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

Influence of endogenous norepinephrine on cerebral blood flow and metabolism

1976 ◽  
Vol 231 (2) ◽  
pp. 489-494 ◽  
Author(s):  
ET MacKenzie ◽  
J McCulloch ◽  
AM Harper
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Cerebral Circulation ◽  
Brain Metabolism ◽  
Cerebral Metabolism ◽  
Cerebral Oxygen ◽  
Brain Norepinephrine ◽  
Cerebral Oxygen Consumption

The influence of brain norepinephrine on cerebral metabolism and blood flow was examined because exogenous norepinephrine, administered in a way that the blood-brain barrier is bypassed, has been shown to effect pronounced changes in the cerebral circulation. Reserpine (40 mug/kg, by intracarotid infusion) was administered in order to release brain norepinephrine in five anesthetized baboons. Reserpine significantly increased cerebral oxygen consumption (23%) and cerebral blood flow (50%). This response lasted for approximately 60 min. In a further five animals, effects of central beta-adrenoreceptor blockade were studied. Pro pranolol (12 mug/kg-min) produced an immediate, significant reduction in both cerebral oxygen consumption (40%) and cerebral glucose uptake (39%). Cerebral blood flow was reduced minimally. However, the responsiveness of the cerebral circulation to induced hypercapnia was severely attenuated from a gradient of 3.22 before, to 1,11 after, administration. These experiments suggest that central norepinephrine can influence the cerebral circulation primarily through noradrenergic effects on brain metabolism.

Cerebral circulation and metabolism in the acute stage of subarachnoid hemorrhage

2000 ◽  
Vol 93 (6) ◽  
pp. 1014-1018 ◽  
Author(s):  
Toshiaki Hayashi ◽  
Akifumi Suzuki ◽  
Jun Hatazawa ◽  
Iwao Kanno ◽  
Reizo Shirane ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Circulation ◽  
Cerebral Blood Volume ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Metabolism ◽  
Aneurysm Rupture ◽  
Acute Stage ◽  
Content Type ◽  
Positron Emission ◽  
Fine Print

Object. The mechanism of reduction of cerebral circulation and metabolism in patients in the acute stage of aneurysmal subarachnoid hemorrhage (SAH) has not yet been fully clarified. The goal of this study was to elucidate this mechanism further.Methods. The authors estimated cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), O2 extraction fraction (OEF), and cerebral blood volume (CBV) preoperatively in eight patients with aneurysmal SAH (one man and seven women, mean age 63.5 years) within 40 hours of onset by using positron emission tomography (PET). The patients' CBF, CMRO2, and CBF/CBV were significantly lower than those in normal control volunteers. However, OEF and CBV did not differ significantly from those in control volunteers. The significant decrease in CBF/CBV, which indicates reduced cerebral perfusion pressure, was believed to be caused by impaired cerebral circulation due to elevated intracranial pressure (ICP) after rupture of the aneurysm. In two of the eight patients, uncoupling between CBF and CMRO2 was shown, strongly suggesting the presence of cerebral ischemia.Conclusions. The initial reduction in CBF due to elevated ICP, followed by reduction in CMRO2 at the time of aneurysm rupture may play a role in the disturbance of CBF and cerebral metabolism in the acute stage of aneurysmal SAH.

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.

PET FDG Study after Severe Head Injury

1996 ◽  
Vol 9 (1) ◽  
pp. 25-35 ◽  
Author(s):  
D. Kaech ◽  
P. Kalvach ◽  
K. Leenders ◽  
U. Roelcke
Keyword(s):  
Head Injury ◽  
Cerebral Metabolism ◽  
Diffuse Axonal Injury ◽  
Brain Perfusion ◽  
Diffuse White Matter ◽  
Significant Attenuation ◽  
Brain Stem Injury ◽  
Materials Used ◽  
The Right

From a series of 10 patients undergoing PET studies of brain metabolism with 18Fluo-ro-Desoxy-Glucose (FDG) between 18 days and 62 months after a major head injury 3 chronic cases examined 25, 33 and 62 months after the accident are presented to illustrate some neuroradiologic aspects. Cortical defects are easily recognised on PET as zones of decreased metabolism after brain laceration corresponding to the residual neurologic deficits. A crossed cerebellar diaschisis is present, reflecting the deafferentation of the cerebellum. In the patient studied 62 months after a left frontotemporal trauma with subdural hematoma and brain swelling, a good correlation between CT, MR, SPECT and PET was found. In the third patient with diffuse axonal injury and predominantly left frontal subdural hygroma 33 months before, the brain perfusion looked normal on SPECT and the cerebral metabolism was only mildly reduced in the right frontal and left parieto-occipital regions on PET. These findings reflect only partially the neuropsychologic sequelae, making the patient unable to work more than 30%. In case of diffuse white matter (and brain stem) injury, the cortical abnormalities shown by PET may not reflect enough the severity of the remaining disability. Finally two materials used for cranioplasty (Palacos® and BOP®) were tested in vitro before the two patients underwent PET examination. There was no significant attenuation of the radiation in vitro and no distinguishable anomalies over the corresponding hemisphere, like in a third patient without bone flap.

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.

Sign in / Sign up

Export Citation Format

Share Document