scholarly journals Novel Neuroprotective Strategies and Targets of Intervention in Epilepsy

10.5772/22781 ◽  
2011 ◽  
Author(s):  
Ryan D. ◽  
Laurie M. ◽  
Patrick G.
Keyword(s):  
Neuroprotective Strategies

Perioperative Neuroprotective Strategies

2008 ◽  
Vol 11 (1) ◽  
pp. 49-56 ◽  
Author(s):  
David P. Nelson ◽  
Dean B. Andropoulos ◽  
Charles D. Fraser
Keyword(s):  
Neuroprotective Strategies

scholarly journals Developing neuroprotective strategies for treatment of HIV-associated neurocognitive dysfunction

2008 ◽  
Vol 2 (3) ◽  
pp. 271-280 ◽  
Author(s):  
Jeffrey A Rumbaugh ◽  
Joseph Steiner ◽  
Ned Sacktor ◽  
Avindra Nath
Keyword(s):  
Neurocognitive Dysfunction ◽  
Neuroprotective Strategies

Cardiopulmonary Bypass Induces Neurologic and Neurocognitive Dysfunction in the Rat

2001 ◽  
Vol 95 (6) ◽  
pp. 1485-1491 ◽  
Author(s):  
G. Burkhard Mackensen ◽  
Yukie Sato ◽  
Bengt Nellgård ◽  
Jose Pineda ◽  
Mark F. Newman ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Water Maze ◽  
Neurologic Outcome ◽  
Spatial Learning And Memory ◽  
Recovery Model ◽  
Neurocognitive Outcome ◽  
Neurocognitive Dysfunction ◽  
Visual Spatial ◽  
Injury Mechanisms ◽  
Neuroprotective Strategies

Background Neurocognitive dysfunction is a common complication of cardiac surgery using cardiopulmonary bypass (CPB). Elucidating injury mechanisms and developing neuroprotective strategies have been hampered by the lack of a suitable long-term recovery model of CPB. The purpose of this study was to investigate neurologic and neurocognitive outcome after CPB in a recovery model of CPB in the rat. Methods Fasted rats (n = 10) were subjected to 60 min of normothermic (37.5 degrees C) nonpulsatile CPB using a roller pump and a membrane oxygenator. Sham-operated controls (n = 10) were not subjected to CPB. Neurologic outcome was assessed on days 1, 3, and 12 after CPB using standardized functional testing. Neurocognitive outcome, defined as the time (or latency) to finding a submerged platform in a Morris water maze (an indicator of visual-spatial learning and memory), was evaluated daily from post-CPB days 3-12. Histologic injury in the hippocampus was also evaluated. Results Neurologic outcome was worse in the CPB versus the sham-operated controls at all three measurement intervals (P < 0.001). The CPB group also had longer water maze latencies compared with the sham-operated controls (P = 0.004), indicating significant neurocognitive dysfunction after CPB. No difference in histologic injury between groups was observed. Conclusions CPB caused both neurologic and neurocognitive impairment in a rodent recovery model. This model could potentially facilitate the investigation of CPB-related injury mechanisms and possible neuroprotective interventions.

scholarly journals Molecular Physiology of Preconditioning-Induced Brain Tolerance to Ischemia

2008 ◽  
Vol 88 (1) ◽  
pp. 211-247 ◽  
Author(s):  
Tihomir Paul Obrenovitch
Keyword(s):  
Defense Mechanisms ◽  
Biological Response ◽  
Tissue Level ◽  
Ischemic Tolerance ◽  
Antioxidant Systems ◽  
Molecular Physiology ◽  
Adaptive Changes ◽  
Functional Changes ◽  
Subsequent Test ◽  
Neuroprotective Strategies

Ischemic tolerance describes the adaptive biological response of cells and organs that is initiated by preconditioning (i.e., exposure to stressor of mild severity) and the associated period during which their resistance to ischemia is markedly increased. This topic is attracting much attention because preconditioning-induced ischemic tolerance is an effective experimental probe to understand how the brain protects itself. This review is focused on the molecular and related functional changes that are associated with, and may contribute to, brain ischemic tolerance. When the tolerant brain is subjected to ischemia, the resulting insult severity (i.e., residual blood flow, disruption of cellular transmembrane gradients) appears to be the same as in the naive brain, but the ensuing lesion is substantially reduced. This suggests that the adaptive changes in the tolerant brain may be primarily directed against postischemic and delayed processes that contribute to ischemic damage, but adaptive changes that are beneficial during the subsequent test insult cannot be ruled out. It has become clear that multiple effectors contribute to ischemic tolerance, including: 1) activation of fundamental cellular defense mechanisms such as antioxidant systems, heat shock proteins, and cell death/survival determinants; 2) responses at tissue level, especially reduced inflammatory responsiveness; and 3) a shift of the neuronal excitatory/inhibitory balance toward inhibition. Accordingly, an improved knowledge of preconditioning/ischemic tolerance should help us to identify neuroprotective strategies that are similar in nature to combination therapy, hence potentially capable of suppressing the multiple, parallel pathophysiological events that cause ischemic brain damage.

Gender differences in the developmental outcomes of children with congenital cardiac defects

2012 ◽  
Vol 22 (5) ◽  
pp. 514-519 ◽  
Author(s):  
Annette Majnemer ◽  
Catherine Limperopoulos ◽  
Michael Shevell ◽  
Charles Rohlicek ◽  
Bernard Rosenblatt ◽  
...  
Keyword(s):  
Gender Differences ◽  
Brain Injury ◽  
Functional Independence Measure ◽  
Early Brain Injury ◽  
Functional Independence ◽  
Receptive Language ◽  
Full Scale ◽  
Fine Motor ◽  
Intellectual Quotient ◽  
Neuroprotective Strategies

AbstractObjectiveThis study compares the developmental and functional outcomes at school entry between boys and girls born with a congenital cardiac defect who required early surgical correction.Study designA prospective cohort of 94 children, including 49 percent boys, were followed up to 5 years of age and assessed for developmental progress. Developmental measures included Wechsler Preschool and Primary Scale of Intelligence – cognitive; Peabody Picture Vocabulary Test – receptive language; Peabody Developmental Motor Scale – motor; and Child Behaviour Checklist – behaviour. Measures of function included the Vineland Adaptive Behavior Scale and Functional Independence Measure for Children (WeeFIM).ResultsThe mean scores of the boys on the WeeFIM subscales, such as self-care, mobility, cognition, were significantly lower than that of the girls. There was a trend for a greater proportion of boys to have abnormalities on neurological examination (boys 37.5 percent abnormal, girls 19.5 percent abnormal). Verbal, performance, and full scale Intellectual Quotients were 5–7 points lower in boys but did not reach significance (full scale Intellectual Quotient: boys 87.7 plus or minus 22.2; girls 93.9 plus or minus 19.3). Boys were more likely to have fine motor delays (50 percent, 82.7 plus or minus 16.5) compared with girls (28.2 percent, 87.0 plus or minus 15.8). There were no gender differences in receptive language or behavioural difficulties.ConclusionsBoys born with congenital heart disease requiring early surgical repair appear to be at enhanced risk for neuromotor impairments and activity limitations. Findings support gender differences in the pathogenesis of early brain injury following hypoxic–ischaemic insults. This has implications for neuroprotective strategies to prevent brain injury.

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