สมองขาดเลือดชั่วคราว Transient Ischaemic Attack (TIA)

สมองขาดเลือดชั่วคราวคืออะไร transient ischaemic attack(TIA )

โรค TIA หรือ โรคอัมพฤกษ์ชั่วคราว คือ โรคที่เกิดจากสมองสูญเสียหน้าที่ชั่วคราว โดยเกือบทั้งหมดเกิดจากเลือดไปเลี้ยงสมองไม่พอเพียงชัวคราว มีส่วนน้อยมากๆที่เกิดจากหลอดเลือดสมองแตก ซึ่งอาการส่วนใหญ่จะผิดปกตินานประมาณ 30 นาที – 1 ชั่วโมง โดยทุกคนจะหายเป็นปกติภายระยะเวลาประมาณใน 24 ชั่วโมง

หากมีการดังกล่าวจะเป็นอาการเตือนว่าโอกาศเกิดอัมพาตสูง

อาการของโรคสมองขาดเลือดชั่วคราวเป็นอย่างไร

อาการของภาวะสมองขาดเลือดชั่วคราว

อาการของภาวะสมองขาดเลือดชั่วคราวขึ้นกับบริเวณสมองที่ขาดเลือด อาการจะเหมือนกับโรคหลอดเลือดสมอง อาการดังกล่าวได้แก่

อ่อนแรง หรือชา แขนขาหรือใบหน้าครึ่งซีก
พูดลำบาก พูดไม่ชัด นึกคำพูดไม่ออก
เวียนศีรษะ ทรงตัวไม่ได้
ตามัว ตามองไม่เห็นเฉียบพลัน
ปวดศีรษะทันที
กลืนลำบาก

อาการดังกล่าวข้างต้นมักจะเกิดแบบเฉียบพลัน

อาการผิดปกติที่เกิดขึ้นจาก TIA มีอะไรบ้าง?

อาการผิดปกติที่พบจาก TIA ก็เหมือนอาการของโรคหลอดเลือดสมอง ได้แก่ แขน ขา อ่อนแรง ด้านใดด้านหนึ่งของร่างกาย ปากเบี้ยว หลับตาไม่สนิท พูดไม่ชัด พูดลำบาก นึกคำพูดไม่ออก วิงเวียนศีรษะ เดินเซ มองเห็นภาพซ้อน

หากเกิดอาการดังกล่าวจะต้องปฏิบัติอย่างไร

หากเกิดอาการเตือนโรคหลอดเลือดสมองดังกล่าวจะต้องรีบไปโรงพยาบาล

What should I do if I think I am having a TIA or mini stroke?

หากอาการดังกล่าวหายไป ยังต้องไปพบแพทย์หรือไม่

เมื่อเกิดอาการเตือนโรคหลอดเลือดสมองต้องรีบไปโรงพยาบาลให้เร็วที่สุด แต่หากอาการหายไปก่อนที่จะไปโรงพยาบาลก็ยังต้องไปโรงพยาบาล

What should I do if the signs go away?

You should seek medical attention immediately even if the signs go away and you feel completely better.

A TIA is a strong warning that a stroke may happen. Stroke can lead to death or long term disability. It can be prevented with changes to your lifestyle or with medication. Talk to your doctor about your treatment options.

What causes a TIA?

A TIA happens when blood going to the brain is stopped and then starts again. Blood is carried to the brain by blood vessels called arteries and a blood clot may cause a blockage that prevents blood moving through an artery. In some cases, a TIA may be caused by a small bleed in the brain.

When blood stops moving, the brain cannot get the oxygen and food it needs and brain cells in the area start to die. These cells usually die within minutes to a few hours after blood flow stops. Once blood flow starts again, the brain once again gets the oxygen and food it needs and the signs of TIA may disappear. Further clots may block blood flow to the brain for a short time (causing another TIA), or permanently (causing a stroke).

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A transient ischaemic attack (TIA) or "mini stroke" is caused by a temporary disruption in the blood supply to part of the brain.

The disruption in blood supply results in a lack of oxygen to the brain. This can cause symptoms similar to those of astroke, such as speech and visual disturbance and numbness or weakness in the arms and legs.

However, a TIA does not last as long as a stroke. The effects only last for a few minutes and are usually fully resolved within 24 hours.

F.A.S.T.

The main signs and symptoms of a TIA can be identified by remembering the word F.A.S.T., which stands for Face-Arms-Speech-Time.

Face – the face may have fallen on one side, the person may be unable to smile, or their mouth or eye may have dropped
Arms – the person may not be able to raise both their arms and keep them there due to weakness or numbness in their arms
Speech – the person may have slurred speech
Time – if any of these signs or symptoms are present, it is time to dial 999 immediately

If the above signs and symptoms last longer than 24 hours, it is regarded as a full stroke.

It is important that a person who has a TIA is checked and treated as soon as possible to minimise the risk of having a further TIA or a full stroke. With treatment, the risk of a further TIA or full stroke can be greatly reduced.

What causes a TIA?

สาเหตุของโรค TIA คือ

เลือดไปเลี้ยงสมองไม่พอเป็นการชั่วคราว โดยมักเกิดจากสาเหตุใหญ่ 3 ประการได้แก่

หลอดเลือดสมองที่แข็งตัว หรือตีบแคบ (โรคหลอดเลือดแดงแข็งAtherosclerosis) ร่วมกับมีการไหลเวียนของเลือดที่ลดลงชั่วคราว หลอดเลือดที่หนาตัวเนื่องจากมีคราบไขมันสะสมอยู่ในผนังหลอดเลือดทำให้หลอดเลือดหนาและแข็งไม่ยืดหยุ่น ทำให้เลือดไหลผ่านไปได้ยาก
เกิดจากมีลิ่มเลือดจากหัวใจขนาดเล็กหลุดมาอุดหลอดเลือดในสมอง
ส่วนน้อยมากๆที่เกิดจากหลอดเลือดขนาดเล็กในสมองแตก

Diagnosing a TIA

As TIAs are often over quickly, you may not have any symptoms by the time you see a healthcare professional.

