scholarly journals Maturation-dependent response of the piglet brain to scaled cortical impact

2000 ◽  
Vol 93 (3) ◽  
pp. 455-462 ◽  
Author(s):  
Ann-Christine Duhaime ◽  
Susan S. Margulies ◽  
Susan R. Durham ◽  
Maureen M. O'Rourke ◽  
Jeffrey A. Golden ◽  
...  
Keyword(s):  
Mechanical Trauma ◽  
Content Type ◽  
Clinical Syndromes ◽  
Contusion Injury ◽  
Different Ages ◽  
Focal Brain Injury ◽  
Maturational Stage ◽  
Cortical Impact ◽  
Focal Injury ◽  
Fine Print

Object. The goal of this study was to investigate the relationship between maturational stage and the brain's response to mechanical trauma in a gyrencephalic model of focal brain injury. Age-dependent differences in injury response might explain certain unique clinical syndromes seen in infants and young children and would determine whether specific therapies might be particularly effective or even counterproductive at different ages.Methods. To deliver proportionally identical injury inputs to animals of different ages, the authors have developed a piglet model of focal contusion injury by using specific volumes of rapid cortical displacement that are precisely scaled to changes in size and dimensions of the growing brain. Using this model, the histological response to a scaled focal cortical impact was compared at 7 days after injury in piglets that were 5 days, 1 month, and 4 months of age at the time of trauma. Despite comparable injury inputs and stable physiological parameters, the percentage of hemisphere injured differed significantly among ages, with the youngest animals sustaining the smallest lesions (0.8%, 8.4%, and 21.5%, for 5-day-, 1-month-, and 4-month-old animals, respectively, p = 0.0018).Conclusions. These results demonstrate that, for this particular focal injury type and severity, vulnerability to mechanical trauma increases progressively during maturation. Because of its developmental and morphological similarity to the human brain, the piglet brain provides distinct advantages in modeling age-specific responses to mechanical trauma. Differences in pathways leading to cell death or repair may be relevant to designing therapies appropriate for patients of different ages.

Atorvastatin reduction of intracranial hematoma volume in rats subjected to controlled cortical impact

2004 ◽  
Vol 101 (5) ◽  
pp. 822-825 ◽  
Author(s):  
Dunyue Lu ◽  
Asim Mahmood ◽  
Changsheng Qu ◽  
Anton Goussev ◽  
Mei Lu ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Functional Improvement ◽  
Intracranial Hematoma ◽  
Imaging Device ◽  
Controlled Cortical Impact ◽  
Content Type ◽  
Tissue Sections ◽  
Male Wistar Rats ◽  
Cortical Impact ◽  
Fine Print

Object. Atorvastatin, a β-hydroxy-β-methylglutaryl coenzyme A reductase inhibitor, has pleiotropic effects such as improving thrombogenic profile, promoting angiogenesis, and reducing inflammatory responses and has shown promise in enhancing neurological functional improvement and promoting neuroplasticity in animal models of traumatic brain injury (TBI), stroke, and intracranial hemorrhage. The authors tested the effect of atorvastatin on intracranial hematoma after TBI. Methods. Male Wistar rats were subjected to controlled cortical impact, and atorvastatin (1 mg/kg) was orally administered 1 day after TBI and daily for 7 days thereafter. Rats were killed at 1, 8, and 15 days post-TBI. The temporal profile of intraparenchymal hematoma was measured on brain tissue sections by using a MicroComputer Imaging Device and light microscopy. Conclusions. Data in this study showed that intraparenchymal and intraventricular hemorrhages are present 1 day after TBI and are absorbed at 15 days after TBI. Furthermore, atorvastatin reduces the volume of intracranial hematoma 8 days after TBI.

Ultrastructural scoring of graded acute spinal cord injury in the rat

2002 ◽  
Vol 97 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Erkan Kaptanoglu ◽  
Selcuk Palaoglu ◽  
H. Selcuk Surucu ◽  
Mutlu Hayran ◽  
Etem Beskonakli
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Behavioral Assessment ◽  
Traumatic Injury ◽  
Significant Negative Correlation ◽  
Content Type ◽  
Cord Injury ◽  
Contusion Injury ◽  
Weight Drop ◽  
Fine Print

Object. There is a need for an accurate quantitative histological technique that also provides information on neurons, axons, vascular endothelium, and subcellular organelles after spinal cord injury (SCI). In this paper the authors describe an objective, quantifiable technique for determining the severity of SCI. The usefulness of ultrastructural scoring of acute SCI was assessed in a rat model of contusion injury. Methods. Spinal cords underwent acute contusion injury by using varying weights to produce graded SCI. Adult Wistar rats were divided into five groups. In the first group control animals underwent laminectomy only, after which nontraumatized spinal cord samples were obtained 8 hours postsurgery. The weight-drop technique was used to produce 10-, 25-, 50-, and 100-g/cm injuries. Spinal cord samples were also obtained in the different trauma groups 8 hours after injury. Behavioral assessment and ultrastructural evaluation were performed in all groups. When the intensity of the traumatic injury was increased, behavioral responses showed a decreasing trend. A similar significant negative correlation was observed between trauma-related intensity and ultrastructural scores. Conclusions. In the present study the authors characterize quantitative ultrastructural scoring of SCI in the acute, early postinjury period. Analysis of these results suggests that this method is useful in evaluating the degree of trauma and the effectiveness of pharmacotherapy in neuroprotection studies.

