Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, April 27, 2024

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 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

WSA(World Stroke Academy) Podcast Series – where knowledge meets action in the fight against stroke

 You can get educated and know more than your doctor.

WSA(World Stroke Academy) Podcast Series – where knowledge meets action in the fight against stroke


Friday, April 26, 2024

Make Stroke a Priority - A manifesto on stroke for the next UK Government

 But you absolutely failed! No request for 100% recovery and a roadmap to get there! What the fuck are you going to do when YOU are the 1 in 4 per WHO that has a stroke?

Make Stroke a Priority - A manifesto on stroke for the next UK Government

Nothing about stroke is recoverable upon demand, quit lying to yourself. Vast amounts of research is needed to get to 100% recovery. And leaders would get there! But you're no leader, are you?

Neuroprotectants? The correct term is neuronal cascade of death!

Never use the word neuroprotection, it has no meaning for survivors and lacks urgency. Use the term; neuronal cascade of death; if your doctor tells you they failed to stop the neuronal cascade of death  in the first week resulting in the death of millions to billions of neurons, your correct response would be: 'WHY ARE YOU SO FUCKING INCOMPETENT IN NOT PREVENTING THAT?'

Neuroprotectants

  • Chapter
  • First Online:
Ischemic Stroke Therapeutics

Abstract

Despite rapid and recent progress in our understanding of numerous new mechanisms regulating neuronal cell physiology and responses to ischemia, no neuroprotective agents have been developed as an adjunctive treatment for acute ischemic stroke. However, with the widespread deployment of acute tissue perfusion-based stroke imaging and endovascular thrombectomy, there is a great therapeutic opportunity to identify patients with salvageable ischemic tissue and provide neuroprotective treatment along with recanalization that significantly improves stroke outcome. In this chapter, we review seminal and recent developments in our understanding of the mechanisms underlying ischemic large vessel stroke injury including bioenergetic failure, excitotoxicity, oxidative stress, regulated cell death, and inflammation. Exciting developments in collaborative translational research efforts will provide investigators with a blueprint for systematically testing the most promising therapies preclinically analogous to clinical trials. Together, these basic, translational, and clinical advances hold the promise of developing novel neuroprotective therapies and greatly improving stroke patient outcomes.

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Study Suggests Treatments that Unleash Immune Cells in the Brain Could Help Combat Alzheimer’s

 Because of your risk of dementia post stroke; is your competent? doctor and hospital closely following this? NO? So you have INCOMPETENT MEDICAL 'PROFESSIONALS'?

Your risk of dementia, has your doctor told you of this?  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:

Study Suggests Treatments that Unleash Immune Cells in the Brain Could Help Combat Alzheimer’s

Posted on by Dr. Monica M. Bertagnolli

A cloud of particles is cleared as antibodies cover receptors on microglia.
In a study, an antibody treatment blocked interaction between APOE proteins and LILRB4 receptors in the brain, enabling microglia immune cells to clear amyloid plaques, a feature of Alzheimer’s. Credit: Donny Bliss/NIH

In Alzheimer’s disease, a buildup of sticky amyloid proteins in the brain clump together to form plaques, causing damage that gradually leads to worsening dementia symptoms. A promising way to change the course of this disease is with treatments that clear away damaging amyloid plaques or stop them from forming in the first place. In fact, the Food and Drug Administration recently approved the first drug for early Alzheimer’s that moderately slows cognitive decline by reducing amyloid plaques.1 Still, more progress is needed to combat this devastating disease that as many as 6.7 million Americans were living with in 2023.

Recent findings from a study in mice, supported in part by NIH and reported in Science Translational Medicine , offer another potential way to clear amyloid plaques in the brain. The key component of this strategy is using the brain’s built-in cleanup crew for amyloid plaques and other waste products: immune cells known as microglia that naturally help to limit the progression of Alzheimer’s. The findings suggest it may be possible to develop immunotherapies—treatments that use the body’s immune system to fight disease—to activate microglia in the brains of people with Alzheimer’s and clear amyloid plaques more effectively.2

In their report, the research team—including Marco Colonna , Washington University School of Medicine in St. Louis, and Jinchao Hou, now at Children’s Hospital of Zhejiang University School of Medicine in Zhejiang Province, China—wrote that microglia in the brain surround plaques to create a barrier that controls their spread. Microglia can also destroy amyloid plaques directly. But how microglia work in the brain depends on a fine-tuned balance of signals that activate or inhibit them. In people with Alzheimer’s, microglia don’t do their job well enough.  

