The symptoms of a transient ischemic attack are temporary and often resolve before the patient can be seen by a health care provider. Patient history is therefore of great importance. History from the family, witnesses, and emergency medical services, as well as the patient, should be obtained. History may include short-term alterations in [2]:

• Behavior
• Speech
• Gait
• Memory
• Movement

Symptoms can vary from individual to individual and by the area of the brain affected. Frequently symptoms include [2] [4]:

• Temporary loss of vision
• Aphasia
• Hemiparesis
• Paresthesia
• Impaired level of consciousness or disorientation
• Dizziness
• Lack of coordination or poor balance
• Temporary partial paralysis of the face and tongue

The symptoms are short-lived, usually lasting less than 15 to 60 minutes. Symptoms vary in severity.

Differential diagnoses to be excluded are [2] [3] [13]:

• Hypoglycemia
• Seizures
• Cranial tumors or lesions
• Migraine with aura
• Peripheral nerve/root disorder
• Demyelinating disease, multiple sclerosis
• Vestibular dysfunction
• Intracranial hemorrhage
• Electrolyte imbalance

The initial workup for individuals presenting with a transient ischemic attack should be aimed at excluding other metabolic or drug-induced causes for the symptoms. Tests that should be done immediately [2]:

• Blood glucose to rule out hypoglycemia
• Complete blood count
• Serum electrolyte levels
• Coagulation studies
• 12-lead electrocardiogram with rhythm strip

A complete neurologic examination is a means of determining the area of neurovascular assault. The examination should include the following [2] [3]:

• Cranial nerve testing
• Motor strength and function
• Sensory testing
• Speech and language evaluation
• Assessment of the cerebellar function, gait and balance

Physical examination should include [2] [3]:

• Vital signs: Temperature, blood pressure, heart rate and rhythm, respiratory rate and pattern, oxygen saturation.
• Overall health and appearance: Hydration status, development, skin color.
• Psychosocial issues: Attentiveness, social interaction, language and memory, cognition.

Further testing may include [2] [3]:

• Erythrocyte sedimentation rate
• Cardiac enzymes
• Lipid profile
• Screening for hypercoagulate states
• Syphilis serology
• Anti-phospholipid antibodies
• Toxicology screening
• Hemoglobin electrophoresis
• Serum protein electrophoresis
• Cerebrospinal fluid examination

Imaging studies [2] [3] [16]:

• Magnetic resonance imaging (MRI) with diffusion-weighted imaging
• Non-contrast computed tomography (CT)
• Vascular imaging: Carotid Doppler ultrasonography of the neck, computed tomography angiography (CTA), or magnetic resonance angiography (MRA)

Recommendations for evaluation and initial interventions for individuals presenting with transient ischemic attacks are [2] [5] [8]:

• Neuroimaging evaluation of the cervical vessels and intracranial vessels is within 24 hours of symptom onset. Magnetic resonance imaging with diffusion sequences are recommended. 
• Electrocardiography as soon as possible with prolonged cardiac monitoring and echocardiography in patients where no vascular etiology identified. 
• Routine blood tests: Complete blood count, electrolytes, fasting blood glucose, renal and liver studies. 
• Hospitalization of patients within 72 hours with an ABCD (2) score > 5 which indicate a high risk of recurrence [5]. 

Antithrombotic therapy, started once intracranial hemorrhage is ruled out, is recommended to prevent subsequent stroke [2]. Most frequently used medications are [1] [2] [13]:

• Aspirin (50-325 mg/day)
• Aspirin plus extended-release dipyridamole
• Clopidogrel

For cardio-embolic transient ischemic attacks long-term anticoagulation therapy is recommended using [1] [2]:

• Heparin (warfarin) titrated to maintain international normalized ratio, INR, at 2-3
• Aspirin 325 mg/day for those unable to take oral anticoagulants or with intracranial stenosis

Maintaining blood pressure below 140/90 mm Hg and total cholesterol below 200 mg/dL may prevent transient ischemic attacks, their recurrence or subsequent stroke [2].

Hospitalization may be required for early lytic therapy and other medical management and secondary prevention [18].

