Implications of the AHA/ASA Updated Definition of Stroke for the 21st Century

Absolutely nothing here will help survivors recover. So useless and a waste of time.

Implications of the AHA/ASA Updated Definition of Stroke for the 21st Century

Abridged from original article by Scott E. Kasner, MD,  and Ralph L. Sacco, MD published 13 July 2018 in World Neurology Vol 28 No. 4

Note: The views expressed by the authors are their own and do not represent an official statement by the American Heart Association/American Stroke Association.

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Stroke was defined by the World Health Organization (WHO) more than 40 years ago as “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.”¹ This was a working definition created for a study assessing the prevalence and natural history of stroke, and it served its purpose at the time.
The ensuing decades have witnessed major advances in basic science, pathophysiology and neuroimaging that have dramatically improved our understanding of ischemia, infarction and haemorrhage in the central nervous system (CNS). There is little doubt that permanent injury occurs well before the 24-hour threshold, and therefore purely time-based definitions are inaccurate and obsolete. Further, neuroimaging has demonstrated that clinically transient symptoms are often associated with evidence of acute cerebral infarction and that infarction may occur without overt symptoms.
In 2009, the American Heart Association/American Stroke Association (AHA/ASA) published a scientific statement redefining transient ischemic attack (TIA) as, “a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia without acute infarction.”² This statement formally addressed only one side of the proverbial coin, but clearly implied that objective evidence of infarction should be considered as a defining feature of stroke.

The new definition harmonizes with our understanding of the pathophysiology of infarction and with the recent redefinition of TIA, but also necessitates the inclusion of silent infarction and silent hemorrhage within the broad definition of stroke.

In the spring of 2013, the AHA/ASA published an expert consensus document with a new definition of stroke to reflect these advances.³ Authors with expertise in the fields of neurology, neurosurgery, neuroradiology, neuropathology, clinical research methods, epidemiology, biomarkers, policy and global public health were invited from within the AHA/ASA, as well as the American Academy of Neurology, the American Association of Neurological Surgeons and Congress of Neurological Surgeons, U.S. Centers for Disease Control and Prevention, the National Institute of Neurological Disorders and Stroke, the European Stroke Organization (ESO), the World Stroke Organization (WSO) and others to establish a universal definition of stroke.
The major fundamental change compared with older definitions is that the new broader definition of stroke includes any objective evidence of permanent brain, spinal cord or retinal cell death due to a vascular cause based upon pathological or imaging evidence with or without the presence of clinical symptoms.  Ultimately, the leaders of the ESO and WSO withdrew from participation and declined to endorse the statement because they disagreed about the inclusion of silent cerebral infarction and silent cerebral haemorrhage within the lexicon of stroke. (See “Stroke Definition in the ICD-11 at the WHO.“)
The AHA/ASA defined CNS infarction based on pathological, imaging or other objective evidence of infarction. In the absence of this evidence, the persistence of symptoms of at least 24 hours or until death remained a method to define stroke. At present, imaging is not always available and also is not perfect. In much of the developing world and in rural parts of more developed regions, neither [CT or MRI] may be available in the acute setting, if at all, which limits the global applicability of an imaging-based definition of stroke.
Silent lesions have been recognized pathologically as infarctions and haemorrhages since the 1960s but were deemed of uncertain importance. However, they may not be entirely asymptomatic, as patients may have subtle cognitive, gait or other functional impairments in the absence of a typical acute presentation. To some extent, the “silence” of an infarction or haemorrhage depends on the eye of the beholder. Patients may not be aware of their symptoms due to neglect, denial or simply may attribute them to another cause and not seek a medical opinion. Physicians and other health care providers may vary in their ability to detect mild neurologic abnormalities, or they, too, may ascribe them to an alternative cause.
The AHA/ASA included silent CNS infarctions and haemorrhages within the broadest definition of stroke for multiple reasons.