The researchers suspected this might have something to do with a protein called apolipoprotein E (APOE). This protein normally helps carry cholesterol and other fats in the bloodstream. But the gene encoding the protein is known for its role in influencing a person’s risk for developing Alzheimer’s, and in the Alzheimer’s brain, the protein is a key component of amyloid plaques. The protein can also inactivate microglia by binding to a receptor called LILRB4 found on the immune cells’ surfaces.

Earlier studies in mouse models of Alzheimer’s showed that the LILRB4 receptor is expressed at high levels in microglia when amyloid plaques build up. This suggested that treatments targeting this receptor on microglia might hold promise for treating Alzheimer’s. In the new study, the research team looked for evidence that an increase in LILRB4 receptors on microglia plays an important role in the brains of people with Alzheimer’s.

To do this, the researchers first studied brain tissue samples from people who died with this disease and discovered unusually high amounts of the LILRB4 receptor on the surfaces of microglia, similar to what had been seen in the mouse models. This could help explain why microglia struggle to control amyloid plaques in the Alzheimer’s brain.

Next, the researchers conducted studies of mouse brains with accumulating amyloid plaques that express the LILRB4 receptor to see if an antibody targeting the receptor could lower amyloid levels by boosting activity of immune microglia. Their findings suggest that the antibody treatment blocked the interaction between APOE proteins and LILRB4 receptors and enabled microglia to clear amyloid plaques. Intriguingly, the team’s additional studies found that this clearing process also changed the animals’ behavior, making them less likely to take risks. That’s important because people with Alzheimer’s may engage in risky behaviors as they lack memories of earlier experiences that they could use to make decisions.

There’s plenty more to learn. For instance, the researchers don’t know yet whether this approach will affect the tau protein, which forms damaging tangles inside neurons in the Alzheimer’s brain. They also want to investigate whether this strategy of clearing amyloid plaques might come with other health risks.

But overall, these findings add to evidence that immunotherapies of this kind could be a promising way to treat Alzheimer’s. This strategy may also have implications for treating other neurodegenerative conditions characterized by toxic debris in the brain, such as Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and Huntington’s disease. The hope is that this kind of research will ultimately lead to more effective treatments for Alzheimer’s and other conditions affecting the brain.

References:

[1] FDA Converts Novel Alzheimer’s Disease Treatment to Traditional Approval. U.S. Food and Drug Administration (2023).

[2] Hou J, et al. Antibody-mediated targeting of human microglial leukocyte Ig-like receptor B4 attenuates amyloid pathology in a mouse model . Science Translational Medicine. DOI: 10.1126/scitranslmed.adj9052 (2024).

NIH Support: National Institute of General Medical Sciences, National Institute on Aging

Stroke could cost UK £75bn by 2035, charity warns

 You could vastly reduce that by having 100% recovery protocols!  Getting people directly back to their old life. But it will require destroying the existing stroke associations since they don't know what the fuck they are doing!

Stroke could cost UK £75bn by 2035, charity warns

By PA News Agency
Juliet Bouverie, chief executive of the Stroke Association, warned that the ‘demand for NHS services will be unsustainable by 2035’ (PA)
Juliet Bouverie, chief executive of the Stroke Association, warned that the ‘demand for NHS services will be unsustainable by 2035’ (PA)(Well, it's simple then, create 100% recovery protocols! ARE YOU THAT BLITHERINGLY STUPID? Please answer, I'll reply with your exact excuse in my blog. Here at: oc1dean@gmail.com))

The number of people suffering a stroke for the first time is expected to rise by more than 50% by 2035, costing the UK more than £75 billion for care and lost productivity, a charity has said.

The Stroke Association urged the next government to invest more in prevention, as well as addressing issues with stroke treatment and rehabilitation services.

Failing to do so could risk demand on NHS services becoming “unsustainable” in 11 years’ time, it said.

151,000
The projected number of new stroke hospital admissions per year by 2035
The Stroke Association

A new manifesto published by the charity estimated that stroke will cost the UK about £43 billion this year, with 100,000 new stroke hospital admissions per year.

This could rise to 151,000 admissions by 2035 – the equivalent of 414 per day – with the number of stroke survivors rising from 1.3 million to 2.1 million.