Platelet-activating factor and progressive brain damage following focal brain injury

1990 ◽  
Vol 73 (2) ◽  
pp. 223-233 ◽  
Author(s):  
Kai U. Frerichs ◽  
Perttu J. Lindsberg ◽  
John M. Hallenbeck ◽  
Giora Z. Feuerstein
Keyword(s):  
Brain Injury ◽  
Brain Damage ◽  
Neuronal Death ◽  
Hippocampal Neurons ◽  
Neuronal Damage ◽  
Platelet Activating Factor ◽  
Secondary Brain Damage ◽  
Content Type ◽  
Focal Brain Injury ◽  
Fine Print

✓ The effects of a platelet-activating factor (PAF) antagonist on brain edema, cortical microcirculation, blood-brain barrier (BBB) disruption, and neuronal death following focal brain injury are reported. A neodymium:yttrium-aluminum-garnet (Nd:YAG) laser was used to induce highly reproducible focal cortical lesions in anesthetized rats. Secondary brain damage in this model was characterized by progressive cortical hypoperfusion, edema, and BBB disruption in the vicinity of the hemispheroid lesion occurring acutely after injury. The histopathological evolution was followed for up to 4 days. Neuronal damage in the cortex and the hippocampus (CA-1) was assessed quantitatively, revealing secondary and progressive loss of neuronal tissue within the first 24 hours following injury. Pretreatment with the PAF antagonist BN 50739 ameliorated the severe hypoperfusion in 12 rats (increasing local cerebral blood flow from a mean ± standard error of the mean of 40.5% ± 8.3% to 80.2% ± 7.8%, p < 0.01) and reduced edema by 70% in 10 rats (p < 0.05) acutely after injury. The PAF antagonist also reduced the progression of neuronal damage in the cortex and the CA-1 hippocampal neurons (decrease of neuronal death from 88.0% ± 3.9% to 49.8% ± 4.2% at 24 hours in the cortex and from 40.2 ± 5.0% to 13.2% ± 2.1% in the hippocampus in 30 rats; p < 0.05). This study provides evidence to support progressive brain damage following focal brain injury, associated with secondary loss of neuronal cells. In this latter process, PAF antagonists may provide significant therapeutic protection in arresting secondary brain damage following cerebral ischemia and neurological trauma.

Thoracic aortic pseudoaneurysm after spine trauma in ankylosing spondylitis

2005 ◽  
Vol 2 (2) ◽  
pp. 218-221 ◽  
Author(s):  
Jason Lifshutz ◽  
Zvi Lidar ◽  
Dennis Maiman
Keyword(s):  
Ankylosing Spondylitis ◽  
Aortic Injury ◽  
Spine Fracture ◽  
Mechanical Trauma ◽  
Early Investigation ◽  
Content Type ◽  
Aortic Pseudoaneurysm ◽  
Increased Risk ◽  
Organ Manifestations ◽  
Fine Print

✓ Ankylosing spondylitis (AS) is a rheumatic disease characterized by consolidation of the articulating surfaces and inflammation of the vertebral column. Because of its associated spine stiffness and secondary osteoporosis, patients with this disorder are at increased risk of vertebral fractures. Ankylosing spondylitis presents a significant challenge to spine surgeons because of its complex effects on the spine, extraarticular organ manifestations, and potential neurological and functional sequelae. Traumatic thoracic and lumbar spine injuries in this patient population may be associated with injury to the aorta either due to direct mechanical trauma or to blunt forces associated with the spine fracture. This complication and association is thought to be the result of pathophysiological changes that cause the aorta to become firmly adherent to the anterior longitudinal ligament. The authors present a case of AS in a patient with a thoracic spine fracture and in whom a delayed thoracic aortic pseudoaneurysm ruptured. To the best of the authors' knowledge, only five cases of this complex condition have been reported since 1980. Recognition of the potential for aortic injury in patients with AS should prompt early investigation of the aorta in cases involving numerous fractures and assist in surgical planning to avoid this lethal injury.

