The impact of bilateral therapy on upper limb function after chronic stroke: a systematic review

 Yeah, we've known of bilateral therapy a long time . This review was fucking worthless! You needed to write up a protocol on its' use and since you didn't; YOU'RE FIRED!

bilateral (29 posts to January 2012)

bilateral arm training (18 posts to December 2020)

bilateral therapy (4 posts to July 2023)

bilateral training (4 posts to February 2021)

bilateral upper limb training (4 posts to July 2021)

The impact of bilateral therapy on upper limb function after chronic stroke: a systematic review

Centre for Physiotherapy Research, University of Otago, Dunedin, New Zealand Accepted November 2009 Abstract Purpose. To determine the evidence for bilateral therapy interventions aimed at improving upper limb (UL) function in adults with a range of UL activity limitations due to a first time chronic stroke. 

Method. 

Seven databases were searched prior to 2008 for articles reporting experimental studies investigating bilateral UL interventions on functional outcome in participants with a first stroke, 6 or more months prior. Included articles were evaluated with the quality index, a tool which evaluates the quality of both randomised and non-randomised studies. Data relating to study design and functional outcome were extracted. 

Results. 

Nine articles were included; three reported on randomised controlled trials (RCT) and six on cohort studies. Eight studies incorporated a mechanical device as their bilateral intervention. Bilateral arm training with rhythmic auditory cueing (BATRAC) was the most commonly used mechanically based intervention, and three of the four uncontrolled BATRAC studies reported significant improvements in UL function post-intervention, however these results were not substantiated by a RCT study of the BATRAC intervention. One study demonstrated significant functional improvements after 6 days of training with a non-mechanical bilateral task. Of the four studies that performed a follow-up assessment, three reported significant improvement in UL function. Quality index ratings of the included studies ranged from 18 to 25 out of 27. 

Conclusion. 

There is some evidence that bilateral therapy improves function in adults with chronic stroke, however more quality RCTs are required to strengthen this evidence. Keywords: Bilateral therapy, upper limb, stroke Introduction Stroke is the third most common cause of mortality and the leading cause of adult disability in the developed world [1]. The current incidence of stroke in western countries is high; approximately 1 million Europeans [2], more than 795,000 Americans [1], and over 60,000 Australians [3] experience a stroke each year. The ongoing social and economic cost of stroke causes additional pressure on health care funding and rehabilitation services. In the United States alone this equates to around $68.9 billion dollars annually [1]. Population growth combined with the ageing population, declining mortality rates and rising stroke incidence suggests that this financial burden will continue to rise [2,4]. As a result, research is focused on the development of cost-effective and efficient approaches to stroke rehabilitation. One of the most important aspects of stroke rehabilitation is the regaining of function in the affected upper limb (UL) as this relates directly to functional independence [5]. A systematic review reported that functional task orientated training appears to have positive effects on functional out- comes, compared with impairment focused interventions [6]. Constraint induced therapy (CIT) is a functional task orientated intervention that has been shown to significantly improve UL function after stroke [7,8]. CIT restricts the use of the non-paretic limb to promote functional movement of the affected UL. The proposed physiological basis underpinning CIT is the reactivation of dormant neuromuscular pathways [9–11]. This notion was first proposed by Taub in 1980 [12], who suggested that encouraging use of the affected limb led to a corresponding increase in cortical representation, which he believed provided the neurological basis for permanent functional gains of the affected extremity. However, a number of limitations regarding the use of CIT exist. For example, CIT requires patients to meet strict inclusion criteria, such as being able to voluntarily achieve at least 108 of wrist extension and thumb abduction of the paretic side, to participate in this type of therapy [13]. In a clinical setting CIT is very personnel and resource intensive, while in the community there are issues of patient safety and reduced functional independence due to constraint of the non-paretic limb [14]. This decreased functional independence may result in reduced patient compliance [14]. Furthermore, many activities of daily living (ADLs) are bimanual in nature and require complimentary and coordi- nated movement of the UL [15,16]. These realisations have prompted the development of a variety of bimanual interventions for UL stroke rehabilitation [16]. Although the concept of bimanual training is not new, the first investigation into the use of bilateral therapy in UL rehabilitation in people with hemi- plegic stroke was conducted by Mudie and Matyas in 1996 [17], with positive results. Bilateral therapy involves the use of both ULs either simultaneously or sequentially [18], whereby the intact UL facilitates relearning of the spatial and temporal parameters required for motor recovery in the paretic UL [19,20]. Importantly, the principles of forced use and task specificity underlying CIT are retained with bilateral therapy without the need to constrain the unaffected UL [5,21]. In addition, it is believed that the performance of bilateral movements may enable activation of the damaged hemisphere by way of inter-hemispheric connections [22–24]. Following stroke it has been shown that using transcranial magnetic stimulation techniques the normal symmetrical transcallosal inhibition is disrupted and an imbalance occurs resulting in over-excitation of the contralesional hemisphere and excessive inhibition of the ipsilesional hemisphere. It is suggested that synchronous bilateral UL movements are a motor- based priming strategy that facilitate a re-balance of these systems. In a sample of 32 adults with chronic stroke, synchronous bilateral UL movements re- sulted in significant increase in ipsilesional hemi- sphere excitability, in transcallosal inhibition from ipsilesional to contralesional hemispheres and in intracortical inhibition within the contralesional hemisphere in the experimental group. Additionally, the experimental group had significant and sustained improvement in UL function [23]. Since the original publication by Mudie and Matyas (1996) [17], there have been numerous studies addressing the effect of bilateral interventions on patients with hemiplegic stroke. Although many studies report positive outcomes using bilateral interventions, some studies failed to demonstrate any functional gains [15]. Rose and Winstein (2004) [25] have suggested that this may be due to the variety of bimanual interventions currently employed in the literature. In this systematic review, we aimed to determine the evidence for bilateral therapy interventions aimed at improving UL function in adults with chronic stroke resulting in a range of UL activity limitations. Previous systematic reviews of bilateral therapy effectiveness have primarily focused on kinematic variables, cortical mapping and patients at various stages of stroke recovery, and not on functional outcome [20,25–27]. As most functional recovery up to six months post-stroke is postulated to occur as a result of spontaneous recovery [28–31], we concen- trated on studies reporting outcome of participants with chronic stroke (more than 6 months post- stroke). 

