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.


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 

 


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.