Hyperventilation early after controlled cortical impact augmented neuronal death in CA3 hippocampus

1998 ◽  
Vol 88 (3) ◽  
pp. 549-556 ◽  
Author(s):  
Michael L. Forbes ◽  
Robert S. B. Clark ◽  
C. Edward Dixon ◽  
Steven H. Graham ◽  
Donald W. Marion ◽  
...  
Keyword(s):  
Functional Outcome ◽  
Neuronal Death ◽  
Hippocampal Neurons ◽  
Secondary Injury ◽  
Controlled Cortical Impact ◽  
Content Type ◽  
Beam Balance ◽  
Cortical Impact ◽  
Normal Ventilation ◽  
Fine Print

Minimizing secondary injury after severe traumatic brain injury (TBI) is the primary goal of cerebral resuscitation. For more than two decades, hyperventilation has been one of the most often used strategies in the management of TBI. Laboratory and clinical studies, however, have verified a post-TBI state of reduced cerebral perfusion that may increase the brain's vulnerability to secondary injury. In addition, it has been suggested in a clinical study that hyperventilation may worsen outcome after TBI. Object. Using the controlled cortical impact model in rats, the authors tested the hypothesis that aggressive hyperventilation applied immediately after TBI would worsen functional outcome, expand the contusion, and promote neuronal death in selectively vulnerable hippocampal neurons. Methods. Twenty-six intubated, mechanically ventilated, isoflurane-anesthetized male Sprague—Dawley rats were subjected to controlled cortical impact (4 m/second, 2.5-mm depth of deformation) and randomized after 10 minutes to either hyperventilation (PaCO2 = 20.3 ± 0.7 mm Hg) or normal ventilation groups (PaCO2 = 34.9 ± 0.3 mm Hg) containing 13 rats apiece and were treated for 5 hours. Beam balance and Morris water maze (MWM) performance latencies were measured in eight rats from each group on Days 1 to 5 and 7 to 11, respectively, after controlled cortical impact. The rats were killed at 14 days postinjury, and serial coronal sections of their brains were studied for contusion volume and hippocampal neuron counting (CA1, CA3) by an observer who was blinded to their treatment group. Mortality rates were similar in both groups (two of 13 in the normal ventilation compared with three of 13 in the hyperventilation group, not significant [NS]). There were no differences between the groups in mean arterial blood pressure, brain temperature, and serum glucose concentration. There were no differences between groups in performance latencies for both beam balance and MWM or contusion volume (27.8 ± 5.1 mm3 compared with 27.8 ± 3.3 mm3, NS) in the normal ventilation compared with the hyperventilation groups, respectively. In brain sections cut from the center of the contusion, hippocampal neuronal survival in the CA1 region was similar in both groups; however, hyperventilation reduced the number of surviving hippocampal CA3 neurons (29.7 cells/hpf, range 24.2–31.7 in the normal ventilation group compared with 19.9 cells/hpf, range 17–23.7 in the hyperventilation group [25th–75th percentiles]; *p < 0.05, Mann—Whitney rank-sum test). Conclusions. Aggressive hyperventilation early after TBI augments CA3 hippocampal neuronal death; however, it did not impair functional outcome or expand the contusion. These data indicate that CA3 hippocampal neurons are selectively vulnerable to the effects of hyperventilation after TBI. Further studies delineating the mechanisms underlying these effects are needed, because the injudicious application of hyperventilation early after TBI may contribute to secondary neuronal injury.

Symptomatic hydrocephalus and reversible spinal cord compression in Listeria monocytogenes meningitis

1989 ◽  
Vol 71 (4) ◽  
pp. 620-622 ◽  
Author(s):  
Eric C. Raps ◽  
David H. Gutmann ◽  
James R. Brorson ◽  
Michael O'Connor ◽  
Howard I. Hurtig
Keyword(s):  
Spinal Cord ◽  
Listeria Monocytogenes ◽  
Cord Compression ◽  
Cervical Cord ◽  
Communicating Hydrocephalus ◽  
Ventricular Drainage ◽  
Central Nervous System Infections ◽  
Content Type ◽  
Clinical Syndromes ◽  
Fine Print

✓ Central nervous system infections with Listeria monocytogenes result in varied clinical syndromes ranging from meningitis to rhomboencephalitis. A case of Listeria meningitis complicated by symptomatic communicating hydrocephalus and hydrostatic cervical cord compression is presented which clinically and radiographically improved with aggressive ventricular drainage.

