Leukotriene production in gerbil brain after ischemic insult, subarachnoid hemorrhage, and concussive injury

1985 ◽  
Vol 62 (6) ◽  
pp. 865-869 ◽  
Author(s):  
Kevin J. Kiwak ◽  
Michael A. Moskowitz ◽  
Lawrence Levine
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Seizure Activity ◽  
Ischemia And Reperfusion ◽  
Ischemic Insult ◽  
Edema Formation ◽  
Content Type ◽  
Gerbil Brain ◽  
Concussive Injury ◽  
Fine Print

✓ A leukotriene-like immunoreactivity was measured by radioimmunoassay in the gerbil forebrain following ischemia and reperfusion, subarachnoid hemorrhage (SAH), or nonlethal concussive brain injury. In each paradigm an increase in immunoreactivity levels was found. Peak levels were reached 15 to 30 minutes after each insult, and slowly returned to baseline over the next 24 hours. The study supports the suggestion that cerebral vessels and circulating blood are capable of producing leukotrienes, and that a major source of production is a nonvascular component within gray matter, possibly the cortical neuron. Leukotrienes may play a role in the pathophysiology of cerebral edema formation, cerebral vasospasm, seizure activity, and other central nervous system abnormalities. These studies are the first to demonstrate leukotriene production in gerbil brain following SAH or concussive brain injury.

Loss of forebrain cholinergic neurons following fluid-percussion injury: implications for cognitive impairment in closed head injury

1995 ◽  
Vol 83 (3) ◽  
pp. 496-502 ◽  
Author(s):  
Richard H. Schmidt ◽  
M. Sean Grady
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Neuron Loss ◽  
Content Type ◽  
Fluid Percussion ◽  
Concussive Injury ◽  
Fine Print

✓ Disturbances in memory, concentration, and problem solving are common after even mild to moderate traumatic brain injury. Because these functions are mediated in part by forebrain cholinergic and catecholaminergic innervation, in this study the authors sought to determine if experimental concussive injury produces detectable morphological damage to these systems. Fluid-percussion head injury, sufficient to cause a 13- to 14-minute loss of righting reflex, was produced in rats that had been anesthetized with halothane. Injury was delivered either at midline or 2 mm off midline and compared with appropriate sham-injured controls. After 11 to 15 days, the rat brains were stained in serial sections for choline acetyltransferase, tyrosine hydroxylase, dopamine β-hydroxylase, acetylcholinesterase, and nicotinamide adenine dinucleotide phosphate diaphorase. Cell counts were determined for the entire population of ventrobasal forebrain cholinergic cells. Midline injury produced a bilateral loss of cholinergic neurons averaging 36% in area Ch1 (medial septal nucleus), 45% in Ch2 (nucleus of the diagonal band of Broca), and 41% in Ch4 (nucleus basalis of Meynart), (p ≤ 0.05). Lateralized injury resulted in cholinergic neuron loss of similar magnitude ipsilaterally (p ≤ 0.05), but a smaller contralateral loss of between 11% and 28%. No loss of neurons was detected in the pontomesencephalic cholinergic groups Ch5 and Ch6. There was no visible effect of head injury on forebrain dopamine or noradrenergic innervation. A significant and apparently selective loss of ventrobasal forebrain cholinergic neurons following brief concussive injury in rats is demonstrated in this study. This type of injury is known to produce significant disturbance in cognitive tasks linked to neocortical and hippocampal cholinergic function. It remains to be determined how this neuron loss occurs, whether it can be prevented with neuroprotective agents, how it affects innervation in target tissues, and whether it occurs in human victims of traumatic brain injury.