More at link.

Cognitive Decline Linked To Seasoning That 90% Overconsume

 Has your competent? doctor instructed the dietician to ensure that all hospital meals fall within this limit? NO? So you don't have a functioning stroke doctor, do you? 

But this:

 

Review finds no proven clinical benefit to strict salt restriction for patients with heart failure

And this:

In many high income countries, approximately 75% of salt in the diet comes from processed foods and meals prepared outside the home. 

Low-Salt Diet Ineffective, Study Finds. Disagreement Abounds. June 2011 

Researchers reveal surprising findings on how salt affects blood flow in the brain

November 2021 

You'll want your competent? doctor to explain these and give you an EXACT PROTOCOL ON SALT!

 

 The latest here:

Cognitive Decline Linked To Seasoning That 90% Overconsume

90% use too much of an everyday substance that can cause inflammation of blood vessels in the brain, which is linked to dementia.

A high-salt diet is linked to cognitive decline and possibly dementia, research finds.

Salt causes the delicate lining of the brain’s blood vessels to inflame, because of signals sent from the gut.

Fully 90 percent of Americans consume above the recommended dietary maximum of 2,300 mg per day.

Dr Costantino Iadecola, study co-author, said:

“We discovered that mice fed a high-salt diet developed dementia even when blood pressure did not rise.

This was surprising since, in humans, the deleterious effects of salt on cognition were attributed to hypertension.”

The effect was quickly reversed by lowering salt intake.

The conclusions come from a study in which mice were fed a high-salt diet that is equivalent to a high-salt diet in humans.

Subsequently, the mice had much worse cognitive function.Their brains showed 28 percent less activity in the cortex and 25 percent less in the hippocampus.

They had problems getting around a maze and did not show the usual interest in new objects placed in their cage.

They also had poorer blood flow in their brains and the integrity of the blood vessels there was worse.

However, these changes were reversed once the mice were returned to a normal diet.

The scientists found that these changes had nothing to do with higher blood pressure.

Worse cognitive functioning in the mice was seen even when the mice had normal blood pressure.

They were the result of signals sent from the gut to the brain.

These activated an immune response in the brain which increased levels of interleukin-17.

This eventually resulted in the inflammation of the delicate lining of the brain’s blood vessels.

Anti-inflammatory diets could lower dementia risk among older individuals with cardiometabolic disorders

 Useless, NOTHING SPECIFIC IN HERE!

If you want to be useful you create an EXACT diet protocol, this does nothing towards that.  

Your chances of getting dementia. YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING THIS!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

Anti-inflammatory diets could lower dementia risk among older individuals with cardiometabolic disorders

In a recent study published in JAMA Network Open, researchers investigated whether anti-inflammatory diets support cognitive functions among cardiometabolic disease (CMD) patients.

Study: Anti-Inflammatory Diet and Dementia in Older Adults With Cardiometabolic Diseases. Image Credit: Elena Eryomenko/Shutterstock.com

Background

CMDs like insulin-independent diabetes, heart disease, and stroke are associated with an elevated dementia risk, particularly when they coexist. Studies associate inflammation with the pathophysiologic features of CMDs and dementia, and dietary habits can modulate systemic inflammation.

Increased levels of inflammatory biomarkers are associated with Western diets heavy on eggs, high-fat dairy, red meat, processed foods, and refined grains.

In contrast, diets rich in fruits, vegetables, whole grains, seafood, and legumes lower inflammatory biomarker levels.

Studies associate lower dietary inflammation with a lower risk of cognitive decline and favorable MRI brain aging indicators. However, the efficacy of anti-inflammatory diets in improving cognition in CMD patients is uncertain.

About the study

The present study researchers explored the potential cognitive benefits of anti-inflammatory diets among older adults with cardiometabolic diseases.

The researchers included 84,342 adult United Kingdom Biobank participants aged 60 years or above, with baseline evaluations conducted between 13 March 2006 and 1 October 2010.

They excluded individuals with dementia, insulin-dependent diabetes, and those with missing CMD data. The primary study outcome was new-onset dementia, identified through medical records and self-reported.

The researchers performed joint effects analysis to assess cardiometabolic disease status and diet-related inflammation concerning the risk of dementia and magnetic resonance imaging (MRI) markers of neurodegeneration and vascular injury in the brain.

In total, 8,917 participants without chronic neurological diseases underwent MRI between 2 May 2014 and 13 March 2020 to provide their gray matter volumes (GMV), total brain volume (TBV), hippocampal volumes (HV), white matter volumes (WMV), and white matter hyperintensity volumes (WMHV)

Researchers ascertained baseline CMDs such as heart disease, stroke, and insulin-independent diabetes from health records.

They calculated Dietary Inflammatory Index (DII) scores based on 31 food nutrients consumed between 8 February 2011 and 15 June 2012, evaluated using the 24-hour Oxford WebQ dietary assessment.

Points up to -1.5 indicated anti-inflammatory, above -1.5 but less than 0.5 indicated neutral, and 0.5 or above indicated pro-inflammatory potential.

Researchers followed the participants through 20 January 2022. They used Cox proportional hazard regressions to calculate the hazard ratios (HR) for analysis. Study covariates included race, education, body mass index (BMI), smoking status, calorie intake, physical activity, socioeconomic status, hypertension, antihypertensive medication use, and apolipoprotein E (APOE) status.

