急性闭合性脑损伤模型的建立与评估

目的建立符合临床的急性闭合性脑损伤模型。方法24只新西兰大耳白兔随机分为4组:A(标准对照组),B、C、D组(均为实验组)。采用800g·cm(100g×8 cm)的打击能量在B、C、D组兔的硬膜外造成脑损伤模型。分别在伤后1、3、5 h测量水肿区脑皮层中水、钠、钙和丙二醛(MDA)的含量及及伤后5 h的病理学改变。结果水肿区脑皮层中水、钠、钙和MDA的含量呈进行性升高并有明显的病理学改变。结论本实验所建立的脑损伤模型符合临床上闭合性颅脑损伤的病理学改变和病理生理特点。     

Effects of ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury

Ｉｎｒｅｃｅｎｔｙｅａｒｓ ,ｉｔｉｓｆｏｕｎｄｔｈａｔｅｘｏｇｅｎｏｕｓｇａｎｇｌｉｏｓｉｄｅＧＭ 1ｎｏｔｏｎｌｙ ｐｒｏｍｏｔｅｃｕｌｔｕｒｅｄｎｅｕｒｏｎｓｔｏｇｅｍｍａｔｅａｎｄａｘｏｎｔｏ ｇｒｏｗｉｎｖｉｔｒｏ ,ｂｕｔａｌｓｏｐａｓｓｅｓｔｈｒｏｕｇｈｂｒａｉｎ ｂｌｏｏｄｂａｒｒｉｅｒｔｏｐｒｏｔｅｃｔｃｅｌｌｕｌａｒｍｅｍｂｒａｎｅｆｕｎｃｔｉｏｎｉｎｔｈｅｅａｒｌｙｓｔａｇｅａｎｄｈａｓｓｉｇｎｉｆｉｃａｎｔｅｆｆｅｃｔｓｏｎｒｅｓｔｏｒａｔｉｏｎｏｆｔｈｅｄａｍａｇｅｄｆｕｎｃｔ…     

Kffects of ganglioside GM1 on kreduction of brain edema and amelioration of metabolism after traumatic brain injury

OBJECTIVE: To observe the effects of ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury (TBI). METHODS: An acute experimental closed TBI model in rats was induced by a fluid-percussion brain injury model. At five and sixty minutes after TBI, the animals were intraperitoneally injected by ganglioside GM1 (30 mg/kg) or the same volume of saline. At the 6th hour after TBI, effects of ganglioside GM1 or saline on changes of mean arterial pressure (MAP), contents of water, lactic acid (LA) and lipid peroxidation (LPO) in the injured cerebral tissues were observed. RESULTS: After TBI, MAP decreased and contents of water, LA and LPO increased in brain injury group; however, MAP was back to normal levels and contents of water, LA and LPO decreased in ganglioside GM1 treated group, compared with those in brain injury group (P < 0.05). No significant difference between the saline treated group and the brain injury group (P > 0.05) was observed. CONCLUSIONS: Ganglioside GM1 does have obvious neuroprotective effect on early TBI.     

The effects of aortic crossclamping and resuscitation on intracranial pressure, cerebral blood flow, and cerebral water content in a model of focal brain injury and hemorrhagic shock

Aortic crossclamping (AOXC) is performed frequently in hypotensive trauma patients who may have had a head injury. The effect of AOXC on the injured brain is unknown. We studied the effect of AOXC on mean arterial pressure (MAP), intracranial pressure (ICP), cerebral blood flow (CBF), cerebral perfusion pressure (CPP), and cerebral water content in a porcine model of focal cryogenic brain injury. Four groups of animals were studied: Group I--brain injury only; Group II--brain injury and AOXC; Group III--brain injury with hemorrhage and AOXC; and Group IV--AOXC only. Focal cryogenic grain injury increased the ICP in Groups I-III. Aortic crossclamping increased MAP, CBF, ICP, and CPP after hemorrhage in Group III. Following declamping and resuscitation there were no differences between the groups in any studied variable. Cerebral water content at the site of the focal brain injury was greater than in nonlesioned cortex but there was no significant difference between groups despite a greater positive fluid balance in hemorrhaged animals. AOXC improved perfusion to the injured brain without a significant increase in ICP. Increased MAP induced by AOXC and large fluid resuscitation appeared to have no detrimental effect on ICP, CBF, cerebral water content, or CPP in this model of brain injury.     