You will be asked in detail about the symptoms you experienced during the TIA. For example, how long they lasted and how they affected you. This will help rule out other conditions.

If a TIA is suspected, you should be referred within seven days of the TIA to a specialist for tests.

Treating a TIA

Following a TIA, you will need treatment to help prevent another TIA or a full stroke.

Your treatment will depend on your individual circumstances, such as your age and medical history.Your healthcare team will discuss the treatment options with you, and tell you about possible benefits and risks.

You may be given medication or asked to make changes to your lifestyle (see the prevention advice below). In some cases, surgery may be needed.

Preventing a TIA

TIAs often occur without warning. If you have a TIA, it is a sign another one may follow and further TIAs can have more serious effects or develop into a full, life-threatening stroke.

Regardless of whether or not you have had a TIA or stroke in the past, there are a number of ways you can lower your risk of having either in the future. These include:

maintaining a healthy weight
eating healthily
taking regular exercise
limiting your alcohol consumption
not smoking

โรคคสมองขาดเลือดมาเลี้ยงชั่วคราว หรือเรียกย่อว่า โรคทีไอเอ (TIA,Transient ischemic attack) หรือที่คนทั่วไปเรียกว่าโรคอัมพฤกษ์ คือ อาการที่ผู้ป่วยมีอาการผิดปกติทางสมองแล้วหายเองได้ ซึ่งอาการดังกล่าว ปัจจุบันถือว่าเป็นปัจจัยเสี่ยงที่สำคัญของการเกิดโรคหลอดเลือดสมองชนิดขาดเลือด หรือโรคอัมพาต บทความนี้มีวัตถุประสงค์เพื่อสร้างความเข้าใจที่ถูกต้องเกี่ยวกับโรค TIA เพราะคนส่วนใหญ่ยังมีความเข้าใจที่ไม่ถูกต้องเกี่ยวกับ TIA หลายประเด็น ส่งผลต่อการรักษาและอาจก่อให้ เกิดความพิการหรือแม้กระทั่งการเสียชีวิตตามมาได้

โรค TIA คืออะไร?

อะไรเป็นสาเหตุให้เกิดโรค TIA?

ใครมีปัจจัยเสี่ยงที่จะเกิดสมองขาดเลือดชั่วคราว?

ปัจจัยเสี่ยงของโรค TIA คือ ปัจจัยเสี่ยงเดียวกับการเกิดโรคอัมพาต ได้แก่ ผู้ป่วยโรคเบาหวาน โรคความดันโลหิตสูง โรคไขมันในเลือดสูง โรคอ้วน ผู้ที่สูบบุหรี่ และ คนที่ไม่ออกกำลังกาย

โรค TIA มีอันตรายหรือไม่?

ถึงแม้ว่าอาการผิดปกติที่เกิดขึ้นดังได้กล่าวแล้วในหัวข้อ อาการ จะหายได้เอง แต่เป็นอันตรายอย่างยิ่ง เนื่องจากผู้ป่วยเป็นโรค TIA นี้มีโอกาสเกิดเป็นโรคอัมพาตจากโรคสมองขาดเลือด สูงถึง 1 ใน 3 ใน 1 เดือน หลังจากเกิดโรค TIA แพทย์วินิจฉัยได้อย่างไรว่าเป็น TIA?

ด้วยโรค TIA นั้น มีโอกาสเป็นอัมพาตได้สูงและที่สำคัญคือ ในขณะที่มีอาการนั้น เราไม่ทราบว่าจะเป็น TIA หรือกลายเป็นอัมพาต การรักษาโรคอัมพาตปัจจุบันนั้นที่เป็นมาตรฐานคือ ควรต้องรักษาภายใน 270 นาทีหลังเกิดอาการ (หรือที่เรียกว่า นาทีชีวิต หรือ Stroke Fast Track) ถ้าผู้ป่วยรอสังเกตอาการ ว่าจะหายหรือไม่หาย ถ้าไม่หายมาพบแพทย์ก็อาจมาช้าเกิน ไป ดังนั้น ถ้ามีอาการผิดปกติดังกล่าวในหัวข้อ อาการ ก็ควรรีบไปพบแพทย์ที่โรงพยาบาลทันที

แพทย์วินิจฉัยได้อย่างไรว่าเป็น TIA?

แพทย์จะทำการวินิจฉัยโรค TIA จากประวัติผู้ป่วยที่มีอาการผิดปกติ การตรวจวัดสัญ ญาณชีพ (ความดันโลหิต การตรวจจับชีพจร อัตราการหายใจ และอุณหภูมิของร่างกาย) และการตรวจร่างกายทางระบบประสาท เช่น แขนขาอ่อนแรงด้านใดด้านหนึ่งของร่างกาย พูดไม่ชัด ปากเบี้ยว โดยอาการผิดปกตินั้นเป็นนานประมาณ 30-60 นาที ถ้านานกว่านั้นก็ไม่เกิน 24 ชั่ว โมง และอาจมีการตรวจอื่นๆเพิ่มเติม ทั้งนี้ขึ้นกับอาการผิดปกติของผู้ป่วยที่แพทย์ตรวจพบและดุลพินิจของแพทย์ เช่น การตรวจเลือดดูปัจจัยเสี่ยงต่างๆ เช่น น้ำตาลในเลือด และ/หรือค่าไข มันในเลือด และการตรวจภาพสมองและ/หลอดเลือดสมองด้วย เอกซเรย์คอมพิวเตอร์ และ/หรือเอมอาร์ไอ

มีวิธีรักษาโรค TIA อย่างไร?

การรักษาโรค TIA คือ การให้ทานยาต้านเกล็ดเลือด หรือยาละลายลิ่มเลือดขึ้นอยู่กับสาเหตุ/ปัจจัยเสี่ยงของการเกิดโรค รวมทั้งการรักษาปัจจัยเสี่ยงข้างต้นที่ได้กล่าวแล้วในหัวข้อ ปัจจัยเสี่ยงถ้าผู้ป่วยมีปัจจัยเสี่ยง เช่น รักษาควบคุมโรคเบาหวาน เป็นต้น

ผู้ป่วยโรค TIA คนไหนที่มีโอกาสเป็นโรคอัมพาต?

