
By showing that visual brain areas are highly excitable following memory reactivation, Sasaki and her colleagues shed light on how new information is incorporated into the memory. And by providing evidence of the role of memory destabilization and reconsolidation in visual perceptual learning, the researchers offer insights into how the brain learns and refines new skills, keeping humans able to adapt in a changing world.
Tuesday, 17 July 2018
Levels of Dopamine | Parkinsons Disease | Towards A Better Tomorrow | Neurology 2018
Arvid Carlsson, the Swedish neuroscientist and Nobel laureate, died on June 29, 2018 at the age of 95. He had devoted his life to understanding how the brain works and was awarded the Nobel for his research into dopamine – an important chemical found in the brain.
So what is dopamine, and why did finding out about it merit the Nobel Prize?
Dopamine is a simple chemical, made in the body from an amino acid called tyrosine. Despite its simplicity, it plays an important role as a neurotransmitter – chemicals that brain cells use to communicate with one another.
What Carlsson did was to reveal exactly how significant dopamine is to the function of the brain. Before his research, most people thought that dopamine was just a precursor of a brain hormone called noradrenaline. By decreasing dopamine levels in the brains of rabbits in his lab in Gothenburg, Carlsson was able to show that if you don’t have the right level of dopamine in your brain, the circuits that determine how the brain controls movement don’t work properly.
Although Carlsson was investigating basic neuroscience, it wasn’t long before scientists and doctors realised that there were similarities between the problems with movement that Carlsson had observed in rabbits and the symptoms of Parkinson’s disease.
Parkinson’s disease is a neurodegenerative disorder, a type of disease where increasing numbers of brain cells die over time, causing patients to develop problems with their movement, including uncontrollable shaking, slowed movement and sudden freezing.
Following on from Carlsson’s research, doctors soon realised that if they examined the brains of people with Parkinson’s there was much less dopamine than you would find in a healthy brain. This is because the cells that make and use dopamine in the brain, dopaminergic neurons, are the cells that die in Parkinson’s disease.
This led researchers to propose a simple solution. If the symptoms of Parkinson’s are caused by too little dopamine, why not boost these levels, with a dopamine pill or injection, to help the brain work again?
Unfortunately, this approach didn’t work, as dopamine isn’t able to cross from the bloodstream into the brain. But providing people with Parkinson’s a precursor to dopamine, a chemical called levodopa that can get into the brain and is converted into dopamine, did work and provided relief from many of the symptoms of Parkinson’s. This was immortalised in the book Awakenings, written by neurologist Oliver Sacks and later made into a film starring Robin Williams and Robert De Niro.
In Awakenings, patients with post-encephalitic Parkinsonism (a viral disease similar to Parkinson’s disease) who were treated with levodopa, had almost miraculous improvements in their symptoms.
Unfortunately, levodopa, and other drugs that target dopamine levels in the brain, only treat the symptoms of Parkinson’s, they don’t slow down the loss of brain cells that underlie the disease. Despite this, and some serious side effects, they remain the frontline drug in our fight against the disease. But we wouldn’t have these frontline drugs if it wasn’t for the important work that Carlsson conducted in the 1950s, and for which he shared the Nobel Prize for Physiology or Medicine in 2000.
Monday, 16 July 2018
Researchers report impairments in the neuroprotective communication between neural blood vessels, astrocytes and neurons may be an early factor in how high blood pressure may impair cognitive function.
The squeeze high blood pressure puts on fragile blood vessels in the brain appears to disrupt a normal, protective process that balances the blood flowing to our brains with the activity of our resting neurons.
In the face of hypertension, as blood flow decreases, neuron-nurturing brain cells called astrocytes may instead tell neurons to increase their activity
These impairments in the neuroprotective communication between brain blood vessels, astrocytes and neurons may be an early factor in how hypertension impairs cognitive function.
Neurons don’t have energy reserves, so their activity is dependent on continuous blood flow.
Untreated hypertension can lead to cognitive impairment but exactly how it happens, we don’t really know. We need to understand the window of change or shift in function in all these different cells. What exactly is happening, in what order and how fast?
