S C Jones, A D Perez-Trepichio, M Xue, A J Furlan, I A Awad
{"title":"Magnetic resonance diffusion-weighted imaging: sensitivity and apparent diffusion constant in stroke.","authors":"S C Jones, A D Perez-Trepichio, M Xue, A J Furlan, I A Awad","doi":"10.1007/978-3-7091-9334-1_56","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_56","url":null,"abstract":"<p><p>Magnetic resonance diffusion-weighted imaging (MR-DWI) is sensitive to the diffusibility of water and may offer characterization and anatomical localization of stroke leading to early tailored therapeutic intervention. We compared DWI, the apparent diffusion constant (ADC), and autoradiographic cerebral blood flow (CBF) in a model of focal cerebral ischemia in the rat. Sprague-Dawley rats were embolized with a single silicone cylinder injected into the internal carotid artery. Both common carotids were permanently ligated. The animals were anesthetized (isoflurane in O2), and paralyzed (gallamine). MR-DWI were obtained with a GE 4.7 T magnet (TE = 3 s, TR = 80 msec, b = 2393.10(-3) mm2/s, slice thickness 3 mm). DWI and CBF autoradiograms were compared visually. ADC was assessed in various regions, including ischemic cortex and a region homologous to ischemic cortex. Imaging times from stroke onset were 50 +/- 6 min (mean +/- SEM) for DWI, 185 +/- 17 min for a second DWI. CBF was determined at 258 +/- 15 min. The specificity was 100% at both 50 min and 185 min, indicating that there were no false positives; in 3 animals ischemia was not present. However, the sensitivity analysis indicated that early DWI yields some false negatives; at 50 min the sensitivity was 60%. We attribute our result of low early sensitivity to small infarcts in relation to the slice thickness. Later, at 185 min, sensitivity was 100%. The first ADCs were higher than the second ADC values in ischemic cortex. For infarcts larger than the slice thickness, early MR-DWI is highly sensitive for imaging evolving ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"207-10"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18970430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
W A van den Brink, B O Santos, A Marmarou, C J Avezaat
{"title":"Quantitative analysis of blood-brain barrier damage in two models of experimental head injury in the rat.","authors":"W A van den Brink, B O Santos, A Marmarou, C J Avezaat","doi":"10.1007/978-3-7091-9334-1_125","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_125","url":null,"abstract":"<p><p>The integrity of the blood-brain barrier was studied in a new model of closed head injury, and in an established model of fluid percussion injury, in the rat. Brain injury in this new model is induced by impact and acceleration of the protected rat skull. Severe hypertension is not a characteristic of this new model as compared to the tremendous surge following direct dural percussion. This is important because of the well known sensitivity of the cerebral microvasculature for acute hypertension. Using a radioactive tracer technique the dysfunction of the barrier was quantified. It is shown that the BBB is temporarily damaged due to trauma, subsequent arterial pressure surge, as seen in the percussed animals, deteriorates the dysfunction of the barrier even further. This study indicates that vascular damage is a key event following head injury. Yet the concomitant basic pathophysiological sequelae of different models must be considered when studying barrier damage and cerebral edema following brain injury. Time window studies of the barrier indicate that the barrier seals within a few hours following severe concussive head injury, and in the absence of a hypertensive surge.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"456-8"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18970444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Expression of basic fibroblast growth factor in astrocytes at the site of cerebral lesions and edematous areas under chronic hypertension.","authors":"E Yamada, H Kataoka, C H Chue, F Hazama","doi":"10.1007/978-3-7091-9334-1_70","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_70","url":null,"abstract":"<p><p>In an attempt to obtain information about changes of the basic fibroblast growth factor (bFGF) in the brain under chronic hypertensive condition, we studied immunohistochemically the distribution of bFGF in the brain of stroke-prone spontaneously hypertensive rats (SHRSP). In the control normotensive rats, only weak immunoreactivity for bFGF was demonstrated in nerve cells and some astrocytes. In SHRSP marked immunoreactivity was demonstrated in the densely packed reactive cells, particularly astrocytes, in and around cerebral lesions. Slightly increased reaction for bFGF was found in the nerve cells around lesions. Astrocytes in the white matter also showed immunoreactivity for bFGF, the localization of which corresponded very well with the site of edema. This finding indicates the possibility that brain edema expresses bFGF in astrocytes and possibly in nerve cells.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"265-7"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-7091-9334-1_70","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18975720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H Kushi, Y Katayama, T Shibuya, T Tsubokawa, T Kuroha