จากเครื่องมือคัดกรองที่เรียกว่า ABCD2 Score มีการทำนายได้ค่อนข้างแม่นยำว่า ใครที่เมื่อเกิดอาการจาก TIA แล้ว มีปัจจัยเสี่ยงสูงต่อการเกิด อัมพาต ซึ่งเครื่องมือคัดกรองนี้ ประ กอบด้วย 5 ปัจจัยสำคัญ ดังต่อไปนี้

Age: อายุ มากกว่า 60 ปี Blood pressure:
ความดันโลหิตสูง มากกว่า 140/90 มม.ปรอท
Clinical sign/อาการผิดปกติที่เกิดขึ้น: มีความผิดปกติทางระบบประสาท คือ แขนขาอ่อนแรง พูดไม่ชัด พูดลำบาก
Duration: ระยะเวลาที่มีอาการนานเท่าไหร่ ยิ่งมีอาการอยู่นาน
ปัจจัยเสี่ยงยิ่งสูง Diabetes: เป็นโรคเบาหวาน

ทั้งนี้โดย อายุตั้งแต่ 60 ปีขึ้นไปมีค่า 1 คะแนน ความดันโลหิตสูงกว่า 140/90 มก.ปรอท มีค่า 1 คะแนน ความผิดปกติทางระบบประสาท แขนขาอ่อนแรงด้านใดด้านหนึ่ง มีค่า 2 คะแนน พูดไม่ชัด พูดลำบากและไม่อ่อนแรง มีค่า 1 คะแนน อื่นๆ มีค่า 0 คะแนน ระยะเวลาที่เกิดอาการ ถ้าสั้นกว่า 10 นาที มีค่า 0 คะแนน 10 – 59 นาที มีค่า 1 คะแนน ตั้งแต่ 60 นาที มีค่า 2 คะแนน ถ้ารวมคะแนนทั้งหมดแล้ว ค่าคะแนนสูง ยิ่งมีโอกาสเกิดโรคอัมพาตได้สูง

หลังจากไปพบแพทย์แล้วก็ปกติดี ควรดูแลสุขภาพอย่างไร?

การดูแลสุขภาพในผู้ป่วย TIA เหมือนกับการดูแลผู้ป่วยเป็นอัมพาต (โรคหลอดเลือดสมอง) เลยครับ คือ ต้องตรวจสุขภาพประจำปี ดูแลรักษา ควบคุม โรคประจำตัวที่เป็นอยู่ เช่น โรคเบาหวาน โรคความดันโลหิตสูง โรคไขมันในเลือดสูง ไม่ควรสูบบุหรี่ ถ้าสูบอยู่ควรต้องเลิกสูบ ไม่ควรดื่มแอลกอฮอล์ ถ้าดื่มอยู่ควรต้องค่อยๆเลิก และเลิกดื่มในที่สุดและ ออกกำลังกายสม่ำเสมอตามควรกับสุขภาพ

ต้องรับประทานยาต้านเกล็ดเลือดหรือไม่? ในโรค TIA จำเป็นต้องรับประทานยาต้านเกล็ดเลือด เพื่อลดโอกาสการเกิดอาการซ้ำ และลดโอกาสเกิดอัมพาต (โรคหลอดเลือดสมอง) ปัจจุบันมีการศึกษา ยืนยันประสิทธิภาพยาแอสไพริน (Aspirin) คู่กับยาโคลพิโดเกล (Clopidogrel) โดยใช้ยานานประมาณ 90 วันนับจากเกิดอาการ และหลังจากนั้นทานแอสไพรินวันละ 1 เม็ด ขนาด 81 มิลลิกรัมตลอดไป เมื่อท่านทราบอย่างนี้แล้วอย่านิ่งนอนใจนะครับ ถ้ามีอาการผิดปกติให้รีบไปโรงพยาบาลพบแพทย์ทันที

ป้องกันโรค TIA ได้อย่างไร?

การป้องกันโรค TIA คือ การควบคุมดูแลรักษาปัจจัยเสี่ยงดังกล่าวข้างต้นในหัวข้อ ปัจจัยเสี่ยงให้ดี และถ้ามีอาการผิดปกติดังกล่าวในหัวข้อ อาการ ต้องรีบมาโรงพยาบาลพบแพทย์

NTRODUCTION — Patients with transient ischemic attack (TIA) or minor (ie, nondisabling) stroke are at increased risk of recurrent stroke, and therefore require urgent evaluation and treatment since immediate intervention may substantially reduce the risk of recurrent stroke.

This topic will review the diagnostic approach and early management of TIA and minor, nondisabling ischemic stroke.

Other aspects of transient cerebral ischemia are discussed separately. (See "Definition of transient ischemic attack" and "Etiology and clinical manifestations of transient ischemic attack" and "Differential diagnosis of transient ischemic attack and stroke".)

The management of patients hospitalized with acute stroke is reviewed elsewhere. (See "Initial assessment and management of acute stroke".)

How is TIA defined? — Transient ischemic attack (TIA) is now defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction [1,2]. The end point, stroke, is biologic (tissue injury) rather than arbitrary (≥24 hours). In keeping with this definition of TIA, ischemic stroke is defined as an infarction of central nervous system tissue.

TIA was originally defined as a sudden onset of a focal neurologic symptom and/or sign lasting less than 24 hours and caused by reversible cerebral ischemia. However, this classic definition of TIA was inadequate for several reasons. Most notably, there is risk of permanent tissue injury (ie, infarction) even when focal transient neurologic symptoms last less than one hour. Furthermore, about one-half of patients with classically defined TIA syndromes (<24 hours in duration) have corresponding appropriate ischemic lesions by brain MRI on diffusion-weighted or perfusion-weighted imaging. (See "Definition of transient ischemic attack", section on 'Relationship of symptom duration and infarction'.)

