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Biomechanics of pediatric head injury
PARKINSON’S DISEASE: WHAT IS THE KEY IN THE PATHOGENESIS? G. bzelci Kavas, M. C. Akbostanci, P. Anbal Kocattirk, F. Tan
CEREBRAL HEMODYNAMICS AFTER TBAUMATIC BBAININJUBY OFIMMATUBEBR4IN William M. Armstead Departments of Anesthesia and Pharmacology, Universiq of Pennsylvania and the Children’s Hospital of Philadelphia, PA, USA
Department of Pathophysiology and Department of Neurology, Faculty of Medicine, Ankara Universiv, Ankara, TURKEY
These studies were designed to characterize the cerebral hemodynamic effects of fluid percussion brain injury (FPI) in the newborn pig equipped with a closed cranial window. Reductions in cerebral blood flow, pial artery diameter, and cerebral oxygenation following FPI were greater in newborn (l-3 days old) vs. juvenile (3-4 weeks old) pigs, suggesting that newborns were exquisitely sensitive to brain injury. Additionally, in piglets, there was decremented dilation to nitric oxide, cGMP, and CAMP dependent stimuli following FPI. The membrane potential of vascular muscle is an important contributor to vascular tone and the activity of Kf channels is an important regulator of membrane potential. Recent studies indicate that altered dilator responsiveness and cerebral hemodynamic control following FPI results from impaired K’ channel function. Mechanisms involved in such impaired K’ channel function may link altered cerebral hemodynamics to neuronal cell damage following FPI.
Although several hypotheses are currently being investigated the cause of Parkinson’s disease (PD) is still UllkIlOWtl. The aim of this study, was to investigate one of the pathogenic endogenous factors in PD. In this preliminary study, 2 1 Parkinsonian patients with the mean age of 61 were compared with the control group in the same age, according to their red cell copper-zinc superoxide dismutase (Cu-Zn SOD) activities, and plasma copper, zinc concentrations. Red cell Cu-Zn SOD activity was measured spectrophotomeuically while plasma copper, zinc concentrations were determined by atomic Correlation between spectrophotometer. absorption UPDRS scoring and HBPNO scoring values and Cu-Zn SOD activities were also studied. The results were analyzed by Student’s t test statistically. The results showed that red cell Cu-Zn SOD activities of the patients increased (5262+774 U/g-I%) in PD and trace element concentrations altered correspondingly but there were not any correlation between the parameters studied. It was concluded that some endogenous factors, beyond the genetic and environmental factors, may lead to PD by causing increased oxidation.
042 BIOMECHANICS OF PEDIATRIC HEAD INJURY F. A. Bandak, T. G. Toridis
ANIMAL MODELS OF TRAUMATIC BRAIN INJURY IN THE DEVELOPING BRAIN P. David Adelson
Department of Neurosurgery Pittsburgh, PA, USA
School of Engineering and Applied Science, The George Washington University Washington DC, USA
Universify of Pittsburgh,
Head trauma is a leading cause of death in children. Even those children who survive their head injuries, often have significant and permanent cognitive and functional deficits. Although numerous studies have characterized the anatomical, neurophysiological, and functional disturbances after traumatic brain injury (TBI) in adults and in adult animal models, little is known about the pathophysiology of TBI in the immature due in part to the relative dearth of information on animal models of TBI in the immature, developing brain. Clinically, there are potentially important clues about the unique response of TBI in children. Children respond differently to severe TBI by more commonly exhibiting diffuse cerebral swelling than adults. The development of diffuse or “malignant” cerebral swelling though is associated with increased mortality and disability when it occurs in both children and adults. The mechanism(s) involved in the development of diffuse swelling remain to be determined, though some have hypothesized that it is a result of acute biochemical cascade of events, cerebrovascular failure with hyperemia and/ or cerebral edema as part of the secondary response to the primary injury. Important information about these pathophysiological events and disturbances after both focal and difise TBI are lacking in immature animals.
Mechanically induced head injuries in children occur under the same biomechanics principles that govern head injuries in adults. Many studies have proposed possible operative mechanical actions that are responsible for head injuries. No consensus exists on the differences between mechanisms of injury in children and adults. Here, we present a brief exposition of some computer techniques used biomechanics analysis of head injury mechanisms and the applicability of these techniques to children. We also present a previously proposed biomechanics-based paradigm for the assessment of the damaging events that are thought to be responsible for head injury in children. Substantiated by biomechanics, these events constitute the history that can be used to help determine causes in unwitnessed head injury cases.
