Transient ischemic attack

A transient ischemic attack (TIA) is a transient episode of neurologic dysfunction caused by ischemia (loss of blood flow) – either focal brain, spinal cord or retinal – without acute infarction (tissue death) 1).

A new clinical concept termed acute cerebrovascular syndrome (ACVS) that includes TIA and acute ischemic stroke has been proposed. With the development of new neuroimaging modalities such as diffusion-weighted image (DWI), the definition of TIA used in the United States has shifted from time-based (less than 24 h) to tissue-based (without acute infarction). High ABCD2 score, carotid artery stenosis, and DWI lesions suggest that patients are at a high risk for early recurrence of ischemic stroke. Recently, it was reported that not only DWI or magnetic resonance angiography(MRA), but also fluid-attenuated inversion recovery (FLAIR) images are useful for evaluating TIA. In Japan, the definition of TIA has not been revised since 1990. To review the definition of TIA and establish a TIA management system that is suitable to domestic healthcare environment, the Japan TIA research group (PI, Kazuo Minematsu) was formed in 2009. The group conducted a nation-wide survey and a retrospective registration study to clarify the current status of clinical practice of TIA. In the group's opinion, TIA is defined as the presence of focal neurological symptoms ascribable to a vascular etiology lasting less than 24 h, irrespective of imaging findings, as classically defined. However, if acute ischemic lesions are found on DWI, it is diagnosed as “TIA with DWI lesions.” The group also made recommendations for hospitalization policies and outpatient management 2).

TIAs have the same underlying cause as strokes: a disruption of cerebral blood flow (CBF), and are often referred to as mini-strokes. This is different from the definition of TIA used before 2009, which was based on the temporal, arbitrary time point of < 24 hours of associated neurological symptoms.

TIAs cause the same symptoms associated with stroke, such as contralateral paralysis (opposite side of body from affected brain hemisphere) or sudden weakness or numbness. A TIA may cause sudden dimming or loss of vision (amaurosis fugax), aphasia, slurred speech (dysarthria) and mental confusion. But unlike a stroke, the symptoms of a TIA can resolve within a few minutes or 24 hours. Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke or a silent stroke.

A silent stroke or silent cerebral infarct (SCI) differs from a TIA in that there are no immediately observable symptoms. An SCI may still cause long lasting neurological dysfunction affecting such areas as mood, personality and cognition. An SCI often occurs before or after a TIA or major stroke.


Watershed infarct

10-15 % of patients with TIA have a stroke within 3 months, 50 % of which occur within 48 hours.


The fourth Auckland Regional Community Stroke study (ARCOS IV) used multiple overlapping case ascertainment methods to identify all hospitalized and nonhospitalized cases of TIA that occurred in people ≥16 years of age usually resident in Auckland (population ≥16 years of age is 1.12 million), during the 12 months from March 1, 2011. All first-ever and recurrent new TIAs (any new TIA 28 days after the index event) during the study period were recorded.

There were 785 people with TIA (402 [51.2%] women, mean [SD] age 71.5 [13.8] years); 614 (78%) of European origin, 84 (11%) Māori/Pacific, and 75 (10%) Asian/Other. The annual incidence of TIA was 40 (95% confidence interval, 36-43), and attack rate was 63 (95% confidence interval, 59-68), per 100 000 people, age standardized to the World Health Organization world population. Approximately two thirds of people were known to be hypertensive or were being treated with blood pressure-lowering agents, half were taking antiplatelet agents and just under half were taking lipid-lowering therapy before the index TIA. Two hundred ten (27%) people were known to have atrial fibrillation at the time of the TIA, of whom only 61 (29%) were taking anticoagulant therapy, suggesting a failure to identify or treat atrial fibrillation.

This study describes the burden of TIA in an era of aggressive primary and secondary vascular risk factor management. Education programs for medical practitioners and patients around the identification and management of atrial fibrillation are required 3).

