Interventional Treatment vs Conservative Management of Unruptured Brain Arteriovenous Malformations

I see no protocols in treating an AVM, so it is your responsibility to not have one until that occurs. Notice how your doctors can keep the monkey off their back.

YOU have to put the monkey(responsibility for your recovery) on their back and never let them transfer it back to you. Tell them you know all about the Harvard Business Review article on monkey on the back tossing. 

The latest here:

 Interventional Treatment vs Conservative Management of Unruptured Brain Arteriovenous Malformations

Endovascular treatment in the multimodality management of brain arteriovenous malformations: report of the Society of NeuroInterventional Surgery Standards and Guidelines Committee

I see no protocols in treating an AVM, so it is your responsibility to not have one until that occurs. Notice how your doctors can keep the monkey off their back.

YOU have to put the monkey(responsibility for your recovery) on their back and never let them transfer it back to you. Tell them you know all about the Harvard Business Review article on monkey on the back tossing.

Endovascular treatment in the multimodality management of brain arteriovenous malformations: report of the Society of NeuroInterventional Surgery Standards and Guidelines Committee

1. Reade De Leacy1,
2. Sameer A Ansari2,
3. http://orcid.org/0000-0003-1743-8781Clemens M Schirmer3,
4. Daniel L Cooke4,
5. Charles J Prestigiacomo5,
6. Ketan R Bulsara6,
7. http://orcid.org/0000-0001-5885-7259Steven W Hetts4
8. SNIS Standards and Guidelines Committee, SNIS Board of Directors

1. Correspondence to Dr Steven W Hetts, Radiology, UCSF, San Francisco, California, USA; steven.hetts@ucsf.edu

Abstract

Background The purpose of this review is to summarize the data available for the role of angiography and embolization in the comprehensive multidisciplinary management of brain arteriovenous malformations (AVMs

Methods We performed a structured literature review for studies examining the indications, efficacy, and outcomes for patients undergoing endovascular therapy in the context of brain AVM management. We graded the quality of the evidence. Recommendations were arrived at through a consensus conference of the authors, then with additional input from the full Society of NeuroInterventional Surgery (SNIS) Standards and Guidelines Committee and the SNIS Board of Directors.

Results The multidisciplinary evaluation and treatment of brain AVMs continues to evolve. Recommendations include: (1) Digital subtraction catheter cerebral angiography (DSA)—including 2D, 3D, and reformatted cross-sectional views when appropriate—is recommended in the pre-treatment assessment of cerebral AVMs. (I, B-NR). (2) It is recommended that endovascular embolization of cerebral arteriovenous malformations be performed in the context of a complete multidisciplinary treatment plan aiming for obliteration of the AVM and cure. (I, B-NR). (3) Embolization of brain AVMs before surgical resection can be useful to reduce intraoperative blood loss, morbidity, and surgical complexity. (IIa, B-NR). (4) The role of primary curative embolization of cerebral arteriovenous malformations is uncertain, particularly as compared with microsurgery and radiosurgery with or without adjunctive embolization. Further research is needed, particularly with regard to risk for AVM recurrence. (III equivocal, C-LD). (5) Targeted embolization of high-risk features of ruptured brain AVMs may be considered to reduce the risk for recurrent hemorrhage. (IIb, C-LD). (6) Palliative embolization may be useful to treat symptomatic AVMs in which curative therapy is otherwise not possible. (IIb, B-NR). (7) The role of AVM embolization as an adjunct to radiosurgery is not well-established. Further research is needed. (III equivocal, C-LD). (8) Imaging follow-up after apparent cure of brain AVMs is recommended to assess for recurrence. Although non-invasive imaging may be used for longitudinal follow-up, DSA remains the gold standard for residual or recurrent AVM detection in patients with concerning imaging and/or clinical findings. (I, C-LD). (9) Improved national and international reporting of patients of all ages with brain AVMs, their treatments, side effects from treatment, and their long-term outcomes would enhance the ability to perform clinical trials and improve the rigor of research into this rare condition. (I, C-EO).

