Transient ischemic attack

Changed by Rohit Sharma, 28 Jun 2017

Updates to Article Attributes

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Transient ischaemic attack (TIA), in the most recent definition, corresponds to a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

Terminology 

In the past TIA was arbitrarily distinguished from stroke by the duration of neurological symptoms of less than 24 hours1. It However, this definition allowed for risk of permanent infarction to be classified as a TIA, and thus the aforementioned tissue-based definition was favoured 1. It is well established nowadays that in most TIAs symptoms resolve in less than one hour but occasionally prolonged episodes may occur 1-2,2

Clinical features

The clinical features are variable and dependent on the mechanism (see below):

  • Low-flow TIA: classic transient focal neurological symptoms, either anterior or posterior circulation symptoms, last only minutes, and are often recurrent 3
  • Embolic TIA: similar presentation to a thromboembolic ischaemic stroke, localised to a specific arterial territory rather than a general circulation, tend to last hours, and do not tend to be recurrent 3
  • Lacunar or small penetrating vessel TIA: similar to low-flow TIAs but the transient neurological symptoms are those of lacunar stroke syndromes, also known as the capsular warning syndrome 4

Pathology

There are three pathophysiological mechanisms:

  • Low-flow TIA: caused by large artery stenosis (e.g. internal carotid artery stenosis1,3
  • Embolic TIA: caused by the same aetiologies of thromboembolic ischaemic stroke1,3
    • There is controversy as to whether these should actually be classified as strokes as per the tissue-based definition
  • Lacunar or small penetrating vessel TIA: caused by either stenosis of intracranial arteries (e.g. middle cerebral artery stenosis) or lipohyalnosis of penetrating arteries 1,4

Radiographic features

There is uncertainty regarding the radiographical features of TIAs given that there is currently no perfect radiographic corollary to detecting minute regions of infarction 1. While CT brain is often unremarkable, there is controversy regarding the significance of regions demonstrating high signal on DWI 5.

It has been proposed that if a region does demonstrate high signal on DWI and if there is no early DWI reversal, then that is a region of infarction and hence should be a stroke and not a TIA 5. However, the confusion lies in a lesion that does in fact demonstrate early DWI reversal, because it has been found that these such lesions may still have infarction, and thus the patient may in fact have a stroke instead of a TIA 6,7. 

Treatment and prognosis

Management is complex but in short, revolves around determining the aetiology of the TIA, risk stratification, and then medical and surgical therapy where appropriate 8.

  • -<p><strong>Transient ischaemic attack (TIA)</strong>, in the most recent definition, corresponds to a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.</p><h4>Terminology </h4><p>In the past TIA was arbitrarily distinguished from <a href="/articles/stroke">stroke</a> by the duration of neurological symptoms of less than 24 hours. It is well established nowadays that in most TIAs symptoms resolve in less than one hour but occasionally prolonged episodes may occur <sup>1-2</sup>. </p><p> </p><h4> </h4>
  • +<p><strong>Transient ischaemic attack (TIA)</strong>, in the most recent definition, corresponds to a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.</p><h4>Terminology </h4><p>In the past TIA was arbitrarily distinguished from <a href="/articles/stroke">stroke</a> by the duration of neurological symptoms of less than 24 hours <sup>1</sup>. However, this definition allowed for risk of permanent infarction to be classified as a TIA, and thus the aforementioned tissue-based definition was favoured <sup>1</sup>. It is well established nowadays that in most TIAs symptoms resolve in less than one hour but occasionally prolonged episodes may occur <sup>1,2</sup>. </p><h4>Clinical features</h4><p>The clinical features are variable and dependent on the mechanism (see below):</p><ul>
  • +<li>Low-flow TIA: classic transient focal neurological symptoms, either anterior or posterior circulation symptoms, last only minutes, and are often recurrent <sup>3</sup>
  • +</li>
  • +<li>Embolic TIA: similar presentation to a thromboembolic <a href="/articles/ischaemic-stroke">ischaemic stroke</a>, localised to a specific arterial territory rather than a general circulation, tend to last hours, and do not tend to be recurrent <sup>3</sup>
  • +</li>
  • +<li>Lacunar or small penetrating vessel TIA: similar to low-flow TIAs but the transient neurological symptoms are those of <a href="/articles/lacunar-stroke-syndrome">lacunar stroke syndromes</a>, also known as the <strong>capsular warning syndrome </strong><sup>4</sup>
  • +</li>
  • +</ul><h4>Pathology</h4><p>There are three pathophysiological mechanisms:</p><ul>
  • +<li>Low-flow TIA: caused by large artery stenosis (e.g. <a href="/articles/carotid-artery-stenosis">internal carotid artery stenosis</a>) <sup>1,3</sup>
  • +</li>
  • +<li>Embolic TIA: caused by the same aetiologies of thromboembolic <a href="/articles/ischaemic-stroke">ischaemic stroke</a> <sup>1,3</sup><ul><li>There is controversy as to whether these should actually be classified as strokes as per the tissue-based definition</li></ul>
  • +</li>
  • +<li>Lacunar or small penetrating vessel TIA: caused by either stenosis of intracranial arteries (e.g. middle cerebral artery stenosis) or lipohyalnosis of penetrating arteries <sup>1,4</sup>
  • +</li>
  • +</ul><h4>Radiographic features</h4><p>There is uncertainty regarding the radiographical features of TIAs given that there is currently no perfect radiographic corollary to detecting minute regions of infarction <sup>1</sup>. While CT brain is often unremarkable, there is controversy regarding the significance of regions demonstrating high signal on DWI <sup>5</sup>.</p><p>It has been proposed that if a region does demonstrate high signal on DWI and if there is no <a href="/articles/early-dwi-reversal-in-ischaemic-stroke">early DWI reversal</a>, then that is a region of infarction and hence should be a stroke and not a TIA <sup>5</sup>. However, the confusion lies in a lesion that does in fact demonstrate <a href="/articles/early-dwi-reversal-in-ischaemic-stroke">early DWI reversal</a>, because it has been found that these such lesions may still have infarction, and thus the patient may in fact have a stroke instead of a TIA <sup>6,7</sup>. </p><h4>Treatment and prognosis</h4><p>Management is complex but in short, revolves around determining the aetiology of the TIA, risk stratification, and then medical and surgical therapy where appropriate <sup>8</sup>.</p>

