The scope of the diabetes problem is vast and diverse, particularly among geographical regions. In 2018, the prevalence of diabetes in the United States varied from 6.6% in Colorado to 13.4% in West Virginia [6]. Genetics, race, age, and lifestyle significantly influence the onset and progression of the disease process [1]. Although all races and ethnicities can develop diabetes, the prevalence is greatest (14.7%) among Native Americans/Alaska Natives. This group also has a risk for development of type 2 diabetes that is nearly two times greater than that of White Americans [1]. The prevalence of diabetes is 12.5% in Hispanic Americans, 11.7% in non-Hispanic Black Americans, 9.2% in Asian Americans/Pacific Islanders, and 7.5% in non-Hispanic White Americans [1]. Compared to non-Hispanic White Americans, African Americans and Hispanics are 40% to 50% more likely to have diabetes [4]. The highest prevalence of diabetes in the United States is observed in Native Americans in certain areas of the Southwest, where more than 30% of the population has the disease [1].

Diabetes is considered to be one of the most important risk factors for ischemic stroke, especially in individuals younger than 65 years of age. Individuals with diabetes who experience an ischemic stroke are typically younger than those without diabetes and often also have signs of hypertension, myocardial infarction (MI), and hyperlipidemia [7]. In 2016, after adjusting for age, the percentage of adults with diabetes who reported stroke was lowest among Hispanics (7.3%) compared with White (7.6%) or Black (9.4%) adults [8].

According to 2022 recommendations from the American Diabetes Association, all adults older than 35 years of age should be screened for type 2 diabetes every three years, or sooner with symptoms or in the presence of risk factors [9]. In addition, individuals of any age who are at risk for or are suspected of having diabetes should be screened. Established risk factors for type 2 diabetes include [9]:

The main cause of cerebrovascular disease in patients with diabetes is atherosclerosis, or thickening of artery walls. It is generally believed that patients with diabetes are at an increased risk for atherosclerosis due to endothelial dysfunction. The endothelium is the biologically active lining of the blood vessel that functions to [12]:

Endothelial dysfunction is the earliest vascular abnormality seen in patients with diabetes and is associated with blood vessel constriction, aggregation of platelets, and a proinflammatory state, with the accumulation of leukocytes and coagulation products on the endothelium [12]. This inflammatory response is mainly caused by the chronic effects of hyperglycemia and specifically the formation of biologically active glycated proteins and lipids that promote inflammation [13]. Visceral obesity, hypertension, and hyperlipidemia also contribute to oxidative stress, which can damage the endothelium [14].

An embolic stroke occurs when an embolus (i.e., any circulating clot or particle originating from a distal point) blocks an artery that supplies oxygen to the brain. Stroke registries indicate that 26% to 29% of ischemic strokes are embolic [21,22]. Emboli include blood clots, fatty deposits, atherosclerotic plaque fragments, and cancerous cells or infectious materials emanating from conditions such as atrial myxoma and endocarditis, respectively. Clinical symptoms of the resulting infarct correspond to the location of the embolus, not its type. The region of the middle cerebral artery is most frequently blocked by emboli [29].

The National Institute of Neurological Disorders and Stroke has identified the following signs and symptoms of stroke [17,30,32]:

Individuals who present with symptoms of cerebrovascular accident should have a full neurologic assessment by a practitioner [30]. After etiology is determined, treatment related to the causative source may be initiated. In thrombotic strokes, treatment is directed at prevention of ischemic injury [15]. Occlusions treated within 90 minutes of the onset of symptoms show the most improvement. Tissue plasminogen activator (t-PA) is recommended for select patients who may be treated within three hours after the onset of symptoms [24,31]. In 2009, the American Heart Association/American Stroke Association (AHA/ASA) revised guidelines for administration of rt-PA after acute stroke, expanding the window of treatment from 3 hours to 4.5 hours. Eligibility criteria for treatment during this later period are similar to those for treatment within three hours, but also include the following exclusion criteria [24,36,37,38]:

Data combined from two large clinical trials suggest that administration of aspirin (160–300 mg) within 48 hours after the onset of stroke slightly reduces mortality and morbidity by preventing early recurrent stroke in some patients [52,53]. A 2014 Cochrane review found that the daily administration of aspirin (160–300 mg) within 48 hours of onset of stroke reduced the risk of early recurrent stroke without a major risk of early hemorrhagic complications. Long-term outcomes were also improved [54]. Although no new data have emerged since the publication of these results, the 2018 AHA guideline recommendations for antiplatelet therapy have changed to include the administration of aspirin in patients with acute ischemic stroke within 24 to 48 hours after onset. For patients treated with IV alteplase, aspirin administration is generally delayed until 24 hours later but might be considered in select patients [24]. Other oral antiplatelet therapies (e.g., ticlopidine, clopidogrel, dipyridamole) have not been tested sufficiently in the setting of acute ischemic stroke. The efficacy of intravenous glycoprotein IIb/IIIa receptor blockers in combination with other interventions or alone is under investigation. These agents may accelerate spontaneous recanalization and improve microvascular patency [55]. If administered alone, these agents have been shown to have an adequate safety profile [56].

Glycemic control is also essential in the prevention of stroke or extension of the injury. Intracellular acidosis resulting from hyperglycemia increases lactate, leading to glial and neuronal membrane damage due to reactive oxygen species generation and impaired vasodilatation. Potentially viable neurons in the ischemic penumbra are more likely to infarct under conditions of hyperglycemia, and research has demonstrated a disruption of the blood brain barrier associated with greater degrees of hemorrhage and cerebral edema. Hyperglycemia with or without a diagnosis of diabetes is associated with transformation from ischemic to hemorrhagic stroke [59]. Therefore, patients with diabetes should be encouraged to monitor their blood glucose levels regularly and remain compliant with prescribed medications.