Conclusions Although the quality of evidence is lower than for more common conditions subjected to multiple randomized controlled trials, endovascular therapy has an important role in the management of brain AVMs. Prospective studies are needed to strengthen the data supporting these recommendations.

http://dx.doi.org/10.1136/neurintsurg-2021-018632

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Introduction

Brain arteriovenous malformations (AVMs), though rare, represent some of the most formidable and complex lesions encountered in neurovascular practice and can be the cause of morbidity and mortality.1 2 Ruptured or unruptured, brain AVMs are the focus of considerable debate regarding optimal management.3 In some instances, the decision for treatment can be controversial. The purpose of this review is not to address the decision on whether or not to treat, since this has been discussed extensively elsewhere in the medical literature.4 The goal of this review is to serve as an overview of the available treatment modalities and their associated outcomes with a focus on the relationship of endovascular therapy to other modalities involved in comprehensive brain AVM management. Recommendations are provided based on the level of medical evidence.

Methods

We systematically reviewed the literature for manuscripts with the key words ‘brain’ and ‘AVM’ or ‘arteriovenous malformation’ as well as any of the following: ‘natural history’, ‘imaging’, ‘management’, ‘treatment’, ‘surgery’, ‘endovascular’, ‘embolization’, ‘radiosurgery’, ‘radiotherapy’, ‘medical therapy’, ‘drug therapy’, ‘standards’, or ‘guidelines’. These terms were chosen to pull in a broad representation of the literature on brain AVMs and their treatment. Individual members of the Society of NeuroInterventional Surgery (SNIS) Standards and Guidelines Committee (S&G Committee) AVM writing group reviewed specific topic areas that form the basis for the narrative sections and recommendations below. The writing group graded evidence using the Oxford Centre for Evidence Based Medicine guidelines5 and the American Heart Association guidelines,6 with the latter being applied to recommendations. The writing group authors presented their findings to the entire S&G Committee to refine recommendations. Subsequent review of the draft guidelines was performed by the SNIS Board of Directors before submission for peer review by the Journal of NeuroInterventional Surgery (JNIS).

Diagnostic and pre-treatment imaging of brain AVMs

Brain AVMs have several angioarchitectural and geographic features that help to predict likelihood of future rupture, identify source of current hemorrhage, and probable morbidity of treatment.7–13 Angioarchitectural features, including feeding artery aneurysms, nidus aneurysms, large-caliber arteriovenous fistulous connections, and venous outflow stenoses, can be visualized to lesser or greater degrees by non-invasive imaging such as MR angiography (MRA) and CT angiography (CTA).14 15 Digital subtraction angiography (DSA), given its higher spatial and temporal resolution, remains superior to non-invasive modalities in identifying relevant AVM angioarchitectural features as compared with non-invasive modalities.16 17 Planar 2D-DSA with high imaging rates (≥7.5 frames per second) can sort out the order in which vessels fill even in high-flow situations. Volumetric 3D-DSA and time-resolved 4D-DSA offer additional structural and combined structural/temporal information, respectively, and can be reformatted in cross-sectional views that better localize the AVM relative to other anatomical structures.18–22 The vessel-selective nature of catheter-based DSA enables the operator to precisely identify individual arterial inputs to the brain AVM; vessel-selective arterial spin-labeling MRA may provide lower-resolution information regarding AVM feeders.23 MRI offers the greatest soft tissue anatomical resolution. Fusion between 3D-DSA and 3D-volumetric MRI has been posited to be the best combined technique for localizing and stratifying the natural history risk and treatment risk in brain AVMs, particularly when combined with clinical information about existing symptoms due to adjacency of the AVM or hemorrhage to eloquent functional regions of the brain.24 Similarly, functional MRI may assist in mapping eloquent regions of the brain that may have shifted location due to a nearby AVM.

RECOMMENDATION 1: Digital subtraction catheter cerebral angiography (DSA)—including 2D, 3D, and reformatted cross-sectional views when appropriate—is recommended in the pre-treatment assessment of cerebral AVMs. (I, B-NR)

Modalities for treatment of brain AVMs

Once the decision for AVM treatment has been made, neurovascular centers typically determine whether single modality or multimodality treatment will be most appropriate. The first consideration is whether the AVM is ruptured or unruptured, as this not only affects the risk of future rupture but also the treatment technique. The goal of treatment—AVM cure (ie, elimination of the nidus and arteriovenous shunting) versus partial treatment with targeting of a high-risk feature in AVMs that does not appear amenable to cure versus palliation of AVM-related symptoms—is a critical up-front discussion point between the patient and the treating team. Angioarchitecture (AVM nidus size, presence of feeding artery aneurysms, presence of nidus aneurysms, large caliber arteriovenous fistulas), location (eloquent vs non-eloquent, deep vs superficial), and local modality-based expertise (microsurgical, endovascular, and radiosurgical) are all key factors to take into account in developing a comprehensive and appropriate treatment plan.25

More at link.