MRI covariates included time between scans, assessment centers, and table and head positions within MRI scanners.

Researchers performed sensitivity analyses applying Fine and Gray's regressions to non-imputed information and limiting participants to those completing at least two dietary evaluations, excluding individuals diagnosed with dementia within five years.

They also determined the association of DII scores with systemic inflammation biomarkers such as serological C-reactive protein (CRP) levels and assessed DII score stability across dietary evaluations.

Results

The mean participant age was 64 years; 51% were female, and 37% had attained at least a college-level education. At baseline, 14,079 (17%) had one or more cardiometabolic diseases.

CMD patients tended to be less educated, older, physically inactive, and more socioeconomically deprived male Asian black smokers with elevated BMI and hypertension. Individuals undergoing MRI had lower age, less socioeconomic deprivation, and better vascular injury risk profiles.

Over 12 years (median) of follow-up, 1,559 individuals (1.90%) received dementia diagnosis. The joint effects analysis yielded an HR of 2.4 for dementia for CMD patients following pro-inflammatory diets and 1.7 for individuals with CMDs consuming foods with anti-inflammatory potential.

Individuals with CMDs consuming anti-inflammatory diets rather than pro-inflammatory diets showed a 31% lower dementia risk (HR, 0.7) among CMD patients consuming anti-inflammatory foods.

Brain MRI scans of individuals consuming anti-inflammatory diets showed significantly higher GMV and lower WMHV values. Using Laplace regressions, CMD patients eating anti-inflammatory foods developed dementia two years after those with CMDs who ate pro-inflammatory foods.

Sensitivity analyses yielded similar results with stable DII scores across dietary evaluations. However, Fine and Gray's regressions yielded attenuated all-cause dementia HR values, indicating that the competing risk of death could influence the results.

Conclusions

The study found that cardiometabolic disease patients consuming anti-inflammatory foods had a decreased incidence of dementia, higher GMV, and lower WMHV values, indicating less neurodegeneration and vascular damage.

The findings suggest that anti-inflammatory diets improve cognitive function in those with cardiometabolic illnesses. Anti-inflammatory foods may reduce systemic inflammation, delaying dementia onset.

Longitudinal brain MRI studies may enhance knowledge of the links between dietary inflammation and brain illness, particularly concerning risk factors like cardiometabolic disorders.

Journal reference:

• Dove A, Dunk MM, Wang J, Guo J, Whitmer RA, Xu W. (2024) Anti-Inflammatory Diet and Dementia in Older Adults With Cardiometabolic Diseases. JAMA Netw Open. 2024;7(8):e2427125. doi:10.1001/jamanetworkopen.2024.27125. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2822212

Eating these foods lowers dementia risk, even with type 2 diabetes and heart disease, study says

 Go ask your competent? doctor to make this useful for you by creating AN EXACT DIET PROTOCOL on this.  At least a competent one would be able to get this done!

YOU DON'T HAVE A COMPETENT DOCTOR, DO YOU?

Your chances of getting dementia. YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING THIS!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

 

Eating these foods lowers dementia risk, even with type 2 diabetes and heart disease, study says

CNN  — 

Eating an anti-inflammatory diet of whole grains, fruits and vegetables instead of an inflammatory diet focused on red and processed meats and ultraprocessed foods, such as sugary cereals, sodas, fries and ice cream, lowered the risk of dementia by 31%, a new study found.

That benefit held true even for people with existing diagnoses of cardiometabolic conditions such as type 2 diabetes, heart disease or stroke, said Abigail Dove, lead author of the study published Monday in the journal JAMA Network Open.

Related article Cut your risk of dementia by 20% with this dietary change

“Following an anti-inflammatory diet was related to lower risk of dementia, even among people with cardiometabolic diseases who are already at elevated risk of dementia,” said Dove, a doctoral student at the Aging Research Center at Karolinska Institutet in Solna, Sweden, in an email.

In fact, people living with type 2 diabetes, stroke or heart disease who ate the most anti-inflammatory foods “developed dementia 2 years later than those with cardiometabolic diseases and a pro-inflammatory diet,” she added.

Brain scans of those who followed an anti-inflammatory diet also showed significantly lower levels of brain biomarkers of neurodegeneration and vascular injury, Dove said.

Even though the study is observational and cannot show cause and effect, the findings reflect existing research that shows a link between dietary inflammation and brain health, said Dr. David Katz, a specialist in preventive and lifestyle medicine who was not involved in the study, via email.

“It is highly likely that a higher quality, less inflammatory diet directly impacts multiple pathways related to brain and neurocognitive health over time,” said Katz, the founder of the nonprofit True Health Initiative, a global coalition of experts dedicated to evidence-based lifestyle medicine.

Anti-inflammatory diets boost nutrients that stave off dementia and chronic disease, studies say.

carlosgaw/E+/Getty Images/File

What is an anti-inflammatory diet?

The exact biological ways foods impact inflammatory pathways is not yet fully understood. However, researchers believe the reliance on sugary, ultraprocessed foods and the abundance of saturated fats from red and processed meats that is common in the Western diet  — along with pollution, cigarette smoke, radiation, plastics and pesticides — may lead to the increased activation of free radicals in the body.

Free radicals are molecules with unpaired electrons. Driven to search for a match, they rob other cells of their electrons, causing cellular damage that can contribute to Alzheimer’s disease and other dementias and chronic diseases.

In addition, researchers believe highly processed and fatty foods can also trigger higher levels of other inflammatory biomarkers such as C-reactive protein, interleukin 6 and tumor necrosis factor α.

Related article Hidden belly fat linked to brain inflammation and dementia, study finds

A November 2020 study found people who ate higher levels of red and processed meats, such as bacon and sausage, as well as sugary, ultraprocessed foods had a 28% higher risk of stroke and a 46% higher risk of heart disease. Just a 10% increase in such foods was significantly associated with a 14% higher risk of death from all causes, according to a February 2019 study.

