İleriye Dönük Bellek Bozukluğu

Bellek, zamana göre kısa süreli bellek ve uzun süreli bellek olarak iki kategoriye ayrılabilir. Uzun süreli belleğimizdeki bilinçli olarak hatırlayabildiğimiz bilgiler bildirimsel bellekte yer almaktadır. Bilinçli olarak hatırlanamayan bilgiler ise bildirimsel olmayan bellekte yer alır. İleriye dönük bellek bozukluğu, bellek bozukluğuna yol açan olaydan itibaren yeni anıların oluşturulamaması anlamına gelmektedir. Bu tür bellek bozukluğuna sahip olan hastalarda genellikle epizodik bellek ve semantik bellek korunmuş durumdadır. İleriye dönük bellek bozukluğu en çok kafa travması sonucu ortaya çıkmaktadır fakat serebrovasküler olaylar, Wernicke-Korsakoff Sendromu, merkezi sinir sistemi enfeksiyonları, anoksi ve çeşitli maddeler de ileriye dönük bellek bozukluğuna yol açabilmektedir. Bu durumla ilişkili temel olarak iki beyin bölgesi bulunmaktadır: Medial temporal lob ve medial diensefalon. Medial temporal lob, hipokampus, amigdala, parahipokampal korteks, peririnal korteks ve entorinal korteksten oluşmaktadır. Hipotalamus, talamus, mamiller cisimcikler ve çeşitli talamik nukleuslar ise medial diensefalonu oluşturmaktadır. Ayrıca forniks ve nadiren serebellum hasarı da ileriye dönük bellek bozukluğu gelişiminde rol oynamaktadır. Epileptik cerrahi ameliyatı nedeniye ileriye dönük bellek bozukluğu gelişen ünlü H.M vakasının ardından hipokampus, bellek araştırmalarının merkezine yerleşmiştir. Literatürde ölümünden sonra beyin dokuları incelenen bellek bozukluğu hastaları ile ilgili birkaç bildirim bulunmaktadır. Bu ölüm sonrası histolojik değerlendirmeler, hipokampal nöron kaybı gibi ortak bazı bulgulara işaret etmektedir. Benzodiyazepinler genellikle kısa süreli ileriye dönük bellek bozukluğuna neden olmaktadır. Benzodiyazepin reseptörleri gama-aminobutirik asit-A (GABA-A) reseptörleri üzerinde bulunan allosterik modülasyon bölgeleridir. GABA-A reseptörleri beş alt birimden oluşmaktadır ve ileriye dönük bellek bozukluğu, alfa 1 alt birimi aracılığıyla ortaya çıkmaktadır. İleriye dönük bellek bozukluğunun hipokampus ve piriform kortekste uzun süreli güçlenme (long term potentiation [LTP]) oluşumunun engellenmesiyle ortaya çıktığı ileri sürülmektedir. İleriye dönük bellek bozukluğunun tedavisinde mevcut nöron kaybı nedeniyle genellikle farmakolojik yöntemler işe yaramamaktadır. Tedavide bildirimsel olmayan bellekten faydalanmak için hastalar günlük rutinlerini belirlemek üzere eğitilmekte ve birkaç eğitim aşamasından sonra işlemsel belleklerinden faydalanmaya alışmaktadırlar. Sosyal ve duygusal desteğin rolü de büyük önem taşımaktadır.

Anahtar Kelimeler:

İleriye dönük bellek bozukluğu, Bildirimsel bellek, Hipokampus

Anterograde Amnesia

Memory can be divided into two categories (i.e. short term memory and long term memory) according to time span. Information at our long term memory that can be remembered with conscious effort are placed in declarative memory. Information that can not be remembered conciously are placed in nondeclarative memory. The definition of anterograde amnesia is inability to generate new memories after the event causing amnesia. Episodic and semantic memories are usually unaffected among patients' who had such amnesia. Anterograde amnesia could mostly result from head trauma but in some cases the cause could be serebrovascular events, Wernicke-Korsakoff Syndrome, santral nervous system enfections, anoxia or various substances. Medial temporal lobe and medial diencephalon are two brain regions mainly related with this condition. Medial temporal lobe is consisted of hippocampus, amygdala, parahippocampal cortex, perirhinal cortex and entorhinal cortex. Hypothalamus, thalamus, mamillary bodies and several thalamic nucleases compose medial diencephalon. Fornix and rarely serebellum damage may also play role in the development of anterograde amnesia. After the famous H.M case, who had anterograde amnesia after an epileptic surgery operation, hippocampus has been placed in the focus of memory researches. In the literature there are several reports evaluating brain tissues of amnesic patients at postmortem stage. Postmortem histological evaluations consistently revealed hippocampal neuronal loss among these patients' brain tissues. Benzodiazepines usually cause short term anterograde amnesia. Benzodiazepine receptors are allosteric modulatory sites on gamma-aminobutyric acid-A (GABA-A) receptors. GABA-A receptors composed of five subunits and anterograde amnesia emerges by means of alfa 1 subunit. Anterograde amnesia has been suggested to occur by the blocking of long term potentiation in hippocampus and piriform cortex. For the treatment of the anterograde amnesia, pharmacological methods usually do not work because of the neuronal loss. In order to make use of the nondeclarative memory in the treatment process, patients are educated to define their daily routines and after several training steps they get used to profit from their procedural memory. The role of social and emotional support is also very important.

Keywords:

Anterograde amnesia, Declarative memory, Hippocampus,

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