Evidence for a window of enhanced plasticity in the human motor cortex following ischemic stroke

Useless. We've known about neuoplasticity for decades. But we still have no understanding of why a neuron drops its' function and takes on a neighboring function. Since we don't know that we can't make neuroplastictity repeatable on demand. NO PROTOCOLS CAN BE WRITTEN ON NEUROPLASTICITY UNTIL WE KNOW THAT. We get useless guidelines instead.  Until we get exact protocols our stroke medical 'professionals' can blame the survivor for not recovering. It's the best 'get out of jail free' card there is. Your stroke medical team has just pushed all responsibility for recovering off their backs and onto yours.

YOU have to put the monkey(responsibility for your recovery) on their back and never let them transfer it back to you. Tell them you know all about the Harvard Business Review article on monkey on the back tossing.

 Evidence for a window of enhanced plasticity in the human motor cortex following ischemic stroke

Neurorehabilitation and Neural Repair , Volume 35(4) , Pgs. 307-320.

NARIC Accession Number: J86353.  What's this?
ISSN: 1545-9683.
Author(s): Hordacre, Brenton ; Austin, Duncan ; Brown, Katlyn E. ; Graetz, Lynton ; Pareés, Isabel ; De Trane, Stefania ; Vallence, Ann-Maree ; Koblar, Simon ; Kleinig, Timothy ; McDonnell, Michelle N. ; Greenwood, Richard ; Ridding, Michael C. ; Rothwell, John C..
Publication Year: 2021.
Number of Pages: 14.

Abstract: 

Study measured synaptic plasticity at a neural level in human stroke survivors to test whether there is an early period of enhanced synaptic plasticity in the weeks and months after ischemic stroke. Continuous theta burst stimulation (cTBS) was used to activate synapses repeatedly in the motor cortex and initiate early stages of synaptic plasticity that temporarily reduces cortical excitability and motor-evoked potential amplitude. Thus, the greater the effect of cTBS on the motor-evoked potential, the greater the inferred level of synaptic plasticity. Data were collected from separate cohorts (Australia and United Kingdom). In each cohort, serial measurements were made in the weeks to months following stroke. Data were obtained for the ipsilesional motor cortex in 31 stroke survivors (Australia) over 12 months and the contralesional motor cortex in 29 stroke survivors (United Kingdom) over 6 months. Depression of cortical excitability by cTBS was most prominent shortly after stroke in the contralesional hemisphere and diminished over subsequent sessions. cTBS response did not differ across the 12-month follow-up period in the ipsilesional hemisphere. Results provide the first neurophysiological evidence consistent with a period of enhanced synaptic plasticity in the human brain after stroke. Behavioral training given during this period may be especially effective in supporting poststroke recovery.
Descriptor Terms: BODY MOVEMENT, BRAIN, ELECTRICAL STIMULATION, HEALTH PROMOTION, INTERNATIONAL REHABILITATION, LIMBS, MOTOR SKILLS, STROKE.


Can this document be ordered through NARIC's document delivery service*?: Y.

Citation: Hordacre, Brenton , Austin, Duncan , Brown, Katlyn E. , Graetz, Lynton , Pareés, Isabel , De Trane, Stefania , Vallence, Ann-Maree , Koblar, Simon , Kleinig, Timothy , McDonnell, Michelle N. , Greenwood, Richard , Ridding, Michael C. , Rothwell, John C.. (2021). Evidence for a window of enhanced plasticity in the human motor cortex following ischemic stroke.  Neurorehabilitation and Neural Repair , 35(4), Pgs. 307-320. Retrieved 6/22/2021, from REHABDATA database.
 

History of stroke may increase risk for late-onset Alzheimer’s disease

So, What the fuck is your doctor doing to prevent that from happening to you?

Throwing their hands up is not an acceptable answer. Screaming in their faces is an acceptable reply from you. YOU have to put the monkey on their back and never let them transfer it back to you. Tell them you know all about the Harvard Business Review article on monkey on the back tossing.

History of stroke may increase risk for late-onset Alzheimer’s disease

Patients with a history of stroke have double the risk for late-onset Alzheimer’s disease in its familial and sporadic forms, researchers reported in JAMA Neurology.

