A use-dependent sodium channel antagonist, 619C89, in reduction of ischemic brain damage and glutamate release after acute subdural hematoma in the rat

1996 ◽  
Vol 85 (1) ◽  
pp. 104-111 ◽  
Author(s):  
Eiji Tsuchida ◽  
John F. Harms ◽  
John J. Woodward ◽  
Ross Bullock
Keyword(s):  
Sodium Channel ◽  
Subdural Hematoma ◽  
Neuronal Damage ◽  
Glutamate Release ◽  
Acute Subdural Hematoma ◽  
Extracellular Glutamate ◽  
Ischemic Brain ◽  
Content Type ◽  
Glutamate Concentration ◽  
Fine Print

✓ Acute subdural hematoma kills or disables more severely head injured patients than any other complication of cranial trauma. The main pathological factor involved is ischemic neuronal damage, which is caused by raised intracranial pressure and local effect. The authors have evaluated the hypothesis that a novel use-dependent sodium channel antagonist, 619C89, could reduce ischemic brain damage in the rat subdural hematoma model. Because previous studies have shown that focal neuronal damage may be mediated by “excitotoxic” mechanisms, and because excitatory amino acid levels have been shown to be markedly elevated after brain trauma in humans, the authors have measured levels of glutamate, aspartate, and threonine within the cortex underneath the hematoma, using in vivo microdialysis before and after induction of hematoma, in both vehicle- and drug-treated rats. Postinjury treatment with 619C89 (30 mg/kg) significantly reduced the volume of hemispheric ischemic damage produced by subdural hematoma, from 99.77 ± 7.51 mm3 in vehicle-treated control rats to 46.07 ± 11.06 mm3 (p = 0.0007) in drug-treated animals. In the vehicle-treated animals, induction of subdural hematoma led to a fourfold increase in glutamate in the first 30 minutes after subdural hematoma occurred. The mean extracellular glutamate concentration in these animals remained 2- to 2.6-fold increased over the following 2.5 hours. In the 619C89-treated animals, the release of glutamate from the cortex underneath the hematoma was significantly attenuated. In these rats, induction of subdural hematoma led to a 2.7-fold increase in the first 30-minute sample, but extracellular glutamate concentration returned to near-basal levels thereafter, compared with vehicle-treated animals (p < 0.05). These results show that 619C89 is highly neuroprotective in this model and that its effects may, in part, be mediated by the inhibiton of glutamate release from the ischemic cortex underneath the hematoma.

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

1991 ◽  
Vol 74 (6) ◽  
pp. 944-950 ◽  
Author(s):  
Min-Hsiung Chen ◽  
Ross Bullock ◽  
David I. Graham ◽  
Jimmy D. Miller ◽  
James McCulloch
Keyword(s):  
Brain Damage ◽  
Subdural Hematoma ◽  
Neuronal Damage ◽  
Nmda Receptor Antagonist ◽  
Acute Subdural Hematoma ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Content Type ◽  
Irreversible Brain Damage ◽  
Slow Injection

✓ 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 µl 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.

Transient glucose hypermetabolism after acute subdural hematoma in the rat

1992 ◽  
Vol 76 (3) ◽  
pp. 471-477 ◽  
Author(s):  
Yasuhiro Kuroda ◽  
Fiona M. Inglis ◽  
Jimmy D. Miller ◽  
James McCulloch ◽  
David I. Graham ◽  
...  
Keyword(s):  
Brain Damage ◽  
Subdural Hematoma ◽  
Excitatory Amino Acids ◽  
Glucose Utilization ◽  
Acute Subdural Hematoma ◽  
Ischemic Brain ◽  
Content Type ◽  
Blood Injection ◽  
High Concentrations ◽  
Fine Print

✓ Ischemic brain damage occurs in most patients with acute subdural hematoma, yet many aspects of the distribution and extent of this damage remain unexplained. Previous studies in rat model, which produces a region of infarction under the hematoma, have implicated an “excitotoxic” mechanism, suggesting that high concentrations of excitatory amino acids may exacerbate ischemic damage. A study is described in which local glucose utilization is measured 2 or 4 hours after induction of acute subdural hematoma in the rat. These changes are compared to those produced by introducing the same volume of inert silicone gel into the subdural space. Massive increases (up to 142%) in glucose utilization occurred throughout both hippocampi and in a variable zone around the ischemic core, but these had normalized by 4 hours after blood injection. Hippocampal hypermetabolism was not seen after introduction of the silicone mass, suggesting that diffusible substances from the clotted blood may be responsible for these changes. This transient hypermetabolism accords with an excitotoxic process, which may amplify brain damage after acute subdural hematoma.