{"title":"Gadolinium DTPA-enhanced magnetic resonance imaging of cerebral contusions.","authors":"H Kushi, Y Katayama, T Shibuya, T Tsubokawa, T Kuroha","doi":"10.1007/978-3-7091-9334-1_129","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_129","url":null,"abstract":"<p><p>The morphological characteristics of cerebral contusions in head trauma patients suggest that an increase in cerebrovascular permeability is responsible for the contusion edema which develops within 1-3 days posttrauma. In the present study, 10 patients with cerebral contusions (mean age, 38 years old; 8 males and 2 females) were examined by gadolinium (Gd)-DTPA enhanced magnetic resonance imaging (MRI) at 1-2 days after trauma. Gd-DTPA (0.3 mmol/kg) was infused intravenously over a period of 30 min. MRIs were taken before, and at 2 and 4 hours after initiation of the Gd-DTPA administration. It was found that contusion edema areas were frequently enhanced by Gd-DTPA at 2 hours. The enhancement diminished at 4 hours. These findings appear to be inconsistent with the results of previously reported similar studies in which enhancement was detected at 6-9 days posttrauma but not during the period earlier than 6 days. This discrepancy may be attributable to the presence of a high blood concentration of Gd-DTPA for a longer period of time and a delay in the time at which MRIs were taken in the present study. The present data indicate that an increased cerebrovascular permeability occurs at as early as 1-2 days posttrauma, and suggest that contusion edema which progresses during the initial 1-3 days may be at least partially vasogenic in nature.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"472-4"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18975724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of protein kinase C activators on Na, K-ATPase activity in rat brain microvessels.","authors":"H Johshita, T Asano, T Matsui, T Koide","doi":"10.1007/978-3-7091-9334-1_29","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_29","url":null,"abstract":"<p><p>In order to study the possible role of C kinase (PKC) on sodium pump of cerebral vessels, we used diacylglycerol (diC8: sn-1,2-dioctanoylglycerol) and phorbol esters (PMA: phorbol 12-myristate 13-acetate; PDA: phorbol 12,13-diacetate; 4 alpha-P: 4-alpha phorbol) as PKC activators, and examined their effects on Na,K-ATPase activity in rat brain microvessels (MVs). Rats were divided into non-treated (control; n = 9), four-vessel occlusion (4VO; 30-30 minutes ischemia and recirculation, n = 5), and middle cerebral artery occlusion (MCAO, n = 3) groups. MVs were passed through nylon meshes and were obtained by ultracentrifuge at 58000 g. Na,K-ATPase activity in MVs was determined by the phosphomolybdate method. DiC8 enhanced Na,K-ATPase activity at 10(-4) M in the control group, the 4VO group and the contralateral hemispheres of the MCAO group (139% +/- 0.06, 135% +/- 0.2, 133% +/- 0.18, mean +/- SE, p < 0.05, p < 0.01, Wilcoxon rank sum) respectively, but had no effects on MVs in the ipsilateral hemispheres of MCAO group (74% +/- 0.04). This activation by diC8 was inhibited by PKC inhibitors, staurosporine (3 x 10(8) M) and H7 (10(-6) M) in the control MVs. By contrast, PMA suppressed Na, K-ATPase at 10(-5) M in the control group (-25% +/- 0.07), but it tended to activate Na,K-ATPase activity in the ipsilateral hemispheres of the MCAO groups (33% +/- 0.09). PDA and 4 alpha-P did not have any consistent effects at the concentration examined. The cause of difference between the effects of diC8 and PMA is unclear at present, but it may stem from the mode of lipid-membrane interaction in these agents and the difference in the condition of cells as well.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"113-5"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18970425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Transdural cortical stabbing facilitates the drainage of edema fluid out of cold-injured brain.","authors":"T L Chiou, Y H Chiang, W S Song, S S Lin","doi":"10.1007/978-3-7091-9334-1_126","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_126","url":null,"abstract":"<p><p>Recent experimental results indicate that cerebral glia lining and glia limitans may be barriers for plasma protein extravasated from injured cerebral microvessels flowing into the adjacent subarachnoid space. Therefore, it has been hypothesized that a transdural cortical stabbing which opens both the pia lining and glia limitans may facilitate drainage of edema fluid into the subarachnoid space and minimize brain edema. This hypothesis was tested in Sprague-Dawley rats with a transdural cold-injury on the right parietal cortex. The animals were sacrificed 24 hours later. One hour before being sacrificed 0.6 ml of 2% Evans blue was intravenously injected to determining the Evans blue distribution area. For measuring the inulin retention volume in the brain, 14C-inulin (10 microCi) in 1 ml of saline was injected intravenously at 10 min before sacrifice. The extent of brain edema was assessed by measuring the water content, the inulin retention volume, and the distribution area of Evans blue in the brain. Our results showed that the transdural cortical stabbing did not alter the water content of the cerebral hemisphere with cold lesion. However, it did effectively diminish the inulin retention volume by 26% as well as the distribution area of Evans blue by 22% in the cerebral hemisphere with cold lesion. In conclusion, a transdural cortical stabbing on the injured cortex may be beneficial for vasogenic brain edema.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"459-61"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18970445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P Mathew, D I Graham, R Bullock, W Maxwell, J McCulloch, G Teasdale
