Deficits In Traumatic Brain Injury Research Articles

Verbal Learning and Memory Deficits in Traumatic Brain Injury: Encoding, Consolidation, and Retrieval

The present study examined the nature of verbal memory deficits in individuals with traumatic brain injury (TBI) compared to healthy controls. The study was designed to control for methodological shortcomings of previous related research. Three groups of participants were used: (a) a head injured sample with moderate to severe traumatic brain injuries (N=55), (b) a control sample matched on age and initial performance on CVLT Trial 5 and Sum of Trials 1 to 5 (N=55), and (c) a control sample matched on age, education, and race, but not on initial CVLT learning performance (N=55). Current findings indicate that: (a) rate of learning was comparable across groups, consistent with no encoding differences, (b) TBI patients have a significantly more rapid rate of forgetting of new information than either acquisition-matched or demographic-matched controls, consistent with consolidation problems in TBI, (c) TBI patients have less proactive interference than demographic-matched control participants, consistent with a consolidation problem in the TBI group, (d) TBI patients and acquisition-matched controls have comparably low rates of proactive interference, consistent with impaired acquisition in both of these groups, and (e) TBI patients and controls do not differ in the benefit experienced from semantic or recognition retrieval cues, consistent with no differences in retrieval processes. These data support an impaired consolidation hypothesis, rather than encoding or retrieval deficits, as the primary deficit underlying memory impairment in TBI.

Acquisition versus retrieval deficits in traumatic brain injury: Implications for memory rehabilitation

DeLuca J, Schultheis MT, Madigan NK, Christodoulou C, Averill A. Acquisition versus retrieval deficits in traumatic brain injury: implications for memory rehabilitation. Arch Phys Med Rehabil 2000;81:1327-33. 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. © 2000 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

Lesion-site specific fMRI activation pattern associated with motor deficits in traumatic brain injury

Lesion-site specific fMRI activation pattern associated with motor deficits in traumatic brain injury

An attempt towards differentiating attentional deficits in traumatic brain injury.

Attentional deficits in patients suffering traumatic brain injury (TBI) can occur with minor to severe impact to the brain. Based on reviews of both the cognitive and neurobehavioral literature, the following three concepts of attention are addressed: (a) arousal/alertness, (b) selective attention, and (c) energetic aspects of attention, which include such components as effort, resource allocation, and speed of processing. Within each concept, definitions are proposed, the underlying brain mechanisms are identified, and the specific deficits associated with TBI are explored. This review combines theoretical perspectives and clinical findings with the objective of leading toward a diagnostic differentiation that in turn will benefit treatment planning.

Protective effect of galanin on behavioral deficits in experimental traumatic brain injury.

The magnitude of behavioral deficits in traumatic brain injury (TBI) has been shown to be partly related to alterations in the balance between excitatory and inhibitory neurotransmitter release. Previous studies have demonstrated that extracellular excitatory neurotransmitter concentrations dramatically increase following experimental TBI. We examined the effects of a neuromodulatory peptide, galanin (GAL), on behavioral morbidity, as measured by sensory motor and memory performance tasks, associated with experimental TBI in the rat. A single intraventricular injection of GAL (1.0 micrograms, n = 8 or 10.0 micrograms, n = 10) or cerebrospinal fluid (CSF) vehicle (n = 10) was administered 5 minutes prior to central fluid percussion TBI in rats. Performance on sensory motor tasks was assessed prior to injury and for 5 days after TBI with beam-balance, beam-walking, and rotarod tasks. Memory performance was assessed on days 11-15 after TBI with the Morris water maze. TBI produced significant motor and memory deficits in the CSF-treated group. GAL-treated rats had significantly less magnitude of deficits compared to CSF-treated rats on beam-balance, beam-walking, and rotarod performance. The 1.0 micrograms GAL dose produced slightly greater protection than the 10.0 micrograms GAL dose. Neither GAL dose affected body weight loss or Morris water maze performance. These results suggest that the physiologic effects of GAL may reduce certain components of TBI morbidity, possibly by modulating neuronal excitability.