Cognitive Mechanisms of Memory Impairment Following Traumatic Brain Injury

Memory impairment is common following traumatic brain injury (TBI). In recent years, researchers have demonstrated that the processes underlying memory formation (working memory, encoding, consolidation, and retrieval) are interrelated but dissociable events.The following study was designed to determine how these processes contribute to memory impairment following experimental TBI in the rat. Experiment 1 indicated thatTBI induces severe working memory deficits in a delayed non-matching-to-place task.Although all animals displayed intact acquisition, only injured animals displayed poor performance as the delay between the sample and choice phases was increased.Experiment 2 was designed to determine if TBI produces a transient period of posttraumatic amnesia (PTA) following TBI. During the early post-injury period, injured animals displayed intact short-term (3min) object recognition memory but impaired long-term (1 and 24hrs) memory. However, during the chronic post-injury period (days 14-17), no recognition memory deficits were observed in injured animals, indicating thatPTA resolves by 14 days post-injury. Experiment 3 was designed to determine the mechanism of anterograde memory impairment following TBI. Animals were injured and then trained to a pre-determined criterion in a 1 -day water maze procedure.Although injured animals required more trials to reach criterion, the rate of forgetting was identical among sham and injured groups up to 24hrs post-training. This suggests that the amount of information encoded into long-term memory, not more rapid forgetting, is the primary mechanism of anterograde memory impairment following TBI. InExperiment 4, animals were trained in the water maze and then injured 1 (recent memory) or 14 (recent memory) days post-training. Fourteen days post-injury, animals were given a retention probe trial followed by a reminding procedure and a second probe trial. Injured animals in both the recent and remote memory conditions displayed impaired performance on the first probe trial. However, injured animals benefited from the reminding procedure, and animals in the remote memory group were identical to shams during the second probe trial. These results indicate that retrograde memory impairment following TBI is mediated primarily by retrieval deficits at the time of testing, while the quality of the memory trace remains largely intact.

Name thesis:degree_name

Doctor of Philosophy

Level thesis:degree_level

Dissertation

Discipline thesis:degree_discipline

Psychology

Year dc:date.available

2007

Author dc:creator

• Whiting, Mark D.

Contributors dc:contributor

• Dr. Robert J. Hamm

• memory
• amnesia
• hippocampus
• information processing
• amnesic disorder
• memory impairment
• cognition
• brain trauma
• Psychology
• Social and Behavioral Sciences

Statement dc:rights

• © The Author

Identifier

https://scholarscompass.vcu.edu/etd/1380

OAI identifier oai:identifier

oai:scholarscompass.vcu.edu:etd-2379