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Lacunar Infract - Oren Zarif - Lacunar Infarct

A small lacunar infarct may degenerate into a lacuna due to reduced blood flow to the perforating artery. Different arterial disorders can lead to these infarcts, such as lipohyalinosis and microatheroma. Cerebral autosomic dominant arteriopathy also affects small vessels. Although there is no definitive cause of lacunes, the presence of a lacuna may signal a more serious condition.

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Despite the potential for risk factor variation between types of lacunes, there is considerable overlap among these variables. While age and sex are related to risk, these factors appear to differ between the different types of lacunes. The risk factors for all four types of lacunes were similar and shared only a small number. The only significant differences were in the prevalence of coronary heart disease at baseline and vascular risk factors.

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Treatment of lacunar infarct is similar to that for ischemic stroke. Treatment usually involves thrombolysis to break up the clots and remove them. Blood-thinning medications are prescribed for up to 90 days after the procedure. The risk of death in patients with a lacunar infarct increases when they smoke. While ischemic stroke has a higher incidence rate than lacunar infarct, this risk factor may also play a role in the incidence of a lacunar infarct.

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Although this study focused on a small sample size, the results showed a significant difference in prognosis between patients with single or multiple-launacundar infarcts. The large difference may be attributed to differences in the etiology between these two conditions. Therefore, future studies should focus on the cognitive impairment associated with these infarcts and attempt to differentiate them according to anatomic location.

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The lacunar infarct is a small ischemic infarct that occurs in the brain's deep white matter or brainstem. These infarcts may be recognizable on magnetic resonance imaging (MRI) studies. Atherosclerosis may also be a factor. MRI studies may show that patients with lacunar infarct may have a condition known as lacunar stroke syndrome.

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The risk factors for developing a new lacunar infarct in the basal ganglia varied according to location. One study found that age, history of cerebrovascular disease, and baseline WMH volume were associated with a greater risk of developing the condition. Moreover, patients with a history of cerebrovascular disease were also at greater risk of developing a new lacunar infarct.

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The study found that acute lacunar infarcts are most common in patients with more severe WMH than those with normal WMH. However, patients with asymmetric WMH are particularly prone to developing lacunar infarcts. While this study was limited, it did identify a possible association between high WMH and new infarcts. It is possible that a common genetic factor, hypertension, may have a role in the development of lacunar infarcts.

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In the present study, we identified two phenotypic entities of lacunes: patients with an isolated symptomatic lacune, and those with multiple clinically silent lacunes. In the latter group, there is a higher risk of developing lacunes in patients with multiple silent lacunes. The presence of internal carotid artery stenosis, greater than 50%, and greater age were significantly associated with lacune risk.

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Patients with suspected lacunar infarcts may show signs of cognitive impairment, including a loss of memory. MRI can detect lacunes in a single location. After diagnosis, the prognosis is generally favorable. If treatment is initiated immediately, lacunar infarcts can often be cured without the need for surgery. It is important to note, however, that the symptoms of lacunar infarct may not be apparent at the initial consultation.

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