Experimental brain injury: successful therapy with the weak base, tromethamine

1984 ◽  
Vol 60 (5) ◽  
pp. 961-971 ◽  
Author(s):  
Michael J. Rosner ◽  
Donald P. Becker
Keyword(s):  
Brain Injury ◽  
Control Group ◽  
Weak Base ◽  
Post Injury ◽  
Content Type ◽  
Ringer’S Solution ◽  
Fluid Percussion Injury ◽  
Lactated Ringer's Solution ◽  
Injury Control ◽  
Fine Print

✓ The presence of lactic acidosis in the cerebrospinal fluid of patients suffering brain injury as the result of trauma, subarachnoid hemorrhage, neoplasia, or ischemia has been well documented. The authors theorized that this acidosis becomes harmful in itself, and that treatment with an alkalinizing agent (tris(hydroxymethyl)aminomethane: tromethamine) capable of penetrating the blood-brain barrier would be efficacious. Fifteen pairs of mongrel cats were subjected to a 2.85-atmosphere fluid-percussion injury (LD80), and were supported by respirators for up to 72 hours prior to being placed in cages for an additional 4 days of observation. Experimental cats underwent continuous infusion of tromethamine (begun 10 minutes after injury); control animals were infused with an equal volume of lactated Ringer's solution. Twenty percent of the control group survived until sacrificed on Day 7 post-injury. Survival in the tromethamine group was 60% (p < 0.05), and morbidity also appeared to be reduced in the treated cats. Intracranial pressure (ICP) in treated cats was 60% (p < 0.05) of that in the control cats after respirator support for 3 days. Tromethamine infusion was associated with improved survival, decreased morbidity, and decreased ICP when compared with results in control animals. The literature with regard to central nervous system acidosis has been reviewed in an attempt to clarify and define this problem.

Comparison of crystalloids and colloids for hemodilution in a model of focal cerebral ischemia

1990 ◽  
Vol 73 (4) ◽  
pp. 576-584 ◽  
Author(s):  
Kazuyoshi Korosue ◽  
Roberto C. Heros ◽  
Christopher S. Ogilvy ◽  
Akio Hyodo ◽  
Yong-Kwang Tu ◽  
...  
Keyword(s):  
Arterial Occlusion ◽  
Acute Stage ◽  
Control Group ◽  
Total Protein Content ◽  
Oncotic Pressure ◽  
Content Type ◽  
Ringer’S Solution ◽  
Arterial Blood ◽  
Lactated Ringer's Solution ◽  
Fine Print

✓ Forty dogs were subjected to 6 hours of occlusion of the left internal carotid and middle cerebral arteries. They were divided into two “hemodilution groups” of 13 dogs each and a control “nonhemodiluted group” of 14 dogs. Thirty minutes after arterial occlusion, isovolemic hemodilution was performed by phlebotomy and infusions of low-molecular weight (MW) dextran in one group and of lactated Ringer's solution in the other group. The animals were sacrificed 1 week after temporary arterial occlusion. Hemodilution reduced the hematocrit to a level of 33% to 34%, which lasted throughout the week in both groups. After hemodilution there was a very significant reduction in blood viscosity, plasma total protein content, and fibrinogen levels in both groups in the acute stage; these levels gradually returned to baseline by the end of the week. In the group with lactated Ringer's solution hemodilution, both osmotic and oncotic pressures were decreased by hemodilution in the acute stage. In the control and low-MW dextran groups, osmotic and oncotic pressure remained unaltered throughout the week. Hemodilution resulted in a slight decrease in mean arterial blood pressure in all groups in the acute stage, but there were no significant changes in central venous, pulmonary arterial, or pulmonary wedge pressures. During the week of study, there were no differences in the cardiac index and total blood volume between the groups, and no significant changes in hematological parameters with the exception of a slight increase in bleeding time immediately after hemodilution with low-MW dextran. Daily neurological assessment showed consistently poorer condition during the first 5 days in the group with lactated Ringer's solution compared to either the control group or the group receiving low-MW dextran. Based on Mann-Whitney U-testing, the infarct volume of the lactated Ringer's solution recipients, expressed as a percentage of the total volume of that hemisphere (median 15.7%, range 6.6% to 25.2%) was significantly larger than that of the group receiving low-MW dextran (median 2.2%, range 0% to 15.8%) and that of the control group (median 11.9%, range 0% to 39.9%). The results indicate that, in this model, hemodilution with colloids was beneficial, whereas hemodilution with crystalloids was deleterious. It is likely that the decrease in oncotic pressure observed after hemodilution with lactated Ringer's solution is one of the most important reasons for its detrimental effect.