Costs associated with the increase could top £75 billion, which includes projected increases in health and social care costs, as well as informal care costs.

About a quarter of strokes impact people of working age, with lost productivity currently costing an estimated £1.6 billion per year.

This too is expected to rise by 136% by 2035, according to the report.

If the next government fails to tackle prevention, treatment, and recovery at the root, then stroke will become the most avoidable burden on the NHS

Juliet Bouverie, Stroke Association

Juliet Bouverie, chief executive of the Stroke Association, warned that the “demand for NHS services will be unsustainable by 2035″.

“If the next government fails to tackle prevention, treatment, and recovery at the root, then stroke will become the most avoidable burden on the NHS,” she added.

The Stroke Association is calling on the Department of Health and Social Care (DHSC) to publish a funded stroke prevention plan to support people of all ages to reduce their risk of stroke.

This includes improving the way people detect and manage conditions that increase the risk of stroke, such as high blood pressure.

The charity also wants all patients to have 24-hour access to thrombectomies – a surgery to remove blood clots from the artery.

The procedure is usually carried out up to six hours after stroke symptoms begin.

The Stroke Association estimates that making thrombectomies universally available could save the health and care system £73 million each year and would allow 1,600 more stroke survivors to be independent.

Thanks to Life After Stroke services, I’ve slowly been rebuilding myself and I am also set to start a phased return to work later this year

Stroke survivor Marwar Uddin

It also called for the Government to address issues in access to rehabilitation and support services, such as the Life After Stroke programme.

Stroke survivor Marwar Uddin, 24, from London, spoke about the long-term impact of the condition and how support services have helped him.

He said: “I need help to go to the toilet. I can’t even dress myself. My voice is different now. I’m a different person. I cry myself to sleep most days. It’s difficult for me.

“Thanks to Life After Stroke services, I’ve slowly been rebuilding myself and I am also set to start a phased return to work later this year.

“If I didn’t have any of this support, I think I would still be in a chair in my living room watching the world go by.”

Ms Bouverie added: “Every stroke is a tragedy, but 151,000 strokes per year, and growing each year, will be a failure of leadership.

“In 2000, stroke was the second leading cause of death in the UK but by making stroke a national priority reflected in local resources, stroke mortality was halved by 2010. So, change is possible.”

Over 90% of acute stroke care providers in England are equipped with artificial intelligence, which can reduce the time it takes to access treatment such as thrombectomy by more than 60 minutes

Department of Health and Social Care

A DHSC spokesperson said: “We’re committed to improving stroke prevention, treatment, and recovery for all.

“Over 90% of acute stroke care providers in England are equipped with artificial intelligence, which can reduce the time it takes to access treatment such as thrombectomy by more than 60 minutes.

“The first ever Long Term Workforce Plan will help to shift more care into the community and invest more in prevention and early intervention, and we’re rolling out a new digital NHS Health Check which could prevent hundreds more strokes.

“We are also taking action to encourage better lifestyle choices, including creating a smoke-free generation and reducing salt intake through food to help prevent the risk of strokes.”

Back in balance: Stroke recovery better for patients who get help fast

 Is your doctor and hospital prepared to deliver tPA in three minutes?

How fast do you have to be to get to 100% recovery? Is it 3 minutes like research in mice proves? Or don't you even fucking know about that research?

Electrical 'storms' and 'flash floods' drown the brain after a stroke

 In this research in mice the needed time frame for tPA delivery is 3 minutes for full recovery.

The latest here:

Back in balance: Stroke recovery better for patients who get help fast

Troy Silvers

Troy Silvers, center, with Robby Mickelson, physical therapy assistant, and Abagail Roque, occupational therapist.

Troy Silvers can walk.

Not so long ago, that task — and many others once taken for granted — were nearly impossible. Following a stroke last summer, the Dalton resident entered Regency Park Health and Rehabilitation, part of Hamilton Health Care System, where he received intense therapy to help him recover from a partially paralyzed right side.

The type of stroke he experienced involving bleeding into the brain tissue is the second most common cause of stroke — between 15 and 30% of all strokes — and the most deadly. After being at Regency Park for several weeks, Silvers continued to make daily improvements toward recovery but has also made significant lifestyle changes, including incorporating exercise into his routine, monitoring his blood pressure, taking medication as prescribed and learning how to better manage stress.