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However, according to the researchers, the effect of CV risk factors on Alzheimer’s disease was mediated by stroke.
Using data from the National Institute on Aging Late-Onset Alzheimer’s Disease/National Cell Repository for Alzheimer’s Disease family study (NIA-LOAD), the researchers assessed the contribution of CV risk factors and history of stroke to late-onset Alzheimer’s disease in large families with multiple family members affected by late-onset Alzheimer’s disease. Data from the Washington Heights-Inwood Columbia Aging Project were used to replicate findings.
The primary endpoint was probable or possible late-onset Alzheimer’s disease based on the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA) criteria. The CV risk factors included in the study were hypertension, type 2 diabetes and CHD.
Giuseppe Tosto, MD, PhD, from Columbia University College of Physicians and Surgeons and NewYork-Presbyterian Hospital, and colleagues calculated a genetic risk score for late-onset Alzheimer’s disease using genome-wide significant single nucleotide polymorphisms except for APOE E4.
Of the 6,553 participants (mean age, 77 years; 62% women) included in the analyses from NIA-LOAD, 3,468 were diagnosed with late-onset Alzheimer’s disease. Of the 5,972 participants (mean age, 77 years; 68% women) in the replication sample, 2,684 had late-onset Alzheimer’s disease.
In the NIA-LOAD analysis, hypertension was associated with a lower risk for late-onset Alzheimer’s disease (OR = 0.63; 95% CI, 0.55-0.72), whereas a history of stroke was associated with twice the risk for late-onset Alzheimer’s disease (OR = 2.23; 95% CI, 1.75-2.83). No associations were observed between late-onset Alzheimer’s disease and type 2 diabetes or CHD.
In the replication study, hypertension did not have an association with late-onset Alzheimer’s disease, nor did any of the other CV risk factors. However, a relationship was again found between late-onset Alzheimer’s disease and history of stroke (OR = 1.96; 95% CI, 1.56-2.46).
According to the researchers, these results highlight the “complex relationship between hypertension and [late-onset Alzheimer’s disease]” as well as the “importance of interventions targeting modifiable risk factors in [late-onset Alzheimer’s disease]. Further studies with longitudinal assessment and a larger set of variables (eg, different classes of treatments) are currently needed.” – by Tracey Romero
Disclosure: Tosto reports no relevant financial disclosures. Please see the full study for a list of all other researchers’ relevant financial disclosures.

WICKED PROBLEM SOLVERS

There are many wicked problems to solve in stroke. But I can guarantee that none of the leaders in stroke will use this article to try to solve them. They have got their heads so far up their asses they haven't seen daylight in decades.  They are lazily WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM.  Dammed lazy assholes. And stroke survivors pay the price for stroke leaders incompetence.

HBR.ORG

JUNE 2016

REPRINT

R1606C

Lessons from successful cross-industry teams

by Amy C. Edmondson

 WICKED PROBLEM SOLVERS
There are problems, and then there are big problems. And the big ones can be wicked, with extraordinary challenges that can be overcome only through partnerships across industries and countries. The tricky part is making these partnerships work despite differences in language, knowledge, values, and culture. In this Harvard Business Review article, Amy Edmondson, Harvard Business School professor and faculty member of Managing Health Care Delivery, presents the four key practices that are essential to team development and cross-industry innovation.

Resilience Is About How You Recharge, Not How You Endure

Just what the fuck is your doctor doing to make sure you have enough resilience to recover from your stroke even when your doctor knows nothing and does nothing? Any stroke protocols at all for this?