Exacerbation of cortical and hippocampal CA1 damage due to posttraumatic hypoxia following moderate fluid-percussion brain injury in rats

1999 ◽  
Vol 91 (4) ◽  
pp. 653-659 ◽  
Author(s):  
Helen M. Bramlett ◽  
Edward J. Green ◽  
W. Dalton Dietrich
Keyword(s):  
Brain Injury ◽  
Head Injuries ◽  
Human Head ◽  
Qualitative Assessment ◽  
Subcortical Structures ◽  
Content Type ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Cortical Contusion ◽  
Fine Print

Object. Patients with head injuries often experience respiratory distress that results in a secondary hypoxic insult. The present experiment was designed to assess the histopathological consequences of a secondary hypoxic insult by using an established rodent model of traumatic brain injury (TBI).Methods. Intubated anesthetized rats were subjected to moderate (1.94–2.18 atm) parasagittal fluid-percussion injury (FPI) to the brain. Following the TBI, the animals were maintained for 30 minutes by using either hypoxic (TBI-HY group, nine animals) or normoxic (TBI-NO, 10 animals) gas levels. Sham-operated animals also underwent all manipulations except for the FPI (sham-HY group, seven animals; and sham-NO group, seven animals). Three days after TBI the rats were killed, and quantitative histopathological evaluation was undertaken. Cortical contusion volumes were dramatically increased in the TBI-HY group compared with the TBI-NO group (p < 0.03). Qualitative assessment of cortical and subcortical structures demonstrated significant damage within the hippocampal areas, CA1 and CA2, of TBI-HY animals compared with the TBI-NO animals (both p < 0.03). There was also a significant increase in the frequency of damaged neuronal profiles within the middle and medial sectors of the CA1 hippocampus (p < 0.03) due to the hypoxic insult.Conclusions. The results of this study demonstrate that a secondary hypoxic insult following parasagittal FPI exacerbates contusion and neuronal pathological conditions. These findings emphasize the need to control for secondary hypoxic insults after experimental and human head injury.

Recovery from mild concussion in high school athletes

2003 ◽  
Vol 98 (2) ◽  
pp. 296-301 ◽  
Author(s):  
Mark R. Lovell ◽  
Michael W. Collins ◽  
Grant L. Iverson ◽  
Melvin Field ◽  
Joseph C. Maroon ◽  
...  
Keyword(s):  
High School ◽  
Mental Status ◽  
Test Performance ◽  
Neuropsychological Test ◽  
Return To Play ◽  
Control Group ◽  
High School Athletes ◽  
Post Injury ◽  
Content Type ◽  
Fine Print

Object. A computerized neuropsychological test battery was conducted to evaluate memory dysfunction and self-reporting of symptoms in a group of high school athletes who had suffered concussion. Methods. Neuropsychological performance prior to and following concussion was compared with the test performance of an age-matched control group. Potentially important diagnostic markers of concussion severity are discussed and linked to recovery within the 1st week of injury. Conclusions. High school athletes who had suffered mild concussion demonstrated significant declines in memory processes relative to a noninjured control group. Statistically significant differences between preseason and postinjury memory test results were still evident in the concussion group at 4 and 7 days postinjury. Self-reported neurological symptoms such as headache, dizziness, and nausea resolved by Day 4. Duration of on-field mental status changes such as retrograde amnesia and posttraumatic confusion was related to the presence of memory impairment at 36 hours and 4 and 7 days post-injury and was also related to slower resolution of self-reported symptoms. The results of this study suggest that caution should be exercised in returning high school athletes to the playing field following concussion. On-field mental status changes appear to have prognostic utility and should be taken into account when making return-to-play decisions following concussion. Athletes who exhibit on-field mental status changes for more than 5 minutes have longer-lasting postconcussion symptoms and memory decline.

Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model

2002 ◽  
Vol 97 (3) ◽  
pp. 643-649 ◽  
Author(s):  
Alois Zauner ◽  
Tobias Clausen ◽  
Oscar L. Alves ◽  
Ann Rice ◽  
Joseph Levasseur ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Tissue ◽  
Cerebral Metabolism ◽  
Acid Base ◽  
Content Type ◽  
Hypoxic Injury ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Feline Model ◽  
Fine Print

Object. Currently, there are no good clinical tools to identify the onset of secondary brain injury and/or hypoxia after traumatic brain injury (TBI). The aim of this study was to evaluate simultaneously early changes of cerebral metabolism, acid—base homeostasis, and oxygenation, as well as their interrelationship after TBI and arterial hypoxia. Methods. Cerebral biochemistry and O2 supply were measured simultaneously in a feline model of fluid-percussion injury (FPI) and secondary hypoxic injury. After FPI, brain tissue PO2 decreased from 33 ± 5 mm Hg to 10 ± 4 mm Hg and brain tissue PCO2 increased from 55 ± 2 mm Hg to 81 ± 9 mm Hg, whereas cerebral pH fell from 7.1 ± 0.06 to 6.84 ± 0.14 (p < 0.05 for all three measures). After 40 minutes of hypoxia, brain tissue PO2 and pH decreased further to 0 mm Hg and 6.48 ± 0.28, respectively (p < 0.05), whereas brain tissue PCO2 remained high at 83 ± 13 mm Hg. Secondary hypoxic injury caused a drastic increase in cerebral lactate from 513 ± 69 µM/L to 3219 ± 490 µM/L (p < 0.05). The lactate/glucose ratio increased from 0.7 ± 0.1 to 9.1 ± 2 after hypoxia was introduced. The O2 consumption decreased significantly from 18.5 ± 1.1 µl/mg/hr to 13.2 ± 2.1 µl/mg/hr after hypoxia was induced. Conclusions. Cerebral metabolism, O2 supply, and acid—base balance were severely compromised ultra-early after TBI, and they declined further if arterial hypoxia was present. The complexity of pathophysiological changes and their interactions after TBI might explain why specific therapeutic attempts that are aimed at the normalization of only one component have failed to improve outcome in severely head injured patients.

Evaluation of endorphin content in the CSF of patients with trigeminal neuralgia before and after Gasserian ganglion thermocoagulation

1981 ◽  
Vol 55 (6) ◽  
pp. 935-937 ◽  
Author(s):  
Giuseppe Salar ◽  
Salvatore Mingrino ◽  
Marco Trabucchi ◽  
Angelo Bosio ◽  
Carlo Semenza
Keyword(s):  
Cerebrospinal Fluid ◽  
Trigeminal Neuralgia ◽  
Control Group ◽  
Gasserian Ganglion ◽  
Content Type ◽  
Group Of Seven ◽  
Idiopathic Trigeminal Neuralgia ◽  
Significant Difference ◽  
Before And After ◽  
Fine Print

✓ The β-endorphin content in cerebrospinal fluid (CSF) was evaluated in 10 patients with idiopathic trigeminal neuralgia during medical treatment (with or without carbamazepine) and after selective thermocoagulation of the Gasserian ganglion. These values were compared with those obtained in a control group of seven patients without pain problems. No statistically significant difference was found between patients suffering from trigeminal neuralgia and those without pain. Furthermore, neither pharmacological treatment nor surgery changed CSF endorphin values. It is concluded that there is no pathogenetic relationship between trigeminal neuralgia and endorphins.

Flushing in relation to a possible rise in intracranial pressure: documentation of an unusual clinical sign

2000 ◽  
Vol 92 (6) ◽  
pp. 1040-1044 ◽  
Author(s):  
Gregory W. Hornig
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intraventricular Hemorrhage ◽  
Pneumococcal Meningitis ◽  
Clinical Importance ◽  
Neurological Deterioration ◽  
Content Type ◽  
Transient Nature ◽  
Fine Print

✓ This report documents clinical features in five children who developed transient reddening of the skin (epidermal flushing) in association with acute elevations in intracranial pressure (ICP). Four boys and one girl (ages 9–15 years) deteriorated acutely secondary to intracranial hypertension ranging from 30 to 80 mm Hg in the four documented cases. Two patients suffered from ventriculoperitoneal shunt malfunctions, one had diffuse cerebral edema secondary to traumatic brain injury, one was found to have pneumococcal meningitis and hydrocephalus, and one suffered an intraventricular hemorrhage and hydrocephalus intraoperatively. All patients were noted to have developed epidermal flushing involving either the upper chest, face, or arms during their period of neurological deterioration. The response was transient, typically lasting 5 to 15 minutes, and dissipated quickly. The flushing reaction is postulated to be a centrally mediated response to sudden elevations in ICP. Several potential mechanisms are discussed. Flushing has clinical importance because it may indicate significant elevations in ICP when it is associated with neurological deterioration. Because of its transient nature, the importance of epidermal flushing is often unrecognized; its presence confirms the need for urgent treatment.

