[Transient global amnesia - benign memory blackout]. / Transiente globale Amnesie ­ gutartiger "Blackout" im Gedächtnis.

Transient global amnesia (TGA) is a typical clinical syndrome characterized by acute, predominantly anterograde amnesia. New epidemiological data assume a significantly higher annual incidence than previously assumed, namely around 15 cases per 100,000 people. Those affected, usually over the age of 50, cannot remember new memory content for longer than 30-180 seconds and therefore ask repetitive questions about current events. All other cognitive functions are unimpaired, and everything previously learnt, e.g. driving or cooking, can be carried out. The episodes are self-limiting and by definition subside within 24 hours. At least 10% of those affected will experience 1-5 recurrences in the future. The punctate lesions in the hippocampus, which are found on MRI in at least 50% of patients after 24-72 hours, are distributed 2/3 unilaterally and 1/3 bilaterally. Using 7 Tesla MRI the frequency of detected lesions increases to 90% compared to 50% with 1.5 or 3 Tesla. Beyond the punctiform hippocampal lesions, other memory-related network disorders, including the default network, are also suggested to be involved in the pathomechanism of TGA. TGA etiology and pathophysiology are not known in detail. Vascular, migraine-like, epilepsy-like, and psychogenic mechanisms are discussed. Triggers of the episodes are often physical exertion with a Valsalva character. Management is aimed at identifying the syndrome based on the typical clinical presentation and ruling out possible differential diagnoses with similar symptoms. During the TGA, the usually anxious relatives should be reassured of the benign and inconsequential nature of the episode.

[Vertigo from a neurological point of view]. / Schwindel aus neurologischer Sicht.

Vertigo has many different causal disorders, ranging from general dizziness and orthostatic regulation disorders to attacks of rotary vertigo. A targeted anamnesis and clinical examination can be used to narrow down the differential diagnosis. Questions about the type of dizziness, the duration and accompanying symptoms must be clarified. Various methods are used for differentiation in clinical examinations: the head impulse test, testing of the vertical divergence of the eyes, positioning maneuvers and the ability to stand and walk. But diagnostic imaging is also important. MRI can be used to confirm or rule out vascular causes (cerebral infarction or minor bleeding) and inflammatory lesions. Because the most serious misdiagnosis of dizziness is overlooking a stroke.

Neurological symptoms in aortic dissection: a challenge for neurologists.

Typically, aortic dissection has to be considered in patients with acute thoracic or abdominal pain and accompanying cardiovascular symptoms. Due to these clinical symptoms, neurologists have not been involved in the routine emergency management of aortic dissection. However, transient or permanent neurological symptoms at onset of aortic dissection are not only frequent (17-40% of the patients), but often dramatic and may mask the underlying condition. Especially in pain-free dissection (which occurs in 5-15%) with predominant neurological symptoms diagnosis of aortic dissection can be difficult and delayed. Affecting the outflow of supra-aortal, spinal as well as extremity arteries leads to a variety of neurological symptoms including disturbances of central or peripheral nervous system. Thrombolysis as an emergency stroke therapy without considering aortic dissection may be life-threatening for these patients. Routine chest X-ray and being alert to physical examination findings such as hypotension, asymmetrical pulses or cardiac murmur may reduce risk of delayed diagnosis or misdiagnosis. Neurological symptoms at onset or in the postoperative course of aortic dissection are not necessarily associated with increased mortality.