In a cohort study, patients with suspected TIA or minor stroke (National Institute of Health Stroke Scale <4) within 7 days after onset were prospectively enrolled and followed for 1 year. The high-risk group was defined as having at least one of the following 5 items at the initial visit: (1) atrial fibrillation, (2) carotid stenosis, (3) crescendo TIA, (4) definite focal brain symptoms, or (5) ABCD2 score of 4 or higher. After the initial assessment, the patients were diagnosed as having acute ischemic cerebrovascular syndrome (AICS) or stroke mimic. AICS was classified into 3 categories including definite, probable, and possible AICS, based on evidence of neurological deficits and brain infarction on the imaging study.

A total of 353 patients were enrolled and 89.8% of the patients were examined by diffusion-weighted imaging at the initial visit. Kaplan-Meier analyses demonstrated a statistically significant difference in subsequent stroke risk when the patients were triaged by the ABCD2 score (P = .031), 5-item high-risk categorization (P = .032), or AICS classification (P = .001).

This study demonstrates that hospitals and clinics with imaging facilities play a major role in triage and that the ABCD2 score, 5-item high-risk categorization, and AICS classification are useful as triage tools for patients with suspected TIA or minor stroke 4).

In ischemic stroke or patients with TIA less than five cerebral microbleeds (CMBs) should not affect antithrombotic decisions, although with more than five CMBs the risks of future ICH and ischaemic stroke are finely balanced, and antithrombotics might cause net harm. In lobar ICH populations, a high burden of strictly lobar CMBs is associated with cerebral amyloid angiopathy (CAA) and high ICH risk; antithrombotics should be avoided unless there is a compelling indication 5).

Among patients with minor stroke or TIA, marginal significant interactions between CYP2C19 *2 and *3 alleles carrier status and clopidogrel efficacy were found in smokers, but not in non-smokers. Among smokers, clopidogrel plus aspirin might decrease the recurrence rate of stroke in noncarriers of *2 and *3 alleles of CYP2C19 compared with aspirin alone. However, more caution should be taken to interpret this findings for several limitations in the study 6).

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; American Heart Association; American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; Interdisciplinary Council on Peripheral Vascular Disease. 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 Jun;40(6):2276-93. doi: 10.1161/STROKEAHA.108.192218. Epub 2009 May 7. Review. PubMed PMID: 19423857.
Sato S, Minematsu K. [Transient ischemic attack: past, present, and future]. Brain Nerve. 2013 Jul;65(7):729-38. Review. Japanese. PubMed PMID: 23832976.
Barber PA, Krishnamurthi R, Parag V, Anderson NE, Ranta A, Kilfoyle D, Wong E, Green G, Arroll B, Bennett DA, Witt E, Rush E, Minsun Suh F, Theadom A, Rathnasabapathy Y, Te Ao B, Parmar P, Feigin VL; ARCOS IV Study Group. Incidence of Transient Ischemic Attack in Auckland, New Zealand, in 2011 to 2012. Stroke. 2016 Sep;47(9):2183-8. doi: 10.1161/STROKEAHA.116.014010. Epub 2016 Jul 28. PubMed PMID: 27470991.
Taguchi H, Hasegawa Y, Bandoh K, Koyasu H, Watanabe Y, Yamashita K, Shimazaki K, Shima H, Miyakawa M, Niwa Y; COMBAT-TIA Study Investigators. Implementation of a Community-Based Triage for Patients with Suspected Transient Ischemic Attack or Minor Stroke Study: A Prospective Multicenter Observational Study. J Stroke Cerebrovasc Dis. 2016 Jan 13. pii: S1052-3057(15)00624-2. doi: 10.1016/j.jstrokecerebrovasdis.2015.11.013. [Epub ahead of print] PubMed PMID: 26775272.
Wilson D, Werring DJ. Antithrombotic therapy in patients with cerebral microbleeds. Curr Opin Neurol. 2016 Nov 24. [Epub ahead of print] PubMed PMID: 27898582.
Wang T, Pan Y, Lin J, Anand R, Wang D, Johnston SC, Meng X, Li H, Zhao X, Liu L, Wang Y, Wang Y; CHANCE investigators. Influence of smoking on CYP2C19 genetic variants and clopidogrel efficacy in patients with minor stroke or TIA. Eur J Neurol. 2019 Apr 11. doi: 10.1111/ene.13962. [Epub ahead of print] PubMed PMID: 30974489.
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