Cerebral Hemodynamics and Metabolism Following Experimental Head Injury

Meyer, John Stirling; Kondo, Akinori; Nomura, Fumio; Sakamoto, K.; Teraura, Tetsuaki

doi:10.3171/jns.1970.32.3.0304

Cited by 75 publications

(14 citation statements)

References 33 publications

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“…However, no correlation could be demonstrated between the degree of diffuse brain swelling, classified according to Marshall et al [25], to metabolic parameters such as cerebral lactate differences and cerebral oxygen extraction, to ICE or to outcome. As confirmed by numerous experimental studies, lactate in brain tissue and CSF is increased by cerebral trauma [5,15,27,29,33,45]. These elevated cerebral levels of lactate may contribute to brain acidosis after' trauma, which has been implicated by several authors as a causative factor in injury to the central nervous system [20,26,28,32,35,38].…”

Section: Discussionmentioning

confidence: 76%

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Cerebral lactate production in relation to intracranial pressure, cranial computed tomography findings, and outcome in patients with severe head injury

Murr

Stummer²,

Schürer

et al. 1996

Acta neurochir

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Severe head injury is frequently associated with focal or global disturbances of cerebral blood flow and metabolism. Routine monitoring of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in these patients does not provide information about critically reduced local or global cerebral blood flow. Measurements of cerebral lactate difference, Lactate-Oxygen-Index (LOI) and cerebral oxygen extraction were evaluated for advanced monitoring by comparing these parameters with ICP, cranial computed tomography (CCT) findings, and outcome in a group of severely head-injured patients. In 21 patients with severe brain trauma (GCS < or = 8), arterial as well as jugular venous lactate levels and oxygen saturation were measured in vitro every 6 h after admission of patients to the intensive care unit (ICU) throughout the acute course of treatment. Arterial blood pressure, blood gases, and ICP were assessed by standard monitoring measurements. CCT was performed initially after admission of the patients to the hospital, during the acute period in the ICU, if indicated, and 10 to 14 days after trauma. Outcome was classified according to the Glasgow outcome scale (GOS) at six months after injury. Data were averaged in each patient for every day after trauma and over the entire monitoring period. Resulting values were tested for correlation by regression analysis. Additionally, the data of the group of patients with normal to minimally elevated mean ICP (ICP < 20 mmHg, n = 12) were compared to those of the patients with increased mean ICP (ICP > 20 mmHg, n = 9). The cerebral lactate difference in all patients on the day of trauma was significantly increased as compared to the later period (0.20 vs. 0.11-0.07 mmol/l, p < 0.05), but was not different with high or normal to minimally elevated ICP. In patients with intracranial hypertension, the cerebral lactate difference remained significantly increased from the first to the fifth day after injury, whereas it normalized in this period in the group with normal to minimally elevated ICP. Averaged over the acute course, patients with increased ICP had significantly higher mean lactate differences (0.18 +/- 0.16 vs. 0.067 +/- 0.025 mmol/l, p = 0.001) and higher mean LOIs (0.072 +/- 0.071 vs. 0.028 +/- 0.013, p = 0.011). There was a significant correlation of increased mean cerebral lactate difference to poor outcome (r = 0.46, p = 0.035). Cerebral oxygen extraction in all patients tended to increase on the day of trauma (36.7% vs. 29.2% to 31.5% during the subsequent course), but this difference was not significant. The initial degree of brain swelling, classified by CCT according to Marshall et al. (1991), showed no correlation with cerebral lactate differences, ICP, O2-extraction, or outcome. Neither was there a correlation of cerebral oxygen extraction to ICP nor to outcome. In conclusion, the severity of brain trauma and outcome of patients was reflected by increased cerebral lactate production. Unchanged values of global cerebral oxygen extraction suggest that the re...

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Section: Discussionmentioning

confidence: 76%

“…Increased cerebral formation of lactate was related to the severity of trauma in experimental as well as clinical investigations [27,36]. In most of the clinical studies, increased cerebral lactate levels were assessed by measurements in cerebrospinal fluid (CSF) [6,8,21,34].…”

Section: Introductionmentioning

confidence: 99%

Cerebral lactate production in relation to intracranial pressure, cranial computed tomography findings, and outcome in patients with severe head injury

Murr

Stummer²,

Schürer

et al. 1996

Acta neurochir

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“…The mean cerebral arteriovenous O2 content difference was within the normal range and did not change after OHP. Due to the low value of the CBF, the mean CMRO2 was low before (1.73 ± 1.32 ml/100 g/ min) and after OHP (1.67 ± 1.53 ml/100 g/min), compared to the accepted normal value of 3.3±0.4 ml/100 g/min [22]. Pre-OHP and post-OHP CMRO2 values did not differ significantly.…”

