Introduction: In 2022 the DGN (Deutsche Gesellschaft für Neurologie) published an updated Transient Global Amnesia (TGA) guideline. TGA is characterized by a sudden onset of retrograde and anterograde amnesia for a period of one to a maximum of 24 h (with an average of 6 to 8 h). The incidence is estimated between 3 and 8 per 100,000 population/year. TGA is a disorder that occurs predominantly between 50 and 70 years. Recommendations: The diagnosis of TGA should be made clinically. In case of an atypical clinical presentation or suspicion of a possible differential diagnosis, further diagnostics should be performed immediately. The detection of typical unilateral or bilateral punctate DWI/T2 lesions in the hippocampus (especially the CA1 region) in a proportion of patients proves TGA. The sensitivity of MRI is considered higher when performed between 24 and 72 h after onset. If additional DWI changes occur outside the hippocampus, a vascular etiology should be considered, and prompt sonographic and cardiac diagnostics should be performed EEG may help to differentiate TGA from rare amnestic epileptic attacks, especially in recurrent amnestic attacks. TGA in patients < 50 years of age is a rarity, therefore it is mandatory to rapidly search for other causes in particular in younger patients. The cause of TGA is still unknown. Numerous findings in recent years point to a multifactorial genesis. Because the pathomechanism of TGA is not yet clearly known, no evidence-based therapeutic or prophylactic recommendations can be made. Conclusions: There is no evidence for chronic sequelae of TGA with respect to cerebral ischemia, chronic memory impairment, or the onset of dementia-related syndromes.

Susceptibility-weighted magnetic resonance imaging (MRI) (SWI) offers additional information on conventional MRI contrasts. Central veins can be identified within lesions, and recently, it has been suggested that multiple sclerosis (MS) lesions with slowly expanding demyelination, so-called smoldering lesions, can be identified by a phase rim surrounding the lesion. We analyzed post-contrast SWI in regard to intrinsic lesion characteristics in a cohort of MS patients. A total of 294 MS patients were evaluated using a 3-T MRI. A comprehensive MRI protocol was used including post-contrast SWI. Lesions of at least 5 mm in size were analyzed on conventional MRI and SWI with a structured reporting scheme with a focus on SWI lesion characteristics. A total of 1,323 lesions were analyzed: 1,246/1,323 (94%) were non-enhancing and 77/1,323 (6%) were contrast-enhancing (CE) lesions. In CE lesions, the following patterns were seen: contrast enhancement was nodular in 34/77, ring-shaped enhancement was present in 33/77, and areas of peripheral enhancement were present in 10/77. In CE lesions, an association with central veins was found in 38/77 (50%). In 75/1,246 (6%) non-enhancing lesions, a central dark dot in keeping with a central vein was seen, whereas 162/1,246 (13%) showed peripheral hypointense dots/rims, 199/1,246 (16%) showed scattered hypointense dots mainly within the lesion area, and in 374/1,246 (30%), no SWI hypointensity was detected. Furthermore, 436/1,246 (35%) lesions showed isointensity to the surrounding tissue and were not visible on SWI. SWI is able to offer additional aspects of MS pathology also when used after the application of a contrast agent. Veins connected to lesions, a potentially useful marker in the differential diagnosis of MS, were seen in about 50% of enhancing lesions. Susceptibility artifacts, suggested to mark the presence of myelin-laden macrophages and smoldering inflammation, were visible in 28% of lesions as hypointense dots in and in the periphery of the lesion. Given those results, SWI may provide practical useful additional information in the evaluation of the lesion status in MS patients.