Model Of Acute Subdural Hematoma Research Articles

Experimental acute subdural hematoma in infant piglets.

Traumatic acute subdural hematoma is associated with high mortality in the pediatric population, yet the pathophysiology remains poorly understood. The objective of this study was to develop a pediatric model of acute subdural hematoma, and to evaluate the resultant histopathological changes in the brain. Ten 3-week-old piglets were studied. A 5-mm craniotomy was made in the right frontal skull. A small silastic tube was inserted through the underlying intact dura into the subdural space. A craniotomy was made posterior to the right coronal suture with underlying dura left intact (closed cranial window model). Injection of 5 ml autologous, nonheparinized blood was accomplished through the silastic tube. Animals were sacrificed after 72 h or 1 week. During the subdural injection, intracranial pressure rose to 62 +/- 8 mm Hg, and returned to baseline within 1 h of surgery. Mean arterial blood pressure increased transiently. Cresyl violet and hematoxylin and eosin staining demonstrated extensive areas of white matter necrosis under the hematoma after 72 h survival (n = 7). Zones of necrosis were also noted in cortex, but were less extensive than those seen in white matter. These results differ from adult rodent models in which cortex is primarily affected. This is the first reported pediatric model of traumatic acute subdural hematoma. This model can be used in future studies to investigate pharmacological or other therapies which may improve outcome after this type of injury.

Effect of neuroprotective N-methyl-D-aspartate antagonists on increased intracranial pressure: studies in the rat acute subdural hematoma model.

Glutamate antagonists are the most powerful neuroprotective drugs in laboratory studies of focal cerebral ischemia. Because the majority of clinical conditions in which focal brain ischemia occurs are associated with high intracranial pressure (ICP), we have used the rat acute subdural hematoma model to evaluate the effects of three glutamate N-methyl-D-aspartate antagonists, MK-801, CGS 19755 (SELFOTEL), D-CPP-ene, and mannitol, upon ICP and also upon the volume of ischemic brain damage. Only mannitol produced a significant reduction in ICP and improved cerebral perfusion pressure. The three glutamate antagonists did not significantly affect ICP or cerebral perfusion pressure, but they were associated with a significantly smaller zone of focal brain damage, when compared to the mannitol and saline groups. N-methyl-D-aspartate antagonists do not increase ICP or jeopardize cerebral perfusion pressure when administered under anesthesia with a controlled PaCO2 level. Further studies in humans are indicated.

Glucose hypermetabolism after acute subdural hematoma is ameliorated by a competitive NMDA antagonist.

Intracranial hematomas occur in almost half of patients who sustain a severe head injury, and outcome is particularly poor in patients with acute subdural hematoma. We have measured regional cerebral glucose metabolism (2-deoxyglucose autoradiography) in a new rat model of acute subdural hematoma and compared the changes to those seen in sham-operated control animals and animals pretreated with a high-affinity competitive NMDA antagonist, D-CPP-ene. At 2 h after inducing the hematoma, a severe reduction in glucose use was seen in the cortex beneath the hematoma (less than 5 mumol/100g/min) consistent with a zone of histologic infarction seen in other studies. A band of markedly increased glucose use was seen in the periischemic zone, surrounding this infarcted tissue and throughout the hippocampus bilaterally (up to 142% increase). Both the zone of reduced glucose use and the volume of tissue with increased glucose metabolism were significantly reduced in the animals pretreated with D-CPP-ene. These data indicate that the neuroprotective effect of NMDA antagonists, seen in this and other models, may be mediated by reducing the increased metabolism that occurs probably due to glutamate release.

Ischemic neuronal damage after acute subdural hematoma in the rat: effects of pretreatment with a glutamate antagonist

The ability of a competitive N-methyl-D-aspartate (NMDA) receptor antagonist (D-CPP-ene) to reduce irreversible brain damage has been examined in a rodent model of acute subdural hematoma. Acute subdural hematoma was produced by the slow injection of 400 microliters homologous blood into the subdural space overlying the parietal cortex in halothane-anesthetized rats. Brain damage was assessed histologically in sections at multiple coronal planes in animals sacrificed 4 hours after induction of the subdural hematoma. Pretreatment with D-CPP-ene (15 mg/kg) significantly reduced the volume of ischemic brain damage produced by the subdural hematoma from 62 +/- 8 cu mm (mean +/- standard error of the mean) in vehicle-treated control rats to 29 +/- 7 cu mm in drug-treated animals. These data demonstrate the anti-ischemic efficacy of NMDA antagonists in an animal model of intracranial hemorrhage in which intracranial pressure is elevated, and suggest that excitotoxic mechanisms (which are susceptible to antagonism by D-CPP-ene) may play a role in the ischemic brain damage which is observed in patients who die after acute subdural hematoma.

Ischemic brain damage in a model of acute subdural hematoma: Miller JD, Bullock R, Graham DI, et al Neurosurgery 27:433–438 Sep 1990

Ischemic brain damage in a model of acute subdural hematoma: Miller JD, Bullock R, Graham DI, et al Neurosurgery 27:433–438 Sep 1990

Ischemic brain damage in a model of acute subdural hematoma

Ischemic brain damage is the most important neuropathological finding in humans who die after acute subdural hematoma; however, its causes are poorly understood. We have produced acute subdural hematoma in the rat by injecting 400 microliters of autologous blood (approximately 20% of intracranial volume) into the subdural space. Extensive areas of ischemic damage, involving 14 to 16% of the volume of the hemisphere, developed in this model at 4 and 24 hours after the lesion. The hematomas were associated with a brief peak in intracranial pressure (51 mm Hg), which remained at three times normal levels (14 mm Hg) for 3 hours. In this model, therefore, ischemic damage appears to be due to the local effects of blood overlying the cortex at 4 hours after the ictus, rather than to globally raised intracranial pressure. The implications for the pathophysiology of acute subdural hematomas in humans are discussed.

Ischemic Brain Damage in a Model of Acute Subdural Hematoma

Ischemic brain damage is the most important neuropathological finding in humans who die after acute subdural hematoma: however, its causes are poorly understood. We have produced acute subdural hematoma in the rat by injecting 400 μl of autologous blood (∽20% of intracranial volume) into the subdural space. Extensive areas of ischemic damage, involving 14 to 16% of the volume of the hemisphere, developed in this model at 4 and 24 hours after the lesion. The hematomas were associated with a brief peak in intracranial pressure (51 mm Hg), which remained at three times normal levels (14 mm Hg) for 3 hours. In this model, therefore, ischemic damage appears to be due to the local effects of blood overlying the cortex at 4 hours after the ictus, rather than to globally raised intracranial pressure. The implications for the pathophysiology of acute subdural hematomas in humans are discussed. (Neurosurgery 27:433-439, 1990)