Evaluation of brain-stem dysfunction following severe fluid-percussion head injury to the cat

1991 ◽  
Vol 74 (2) ◽  
pp. 270-277 ◽  
Author(s):  
Katsuji Shima ◽  
Anthony Marmarou
Keyword(s):  
Brain Stem ◽  
Content Type ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Brain Stem Injury ◽  
Group 2 ◽  
High Level ◽  
Subarachnoid Hemorrhages ◽  
Fine Print ◽  
Group 1

✓ The degree of brain-stem dysfunction associated with high-level fluid-percussion injury (3.0 to 3.8 atm) was investigated in anesthetized cats. Measurements were made of the animals' intracranial pressure (ICP), pressure-volume index (PVI), far-field brain-stem auditory evoked responses (BAER's), and cerebral blood flow (CBF). The animals were classified into two groups based on the severity of neuropathological damage to the brain stem after trauma: Group 1 had mild intraparenchymal and subarachnoid hemorrhages and Group 2 had severe intraparenchymal and subarachnoid hemorrhages. The ICP values in Group 1 were insignificantly lower than those in Group 2, while the PVI values in Group 2 were clearly lower (p < 0.05). Immediately after the injury, peaks II, III, and IV of the BAER's demonstrated a transitory and marked suppression. One Group 1 and two Group 2 animals showed the disappearance of peak V. In Group 1, the latencies of peak II, III, and IV gradually increased until 60 to 150 minutes postinjury, then returned to 95% of baseline value at 8 hours; however, the animals in Group 2 showed poor recovery of latencies. Two hours after brain injury, the CBF decreased to 40% of the preinjury measurement in both groups (p < 0.001). In contrast to Group 2, the CBF in Group 1 returned to 86.8% of the preinjury measurement by 8 hours following the injury. Changes in PVI, BAER, and CBF correlated well with the degree of brain-stem injury following severe head injury'- These data indicate that high-level fluid-percussion injury (> 3.0 atm) is predominantly a model of brain-stem injury.

scholarly journals Direct evidence for a key role of protein kinase C in the development of vasospasm after subarachnoid hemorrhage

1992 ◽  
Vol 76 (4) ◽  
pp. 635-639 ◽  
Author(s):  
Shigeru Nishizawa ◽  
Nobukazu Nezu ◽  
Kenichi Uemura
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Direct Evidence ◽  
Control Group ◽  
Content Type ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Fine Print

✓ Vascular contraction is induced by the activation of intracellular contractile proteins mediated through signal transduction from the outside to the inside of cells. Protein kinase C plays a crucial role in this signal transduction. It is hypothesized that protein kinase C plays a causative part in the development of vasospasm after subarachnoid hemorrhage (SAH). To verify this directly, the authors measured protein kinase C activity in canine basilar arteries in an SAH model with (γ-32P)adenosine triphosphate and the data were compared to those in a control group. Protein kinase C is translocated to the membrane from the cytosol when it is activated, and the translocation is an index of the activation; thus, protein kinase C activity was measured both in the cytosol and in the membrane fractions. Protein kinase C activity in the membrane in the SAH model was remarkably enhanced compared to that in the control group. The percentage of membrane activity to the total was also significantly greater in the SAH vessels than in the control group, and the percentage of cytosol activity in the SAH group was decreased compared to that in the control arteries. The results indicate that protein kinase C in the vascular smooth muscle was translocated to the membrane from the cytosol and was activated when SAH occurred. It is concluded that this is direct evidence for a key role of protein kinase C in the development of vasospasm.