“His physical limitations have not stopped him from joining his wife with daily walks and visits to their garden,” said Cherryl Berdos, rehabilitation director at Regency Park. “Recovering from a stroke can be a long and frustrating experience. It is normal to face difficulties along the way, but Mr. Troy’s dedication and willingness to work toward improvement helped him a lot.”

When he entered Regency Park, Silvers struggled to stand, walk, dress, eat and perform other daily tasks without assistance. Because his body was working so hard to compensate for the impairments, once-simple tasks became an exercise in frustration, and fatigue was a constant companion.

Berdos said he was often tempted to use only his unaffected side to improve efficiency.(But didn't his competent? doctor tell him of the research on using the good side recovers the bad side? NO! So not a competent doctor?

Exercising the good side to recover the 'bad' side. December 2012)

At first, he needed a walker to get around, plus two individuals to ensure safety. One would hold onto him while another followed with a wheelchair.

Now he can walk, climb stairs, bathe, dress and eat all on his own, and he continues to make daily efforts toward regaining more function. Silvers said he especially wants to thank Robby Mickelson and Abagail Roque who provided his physical and occupational therapy and worked with his entire treatment team.

When Silvers started rehab, he felt “100%” optimistic about his outcomes and was determined to get better every day. Today, he advises anyone going through a similar situation to “take care of your health, exercise (and) eat healthy.” Berdos said Silvers has also become an encouragement for other patients.

All Regency Park patients receive intensive rehab aligned with their level of healing and as determined by their physician.

“We create a personalized care plan, emphasizing your quality of life, dignity and comfort, which will help you reach your goals or help you manage an ongoing illness, chronic medical condition or disability,” said Berdos.

Act FAST (for face, arms, speech, time)

Time is of the essence when someone is experiencing stroke symptoms. If you or someone you know is experiencing face drooping, arm weakness or speech difficulty, call 911 immediately. By the time the ambulance reaches the emergency department, the responders will have started an IV and notified the medical facility that they are on the way with a possible stroke patient.

React to this story:

World Stroke Academy: Let’s keep enhancing stroke care together🧠 We are delighted to announce our new #eLearning module:

 THIS IS WHY STROKE NEVER GETS SOLVED! The WSO only works on 'care'. They need to be completely destroyed and run by survivors! Survivors would produce recovery and results instead of this lazy crapola. And for proof there is this shit:

I don't need to hear any lies about this meme from World Stroke Day a couple of years ago.

What a lying piece of shit.

 



A self-management program increases the dosage of inpatient rehabilitation by 26 minutes per day: a process evaluation

 For stroke 100% recovery, it is incredibly simple, your stroke medical 'professionals' provide EXACT 100% RECOVERY PROTOCOLS and your patient will not stop until 100% recovery is achieved! The RESPONSIBILITY is on the 'professionals' to do this, not dump everything onto survivors! If your stroke medical 'professionals' don't understand and do this; FIRE THEM!

A self-management program increases the dosage of inpatient rehabilitation by 26 minutes per day: a process evaluation

Received 29 Sep 2023, Accepted 01 Apr 2024, Published online: 16 Apr 2024

Abstract

Purpose

To evaluate the implementation of a self-management program, My Therapy, designed to increase inpatient rehabilitation therapy dosage via independent practice.

Materials and methods

A process evaluation of My Therapy for adult patients admitted for rehabilitation for any condition supervised by physiotherapists and occupational therapists across eight rehabilitation wards compared usual care. Outcomes included reach, dosage, fidelity and adaptation.

Results

The mean (SD) age of the process evaluation sample (n = 123) was 73 (11) years with a mean (SD) length of stay of 14.0 (6.6) days. The My Therapy program reached 68% of participants (n = 632/928), and resulted in an average increase in therapy dosage of 26 (95% CI 12 to 40) minutes/day of independent practice. All My Therapy audited programs (n = 28) included body function/structure impairment-based exercises, and half (n = 13/28) included activity/participation-based exercises. On average, participants completed programs 1.8 (SD 1.2) times/day, which were prescribed in accordance with the My Therapy criteria, demonstrating fidelity. There were no between-group differences in daily steps or standing time, however, My Therapy participants spent more time sitting (p ≤ 0.05). Implementation adaptations were minimal.

Conclusion

A self-management rehabilitation program was implemented with fidelity for two in three rehabilitation patients, resulting in increased therapy dosage with minimal adaptations.

