scholarly journals 52. Experimental Studies of Cerebral Circulation and Cerebral Metabolism in the Early Stage after Severe Head Injury

1962 ◽  
Vol 4 (0) ◽  
pp. 183-183
Author(s):  
Kazuo KOJIMA ◽  
Setsuo ONO ◽  
Humio NOMURA ◽  
Futoshi MOCHIKI
Keyword(s):  
Head Injury ◽  
Cerebral Circulation ◽  
Severe Head Injury ◽  
Early Stage ◽  
Cerebral Metabolism ◽  
Experimental Studies

scholarly journals Cerebral arteriovenous oxygen difference: a predictor of cerebral infarction and outcome in patients with severe head injury

1997 ◽  
Vol 2 (5) ◽  
pp. E1
Author(s):  
Peter D. Le Roux ◽  
David W. Newell ◽  
Arthur M. Lam ◽  
M. Sean Grady ◽  
H. Richard Winn
Keyword(s):  
Head Injury ◽  
Cerebral Infarction ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Cerebral Metabolism ◽  
Jugular Bulb ◽  
Group A ◽  
The Mean ◽  
Group B ◽  
Oxygen Difference

Jugular bulb oxygen monitoring can be used to estimate the adequacy of cerebral blood flow to support cerebral metabolism after severe head injury. In the present study, the authors studied the cerebral arteriovenous oxygen difference (AVDO2) before and after treatment in 32 head-injured patients (Glasgow Coma Scale scores ¾ 8) to examine the relationships among AVDO2 and cerebral perfusion pressure (CPP), delayed cerebral infarction, and outcome. Fifteen patients (Group A) underwent craniotomy for hematoma evacuation and 17 (Group B) received mannitol for sustained intracranial hypertension (intracranial pressure > 20 mm Hg, > 10 minutes). Radiographic evidence of delayed cerebral infarction was observed in 14 patients. Overall, 17 patients died or were severely disabled. Cerebral AVDO2 was elevated before craniotomy or mannitol administration; the mean AVDO2 for all patients before treatment was 8.6 ± 1.8 vol%. Following craniotomy or mannitol administration, the AVDO2 decreased in 27 patients and increased in five patients (mean AVDO2 6.2 ± 2.1 vol% in all patients; 6 ± 1.9 vol% in Group A; and 6.4 ± 2.4 vol% in Group B). The mean CPP was 75 ± 9.8 mm Hg and no relationship with AVDO2 was demonstrated. Before treatment, the AVDO2 was not associated with delayed cerebral infarction or outcome. By contrast, a limited improvement in elevated AVDO2 after craniotomy or mannitol administration was significantly associated with delayed cerebral infarction (Group A: p < 0.001; Group B: p < 0.01). Similarly, a limited improvement in elevated AVDO2 after treatment was significantly associated with an unfavorable outcome (Group A: p < 0.01; Group B: p < 0.001). In conclusion, these findings strongly indicate that, despite adequate cerebral perfusion, limited improvement in elevated cerebral AVDO2 after treatment consisting of either craniotomy or mannitol administration may be used to help predict delayed cerebral infarction and poor outcome after traumatic brain injury.

scholarly journals 72. Cerebral Metabolism Following Severe Head Injury

1971 ◽  
Vol 11 ◽  
pp. 172-173
Author(s):  
Takao MINAMI ◽  
Kikushi KATSURADA ◽  
Ryohei YAMADA ◽  
Ichiro TAHARA ◽  
Tsuyoshi SUGIMOTO
Keyword(s):  
Head Injury ◽  
Severe Head Injury ◽  
Cerebral Metabolism

Cerebral arteriovenous oxygen difference: a predictor of cerebral infarction and outcome in patients with severe head injury

1997 ◽  
Vol 87 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Peter D. Le Roux ◽  
David W. Newell ◽  
Arthur M. Lam ◽  
M. Sean Grady ◽  
H. Richard Winn
Keyword(s):  
Head Injury ◽  
Cerebral Infarction ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Cerebral Metabolism ◽  
Content Type ◽  
Group A ◽  
The Mean ◽  
Group B ◽  
Oxygen Difference