Implications for World Neurology

The new tissue-based definition of CNS infarction depends on either early objective (currently neuroimaging) evidence of infarction or persistence of symptoms for at least 24 hours. If early imaging is not available, then clinicians are left with a diagnostic dilemma in those first 24 hours since the event cannot be clearly classified as stroke.
Ultimately, diagnostic techniques and/or time will help define infarct or haemorrhage based on objective imaging, or TIA in the absence of positive imaging and resolution of symptoms within 24 hours from onset. A major challenge for the future will be the achievement of access to diagnostic and treatment tools in the developing world, where a substantial portion of the global burden of stroke occurs.
The inclusion of silent infarcts and microhemorrhages within the AHA/ASA definition of stroke opens many questions for clinicians. In regions with little or no access to neuroimaging, this change in definition may prove irrelevant for many years to come. However, for those with such access, silent lesions are likely to be detected as a result of the widespread use of MRI for non-cerebrovascular symptoms such as headache or dizziness.
Updating the definition of the disease can have prominent effects on disease surveillance and assessments of public health.  In the case of adding a large number of silent infarction cases to the existing number of stroke cases, this will increase the total number of stroke cases while likely decreasing the mortality rate due to the addition of a number of minor/silent cases.⁴ Updating the definition of stroke could result in reclassification of stroke cases for incidence, prevalence, and mortality in national and international statistics, disease classification coding systems and existing health surveys. This is particularly problematic if definitions are applied differently in each region of the globe, and this is a major concern of all stroke organizations. Therefore, the AHA/ASA recommended that symptomatic and silent infarctions and haemorrhages should be counted separately to allow for valid analyses of temporal and geographic trends in stroke. Although the WSO, ESO and WHO will not include the silent lesions within the definition of stroke, they recognize their importance and are going to start counting them within the scope of cerebrovascular disorders in the ICD-11.

Read the full article 

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At the time of print, Kasner is with the University of Pennsylvania and Sacco is with the University of Miami.
References

1. Aho K, Harmsen P, Hatano S, Marquardsen J, Smirnov VE, Strasser T. Cerebrovascular disease in the community: results of a WHO collaborative study. Bull World Health Organ. 1980;58:113-130.
2. Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E, Hatsukami TS, Higashida RT, Johnston SC, Kidwell CS, Lutsep HL, Miller E, Sacco RL. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009;40:2276-2293.
3. Sacco RL, Kasner SE, Broderick JP, Caplan LR, Connors JJ, Culebras A, Elkind MS, George MG, Hamdan AD, Higashida RT, Hoh BL, Janis LS, Kase CS, Kleindorfer DO, Lee JM, Moseley ME, Peterson ED, Turan TN, Valderrama AL, Vinters HV. An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013;44:2064-2089.
4. Pia Sormani M. The Will Rogers phenomenon: the effect of different diagnostic criteria. J Neurol Sci. 2009;287 Suppl 1:S46-49.

Rehabilitation of Severe Stroke

With all the problems of rehabbing severe strokes it would seem obvious to all except for those blind idiots in the stroke world that stopping the neuronal cascade of death will result in less severe strokes.
http://www.ebrsr.com/uploads/Chapter-23_Severe-Stroke_FINAL_16ed.pdf

Abstract

Severe strokes often result in multiple disabilities and constitute not only the most disabled group of stroke patients but also the greatest rehabilitation challenge. On a per-person basis, severe stroke patients incur the greatest costs to the healthcare system, primarily due to increased length of stay(LOS) in hospital and the frequent need for expensive long-term care or institutionalization

(Navarrete-Navarro et al. 2003)

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Research relating to the definition, classification, neuro

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recovery and rehabilitation

of severe strokes is provided in this review. Clinical evidence

for various severe stroke rehabilitation models are discussed(including slow-stream, intensive care unit (ICU), and specialized interdisciplinary stroke rehabilitation).

Ethical dialogue pertaining to severe stroke is also presented.

An Updated Definition of Stroke for the 21st Century

Great, our medical team doesn't even have a definition of stroke. How the hell do we expect them to solve all the problems in stroke rehab, prevention, research?
Written about in 1999;
Stroke is the wrong term to use

The term ‘stroke’ is obscurantist, reductionist, and redundant. It has connotations that are unhelpful to both the general public and the medical profession. Better terms exist that either do not pretend to be a diagnosis (eg, ‘brain attack’), or that have some pathophysiological significance. ‘Stroke’ should be consigned to the dustbin of medical usage.