Thus, the benign connotation of the term TIA has been replaced by an understanding that even relatively brief ischemia can cause permanent brain injury.

Although the revised tissue-based definition is favored by guidelines, the traditional time-based definition of TIA is still widely used in clinical practice.

How is minor stroke defined? — Minor ischemic stroke has been defined in various ways, most often by a low score on the National Institutes of Health Stroke Scale (NIHSS) [3,4], and there is no unified definition. We prefer to define minor stroke by the absence of a persistent neurologic deficit that is potentially disabling. Any of the following should be considered disabling deficits [5]:

●Complete hemianopia: ≥2 on the NIHSS question 3 (table 1)

●Severe aphasia: ≥2 on NIHSS question 9

●Visual or sensory extinction: ≥1 on NIHSS question 11

●Any weakness limiting sustained effort against gravity: ≥2 on NIHSS question 5 or 6

●Any deficits that lead to a total NIHSS >5 (calculator 1)

●Inability to walk

●Any remaining deficit considered potentially disabling by the patient, family, or the treating practitioner

Patients who present within the appropriate time window after ischemic symptom onset with a persistent neurologic deficit that is potentially disabling, despite improvement of any degree, should be treated with intravenous thrombolysis in the absence of other contraindications (table 2). (See "Intravenous fibrinolytic (thrombolytic) therapy in acute ischemic stroke: Therapeutic use".)

The presence of persistent but minor, nondisabling neurologic deficits is the main factor that distinguishes minor ischemic stroke from TIA. However, both are associated with an increased risk of recurrent ischemic stroke [6,7]. This increased risk of stroke may be more related to the presence of infarction on diffusion-weighted MRI studies than to the duration of minor neurologic deficit.

URGENT EVALUATION — Patients who have a suspected transient ischemic attack (TIA) require urgent evaluation (algorithm 1) due to the high stroke risk associated with TIA [1]. Furthermore, immediate intervention after a TIA may prevent a significant number of strokes. (See 'Risk of recurrent stroke' below and'Immediate treatment' below.)

The diagnosis of TIA (defined by the absence of tissue infarction) is clinical, and is based upon a determination that the symptoms of the attack are more likely caused by brain ischemia than another cause. This determination can be challenging and is usually subjective because the symptoms of TIA are transient, highly variable (table 3), and often minor. (See "Differential diagnosis of transient ischemic attack and stroke", section on 'Symptoms of TIA' and "Differential diagnosis of transient ischemic attack and stroke", section on 'Distinguishing transient attacks'.)

The initial evaluation of suspected TIA and minor (ie, nondisabling) ischemic stroke includes basic laboratory studies that are suggested by the history and physical examination, an electrocardiogram, brain imaging, and neurovascular imaging. Laboratory testing is helpful in ruling out metabolic and hematologic causes of neurologic symptoms, including hypoglycemia, hyponatremia, and thrombocytosis.

Several neurologic disorders give rise to transient focal neurologic symptoms, and these should be considered before establishing a diagnosis of TIA. In addition to TIAs, the most important and frequent causes of discrete self-limited attacks include:

●Seizures

●Migraine auras

●Syncope

Less frequent causes include:

●Peripheral vestibulopathies that cause transient episodic dizziness

●Pressure- or position-related peripheral nerve or nerve root compression that causes transient paresthesia and numbness

●Metabolic perturbations such as hypoglycemia and hepatic, renal, and pulmonary encephalopathies that can produce temporary aberrations in behavior and movement

●Transient global amnesia

The differential diagnosis is discussed in greater detail elsewhere. (See "Differential diagnosis of transient ischemic attack and stroke".)

Hospital or outpatient evaluation? — Whether hospitalization is required for TIA evaluation is not clear, but urgent assessment and management is essential regardless of inpatient or outpatient status [1,8-12]. Possible advantages of hospitalization include facilitated early use of thrombolytic therapy and other medical management if symptoms recur, expedited TIA evaluation, and expedited institution of secondary prevention [8].

We suggest hospitalization for patients with a first TIA within the past 72 hours if any of the following conditions are present:

●High risk of early stroke after TIA as suggested by:

•The presence of a known cardiac, arterial, or systemic etiology of brain ischemia that is amenable to treatment

•The presence of acute infarction on diffusion-weighted MRI (see 'Importance of infarction' below)

•Certain other clinical and imaging features (table 4) (see 'Risk stratification' below)

●Uncertainty that the diagnostic workup can be completed within two days as an outpatient

●Concurrent serious acute medical issues

Patients who need urgent evaluation and are not hospitalized should have rapid access to the following studies:

●Brain imaging with head CT and/or MRI

●Neurovascular studies such as CT angiography (CTA), MR angiography (MRA), and/or ultrasound

●Electrocardiogram (ECG)

All patients with a TIA within the past two weeks who are not hospitalized should undergo investigations within 24 to 48 hours to determine the mechanism of ischemia and subsequent preventive therapy. Patients who are not admitted should be informed that they need to go to an Emergency Department immediately if symptoms recur.

The 2009 American Heart Association and American Stroke Association (AHA/ASA) guidelines for the definition and evaluation of TIA state that it is reasonable to hospitalize patients with TIA who present within 72 hours of symptom onset and meet any of the following criteria [1]:

●ABCD2 score (table 5) of ≥3

●ABCD2 score of 0 to 2 and uncertainty that the diagnostic workup can be completed within two days as an outpatient

●ABCD2 score of 0 to 2 and other evidence that the event was caused by focal ischemia

The ABCD2 score (ie, ABCD squared, for Age, Blood pressure, Clinical features, Duration of symptoms, and Diabetes) is a simple prognostic assessment tool with moderate predictive accuracy that was designed to identify patients at high risk of ischemic stroke in the first two days after TIA, as discussed later in detail (table 5). (See 'Risk stratification' below.)