Traumatic shock and head injury: effects of fluid resuscitation on the brain

The effects of resuscitation of traumatic-hemorrhagic shock on the brain are unknown. Traumatic shock in sheep (fracture/crush injury, 2-hr hemorrhage to 40 mm Hg) was followed by resuscitation to baseline mean arterial pressure. Two groups without brain injury were resuscitated with lactated Ringer's (LR1, n = 7) or albumin (ALB1, n = 6). Focal brain injury was added in two further groups (LR2, n = 6; ALB2, n = 6). Hemodynamics, intracranial pressure (ICP), EEG, and colloid osmotic pressure (COP) were followed. Brain water (BW) and cerebral blood volume (CBV) were compared to those of controls (C, n = 7). Results: ICP rose in all groups. Animals without brain injury did not have increased brain water. Below are results for brain-injured animals after resuscitation (mean +/- SEM). (table; see text) Maintaining COP during initial resuscitation does not minimize cerebral edema: the effects of LR and ALB were similar in this setting. Focal brain injury causes edema but does not cause large increases in ICP with initial resuscitation.     

肢体关节爆炸伤并海水浸泡后的创伤反应

目的观察肢体关节爆炸伤并海水浸泡后的肢体创伤反应。方法新西兰白兔24只,随机分为对照组(A组n=12)和实验组(B组n=12)。0.9g铜壳单质猛炸药以海绵间隔6cm,绑于实验下肢膝关节前外侧,麻醉后电引爆分组实验。A组伤口包扎后陆地放置1h,B组伤口包扎后下肢浸入海水中1h,各组分别于麻醉后及实验后分别测血白细胞(WBC)、血清C反应蛋白(CRP)、白细胞介素-1、6(IL-1、IL-6)、肿瘤坏死因子(TNF)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活力。结果爆炸后1h血WBC、SOD均下降,差异有显著性意义(P<0.05、P<0.001);CRP、IL-1变化差异无显著性意义(P>0.05);MDA、IL-6、TNF均升高且差异有显著性意义(P<0.05、P<0.001)。组间比较MDA、SOD、IL-6值差异有显著性意义(P<0.05)。结论肢体关节爆炸伤后机体创伤反应严重,脂质过氧化反应增强、WBC减少、IL-6、TNF表达增强。海水浸泡肢体进一步加重创伤反应,MDA、IL-6值显著增高,SOD值显著降低。     

深低温停循环逆行脑灌注脑组织自由基变化的实验研究

研究深低温停循环（ＤＨＣＡ）与逆行脑灌注（ＲＣＰ）时脑组织自由基的变化。健康杂种犬１４只，随机等分为ＤＨＣＡ组和ＲＣＰ组，在停循环前（Ａ点）、ＤＨＣＡ／ＲＣＰ３０分（Ｂ点）、ＤＨＣＡ／ＲＣＰ６０分（Ｃ点）ＤＨＣＡ／ＲＣＰ９０分（Ｄ眯）和复温再灌注３０分（Ｅ点）取脑皮层ｌｇ，检测丙二醛（ＭＤＡ）和超氧化物歧化酶（ＳＯＤ）水平。结果见两组在Ａ点ＭＤＡ和ＳＯＤ无差别。在Ｂ、Ｃ、Ｄ、Ｅ点，ＤＨＣＡ组ＭＤＡ     

Acute effects of changing plasma osmolality and colloid oncotic pressure on the formation of brain edema after cryogenic injury