By the time patients are symptomatic, a lot of the physiology of the vasculature has deteriorated so the question is: How can we diagnose impairments in vascular function way before that, years before cognitive impairments are established and become symptomatic.
Regulation of blood flow, both up and down, is a normal, relentless function in our bodies. Certainly, that is true in the closed confines of the skull where there is literally little wiggle room, plus the brain just doesn’t like extreme ups or downs. In fact, fine adjustments are even made each time we stand up or sit. Your brain autoregulates to maintain flow relatively constantly,which is a good thing.
Huge increases in flow, for example, can result in dangerous swelling, particularly if blood pressure also happens to go up. Conversely, lower pressure and less blood flow mean less energy for neurons, which pretty much operate with an empty cupboard that requires the continuous flow of blood and the oxygen and nutrients it contains to function.
Neurons don’t have energy reserves so their activity is dependent on continuous blood flow. That’s why brain cells can die so quickly in the aftermath of a stroke or head trauma and why they probably don’t function well with chronic hypertension. A lot of these things get activated as a protective mechanism, but chronically they can shift into being more deleterious.
High blood pressure makes the thin-walled parenchymal arterioles that carry the blood neurons need constrict, so they carry less blood. Astrocytes, whose finger-like appendages cover most of the surface of these blood vessels, sense the increased pressure.
They had shown that the increased arteriole constriction they sense appears to trigger an increase in calcium inside the astrocytes, an indicator that their activity level has gone up. The increased calcium can lead to many things but in this case, researchers think the calcium overload turns normally protective astrocytes bad. They appear to both increase constriction – apparently by tightening their grip on the blood vessels – and promote inflammation.
It can shift who these astrocytes become, One of the many things they are further exploring is what happens, in turn, to the neurons.
They have evidence that one message neurons are not getting from these altered astrocytes is to reduce their resting activity even though less sustenance is available, creating an unhealthy balance for the brain.
A lot of these things get activated as a protective mechanism, but chronically they can shift into being more deleterious.
Over time, high blood pressure also results in a remodelling and stiffening of previously agile blood vessel walls so there is even less blood flowing. The unhealthy remodelling further alters the protective conversations the vessels, astrocytes and neurons should be having.
Eventually, communication appears to get reset so that resting blood flow and resting neuronal activity that enable basics like breathing are out of balance. There is a rightward shift,
This imbalance may also eventually decrease the normal ability to increase blood flow and neuronal activity when it’s time to solve a math problem or to have that significant conversation with a friend.
To better understand what goes bad, they are looking again at how a healthy balance happens and what hypertension does to it.
They are looking at what happens to calcium levels inside astrocytes in response to higher and lower pressures in the parenchymal arterioles in the brains of both normal mice and those that already have impaired blood flow. They also want to know what precisely mediates any change.
They are looking, both in brain slices and lab animals, at how pressure and flow changes in the fragile arterioles impact the resting activity of neurons in both the presence and absence of cardiovascular disease.
They want to know if at least one way a healthy balance occurs is by astrocytes recruiting GABAergic interneurons, which are known to play a role in inhibiting neuronal activity. They also are looking at which specific interneuron subtype drives neuronal response in the face of cardiovascular disease, suspecting it instead drives neuronal activity upward.
High blood pressure is a well-established risk factor for stroke and for cognitive function, in fact, a recent study published in Frontiers in Aging Neuroscienceindicates that hypertension accelerates Alzheimer’s development and that midlife control of high pressures may delay onset.
Rest is relative for neurons, which always are working at some level to maintain our basic functions. In fact, the majority of the brain’s energy goes to maintain resting activity that enables basics like breathing.
Functionally evoked changes in blood flow – like when you are actively thinking or doing – temporarily override cerebral autoregulation that in a healthy state balances basal blood flow and resting neuronal activity.
Thursday, 12 July 2018
Tiny particles called quantum dots reduce symptoms in mice primed to develop a type of Parkinson’s disease and also block the formation of the toxic protein clumps in Alzheimer’s. They could one day be a novel treatment for these brain disorders, although tests in people are some years away.
Quantum dots are just a few nanometres in size – so small they become subject to some of the strange effects of quantum physics. They have useful electronic and fluorescent properties and are found in some TV screens and LED lights.