References changed:

  • 2. Kidwell CS, Alger JR, Di Salle F et-al. Diffusion MRI in patients with transient ischemic attacks. Stroke. 1999;30 (6): 1174-80. <a href="http://dx.doi.org/10.1161/01.STR.30.6.1174">doi:10.1161/01.STR.30.6.1174</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/10356095">Pubmed citation</a><span class="auto"></span>
  • 4. Donnan GA, O'Malley HM, Quang L, Hurley S, Bladin PF. The capsular warning syndrome. Neurology. 43 (5): 957. <a href="https://doi.org/10.1212/WNL.43.5.957">doi:10.1212/WNL.43.5.957</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/8492952">Pubmed</a> <span class="ref_v4"></span>
  • 5. C. Oppenheim, C. Lamy, E. Touzé, D. Calvet, M. Hamon, J.-L. Mas, J.-F. Méder. Do Transient Ischemic Attacks with Diffusion-Weighted Imaging Abnormalities Correspond to Brain Infarctions?. American Journal of Neuroradiology. 27 (8): 1782. <a href="https://www.ncbi.nlm.nih.gov/pubmed/16971636">Pubmed</a> <span class="ref_v4"></span>
  • 6. Inoue M, Mlynash M, Christensen S et-al. Early diffusion-weighted imaging reversal after endovascular reperfusion is typically transient in patients imaged 3 to 6 hours after onset. Stroke. 2014;45 (4): 1024-8. <a href="http://dx.doi.org/10.1161/STROKEAHA.113.002135">doi:10.1161/STROKEAHA.113.002135</a> - <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4396865">Free text at pubmed</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/24558095">Pubmed citation</a><span class="auto"></span>
  • 7. Campbell BC, Purushotham A, Christensen S et-al. The infarct core is well represented by the acute diffusion lesion: sustained reversal is infrequent. J. Cereb. Blood Flow Metab.32 (1): 50-6. <a href="http://dx.doi.org/doi:10.1038/jcbfm.2011.102">doi:doi:10.1038/jcbfm.2011.102</a> - <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3323290">Free text at pubmed</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/21772309">Pubmed citation</a><span class="auto"></span>
  • 1. Easton JD, Saver JL, Albers GW et-al. 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 (6): 2276-93. <a href="http://dx.doi.org/10.1161/STROKEAHA.108.192218">doi:10.1161/STROKEAHA.108.192218</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/19423857">Pubmed citation</a><span class="auto"></span>
  • 3. Javaid A, Alfishawy M. Internal Carotid Artery Stenosis Presenting with Limb Shaking TIA. Case reports in neurological medicine. 2016: 3656859. <a href="https://doi.org/10.1155/2016/3656859">doi:10.1155/2016/3656859</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/27840754">Pubmed</a> <span class="ref_v4"></span>
  • 8. Walter N. Kernan, Bruce Ovbiagele, Henry R. Black, Dawn M. Bravata, Marc I. Chimowitz, Michael D. Ezekowitz, Margaret C. Fang, Marc Fisher, Karen L. Furie, Donald V. Heck, S. Claiborne (Clay) Johnston, Scott E. Kasner, Steven J. Kittner, Pamela H. Mitchell, Michael W. Rich, DeJuran Richardson, Lee H. Schwamm, John A. Wilson. Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack. Stroke. 45 (7): 2160. <a href="https://doi.org/10.1161/STR.0000000000000024">doi:10.1161/STR.0000000000000024</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/24788967">Pubmed</a> <span class="ref_v4"></span>
  • 2. Easton JD, Saver JL, Albers GW et-al. 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 (6): 2276-93. <a href="http://dx.doi.org/10.1161/STROKEAHA.108.192218">doi:10.1161/STROKEAHA.108.192218</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/19423857">Pubmed citation</a><span class="auto"></span>
  • 1. Kidwell CS, Alger JR, Di Salle F et-al. Diffusion MRI in patients with transient ischemic attacks. Stroke. 1999;30 (6): 1174-80. <a href="http://dx.doi.org/10.1161/01.STR.30.6.1174">doi:10.1161/01.STR.30.6.1174</a> - <a href="http://www.ncbi.nlm.nih.gov/pubmed/10356095">Pubmed citation</a><span class="auto"></span>

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