IMPLICATIONS FOR REHABILITATION

  • The My Therapy self-management program was implemented with good reach (68% of participants received My Therapy) across four public and private inpatient rehabilitation services.

  • Under My Therapy conditions, the dosage of inpatient rehabilitation therapy participation increased by an average of 26 minutes per day, which will help close the evidence-practice gap between the current rehabilitation dosage of about 1-hour per day, and the recommended rehabilitation dosage of 3-hours per day.

  • My Therapy programs most frequently included impairment-based exercises that were completed in sitting, and did not increase time spent standing and walking.

  • Consideration should be given to prescribing My Therapy (content and dosage) at an optimal level to promote patient functional independence, while maintaining safety.

Introduction

Adult physical rehabilitation encompasses a range of services delivered through multidisciplinary teams, aiming to deliver person centred care using evidence based interventions and evaluating progression towards meaningful goals [Citation1]. Rehabilitation can be delivered within traditional bed-based settings in a hospital, as well as home-based services, whereby rehabilitation is delivered to patients within the community environment [Citation1–3]. There is evidence that rehabilitation outcomes are influenced by the amount of therapy the person receives [Citation4] and one way to increase dosage is to increase therapy staffing levels [Citation5]. However budgetary constraints often limit additional staffing resources, despite the known benefits and the ever increasing complexity of the inpatient rehabilitation cohort [Citation6]. Clinicians, health service managers, and policy makers need to think creatively of ways to increase the dosage of evidence-based therapy interventions to promote functional recovery during rehabilitation. One solution to the problem of providing a sufficient dosage of therapy is through patient therapy self-management, that is, re-directing some of the idle time rehabilitation patients have between supervised therapy sessions into meaningful self-directed therapy activities [Citation7].

An example of this is My Therapy, a consumer driven self-management program, that focuses on occupational therapy and physiotherapy exercises and tasks that can be completed outside of supervised therapy sessions [Citation8]. Pilot work has shown that My Therapy can increase rehabilitation therapy participation by up to 14 min per day [Citation8]. In 2021-22, the My Therapy intervention was evaluated via a multi-site stepped wedge cluster randomised control trial conducted over eight wards at four health services (two public and two private). The trial included 2550 (control conditions, n = 1458; My Therapy conditions n = 1092) rehabilitation participants admitted to a rehabilitation ward, as well as, 788 geriatric evaluation and management participants (control conditions, n = 388; My Therapy conditions n = 400) admitted to a rehabilitation ward giving a total of 3,338 participants (unpublished data).

Process evaluations are increasingly being used alongside clinical and economic evaluations, to help understand the factors that may positively or negatively influence trial results [Citation9,Citation10]. Guided by the Medical Research Council (MRC) framework, process evaluations aim to: capture reach and determine the extent the intended population came into contact with the intervention; determine the dosage and quantity of intervention delivery; determine fidelity by understanding if the intervention was delivered as intended and how it was delivered; and determine if any adaptations were required to the intervention from what was planned [Citation10]. Process evaluations, can provide valuable insights into unexpected or unanticipated results (clinical or economic), and can provide a clear description of intervention implementation to allow the intervention to be scaled up or replicated elsewhere should desired results be achieved [Citation10]. The aim of this study was to evaluate the reach, dosage, fidelity and adaptations of the implementation of My Therapy into inpatient rehabilitation, as part of a larger stepped wedge cluster randomised trial.

Methods

Context: My Therapy intervention

My Therapy is a “consumer driven, self-management program designed to increase the dosage of therapy participation during physical rehabilitation, through independent practice of exercise and activity, in addition to usual care” [Citation11]. Implementation was intended to be additional to usual care, and not as a substitution of supervised therapy. My Therapy was delivered by occupational therapists and physiotherapists on the ward through provision of a subset of therapy activities to be practised independently where safe and appropriate using an online exercise prescription program PTX (www.physiotherapyexercises.com). Discussion and input from the participants, alongside occupational therapy and physiotherapy collaboration, were key to developing the individualised My Therapy programs delivered in paper format. While a recommended goal of exercise/additional therapy dosage was set by prescribing therapists, the quantity and frequency to complete activities were at the participant’s discretion [Citation11]. My Therapy is based on four criteria/pillars: i) the provision of a written self-management program (delivered electronically or in paper format); (ii) ensuring programs are documented by the therapist in the medical record; (iii) providing a feedback mechanism between the patient and the therapist (such as an activity/exercise completion tick sheet); and (iv) ensuring programs are actively monitored and progressed, as clinically indicated [Citation12]. At a practical level, My Therapy was designed to be provided to all participants on the ward where deemed safe and appropriate by the treating occupational therapist or physiotherapist. Any additional items (such as weights) that were required for the participant to complete their program were provided for use on provision of the My Therapy program by the therapist. Recommendations were made to the participant by their treating therapist to complete the My Therapy program outside of structured therapy sessions with health professionals (e.g. occupational therapists and physiotherapists).