Unlike most medicines, their tiny size means they can pass from the bloodstream into the brain. Byung Hee Hong of Seoul National University in South Korea and his colleagues wondered if they would affect the molecules involved in Parkinson’s or other brain disorders.
Parkinson’s disease involves gradually worsening tremors and movement problems. It is thought to be caused by a protein called synuclein found in nerve cells folding into the wrong shape, which triggers a chain reaction of misfolding in nearby synuclein molecules. This leads to a build-up of long strands or “fibrils” of the protein, killing neurons.
Hong’s team found that in a dish, quantum dots made from graphene – a form of carbon – bind to synuclein, and not only stop it from clumping into fibres, but also cause existing fibres to break up into individual molecules. “We didn’t expect the quantum dots to induce disaggregation of fibrils,” says Hong.
Next, the team injected quantum dots into mice dosed with fibrils, which normally trigger gradually worsening movement problems. Six months later, the mice showed improvement on two different physical tests.
If the treatment affects people the same way, Hong says it is unclear how much benefit this would bring. “It’s hard to translate the results in mice to actual patients, whose systems are way more complicated. But we do believe quantum dots can make positive impacts to some extent.”
Another team has found that quantum dots show promise for Alzheimer’s disease; in a similar fashion, they bind to a protein called amyloid, and reduce it from clumping together, a process thought to be involved in this dementia. However, tests in an animal version of Alzheimer’s haven’t yet been reported.
“This might be a universal effect on any kind of fibrillation process related to disease,” says Hong. His team is investigating using quantum dots in Alzheimer’s and motor neuron disease – the condition that affected Stephen Hawking – which also involves protein clumping.
Sebastien Paillusson of King’s College London, who was not involved in the work, says the findings in mice are promising, but should not raise anyone’s hopes until the approach has been tested in people. “Unfortunately in Parkinson’s, there have been a lot of compounds shown to work in mice but not in humans.”
Paillusson added, though, that it was unusual for anything to reverse the fibre-forming process. “This is a very novel approach.”
Hong says if safety tests in animals go well, they hope to start trials in people in about two years
Wednesday, 11 July 2018
Neurotransmitter | Noradrenaline | Sensory Perceptions | Brain | Neurology2018 | Berlin
A new study reveals noradrenaline plays a vital role in early stages of perception. Researchers report later processing of visual information occurs in the cerebral cortex and is affected by noradrenaline to determine if an image will enter our stream of consciousness.
A new study published in Current Biology suggests that noradrenaline, a neurotransmitter responsible for arousal in the brain, plays a vital role in our early sensory perceptions of the world.
Until now, medical science believed that noradrenaline is involved in alertness, stress, attention and decision making, says senior author Dr. Yuval Nir, of TAU’s Sackler Faculty of Medicine and Sagol School of Neuroscience. Our study shows that, in fact, noradrenaline plays a vital role in earlier stages of perception, determining our ability to perceive events around us.
The research was jointly led by Dr. Hagar Gelbard-Sagiv and Efrat Magidov of TAU’s Sackler Faculty of Medicine and Sagol School of Neuroscience,
The scientists ran a series of experiments on 30 participants at the Sagol Brain Institute at Tel Aviv Medical Center. Subjects took part in three different sessions in which they received (1) drugs that lowered noradrenaline levels; (2) drugs that increased those levels; or (3) a placebo. After taking the medication, the participants were asked to perform visual tasks such as detecting and discriminating between low-contrast images, while the researchers measured their brain activity by EEG or fMRI. The researchers hoped to determine how various levels of noradrenaline affected visual perception and the way the brain responds to images.
We determined that noradrenaline affected the participants’ ability to detect low-contrast images. Even though the images were identical in each case, their visibility changed across sessions. We could predict whether the subjects could perceive those images by examining the levels of noradrenaline in their systems,”says Dr. Gelbard-Sagiv.
Our measurements of brain activity show that the first stages of visual processing are quite automatic, but late processing in the cerebral cortex is affected by noradrenaline and determines if an image will enter our stream of consciousness,” adds Magidov.
“Many people suffer from difficulties in initiating and maintaining sleep,” Dr. Nir concludes. “We hope to follow up on these results and test whether noradrenaline also determines if sensory stimuli such as sounds wake us up from sleep.