Hospital admission for TIA may be cost effective compared with no admission or specific intervention, particularly for high-risk patients eligible for intravenous (IV) tPA treatment. Supporting evidence comes from a cost-utility analysis of 24-hour hospitalization in the United States for patients diagnosed with recent TIA [13]. The study assumed that only those patients without absolute contraindications for IV tPA treatment would be admitted, and that hospitalized patients who developed a new stroke would be identified and treated with tPA within one hour of stroke onset. The overall cost effectiveness ratio was 55,044 dollars per quality adjusted life year, a value considered borderline cost effective. However, admission was cost effective for patients with a 24-hour stroke risk >5 percent. In contrast, a subsequent report found that hospital admission for TIA was not cost effective in the United States compared with urgent (same-day) outpatient clinic evaluation [14], despite increased access to tPA in the hospital.

Brain imaging studies — Brain imaging with MRI or CT is indicated in all patients with suspected TIA or minor (nondisabling) stroke as soon as possible, particularly those with symptoms suggestive of hemispheric TIA [1,8]. Brain MRI with diffusion-weighted imaging has a greater sensitivity than CT for detecting small infarcts in patients with TIA; thus CT is a suboptimal alternative. The 2009 AHA/ASA guidelines recommend neuroimaging within 24 hours of symptom onset and further recommend MRI and diffusion-weighted MR imaging as preferred modalities [1]. Head CT is recommended if MRI cannot be performed.

The presence of a brain infarct on MRI or CT scan located in an area suggested by the anatomy of the TIA or stroke (eg, in the left precentral gyrus or left internal capsule in a patient with transient right arm and leg weakness) identifies a vascular etiology of symptoms. Many patients whose clinical history and neurologic examination suggest that an attack was transient have infarcts in brain areas appropriate to the neurologic symptoms. (See "Definition of transient ischemic attack", section on 'Relationship of symptom duration and infarction'.)

Infarction is more likely to be identified acutely on MRI than on CT. Diffusion-weighted MRI imaging (DWI) and the apparent diffusion coefficient (ADC) map that is derived from DWI can discriminate tissue injury very early after the onset of ischemic symptoms. In most but not all cases of TIA and minor (nondisabling) stroke, early DWI and ADC can confirm whether only ischemia has occurred or if there has also been an element of infarction, thereby differentiating stroke from TIA within the first hours after symptom onset. (See "Neuroimaging of acute ischemic stroke", section on 'CT versus MRI techniques in hyperacute stroke'.)

Other diseases that mimic TIAs may be identified by neuroimaging techniques, although pathological biopsy examination is occasionally needed (eg, temporal artery biopsy or examination of the cerebrospinal fluid). In rare cases, brain biopsy is indicated. (See "Differential diagnosis of transient ischemic attack and stroke".)

Neurovascular evaluation — The single most important issue to resolve in the initial evaluation of TIA and ischemic stroke is whether or not there is an obstructive lesion in a larger artery supplying the affected territory. Noninvasive options for evaluation of large vessel occlusive disease include magnetic resonance angiography (MRA), computed tomography angiography (CTA), carotid duplex ultrasonography (CDUS), and transcranial Doppler ultrasonography (TCD). The choice among these depends upon local availability and expertise as well as individual patient characteristics and preference [1]. (See "Neuroimaging of acute ischemic stroke".)

The 2009 AHA/ASA guidelines recommend routine noninvasive imaging of the cervicocephalic vessels as part of the evaluation of patients with suspected TIA [1]. The guidelines note that it is reasonable to obtain noninvasive testing of the intracranial vasculature if knowledge of an intracranial stenosis or occlusion will alter management.

Although noninvasive studies are considered reliable for the exclusion of intracranial stenosis, the 2009 AHA/ASA guidelines conclude that reliable diagnosis of the presence and degree of intracranial stenosis requires evaluation with catheter angiography to confirm abnormalities detected with noninvasive testing [1].

A focused Doppler and neuroimaging test (eg, MRA or CTA) can be used to establish an arterial source of the embolism or low flow. These tests can exclude an arterial source in cases where the symptoms are due to proximal embolism from the heart, aorta, or an unknown source, and in cases where the symptoms are due to small vessel disease (see "Evaluation of carotid artery stenosis"). The following are important aspects regarding such testing:

●Duplex ultrasound and transcranial Doppler studies require considerable technical skill to perform and an experienced interpreter. They should be used only if there is adequate confidence that the testing and interpretation is reliable.

●Conventional angiography is associated with a small risk of stroke and should be performed by experienced physicians. It should only be considered when the diagnosis is uncertain by noninvasive methods, and when proof of the diagnosis is essential for proper stroke preventive therapy. As an example, if one of the stroke-producing arterial lesions noted above is suspected but not confirmed by conventional noninvasive Doppler, MRI, or CT methods, then angiography can be considered.

The distinction between artery-to-artery and other (mainly cardiac) sources of embolism can be difficult. Suspicion of the former typically arises once vascular pathology in a large vessel has been identified (eg, with noninvasive testing). Repetitive spells within a single vascular territory are also suggestive of an artery-to-artery source, as is a normal echocardiogram.

Cardiac evaluation — A possible cardiac source should be considered in patients with TIA or ischemic stroke caused by embolism. At minimum, such patients should have a standard 12-lead electrocardiogram as soon as possible after symptom onset [1].

Cardiac monitoring is an essential part of evaluation to exclude atrial fibrillation in the setting of embolic TIA or stroke. Cardiac rhythm monitoring with inpatient telemetry or Holter monitor is useful for patients without a clear etiology after initial brain imaging and electrocardiography [1]. For patients with a cryptogenic TIA and no evidence of atrial fibrillation on ECG and 24-hour cardiac monitoring, we suggest ambulatory cardiac monitoring for several weeks [2]. (See "Overview of the evaluation of stroke", section on 'Monitoring for occult atrial fibrillation'.)