{"title":"Focal brain injury: histological evidence of delayed inflammatory response in a new rodent model of focal cortical injury.","authors":"P Mathew, D I Graham, R Bullock, W Maxwell, J McCulloch, G Teasdale","doi":"10.1007/978-3-7091-9334-1_116","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_116","url":null,"abstract":"<p><p>Cortical contusions are one of the most common characteristics in head injury and are regarded by many as the hallmark of significant injury. No experimental study has clarified the roles of mechanical forces, haemorrhage and ischaemia in the process of progressive acute brain damage and later neurobehavioural dysfunction. We have devised a new, simple reproducible rodent model of focal cortical injury which employs a 'pure' mechanical/physical force applied through the intact dura. Using this model we have investigated the time course and pattern of changes in neurons, glia and microvasculature. With the exception of haemorrhage, this model closely reproduces the light- and electron microscopy features of human contusion. In the absence of perivascular haemorrhage we have demonstrated delayed perivascular protein leakage and polymorphonuclear-leukocyte infiltration of the damaged cortex. We postulate that a component of the delayed blood brain barrier breakdown demonstrated in human focal head injury (which may contribute to swelling and brain damage) is due to an acute inflammatory response, the magnitude of which is dependent on the amount of tissue injury.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"428-30"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R Hata, M Matsumoto, K Yamamoto, T Ohtsuki, S Ogawa, N Handa, T Kubo, T Matsunaga, T Nishimura, T Kamada
{"title":"An ischemic opening of the blood-brain barrier may deteriorate brain stem auditory evoked potentials following transient hindbrain ischemia in gerbils.","authors":"R Hata, M Matsumoto, K Yamamoto, T Ohtsuki, S Ogawa, N Handa, T Kubo, T Matsunaga, T Nishimura, T Kamada","doi":"10.1007/978-3-7091-9334-1_53","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_53","url":null,"abstract":"<p><p>To clarify the effect of vasogenic brain edema on the brainstem, the relationships between waveform changes in brainstem auditory evoked potentials (BAEP) and blood-brain barrier (BBB) disturbance following transient hindbrain ischemia were investigated. Hindbrain ischemia was induced in gerbils by bilateral occlusion of the vertebral arteries. The animals were divided into three groups subjected to 0, 5, and 30 min of bilateral vertebral occlusion (BVO-0',-5', and -30' groups; n = 4 in each group). Two hours after recirculation, Evans blue (EB) solution was injected into the saphenous vein. The brains were removed after 30 min of circulation, and all areas stained macroscopically by EB were noted and recorded. During hindbrain ischemia, BAEP disappeared within 3 min. In the BVO-5' group, BAEP reappeared and returned to normal within 10 min after reperfusion, whereas in the BVO-30' group, BAEP never returned to normal and finally disappeared within 30 min after reperfusion. In the BVO-5' group, no EB staining was visible. On the other hand, in the BVO-30' group, EB staining was seen in the medial part of the tegmentum in the midbrain in two animals, and around the vestibular nucleus in the lateral parts of the pons in three. These results demonstrate the close relationship between the reversibility of ischemia-induced changes in BAEP and BBB disturbance in the brainstem.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"197-9"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-7091-9334-1_53","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tirilazad reduces brain edema after middle cerebral artery ligation in hypertensive rats.","authors":"A Karki, I Westergren, H Widner, B Johansson","doi":"10.1007/978-3-7091-9334-1_83","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_83","url":null,"abstract":"<p><p>Tirilazad (3 mg/kg i.v.) or vehicle was given 10 min, 3 and 12 hours after ligation of the right middle cerebral artery in male spontaneously hypertensive rats (n = 12 in each group). Brain specific gravity was determined in 23 predetermined cortical regions covering the core and penumbra areas 24 hours after the occlusion. The specific gravity was significantly higher in tirilazad-treated rats than in controls (p < 0.0001). When individual regions of the two groups were compared, the difference was significant in 9 of the 23 samples predominantly, but not exclusively, in the penumbra zone.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"310-3"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Riboflavin reduces edema in focal cerebral ischemia.","authors":"A L Betz, X D Ren, S R Ennis, D E Hultquist","doi":"10.1007/978-3-7091-9334-1_84","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_84","url":null,"abstract":"<p><p>Oxidized irwN has been proposed as a mediator of the free radical-induced damage that occurs during cerebral ischemia. Dihydroriboflavin, a compound produced from riboflavin (B2) by NADPH-dependent flavin reductase, rapidly reduces oxidized iron. Since treatment with riboflavin offers protection from ischemic injury in other tissues, we tested the effect of pretreatment with B2 on brain edema formation during focal ischemia. Two different models of middle cerebral artery occlusion (MCAO) in rats were tested: transcranial electrocautery and intracarotid occlusion with a nylon thread. Groups of 6-8 animals were treated with 7.5 mg of B2/kg or saline vehicle 1 h before MCAO and brain water content was determined after 4 h of ischemia. Pretreatment with B2 reduced total hemisphere edema formation from 0.37 +/- 0.05 to 0.19 +/- 0.05 mg/g dry wt. (48% protection, p < 0.01) following transcranial MCAO. Edema was greater following MCAO with the intra-carotid thread (0.54 +/- 0.05 ml/g) but protection by B2 was less (21%). We conclude that pretreatment with B2 reduces ischemic brain injury, perhaps by reacting with oxidized iron. However, the larger stroke produced by the thread MCAO method makes it more difficult to observe protection following brief ischemia in this model.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"314-7"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-7091-9334-1_84","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}