Resilience Is About How You Recharge, Not How You Endure

As constant travelers and parents of a 2-year-old, we sometimes fantasize about how much work we can do when one of us gets on a plane, undistracted by phones, friends, and Finding Nemo. We race to get all our ground work done: packing, going through TSA, doing a last-minute work call, calling each other, then boarding the plane. Then, when we try to have that amazing work session in flight, we get nothing done. Even worse, after refreshing our email or reading the same studies over and over, we are too exhausted when we land to soldier on with the emails that have inevitably still piled up.
Why should flying deplete us? We’re just sitting there doing nothing. Why can’t we be tougher — more resilient and determined in our work – so we can accomplish all of the goals we set for ourselves? Based on our current research, we have come to realize that the problem is not our hectic schedule or the plane travel itself; the problem comes from a misunderstanding of what it means to be resilient, and the resulting impact of overworking.
We often take a militaristic, “tough” approach to resilience and grit. We imagine a Marine slogging through the mud, a boxer going one more round, or a football player picking himself up off the turf for one more play. We believe that longer we tough it out, the tougher we are, and therefore the more successful we will be. However, this entire conception is scientifically inaccurate.
The very lack of a recovery period is dramatically holding back our collective ability to be resilient and successful. Research has found that there is a direct correlation between lack of recovery and increased incidence of health and safety problems. And lack of recovery — whether by disrupting sleep with thoughts of work or having continuous cognitive arousal by watching our phones — is costing our companies $62 billion a year (that’s billion, not million) in lost productivity.
And just because work stops, it doesn’t mean we are recovering. We “stop” work sometimes at 5PM, but then we spend the night wrestling with solutions to work problems, talking about our work over dinner, and falling asleep thinking about how much work we’ll do tomorrow. In a study released last month, researchers from Norway found that 7.8% of Norwegians have become workaholics. The scientists cite a definition of “workaholism” as “being overly concerned about work, driven by an uncontrollable work motivation, and investing so much time and effort to work that it impairs other important life areas.”
We believe that the number of people who fit that definition includes the majority of American workers, including those who read HBR, which prompted us to begin a study of workaholism in the U.S. Our study will use a large corporate dataset from a major medical company to examine how technology extends our working hours and thus interferes with necessary cognitive recovery, resulting in huge health care costs and turnover costs for employers.

You Need An Innovation Strategy but stroke doesn't

Only 12 pages from Harvard Business Review. But our fucking failures of stroke associations have no need for this because they would rather stick to small ideas like F.A.S.T. and prevention press releases.

RECOMMENDED READING

YOU NEED AN INNOVATION STRATEGY Innovation, by definition, means trying something new. So it's a bit ironic that many companies pursue it by adhering to accepted innovation practices or mimicking the actions of other innovators. And it's not surprising that many of these initiatives fail. In this Harvard Business Review article, HBS Professor Gary P. Pisano examines the importance of developing a clear and comprehensive innovation strategy. To maximize value, he contends, a company's innovation strategy must be consistent with its business model and technical capabilities.

THE STRATEGY THAT WILL FIX HEALTH CARE - Harvard Business Review

This first line is not occurring in stroke health care:

PROVIDERS MUST LEAD THE WAY IN MAKING VALUE THE OVERARCHING GOAL 

The crisis in stroke is simple; nothing is available or works. Our providers have been failing for so long they don't even know what the goal is. Only 19 pages that your hospital should be able to implement in the next 50 years. If you want it sooner you'll have to install your own stroke department head.
http://go.questexweb.com/de0QRDLuwG0F200Q2p410M0 
What's the solution to the world's seemingly intractable health care crisis? It starts with a clear and achievable goal—better value—supported by an innovative strategy that's driven by the needs of patients, not providers. In this Harvard Business Review article, Harvard Business School Faculty Chair Michael Porter and his co-author outline such a strategy. They present a groundbreaking approach to high-value health care that focuses on six components: medical conditions, measurement of costs and outcomes(not done in stroke), bundled pricing, integrated care delivery, geographically expanded service, and an enabling IT platform. 

What is Neural Plasticity?

You can make up your own mind whether any of this is specific enough to actually be able to accomplish this on command.

I would have to say this is a complete cop-out. 'We know this works but we don't know exactly how to tell you to accomplish this'. Saying the mantra, 'exercise and move' doesn't help anyone except for the stroke medical person because they have then successfully dumped the monkey on the stroke survivors back. Thus successfully being able to 'blame the patient' for not recovering.

 What is Neural Plasticity? from StrokeSmart magazine

You could try reading this dense one which doesn't help understand it at all.

Molecular control of brain plasticity and repair

3 Strategies for Combating Post-stroke Fatigue

NO, NO, NO  This is putting all the responsibility for combatting fatigue on the patient. Dump that fucking monkey directly on your doctors' back. They need to actually do some work for once. Quote this Harvard Business Review article to them and never let a stroke recovery problem be allowed to stay on your back overnight.

Who's Got the Monkey?

3 Strategies for Combating Post-stroke Fatigue

1. Keep a fatigue diary.
2. Plan Your Activities. 
3.Adjust Your Diet.