In the six weeks prior to cross over to My Therapy conditions, implementation preparation occurred. This allowed for education of the My Therapy intervention through formal verbal education to clinical staff, interactive group discussions to co-design local implementation strategies and provision of written explanatory materials for occupational therapy and physiotherapy staff. Other members of the rehabilitation team were engaged in the pre-implementation phase by raising awareness with their role when under My Therapy conditions, but this was limited to encouraging participants to complete their My Therapy programs and not to supervise the program. To support implementation at each of the four health services, there was regular collaboration between site co-ordinators at each of the sites through online meetings and email correspondence. This provided an opportunity for shared resources between participating sites and tailoring to meet local needs.

Study design and setting

This observational process evaluation study, completed alongside a stepped wedge cluster randomised trial, has been reported in accordance with the STROBE checklist [Citation13]. The process evaluation was conducted from April 2021 to April 2022. The protocol for the main clinical trial and the process evaluation have been previously published [Citation11,Citation12]. For this process evaluation, a quantitative dominant design was used. The evaluation was undertaken in eight rehabilitation wards across two public and two private Victorian health networks in Australia, with two of the public health wards located in the community (i.e., home-based wards). Multi-site ethics approval was received from Alfred Hospital Human Research Ethics Committee (HREC) (ID: 69610), followed by site specific approvals at each of the participating health services (Alfred Hospital, ID 758/20; Eastern Health, ID S21-004-69610; Cabrini Health, ID 11-04-03-21; Healthscope via La Trobe HREC, ID 758/20).

The four study components aligned with the study aims are: i) capture reach and determine the extent the intended population came into contact with the intervention; ii) determine the dosage and quantity of intervention delivery, including the amount of supervised therapy participation as part of usual care, and My Therapy program content, mapped to the International Classification of Function (ICF) [Citation14]; iii) determine fidelity (patient adherence as well as therapist engagement) by understanding if the intervention was delivered as intended, how it was delivered and physical activity levels in sitting, standing and stepping; and iv) determine if any adaptations were required to the intervention from what was planned (Appendix A, Supplementary Material) [Citation11,Citation12].

All participants included in this process evaluation were subgroups of the participants included in the stepped wedge cluster randomised trial (

). The first group (group 1), recruited to evaluate program reach, included a subgroup of participants admitted in each block of the main trial (n = 3,338). The second group (group 2) recruited for the evaluation of dosage and fidelity were recruited over three time points (month 1/block 1 (April 2021), 6/block 5 (September 2021) and 12/block 9 (March 2022) of the 12-month/block 9 clinical trial), and were a subgroup of group 1. The third group (group 3) recruited for a detailed evaluation of dosage were a subgroup of participants from group 2. The fourth group (group 4) recruited for a detailed evaluation of fidelity were a subgroup of participants from group 2.

Figure 1. Participant flow.

Figure 1. Participant flow.

Group 1 (reach) included all eight participating rehabilitation wards in the clinical trial, capturing all admitted participants including but not limited to diagnoses, such as orthopaedic, neurological, reconditioning, and respiratory, with and without a cognitive impairment. For group 2 (dosage and fidelity), the aim was to recruit a consecutive sample of 120 participants already consented to the main clinical trial, meeting the eligibility criteria of being over 18 years, admitted for rehabilitation for any reason and having access to Medicare (Australian universal health care program). Participants in group 2 (dosage and fidelity), met the additional eligibility criteria of not having a cognitive impairment (limiting ability to complete data collection tools) and being English speaking. Participants were approached by a member of the research team, their involvement in the study explained and written consent was gained. For groups 3 (dosage) and 4 (fidelity), convenience sampling was used from participants already recruited in group 2 with group 3 only including participants with a My Therapy program. Participants under control conditions receiving usual care only were included in groups 1 (reach), 2 (dosage and fidelity) and 4 (fidelity).