In this talk, the speaker will introduce the available models of TBI in developing animals and some of the studies to date
that have attempted to these pathophysiologic disturbances unique to the immature brain. Some of the early findings of these new models as well as their future applications and directions will also be discussed.
235
CEREBRAL HEMODYNAMICS AFTER TBAUMATIC BBAININJUBY OFIMMATUBEBR4IN William M. Armstead Departments of Anesthesia and Pharmacology, Universiq of Pennsylvania and the Children’s Hospital of Philadelphia, PA, USA
Department of Pathophysiology and Department of Neurology, Faculty of Medicine, Ankara Universiv, Ankara, TURKEY
These studies were designed to characterize the cerebral hemodynamic effects of fluid percussion brain injury (FPI) in the newborn pig equipped with a closed cranial window. Reductions in cerebral blood flow, pial artery diameter, and cerebral oxygenation following FPI were greater in newborn (l-3 days old) vs. juvenile (3-4 weeks old) pigs, suggesting that newborns were exquisitely sensitive to brain injury. Additionally, in piglets, there was decremented dilation to nitric oxide, cGMP, and CAMP dependent stimuli following FPI. The membrane potential of vascular muscle is an important contributor to vascular tone and the activity of Kf channels is an important regulator of membrane potential. Recent studies indicate that altered dilator responsiveness and cerebral hemodynamic control following FPI results from impaired K’ channel function. Mechanisms involved in such impaired K’ channel function may link altered cerebral hemodynamics to neuronal cell damage following FPI.
Although several hypotheses are currently being investigated the cause of Parkinson’s disease (PD) is still UllkIlOWtl. The aim of this study, was to investigate one of the pathogenic endogenous factors in PD. In this preliminary study, 2 1 Parkinsonian patients with the mean age of 61 were compared with the control group in the same age, according to their red cell copper-zinc superoxide dismutase (Cu-Zn SOD) activities, and plasma copper, zinc concentrations. Red cell Cu-Zn SOD activity was measured spectrophotomeuically while plasma copper, zinc concentrations were determined by atomic Correlation between spectrophotometer. absorption UPDRS scoring and HBPNO scoring values and Cu-Zn SOD activities were also studied. The results were analyzed by Student’s t test statistically. The results showed that red cell Cu-Zn SOD activities of the patients increased (5262+774 U/g-I%) in PD and trace element concentrations altered correspondingly but there were not any correlation between the parameters studied. It was concluded that some endogenous factors, beyond the genetic and environmental factors, may lead to PD by causing increased oxidation.
042 BIOMECHANICS OF PEDIATRIC HEAD INJURY F. A. Bandak, T. G. Toridis
ANIMAL MODELS OF TRAUMATIC BRAIN INJURY IN THE DEVELOPING BRAIN P. David Adelson
Department of Neurosurgery Pittsburgh, PA, USA
School of Engineering and Applied Science, The George Washington University Washington DC, USA
Universify of Pittsburgh,
Head trauma is a leading cause of death in children. Even those children who survive their head injuries, often have significant and permanent cognitive and functional deficits. Although numerous studies have characterized the anatomical, neurophysiological, and functional disturbances after traumatic brain injury (TBI) in adults and in adult animal models, little is known about the pathophysiology of TBI in the immature due in part to the relative dearth of information on animal models of TBI in the immature, developing brain. Clinically, there are potentially important clues about the unique response of TBI in children. Children respond differently to severe TBI by more commonly exhibiting diffuse cerebral swelling than adults. The development of diffuse or “malignant” cerebral swelling though is associated with increased mortality and disability when it occurs in both children and adults. The mechanism(s) involved in the development of diffuse swelling remain to be determined, though some have hypothesized that it is a result of acute biochemical cascade of events, cerebrovascular failure with hyperemia and/ or cerebral edema as part of the secondary response to the primary injury. Important information about these pathophysiological events and disturbances after both focal and difise TBI are lacking in immature animals.
Mechanically induced head injuries in children occur under the same biomechanics principles that govern head injuries in adults. Many studies have proposed possible operative mechanical actions that are responsible for head injuries. No consensus exists on the differences between mechanisms of injury in children and adults. Here, we present a brief exposition of some computer techniques used biomechanics analysis of head injury mechanisms and the applicability of these techniques to children. We also present a previously proposed biomechanics-based paradigm for the assessment of the damaging events that are thought to be responsible for head injury in children. Substantiated by biomechanics, these events constitute the history that can be used to help determine causes in unwitnessed head injury cases.
In this talk, the speaker will introduce the available models of TBI in developing animals and some of the studies to date
that have attempted to these pathophysiologic disturbances unique to the immature brain. Some of the early findings of these new models as well as their future applications and directions will also be discussed.
235