No abstract

Affective experience colours everyday perception and cognition, yet its fundamental and neurobiological basis is poorly understood. The current debate essentially centers around the communalities and specificities across individuals, events, and emotional categories like anger, sadness, and happiness. Using fMRI during the experience of these emotions, we critically compare the two dominant conflicting theories on human affect. Basic emotion theory posits emotions as discrete universal entities generated by dedicated emotion category-specific neural circuits, while psychological construction theory claims emotional events as unique, idiosyncratic, and constructed by psychological primitives like core affect and conceptualization, which underlie each emotional event and operate in a predictive framework. Based on the findings of 8 a priori-defined model-specific prediction tests on the neural response amplitudes and patterns, we conclude that the neurobiological basis of affect is primarily characterized by idiosyncratic mechanisms and a common neural basis shared across emotion categories, consistent with psychological construction theory. The findings provide further insight into the organizational principles of the neural basis of affect and brain function in general. Future studies in clinical populations with affective symptoms may reveal the corresponding underlying neural changes from a psychological construction perspective.

IzvlečekV razvitem svetu ima 5-10 % prebivalstva nad 65 let demenco, katere pojavnost še vedno narašča. Demence zaradi možganskih žilnih bolezni -vaskularna demenca (VaD) predstavljajo dobro petino vseh vzrokov za demenco. Milejša oblika je vaskularni kognitivni upad (VaKU). Za postavitev diagnoze VaD je pomembno, da sta upad spoznavnih sposobnosti in možgansko-žilna bolezen jasno časovno povezana ter ni popravljivih vzrokov za kognitivni upad. Pri postavitvi diagnoze uporabimo nevropsihološko testiranje in slikovne preiskave.Glavni dejavniki tveganja za VaKU in VaD so starost, ateroskleroza, sladkorna bolezen in arterijska hipertenzija, ki sprožijo kaskado dogodkov v patogenezi kognitivne okvare. Ta je zelo raznolika in poteka z ali brez pridruženih nevroloških simptomov. Klinična slika je odvisna od področja in velikosti možganske spremembe.Pri zdravljenju VaKU in VaD je najbolj pomembna primarna preventiva. Za zdravljenje simptomov VaKU in VaD se uporabljajo enaka zdravila kot za zdravljenje simptomov Alzheimerjeve bolezni. Pomembni sta še rehabilitacija in sekundarna preventiva ponovne možganske kapi. AbstractIn the developed world, five to ten percent of people older than 65 years have dementia. One fifth of dementia etiologies are due to vascular brain lesions (VaD -vascular dementia). A milder form is called vascular cognitive impairment (VCI). The main clinical criteria for VaD are: 1. cognitive decline verified with standardized cognitive test/scale, 2. evidence of the associated vascular brain lesion, 3. excluded reversible causes of cognitive decline.The main risk factors for VaD are age, atherosclerosis, diabetes and hypertension. They play a key role in pathogenesis of the cognitive impairment. Depending on the damaged brain region, different cognitive domains may be affected with or without other neurological signs. These diversities in the clinical picture challenge the correct diagnosis. Unique feature of VaD is its progression, which can be stopped, if patients receive an appropriate treatment.The treatment of VCI and VaD symptoms is similar to that in Alzheimer's disease. More importantly, VCI may be slowed down or even stopped with proper secondary stroke prevention and good rehabilitation. The most efficient is primary stroke prevention with healthy lifestyle and treatment of acquired risk factors.