Lacunar Infract - Oren Zarif - Lacunar Infarct
A lacunar infarct is a small, non-contiguous infarct in the brain. A lacunar infarct is less than 15 mm in diameter and characterized by a cobweb-like network of fibrous strands. It can be either chronic or acute. There are several possible causes of lacunar infarct. There are many ways to diagnose a lacunar infarct, including an MRI or CT.
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The mechanism of lacunes is still being studied. Embolic material from larger arteries or the heart could cause them. Studies on animal models cannot prove causality, but they do demonstrate that a significant percentage of lacunar infarcts are caused by emboli. Other studies, which used symptomatic patients, could not prove the mechanism. In order to distinguish between these two possibilities, the CHS provides an excellent opportunity to study risk factors and their interaction with the presence of lacunes.
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The incidence of ischemic infarcts in the elderly population is high. In the Cardiovascular Health Study (CHS), 3660 older adults were evaluated for MRI and 1131 had an ischemic infarct and 841 had a lacunar infarct. Although the majority of participants in both studies denied any stroke history, the study found that those with MRI-defined lacunes had a higher risk of developing a TIA and lower-extremity strokes than those with a non-laued infarct.
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A small lacunar infarct in the white matter of the brain is often associated with occlusive carotid artery disease, which is one of the causes of stroke. This condition may also be caused by other vascular conditions, such as arteriolosclerosis or a familial form of cerebrovascular disease. Interestingly, both types of infarcts are characterized by an increased risk of white matter lesions in the brain.
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Although the frequency of lacunar strokes has decreased, there are still some cases that have a vascular etiology and are attributed to ischemic disease. Treatment for these patients can include antiplatelet medications and the control of vascular risk factors, including hypertension and lipidemia. However, antiplatelet drugs do not work as well as clot-busters. So, what are the best options?
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Compared to ischemic stroke, the treatment for lacunar infarct is similar to that for ischemic stroke. Both types of treatment involve breaking up blood clots. In addition to medications, thrombectomy may be performed. If this treatment is unsuccessful, the patient must take blood-thinning medications for 90 days. If treatment is not successful, they will need to undergo a more intensive treatment.
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Although there are several factors associated with vascular risk, there are few studies that specifically look at the risk factors for lacunar infarcts. Age and sex, as well as baseline white matter hyperintensity volume, are factors to consider. In the study, the authors hypothesized that there may be a difference in risk factors for patients with lacunar infarcts in deep white matter and the basal ganglia.
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NCCT and CTA have high sensitivity and specificity for detecting lacunar infarcts. However, NCCT/CTA did not detect lacunar infarcts in patients with thalamus and basal ganglia, which is a major concern. This study shows that CT/CT is superior to NCCT/CTA for identifying lacunar infarcts.
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A patient with a lacunar infarct will require extensive rehabilitation. Physical therapy can help manage the deficits caused by spasticity, and medications may reduce the need for muscle relaxants. Pharmacists play a vital role for patients with multiple medications. The rehabilitation process needs to continue as long as necessary to maximize neurological function. In the event of a subsequent stroke, intensive antihypertensive therapy and lipid management may be required to protect the brain against future damage.