Hospitalization is required for [16] [17]:

• Crescendo transient ischemic attacks
• Symptoms lasting longer than 1 hour
• Internal carotid stenosis greater than 50%
• Atrial fibrillation
• Hypercoagulate status

Angioplasty or stent placement to treat transient ischemic attacks are currently being investigated, but their usefulness is not yet known [18]. Endarterectomy versus medical treatment alone has shown that surgery reduced the risk of stroke in patients with carotid stenosis, but the benefits were substantially less when surgery was delayed more than two weeks [13].

Recombinant human Interleukin-1ra (IL-1ra) administered intravenously has been shown to effectively reduce inflammation after a transient ischemic event. Though safe, its efficacy in the early hours after the ischemic episode are limited by its slow uptake. Further research is needed to find better therapeutic agents [15].

Research has shown transient ischemic attacks to be a very strong predictor of subsequent stroke and death [6]. Early identification, immediate treatment, and institution of stroke prevention techniques are imperative to preventing further morbidity and mortality [2] [3].

Transient ischemic attacks are episodes of temporary, focal cerebral dysfunction due to vascular occlusion and tissue ischemia [2] [7]. Onset is acute and abrupt and the event is of short duration, from 15 minutes to 24 hours. Resolution of symptoms is rapid as well. Transient ischemic attacks leave no residual neurological deficit [2] [8]. Differentials diagnoses include [7] migraine, epilepsy, syncope, or even neurosis. 

Transient ischemic attacks are classified and initially evaluated using the ABCD (2) score [9]. This evaluation tool is based on five criteria: Age > 60 years (1 point), blood pressure > 140/90 mm Hg (1 point), clinically unilateral weakness (2 points), speech impairment without weakness (1point), duration > 60 min (2 points) or 10 to 59 min (1 point) and diabetes (1 point) [10]. The higher the score the higher the risk for recurrence of transient ischemia and/or eminent stroke [9] [10]. 

Patients are classified as follows [9] [10]:

• High risk with a score of 6-7; stroke risk 8.1%, 
• Moderate risk with a score of 4-5; stroke risk 4.1%, 
• Low risk with score of 0-3; stroke risk 1.0%.

Transient ischemic attacks may also be classified as typical transient ischemia or nonspecific transient neurological attacks [4] [7]. Typical transient ischemic attacks are the result of temporary vascular occlusion. Nonspecific transient neurological attacks may be due to cardiac abnormalities, such as arrhythmias [7]. The non-specific form accounts for less than half of patients and studies have shown them to be at lower risk of subsequent stroke [4] [7].

The incidence of transient ischemic attacks is approximately 1 per 1000 population in the United States, accounting for 200,000-500,00 cases a year [2] [11] [12]. The reported incidence is lower in other developed countries [5] [13].

Approximately 15% of strokes occur in individuals with a history of previous transient ischemic attacks [2] [4] [13]. The incidence of transient ischemic attacks increases with age. The incidence is significantly higher in men than in women, approximately 1.5 to 1 [6].

The incidence in blacks is 1.5 times higher than that in whites [1] [6]. This may, in part, be due to an increased prevalence of diabetes and cardiovascular disease in this population group [6].

Transient ischemic attacks are the result of a temporary decrease or cessation of cerebral blood flow to a portion of the brain [4] [8]. They may be due to an acute thromboembolic event or chronic vascular stenosis. Cerebrovascular disease and atherosclerosis are the primary causes of the syndrome, and are a group of conditions that affect the blood vessels supplying the brain [14]. Symptoms vary according to the area of the brain affected.

Other possible causes include [8] [14]:

• Atherosclerosis
• Embolic cardiac disorders
• Valvular disease
• Atrial fibrillation, aortic arch disease, or atrial-septal defect
• Arterial dissection
• Arteritis and vasculitis
• Sympathomimetic drugs such as cocaine
• Tumors or hematomas
• Hypercoagulation states, clotting disorders
• Congenital heart disease
• Central nervous system infection
• Neurofibromatosis and fibromuscular dysplasia
• Marfan syndrome
• Sickle cell disease

The pathophysiology of brain ischemia is related to the action of neuro-inflammatory mediators that increase the progression of tissue damage [15]. With ischemia, increased levels of cytokines and chemokines cause the adhesion of white blood cells to the vascular endothelium [15]. This process further impairs cerebral blood flow resulting in further damage and the increased risk of subsequent stroke.