“We hope that in the future our findings will open new avenues for the development of better anesthetics and new tools for early detection of dangerous situations, such as lapses while driving or flying.”
Tuesday, 10 July 2018
A new nomenclature for genetic movement disorders.
A Task Force was created by the International Parkinson and Movement Disorders Society with the aim of analysing apparent problems and providing solutions regarding the current nomenclature of genetic movement disorders.
Their suggestions have been published,
1. Aim to tackle several drawbacks of the current locus assignment system, such as 1) the inability to distinguish disease-causing mutations from genetic risk factors, 2) inconsistent associations with phenotype, 3) failure to assign a locus symbol in some established movement disorders, 4) more than one symbol being assigned for the same disorder, 5) unconfirmed genotype-phenotype associations, 6) erroneous labels and 7) symbol designation in the absence of known locus or gene.
The proposed nomenclature suggests that a disorder should be listed only if the causative gene is already known (i.e. genetic testing is possible), and appropriate prefixes should be assigned according to the core phenotypic feature, followed by the causative gene (e.g. DYT-gene1, PARK-gene2, HSP-gene3). Thus, currently used locus numbers are eliminated from future medical terminology (e.g. DYT1, PARK6,…). Suggested designations derive from primary clinical phenomenology: genetically determined parkinsonism, dystonia, chorea, paroxysmal movement disorders, dominant cerebellar ataxia, and spastic paraplegia.
Two groups of genetically determined disorders are prefixed not according to phenotype but typical imaging instead: primary familial brain calcification (PFBC-gene1, PFBC-gene2,…) and neurodegeneration with brain iron accumulation (NBIA-gene1, NBIA-gene2,…). Rules have been defined for disorders featuring mixed core characteristics. Future work will focus on as yet not approached disorders such as myoclonus, as well as x-linked, recessive, and congenital ataxias.
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Sunday, 8 July 2018
Obesity and overweight linked to long-term health problems after traumatic brain injury
High Body Weight Linked to Health Problems after Acute Rehabilitation for TBI
The study included 7,287 adults with TBI who had undergone inpatient acute rehabilitation. Inpatient rehabilitation consists of intensive therapy, provided by a team of specialists, designed to improve physical and mental functioning. Care was provided by rehabilitation centers participating in the the Traumatic Brain Injury Model Systems (TBIMS) program, sponsored by the National Institute on Disability, Independent Living, and Rehabilitation Research.
About three-fourths of patients were men; the average age was 46 years. The relationship between body weight and functional and health outcomes was assessed from one to 25 years after TBI. At the most recent follow-up, 23 percent of TBI survivors were classified as obese, 36 percent as overweight, 39 percent as normal weight, and three percent as underweight.
Overweight and obesity were less likely for patients under age 30, as well as those aged 80 years or older. While the percentage of overweight patients was relatively stable, the obesity rate increased over time especially five years or longer after TBI.
Being overweight or obese was strongly associated with several chronic health conditions, including high blood pressure, heart failure, and diabetes. Overweight/obese patients also rated themselves as having poorer general health. The frequency of seizures -- a common problem among TBI survivors was also related to differences in body weight and health status.
The overall rate of overweight/obesity in the TBI patients (59 percent) was lower than reported in the general US population (over 70 percent). This may be attributed to several reasons in need of further examination -- for example, a higher rate of health complications, rehospitalizations, medication side effects, or death among individuals who were already obese at the time of TBI and thus were excluded from the follow-up study.
Achieving and maintaining a healthy diet and engaging in regular physical activity following a TBI are critical goals for recovery, Dr. Dreer and coauthors write. During the early recovery period, patients may lose weight due to increased metabolic rate and other physical effects of TBI. In the later phases, weight gain may occur due to a wide range of factors including medical conditions, medications, cognitive or behavioural changes, physical limitations, and lack of transportation or other resources.
Based on the large-scale TBIMS database, the new study confirms that being overweight or obese is associated with significant health problems for survivors of moderate to severe TBI who require acute rehabilitation. The researchers note some important limitations of their study, including the lack of information on the timing of weight problems and associated health conditions.