✓ Jugular bulb oxygen monitoring can be used to estimate the adequacy of cerebral blood flow to support cerebral metabolism after severe head injury. In the present study, the authors studied the cerebral arteriovenous oxygen difference (AVDO2) before and after treatment in 32 head-injured patients (Glasgow Coma Scale scores ≤ 8) to examine the relationships among AVDO2 and cerebral perfusion pressure (CPP), delayed cerebral infarction, and outcome. Fifteen patients (Group A) underwent craniotomy for hematoma evacuation and 17 (Group B) received mannitol for sustained intracranial hypertension (intracranial pressure > 20 mm Hg, > 10 minutes). Radiographic evidence of delayed cerebral infarction was observed in 14 patients. Overall, 17 patients died or were severely disabled. Cerebral AVDO2 was elevated before craniotomy or mannitol administration; the mean AVDO2 for all patients before treatment was 8.6 ± 1.8 vol%. Following craniotomy or mannitol administration, the AVDO2 decreased in 27 patients and increased in five patients (mean AVDO2 6.2 ± 2.1 vol% in all patients; 6 ± 1.9 vol% in Group A; and 6.4 ± 2.4 vol% in Group B). The mean CPP was 75 ± 9.8 mm Hg and no relationship with AVDO2 was demonstrated. Before treatment, the AVDO2 was not associated with delayed cerebral infarction or outcome. By contrast, a limited improvement in elevated AVDO2 after craniotomy or mannitol administration was significantly associated with delayed cerebral infarction (Group A: p < 0.001; Group B: p < 0.01). Similarly, a limited improvement in elevated AVDO2 after treatment was significantly associated with an unfavorable outcome (Group A: p < 0.01; Group B: p < 0.001). In conclusion, these findings strongly indicate that, despite adequate cerebral perfusion, limited improvement in elevated cerebral AVDO2 after treatment consisting of either craniotomy or mannitol administration may be used to help predict delayed cerebral infarction and poor outcome after traumatic brain injury.

The effect of glucose administration on carbohydrate metabolism after head injury

1991 ◽  
Vol 74 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Claudia S. Robertson ◽  
J. Clay Goodman ◽  
Raj K. Narayan ◽  
Charles F. Contant ◽  
Robert G. Grossman
Keyword(s):  
Head Injury ◽  
Severe Head Injury ◽  
Ketone Bodies ◽  
Cerebral Metabolism ◽  
Saline Group ◽  
Early Recovery ◽  
Energy Substrates ◽  
Blood Concentrations ◽  
Effect Of Glucose ◽  
Glucose Group

✓ The role of intravenous infusion of glucose in limiting ketogenesis and the effect of glucose on cerebral metabolism following severe head injury were studied in 21 comatose patients. The patients were randomly assigned to alimentation with or without glucose. Systemic protein wasting, arterial concentrations of energy substrates, and cerebral metabolism of these energy substrates were monitored for 5 days postinjury. Both groups were in negative nitrogen balance, and had wasting of systemic proteins despite substantial protein intake. Blood and cerebrospinal fluid (CSF) glucose concentrations were highest on Day 1, but remained higher than normal fasting levels on all days of study, even in the patients who received no exogenous glucose. Although there were no differences in blood or CSF glucose concentrations in the two groups of patients, the glucose group had higher plasma insulin levels, with a mean ± standard deviation of 14.8 ± 7.3 µU/ml compared to 10.3 ± 4.2 µU/ml in the saline group. The blood concentrations of β-hydroxybutyrate, acetoacetate, pyruvate, glycerol, and the free fatty acids were higher in the saline group than in the glucose group. Cerebral oxygen consumption was similar in the two groups, while the cerebral metabolism of glucose and of the ketone bodies was dependent on whether glucose was administered. In the glucose group, glucose was the only energy substrate utilized by the brain. In the saline group, the ketone bodies β-hydroxybutyrate and acetoacetate replaced glucose to the extent of 16% of the brain's total energy production. Cerebral lactate production and CSF lactate concentration were lower in the saline group. These studies suggest that administration of glucose during the early recovery period of severe head injury is a major cause of suppressed ketogenesis, and may increase production of lactic acid by the traumatized brain by limiting the availability of nonglycolytic energy substrates.

scholarly journals g-11. Effects on Cerebral Circulation and Cerebral Metabolism of Various Kinds of Treatment for Head Injury

1968 ◽  
Vol 10 ◽  
pp. 160-161
Author(s):  
Yoshitoki MURASE ◽  
Katsuro TAKEUCHI ◽  
Kazuki SAKATA ◽  
Takao TAKEMOTO
Keyword(s):  
Head Injury ◽  
Cerebral Circulation ◽  
Cerebral Metabolism ◽  
G 11

Usefulness of RemiPro for pediatric neurorehabilitation in severe head injury: A case report

2011 ◽  
Vol 42 (S 01) ◽  
Author(s):  
M Hessenauer ◽  
E Romein ◽  
S Berweck ◽  
G Kluger ◽  
M Staudt
Keyword(s):  
Case Report ◽  
Head Injury ◽  
Severe Head Injury

Severe Head Injury linked to Subsequent Development of Malignant Brain Tumour within a Short Period- A Case Report

2018 ◽  
Vol 3 (2) ◽  
Keyword(s):  
Head Injury ◽  
Brain Tumour ◽  
Severe Head Injury ◽  
Case Reports ◽  
Subsequent Development ◽  
Malignant Brain Tumour ◽  
Tumour Development ◽  
Short Period ◽  
The Brain

There have been a few case reports of head injury leading to brain tumour development in the same region as the brain injury. Here we report a case where the patient suffered a severe head injury with contusion. He recovered clinically with conservative management. Follow up Computed Tomography scan of the brain a month later showed complete resolution of the lesion. He subsequently developed malignant brain tumour in the same region as the original contusion within a very short period of 15 months. Head injury patients need close follow up especially when severe. The link between severity of head injury and malignant brain tumour development needs further evaluation. Role of anti-inflammatory agents for prevention of post traumatic brain tumours needs further exploration.

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