Outcomes

Data were collected and managed using REDCap (Research Electronic Data Capture) electronic data capture tools, that were hosted at Monash University and managed by Helix [Citation15,Citation16].

For this process evaluation, independent groups of participants were classified as receiving usual care (during control blocks of the stepped wedge cluster randomised trial, termed control conditions) or receiving My Therapy plus usual care (during intervention blocks of the stepped wedge cluster randomised trial, termed intervention conditions). If participants completed a self-management program under the control conditions this has been called a “self-management program”; if participants completed a self-management program under the intervention conditions this has been called a “My Therapy program” with both self-management and My Therapy programs needing to meet the four My Therapy criteria/pillars [Citation12]. It was recognised that some participants may not agree to participate in a My Therapy program or be unable to be provided a program, for example, due to safety considerations. However, the intention was that every patient on the ward would be assessed for a My Therapy program during the intervention blocks, and if appropriate, be provided with a program.

Reach: Data collection was completed on eight participating wards across the four health services over nine time points (once every six-weeks midway through each block during the 12-month clinical trial by site co-ordinators/associate investigators). To understand the reach of a self-management program under control and intervention conditions, medical files were audited to determine whether a self-management program had been prescribed, supplemented with discussion with treating therapists (group 1 (reach)). My Therapy was only considered to have been implemented when all four My Therapy criteria/pillars were fulfilled. On a single day, the ward audit was completed for the participating ward, capturing all admitted participants. Within the ward audit, there were no exclusion criteria applied, thereby capturing all participants on the ward. Individual participants were not able to be identified within the ward audit. Data were uploaded by the site co-ordinator to a customised form on REDCap that was blinded to the researcher. An apriori target for reach was not set. While a 100% reach would be ideal considering the whole of ward approach, researchers recognised this may not always be achievable, and note that the My Therapy feasibility study achieved a 72% reach [Citation8].

Dosage and fidelity were measured over three time points (month 1/Block 1 (April 2021), 6/Block 5 (September 2021) and 12/Block 9 (March 2022) of the 12-month clinical trial). Participants were classified as receiving usual care (control conditions) or receiving My Therapy plus usual care (intervention conditions).

  • Dosage: Group 2 (dosage and fidelity) participants, were audited using the therapy timetable by capturing the scheduled and completed duration of occupational therapy and physiotherapy sessions and delivery mode. The audit of the therapy timetable was completed by a researcher. If provided a My Therapy program, participants completed a daily written activity log capturing time spent and the number of times and the number of activities/exercises completed, as well as the recommended amounts from the therapist. The audit was completed midway through each block.

  • Fidelity: Group 2 (dosage and fidelity) participants with a My Therapy program, the activity log described above captured My Therapy patient adherence to the prescribed program by recording the recommended amount and the number of activities and amounts actually completed. For participants with a My Therapy program, all My Therapy programs provided across the seven-day data collection period were audited to capture therapist My Therapy engagement (occupational therapy and physiotherapy prescription and frequency of review of the program). The audit was completed midway through each block.

  • Dosage: The My Therapy programs of group 3 (dosage) participants was audited capturing the focus of the exercise/activities recommended (classified as an exercise) to address: i) body function/structure impairment tasks (e.g. strengthening exercises); or ii) activity/participation based tasks which were considered the practice of functional activities repetitively (e.g. task specific training [Citation17] such as walking or dressing practice) according to the ICF [Citation14]; who recommended the activities/exercises (i.e. occupational therapy or physiotherapy) and the position in which the activities were to be completed (i.e. standing, sitting, lying). The audit was completed midway through each block.

  • Fidelity: Group 4 (fidelity) participants under control and intervention conditions, wore activity monitors capturing physical activity levels in sitting, standing and stepping. Participants were asked to wear an accelerometer-based activity monitor (activPAL, PAL Technologies Limited). Participants were asked to wear monitors for 24 hours per day over seven consecutive days. Monitors were placed on the anterior middle thigh in a zip lock bag, placed on a small piece of gauze to protect the skin and covered by a waterproof dressing

Evaluation of adaptations: The adaptations log was based on the service profile audit completed on each of the participating wards which captured any major deviations to planned implementation (once every six-weeks at the start of each block, capturing information for the previous block, Appendix A, Supplementary Material).

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