There is a way to fight back: Research has suggested that anti-inflammatory elements such as vitamins, carotenoids and flavonoids in foods such as fruits and vegetables may neutralize free radicals and other inflammatory markers and reduce the stress on the body, according to the Mayo Clinic.

Better brains with anti-inflammatory foods

The new study analyzed the dietary patterns of over 84,000 dementia-free adults older than age 60 with a diagnosis of type 2 diabetes and/or heart disease or stroke who were part of the UK Biobank, a longitudinal study that includes participants from England, Scotland and Wales.

Each person was asked five times about their consumption of 206 foods and 32 drinks that were divided into levels of inflammatory and anti-inflammatory nutrients. Medical records were examined over the next 15 years to discover whether there were any associations between eating the least and the most amounts of inflammatory foods and diagnoses of dementia. In addition, nearly 9,000 of the participants also underwent magnetic resonance imaging, or MRI, brain scans.

Related article Foods that cause inflammation

Scans found people with cardiometabolic diseases who ate the most anti-inflammatory foods had larger gray matter volume — indicating less neurodegeneration — and lower white matter intensities, which are signs of vascular injury in the brain, compared with people who ate an inflammatory diet.

While more research needs to be done, overall, “the signal is clear above the background noise,” Katz said.

“Even after one is contending with a chronic, cardiometabolic condition, the adoption of a higher quality diet appears to offer some protection to the brain, reducing and delaying both functional and anatomical signs of degradation.”

Interaction effect between blood selenium levels and stroke history on all-cause mortality: a retrospective cohort study of NHANES

 Is your competent? doctor currently preparing protocols on selenium based on these two recent research articles? NO? So your don't have a functioning stroke doctor?

Selenium-containing compounds: a new hope for innovative treatments in Alzheimer’s disease and Parkinson’s disease June 2024 

 

The Role of Gut Microbiota in the Neuroprotective Effects of Selenium in Alzheimer’s Disease July 2024

 

Interaction effect between blood selenium levels and stroke history on all-cause mortality: a retrospective cohort study of NHANES

Yanli LiLanqun LiuZufu YangJimin Xu^*

• Department of Traditional Chinese Medicine, Beijing Boai Hospital, China Rehabilitation Research Center, School of Rehabilitation Medicine, Capital Medical University, Beijing, China

Aim: The study aimed to investigate the interaction effect between blood selenium levels and stroke history on all-cause mortality.

Methods: In this retrospective cohort study, participant data were obtained from the National Health and Nutrition Examination Survey (NHANES) 2011–2018. The covariates were screened via the backward selection method in weighted univariate and multivariate Cox regression models. Weighted univariate and multivariate Cox regression models were conducted to investigate the association of blood selenium and stroke history with all-cause mortality. The results were expressed as hazard ratios (HRs) and 95% confidence intervals (CIs). The synergy index (SI) was used to assess the assistive interaction. The association was further explored in different gender groups.

Results: Totally, 8,989 participants were included, of whom 861 (9.57%) died. Participants with blood selenium ≥192.96 ug/L were associated with lower odds of all-cause mortality (HR = 0.70, 95% CI: 0.58–0.84), whereas those with a stroke history were associated with a higher risk of all-cause mortality (HR = 1.57, 95% CI: 1.15–2.16). Compared to participants with blood selenium ≥192.96 ug/L and non-stroke history, participants with both blood selenium < 192.96 ug/L and stroke history had a higher all–cause mortality risk (HR = 2.31, 95% CI: 1.62–3.29; SI = 0.713, 95% CI: 0.533–0.952). All participants with blood selenium < 192.96 ug/L and stroke history were related to higher all–cause mortality risk (HR = 1.61, 95% CI: 1.21–2.13). In males, the interaction effect of blood selenium and stroke history on all–cause mortality (HR = 2.27, 95% CI: 1.50–3.46; SI = 0.651, 95% CI: 0.430–0.986) increased twice.

Conclusion: Blood selenium and stroke history have an interaction effect on all-cause mortality. Increasing selenium-rich food or supplement intake, especially for individuals with a stroke history, may improve poor prognosis.(Well, then, do the research that creates a protocol for selenium!)

Introduction

Stroke, a neurological emergency, is the second leading cause of death and a major contributor to disability worldwide (1). Stroke affects 13.7 million people and causes 5.5 million deaths (2). Stroke is also responsible for about 140,000 deaths in the U.S. every year, which is about one out of every 20 deaths in the country (3). Stroke history is an independent risk factor for poor prognosis in ischemic stroke patients (4). Oxidative stress and inflammation play significant roles in the pathogenesis of stroke (5–7).

Selenium, an essential trace element, plays a critical role in various physiologic processes, including oxidative stress, thyroid hormone metabolism, and immune function (8, 9). Lower circulating selenium levels have been linked to an elevated risk of cardiovascular disease, increased risk of ischemic stroke, and all-cause mortality (10). In patients with heart failure, blood selenium was independently associated with a 50% higher mortality rate (11). A lower concentration of selenium could increase the risk of ischemic stroke (12). And Wang et al. reported that plasma selenium was inversely associated with the risk of a first ischemic stroke (13). Zhao et al. (14) also found a negative relationship between blood selenium levels and stroke. In addition, the modifying effect of selenium was observed in metabolic disease, cardiovascular disease (CVD), and neurologic symptoms (15–17). We hypothesize that blood selenium level and stroke history may have an interaction with the long-term prognosis of participants.

Thus, this study aimed to investigate the interaction effect of blood selenium and stroke on all-cause mortality. The findings of this study will contribute to existing knowledge on the role of blood selenium in stroke prognosis and provide guidelines for the development of targeted interventions to improve outcomes for individuals with stroke histories.

More at link.