Risk of late stroke and survival following carotid endarterectomy procedures for symptomatic patients

1990 ◽  
Vol 73 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Dennis A. Turner ◽  
Jay Tracy ◽  
Stephen J. Haines
Keyword(s):  
Carotid Endarterectomy ◽  
Life Table ◽  
Stroke Risk ◽  
Neurological Symptoms ◽  
Treatment Modalities ◽  
Control Group ◽  
Content Type ◽  
Postoperative Stroke ◽  
Fine Print

✓ The long-term outcome following carotid endarterectomy for neurological symptoms was analyzed using a retrospective life-table approach in 212 patients who had undergone 243 endarterectomy procedures. The postoperative follow-up period averaged 38.9 ± 2.1 months (mean ± standard error of the mean). The endpoints of stroke and death were evaluated in these patients. Patient groups with the preoperative symptoms of amaurosis fugax, transient ischemic attack, and prior recovered stroke were similar in terms of life-table outcome over the follow-up period. Sixty-two percent of symptomatic patients were alive and free of stroke at 5 years. The late risk of stroke (after 30 days postoperatively) averaged 1.7% per year based on a linear approximation to the hazard at each life-table interval (1.3% per year for ipsilateral stroke). The trend of late stroke risk was clearly downward, however, and could be fitted more accurately by an exponential decay function with a half-life of 33 months. Thus, the risk of stroke following carotid endarterectomy for neurological symptoms was highest in the perioperative period, slowly declined with time, and occurred predominantly ipsilateral to the procedure. The definition of a prospective medical control group remains crucial for a critical analysis of treatment modalities following the onset of premonitory neurological symptoms. In the absence of an adequate control group for this series, the calculated perioperative and postoperative stroke risk from this study was compared to data obtained from the literature on stroke risk in medically treated symptomatic patients. This uncontrolled comparison of treatment modalities suggests the combined perioperative and postoperative stroke risk associated with carotid endarterectomy to be modestly improved over medical treatment alone.

Effect of sympathectomy on spinal blood flow autoregulation and posttraumatic ischemia

1982 ◽  
Vol 56 (5) ◽  
pp. 706-710 ◽  
Author(s):  
Wise Young ◽  
Vincent DeCrescito ◽  
John J. Tomasula
Keyword(s):  
Blood Flow ◽  
Spinal Injury ◽  
Sympathetic Ganglia ◽  
Control Group ◽  
Content Type ◽  
Systemic Pressure ◽  
Sympathetic Regulation ◽  
Mean Systemic Pressure ◽  
Paravertebral Sympathetic Ganglia ◽  
Fine Print

✓ The hypothesis that the paravertebral sympathetic ganglia play a role in spinal blood flow regulation was tested in cats. Five cats were subjected to paravertebral sympathectomy, two to combined sympathectomy-adrenalectomy, three to adrenalectomy alone, and five controls received no treatment. Laminectomy was carried out to expose the T4–10 cord, and autoregulation was tested by measuring blood flow from the lateral columns with the hydrogen clearance technique during manipulation of systemic pressure with intravenous saline infusion and nitroprusside administration. The cord was then contused at T-7 with a 400 gm-cm impact injury. Posttraumatic blood flow was recorded, and neurophysiological function was assessed with somatosensory evoked potential (SEP) monitoring. Before injury, blood flow in the untreated (control) group had no consistent relationship with mean systemic pressure over the range 80 to 160 mm Hg. In contrast, in all cats with paravertebral sympathectomy, whether accompanied by adrenalectomy or not, blood flows increased with systemic pressure (correlation coefficient 0.86, p < 0.01). After injury, the control and adrenalectomized cats showed blood flow decreases of > 60% to 4 to 6 ml/100 gm/min (p < 0.01) by 2 to 3 hours. However, cats with paravertebral sympathectomy maintained blood flow above 9 ml/100 gm/min for up to 3 hours after injury. All the sympathectomized cats recovered their SEP by the 3rd hour after injury, compared with none of the controls. Thus, in the absence of the paravertebral sympathetic ganglia, spinal blood flow autoregulation was impaired and the typical posttraumatic loss in blood flow did not occur. The sympathectomy also protected the spinal cords from the neurophysiological loss usually seen in 400 gm-cm injury. The data suggest the need for caution in using acetylcholine blocking agents to paralyze animals in experimental spinal injury, since these agents alter sympathetic activity and may influence the injury process. The spinal cord is an excellent model in which to investigate sympathetic regulation of central nervous system blood flow.

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