Effect of perfluorocarbons on brain oxygenation and ischemic damage in an acute subdural hematoma model in rats

2005 ◽  
Vol 103 (4) ◽  
pp. 724-730 ◽  
Author(s):  
Taek Hyun Kwon ◽  
Dong Sun ◽  
Wilson P. Daugherty ◽  
Bruce D. Spiess ◽  
M. Ross Bullock
Keyword(s):  
Brain Tissue ◽  
Brain Damage ◽  
Subdural Hematoma ◽  
Histological Study ◽  
Acute Subdural Hematoma ◽  
Brain Oxygenation ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Content Type ◽  
Fine Print

Object. This study was conducted to determine whether perfluorocarbons (PFCs) improve brain oxygenation and reduce ischemic brain damage in an acute subdural hematoma (SDH) model in rats. Methods. Forty adult male Sprague—Dawley rats were allocated to four groups: 1) controls, acute SDH treated with saline and 30% O2; 2) 30-PFC group, acute SDH treated with PFC infusion in 30% O2; 3) 100-O2 group, acute SDH treated with 100% O2; and 4) 100-PFC group, acute SDH treated with PFC plus 100% O2. Ten minutes after the induction of acute SDH, a single dose of PFC was infused and 30% or 100% O2 was administered simultaneously. Four hours later, half of the rats were killed by perfusion for histological study to assess the extent of ischemic brain damage. The other half were used to measure brain tissue oxygen tension (PO2). The volume of ischemic brain damage was 162.4 ± 7.6 mm3 in controls, 165.3 ± 11.3 mm3 in the 30-PFC group, 153.4 ± 17.3 mm3 in the 100-O2 group, and 95.9 ± 12.8 mm3 in the 100-PFC group (41% reduction compared with controls, p = 0.002). Baseline brain tissue PO2 values were approximately 20 mm Hg, and after induction of acute SDH, PO2 rapidly decreased and remained at 1 to 2 mm Hg. Treatment with either PFC or 100% O2 improved brain tissue PO2, with final values of 5.14 and 7.02 mm Hg, respectively. Infusion of PFC with 100% O2 improved brain tissue PO2 the most, with a final value of 15.16 mm Hg. Conclusions. Data from the current study demonstrated that PFC infusion along with 100% O2 can significantly improve brain oxygenation and reduce ischemic brain damage in acute SDH.

Acute subdural hematoma

1982 ◽  
Vol 57 (2) ◽  
pp. 254-257 ◽  
Author(s):  
Henry A. Shenkin
Keyword(s):  
Computerized Tomography ◽  
Subdural Hematoma ◽  
Neurological Status ◽  
Neurological Dysfunction ◽  
Acute Subdural Hematoma ◽  
Consecutive Series ◽  
Content Type ◽  
Subdural Hematomas ◽  
Fine Print

✓ In a consecutive series of 39 cases of acute subdural hematoma (SDH), encountered since computerized tomography diagnosis became available, 61.5% were found to be the result of bleeding from a small cortical artery, 25.6% were of venous origin, 7.7% resulted from cerebral contusions, and 5% were acute bleeds into chronic subdural hematomas. Craniotomy was performed promptly on admission, but there was no difference in survival (overall 51.3%) between patients with arterial and venous bleeds. The only apparent factor affecting survival in this series was the preoperative neurological status: 67% of patients who were decerebrate and had fixed pupils prior to operation died. Of patients with less severe neurological dysfunction, only 20% failed to survive.

Chronic subdural hematoma in infancy

1990 ◽  
Vol 73 (2) ◽  
pp. 201-205 ◽  
Author(s):  
Nobuhiko Aoki
Keyword(s):  
Computerized Tomography ◽  
Subdural Hematoma ◽  
Treatment Protocol ◽  
Chronic Subdural Hematoma ◽  
Neurological Deficits ◽  
Acute Subdural Hematoma ◽  
Hemorrhagic Diathesis ◽  
Content Type ◽  
Fine Print ◽  
Subdural Tapping

✓ The cases of 30 infants with chronic subdural hematoma treated surgically between 1978 and 1987 (after the introduction of computerized tomography) were reviewed. This series was limited to infants presenting with increased intracranial pressure, neurological deficits, or developmental retardation. Nineteen patients were male and 11 were female, ranging in age from 1 to 14 months (average 6.1 months). The surgical treatment was initiated with percutaneous subdural tapping which was repeated periodically, if indicated, for 2 weeks. If the patients failed to respond to subdural tapping, subdural-peritoneal shunting was installed. The follow-up periods were from 3 months to 9 years 8 months (average 4 years 10 months). Computerized tomography at that time disclosed disappearance or minimal collection of subdural fluid in 28 cases (93%) and a significant collection (> 5 mm) in two (7%). Neurological examination revealed that the patients were “normal” in 17 cases (57%), “mildly or moderately disabled” in nine (30%), and “severely disabled” in four (13%). The majority of disabled patients had lesions secondary to infantile acute subdural hematoma, child abuse, or hemorrhagic diathesis. These results indicate that the treatment protocol in the present series is acceptable for the elimination of subdural hematoma. Together, early diagnosis and treatment of the etiological conditions causing the lesion are indispensable for obtaining a satisfactory neurological outcome.

