History and exam
Key diagnostic factors
common
patient/caregiver report of focal neurologic deficit
TIA is fundamentally a clinical diagnosis. Therefore, an accurate history, informed by the patient/caregiver's report of focal neurologic deficit, is key.
sudden onset and brief duration of symptoms
TIA symptoms are typically brief and the majority will resolve within the first hour.
Persistent symptoms at presentation should be treated as stroke, and therapy should not be delayed in the hope of spontaneous recovery.[43]
Other diagnostic factors
common
history of extracranial atherosclerosis
Diagnosis of atherosclerosis in other parts of the body suggests the likelihood of cerebrovascular atherosclerotic disease.
Presence of coronary artery disease, carotid stenosis, or peripheral vascular disease increases likelihood that transient neurologic events are due to atherosclerotic ischemic cerebral insult.
history of cardiac disease
The presence of atrial fibrillation, valve disease, valvular prosthesis, cardiac shunts, or severely impaired contractility increases the probability that transient neurologic events are due to embolic ischemic cerebral insult.
Occurrence of symptoms during Valsalva increases probability of paradoxical emboli across cardiac shunt.
unilateral symptoms
In general, TIAs represent ischemia in an area of brain controlling function on the contralateral side of the body.[7] Lacunar symptoms tend to give isolated sensory or isolated motor deficits but also a number of less common symptom complexes.[9]
Bilateral symptoms suggest central emboli with multiple areas of ischemia, or brainstem ischemia that classically causes "crossed symptoms."[50] Bilateral symptoms from central embolization may, on close examination, be multiple events over time rather than a single event. More often, bilateral symptoms suggest nonischemic explanation for neurologic deficits.
dysphasia
Common in anterior circulation ischemia.[50] Usually indicates left-sided cerebral hemisphere ischemia.
ataxia, vertigo, or loss of balance
Common in posterior circulation TIAs.[70]
vision loss or visual field deficit
Monocular vision loss may occur and is often transient.[51] This is a common early warning signal for cervical carotid stenosis. It can present as amaurosis fugax or retinal stroke (branch or central retinal artery occlusion); recognize and investigate with the same urgency. Vision loss may occur in patients with posterior circulation ischemia.
When visual field loss is unilateral, this sign may reflect either carotid or vertebrobasilar ischemia, whereas bilateral visual field loss is usually due to vertebrobasilar ischemia.
binocular diplopia
Common in posterior circulation TIAs.[70]
increased BP on presentation
BP frequently rises acutely after a cerebral ischemic event, which may have a protective effect by increasing cerebral blood flow.
Hypertension itself is a risk factor for stroke and increases pretest probability that deficits are from an ischemic (or hemorrhagic) mechanism.
absence of positive symptoms (shaking, scotoma, spasm)
Most cerebrovascular ischemic events have a deficit.
The presence of positive symptoms such as shaking, scotomata, or spasm should suggest alternative etiology (e.g., seizure, migraine, conversion disorder, or dystonia).[50]
uncommon
family or personal history of premature stroke, miscarriage, or venous thromboembolism
carotid bruit
The presence of a carotid bruit is both poorly sensitive and poorly specific for significant stenosis.
Risk factors
strong
atrial fibrillation
In patients with atrial fibrillation without valvular disease, the relative risk for TIA is 2.5- to 5-fold higher than in patients without atrial fibrillation. There is a dramatically higher risk when associated with valve abnormality.[19][20]
Persistent atrial fibrillation appears to have a higher risk than intermittent fibrillation.[20]
Atrial fibrillation causes stasis in the left atrium, which increases the chance of thrombus formation in the left atrial appendage.[21] Thrombus once formed inside the heart can embolize, creating TIA or stroke.
valvular disease
carotid stenosis
Strong for high-grade stenosis. Risk of stroke, TIA, or death in asymptomatic stenosis ranges from 11% to 21% with medical management only.[22] Higher rates of stenosis (>70%) are associated with significantly increased risk compared with moderate stenosis (50% to 69%).
intracranial stenosis
Symptomatic intracranial atherosclerotic arterial stenosis is one of the most common causes of stroke worldwide and is associated with a high risk of recurrent stroke.[23] Large artery intracranial occlusive disease affecting the middle cerebral artery, intracranial portion of the internal carotid artery, vertebrobasilar artery, and posterior and anterior cerebral arteries is more common in Asian patients.[24]
congestive heart failure
This may be due either to stasis, leading to increased risk of cardioembolic events, or via common risk factors for cerebrovascular disease and ischemic heart failure. The odds ratio for congestive heart failure and TIA is 2.4.[20]
hypertension
The most common risk factor for cerebrovascular disease.
