Transient ischemic attack
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At the time the article was created Bruno Di Muzio had no recorded disclosures.View Bruno Di Muzio's current disclosures
At the time the article was last revised Henry Knipe had the following disclosures:
- Radiopaedia Events Pty Ltd, Speaker fees (past)
- Integral Diagnostics, Shareholder (ongoing)
- Micro-X Ltd, Shareholder (ongoing)
These were assessed during peer review and were determined to not be relevant to the changes that were made.View Henry Knipe's current disclosures
Transient ischemic attacks (TIAs), in the most recent definition, correspond to a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.
In the past, TIA was arbitrarily distinguished from stroke by the duration of neurological symptoms of less than 24 hours 1. However, this definition allowed for risk of permanent infarction to be classified as a TIA, and thus the aforementioned tissue-based definition was favored 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.
The incidence increases with age, with approximately 0.1 million new cases per year reported world wide. A male gender predominance noted in an American population 10.
Risk factors are essentially typical vascular risk factors, such as hypertension, cigarette smoking, and diabetes mellitus 10.
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 ischemic stroke, localized 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: also known as the capsular warning syndrome, these are similar to low-flow TIAs but the transient and recurrent neurological symptoms are those of lacunar stroke syndromes 4
There are three pathophysiological mechanisms:
low-flow TIA: caused by large artery stenosis (e.g. internal carotid artery stenosis) 1,3
embolic TIA: caused by the same etiologies of thromboembolic ischemic stroke 1,3
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 lipohyalinosis of penetrating arteries 1,4
There is uncertainty regarding the radiographic features of TIAs given that there is currently no perfect radiographic corollary to the pathology, especially when even minute regions of infarction could differentiate a stroke from a TIA 1. While CT brain is often unremarkable, there is controversy regarding the significance of regions demonstrating high signal on DWI, a finding present in approximately half of all TIAs 5.
It has been proposed that if a region demonstrates high signal on DWI, and especially 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 if a lesion demonstrates early DWI reversal, because it has been found that these such lesions may still have some degree of infarction, and thus the patient may, in fact, have had a stroke instead of a TIA 6,7. Thus, determining which, or determining if all, "DWI-positive" TIAs should, in fact, be classified as strokes remains unclear and a subject of ongoing research 5.
Treatment and prognosis
Management is complex, but in short, revolves around determining the etiology of the TIA, risk stratification, and then medical (e.g. aspirin) and/or surgical therapy (e.g. carotid endarterectomy) where appropriate 8.
History and etymology
The term transient ischemic attack was coined by Charles Miller Fisher (1913-2012), a renowned Canadian neurologist, in 1951 9. The term capsular warning syndrome was coined by Geoffrey Donnan, Australian neurologist, and colleagues in 1993 4.
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- 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. doi:10.1161/STROKEAHA.113.002135 - Free text at pubmed - Pubmed citation
- 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. doi:doi:10.1038/jcbfm.2011.102 - Free text at pubmed - Pubmed citation
- 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. doi:10.1161/STR.0000000000000024 - Pubmed
- 9. Louis R. Caplan, Jay P. Mohr, Robert H. Ackerman. In Memoriam: Charles Miller Fisher, MD (1913-2012). (2012) Archives of Neurology. 69 (9): 1208. doi:10.1001/archneurol.2012.1743 - Pubmed
- 10. Wolfgang Dähnert. Radiology Review Manual. (2020) ISBN: 9781609139438