Ischemic Brain Damage in a Model of Acute Subdural Hematoma

Miller, J. D.; Bullock, Ross; Graham, David I.; Teasdale, Graham M.

doi:10.1227/00006123-199009000-00016

Cited by 139 publications

(36 citation statements)

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“…The rat subdural hematoma model has demonstrated a consistent zone of ischémie brain damage within the hemisphere beneath the subdural hematoma, as is found in some humans with subdural hematoma (Miller et al, 1990). Using this model, it has previously been possible to demonstrate many of the features of the "excitotoxic" process, and a consistent neuroprotective effect has been found with /V-methyl-D-aspartate (NMDA) antagonists, both in pretreatment and in posttreatment paradigms with this model Chen et al, 1991;Kuroda et al, 1994).…”

Section: Introductionmentioning

confidence: 64%

“…This has not been frequently observed in patients with acute subdural hematoma (Schröder et al, 1994). Miller et al (1990) described a model of acute subdural hematoma in the rat, in which an extensive zone of underlying ischémie damage, involving 14 to 16% of the volume of the hemisphere, could be produced. The pattern of ischémie damage observed in this model is similar to the focal ischémie damage observed in humans who die after acute subdural hematoma Macpherson and Graham, 1978).…”

Section: Subdural Hematomamentioning

confidence: 99%

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The Effect of the Glycine Site-Specific N-Methyl-d-Aspartate Antagonist ACEA1021 on Ischemic Brain Damage Caused by Acute Subdural Hematoma in the Rat

Tsuchida

Bullock

1995

Journal of Neurotrauma

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Acute subdural hematoma (SDH) complicates about 20% of severely head-injured patients, and death and severe disability frequently result, yet over half of these patients may have been conscious, at some time after injury, implying secondary mechanisms of brain damage. Drugs that block the "excitotoxic" effects of glutamate at the N-methyl-D-aspartate (NMDA) receptor have generally been effective in reducing ischemic brain damage associated with SDH in animal models, yet these agents all appear to be associated with major behavioral side effects, in conscious patients, at neuroprotective doses. We therefore evaluated the effects of treatment with a novel antagonist for the glycine binding site of the NMDA receptor (ACEA1021) upon ischemic brain damage, in the rat SDH model. ACEA1021 may be free of psychomotor effects, and may thus permit high dose therapy in conscious trauma and stroke patients. SDH was produced by the slow injection of 0.4 mL autologous blood into the subdural space overlying the parietal cortex. brain damage was assessed histologically at 8 coronal planes, in animals sacrificed 4 h after induction of hematoma. Both pre- and posttreatment with ACEA1021 significantly reduced hemispheric ischemic damage produced by SDH. The magnitude of neuroprotection with this compound (26 to 39% reduction in infarct size) is similar to other NMDA antagonists, and the robust posttreatment effect implies that human studies with this compound should be performed in head injured patients, subject to completion of toxicology testing.

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Section: Introductionmentioning

confidence: 64%

Section: Subdural Hematomamentioning

confidence: 99%

The Effect of the Glycine Site-Specific N-Methyl-d-Aspartate Antagonist ACEA1021 on Ischemic Brain Damage Caused by Acute Subdural Hematoma in the Rat

Tsuchida

Bullock

1995

Journal of Neurotrauma

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“…We have shown that production of an ASDH in rats produces an underlying extensive zone of ischémie brain damage (Miller et al, 1990), reduced CBF , and increased intracranial pressure resulting from edema (Kuroda et al, 1994), as in humans. This model is therefore appropriate to study the pathogenesis of the ischémie process and to evaluate the effect of neuroprotective agents on ischémie brain damage underneath the ASDH (Bullock and Fujisawa, 1992;Chen et al, 1991;Tsuchida et al, 1997).…”

Section: Introductionmentioning

confidence: 83%

Detection of Ultra-Early Brain Damage After Acute Subdural Hematoma in the Rat by Magnetic Resonance Imaging

Tsuchida¹,

Alessandri²,

Corwin³

et al. 1999

Journal of Neurotrauma

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We measured serial changes in diffusion-weighted magnetic resonance imaging (DW) and in apparent diffusion coefficient (ADC) 1 to 3 hours after induction of acute subdural hematoma (ASDH) in rats, to assess the rate of development of cytotoxic edema and ischemic brain damage observed in this model. Cortical ADC values underneath the hematoma in ASDH rats (n = 12) were significantly lower than those in sham-operated rats (n = 5) at 1 hour. By 3 hours, the area of ADC abnormality had further increased. The lesion areas, as percentage of hemispheric areas on 1- and 3-hour ADC maps, correlated significantly with those on the histologic sections stained with hematoxylin and eosin. The results indicate that DWI with ADC mapping may provide a valuable diagnostic tool for monitoring of early pathologic changes following subdural hematoma in head-injured patients.

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“…When autologous, nonheparinized blood is injected through the dorsal burr hole through the dura mater, it typically forms a clot over the dorsal surface of the brain mimicking a posttraumatic subdural hematoma, similar to the management of human subdural hematomas, the experimental protocol involves surgical removal of the clot at a specified time followed by histological measurement of ischemic damage caused by the hematoma [17]. …”

Section: Acute Neurological Injury Modelsmentioning

confidence: 99%