Interleukin-1 (IL-1) is a group of cytokines that regulate the immune and inflammatory responses in the body. Recent research suggests that these substances may reduce brain injury by decreasing the inflammatory progression occurring post-ischemic episode [15].

After a transient ischemic attack, reducing stroke risk has an impact on subsequent morbidity and mortality. This will require extensive public education about the symptoms of these events and the importance of immediate evaluation, no matter the duration [11].

Maintaining blood pressure below 140/90 mm Hg and total cholesterol below 200 mg/dL, weight loss and maintenance of normal body mass index may be preventive of transient ischemic attacks [17].

Transient ischemic attacks (TIA) are defined as temporary neurologic events that last less than 24 hours. They are due to short-term cerebral, spinal cord, or retinal ischemia [1] [2] and not associated with tissue infarction and subsequent damage [2] [3]. However, better imaging techniques have indicated that minimal tissue damage may occur in the shortest of episodes [1] [3].

Usual symptoms of transient ischemic attacks include hemiparesis, hemiparesthesia, dysphasia, diplopia and monocular blindness, imbalance and gait disturbances, and possible disorientation [1] [2] [4].

The incidence of subsequent stroke in individuals who have had a transient ischemic attack may be as high as 10% within 3 months and 11 to 25% in the next 5 years [2] [5] [6].

What is transient ischemic attack?

A transient ischemic attack refers to a temporary sudden decrease in blood supply to the brain resulting in short-term neurological symptoms. The cause of this disorder is a sudden decrease in blood supply to a part of the brain.

What are the symptoms?

The symptoms of transient ischemic attack include:

• Temporary loss of vision
• Difficulty speaking
• Weakness on one side of the body
• Numbness or tingling 
• Impaired level of consciousness or disorientation
• Dizziness
• Lack of coordination or poor balance

What causes transient ischemic attack?

Transient ischemic attacks are caused by interference with the blood supply to the brain. Reasons for this include:

• Atherosclerosis
• Cardiac disorders: Valvular disease, atrial fibrillation
• Inflammation of the blood vessels
• Drugs such as cocaine
• Tumors or hematomas
• Clotting disorders
• Congenital heart disease
• Central nervous system infection
• Sickle cell disease

It is believed that much of the damage and the increased risk of stroke caused by transient ischemic attacks is due to inflammation of brain tissue as a result of ischemia, decreased oxygen supply.

Who gets transient ischemic attack?

Anyone who has cerebrovascular disease or disorders is at risk for transient ischemic attacks. The risk increases with age. The incidence is higher in men than in women and in blacks than in whites.  Those at particular risk are individuals with high blood pressure, high cholesterol, diabetes, elevated body mass index (BMI), and atherosclerosis.

How is it diagnosed?

The symptoms of the disorder are of such short duration, often 1 to 60 minutes, that they may be gone before the individual can be seen by a healthcare provider. Transient ischemic attacks are diagnosed initially by the history of the event, symptoms, duration, and residual effects. Diagnosis is then a matter of excluding other possible diagnoses such as migraines, seizures, and hypoglycemia. Once it is determined that the symptoms are caused by a transient ischemic episode, the underlying cause of the decreased blood flow must be identified and that issued needs to be treated.

How is transient ischemic attack treated?

If it is determined that the transient ischemic attack is due to an embolism or clotting problem medications to decrease the formation of clots can be effective. These medications include warfarin (Coumadin) or heparin in the acute phase, and/ aspirin.
If the underlying cause is occlusion due to embolus or stenosis (clot or narrowing of blood vessel) surgical intervention may be needed. New medications are currently being researched for use in transient ischemic events. These medication reduce the inflammation caused by brain ischemia and may help to prevent subsequent strokes.