And 13 years later we might get some definition. We are working with sloths but that would denigrate sloths.
http://stroke.ahajournals.org/content/early/2013/05/07/STR.0b013e318296aeca

Abstract

Despite the global impact and advances in understanding the pathophysiology of cerebrovascular diseases, the term “stroke” is not consistently defined in clinical practice, in clinical research, or in assessments of the public health. The classic definition is mainly clinical and does not account for advances in science and technology. The Stroke Council of the American Heart Association/American Stroke Association convened a writing group to develop an expert consensus document for an updated definition of stroke for the 21st century. Central nervous system infarction is defined as brain, spinal cord, or retinal cell death attributable to ischemia, based on neuropathological, neuroimaging, and/or clinical evidence of permanent injury. Central nervous system infarction occurs over a clinical spectrum: Ischemic stroke specifically refers to central nervous system infarction accompanied by overt symptoms, while silent infarction by definition causes no known symptoms. Stroke also broadly includes intracerebral hemorrhage and subarachnoid hemorrhage. The updated definition of stroke incorporates clinical and tissue criteria and can be incorporated into practice, research, and assessments of the public health.

Tissue Injury Has Lead in New Stroke Definition

This is long past due. This is actually a great occurence.
1. Your insurance company will not pay for therapy until it is objectively proven you had a stroke.
2. This will lead to multiple CT/MRI scans in the first week since the very first scan may not show up.
3. This leads to objective proof of how the neuronal cascade of death resolves over the first week.
4. Proving to the stroke medical world that the number one focus needs to be stopping the neuronal cascade of death.
5. This objective scan of dead and dying areas will force neurologists/PMR doctors to use them in telling the therapists what protocols to use.
6. Neurologists/PMR doctors will be required to actually create and understand therapy protocols for recovery.
7. No more lying about recovery prospects.
8. Therapists will finally be able to do clinical research since they now will have a repeatable starting point.
9. You will be able to have a 3d mappable damage area to deficits.
http://www.medpagetoday.com/Cardiology/Strokes/39125?
If neuroimaging shows brain tissue injury, the insult should be called a stroke, even if no symptoms exist, according to an expert consensus document from the American Heart Association/American Stroke Association (AHA/ASA).
"A tissue-based definition of ischemic stroke and transient ischemic attack enhances diagnostic criteria and relies on utilization of various imaging techniques in the acute phase of the stroke," according to writing committee co-chair Scott E. Kasner, MD, of the University of Pennsylvania in Philadelphia, and colleagues.
The experts correlated the updated stroke definition with a similar update to the definition of myocardial infarction, in which the term "acute coronary syndrome" is used before the determination of infarction has been made.
"Nevertheless, these [cardiac] patients receive urgent evaluations and treatments intended to avert or minimize permanent myocardial tissue damage," they wrote in the statement published online in Stroke: Journal of the American Heart Association

More at link.

What has gone wrong in stroke research?

I wonder who answered this? From BMJ in 1999. If this was asked about way back in 1999 why am I still asking the same questions?
http://pmj.bmj.com/content/75/886/449.full

• Accepted 19 April 1999

There have been two main approaches to the acute treatment of stroke, thrombolysis and neuroprotection. After a number of disappointing thrombolytic trials using either streptokinase1-3 or an inappropriately long time-window,4 tissue plasminogen activator (t-PA) was demonstrated to improve clinical outcome at three months.5Patients who received t-PA within 3 hours of onset were 30% more likely to have minimal or no disability at 3 months when compared with placebo. This was at the price of 6.4% of patients, who received t-PA and developed symptomatic intracerebral haemorrhage, producing a non-statistical benefit in terms of mortality (17%vs 21%). For many patients, disability is a more important issue than death and t-PA reduces disability, but will cause some deaths from haemorrhage.

Normal cerebral blood flow is approximately 100 ml/100 g of brain tissue per minute. In cerebral infarction there is a core of tissue with blood flows in the 0–10 ml/100 g/min range where neuronal death will occur within an hour and the damage is irreversible. Around this is an area of brain called the penumbra,6 where blood flow is in the 10–20 ml/100 g/min range. In the penumbra there is electrical failure and large scale release of the excitatory amino acids, glutamate and aspartate. This release of amino acids is associated with calcium influx into the neurones and a cascade of deleterious biochemical events that leads to cell death. The theoretical basis for neuroprotection lies in interrupting this process within the penumbra and reducing the final size of the ischaemic injury. There were initially great hopes for glutamate antagonists, particularly theN-methyl-D-aspartate receptor antagonists.7 A number of neuroprotectants remain in late clinical development,8 but many have fallen by the wayside, either through unacceptable side-effects or lack of efficacy.9 The latest, lubeluzole, a NO modifier, produced conflicting results in very similar trials performed on either side of the Atlantic.10 11 Thus far, neuroprotective agents have failed to live up to their promise from animal studies and phase II studies, by not delivering efficacy in phase III.