Echocardiography is reasonable when no cause for TIA or ischemic stroke has been identified by other aspects of the work-up [1]. TTE is the preferred initial test for the majority of patients with a suspected cardiac or aortic source of emboli, including (see "Echocardiography in detection of cardiac and aortic sources of systemic embolism", section on 'Choosing between TTE and TEE'):

●Patients ≥45 years with a cerebrovascular event

●Patients with a high suspicion of left ventricular thrombus

●Patients in whom TEE is contraindicated (eg, esophageal stricture, unstable hemodynamic status) or who refuse TEE

TEE is the preferred initial test to localize the source of embolism in the following circumstances:

●Patients <45 years without known cardiovascular disease (ie, absence of myocardial infarction or valvular disease history)

●Patients with a high pretest probability of a cardiac embolic source (table 6) in whom a negative TTE would be likely to be falsely negative

●Patients with atrial fibrillation and suspected left atrial or left atrial appendage thrombus, especially in the absence of therapeutic anticoagulation, but only if the TEE would impact management

●Patients with a mechanical heart valve

●Patients with suspected aortic pathology

The use of echocardiography for the detection of cardiac sources of embolism is discussed in greater detail separately. (See "Echocardiography in detection of cardiac and aortic sources of systemic embolism".)

Blood cultures, an erythrocyte sedimentation rate, or antinuclear antibody testing are indicated if bacterial or nonbacterial endocarditis is suspected.

Blood tests — In patients with suspected TIA, the following blood tests should be considered [1,8,15]:

●Complete blood count (CBC)

●Prothrombin time and partial thromboplastin time

●Serum electrolytes and creatinine

●Fasting blood glucose and lipids

●Erythrocyte sedimentation rate (ESR)

Suspicion for blood disorders as potential sources of cerebral ischemia should be raised in the following settings [15]:

●Cryptogenic stroke or TIA

●Age 45 or younger

●History of clotting dysfunction

●Multiple venous and arterial occlusions

●Suspected or confirmed cancer

●Family history of thrombotic events

In these settings, additional blood and coagulation studies should be considered. This topic is discussed elsewhere. (See "Overview of the evaluation of stroke", section on 'Blood tests'.)

RISK OF RECURRENT STROKE — TIA is a neurologic emergency because patients with TIA and minor (ie, nondisabling) stroke are at increased risk of recurrent stroke. This risk is illustrated by the following studies:

●A meta-analysis of 11 observational studies published through December 2006 found that the risk of stroke at 2 days, 30 days, and 90 days after TIA was 3.5, 8.0, and 9.2 percent, respectively [16]. In the three studies that used active ascertainment of stroke outcome (ie, face-to-face evaluation by a practitioner at three months rather than use of administrative data), the 2, 30, and 90 day risk of stroke after TIA was even higher (9.9, 13.4, and 17.3 percent, respectively). Similar findings were reported in a meta-analysis of 18 cohorts published through June 2007 [17].

●A well-designed prospective cohort study of 2447 participants from the Dutch TIA trial, published in 2005, found that the risk for major vascular events and stroke was highest shortly after TIA or minor stroke, declined to its lowest point at about three years, and then progressively increased over the remainder of the 10-year follow-up (figure 1) [18]. In contrast, the risk for mortality gradually rose throughout the study. By 10 years, 60 percent had died and 54 percent had experienced new vascular events (stroke and myocardial infarction). Event-free survival was 48 percent. Predictive factors for risk of vascular events and death included age over 65 years, diabetes, claudication, previous vascular surgery, and pathologic Q waves on baseline electrocardiogram.

●In a 2016 report from the TIAregistry.org project, a prospective multinational registry of over 4700 patients with TIA or minor stroke (defined by a modified Rankin scale score of 0 or 1 when first evaluated), the estimated risks of stroke at days 2, 30, 90, and 365 after the index event were 1.5, 2.8, 3.7, and 5.1 percent, respectively [19]. These rates are lower than those previously reported, possibly due to the more rapid implementation of newer and more effective strategies for the secondary prevention of ischemic stroke; the registry included only sites with dedicated systems for the urgent evaluation of TIA, and most patients were seen by a stroke specialist within 24 hours of symptom onset. Independent risk factors for recurrent stroke were multiple infarctions on brain imaging, large artery atherosclerosis, and an ABCD2 score of 6 or 7. (See 'Risk stratification' below.)

The urgency associated with TIA derives also from the observation that TIAs are most likely to occur in the hours and days immediately preceding ischemic stroke. As an example, a study that analyzed four cohorts of patients who had recent ischemic stroke found that TIAs occurred most often in the 48 hours prior to the stroke [20]. Another study found that the risk of ischemic stroke occurring within 24 hours of a probable or definite TIA was approximately 5 percent [21]. Of all ischemic strokes during the 30 days after a first TIA, 42 percent occurred within the first 24 hours. This may be an overestimate related to the difficulty distinguishing a single ischemic event (stroke) with fluctuating symptoms from separate events (TIA followed by stroke) within a short period of time. Nevertheless, these observations underscore the high early risk of developing a permanent deficit after transient ischemic symptoms and the importance of urgent assessment, risk stratification, and treatment.

Given this short time window and high risk of stroke (1.5 to 3.5 percent in the first 48 hours after TIA [16,19]) neurologic evaluation of and intervention for TIA should occur urgently. Furthermore, clinical TIAs associated with evidence of infarction by neuroimaging may be a marker of particularly high risk for ischemic stroke. (See "Definition of transient ischemic attack".)

Recognition and urgent evaluation of TIAs can identify patients who may benefit from preventive therapy or from revascularization of large vessels such as the carotid artery. As examples, premonitory carotid territory TIAs occur in approximately 50 to 75 percent of patients with ischemic stroke from extracranial carotid disease [22-24], and vertebrobasilar TIAs are associated with a risk of subsequent stroke or death that is similar to or possibly higher than that seen with carotid TIAs [25].

TIA etiology — TIA caused by vascular pathologies (ie, large artery atherosclerosis and small vessel disease) appears to confer a higher risk of subsequent stroke than cardiac and other nonvascular subtypes of TIA. However, the available evidence is not entirely consistent:

●In a prospective series of 410 patients with TIA, the large artery atherosclerosis subtype of TIA was associated with a higher risk of stroke recurrence at 7 and 90 days than other TIA subtypes (cardioembolism, small vessel disease, undetermined, or other determined cause) [26]. In addition, the prospective TIAregistry.org project found that large artery atherosclerosis was an independent risk factor for recurrent stroke [19].