The cerebral effects of alterations in plasma osmolality (Osm) and colloid oncotic pressure (COP) were examined in normocarbic, normothermic, pentobarbital-anesthetized rabbits that had been subjected to cryogenic brain injury. Monitored variables in all animals included mean arterial, right atrial, and intracranial pressures (MAP, CVP, and ICP), electroencephalographic (EEG) recordings, and cerebral blood flow (CBF). When surgical preparation was complete, a left parietal lesion was produced with liquid nitrogen. Group 1 (control, n = 8) animals subsequently received only maintenance fluids [lactated Ringer's solution (LR)]. One hour after injury, 3 other groups of animals underwent 45 minutes of plasmapheresis, carried out by arterial phlebotomy (packed red cells returned), with separated plasma being replaced by one of three fluids given in amounts sufficient to maintain MAP and CVP at baseline values. The three fluids were 1) 6% hetastarch in hypo-osmotic LR [Group 2 (Hypo-Osm), n = 6; COP = 21 mm Hg, Osm = 130 mOsm/kg]; 2) iso-osmotic LR [Group 3 (Hypo-COP), n = 8; COP = 0; Osm = 305]; and 3) 6% hetastarch in iso-osmotic LR [Group 4 (Iso-Osm/COP), n = 8; COP = 21, Osm = 310]. The animals were killed by exsanguination 25 minutes after completion of plasmapheresis. The brain was removed, the hemispheres separated, weighed, and sliced, and the specific gravities (SpGr) of the regional tissue determined. There were no differences in MAP, CVP, regional CBF, or EEG activity among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

缺血预适应对缺血脊髓保护作用的实验研究

目的：探讨缺血预适应对缺血脊髓的保护作用及其可能机制。方法：48只成年大耳白兔随机分为两组，每组24只，建立脊髓缺血模型。缺血预适应组（IPC组）采用腹主动脉阻断5min，开放15min的预适应方案后，再阻断40min后开放。对照组常规阻断腹主动脉40min后开放。分别于阻断前、阻断40min后、开放后2、8、24和72h，测定脑脊液超氧化物歧化酶（SOD）、脊髓脂质过氧化物酶（LPO）及脊髓组织含水量，并行双后肢神经功能评分。结果：IPC组各时相脑脊液SOD活性及神经功能评分显著优于对照组（P＜0．05），脊髓LPO含量及组织含水量明显低于对照组（P＜0．05）。结论：缺血预适应通过调动与增强脊髓组织内源性抗损害机制对缺血脊髓发挥保护作用。     

An experimental study of tissue injury associated with reperfusion in ischemic limbs

Twenty adult mongrel dogs were divided into three groups. Group I: control (n = 7), group II: limb ischemia for 6 hours followed by reperfusion (n = 6), and group III: administration of alpha-tocopherol after 6 hours of ischemia, and reperfusion (n = 7). In group II, serum CPK and LPO increased after reperfusion with peak levels of 38,000 +/- 9,800 mU/ml and 20.4 +/- 3.7 nmol/ml respectively, which were significantly higher than those in group I. (CPK: p less than 0.02, LPO less than 0.03). In group III, the peak levels of serum CPK and LPO were regulated to the low level of 1,060 +/- 290 mU/ml and 9.2 +/- 4.5nmol/ml, respectively, which were significantly lower than those in group II. (CPK: p less than 0.02, LPO less than 0.04). Additional 13 dogs were divided into two groups in order to assess tissue LPO in the limb, liver, and kidney. Group A: control (n = 5), group B: reperfusion after 6 hours of ischemia (n = 8). Tissue LPO level of 1.89 +/- 0.74nmol/mg-protein in the gastrocnemius muscle in group B was significantly higher than that in group A (p less than 0.02), although there was no significant difference in the gracilis muscle, liver, and kidney. These results prove indirectly the participation of lipid peroxidative reaction by active oxygen in the mechanism of development of reperfusion injury, and suggest the preventive effect of alpha-tocopherol to reperfusion injury.     

A comparison of the effects of halothane, isoflurane, and pentobarbital anesthesia on intracranial pressure and cerebral edema formation following brain injury in rabbits

