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|LETTER TO EDITOR
|Year : 2017 | Volume
| Issue : 4 | Page : 889-890
Fluctuation of diffusion-weighted imaging and apparent diffusion coefficient in acute stroke following tissue plasminogen activator administration
Aníbal S Chertcoff1, Juan Chomont2, Lucrecia Bandeo1, Fátima Pantiu1, Claudia Uribe Roca1, Pablo Bonardo1, Carlos Rugilo2, Ricardo Reisin1
1 Department of Neurology, Buenos Aires British Hospital, Ciudad Autónoma de Buenos Aires, Argentina
2 Department of Radiology, Buenos Aires British Hospital, Ciudad Autónoma de Buenos Aires, Argentina
|Date of Web Publication||5-Jul-2017|
Aníbal S Chertcoff
Perdriel 74, 1280, Ciudad Autónoma de Buenos Aires
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Chertcoff AS, Chomont J, Bandeo L, Pantiu F, Roca CU, Bonardo P, Rugilo C, Reisin R. Fluctuation of diffusion-weighted imaging and apparent diffusion coefficient in acute stroke following tissue plasminogen activator administration. Neurol India 2017;65:889-90
|How to cite this URL:|
Chertcoff AS, Chomont J, Bandeo L, Pantiu F, Roca CU, Bonardo P, Rugilo C, Reisin R. Fluctuation of diffusion-weighted imaging and apparent diffusion coefficient in acute stroke following tissue plasminogen activator administration. Neurol India [serial online] 2017 [cited 2019 Aug 19];65:889-90. Available from: http://www.neurologyindia.com/text.asp?2017/65/4/889/209477
Acute cerebral infarction can be rapidly identified by magnetic resonance imaging (MRI) through the finding of diffusion-weighted imaging (DWI) hyperintensity with associated reduction in apparent diffusion coefficient (ADC) signal. Under ischemic conditions, DWI restriction occurs within minutes and usually persists for 7–10 days. ADC values begin to increase 5–10 days after the onset of stroke. Traditionally, alterations in both sequences have been considered a surrogate marker of irreversible infarct core. However, there have been reports showing partial or complete reversal of abnormalities on DWI and ADC after early reperfusion during the first 24 hours of stroke onset.,, We report the case of a 46-year old woman who experienced sudden-onset aphasia, mild right-sided hemiparesis, and dysarthria. She presented to the emergency department within 3 hours of symptom onset, and her National Institute of Health Stroke Scale score (NIHSS) on admission was 5. MRI revealed a hyperintense signal on DWI involving the left insular cortex with a severely reduced value of ADC (mean diffusivity: 377 × 10−6 mm 2/s) [Figure 1]; her brain MR angiography showed a proximal occlusion of the middle cerebral artery (MCA). Intravenous tissue plasminogen activator (t-PA) was administered resulting in significant symptomatic improvement after infusion (NIHSS 1). A second MRI performed 11 hours after the symptom onset displayed reduction of the hyperintense lesion on DWI and normalization of the ADC signal (mean diffusivity: 761 × 10−6 mm 2/s) [Figure 1]. Recanalization of MCA was also observed. During hospitalization, a pulmonary embolism and a patent foramen ovale were diagnosed; stroke was interpreted as being due to paradoxical embolism. At 72 hours after stroke onset, a third MRI exhibited enlargement of the DWI lesion and a new decrease in ADC values (mean diffusivity: 524 × 10−6 mm 2/s) [Figure 1]. Normal flow signal on the MCA persisted. Despite the fluctuation being visible on neuroimaging, the patient remained clinically stable.
|Figure 1: DWI, ADC, fluid-attenuated inversion recovery (FLAIR) and magnetic resonance angiography (MRA) at 3, 11 and 72 hours after symptom onset. The DWI hyperintense lesion observed on admission initially decreased in size and then augmented; ADC hypointense signal normalizes after t-PA and reappeared at 72 hours. A normal FLAIR sequence was noticed on admission, a hyperintense signal appeared at 11 and 72 hours. MRA exhibited occlusion of the left middle cerebral artery on admission. After t-PA, recanalization was observed at 11 hours and persisted on the latter MRA|
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DWI hyperintensity in acute ischemic stroke was once considered to represent irreversible tissue damage due to ischemia. Nevertheless, as seen in our presented case, recent studies have shown that abnormalities in diffusion during the first few hours of ischemic stroke might have a fluctuating course in patients receiving tissue plasminogen activator (t-PA). A study analyzing ADC reversal in stroke patients treated with local arterial thrombolysis divided the patients into two groups based upon whether or not they achieved satisfactory recanalization. The study revealed that ADC and DWI signal reversal after treatment correlated with angiographic recanalization. A conclusion was drawn that both sequences could be useful not only to show a fixed ischemic lesion but also the dynamic processes such as reperfusion after thrombolysis. Other studies also suggest that early DWI lesion reversal could be related to rapid recanalization and reperfusion. In one study, DWI reversal was observed only in 7% of patients receiving t-PA, although most of them, as in our case, later exhibited lesion reappearance. The mechanisms probably involved in the DWI lesion reappearance include early T2 “shine-through phenomenon” and ADC decline due to late secondary ischemic injury. The phenomenon of late secondary injury has been extensively described in animal models of transient brain ischemia and has been related to the severity and duration of tissue hypoxia leading to neuronal necrosis due to late energy failure, cellular apoptosis, and reperfusion-associated injury. In the presented case, a late ADC decline was observed and may have been responsible for the variability in imaging. Neurologists should be aware that fluctuations on DWI and ADC could be found in patients with acute stroke during the first days after reperfusion.
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