Acute brain edema in fatal head injury: analysis by dynamic CT scanning

1985 ◽  
Vol 63 (6) ◽  
pp. 830-839 ◽  
Author(s):  
Eiji Yoshino ◽  
Tarumi Yamaki ◽  
Toshihiro Higuchi ◽  
Yoshiharu Horikawa ◽  
Kimiyoshi Hirakawa
Keyword(s):  
Head Injury ◽  
Brain Edema ◽  
Subdural Hematoma ◽  
Ct Scans ◽  
Acute Subdural Hematoma ◽  
Dynamic Ct ◽  
Content Type ◽  
Injured Patients ◽  
Fine Print ◽  
Diffuse Brain

✓ Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p < 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.

Acute subdural hematoma and death following lateral cervical spinal puncture

1983 ◽  
Vol 58 (2) ◽  
pp. 284-286 ◽  
Author(s):  
Larry A. Rogers
Keyword(s):  
Vertebral Artery ◽  
Subdural Hematoma ◽  
Posterior Cranial Fossa ◽  
Acute Subdural Hematoma ◽  
Content Type ◽  
Spinal Puncture ◽  
Cranial Fossa ◽  
Fine Print

✓ An acute subdural hematoma dissecting into the posterior cranial fossa and resulting in death is reported. The patient had undergone spinal puncture by the lateral cervical technique prior to development of the hematoma. Autopsy demonstrated that the source of hemorrhage was an anomalous intraspinal vertebral artery.

Infantile acute subdural hematoma

1984 ◽  
Vol 61 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Nobuhiko Aoki ◽  
Hideaki Masuzawa
Keyword(s):  
Head Trauma ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma ◽  
Minor Head Trauma ◽  
Cerebral Contusion ◽  
Content Type ◽  
Male Predominance ◽  
Funduscopic Examination ◽  
Fine Print ◽  
Subdural Tapping

✓ Twenty-six cases of infantile acute subdural hematoma treated between 1972 and 1983 were reviewed. The series was limited to infants with acute subdural hematoma apparently due to minor head trauma without loss of consciousness, and not associated with cerebral contusion. Twenty-three of the patients were boys, and three were girls, showing a clear male predominance. The patients ranged in age between 3 and 13 months, with an average age of 8.1 months, the majority of patients being between 7 and 10 months old. Most of the patients were brought to the hospital because of generalized tonic convulsion which developed soon after minor head trauma, and all patients had retinal and preretinal hemorrhage. The cases were graded into mild, intermediate, and fulminant types, mainly on the basis of the level of consciousness and motor weakness. Treatment for fulminant cases was emergency craniotomy, and that for mild cases was subdural tapping alone. For intermediate cases, craniotomy or subdural tapping was selected according to the contents of the hematoma. The follow-up results included death in two cases, mild physical retardation in one case, and epilepsy in one case. The remaining 23 patients showed normal development. The relationship between computerized tomography (CT) findings and clinical grading was analyzed. Because some mild and intermediate cases could be missed on CT, the importance of noting the characteristic clinical course and of funduscopic examination is stressed.

Long-term follow-up review of patients with acute and subacute subdural hematomas

1978 ◽  
Vol 48 (3) ◽  
pp. 345-349 ◽  
Author(s):  
Jarl Rosenørn ◽  
Flemming Gjerris
Keyword(s):  
Survival Rate ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma ◽  
Content Type ◽  
Subdural Hematomas ◽  
Long Term Follow Up ◽  
Fine Print ◽  
Back To Work

✓ The authors present 149 patients suffering from acute (112) and subacute (37) subdural hematomas admitted during the 10-year period 1965 to 1974, with a follow-up period of 2 to 12 years. During the time of observation, 104 patients died and 45 survived; 73% of the patients with acute and 27% with subacute subdural hematomas died. Of the patients with an acute subdural hematoma, 11% went back to work, as against 32% of those with subacute subdural hematomas. The 5-year survival rate was 28% in patients with acute and 76% in patients with subacute subdural hematomas.

Complication of a large cranial defect

1976 ◽  
Vol 44 (4) ◽  
pp. 506-508 ◽  
Author(s):  
Kamran Tabaddor ◽  
James LaMorgese
Keyword(s):  
Intracranial Pressure ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma ◽  
Content Type ◽  
Cranial Defect ◽  
Early Cranioplasty ◽  
Fine Print

✓ A patient with acute subdural hematoma was successfully treated with hemicraniectomy. He developed contralateral weakness 4 months after surgery which was reversed by cranioplasty. The presumptive mechanism is a gradient between atmospheric and intracranial pressure. Early cranioplasty is suggested to prevent this phenomenon.

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