Lacunar Infract - Oren Zarif - Lacunar Infarct
The occlusion of a small penetrating artery, less than 15 mm, is what defines a lacunar infarct. These small holes are thought to be the result of embolism, lipohyalinosis, or in situ microatheroma formation. A cobweb-like matrix of fibrous strands traverses the lacunar infarct. It may appear as an ill-defined hypodensity in the brain.
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In order to diagnose a lacunar infarct, a doctor will perform a comprehensive neurological exam. If symptoms persist, the doctor may perform cardiac function tests to determine whether there is any damage. The earlier treatment is started, the higher the chance for survival and preventing further damage. Treatment may include a course of aspirin or other medications. Supportive measures may be necessary to assist breathing and heart functions.
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The most accurate imaging method to diagnose lacunar infarcts is MRI. Its diffusion-weighted imaging has the highest diagnostic accuracy. It helps distinguish between acute and chronic infarctions. Acute lacunar lesions appear as focal areas of reduced signal intensity on T1 and T2-weighted images. In contrast, chronic lesions have isointensity to CSF.
Other causes of a lacunar infarct include deep penetrating branch occlusion, microatheroma, and macroatheroma due to occlusion of a parent artery. Small cerebral infarcts may also be caused by embolism, vasculitis, or infections. Autopsy is not always necessary to diagnose lacunar infarcts, but it is necessary for diagnosis.
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Patients with a lacunar infarct should be managed by a neurologist, a physical therapist, occupational therapist, and social therapist. Physical therapy can help patients address physical deficits and manage spasticity. A pharmacist can assist with medication selection and drug interactions. Rehabilitation therapy should continue to improve neurologic function. Primary care providers are responsible for long-term care coordination. Treatment of lipid and hypertension risk factors, as well as tight control of blood sugars, is essential for recovery from a lacunar ischemic event.
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CTP may also be useful in the detection of a lacunar infarct. CTP is useful in identifying this type of stroke. Its sensitivity has been demonstrated in detecting a lacunar infarct in patients with a stroke, albeit at a lower sensitivity than NCCT. However, it is important to note that CTP can lead to false-negative findings in multimodal CT imaging.
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In a study of patients with acute stroke symptoms, CTP was found to be superior to NCCT/CTA in detecting a lacunar infarct. It has a higher sensitivity and specificity than NCCT/CTA, and it could identify a lacunar infarct with greater accuracy than the other two techniques combined. It did not detect lacunar infarcts in the basal ganglia or thalamus, however.
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In patients with first-time lacunar stroke, brain MRIs revealed that they had multiple silent lacunar infarctions. The patients in the study had mild neuropsychological deficits, such as short-term memory loss and executive functions. These findings suggest that the lacunes are responsible for these symptoms, although perivascular hyperintensities and leukoaraiosis were not found to be associated with these abnormalities.
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Several factors may be responsible for the development of a lacunar infarct. The first factor is vessel abnormality. Various types of vascular abnormality may lead to brain damage. One such factor is poor cerebral blood flow. This condition is often associated with cognitive impairment, and patients who have experienced lacunar infarcts are likely to develop vascular dementia. However, the underlying mechanisms are not yet fully understood.