Elucidating the pivotal molecular mechanisms, therapeutic and neuroprotective effects of lithium in traumatic brain injury

You can ask your competent? doctor what has been done with all this earlier research. No knowledge you need to fire your doctor.

I've got 14 posts on lithium back to 2011 and I bet your stroke medical 'professionals' have not done one damn thing. WHOM will create protocols for lithium?

 Elucidating the pivotal molecular mechanisms, therapeutic and neuroprotective effects of lithium in traumatic brain injury

Received: 9 January 2024 Revised: 17 May 2024 Accepted: 26 May 2024
DOI: 10.1002/brb3.3595

Seidu A. Richard1,2
1 Department of Medicine, Princefield
University, Ho, Ghana
2 Institute of Neuroscience, Third Affiliated
Hospital, Zhengzhou University, Zhengzhou,
China
Correspondence
Seidu A. Richard, Department of Medicine,
Princefield University, P. O. Box MA 128,
Ho-Volta Region, Ghana.
Email: gbepoo@gmail.com

Abstract

Introduction: 

 

Traumatic brain injury (TBI) refers to damage to brain tissue by mechan-
ical or blunt force via trauma. TBI is often associated with impaired cognitive abilities,
like difficulties in memory, learning, attention, and other higher brain functions, that
typically remain for years after the injury. Lithium is an elementary light metal that
is only utilized in salt form due to its high intrinsic reactivity. This current review
discusses the molecular mechanisms and therapeutic and neuroprotective effects of
lithium in TBI.
Method: 

 

The “Boolean logic” was used to search for articles on the subject matter in
PubMed and PubMed Central, as well as Google Scholar.
 

Results: 

Lithium’s therapeutic action is extremely complex, involving multiple effects
on gene secretion, neurotransmitter or receptor-mediated signaling, signal trans-
duction processes, circadian modulation, as well as ion transport. Lithium is able to
normalize multiple short- as well as long-term modifications in neuronal circuits that
ultimately result in disparity in cortical excitation and inhibition activated by TBI. Also,
lithium levels are more distinct in the hippocampus, thalamus, neo-cortex, olfactory
bulb, amygdala as well as the gray matter of the cerebellum following treatment of TBI.
 

Conclusion: 

Lithium attenuates neuroinflammation and neuronal toxicity as well as
protects the brain from edema, hippocampal neurodegeneration, loss of hemispheric
tissues, and enhanced memory as well as spatial learning after TBI.

This Diet Wipes Out Memory And Learning

 Does your competent? doctor have enough functioning brain cells to get the nutritionist to create EXACT DIET PROTOCOLS to prevent this problem?

This Diet(Western style) Wipes Out Memory And Learning

Gamma oscillations and their role in orchestrating balance and communication following stroke

Didn't your competent? doctor start creating protocols on this years ago? NO? So you DON'T have a competent doctor? Why are you there? Now if we just had someone in stroke with two functioning neurons to rub together we could easily get a protocol written on this and get survivors recovered! BUT WE HAVE NO ONE WITH BRAINS WORKING IN STROKE! You'll probably have to read the conclusion yourself and come up with your own protocols since everyone in stroke is a complete fucking failure!

• gamma oscillations (13 posts to May 2012)

  • gamma oscillations (5 posts to May 2021)

   

 Gamma oscillations and their role in orchestrating balance and communication following stroke