To evaluate the impact of anesthetics on the evolution of a cerebral injury, 33 rabbits were subjected to a cryogenic brain lesion, followed by 10 h of anesthesia with 1 MAC halothane or isoflurane (n = 11 each) or with an equipotent dose of pentobarbital (n = 11). The lungs were ventilated to a PaCO2 = 30-35 mmHg with O2/air and normothermia was maintained. Intracranial pressure (ICP), mean arterial pressure (MAP), central venous pressure (CVP), arterial blood gases, and pH, osmolality, and other blood chemistries were recorded. Fifteen minutes after surgery, a left parietal injury was produced with liquid N2. A MAP greater than 70-75 mmHg was maintained throughout the study, using angiotensin II as needed, and CSF was removed if severe intracranial hypertension (ICP greater than 30 mmHg) threatened to reduce cerebral perfusion pressure (CPP = MAP-ICP) below 40 mmHg. 10 h after injury, the animals were killed, and edema formation assessed by: A) the wet weight of the two hemispheres; B) water content (%H2O; wet-dry weight) of the posterior aspect of the hemispheres; and C) specific gravity (SpGr) of tissue samples taken adjacent to and distant from the lesion. Animals given pentobarbital had higher MAP's until 3 h after the lesion had been induced. There were no subsequent intergroup differences in MAP, and no differences at any time in CVP, PaO2, PaCO2, pH, total fluids, or urine output. ICP increased in all animals, but with no significant intergroup differences (ICP in halothane animals was numerically lower). There were no clear differences in the incidence of ventricular drainage (1 halothane, 5 isoflurane, 3 pentobarbital; P = 0.16). In spite of CSF drainage and angiotensin, CPP     

The effects of 30% and 60% xenon inhalation on pial vessel diameter and intracranial pressure in rabbits

Xenon may increase cerebral blood flow and intracranial pressure (ICP). To evaluate the effects of xenon on brain circulation, we measured pial vessel diameter changes, CO(2) reactivity, and ICP during xenon inhalation in rabbits. Minimum alveolar anesthetic concentration (MAC) for xenon was established in rabbits (n = 6). By using a cranial window model, pial vessel diameters were measured at 30% and 60% xenon inhalation and in time control groups (n = 15). ICP, mean arterial blood pressure, and heart rate were recorded during 30% and 60% xenon inhalation (n = 5). Pial vessel diameters were measured during hypocapnia and hypercapnia conditions in 60% Xenon and Control groups (n = 14). MAC for xenon was 85%. Xenon (0.35 and 0.7 MAC) dilated the arterioles (10% and 18%, respectively) and venules (2% and 4%, respectively) (P < 0.05). Dilation of arterioles was more prominent than that of venules. ICP, mean arterial blood pressure, and heart rate did not change during xenon inhalation. No difference in CO(2) reactivity was observed between Xenon and Control groups (P = 0.79). Sixty percent xenon (0.7 MAC) dilated brain vessels, but venule changes were small. Xenon did not increase ICP and preserved CO(2) reactivity of the brain vessels. IMPLICATIONS: Xenon might increase cerebral blood flow; however, 0.7 minimum alveolar anesthetic concentration xenon preserved both low intracranial pressure and CO(2) reactivity of the cerebral vessels in the normal rabbit.     

肝素对顿抑心肌功能影响的实验研究

目的：探讨肝素化剂量肝素对在体家兔短暂缺血－再灌注顿抑心肌的功能的影响。方法：23只雄性家兔，分为实验（A）组和对照（B）组，建立在体心肌短暂缺血（15min）－再灌主（60min）损伤模型。A组于前降支阻断前20min给予肝素（700U／kg）。分别于给药前、缺血前、再灌注期间，检测2组NO、ET－1、MDA、SOD水平，测定血流动力学指标变化，对心肌超微结构做定性观察。结果：A组在给药后20min，NO含量即较给药前明显升高（P＜0．05），且在整个再灌注期较B组有显著性差别（P＜0．05），心功能、超微结构明显改善。结论：肝素参与短暂缺血－再灌注顿抑心肌功能的保护，机制可能是通过药物性预适应，增强内皮源性NO的产生，从而减轻心肌缺血－再灌注损伤。     

The cerebral effects of pancuronium and atracurium in halothane-anesthetized dogs