However, these findings do highlight the potential importance of surveillance, prevention, and management of weight and related health conditions during the years postinjury, Dr Dreer and colleagues conclude.Lifestyle and health behaviours related to weight gain will need to be a component of any proactive approach to managing TBI as a chronic health condition.
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Saturday, 7 July 2018
Friday, 6 July 2018
Researchers report both those who received voluntary and involuntary electroconvulsive therapy reported their symptoms were much improved following treatment.
The findings, which have just been published in the July issue of the journal Brain Stimulation, are based on the largest study of its kind internationally and one of very few studies to report on people requiring involuntary treatment, who are rarely able to take part in clinical research. The results provide reassurance for people who have had involuntary ECT, their families and healthcare providers, according to Professor of Psychiatry Declan McLoughlin from Trinity’s Department of Psychiatry and Trinity Institute of Neuroscience.
The study found that people who have involuntary ECT were more severely unwell before treatment than those having voluntary ECT and were more likely to have psychotic symptoms such as hallucinations and delusions, and have more physical deterioration as a result of severe self-neglect.
Depression is one of the leading causes of disability worldwide. People who suffer from severe depression may lose the capacity to make decisions and require treatment under mental health law in order to recover. ECT is the most effective acute treatment for severe depression and is sometimes administered as an involuntary treatment. In Ireland, approximately fifty people require involuntary ECT each year.
The research team, led by Professor McLoughlin, studied the records of five years of involuntary ECT treatment at St Patrick’s Mental Health Services, Dublin, Ireland. The team reported on 48 involuntary ECT courses and compared these with 96 courses of voluntary ECT administered to people of the same age and sex at the same time.
The results shed light on a group about which little is known and provide a stronger evidence base for patients receiving involuntary ECT under the provisions of mental health legislation, according to Professor McLoughlin.
People who require involuntary ECT are among the most severely unwell in our mental health services. Yet, because they generally lack decision-making capacity and cannot take part in research, we do not know for sure if we can apply research advances to persons having involuntary ECT. Our knowledge of how best to use ECT to help someone recover from severe depression is based on research samples comprised entirely of people choosing to have voluntary ECT.
Our results are reassuring for people who have had involuntary ECT and their families. It’s also a relief to mental health professionals to know that the research results on which we base treatment decisions for voluntary treatment can now be used with greater confidence to also guide treatment for people having involuntary ECT.”
He cautioned, however, that “although ECT is a safe and highly effective evidence-based treatment, ongoing research is essential to understand who will benefit most from the treatment, and how to help people with depression stay well after recovery”.
Wednesday, 4 July 2018
Neurology Conference | Parkinson's disease | Intestine | Research Topics | Neurology 2018 | Call For Papers |
Parkinson's disease | Intestine | Research Topics | Neurology 2018
In the early stages of the disease, other types of complications have been observed, including constipation and gastrointestinal disorders. Constipation is one of the most common non-motor symptoms of the disease. It was documented for more than 200 years by James Parkinson in the first report of the disease. In 2010, researchers from the National Institute of Neurology and Neurosurgery in Mexico City reported that 30% of Parkinson's patients studied suffer from gastrointestinal disorders.
In recent years, various investigations have linked Parkinson's Disease with an alleged origin in the intestine. This is due to the findings of a possible transmission of the intestine to the brain. Here I will present the main mechanisms that are proposed to explain this relationship between these parts of the body.
1. Transmission of the intestine to the brain
In 2003, Heiko Braak and colleagues published extensive research that analyzed brain tissue from 168 samples of cases diagnosed with Parkinson's disease, cases with indications of the disease and individuals without neurological disorders. The objective was to compare the lesions in the samples and establish a pattern of Parkinson's progression. One of the key lesions in the disease is the toxic buildup of a protein called alpha-synuclein in affected neurons. They found in the patients studied the accumulation of alpha-synuclein in a part of the vagus nerve, which is responsible for intestinal functions. Braak suggested a new mechanism combining his observations with other reports of defective alpha-synuclein in the intestinal tract of Parkinson's patients. It was speculatively suggested that the disease was following a progression similar to that of a "pathogen" and that the entry route could be the intestine. Although this work continues to be a benchmark for Parkinson's research, many other studies have shown that not all patients follow the stages of progression suggested by Braak et al. There are reports of up to 50% of patients studied that do not agree with the pathological signs described in the Braak stage system (Kalaitzakis, 2008).