The early mortality in cerebral ischaemia is predominantly due to swelling of the brain and the development of fatal raised intracranial pressure. This swelling is due to oedema developing in the dead and dying ischaemic areas. A decade ago glycerol was demonstrated to reduce the mortality associated with oedema without increasing the number of disabled survivors.12 Even more heroic measures such as decompressive surgery for hemispheric infarction have been tried13 with initially encouraging results (mortality reduced from two thirds to a third).

While in the US thrombolysis is standard treatment for those lucky stroke victims who get to hospital early enough and have no changes on computed tomography, in Europe there is no consensus on acute therapy for stroke. The European license for t-PA use in cerebral infarction is currently under consideration. Why have acute treatments for a relatively simple problem of a blocked pipe in the brain been so problematic?

The terminology has seduced us into believing the problem is simple. The term ‘stroke’ should be exorcised from the medical literature. A stroke is defined as an acute neurological event caused either by cerebral infarction or intracerebral haemorrhage in which symptoms persist for longer than 24 hours or which results in death. The WHO has included subarachnoid haemorrhage as a form of stroke,14 15 but many authors do not. From a neuroscientific point of view, the term ‘stroke’ is unsatisfactory in that it includes a number of pathologies whose management and prognosis are different. By using the term there is thus a danger of over simplifying a complex area. Adding qualifiers helps little. Haemorrhagic stroke, which means primary intraparenchymal haemorrhage, is often confused with secondary haemorrhagic transformation of an infarct. The term ischaemic stroke is equivalent to cerebral infarction, but fails to convey the heterogenous nature of the pathology.

When assessing the nature of an acute cerebrovascular event there are several pertinent questions to be answered. First, it must be decided whether it is an infarct or a haemorrhage. If it is a haemorrhage then the underlying cause (hypertensive, arteriovenous malformation, amyloid angiopathy, etc) must be ascertained. If it is an infarct, the first step is to identify the blood vessel concerned. This involves territory (anterior vs posterior) and size (large artery vs arteriole). Ischaemic events are either transient (symptoms resolving within 24 hours) or not. The second step is to infer the probable mechanism; whether it is likely to be due to hypoperfusion or is embolic or thrombotic. The third step, and most important for long-term secondary prevention, is to identify the underlying pathological process, such as atheroma or hyaline degeneration secondary to hypertension (table). The discharge diagnosis on a patient would then be, for example: “cerebral infarction in the middle cerebral artery territory, presumed to be embolic in nature, secondary to atheromatous disease”. Such a classification requires clinical acumen and access to neuroimaging. A recent audit in our hospital revealed that the assessment by the admitting doctor went no further than ‘stroke’ in 60% of cases (Clinical Audit Department, North Staffordshire Hospital NHS Trust, 1996).

The danger from a clinical point of view of talking about stroke or cerebrovascular disease is that the terms presume a unitary phenomenon. Unsophisticated studies into ‘stroke’ can produce results that are difficult to apply to individual patients.16

Meta-analyses demonstrating that organised stroke unit care reduces death, dependency and the need for institutional care,17 18 are examples of two heterogenous terms (stroke and stroke unit) held together by p<0.0001. What is it about organised care and which patients benefit? As meta-analysis failed to find any sub-group of patients or model of stroke unit care particularly associated with benefit,18 one might be tempted to conclude that the advantage was attributable to a general effect, such as staff morale and dedication.

In the general population the word ‘stroke’ raises feelings of doom and passivity. Only 60% of the US population over 50 years old realise that a stroke occurs in the brain.19 If the potential advantages of thrombolysis and neuroprotective agents are to be realised, patients have to receive medical attention rapidly. In order to raise awareness of the urgent nature of the situation the term ‘brain attack’ aptly describes the situation without pretending to be a diagnosis.

The term ‘stroke’ is obscurantist, reductionist, and redundant. It has connotations that are unhelpful to both the general public and the medical profession. Better terms exist that either do not pretend to be a diagnosis (eg, ‘brain attack’), or that have some pathophysiological significance. ‘Stroke’ should be consigned to the dustbin of medical usage.

Those interested in the management of ‘stroke’ were lulled into intellectual complacency by an uncritical acceptance of analogies with myocardial infarction. Cerebral infarction is a much more complex process and requires a more sophisticated approach; a preliminary and necessary step is the discarding of simplistic terminology. We can then concentrate on therapeutic interventions in subpopulations defined by pathology and time from onset.