●A prospective population-based study from Ireland found that carotid stenosis ≥ 50 percent was an independent predictor of stroke at 90 days after TIA, whereas no association was observed between atrial fibrillation and subsequent stroke [27].

●Another prospective population-based study from the United Kingdom reported that TIA due to small vessel vasculopathy was associated with a higher risk of early stroke than TIA due to other causes [28]. The stroke risk was particularly elevated after multiple stereotyped small vessel TIAs occurring in a brief period of time and characterized by motor or sensory symptoms but no cortical signs, the so-called "capsular warning syndrome" [29] or "stuttering lacunar syndrome." Although data are limited, the risk of early (within seven days) stroke after such events may be >40 percent [28,29].

Risk stratification — Methods that can reliably assess the risk of stroke after TIA in individual patients would be useful for triaging patients. The discussion that follows applies to the traditional time-based definition of TIA, which is characterized clinically by the temporary nature (<24 hours) of the associated neurologic symptoms.

A simple though imperfect assessment called the ABCD2 score (ie, ABCD squared, for Age, Blood pressure, Clinical features, Duration of symptoms, and Diabetes) was designed to identify patients at high risk of ischemic stroke in the first seven days after TIA [30]. The ABCD2 score is tallied as follows:

●Age (≥60 years = 1 point)

●Blood pressure elevation when first assessed after TIA (systolic ≥140 mmHg or diastolic ≥90 mmHg = 1 point)

●Clinical features (unilateral weakness = 2 points; isolated speech disturbance = 1 point; other = 0 points)

●Duration of TIA symptoms (≥60 minutes = 2 points; 10 to 59 minutes = 1 point; <10 minutes = 0 points)

●Diabetes (present = 1 point)

The ABCD2 score was based upon two earlier prognostic scores for TIA (the California score [31] and the ABCD score [32]) and was derived and validated using independent study populations (two derivation and four validation cohorts) from the US (California) and the UK (Oxford) that included 4809 patients with TIA [30]. The unified ABCD2 score was a slightly more accurate predictor of stroke risk than either of its predecessors in these populations.

Estimated two-day stroke risks determined by the ABCD2 score in the combined derivation and validation cohorts were as follows [30]:

●Score 6 to 7: High two-day stroke risk (8 percent)

●Score 4 to 5: Moderate two-day stroke risk (4 percent)

●Score 0 to 3: Low two-day stroke risk (1 percent)

The ABCD2 score was designed to be used in primary care settings to stratify patients according to stroke risk and thus identify those who required emergency assessment by specialists. However, its predictive performance is not optimal, as illustrated by the following observations:

●A systematic review and meta-analysis of 29 studies that included over 13,700 patients with TIA found that the ABCD2 score did not reliably distinguish those with a low and high risk of recurrent stroke, or those with TIAs and TIA mimics [33].

●An earlier meta-analysis found that the score performance was poor in settings of low baseline risk and in TIA diagnosed by nonspecialists [34].

●The predictive power of the ABCD2 score is generally lower in hospital settings compared with population-based settings, thus limiting its utility for high-risk populations [30,35,36].

Importance of infarction — There is accumulating evidence suggesting that the findings of acute infarction on diffusion-weighted MRI (DWI) [37-41] or acute or chronic ischemic lesions on CT [42] after a transient ischemic event are important predictors of stroke. In patients with an imaging-positive transient event, the 90 day risk of stroke appears to be as high as 14 percent [37-39,43]. In contrast, after an imaging-negative transient event, the corresponding risk is <1 percent.

Risk models that combine information from acute DWI, noninvasive angiography, and presumed TIA etiology improve the accuracy of stroke risk prediction after TIA [37,38,44-48]. There are a number of examples:

●Several scores are based upon the conventional ABCD2 score:

•The Clinical- and Imaging-based Prediction (CIP) model incorporates diffusion-weighted MRI findings with a dichotomized ABCD2 score [37].

•The ABCD2I score adds information about brain infarction on diffusion-weighted MRI or CT [44].

•The ABDC3-I score assigns points for an earlier TIA within seven days of the index event and further incorporates data from initial diagnostic brain and carotid imaging [45].

●The Recurrence Risk Estimator (RRE) score combines clinical (recent history of stroke or TIA plus admission stroke subtype) and imaging information [46] for predicting recurrent stroke following traditionally defined ischemic stroke and following TIA with infarction [49,50]. The RRE score was externally validated in a multicenter cohort of over 1400 patients with acute ischemic stroke [51].

Additional research and validation of these models is needed to determine whether these stroke risk stratification models have any utility for clinical practice. The requirement for MRI limits the widespread applicability of advanced risk prediction models.

IMMEDIATE TREATMENT — We recommend that appropriate diagnostic evaluation and stroke prevention treatment be implemented without delay, preferably within one day of the ischemic event, for patients who present with TIA or minor (nondisabling) ischemic stroke.

Accumulating evidence suggests that immediate intervention after a TIA or minor (nondisabling) ischemic stroke can reduce the risk of recurrent stroke compared with delayed intervention. This point is illustrated by the following reports:

●The prospective EXPRESS study evaluated the impact of expediting outpatient treatment for TIA or minor ischemic stroke [52]. In order to compare traditional with expedited treatment, the study was conducted in two phases. In phase one, 323 patients were seen in a traditional clinic setting where evaluation required a scheduled appointment and treatment recommendations were made to referring physicians. In phase two, 297 patients were seen in an urgent walk-in stroke clinic without having to arrange an appointment, and treatment was implemented immediately by clinic practitioners. In both phases, treatment of confirmed TIA or stroke was individualized according to patient characteristics, but generally included antiplatelet or anticoagulant therapy, statin therapy, antihypertensive medication, and carotid endarterectomy as required. Although EXPRESS was not a randomized trial, the study was nested in an ongoing population-based study of stroke and TIA, thus minimizing the potential problems of incomplete ascertainment and selection bias that complicate observational studies. The following observations were reported [52]:

•The median delay to assessment in the outpatient clinic was significantly reduced from phase one to phase two (3 days versus <1 day), as was the median delay to first prescription of treatment (20 days versus 1 day)

•The risk of recurrent stroke at 90 days was significantly lower for patients seen in phase two than for those seen in phase one (2.1 versus 10.3 percent; adjusted hazard ratio 0.20, 95% CI 0.08-0.49)

●The observational SOS-TIA study analyzed the rapid assessment of 1085 patients with suspected TIA in a hospital-based clinic with 24 hour access [53]. Patients were evaluated within four hours of admission, and those with a final diagnosis of confirmed or possible TIA (n = 845) received immediate treatment with a stroke prevention program that included antiplatelet or anticoagulant treatment and/or carotid revascularization as appropriate. At 90 days, the observed stroke rate was much lower than an expected stroke rate predicted by the ABCD2 scores (1.24 versus 5.96 percent). (See 'Risk stratification' above.)

The results of this study should be interpreted with caution because of methodologic limitations, including the use of ABCD2 scores to predict stroke risk, rather than determination of stroke risk in a control population [54].

Early evaluation and intervention for symptomatic carotid artery disease may be an important aspect of stroke prevention. Supporting evidence comes from a pooled analysis of the NASCET and ECST trials, which found that early carotid endarterectomy (within two weeks of a nondisabling stroke or TIA) significantly improved outcome compared with later surgery [55]. Thus, early identification of symptomatic carotid disease is critical. (See "Management of symptomatic carotid atherosclerotic disease", section on 'Timing of surgery'.)

Treatment by etiology — The preferred approach to the management of TIA and ischemic stroke is to determine the pathophysiology of the event and treat accordingly. This is reviewed here briefly and discussed in detail elsewhere. (See "Secondary prevention for specific causes of ischemic stroke and transient ischemic attack".)

●Options for the secondary prevention of TIA or ischemic stroke caused by large artery disease include revascularization (mainly for symptomatic cervical internal carotid artery stenosis) and intensive medical therapy (ie, antiplatelet, antihypertensive, and statin therapy) for multifactorial risk reduction. (See"Secondary prevention for specific causes of ischemic stroke and transient ischemic attack", section on 'Large artery disease'.)

●Selected patients with recently symptomatic cervical internal carotid stenosis of 50 to 99 percent who have a life expectancy of at least five years are generally treated with carotid endarterectomy. For patients with TIA or ischemic stroke having carotid endarterectomy, we recommend aspirin at a dose of 81 to 325mg/day started before surgery. (See "Management of symptomatic carotid atherosclerotic disease" and "Carotid endarterectomy", section on 'Aspirin'.)

●For patients with TIA or stroke caused by small vessel disease, medical management (ie, antiplatelet, antihypertensive, and statin therapy) is the mainstay for secondary stroke prevention. (See "Secondary prevention for specific causes of ischemic stroke and transient ischemic attack", section on 'Small artery occlusion'.)

●For patients with TIA or ischemic stroke of atherothrombotic, lacunar (small vessel occlusive), or cryptogenic type, we recommend treatment with an antiplatelet agent. This issue and the choice among specific antiplatelet agents (ie, aspirin, the combination aspirin-extended-release dipyridamole, orclopidogrel) are discussed separately. (See "Antiplatelet therapy for secondary prevention of stroke".)

●For most patients with atrial fibrillation and a recent ischemic stroke or TIA, we recommend oral anticoagulation. We recommend aspirin for patients with atrial fibrillation and cardioembolic stroke who have contraindications to anticoagulant therapy. (See "Atrial fibrillation: Anticoagulant therapy to prevent embolization".)

Risk factor management — Risk factor management is appropriate for all patients with ischemic stroke or TIA, and most patients should be treated with all available risk reduction strategies. Currently viable strategies include blood pressure reduction, statins, antithrombotic therapy, and lifestyle modification, including smoking cessation. These interventions are discussed in greater detail separately. (See "Overview of secondary prevention of ischemic stroke".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient information: Stroke (The Basics)" and "Patient information: Transient ischemic attack (The Basics)")

●Beyond the Basics topics (see "Patient information: Stroke symptoms and diagnosis (Beyond the Basics)" and "Patient information: Transient ischemic attack (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●The initial evaluation of suspected TIA and minor (ie, nondisabling) ischemic stroke includes urgent brain imaging, neurovascular imaging, and a cardiac evaluation (algorithm 1). Laboratory testing is helpful in ruling out metabolic and hematologic causes of neurologic symptoms. (See 'Urgent evaluation' above.)

●TIA and minor ischemic stroke are associated with a high early risk of recurrent stroke. The stroke risk in the first two days after TIA is approximately 4 to 10 percent. The ABCD2 score (table 5) was designed to identify patients at high risk of ischemic stroke in this time period, but its predictive performance is not optimal. Risk stratification models that combine information from brain imaging, neurovascular imaging, and presumed TIA etiology in addition to the clinical ABCD2 score may improve the accuracy of stroke risk prediction after TIA. (See 'Risk of recurrent stroke' above.)

●Accumulating evidence suggests that immediate evaluation and intervention after a TIA or minor ischemic stroke reduces the risk of recurrent stroke. For patients who present with TIA or minor ischemic stroke, we recommend implementation of appropriate diagnostic evaluation and stroke prevention treatment without delay, preferably within one day of the ischemic event (Grade 1B). (See 'Immediate treatment' above.)

●Risk factor management is appropriate for all patients with ischemic stroke or TIA, and most patients should be treated with all available risk reduction strategies. Currently viable strategies include blood pressure reduction, statins, antiplatelet therapy, and lifestyle modification, including smoking cessation. These interventions are discussed in greater detail separately. (See "Overview of secondary prevention of ischemic stroke".)

●An overview of the treatment for specific causes of TIA and ischemic stroke is provided separately. (See "Secondary prevention for specific causes of ischemic stroke and transient ischemic attack".)