Stroke ranks fifth among all causes of death in the United States, accounting for one out of every 19 deaths, with costs of more than $100 billion annually. Cumulative all-cause mortality after a stroke is estimated to be 10.5% at 30 days and 21.2% at one year. An estimated 7.6 million Americans are self-reported to have experienced a transient ischemic attack (TIA) or stroke, with a climbing projection of an additional 3.4 million by 2030. The incidence of stroke is approximately 795,000 people per year, and 25% of these occurrences are recurrent episodes.1
Traditionally, stroke was defined as a focal injury to the central nervous system (CNS) caused by a vascular etiology lasting more than 24 hours, which primarily made this disease a clinical diagnosis. Given advancements in the understanding of cerebrovascular disease as a process and the widespread availability of rapid imaging, a more universal definition has emerged, defining stroke broadly as a concept encompassing CNS infarctions and hemorrhages based on imaging and pathologic and clinical findings.2
Clinical symptoms of neurologic dysfunction accompanied by evidence of infarction on brain imaging are classified as ischemic stroke, whereas transient symptoms without evidence of infarction are classified as TIA.
Rapid diagnosis and prompt treatment of stroke with consideration for use of recombinant tissue plasminogen activator (rtPA) can significantly reduce mortality and morbidity; risk factor modification can reduce recurrence.
Numerous risk factors contribute to stroke. Approximately 87% of stroke risk is attributable to modifiable risk factors such as adiposity, diabetes mellitus, hypertension, and dyslipidemia. Behavioral factors such as smoking, sedentary lifestyle, and unhealthy dietary choices account for about 47% of these modifiable risk factors.1
Depending on the type of stroke, risk factors have variable associations. Diabetes increases the risk of an ischemic stroke but decreases the risk of a subarachnoid hemorrhage. Adiposity appears to increase the risk of ischemic stroke; however, its association with hemorrhagic stroke is unclear. Hypertension increases the risk of all types of stroke, but the risk tends to be higher with hemorrhagic vs. ischemic stroke.3
Radiographic findings of previous stroke are the greatest predictor of future stroke.4
Classification of Strokes
Stroke classification is based on the underlying pathologic process and vascular distribution. Appropriate classification of a stroke assists in formulating definitive treatment decisions and communicating potential short- and long-term prognoses. In the United States, approximately 87% of all strokes are ischemic, 10% are intracerebral hemorrhages, and 3% are subarachnoid hemorrhages.1
An ischemic stroke is defined as an episode of neurologic dysfunction secondary to a focal CNS infarction. A silent ischemic infarction is defined as imaging or neuropathologic evidence of an infarction without neurologic dysfunction.
Intracerebral and spontaneous subarachnoid hemorrhages are defined as rapidly developing neurologic dysfunction secondary to the focal accumulation of blood in the brain parenchyma and in the subarachnoid space, respectively, and are not precipitated by trauma. A silent cerebral hemorrhage is similar to a silent ischemic stroke in that both are without clinical symptoms. Imaging shows a focal collection of blood within the brain parenchyma or ventricular system, often presenting in the form of microhemorrhages.2
A stroke caused by cerebral venous thrombosis is an infarction or hemorrhage in the brain, spinal cord, or retina due to thrombosis of a cerebral venous structure and represents 0.5% to 1% of all strokes. A stroke classified as “not otherwise specified” is defined as acute neurologic dysfunction presumed to be caused by ischemia or hemorrhage that persists for more than 24 hours or until death, but with indeterminate evidence to be classified as any other type of stroke.2
Attempting to localize the vascular distribution of a stroke based on clinical assessment has traditionally been used to assist in diagnosis and treatment and for rehabilitation purposes.
The history is key in the initial assessment of stroke and should focus on the symptoms and signs of focal neurologic injury, such as unilateral weakness or sensory deficit, facial droop, dysarthria, or aphasia (Table 1)
Patients typically present with a sudden and maximal focal neurologic deficit that is consistent with a vascular territory.6
The timing of events or symptom onset, specifically the last known well or baseline state, is crucial for assessment and determining treatment options.