Olfactory glia transplantation into cervical spinal cord contusion injuries

2005 ◽  
Vol 3 (4) ◽  
pp. 308-317 ◽  
Author(s):  
Jorge E. Collazos-Castro ◽  
Vilma C. Muñetón-Gómez ◽  
Manuel Nieto-Sampedro
Keyword(s):  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Axonal Growth ◽  
Cell Transplant ◽  
Tracer Injection ◽  
Neural Repair ◽  
Content Type ◽  
Cord Injury ◽  
Contusion Injury ◽  
Fine Print

Object. The results of olfactory ensheathing cell (OEC) transplantation have raised great expectations as a potential treatment for spinal cord injury (SCI). Its capacity to promote functional neural repair, however, remains unclear. The authors studied axonal growth and locomotor recovery after C-7 contusion injury and OEC transplantation in adult rats. Methods. Twenty-four male Wistar rats underwent a mild C-7 contusion injury that completely disrupted the dorsal corticospinal tract (DCST). In 14 rats OECs were transplanted into the lesion, and 10 were used as controls. At 3 months postcontusion, the kinematics of locomotion were assessed, and the CST was traced by injecting dextran tetramethylrhodamine bilaterally into the cerebral cortex. The animals were killed 2 weeks after tracer injection, and their spinal cords were studied immunohistochemically. Although the survival of transplanted cells varied, they were present in all cases. The authors observed neither OEC migration nor DCST axon regeneration in any of the cell transplant—treated rats. Corticospinal axons ended in retraction bulbs at the proximal edge of the lesion or, exceptionally, a few micrometers inside the transplant. The results of neurofilament immunohistochemical analysis provided evidence of neurites from systems other than the DCST growing into the transplant, but in some cases these neurites formed loops of pathological appearance. Contusion injury of C-7 caused chronic locomotor deficits that did not improve after OEC transplants. Conclusions. The findings in this study indicate that OEC transplants alone are not sufficient for neural repair and functional recovery after SCI. In addition, OECs can induce abnormal axonal growth, making further studies necessary before considering their clinical use.

Experience with Arnold-Chiari malformation, 1960 to 1970

1976 ◽  
Vol 45 (4) ◽  
pp. 416-422 ◽  
Author(s):  
Ruben J. Saez ◽  
Burton M. Onofrio ◽  
Takehiko Yanagihara
Keyword(s):  
Retrospective Study ◽  
Neurological Deficit ◽  
Chiari Malformation ◽  
Prognostic Significance ◽  
Cerebellar Dysfunction ◽  
Content Type ◽  
Arnold Chiari Malformation ◽  
Clinical Syndromes ◽  
Suboccipital Decompression ◽  
Fine Print

✓ A retrospective study of 60 adult patients with Arnold-Chiari malformation revealed that certain presenting clinical syndromes, although not pathognomonic, seemed to have definite prognostic significance. Surgical management by suboccipital decompression led to remarkable and enduring improvement in 65% of patients followed for as long as 14 years. In some patients, however, the initial postoperative benefit tended to fade into an insidious progression of neurological deficit. Despite operation, 18.6% of patients eventually experienced progressive neurological deterioration. Patients who presented with paroxysmal intracranial hypertension or cerebellar dysfunction had the best prognosis. Evidence of central cord involvement was the single most detrimental factor to neurological recovery.

In situ fixation of the spinal cord using microwave radiation

1988 ◽  
Vol 69 (5) ◽  
pp. 719-722 ◽  
Author(s):  
David J. Gower ◽  
Carol Hollman ◽  
K. Stuart Lee ◽  
Michael Tytell
Keyword(s):  
Spinal Cord ◽  
Mechanical Trauma ◽  
Tissue Fixation ◽  
Easy Method ◽  
Content Type ◽  
In Situ Fixation ◽  
Tissue Degradation ◽  
Perfusion Fixation ◽  
Fine Print

✓ Due to its investiture with bone, the spinal cord can be difficult to study anatomically and histologically. Tissue degradation during immersion fixation or mechanical trauma during extraction of unfixed tissue often produces confusing artifacts. Perfusion fixation eliminates many of these problems, but it is a slow, tedious, and technically demanding procedure. This report demonstrates that microwave irradiation of the spinal cord before its removal from the spine is a rapid and easy method of tissue fixation with an absence of artifacts comparable to that with perfusion fixation.

Relative susceptibility of elements of the cerebral cortex to mechanical trauma in the rat

1971 ◽  
Vol 35 (5) ◽  
pp. 517-522 ◽  
Author(s):  
Melvin H. Epstein
Keyword(s):  
Central Nervous System ◽  
Tissue Culture ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Nutrient Medium ◽  
Model System ◽  
Mechanical Trauma ◽  
Content Type ◽  
The Central Nervous System ◽  
Fine Print

✓ A model system for the study of trauma to elements of the central nervous system is described. It consists of floating samples of cortex (1 mm3) in nutrient medium. After variable amounts of trauma the cortical samples are allowed to grow in tissue culture, or their individual cytoarchitectonic layers are studied metabolically in the Cartesian diver. The results indicate that neurons are the most labile cellular elements when the cerebral cortex is exposed to mechanical trauma. The glia are the next most vulnerable to damage while the fibroblastic series are highly resistant to concussive forces.

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