Amnesia pathophysiology: Difference between revisions
No edit summary |
No edit summary |
||
Line 7: | Line 7: | ||
==Pathophysiology== | ==Pathophysiology== | ||
Memory is disrupted by damage that may occur in different parts of the brain such as the [[medial temporal lobe]], the [[hippocampus]], the [[cortex]] and the [[frontal lobe]]. Injury to any of these areas may lead to specific disruptions in the processes of acquiring and recalling memories. For instance, damage to the medial [[temporal lobe]] and [[hippocampus]] can sharply reduce the ability to acquire new [[declarative memory]] whereas damage to the storage areas in the cortex can disrupt retrieval of old memories and interfere with the acquisition of new memories. | Memory is disrupted by damage that may occur in different parts of the brain such as the [[medial temporal lobe]], the [[hippocampus]], the [[cortex]] and the [[frontal lobe]]. Injury to any of these areas may lead to specific disruptions in the processes of acquiring and recalling memories. For instance, damage to the medial [[temporal lobe]] and [[hippocampus]] can sharply reduce the ability to acquire new [[declarative memory]] whereas damage to the storage areas in the cortex can disrupt retrieval of old memories and interfere with the acquisition of new memories. | ||
Anterograde amnesia can result from damage to the [[hippocampal formation|hippocampus]], [[Fornix of brain|fornix]], or [[mammillary bodies]], thus lending credence to the theory that these structures are primarily responsible for laying down long-term memories. However, the condition can also arise from damage to the [[basal forebrain]] (which produces [[acetylcholine]]) or a set of brain structures called the [[diencephalon]]. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} |
Revision as of 14:08, 15 February 2013
Amnesia Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Amnesia pathophysiology On the Web |
American Roentgen Ray Society Images of Amnesia pathophysiology |
Risk calculators and risk factors for Amnesia pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Overview
Amnesia results from damage to different memory centers in the brain, such as the medial temporal lobe and the hippocampus, which are involved in acquiring and restoring memory.
Pathophysiology
Memory is disrupted by damage that may occur in different parts of the brain such as the medial temporal lobe, the hippocampus, the cortex and the frontal lobe. Injury to any of these areas may lead to specific disruptions in the processes of acquiring and recalling memories. For instance, damage to the medial temporal lobe and hippocampus can sharply reduce the ability to acquire new declarative memory whereas damage to the storage areas in the cortex can disrupt retrieval of old memories and interfere with the acquisition of new memories.
Anterograde amnesia can result from damage to the hippocampus, fornix, or mammillary bodies, thus lending credence to the theory that these structures are primarily responsible for laying down long-term memories. However, the condition can also arise from damage to the basal forebrain (which produces acetylcholine) or a set of brain structures called the diencephalon.