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.

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.

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.

Functional outcome after surgical treatment of spontaneous and nonspontaneous spinal subdural hematomas

2005 ◽  
Vol 3 (1) ◽  
pp. 12-16 ◽  
Author(s):  
Ruth Thiex ◽  
Armin Thron ◽  
Joachim M. Gilsbach ◽  
Veit Rohde
Keyword(s):  
Functional Outcome ◽  
Symptom Onset ◽  
Neurological Deficits ◽  
Content Type ◽  
Sensorimotor Deficits ◽  
Subdural Hematomas ◽  
Long Term Survivors ◽  
Postoperative Improvement ◽  
Fine Print

Object. Because of the rarity of spinal subdural hematomas (SDHs), the literature offers scarce estimates of the outcome and predictive factors in patients suffering from these lesions. In addition, single-institution surgical series are still lacking. Therefore, the authors retrospectively evaluated the early and long-term functional outcomes measured in eight patients with spontaneous and nonspontaneous spinal SDHs in whom the clot had been evacuated. Methods. The patients' charts were evaluated for origin of the lesion, risk factors, and neurological deficits at symptom onset and at 28 days after extirpation of the spinal SDH. Long-term clinical outcome (Barthel Index [BI]) was evaluated by administering a telephone questionnaire to the patient or a relative. Only one patient with a spontaneous spinal SDH was identified. Four patients were undergoing anticoagulant therapy, and three patients had undergone a previous anesthetic/diagnostic spinal procedure. Twenty-eight days postoperatively, neurological deficits improved in six of eight patients; however, in two of the six patients, the improvement did not allow the patients to become independent again. In two patients, surgery did not affect the complete sensorimotor deficits. In the long-term survivors (median 45 months) a median BI of 55 was achieved. The latency between symptom onset and surgery did not correlate with functional outcome in this series. The preoperative neurological condition and location of the hematoma correlated positively with early and long-term functional outcome. Conclusions. To the best of their knowledge, the present study is the largest single-institutional study of patients with surgically treated spinal SDHs. Despite some postoperative improvement of sensorimotor deficits in most patients, the prognosis is poor because 50% of the patients remain dependent. Their outcome was determined by the preoperative sensorimotor function and spinal level of the spinal SDH.

Improved motor outcome in response to magnesium therapy received up to 24 hours after traumatic diffuse axonal brain injury in rats

1999 ◽  
Vol 90 (3) ◽  
pp. 504-509 ◽  
Author(s):  
Deanne L. Heath ◽  
Robert Vink
Keyword(s):  
Brain Injury ◽  
Untreated Control ◽  
Repeated Administration ◽  
Therapeutic Window ◽  
Motor Deficits ◽  
Content Type ◽  
Assessment Period ◽  
Motor Outcome ◽  
The Impact ◽  
Fine Print

Object. The goal of this study was to establish the therapeutic window during which delayed therapy with MgSO4 improves neurological motor outcome in rats that have suffered severe traumatic axonal brain injury.Methods. Severe brain injury was induced in male Sprague—Dawley rats by using the impact—acceleration model of severe traumatic diffuse axonal brain injury. Injured animals were subsequently treated with MgSO4 (750 µmol/kg) infused intramuscularly at 30 minutes or at 8, 12, or 24 hours after trauma and were tested for neurological motor outcome during the following week by using the rotarod test. Injured untreated (control) animals demonstrated highly significant (p < 0.001) neurological motor deficits that were sustained over the 1-week assessment period. Animals treated with MgSO4 at 30 minutes or at 8 or 12 hours postinjury demonstrated significantly improved motor outcomes compared with untreated control animals at all time points (0.001 < p < 0.05). Animals treated with MgSO4 at 24 hours had motor scores that were similar to those of untreated control animals early in the week, but demonstrated a significantly more rapid recovery in function and, by the end of the assessment period, they demonstrated significantly improved motor scores (p < 0.01). Repeated administration of MgSO4 over the 1-week observation period did not further improve outcome.Conclusions. The present results demonstrate that Mg++ plays a neuroprotective role following severe diffuse traumatic axonal brain injury. Moreover, Mg++ therapy significantly improved motor outcome when administered up to 24 hours after injury, with early treatments providing the most significant benefit. Repeated administration beyond 24 hours postinjury did not provide additional neuroprotection.

Dimethyl sulfoxide in the treatment of experimental brain compression

1973 ◽  
Vol 38 (3) ◽  
pp. 345-354 ◽  
Author(s):  
J. C. de la Torre ◽  
D. W. Rowed ◽  
H. M. Kawanaga ◽  
S. Mullan
Keyword(s):  
Brain Injury ◽  
Head Injury ◽  
Mortality Rate ◽  
Dimethyl Sulfoxide ◽  
Rhesus Monkeys ◽  
Neurological Deficits ◽  
Content Type ◽  
Brain Compression ◽  
The Brain ◽  
Fine Print

✓ Forty rhesus monkeys were subjected to acute experimental head injury by extradural balloon compression of the brain. A critical endpoint in the compression was used to inject either saline, urea, or dimethyl sulfoxide (DMSO). All saline-treated animals died. Ten of 15 urea-treated animals survived, while 14 of 15 DMSO-injected monkeys survived. The incidence of neurological deficits seen in survivors was four for urea and one for DMSO. It is concluded that DMSO is capable of modifying the mortality rate and posttraumatic sequelae of brain injury in the experimental model used.

