Imaging of Stroke: Part 2, Pathophysiology at the Molecular and Cellular Levels and Corresponding Imaging Changes

Abstract

The pathophysiology of stroke has several complex mechanisms. Understanding these mechanisms is essential to derive neuroprotective agents that limit neuronal damage after ischemia. Imaging and clinical strategies aimed at extending the therapeutic window for reperfusion treatment with mechanical and pharmacologic thrombolysis will add value to existing treatment strategies. Acute ischemic stroke is defined as abrupt neurologic dysfunction due to focal brain ischemia resulting in persistent neurologic deficit accompanied by characteristic abnormalities on brain imaging. Knowledge of the pathophysiologic mechanisms of neuronal injury in stroke is essential to target treatment. Neuroprotective and thrombolytic agents have been shown to improve clinical outcome. Physiologic imaging with diffusion-weighted imaging (DWI) and perfusion CT and MRI provide a pathophysiologic substrate of evolving ischemic stroke.

MRI of Cerebellar Infarction

“…Common risk factors for venous sinus thrombosis include puerperium, oral contraceptives, protein C of factor V Leiden deficiency and dehydration [28,29,30]. …”

“…1, 3, 4, and 6) are usually readily recognised as bright areas on DWI with low signal on apparent diffusion coefficient (ADC) maps due to restricted diffusion, although it should be noted that infarcts in the posterior circulation may be more often DWI negative than those in the anterior circulation [36,37,38]. DWI becomes positive within minutes after the onset of infarction because of cytotoxic oedema [1,30]. In the following hours, infarcts become hyperintense on FLAIR and T2-weighted images (T2WI).…”

“…Brain swelling peaks at about 3 days, and infarct volume in the acute stage on DWI is therefore not a reliable indicator of the final infarct size [30]. In the second half of the first week, infarcts considerably diminish in size and diffusion (pseudo-)normalises after around 10 days (1-4 weeks) [30].…”

“…In the second half of the first week, infarcts considerably diminish in size and diffusion (pseudo-)normalises after around 10 days (1-4 weeks) [30]. Thus, MRI provides the greatest diagnostic yield when performed as soon as possible (certainly within a few days) of symptom onset, especially in minor stroke.…”

Harnessing the Potential of Biomaterials for Brain Repair after Stroke

“…The last phase of a stroke is the delayed injury or chronic phase, occurring in the weeks following the initial occlusion (Heiss, 2012;Kanekar et al, 2012). In this phase, there is widespread edema and activation of proteases and cytokines.…”