Montana Samantzis#, Cong Wang#, Matilde Balbi

Induced brain oscillations in the gamma range have recently garnered attention due to their reported neuroprotective effects in the treatment of Alzheimer’s disease. This method differs from pharmacological approaches by tapping into the neuronal population dynamics that underlie the homeostatic processes in the brain that are crucial for the recovery of function. Recently,induced gamma-range oscillations have been used to improve cerebral blood flow, motor function, and synaptic plasticity in a mouse model of focal stroke, highlighting the broad potential of recruiting intrinsic recovery processes for the treatment of neurological conditions. Addressing open questions, such as the frequency specificity of the benefits, will shed light on the intrinsic processes involved and allow clinicians to optimize recovery after stroke. Interneurons play a crucial role in orchestrating the coordinated activity of adjacent neurons through inhibitory mechanisms and are instrumental in the generation of oscillatory activity within the brain.In particular, the generation of gamma oscillations,rhythmic patterns of activity that occur within the frequency range of 25–100 Hz, is tied to the firing activity of parvalbumin interneurons (Cardin et al.,2009). In the cortex, parvalbumin neurons inhibit excitatory pyramidal neurons, and their inhibitory postsynaptic potentials are phase-locked to gamma oscillations (Guan et al., 2022). Gamma oscillations are proposed to play a key role in maintaining homeostatic brain processes including synchronization of other oscillatory bands, inter- and intra-regional communication,and maintenance of excitatory and inhibitory activation within the brain (Guan et al., 2022). Disruption of gamma oscillations occurs in several pathological and non-pathological conditions which can lead to disruption of metabolic,cognitive, and behavioral processes. New evidence has proposed that entrainment of these oscillations may facilitate functional recovery,making this a promising target for therapeutic intervention (Adaikkan and Tsai, 2020; Balbi et al.,2021; Wang et al., 2023). Following ischemic stroke, there is an increased disruption of low gamma oscillations (30–50 Hz) in the region surrounding the ischemic core (Hazimeet al., 2021). Optogenetic targeting of fast-spiking parvalbumin inhibitory neurons at 40 Hz has been shown to increase the power of gamma oscillations (Cardin et al., 2009), and in the context of ischemic stroke, stimulation of inhibitory neurons at this frequency has shown remarkable improvements to functional recovery (Balbi etal., 2021). The precise mechanism by which the targeted modulation of inhibitory neuronal activity through gamma oscillations contributes to enhanced recovery following a stroke remains elusive.In this perspective, we discuss our recent findings proposing that this phenomenon can be attributed to facilitating interregional communication between brain regions and inducing functional plasticity (Wang et al., 2023).Gamma frequency stimulation of inhibitory neurons regulates the inhibitory-excitatory balance: Targeting oscillatory dynamics using brain stimulation techniques is an emerging toolfor promoting recovery post stroke, however,has had varying results (reviewed in Storch etal., 2021). Gamma oscillations in particular are thought to be key in order to maintain a healthy balance between excitatory and inhibitory activity within the brain, which is essential for information processing. Targeting inhibitory neurons either ipsi- or contra-lesionally within the gamma frequency preferentially facilitates behavioral recovery following stroke (Balbi et al.,2021). Ipsilesional 40 Hz stimulation immediately following stroke also aided in restoration of blood flow and reduced lesion size, whilst optogenetic stimulation at 10 Hz or whisker stimulation at 4 Hz did not improve outcomes (Balbi et al., 2021). While investigating how gamma oscillations modulate neuronal assemblies, we found that 40Hz stimulation of interneurons leads to synaptic current changes in pyramidal neurons, meaning that they receive direct inputs from interneurons to regulate their activity (Wang et al., 2023). We observed synchronized but anticorrelated activity of excitatory and inhibitory signals whereby interneuron firing occurred during the peak phase of the gamma rhythm, and pyramidal neurons fired during the trough phase. These modulatory effects were observed exclusively during 40 Hz stimulation where the firing rate of both pyramidal neurons and interneurons was affected, whilst10 Hz stimulation of interneurons had no effect on the firing rate of either cell type (Wang etal., 2023). By stimulating inhibitory neurons at their resonating frequency, we are therefore able to increase their activity whilst simultaneously reducing possible over-excitation caused by stroke.Thus, this induction of gamma oscillations may restore the harmony between inhibitory and excitatory activity in the brain. We hypothesize that by rescuing this balance in local networks,we may be able to mitigate damage to long-range connections between brain regions.Induction of gamma oscillations leads to improved inter-regional communication: Theta-gamma coupling refers to the synchronization between neuronal oscillatory rhythms in the theta (4–8 Hz) and gamma range. This coupling showcases the regulatory role of low-frequency brain activity in orchestrating information exchange between different brain regions by modulating the amplitude of high-frequency oscillations. This dynamic interplay between theta and gamma oscillations is thought to play a crucial role in coordinating cognitive functions by enhancing communication between different brain regions.Theta-gamma cross-frequency coupling is disrupted following stroke, making it a clear target for improving recovery (Zheng et al.,2020; Rustamov et al., 2022; Wang et al., 2023).Furthermore, this coupling is increased during the generation and execution of motor functions,Montana Samantzis#, Cong Wang#, Matilde Balbi*and an improvement of theta-gamma coupling has been reported as a potential biomarker of recovery in patients during the chronic phase of stroke, correlating with improved motor performance (Rustamov et al., 2022). Deficits in theta-gamma coupling that are observed within two weeks following hippocampal ischemia can be rescued following repeated 40 Hz visual stimulation (Zheng et al., 2020). Interestingly, our recent work builds upon this evidence and shows that 40 Hz stimulation also enhances theta-gamma coupling and motor performance in the acute phase following stroke, suggesting that this may also be a useful biomarker for recovery of motor function acutely following injury (Balbi et al., 2021;Wang et al., 2023).On a wider scale, gamma oscillations facilitate inter-regional communication, potentially through enhancing the coherence of gamma oscillations between regions. Following stroke,there is a decrease in evoked gamma synchronicity which has been shown to correlate with worse clinical outcomes (Pellegrino et al., 2019). By optogenetically targeting inhibitory neurons at 40 Hz in the acute phase after stroke, we recently demonstrated increased interregional communication between the primary motor cortex and the posterior temporal area. Interestingly,this increase in functional connectivity was still observed 24 hours following stimulation (Wang etal., 2023). This restoration of coordinated network activity between regions is a key for facilitating communication following stroke and may allow for compensation of lost activity within the stroke core, thus helping to promote motor function.Functional plasticity following ischemia can be facilitated by inducing gamma oscillations: Neuroplasticity refers to the nervous system’s ability to change itself by reorganizing its connections, functions, or structures in response to internal or external stimuli. Following ischemia,there is damage to one or more brain regions,causing the brain to compensate for lost functions and reorganize its network structure. As gamma oscillations are heavily involved in the coordination of network activity, they may also play a key role in the regulation of plasticity processes following disruption to natural communication patterns.As previously mentioned, we have demonstrated that induced gamma oscillations phase locks the activity of both inhibitory and excitatory activity,which we postulate can synchronize the timing of both pre- and post-synaptic activities (Wang et al.,2023). The physiological process underlying the link between synchronous neuronal activity and neuroplasticity may be an instance of Hebbian theory such as spike-timing-dependent plasticity(Dan and Poo, 2004).We also recently observed a decrease in the number of pairwise functional synaptic connections as determined by cross correlogram analysis following ischemic stroke (Wang et al.,2023). Remarkably, following 40 Hz stimulation this functional connectivity is rescued to baseline levels 24 hours following ischemia (Wang et al., 2023).40 Hz visual stimulation has also been shown to increase postsynaptic long-term potentiations,  presynaptic short-term plasticity, and spine density following hippocampal ischemia (Zheng et al.,2020). In addition to functional changes, several key proteins related to synaptic plasticity have changes to expression levels as a result of 40 Hz stimulation, namely, postsynaptic density protein95, glutamate transport ATP-binding protein,and regulator of G protein signaling 12 (Zhenget al., 2020; Wang et al., 2023). Increases in these protein levels further support the idea that gamma frequency stimulation may have effects on both pre- and post-synaptic plasticity. However,further exploration of potential pathways of action is needed in order to fully understand the role of these oscillations in this fundamental plasticity process. In future studies, it will also be important to ascertain the extent to which 40 Hz stimulation can affect pre- and post-synaptic plasticity when the stimulation site is not directly next to the stroke region.

