Background: Angioedema (AE) in stroke has been reported exclusively after thrombolysis with recombinant tissue-type plasminogen activator (rtPA). Previous studies proposed the insular cortex to play a specific role in the development of AE after stroke. We evaluated the incidence of AE in acute stroke and tried to identify the predominantly involved brain structures. Methods: We performed a retrospective search of our stroke database for patients with an AE. MRI data were analyzed by adapting the images to a standard size and superimposing the infarctions. The areas of overlap were assumed to represent the areas of interest. Results: 865 of 4,789 (18.1%) consecutive patients with acute stroke received IV rtPA, 20 of them (2.3%) developed AE. One patient developed AE without prior thrombolysis. The odds ratio for AE after rtPA was 93 (95% CI: 12-693). Of the 21 AE patients, 15 (71.4%) had ACE-inhibitor treatment (ACEi) and 7 (33.3%) had diabetes. In all but one patient, AE was clearly lateralized; then the AE was contralateral to the side of the ischemia in 18 of 20 patients (90.0%). An insular/peri-insular involvement was detected in 17/21 (81.0%). About 80.0% of the patients had a suspected MCA branch occlusion. Conclusions: In contrast to AE in other conditions, AE in stroke seems to feature a unique cerebral pathology because it is mostly lateralized (contralateral to an infarction), is associated with a distinct brain area, may even occur without rtPA, and is far more frequent than after thrombolysis for other indications. rtPA is the major risk factor. Similar to prior studies, we identified ACEi to be another risk factor, and a diabetic autonomic instability might further increase the risk. Central pathways involving the insular and peri-insular cortex seem to play a major role in the pathophysiology of AE in stroke.

Since the beginning oft he Covid-19 pandemic we have observed an increased incidence of transient global amnesia, possibly related to emotional stress as a trigger factor.

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<b><i>Background:</i></b> Transient global amnesia (TGA) is a syndrome featuring acute anterograde amnesia as the most striking clinical symptom. Its etiology is still a matter of debate. Most neurological guidelines allow the diagnosis on the basis of clinical criteria only; a more extensive evaluation is recommended only for patients with “red flags” like severe headache, nausea or vomiting, or metabolic abnormalities. The aim of our study was to assess the frequency of a severe underlying disease or alternative diagnoses (mimics) in patients fulfilling the clinical criteria. <b><i>Methods:</i></b> We evaluated the medical records and the imaging data of an unselected consecutive cohort of patients with suspected TGA over a 7-year period. All patients were hospitalized and received a neurological workup including brain imaging, color-coded duplex sonography of the brain supplying arteries, electroencephalography, and laboratory studies of blood and (in selected cases) cerebrospinal fluid. <b><i>Results:</i></b> 163 patients with 166 episodes of suspected TGA were hospitalized (3 patients twice). After the workup, the diagnosis of TGA was confirmed in 148/166 (89.2%) episodes (“simple TGA”). Eighteen patients (10.8%) either had an alternative diagnosis or a severe comorbidity that was assumed to have had an impact on the occurrence of the amnestic episode (“complicated TGA/mimic”). The most important differential diagnosis was stroke (11 patients, 6.6% of all TGA suspects and 61.1% of the complicated TGA/mimic group). Other mimics were transient epileptic amnesia (2 patients) and steroid-induced delirium (1 patient). Important comorbidities that had not been obvious at the time of presentation were severe sleep apnea (2 patients), triptan overuse (1 patient), and an involuntary amlodipine intoxication during TGA. <b><i>Conclusion:</i></b> As approximately every tenth patient with suspected TGA either had an alternative diagnosis or a severe comorbidity, which had not been obvious at the time of admission, we consider in-patient treatment of all suspected TGA cases as appropriate, preferably in the setting of a stroke unit, as ischemic stroke was the by far most important diagnosis mimicking TGA.