Currently an "unknown pathogen" is not the first line of research as the origin of the disease. Environmental factors that use the vagus nerve as a transport route have also been suggested as possible initiators or catalysts. But there are still questions about this mechanism of propagation of Parkinson's disease, such as Why is the distribution of alpha-synuclein accumulations so variable once they reach the brain of patients? o Why would alpha-synuclein begin to accumulate defectively in the intestine in the first place? Till the date,
2. The intestinal flora and its possible role in the disease
Different research groups have studied the changes in intestinal flora in patients with Parkinson's. For example, some groups have described a greater abundance of bacterial families in Parkinson's patients than in people without the disease.
Other groups have associated the presence of certain bacteria with worsening of symptoms in patients. Some groups began to observe that the intestinal flora of Parkinson's patients with motor complications has more abundance of some types of bacteria, compared with patients who do not develop those specific symptoms. It was also reported that patients with Parkinson's who suffer gastrointestinal infections caused by the bacterium Helicobacter pylori present more serious motor symptoms. Recently, a research group led by Sarkis Mazmanian showed that metabolites produced by certain bacteria can worsen the motor symptoms and brain pathology of model mice of this disease.
Changes in bacterial flora have also been associated with specific drugs that are used to treat patients (Scheperjans, 2015). However, it is still unclear if the prevalence of certain bacteria can influence the metabolism of drugs and affect the regulation of motor symptoms.
Although all these investigations present a relation between intestinal flora and Parkinson's disease, the evidence is very limited to issue conclusions about the relevance of treatments that involve the intestinal flora for the disease. These studies have not made clear whether changes in the intestinal flora are a cause or consequence of Parkinson's disease. Therefore, the relationship between certain types of bacteria in the intestinal flora and the processing of medications administered to patients should be properly investigated before proposing the intestinal flora as a target for treatment.
3. Inflammation, key process for a new model
In recent years, a model of disease progression that involves inflammation in the intestine has become more important. This model tries to combine evidence of reports of patients with intestinal inflammation, associations of Parkinson's disease with other intestinal diseases and the implication of important agents for Parkinson's disease with immunological processes in our body. A greater probability (28%) of developing Parkinson's disease was reported in a considerable number of patients with inflammatory bowel diseases. One of these diseases is Crohn's disease, an intestinal disorder related to Parkinson's disease due to a gene ( LRRK2 ) associated with these two diseases, which has a role in the regulation of inflammatory processes.
Do you remember alpha-synuclein? now more studies relate it to processes of immune response and inflammation. Increased inflammatory activity may increase alpha-synuclein levels in the intestine and in the brain. It has also been observed that alpha-synuclein stimulates inflammatory responses by promoting a cycle that further complicates the disease and would help the spread to other organs and tissues.
The model now suggested indicates that an external factor could trigger an immune response of chronic inflammation, which, when not regulated by the organism, would affect the intestinal flora and the production of proteins such as alpha-synuclein. The accumulation of defective alpha-synuclein would spread from the intestine to the brain through the vagus nerve and from there it would affect different neurons, including those that produce dopamine, to give rise to Parkinson's disease.
Although this model combines Braak's observations with recent findings about the disease, it still does not conclude whether intestinal complications are a cause or consequence of the disease. It is known that the intestinal symptoms of the disease precede the motor, but this does not indicate that the cause of the disease is in the intestine. Nor does it explain why a proportion of patients do not present intestinal disorders, nor does it resolve the aforementioned inconsistencies of the Braak system. In addition, this new model does not exclude the possible existence of an external factor that would cause intestinal inflammation, so in this case the intestinal anomalies would not represent the true origin.
All these studies begin to give more indications of the different faults in the organism that occur in Parkinson's disease. As mentioned above, it is possible that Parkinson's disease has different origins, which explains the different symptoms and patterns of progression in each of the patients. This also agrees with the difficulties that exist to establish an effective treatment for this disease, since each patient develops differently.
July 4, 2018 by Melissa Leija Salazar
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