Search results
Results from the WOW.Com Content Network
Anterograde amnesia can also be caused by alcohol intoxication, a phenomenon commonly known as a blackout. Studies show rapid rises in blood alcohol concentration over a short period of time severely impair or in some cases completely block the brain's ability to transfer short-term memories created during the period of intoxication to long ...
Patient N.A. (born July 9, 1938) was an anonymous man from the United States who developed anterograde amnesia due to a fencing accident. The cause of his amnesia was found to be a thalamic lesion extending to the hypothalamus. Damage to the temporal cortex was also found and was suspected to be a result of an exploratory surgery. [1]
In 1981, Cochrane was involved in a motorcycle accident that left him with severe anterograde amnesia, as well as temporally graded retrograde amnesia. Like other amnesic patients (patient HM, for example), Cochrane had his semantic memory intact, but lacked episodic memory with respect to his entire past. [2]
For example, anterograde amnesia, from damage of the medial temporal lobe, is an impairment of declarative memory that affects both episodic and semantic memory operations. [16] Originally, Tulving proposed that episodic and semantic memory were separate systems that competed with each other in retrieval.
Amnesia is an abnormal mental state in which memory and learning are affected out of all proportion to other cognitive functions in an otherwise alert and responsive patient. [5] There are two forms of amnesia: Anterograde amnesia and retrograde amnesia, that show hippocampal or medial temporal lobe damage.
Individuals with retrograde amnesia may partially regain memory later, but memories are not regained with anterograde amnesia because they were not encoded properly. [ 8 ] The term "post-traumatic amnesia" was first used in 1940 in a paper by Symonds to refer to the period between the injury and the return of full, continuous memory, including ...
Another example demonstrated by some patients, such as K.C. and H.M, who have medial temporal damage and anterograde amnesia, still have perceptual priming. Priming was accomplished in many different experiments of amnesia, and it was found that the patients can be primed; they have no conscious recall of the event, but the response is there. [20]
Systematic studies of anterograde amnesia started to emerge in the 1960s and 1970s. The case of Henry Molaison, formerly known as patient H.M., became a landmark in studies of memory as it relates to amnesia and the removal of the hippocampal zone and sparked massive interest in the study of brain lesions and their effect on