Evaluation of the hyperintense acute reperfusion marker for the detection of ischemia in anterior and posterior circulation in patients with transient ischemic /neurological attack

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In the present research project we aim to evaluate the incidence of the hyperintense acute reperfusion marker (HARM) in patients with transient ischemic attack (TIA) or transient neurological attack (TNA). Initially, HARM was described after acute ischemic stroke and is caused by impairment of the blood-brain barrier after recanalization of an acute vessel occlusion and consecutive reperfusion. Disruption of the blood-brain barrier results in the accumulation of contrast agent in the subarachnoid space, which can be demonstrated superbly on fluid attenuated inversion recovery (FLAIR) images.Transient ischemic attacks are defined as a transient focal neurological deficit with a likely cerebrovascular cause. In contrast to this, transient neurological attacks are defined as a transient non-focal neurological deficit with various etiologies, which however also include cerebrovascular causes. The clinical diagnosis of a TIA is often incorrect and the differentiation of TIA and TNA can also be difficult. The MRI is the most important diagnostic procedure for the detection or exclusion of acute cerebral ischemia in patients with TIA/TNA. Acute ischemic lesions can be detected in approximately two thirds of all TIA cases and only in about one-fifth of TNA cases on diffusion-weighted imaging (DWI). Additional perfusion-weighted imaging (PWI) can only slightly increase this proportion. The hyperintense acute reperfusion marker could be complementary to DWI and PWI and could reduce the existing diagnostic gap. In particular, in the case of a TNA this could be of major clinical relevance, in order to avoid mistreatment or even dismissal without further diagnostic testing after unremarkable MRI.Therefore, the aim of this study is to evaluate the incidence of HARM in a statistically relevant number of patients with TIA and TNA and to investigate associations with symptom duration and anatomical localization. In addition, the dynamics of contrast agent accumulation in the subarachnoid space in the case of HARM will be analyzed in detail.