Contribution of polyamine oxidase to brain injury after trauma

1999 ◽  
Vol 90 (6) ◽  
pp. 1078-1082 ◽  
Author(s):  
Aclan Doğan ◽  
a. Muralikrishna Rao ◽  
Muştafa K. Baskaya ◽  
James Hatcher ◽  
Cuneyt Temiz ◽  
...  
Keyword(s):  
Brain Injury ◽  
Traumatic Injury ◽  
Polyamine Oxidase ◽  
Cresyl Violet ◽  
Sprague Dawley ◽  
Edema Formation ◽  
Content Type ◽  
Sprague Dawley Rats ◽  
Mdl 72527 ◽  
Fine Print

Object. The possible role of the polyamine interconversion pathway on edema formation, traumatic injury volume, and tissue polyamine levels after traumatic brain injury (TBI) was studied using an inhibitor of the interconversion pathway enzyme, polyamine oxidase.Methods. Experimental TBI was induced in Sprague—Dawley rats by using a controlled cortical impact device at a velocity of 3 m/second, resulting in a 2-mm deformation. Immediately after TBI was induced, 100 mg/kg of N1,N4-bis(2,3-butadienyl)-1,4-butanediamine 2HCl (MDL 72527) or saline was injected intraperitoneally. Brain water content and tissue polyamine levels were measured at 24 hours after TBI. Traumatic injury volume was evaluated using 2% cresyl violet solution 7 days after TBI occurred. The MDL 72527 treatment significantly reduced brain edema (80.4 ± 0.8% compared with 81.2 ± 1.2%, p < 0.05) and injury volume (30.1 ± 6.6 mm3 compared with 42.7 ± 13.3 mm3, p < 0.05) compared with the saline treatment. The TBI caused a significant increase in tissue putrescine levels at the traumatized site (65.5 ± 26.5 pmol/g in the cortex and 70.9 ± 22.4 pmol/g in the hippocampus) compared with the nontraumatized site (7 ± 2.4 pmol/g in the cortex and 11.4 ± 6.4 pmol/g in the hippocampus). The increase in putrescine levels in both the traumatized and nontraumatized cortex and hippocampus was reduced by a mean of 60% with MDL 72527 treatment.Conclusions. These results demonstrate, for the first time, that the polyamine interconversion pathway has an important role in the increase of putrescine levels after TBI and that the polyamine oxidase inhibitors, blockers of the interconversion pathway, can be neuroprotective against edema formation and necrotic cavitation after TBI.

Attenuation of intracerebral hemorrhage and thrombin-induced brain edema by overexpression of interleukin-1 receptor antagonist

2001 ◽  
Vol 95 (4) ◽  
pp. 680-686 ◽  
Author(s):  
Tetsuya Masada ◽  
Ya Hua ◽  
Guohua Xi ◽  
Guo-Yuan Yang ◽  
Julian T. Hoff ◽  
...  
Keyword(s):  
Brain Injury ◽  
Basal Ganglia ◽  
Intracerebral Hemorrhage ◽  
Receptor Antagonist ◽  
Brain Edema ◽  
Inflammatory Reaction ◽  
Interleukin 1 ◽  
Edema Formation ◽  
Content Type ◽  
Fine Print

Object. Adenovirus-mediated overexpression of interleukin-1 receptor antagonist (IL-1ra) attenuates the inflammatory reaction and brain injury that follows focal cerebral ischemia. Recently, an inflammatory reaction after intracerebral hemorrhage (ICH) was identified. In this study the authors examine the hypothesis that overexpression of IL-1ra reduces brain injury (specifically edema formation) after ICH. Methods. Adenoviruses expressing IL-1ra (Ad.RSVIL-1ra) or LacZ, a control protein (Ad.RSVlacZ), or saline were injected into the left lateral cerebral ventricle in rats. On the 5th day after virus injection, 100 µl of autologous blood or 5 U thrombin was infused into the right basal ganglia. Rats with ICH were killed 24 or 72 hours later for measurement of brain water and ion content. Thrombin-treated rats were killed 24 hours later for edema measurements and an assessment of polymorphonuclear leukocyte (PMNL) infiltration by myeloperoxidase (MPO) assay, as well as histological evaluation. Compared with saline-treated and Ad.RSVlacZ—transduced controls, Ad.RSVIL-1ra-transduced rats had significantly attenuated edema in the ipsilateral basal ganglia 3 days after ICH (81.5 ± 0.3% compared with 83.4 ± 0.4% and 83.3 ± 0.5% in control animals). Thrombin-induced brain edema was also reduced in Ad.RSVIL-1ra—treated rats (81.3 ± 0.4% compared with 83.2 ± 0.4% and 82.5 ± 0.4% in control rats). The reduction in thrombin-induced edema was associated with a reduction in PMNL infiltration into the basal ganglia, as assessed by MPO assay (49% reduction) and histological examination. Conclusions. Overexpression of IL-1ra by using an adenovirus vector attenuated brain edema formation and thrombin-induced intracerebral inflammation following ICH. The reduction in ICH-induced edema with IL-1ra may result from reduction of thrombin-induced brain inflammation.