What are the complications of transient ischemic attack?

The main complication of transient ischemic attacks is cerebral vascular accidents or stroke. Research has shown that 15-25% of people who experience a transient ischemic attack will experience a stroke within 3 months to 5 years. Strokes result in permanent disability or death.

How can transient ischemic attacks be prevented?

After a transient ischemic attack, reducing stroke risk has an impact on subsequent morbidity and mortality. Maintaining blood pressure below 140/90 mm Hg and total cholesterol below 200 mg/dL, weight loss and maintenance of normal body mass index may help to preventive transient ischemic attacks and stroke.

1. Albers GW, Caplan LR, Easton JD, Fayad PB, Mohr JP, Saver JL, et al. Transient ischemic attack--proposal for a new definition. N Engl J Med. 2002;347(21):1713-6.
2. Bray JE, Coughlan K, Bladin C. Can the ABCD Score be dichotomised to identify high-risk patients with transient ischaemic attack in the emergency department?. Emerg Med J. 2007;24(2):92-5.
3. Edlow JA, Kim S, Pelletier AJ, Camargo CA. National Study on Emergency Department Visits for Transient Ischemic Attack, 1992–2001. Academic Emergency Medicine. 2006; 13:666–672.
4. Bos MJ, van Rijn MJ, Witteman JC, Hofman A, Koudstaal PJ, Breteler MM. Incidence and prognosis of transient neurological attacks. JAMA. 2007;298(24):2877-85. 
5. Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2009;40(6):2276-93.
6. Kleindorfer D, Panagos P, Pancioli A. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. 2005;36(4):720-3.
7. Bots ML, van der Wilk EC, Koudstaal PJ, Hofman A, Grobbee DE. Transient neurological attacks in the general population. Prevalence, risk factors, and clinical relevance. Stroke. 1997;28(4):768-73.
8. Giles MF, Albers GW, Amarenco P, Arsava EM, Asimos AW, Ay H, et al. Early stroke risk and ABCD2 score performance in tissue vs time-defined TIA: A multicenter study. Neurology. 2011;77(13):1222-8.
9. Fothergill A, Christianson TJ, Brown RD Jr, Rabinstein AA. Validation and refinement of the ABCD2 score: a population-based analysis. Stroke. 2009;40(8):2669-73.
10. Johnston SC, Rothwell PM, Nguyen-Huynh MN, Giles MF, Elkins JS, Bernstein AL, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. 2007;369(9558):283-92.
11. Johnston SC, Fayad PB, Gorelick PB, Hanley DF, Shwayder P, van Husen D, et al. Prevalence and knowledge of transient ischemic attack among US adults. Neurology. 2003;60(9):1429-34.
12. Chandratheva A, Lasserson DS, Geraghty OC, Rothwell PM. Population-based study of behavior immediately after transient ischemic attack and minor stroke in 1000 consecutive patients: lessons for public education. Stroke. 2010;41(6):1108-14.
13. Halliday AW, Lees T, Kamugasha D. Waiting times for carotid endarterectomy in UK: observational study. BMJ. 2009;338:b1847.
14. Andrade SE, Harrold LR, Tjia J, Cutrona SL, Saczynski JS, Dodd KS, et al. A systematic review of validated methods for identifying cerebrovascular accident or transient ischemic attack using administrative data. Pharm Epidem and Drug Safety. 2012; 21(S1): 100–128.
15. Amantea D, Nappi G, Bernardi G, Bagetta G, Corasaniti MT. Post-ischemic brain damage: pathophysiology and role of inflammatory mediators. FEBS Journal. 2009;276:13–26.
16. White H, Boden-Albala B, Wang C, Elkind MS, Rundek T, Wright CB, et al. Ischemic stroke subtype incidence among whites, blacks, and Hispanics: the Northern Manhattan Study. Circulation. 2005;111(10):1327-31.
17. Johnston SC, Nguyen-Huynh MN, Schwarz ME, Fuller K, Williams CE, Josephson SA, et al. National Stroke Association guidelines for the management of transient ischemic attacks. Ann Neurol. 2006;60(3):301-13.