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.

Deferoxamine-induced attenuation of brain edema and neurological deficits in a rat model of intracerebral hemorrhage

2004 ◽  
Vol 100 (4) ◽  
pp. 672-678 ◽  
Author(s):  
Takehiro Nakamura ◽  
Richard F. Keep ◽  
Ya Hua ◽  
Timothy Schallert ◽  
Julian T. Hoff ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Oxidative Dna Damage ◽  
Iron Accumulation ◽  
Neurological Deficits ◽  
Content Type ◽  
Autologous Whole Blood ◽  
Fine Print

Object. Previous studies undertaken by the authors have indicated that iron accumulation and oxidative stress in the brain contribute to secondary brain damage after intracerebral hemorrhage (ICH). In the present study the authors investigate whether deferoxamine, an iron chelator, can reduce ICH-induced brain injury. Methods. Male Sprague—Dawley rats each received an infusion of 100 µl of autologous whole blood into the right basal ganglia and were killed 1, 3, or 7 days later. Iron distribution was examined histochemically (enhanced Perls reaction). The effects of deferoxamine on ICH-induced brain injury were examined by measuring brain edema and neurological deficits. Immunohistochemical analysis was performed to investigate 8-hydroxyl-2′-deoxyguanosine (8-OHdG), a marker of oxidative DNA damage, and Western blot analysis was performed to measure the amount of apurinic/apyrimidinic endonuclease/redox effector factor—1 (APE/Ref-1), a repair mechanism for DNA oxidative damage. Iron accumulation was observed in the perihematomal zone from 1 day after ICH. Deferoxamine attenuated brain edema, neurological deficits, and ICH-induced changes in 8-OHdG and APE/Ref-1. Conclusions. Deferoxamine and other iron chelators may be potential therapeutic agents for ICH. They may act by reducing the oxidative stress caused by the release of iron from the hematoma.

A fatal, chronically growing basilar artery: a new type of dissecting aneurysm

1996 ◽  
Vol 84 (6) ◽  
pp. 962-971 ◽  
Author(s):  
Tohru Mizutani
Keyword(s):  
Mr Imaging ◽  
Basilar Artery ◽  
Dissecting Aneurysm ◽  
Neurological Deficits ◽  
Vertebrobasilar Insufficiency ◽  
Content Type ◽  
Asymptomatic Patients ◽  
Basilar Arteries ◽  
Fine Print

✓ A long-term follow-up study (minimum duration 2 years) was made of 13 patients with tortuous dilated basilar arteries. Of these, five patients had symptoms related to the presence of such arteries. Symptoms present at a very early stage included vertebrobasilar insufficiency in two patients, brainstem infarction in two patients, and left hemifacial spasm in one patient. Initial magnetic resonance (MR) imaging in serial slices of basilar arteries obtained from the five symptomatic patients showed an intimal flap or a subadventitial hematoma, both of which are characteristic of a dissecting aneurysm. In contrast, the basilar arteries in the eight asymptomatic patients did not show particular findings and they remained clinically and radiologically silent during the follow-up period. All of the lesions in the five symptomatic patients gradually grew to fantastic sizes, with progressive deterioration of the related clinical symptoms. Dilation of the basilar artery was consistent with hemorrhage into the “pseudolumen” within the laminated thrombus, which was confirmed by MR imaging studies. Of the five symptomatic patients studied, two died of fatal subarachnoid hemorrhage (SAH) and two of brainstem compression; the fifth patient remains alive without neurological deficits. In the three patients who underwent autopsy, a definite macroscopic double lumen was observed in both the proximal and distal ends of the aneurysms within the layer of the thickening intima. Microscopically, multiple mural dissections, fragmentation of internal elastic lamina (IEL), and degeneration of media were diffusely observed in the remarkably extended wall of the aneurysms. The substantial mechanism of pathogenesis and enlargement in the symptomatic, highly tortuous dilated artery might initially be macroscopic dissection within a thickening intima and subsequent repetitive hemorrhaging within a laminated thrombus in the pseudolumen combined with microscopic multiple mural dissections on the basis of a weakened IEL. The authors note and caution that symptomatic, tortuous dilated basilar arteries cannot be overlooked because they include a group of malignant arteries that may grow rapidly, resulting in a fatal course.

Progressive neurological deficits with benign intracerebral cysts

1986 ◽  
Vol 65 (5) ◽  
pp. 706-709 ◽  
Author(s):  
Yoko Nakasu ◽  
Jyoji Handa ◽  
Kazuyoshi Watanabe
Keyword(s):  
Histological Examination ◽  
Computerized Tomography ◽  
Cyst Wall ◽  
Benign Lesion ◽  
Ct Scanning ◽  
Neurological Deficits ◽  
Review Of The Literature ◽  
Content Type ◽  
Ct Findings ◽  
Fine Print

✓ Two patients with benign intracerebral cysts are reported and a brief review of the literature is given. Although computerized tomography (CT) scanning is useful in detecting a variety of intracerebral cysts, the CT findings are not specific for any lesion. An exploratory operation with establishment of an adequate route of drainage and a histological examination of the cyst wall are mandatory in the management of patients with a progressive but benign lesion.

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