Treatment window for hypothermia in brain injury

2001 ◽  
Vol 95 (6) ◽  
pp. 979-983 ◽  
Author(s):  
Carrie G. Markgraf ◽  
Guy L. Clifton ◽  
Melanie R. Moody
Keyword(s):  
Brain Injury ◽  
Functional Outcome ◽  
Dry Weight ◽  
Water Levels ◽  
Neurological Deficits ◽  
Therapeutic Window ◽  
Edema Formation ◽  
Content Type ◽  
Hypothermia Treatment ◽  
Fine Print

Object. The goal of this study was to evaluate the therapeutic window for hypothermia treatment following experimental brain injury by measuring edema formation and functional outcome. Methods. Traumatic brain injury (TBI) was produced in anesthetized rats by using cortical impact injury. Edema was measured in the ipsilateral and contralateral hemispheres by subtracting dry weight from wet weight, and neurological function was assessed using a battery of behavioral tests 24 hours after TBI. In injured rats, it was found that brain water levels were elevated at 1 hour postinjury, compared with those in sham-injured control animals, and that edema peaked at 24 hours and remained elevated for 4 days. Hypothermia (3 hours at 30°C) induced either immediately after TBI or 60 minutes after TBI significantly reduced early neurological deficits. Delay of treatment by 90 or 120 minutes postinjury did not result in this neurological protection. Immediate administration of hypothermia also significantly decreased the peak magnitude of edema at 24 hours and 48 hours postinjury, compared with that in normothermic injured control animals. When delayed by 90 minutes, hypothermia did not affect the pattern of edema formation. Conclusions. When hypothermia was administered immediately or 60 minutes after TBI, injured rats showed an improvement in functional outcome and a decrease in edema. Delayed hypothermia treatment had no effect on functional outcome or on edema.

Cytidinediphosphocholine treatment to decrease traumatic brain injury—induced hippocampal neuronal death, cortical contusion volume, and neurological dysfunction in rats

2003 ◽  
Vol 98 (4) ◽  
pp. 867-873 ◽  
Author(s):  
Robert J. Dempsey ◽  
Vemuganti L. Raghavendra Rao
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Death ◽  
Hippocampal Neurons ◽  
Neurological Dysfunction ◽  
Adult Rats ◽  
Edema Formation ◽  
Content Type ◽  
Cortical Contusion ◽  
Fine Print

Object. In previous studies at their laboratory the authors showed that cytidinediphosphocholine (CDP-choline), an intermediate of phosphatidylcholine synthesis, decreases edema formation and blood—brain barrier disruption following traumatic brain injury (TBI). In the present study the authors investigate whether CDP-choline protects hippocampal neurons after controlled cortical impact (CCI)—induced TBI in adult rats. Methods. After adult male Sprague—Dawley rats had been anesthetized with halothane, a moderate-grade TBI was induced with the aid of a CCI device set at a velocity of 3 m/second, creating a 2-mm deformation. Sham-operated rats, which underwent craniectomy without impact served as controls. The CDP-choline (100, 200, and 400 mg/kg body weight) or saline was injected into the animals twice (once immediately postinjury and once 6 hours postinjury). Seven days after the injury, the rats were neurologically evaluated and killed, and the number of hippocampal neurons was estimated by examining thionine-stained brain sections. By 7 days postinjury, there was a significant amount of neuronal death in the ipsilateral hippocampus in the CA2 (by 53 ± 7%, p < 0.05) and CA3 (by 59 ± 9%, p < 0.05) regions and a contusion (volume 34 ± 8 mm3) in the ipsilateral cortex compared with sham-operated control animals. Rats subjected to TBI also displayed severe neurological deficit at 7 days postinjury. Treating rats with CDP-choline (200 and 400 mg/kg, intraperitoneally) significantly prevented TBI-induced neuronal loss in the hippocampus, decreased cortical contusion volume, and improved neurological recovery. Conclusions. Treatment with CDP-choline decreased brain damage following TBI.