Section: Changes In Cmro> Cmrgl and Cmrlactmentioning

confidence: 91%

“…This is in keeping with the results in our three patients with bilateral hemispheric lesions and low CBF: two of them, with a total of four studies, showed an increased flow after OHP, while the third patient was uninfluenced. Indirect evidence for this effect of OHP on low CBF can be found in its demonstrated capacity of reducing increased intracranial pressure [10,23,25,26,28,29], and experi mental brain edema [29], two major factors of brain posttraumatic ischemia [7,20,22], Regarding CMRO2, CMRGL and CMRLact, the disparate patterns of response to OHP primarily reflect the diverse pathological and circulatory status of the brain region covered by the probe. However, the relative inaccuracy of this usual method for measuring cerebral metabolic rates must be borne in mind.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Blood Flow, Cerebral Metabolism and Cerebrospinal Fluid Biochemistry in Brain-Injured Patients after Exposure to Hyperbaric Oxygen

Artru¹,

Philippon²,

Gau³

et al. 1976

Eur Neurol

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A series of head-injured patients, in coma, were treated with hyperbaric oxygen (OHP) at 2.5 atm. Cerebral blood flow (CBF), cerebral metabolic rates of oxygen (CMRO₂), glucose (CMRGL), and lactate (CMRL act), and various cerebrospinal fluid (CSF) parameters were measured before and 2 h after the treatment. Pre-OHP and post-OHP average values of arterial blood and CSF lactate, and CMRL act were higher than normal, while CBF, CMRO₂ and CSF oxygen pressure (PO₂) were lower. CBF tended to increase after OHP in some patients and to decrease in others. This discrepancy and the conflicting results of the literature can be tentatively explained in assuming that there is a different effect of OHP on normal brain circulation as compared to impaired brain circulation. Changes of cerebral metabolic rates were inconsistent and did not relate to changes of CBF, except with repeated studies of the same patient. A correlation was found between the variations of CMRGL and those of arterial blood and CSF glucose content. CSF PO₂, CSF acid-base balance, and CSF lactate content did not vary, and arterial PO₂ showed a consistent fall. In two patients who were neurologically improved after OHP exposure, the CBF and metabolic changes were not the same.

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“…Meyer etal. [11] have reported significant CBF reduction following severe concussion or contusion produced by an airgun in baboons, with only a slight increase in CBF during the first minute following mild concussions. Nilsson and Nordstrom [12] have observed an immediate 50% increase in CBF following concussion produced by an accelerated piston in rats, followed by a marked reduction for 40 rain, after which CBF tended to recover toward baseline.…”

Section: Cerebral Blood Flow Responses To Injurymentioning

confidence: 99%

Changes in ICBF, morphology and related parameters by fluid percussion injury

et al. 1996

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We investigated the pathophysiological and morphological responses of anaesthetized rats to fluid percussion brain injury generated by an original midline fluid percussion injury device. Following different grades of trauma, lCBF was measured continuously in the right parietal cortex through a burr hole using laser Doppler flowmeter, and physiological parameters were monitored. Pathological changes also were evaluated microscopically. During the first 2 hours following trauma, we found four patterns of cerebral circulatory responses. Little measurable pathophysiological response occurred after percussion pulses of less than 1.33 atmospheres (atm). In animals subjected to pulses of greater than 4.30 atm, lCBF increased synchronously with blood pressure, and then both parameters decreased continuously until death. In animals subjected to pulses of 1.53 to 2.33 atm, trauma produced a transient increase in lCBF with no synchronous rise in blood pressure. In animals subjected to pulses of 2.70 to 3.87 atm, lCBF increased synchronously with blood pressure immediately following the injury, but had decreased markedly by 60 seconds and remained below the pre-injury baseline. Blood pressure recovered to baseline within 4 minutes of the injury. The transient increase in lCBF occurred within 5 seconds following percussion pulses of greater than 1.53 atm and appeared to be independent of the rise in systemic blood pressure. Apnoea occurred in animals subjected to pulses of greater than 1.53 atm, and the duration of apnoea and mortality rate correlated with the magnitude of the applied injury. A power decrease in the electroencephalogram post-injury and a delay in its recovery, both depended on the magnitude of the injury with few regional differences in the beta-2 band power. The distribution and extent of blood-brain barrier disruption and small haemorrhages also correlated with the magnitude of the injury. The number of neurons decreased significantly in both hippocampi by 2 weeks following moderate trauma. The four patterns of lCBF changes demonstrated in the present study, as well as the other responses to injury, may be useful for studying graded models of various diffuse brain injuries.

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Cerebral Hemodynamics and Metabolism Following Experimental Head Injury

Cited by 75 publications

References 33 publications

Cerebral lactate production in relation to intracranial pressure, cranial computed tomography findings, and outcome in patients with severe head injury

Cerebral lactate production in relation to intracranial pressure, cranial computed tomography findings, and outcome in patients with severe head injury

Cerebral Blood Flow, Cerebral Metabolism and Cerebrospinal Fluid Biochemistry in Brain-Injured Patients after Exposure to Hyperbaric Oxygen

Changes in ICBF, morphology and related parameters by fluid percussion injury

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