امراض نظري 3.docx

**MRI** MRI is more time consuming and less available than CT [but has] [significantly higher sensitivity and specificity in the diagnosis of] [acute ischemic infarction in the first few hours after onset.] Early hyperacute ================ Within minutes of arterial occlusion, DWI([[diffusion-we...

**MRI** MRI is more time consuming and less available than CT [but has] [significantly higher sensitivity and specificity in the diagnosis of] [acute ischemic infarction in the first few hours after onset.] Early hyperacute ================ Within minutes of arterial occlusion, DWI([[diffusion-weighted] [MRI:assessment of hypoperfsion on cellular function,indicating] [imminent cell death)] [ ]](https://radiopaedia.org/articles/diffusion-weighted-imaging-in-acute-ischaemic-stroke?lang=us) demonstrates increased signal and reduced ADC(apperant diffusion coefficient :is ameasure of magnitude of diffusion within the tissue) values. At this stage, the affected parenchyma appears normal on other sequences, although changes in flow will be detected (occlusion on MRA) and the thromboembolism may be detected. If infarction is incomplete then cortical contrast enhancement may be seen as early as 2 to 4 hours. In a minority of cases, DWI may be normal (please refer to [[DWInegative acute ischemic stroke]](https://radiopaedia.org/articles/diffusion-negative-acute-ischaemic-stroke?lang=us) for more details). Late hyperacute =============== Generally, after 6 hours, high T2 signal will be detected, initially more easily seen on FLAIR. This change continues to increase over the next day or two. T1 hypointensity is only seen after 16 hours and persists.  Acute ===== During the first week, the infarcted parenchyma continues to demonstrate high DWI signal and low ADC signal, although by the end of the first week ADC values have started to increase. The infarct remains hyperintense on T2 and FLAIR, with T2 signal progressively increasing during the first 4 days. T1 signal remains low, although some cortical intrinsic high T1 signal may be seen as early as 3 days after infarction. After day 5 the cortex usually demonstrates contrast enhancement. Less common patterns of enhancement include arterial enhancement, encountered in approximately half of strokes and becomes evident after 3 days, and meningeal enhancement which is uncommon and is usually seen between 2 and 6 days. Hemorrhage, most easily seen on susceptibility-weighted imaging (SWI:used to identiy small hemorrhage and calcium. Although most commonly seen after 12 hours and within the first few days, it may occur earlier or as late as 5 days. Subacute ======== ADC demonstrates pseudonormalization typically occurring between 10-15 days. As ADC values continue to rise, infarcted tissue progressively gets brighter than normal parenchyma. In contrast, DWI remains elevated due to persistent high 2/FLAIR signal ([[T2 shine through;](https://radiopaedia.org/articles/t2-shine-through?lang=us)it is phenomenon cause increase DWI]), unless hemorrhage ([[T2 blackout:](https://radiopaedia.org/articles/t2-blackout-effect?lang=us)hypointensity on DWI]) or cystic encephalomalacia. Cortical enhancement is usually present throughout the subacute period. T1 weighted sequences continue to show hypointensity throughout the area of infarct with cortical intrinsic high T1 signal due to the liquefactive necrosis and influx of monocytes as a response. The terms \"cortical laminar necrosis\" or \"pseudolaminar necrosis\" are occasionally, but incorrectly, used to describe this appearance in the context of thromboembolic stroke, but should be restricted to use in cases of isolated cortical necrosis. Chronic ======= T1 signal remains low with intrinsic high T1 in the cortex if cortical necrosis is present T2 signal is high. Cortical contrast enhancement usually persists for 2 to 4 months. Importantly if parenchymal enhancement persists for more than 12 weeks the presence of an underlying lesion should be considered. ADC values are high. DWI signal is variable, but as time goes on signal progressively decreases. Transcranial Doppler ultrasound =============================== Often described as an emerging application of [[point-of-care] [ultrasonography],](https://radiopaedia.org/articles/point-of-care-ultrasound-curriculum?lang=us) use of [[transcranial Doppler (TCD)] [sonography]](https://radiopaedia.org/articles/transcranial-doppler-sonography-ultrasound-1?lang=us) has been utilized for the diagnosis of intracranial [vessel occlusion], as well as the [differentiation between ischemic] [and hemorrhagic stroke.] In the context of a CT negative for intracerebral hemorrhage and a clinically suspicious patient presentation, diagnostic criteria for occlusion of an isolated vessel are as follows: - complete absence of [[color flow Doppler]](https://radiopaedia.org/articles/color-flow-doppler-ultrasound?lang=us) signals - absence of [[pulsed-wave Doppler]](https://radiopaedia.org/articles/spectral-doppler-ultrasound?lang=us) signals - concurrent adequate visualization of surrounding parenchyma and vessels. color flow and pulsed wave Doppler signals must be demonstrated adequately in the remainder of the circle of Willis. Sonographic monitoring of the complications of ischemic stroke is also possible, including the detection of: measurement of the optic nerve sheath diameter ([[ONSD])](https://radiopaedia.org/articles/optic-nerve-sheath-diameter?lang=us) in common use as an intracranial pressure surrogate. Treatment and prognosis ======================= Acute treatment focuses on prompt application of reperfusion therapies: - intravenous or intra-arterial thrombolysis (e.g. alteplase, tenecteplase) - [[mechanical] [thrombectomy]](https://radiopaedia.org/articles/endovascular-clot-retrieval-ecr?lang=us) Neurosurgical intervention can also be pursued in certain cases, to allow patients to survive the period of maximal swelling by performing decompressive craniotomies (with or without duroplasty), particularly in younger patients with either large MCA infarcts or posterior fossa infarcts. Additionally, supportive care should be provided, including caring for patients in dedicated inpatient stroke units and attempting to prevent the numerous complications which are encountered by patients with neurological impairment from stroke (e.g. [[aspiration] [pneumonia],](https://radiopaedia.org/articles/aspiration-pneumonia?lang=us) [[pressure ulcers],](https://radiopaedia.org/articles/missing?article%5btitle%5d=pressure-ulcers&lang=us) etc.).