Aneurysm-induced third nerve palsy

1972 ◽  
Vol 36 (5) ◽  
pp. 548-551 ◽  
Author(s):  
Iftikhar A. Raja
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Functional Recovery ◽  
Poor Prognosis ◽  
Nerve Palsy ◽  
Nerve Function ◽  
Content Type ◽  
Third Nerve Palsy ◽  
Carotid Ligation ◽  
Third Nerve ◽  
Fine Print

✓ Forty-two patients with aneurysm-induced third nerve palsy are described. After carotid ligation, 58% showed satisfactory and 42% unsatisfactory functional recovery. In some patients the deficit continued to increase even after carotid ligation. Early ligation provided a better chance of recovery of third nerve function. Patients in whom third nerve palsy began after subarachnoid hemorrhage had a poor prognosis. No relationship was noted between the size of the aneurysm and the recovery of third nerve function.

Arteriovenous malformation of choroid plexus

1975 ◽  
Vol 42 (4) ◽  
pp. 457-461 ◽  
Author(s):  
Charles J. Hodge ◽  
Robert B. King
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Arteriovenous Malformation ◽  
Choroid Plexus ◽  
Content Type ◽  
Fine Print

✓ The authors describe a patient with subarachnoid hemorrhage from an arteriovenous malformation of the choroid plexus and present a brief review of related reports.

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.

Surgical experiences with giant intracranial aneurysms

1984 ◽  
Vol 61 (6) ◽  
pp. 1009-1028 ◽  
Author(s):  
Lindsay Symon ◽  
Janos Vajda
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Mortality Rate ◽  
Intracranial Aneurysms ◽  
Visual Loss ◽  
Considerable Improvement ◽  
Brain Circulation ◽  
Content Type ◽  
Space Occupying Lesion ◽  
Fine Print

✓ A series of 35 patients with 36 giant aneurysms is presented. Thirteen patients presented following subarachnoid hemorrhage (SAH) and 22 with evidence of a space-occupying lesion without recent SAH. The preferred technique of temporary trapping of the aneurysm, evacuation of the contained thrombus, and occlusion of the neck by a suitable clip is described. The danger of attempted ligation in atheromatous vessels is stressed. Intraoperatively, blood pressure was adjusted to keep the general brain circulation within autoregulatory limits. Direct occlusion of the aneurysm was possible in over 80% of the cases. The mortality rate was 8% in 36 operations. Six percent of patients had a poor result. Considerable improvement in visual loss was evident in six of seven patients in whom this was a presenting feature, and in four of seven with disturbed eye movements.

Circling and rotational automatisms in patients with frontotemporal cortical and subcortical lesions

1971 ◽  
Vol 35 (5) ◽  
pp. 554-563 ◽  
Author(s):  
Richard C. Schneider ◽  
Hazel D. Calhoun ◽  
Kenneth A. Kooi
Keyword(s):  
Electrical Activity ◽  
Seizure Activity ◽  
Cerebrovascular Insufficiency ◽  
Normal Pattern ◽  
Content Type ◽  
Depressed Fracture ◽  
Intracranial Lesions ◽  
Fine Print

✓ The authors report five patients who had circling or rotational automatisms similar to movements described in monkeys following epileptogenic lesions. All patients were found to have intracranial lesions in the frontotemporal junction: two had tumors, one had demonstrated cerebrovascular insufficiency, one had an extensive depressed fracture, and one an aneurysm. In all patients, EEG's were performed and foci identified along with the degree of spread of electrical activity. Three were treated conservatively and two surgically, with good results; seizure activity subsided and the EEG's reverted to a more normal pattern. The importance of electroencephalographic and electrocorticographic studies is emphasized.

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