 

Conclusion and perspective: 

 

There is currently substantial evidence that gamma frequency stimulation may be beneficial in a range of neurodegenerative disorders; however, our understanding of the mechanisms of action is lacking. Recent findings show that entraining inhibitory activity in the gamma frequency range leads to synchronicity and functional plasticity following stroke (Figure 1). This evidence suggests that entrainment of gamma oscillations may be a promising treatment for other neurological disorders where gamma therapies are disrupted.The neurovascular unit encapsulates the highly complex synchronization between brain cells and the vasculature. Communication between different components of the neurovascular unit is a cornerstone for healthy brain functioning,including the generation of oscillatory activity.The coupling of the components of this unit is an intricate process involving a series of coordinated responses to changes in blood flow or neuronal activity, and disruption to either of these processes can be detrimental to the function of the unit as a whole. In addition to interneurons, astrocytes are a key component of the neurovascular unit that plays a role in the maintenance of gamma oscillations (Lee et al., 2014). The loss of blood flow following ischemia interferes with the activity within these crucial components and disrupts neurovascular function. We propose that induction and restoration of oscillatory activity in the gamma range in the stroke region can provide a substitute for naturally occurring oscillatory activity that is needed during a critical time window.This work was supported by the Brazil Family Program for Neurology (to MB), Alastair Rushworth Research Fund (to MS), Australian Government Research Training Program Scholarship (to MS),the National Natural Science Foundation of China(82202787) (to CW). Montana Samantzis#, Cong Wang#,Matilde Balbi*Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia(Samantzis M, Wang C, Balbi M)Engineering Research Centre of Traditional ChineseMedicine Intelligent Rehabilitation, Ministry of Education, Shanghai, China (Wang C)*Correspondence to: Matilde Balbi, PhD,m.balbi@uq.edu.au.https://orcid.org/0000-0003-4590-5447(Matilde Balbi)#Both authors contributed equally to this article.Date of submission: January 31, 2024Date of decision: March 4, 2024Date of acceptance: March 20, 2024Date of web publication: April 16, 2024https://doi.org/10.4103/NRR.NRR-D-24-00127How to cite this article: Samantzis M, Wang C,Balbi M (2024) Gamma oscillations and their role in orchestrating balance and communication following stroke. Neural Regen Res 19(0):000-000

Effect of high-frequency (5Hz) rTMS stimulating left DLPFC combined with galantamine on cognitive impairment after ischemic stroke and serum homocysteine and neuron-specific enolase

 Your doctor should have been familiar with galantamine for a decade already

• galantamine (5 posts to August 2013)

And with these positive effects your doctor should immediately create a protocol on this!

Effect of high-frequency (5Hz) rTMS stimulating left DLPFC combined with galantamine on cognitive impairment after ischemic stroke and serum homocysteine and neuron-specific enolase

Guojin HuLi ZhangXiuli Sun^*Lin Wang^*Qian XuQin LiWei HuangYao Xiao

• Department of Geriatric Rehabilitation, Shanghai Second Rehabilitation Hospital, Shanghai, China

Objective: To investigate the efficacy of high-frequency repetitive transcranial magnetic stimulation (HF-rTMS) combined with galantamine in patients with cognitive impairment after stroke and its effect on serum homocysteine (Hcy) and neuron-specific enolase (NSE) levels.

Methods: A total of 90 patients with cognitive impairment after the first ischemic stroke were enrolled. They were randomly divided into rTMS+ cognitive rehabilitation group, Galantamine + cognitive rehabilitation group, and rTMS+ Galantamine + cognitive rehabilitation group. All groups received routine medical treatment and limb rehabilitation treatment. The rTMS stimulation site was the left dorsolateral prefrontal cortex (left DLPFC), the magnetic stimulation frequency was 5 Hz, the magnetic stimulation intensity was 80% of the motor threshold level, and 3,000 pulses were given every day. The Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Fugl-Meyer scale, and modified Barthel index, as well as rehabilitation scale and serum NSE and Hcy were evaluated before and after treatment (after 4 weeks).

Results: After 4 weeks of treatment, the scores of MMSE, MoCa scale, Fugl-Meyer scale, and modified Barthel index in the three groups were significantly higher than those before treatment (all p < 0.05), while the serum NSE and Hcy levels of the three groups were decreased. rTMS+ Galantamine + cognitive rehabilitation group had higher scale scores, and the difference between the three groups was statistically significant compared with the other two groups (all p < 0.05).

Conclusion: Cognitive rehabilitation combined with HF-rTMS and galantamine could improve the cognitive function of patients to the greatest extent, promote the recovery of physical activity, improve the self-care ability of daily life, and effectively reduce the serum HCY and NSE levels in patients with cognitive impairment after stroke. No randomized controlled trials of similar combination treatments have been reported. The better therapeutic effect may be related to the fact that galantamine combined with repetitive transcranial magnetism can activate the brain cholinergic system more extensively, promote brain neural remodeling through long-term potentiation and inhibit local neuroinflammatory responses in brain injury.

1 Introduction

Post-stroke cognitive impairment (PSCI), especially post-stroke dementia, seriously affects patients’ functional recovery, daily activities, and social functioning. PSCI is an independent risk factor affecting the prognosis of stroke. Professor Hachinski’s survey published in “Stroke” in 2006 showed that as many as 64% of stroke patients have varying degrees of cognitive impairment, and 1/3 will develop obvious dementia (1). A systematic review of epidemiological characteristics of post-stroke cognitive impairment in China in 2013 showed that the incidence rates of PSCI and post-stroke dementia (PSD) within 3 months after stroke were 56.6 and 23.2%, respectively (2). Compared with those without dementia, physical function of PSCI patients, their mental health status, and social functioning undergo more significant decline. Also, their functional independence is weakened, social participation ability is worsened, life satisfaction drastically decreases, and the 5-year survival rate is significantly lowered (3, 4). PSCI also seriously hinders the improvement of patients’ motor function, psychological state, self-care ability, and ability to participate in social activities and reduces life expectancy.

