No abstract

Working memory is frequently impaired after traumatic brain injury (TBI). The present study aimed to investigate working memory deficits in patients with diffuse axonal injury and to determine the contribution of cerebral activation dysfunctions to them. Eighteen patients with severe TBI and 14 healthy controls matched for age and gender were included in the study. TBI patients were selected according to signs of diffuse axonal injury on computed tomography (CT) and without any evidence of focal lesions on MRI clinical examination. Functional magnetic resonance (fMRI) was used to assess brain activation during n-back tasks (0-, 2-, and 3-back). Compared to controls, the TBI group showed significant working memory impairment on the Digits Backwards (p=0.022) and Letter-Number Sequencing subtests from the WAIS-III (p<0.001) under the 2-back (p=0.008) and 3-back (p=0.017) conditions. Both groups engaged bilateral fronto-parietal regions known to be involved in working memory, although patients showed less cerebral activation than did controls. Decreased activation in TBI patients compared to controls was observed mainly in the right superior and middle frontal cortex. The correlation patterns differed between patients and controls: while the control group showed a negative correlation between performance and activation in prefrontal cortex (PFC), TBI patients presented a positive correlation in right parietal and left parahippocampus for the low and high working memory load, respectively. In conclusion, severe TBI patients with diffuse brain damage show a pattern of cerebral hypoactivation in the right middle and superior frontal regions during working memory tasks, and also present an impaired pattern of performance correlations.

This study shows that memory problems are the most prominent and relevant impairment, although all other cognitive functions are also impaired, affecting both memory itself and general behaviour. Statistical analysis also provides preliminary evidence on the different profile of memory impairment whether cerebral anoxia had hypoxic or ischemic origin.

Objectives: How brain damage after stroke is related to specific clinical manifestation and recovery is incompletely understood. We studied cognitive reserve (CR) in stroke patients by two types of measurements: (i) objectively verifiable static proxies (i.e., education, occupational attainment), and (ii) subjective, dynamic proxies based on patient testimony in response to a questionnaire. We hypothesized that one or both of these types of CR measurements might correlate positively with patient cognitive performance during the post-acute and chronic phases of recovery. Method: Thirty-four stroke patients underwent neuropsychological assessment at 2, 6 and 24 months after stroke onset. In chronic stage at 24+ months, self-rating assessments of cognitive performance in daily life and social integration were obtained. CR before and after stroke was estimated using static proxies and dynamic proxies were obtained using the Cognitive Reserve Scale (CRS-Pre-stroke, CRS-Post-stroke). Results: CRS-Pre-stroke and CRS-Post-stroke showed significant mean differences. Dynamic proxies showed positive correlation with self-assessment of attention, metacognition, and functional ability in chronic stage. In contrast, significant correlations between static proxies and cognitive recovery were not found. Conclusions: Dynamic proxies of CR were positively correlated with patients’ perception of their functional abilities in daily life. To best guide cognitive prognosis and treatment, we propose that dynamic proxies of CR should be included in neuropsychological assessments of patients with brain damage.