This inability to recall if an episodic memory was real or imagined only compounds the dangers of W-K Syndrome and puts not only the W-K patient but others at risk. Damage to the frontal lobes due to ethanol neurotoxicity, may inhibit ones ability to distinguish between ones internal or external gathered information thus influencing a confusion between imagined and reality when recalling a memory. The etiology of IIE may be causally rooted in brain damage to the prefrontal cortex and anterior thalamic region due to AUD. Pfefferbaum, SRI InternationalĪUD and its consequences such as W-K Syndrome, anterograde, and retrograde amnesia, pose a serious threat to the basic functions of ones life especially when IIE is involved. Larger ventricles are seen in patients with W-K Syndrome because of the bodies inability to maintain, rebuild and repair.Ĭredit: Adapted from a figure by A. Magnetic resonance imaging (MRI) scans have shown the degradation of brain mass associated with Wernicke-Korsakoff Syndrome. IIE due to W-K Syndrome may disrupt an individuals life at the most basic level such as their inability to recall episodic memories such as whether or not they turned off the stove or locked their door, pose a threat to safety. Episodic memories are memories that have been encoded in a temporal way from events in ones life that you can recall (Canvas, 2023). The result of AUD and thiamine deficiency / ethanol neurotoxicity may cause such damage to important brain regions that will cause individuals to confabulate and falsely remember episodic memories (El Haj & Robin, 2020). These disruptions to the biology of the brain such as the thalamus, hypothalamus, hippocampus, and cerebellum are known to have negative and in most cases, irreversible consequences to ones memory.Īdditional to anterograde and retrograde amnesia, Wernicke-Korsakoff’s Syndrome patients may display a form of memory distortion called the imagination inflation effect. Thiamine deficiency can disrupt processes like the synthesis of neurotransmitters, maintenance of membrane potential, and myelination. Wernicke-Korsakoff syndrome is caused by a thiamine (vitamin B1) deficiency most commonly found in individuals with Alcohol Use Disorder (AUD) and associated diets that lack proper nutrition, in this case, thiamine (“Wernicke-Korsakoff Syndrome”, n.d.). Individuals will have severely impaired abilities to form new memories and the recall of previously formed memories (retrograde amnesia). Wernicke-Korsakoff’s Syndrome involves extensive memory deficits such as anterograde amnesia as well as a number of cognitive and behavioral changes. These molecular mechanisms of memory have a biological basis that can be affected by conditions such as Wernicke encephalopathy or its more advanced, irreversible stage, Korsakoff’s syndrome. Building such a network by way of long-term potentiation, has been hypothesized to share the same mechanisms as long-term memory. The article includes the imagination inflation effect which is seen in individuals suffering from Wernicke-Korsakoff Syndrome and will be included in my post.Įncoding memories on the synaptic level has been observed to strengthen the connection between neighboring cells (Canvas, 2023). The article was published by Mohamad El Haj of the University of Nantes and Hospital of Tourcoing, Tourcoing, France and Frédérique Robin of the University of Nantes. This syndrome, and its relation to long term memory (LTM), is discussed in an article that I have found interesting. The topics that I have chosen involve lesson 8: long-term memory: encoding and retrieval and the detriments of Wernicke-Korsakoff Syndrome. Keywords: Anterograde Amnesia, Anosognosia, Alcohol Use Disorder (AUD), Imagination Inflation Effect (IIE), Long Term Memory (LTM), Thiamine Deficiency, Nutrition, Retrograde Amnesia. Topic: Long-term memory: encoding and retrieval and the detriments of Wernicke-Korsakoff Syndrome.
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