In recent years, non-invasive brain stimulation technology has developed rapidly, among which repetitive transcranial magnetic stimulation (rTMS) technology has received the greatest attention from researchers. rTMS acts on the central nervous system, mainly the brain, through a pulsed magnetic field, changing the membrane potential of neurons in the cerebral cortex, causing them to generate induced currents, affecting intramembrane metabolism and neural electrical activity, and inducing a series of physiological and biochemical changes. As a result, this technology has been widely investigated in recent years, producing positive effects on depression, cognitive impairment, post-stroke movement disorders, aphasia, etc. (5–7).

rTMS alters the excitability of cortical and subcortical neurons. Among them, high-frequency (>1 Hz) stimuli produce excitatory effects, and low-frequency (≤1 Hz) stimuli produce inhibitory effects. rTMS can act on synapses to produce long-term potentiation or long-term inhibitory effects and promote the excitation or inhibition of cortical neural circuits. Moreover, the physiological effects are persistent (8).

A large amount of available data indicates that TMS technology has a very unique role in the rehabilitation treatment of dementia, including degenerative dementias such as Alzheimer’s disease, as well as secondary dementias (mainly caused by vascular factors). Transcranial magnetic field can not only predict the risk of dementia in the brain, but also improve cognitive function by stimulating treatment to activate cholinergic neural pathways and promote brain injury remodeling. Existing transcranial magnetic studies have shown that patients with vascular dementia have increased motor cortex excitability (decreased resting motor threshold), which is consistent with patients with Alzheimer’s disease (9, 10). This may be part of a mechanism to compensate for plasticity after neuron loss and/or ischemic injury in the brain, with increased excitability helping to protect cognitive function. Abnormal resting motor threshold can be used as a “neurophysiological boundary point” to distinguish patients with normal cognition, non-demented vascular cognitive impairment, and vascular dementia (11). At the same time, the short-latency input inhibition measured by transcranial magnetic can reflect the function of cholinergic circuit in the central nervous system, which is closely related to cognitive function. Although there are some conflicting data in vascular dementia studies (12–14), this may be related to the variable location of subcortical infarctions in patients with vascular cognitive impairment and the significant differences in the distribution and extent of cholinergic denervation caused by them. Nevertheless, short latency inhibition holds great promise in the diagnosis and prognosis of different dementia processes and in the identification of acetylcholinesterase inhibitors for the treatment of sensitive individuals (15).

Transcranial magnetic therapy has a pleiotropic effect, although in a small number of experiments, the effects of high-frequency rTMS on mood, cognition, cortical microcircuits, neurotrophic/growth factors, and cerebral blood flow were not detected. This may be related to the selection of stimulus intensity, total pulse number, test sample size, sex selection, and the unclear mechanism of how ischemic brain injury affects plasticity induced by transcranial magnetic stimulation (16).

At present, there are many studies on the clinical application of rTMS in the treatment of post-stroke dementia, and gratifying results have been achieved (17, 18). Cha et al. (19) performed high-frequency transcranial magnetic therapy in patients with PSCI and assessed cognitive and emotional abilities at 2 and 14 weeks of treatment. The results showed that after rTMS treatment, the cognitive function of the patients was improved, and the proinflammatory cytokines in peripheral blood were decreased. These improvements lasted for three months. The meta-analysis by Li et al. (18) showed that the left dorsolateral prefrontal cortex of PSCI patients was stimulated by high-frequency rTMS, and the number symbol test, Rivermead behavioral memory test and the patients’ attention were significantly improved.

Galantamine hydrobromide is a second-generation cholinesterase inhibitor, initially used for the treatment of AD, which is highly selective for AChE in the central nervous system. It mainly inhibits cholinesterase at the synaptic cleft between the presynaptic membrane and the posterior membrane of brain cholinergic nerve cells, delays the degradation of acetylcholine, increases the content of available acetylcholine, stimulates and improves the function of the remaining acetylcholine receptors (20). The same time, after oral administration of Galantamine, the nicotinic cholinergic receptors in patients with vascular dementia can be regulated to a certain extent (allosteric regulation), and this change can promote a large amount of cholinergic nervous system in patients, releasing acetylcholine, promote its central nervous system into an excited state, and correct its memory and cognitive dysfunction. This unique dual action is beneficial for improving cognitive deficits in dementia patients.

Studies have shown that Galantamine has a good curative effect on patients with vascular dementia. In 2007, Auchus et al. (21) conducted a randomized, double-blind, and placebo-controlled clinical study involving multiple countries. Their results showed that the Galantamine group had significantly improved cognitive function and executive ability compared to the placebo group. In terms of improving activities of daily living, there was little difference between the two groups. The meta-analysis conducted by Yu-Dan et al. (22) showed that the treatment with donepezil and galantamine could significantly improve the Alzheimer’s disease cognitive scale (ADAS cog) score in patients with vascular dementia, with mild adverse reactions and high safety.

The treatment of PSCI requires early screening and detection and timely comprehensive intervention. Comprehensive intervention includes intervention and prevention of known risk factors, drug treatment, and rehabilitation. In addition, the recovery of cognitive function after stroke depends on repairing damaged nerve cells and cortical reconstruction, and intensive cognitive training can accelerate the process of cortical reconstruction. There is no ideal method for the treatment of PSCI, and the current treatment methods have poor efficacy. We attempted to combine high-frequency repetitive transcranial magnetic stimulation and galantamine oral therapy on the basis of cognitive rehabilitation therapy for PSCI patients, achieving better efficacy than the control group. The following report is presented.

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