OBJECTIVE: To examine whether impaired memory in persons with traumatic brain injury (TBI) is caused by impaired initial acquisition or compromised retrieval from long-term storage. DESIGN: Prospective matched controlled trial. SETTING: Postacute rehabilitation institute. PARTICIPANTS: Patients with moderate to severe TBI (n = 28) and 21 matched, healthy controls (HCs). MAIN OUTCOME MEASURES: Patients with TBI and HC subjects were equated on initial acquisition on a verbal list-learning task. Recall and recognition performance was then evaluated at 30- and 90-minutes after learning. RESULTS: All HC subjects and 20 subjects with TBI (TBI-MET) were able to meet the learning criterion, but the TBI-MET group took significantly more trials than HC subjects to do so. However, after equating groups on acquisition, the TBI-MET group did not differ from controls on recall and recognition at both the 30- and 90-minute delays. Eight TBI subjects showed severe learning deficits (TBI-NOT MET) because they never learned the task, and showed significantly impaired recall and recognition performance. The 2 TBI groups did not differ on measures of severity of injury, but the TBI-NOT MET group performed significantly below the TBI-MET group on executive functioning. Rate of forgetting did not differ across the 3 groups. CONCLUSIONS: Results suggest that memory impairment after TBI is caused primarily by deficiencies in initial acquisition of verbal information rather than in compromised retrieval. The findings have significant implications for the rehabilitation and treatment of individuals with TBI.
OBJECTIVE: To examine whether impaired memory in persons with traumatic brain injury (TBI) is caused by impaired initial acquisition or compromised retrieval from long-term storage. DESIGN: Prospective matched controlled trial. SETTING: Postacute rehabilitation institute. PARTICIPANTS: Patients with moderate to severe TBI (n = 28) and 21 matched, healthy controls (HCs). MAIN OUTCOME MEASURES: Patients with TBI and HC subjects were equated on initial acquisition on a verbal list-learning task. Recall and recognition performance was then evaluated at 30- and 90-minutes after learning. RESULTS: All HC subjects and 20 subjects with TBI (TBI-MET) were able to meet the learning criterion, but the TBI-MET group took significantly more trials than HC subjects to do so. However, after equating groups on acquisition, the TBI-MET group did not differ from controls on recall and recognition at both the 30- and 90-minute delays. Eight TBI subjects showed severe learning deficits (TBI-NOT MET) because they never learned the task, and showed significantly impaired recall and recognition performance. The 2 TBI groups did not differ on measures of severity of injury, but the TBI-NOT MET group performed significantly below the TBI-MET group on executive functioning. Rate of forgetting did not differ across the 3 groups. CONCLUSIONS: Results suggest that memory impairment after TBI is caused primarily by deficiencies in initial acquisition of verbal information rather than in compromised retrieval. The findings have significant implications for the rehabilitation and treatment of individuals with TBI.
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