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.

Showing posts with label see no evil;speak no evil;do no evil. Show all posts
Showing posts with label see no evil;speak no evil;do no evil. Show all posts

Tuesday, March 30, 2021

Unique diagnostic signatures of concussion in the saliva of male athletes: the Study of Concussion in Rugby Union through MicroRNAs (SCRUM)

I can very obviously see a possible use for this in stroke and TBI, but no one in stroke leadership will do anything with this. Their motto must be hear no research, see no research, do no research!

hear no evil,see no evil,speak no evil


 

 

 

 

 

 

Unique diagnostic signatures of concussion in the saliva of male athletes: the Study of Concussion in Rugby Union through MicroRNAs (SCRUM)

  1. Valentina Di Pietro1,2,3,
  2. Patrick O'Halloran1,3,
  3. Callum N Watson1,
  4. Ghazala Begum3,
  5. Animesh Acharjee2,4,5,
  6. Kamal M Yakoub2,
  7. Conor Bentley2,
  8. David J Davies1,2,
  9. Paolo Iliceto6,
  10. Gabriella Candilera6,
  11. David K Menon7,
  12. Matthew J Cross8,9,
  13. Keith A Stokes8,10,
  14. Simon PT Kemp10,11,
  15. Antonio Belli1,2,3
  1. Correspondence to Dr Valentina Di Pietro, University of Birmingham, Institute of Inflammation and Ageing, Birmingham 9,000, UK; v.dipietro@bham.ac.uk

Abstract

Objective To investigate the role of salivary small non-coding RNAs (sncRNAs) in the diagnosis of sport-related concussion.

Methods Saliva was obtained from male professional players in the top two tiers of England’s elite rugby union competition across two seasons (2017–2019). Samples were collected preseason from 1028 players, and during standardised head injury assessments (HIAs) at three time points (in-game, post-game, and 36–48 hours post-game) from 156 of these. Samples were also collected from controls (102 uninjured players and 66 players sustaining a musculoskeletal injury). Diagnostic sncRNAs were identified with next generation sequencing and validated using quantitative PCR in 702 samples. A predictive logistic regression model was built on 2017–2018 data (training dataset) and prospectively validated the following season (test dataset).

Results The HIA process confirmed concussion in 106 players (HIA+) and excluded this in 50 (HIA−). 32 sncRNAs were significantly differentially expressed across these two groups, with let-7f-5p showing the highest area under the curve (AUC) at 36–48 hours. Additionally, a combined panel of 14 sncRNAs (let-7a-5p, miR-143-3p, miR-103a-3p, miR-34b-3p, RNU6-7, RNU6-45, Snora57, snoU13.120, tRNA18Arg-CCT, U6-168, U6-428, U6-1249, Uco22cjg1,YRNA_255) could differentiate concussed subjects from all other groups, including players who were HIA− and controls, immediately after the game (AUC 0.91, 95% CI 0.81 to 1) and 36–48 hours later (AUC 0.94, 95% CI 0.86 to 1). When prospectively tested, the panel confirmed high predictive accuracy (AUC 0.96, 95% CI 0.92 to 1 post-game and AUC 0.93, 95% CI 0.86 to 1 at 36–48 hours).

Conclusions SCRUM, a large prospective observational study of non-invasive concussion biomarkers, has identified unique signatures of concussion in saliva of male athletes diagnosed with concussion.

https://creativecommons.org/licenses/by/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/.

 

Monday, May 8, 2017

Improving Stroke Diagnosis Accuracy: An Interview With David Newman-Toker, MD, PhD

How often does your stroke hospital misdiagnose stroke? If they don't even know that they should be closed. Not measuring missed diagnosis is actually a feature of stroke hospitals. That way they can be willfully blind, See no evil, hear no evil, speak/do no evil.

Improving Stroke Diagnosis Accuracy: An Interview With David Newman-Toker, MD, PhD