Relative risk for TIA is approximately 2- to 5-fold in the presence of hypertension.[19][20] The higher the chronic BP elevation, the more this risk factor is important for cerebral ischemia, forming a continuous risk association.
Mechanism is via increasing likelihood of atherosclerotic vascular disease.
hyperlipidemia
There is a direct relationship between elevated total cholesterol and LDL-cholesterol and increased risk of ischemic stroke. The relationship between other lipid profile components and stroke is more complex. Primary stroke prevention trials show 11% to 40% reduction in risk of stroke with statin therapy.[25]
diabetes mellitus
Diabetes is a potent risk factor for atherosclerotic disease and has been reported to be present in up to one third of patients who present with cerebral ischemia.[21][26] The presence of diabetes increases the risk for TIA by an odds ratio of 1.5 to 2.[19][20][27]
Diabetes is frequently associated with other atherosclerotic risk factors in the metabolic syndrome. It is recommended that the patient with diabetes be recognized to be at greater than average risk for cerebrovascular disease. As a result, patients with diabetes are felt to merit aggressive management of other modifiable risk factors.
cigarette smoking
Tobacco abuse is one of the most important modifiable risk factors for cerebrovascular disease, and smokers have 1.5 to 2 times the risk of nonsmokers for cerebrovascular events.[19][21][28]
Tobacco smoke may increase blood viscosity and increase coagulability.
The increased risk wanes with smoking cessation, but some increased risk remains, likely associated with lasting atherosclerotic vascular changes.
The association between smoking and ischemic stroke is strongest in younger patients.[28]
alcohol abuse
Alcohol abuse is strongly associated with increased risk for stroke.[21] The association varies by pattern of consumption, with increased risk in heavy episodic ("binge") drinking (odds ratio 1.39) and heavy alcohol use (odds ratio 1.57). Geographic region also plays a role, with low levels of alcohol consumption associated with reduced risk of stroke in western Europe and North America only (odds ratio 0.66).[29] Alcohol consumption is associated with elevated blood pressure, and increases the risk of other cardiovascular disease.[30][31]
advanced age
TIAs are more common in middle age and in older people.[1] Symptoms in a young patient increase the possibility of alternative diagnosis or a less common etiology for ischemia, such as congenital heart disease, paradoxical emboli, drug use, or hypercoagulability.
weak
patent foramen ovale (PFO)
In selected cases, such as the young TIA patient with a PFO, atrial septal aneurysm, and significant shunt, there may be an association with stroke.[32] For the unselected general population, the presence of a PFO does not significantly increase the risk of cerebral ischemia. The relationship between PFO and TIA is complicated by the commonness of PFO in the population and a clear causal relationship has not been established: it is estimated that approximately 25% of the population has a PFO, but in approximately 80% of patients with PFO and stroke, the PFO is incidental.[33][34] However, in patients with cryptogenic stroke, closure of PFOs has been shown to reduce recurrent stroke rates.[35]
inactivity
It appears that vigorous physical activity may be protective against later cerebrovascular events.[36] Data from a large prospective study demonstrate that moderate to vigorous exercise four times per week may be protective against stroke, and show a possible association between self-reported physical inactivity and stroke (hazard ratio 1.20).[37]
obesity
Obesity, particularly abdominal obesity, is weakly associated with cerebrovascular disease. In population studies, obesity has been shown to increase risk for ischemic stroke by 50% to 100% compared with patients who have a normal weight.[21] The causal pathway from obesity to stroke risk is mediated by factors that track closely with weight, particularly elevated blood pressure, atrial fibrillation, dyslipidemia, and hyperglycemia.[21][38]
hypercoagulability
The majority of TIAs occur in patients who lack any hypercoagulability, with only 1% to 4.8% of strokes being due to coagulation disorders.[9]
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