In the United States, more than 12 million people receive an inaccurate medical diagnosis annually, and nearly every individual is likely to be misdiagnosed at least once.1,2 It is estimated that at least 40,000 to 80,000 deaths per year result from such errors, and 47% of hospital misdiagnoses lead to serious disability.3,4
More than half of malpractice cases pertaining to emergency departments (EDs) stem from diagnostic errors, and some findings indicate these may be disproportionately high for neurologic conditions, and especially stroke.5 Other research shows that misdiagnosis leads to death significantly more often with cerebrovascular events compared with myocardial infarction (45% vs 1%; P <.001).6
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Although multiple studies have found elevated rates of stroke misdiagnosis, including a study from 2014 demonstrating that up to 12.7% of hospital stroke admissions were misdiagnosed initially, the precise numbers are unclear because of wide variation in reported rates.7 More accurate "estimates would help clarify the burden of harms from misdiagnosis and could help identify subgroups for which misdiagnosis-reduction interventions should be sought," wrote Alexander Andrea Tarnutzer, MD, from the University Hospital Zurich, Switzerland, and colleagues in a new article published in Neurology.8
To that end, they conducted a meta-analysis of 23 studies on diagnostic accuracy pertaining to ischemic stroke, transient ischemic attack, or subarachnoid hemorrhage, with a total of 15,721 patients. Their findings show that nearly 8.7% of cerebrovascular events are initially misdiagnosed in the ED, and rates are substantially higher for patients with symptoms that are:
  • Milder (subarachnoid hemorrhage with normal vs abnormal mental state; false-negative rate, 23.8% vs 4.2%; odds ratio [OR], 7.03; 95% CI, 4.80-10.31),
  • Nonspecific (dizziness vs motor findings; false-negative rate, 39.4% vs 4.4%; OR, 14.22; 95% CI, 9.76-20.74), or
  • Transient (transient ischemic attack vs ischemic stroke; false discovery rate, 59.7% vs 11.7%; OR, 11.21; 95% CI, 6.66-18.89).
To learn more about these results and how physicians might help reduce the frequency of such misdiagnoses, Neurology Advisor spoke with the study's senior investigator, David E. Newman-Toker, MD, PhD, professor of neurology, ophthalmology, and otolaryngology at Johns Hopkins University School of Medicine in Baltimore, Maryland; director of the Division of Neuro-Visual & Vestibular Disorders; and director of the Armstrong Institute Center for Diagnostic Excellence.
Neurology Advisor: What are the likely reasons for your finding that nearly 9% of patients with stroke admitted to the ED are misdiagnosed?
Dr Newman-Toker: The patients most likely to be misdiagnosed are those with atypical stroke symptoms. Most often these are common, nonlateralizing symptoms such as dizziness, vertigo, headaches, confusion, or decreased level of consciousness. Roughly 95% of patients presenting with such symptoms to acute care settings do not have strokes as a cause, so finding these strokes requires the ability to separate them from more common causes with high accuracy.
False-negative neuroimaging is more common than often imagined: computed tomography misses >80%, and magnetic resonance imaging misses 10-20% of acute ischemic strokes in the first 48 hours, especially with posterior fossa infarctions. Many of the bedside techniques to differentiate dangerous from benign causes (eg, vestibular neuritis vs cerebellar stroke) rely on tests unfamiliar to most emergency physicians and many neurologists, such as the head impulse test of vestibulo-ocular reflex function as part of the HINTS (Head-Impulse-Nystagmus-Test-of-Skew) bedside test battery.
Neurology Advisor: What is the potential effect of these inaccurate diagnoses?
Dr Newman-Toker: Patients can suffer harms from delayed or missed diagnosis through missed opportunities for acute stroke treatments such as thrombolysis, critical care management of delayed stroke complications, or early secondary stroke prevention. As a result, some patients are left dead or disabled. Disproportionately, these harms affect women, minorities, and especially younger patients. Patients aged 18-45 years are 7-fold more likely to be missed than those older than 75 years. One 18-year-old patient I know, for example, is still trying to recover from locked-in syndrome after his initial presenting symptoms of vertigo and vomiting from vertebral artery dissection were misattributed to recreational drug use.
Neurology Advisor: What can neurologists do to improve stroke assessment and avoid misdiagnosis?
Dr Newman-Toker: Most patients with stroke are never seen by a neurologist, so diagnosis relies largely on the neurologic diagnostic skills of frontline care providers. This means neurologists need to engage their emergency medicine colleagues, working together to identify protocols and pathways for when to trigger appropriate neurological consultation or initiate acute stroke therapies. It also means neurologists must play a critical role in directly educating frontline physicians and providing feedback when errors occur.
Neurology Advisor: What should be the next steps in terms of research in this area?
Dr Newman-Toker: Surprising as it may be, there is no systematic monitoring of diagnostic accuracy or missed stroke. The critical next step is to begin operationally monitoring our diagnostic performance in differentiating strokes from stroke mimics. This will facilitate further studies to identify causes, develop and implement systems solutions, and monitor impact of these interventions.