Pancuronium decreases the minimal alveolar anesthetic concentration (MAC) of halothane in humans, while atracurium has a metabolite, laudanosine, which is a known cerebral stimulant. To determine if these muscle relaxants significantly alter cerebral function, their effects on cerebral metabolic rate (CMRo2), cerebral blood flow (CBF), intracranial pressure (ICP), EEG, and the cerebral energy state were studied in halothane-anesthetized dogs. Group A dogs (n = 6) were maintained at 0.86% end-expired (1.0 MAC) halothane. Thereafter, a sequence of 1) pancuronium 0.1 mg . kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; and 3) pancuronium 0.2 mg . kg-1 produced no changes in CMRo2, CBF, ICP, or EEG. Group B dogs (n = 6) also were maintained at 0.86% end-expired halothane and received the following in sequence: 1) atracurium 0.5 mg . kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; 3) atracurium 1.0 mg . kg-1; and 4) atracurium 2.5 mg . kg-1. There were no changes in CMRo2, CBF, or ICP; EEG evidence of cerebral arousal occurred in only one dog with the final dose of atracurium. Group C dogs (n = 6) received tetracaine spinal anesthesia and the minimal halothane concentration (mean +/- SE = 0.69 +/- 0.03% end-expired) that would maintain an "anesthetic" EEG pattern. Each Group C dog received the following in sequence: 1) atracurium 1.0 mg . kg-1, and 2) atracurium 2.5 mg . kg-1. EEG evidence of cerebral arousal occurred in all six Group C dogs. Arousal was not accompanied by significant increases in CBF, CMRo2, or ICP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Distribution of cerebral flow using retrograde versus antegrade cerebral perfusion.

BACKGROUND: This study compared flow to the brain with retrograde and antegrade cerebral perfusion during circulatory arrest. METHODS: Twenty-four rabbits were injected with 5 mCi of technetium-99 macroaggregated albumin, a tracer trapped in the capillaries. Group I (n = 6) were maintained normothermic, and the tracer was injected into the ascending aorta. Group II (n = 6) were maintained normothermic, and underwent cannulation of the superior vena cava (SVC), exsanguination through the aorta, and injection of the tracer into the SVC, which was proximally occluded. In group III (n = 6), the animal was cooled to 25 degrees C. The animal was exsanguinated through the aorta and tracer was injected into the ascending aorta. In group IV (n = 6), animals were cooled to 25 degrees C. The animal was exsanguinated through the ascending aorta and tracer was injected into the SVC. Three animals (group V) were exsanguinated through the ascending aorta and a retrograde venogram of the SVC was performed. Scintigraphy of groups I to IV was carried out on a digital gamma camera. Brain trapping of tracer was graded from 0 to 5, with 0 being no tracer in the brain and 5 being dominant tracer trapping in the brain. RESULTS: Tracer trapping in the brain showed group I, 3.67+/-0.82; group II, 0; group III, 4.67+/-0.41; group IV, 0.17+/-0.41 (p<0.0001). Retrograde venogram of the SVC showed flow into the cerebral veins. CONCLUSIONS: Retrograde flow through the SVC reaches the cerebral venous system. Flow arriving in retrograde fashion does not go through the capillary system.     

高渗氯化钠羟乙基淀粉注射液输注对急性颅内高压伴失血性休克犬脑组织病理学及氧自由基的影响

目的 观察高渗氯化钠羟乙基淀粉40注射液(HSH)在犬急性颅内高压伴失血性休克模型中恢复循环血容量、减轻脑组织水肿和降低脑组织氧自由基含量的作用.方法 健康杂种犬20只,采用硬膜外球囊注水和动脉放血的方法复制急性颅内高压伴失血性休克模型.动物随机分为羟乙基淀粉溶液组(HES组),乳酸盐林格液组(RL组),7.5%氯化钠溶液组(HS组)和高渗氯化钠羟乙基淀粉40注射液组(HSH组),在休克后1 h分别输入相应液体.监测平均动脉压(MAP)、中心静脉压(CVP)、心率(HR)、颅内压(ICP),检测脑组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力,脑组织标本行病理学检查.结果 复苏后4组液体均能有效地升高MAP(P<0.05),但HES组和RL组的ICP上升明显(P<0.05),复苏后2 h,HS组的MAP开始下降(P<0.05).至复苏后4 h,仅HSH组能维持理想的MAP及较低的ICP,HSH组脑组织氧自由基含量较其他组明显减少(P<0.05).病理学检查显示复苏后4 h,HSH组的脑组织损伤较其他组轻.结论 高渗氯化钠羟乙基淀粉40注射液可有效地复苏失血性休克,降低ICP及氧自由基的生成,减轻脑组织缺血/再灌注的损伤.     

联合应用异博定和还原型谷胱甘肽对兔供肺的保护作用

目的 观察联合应用异博定和还原型谷胱甘肽对兔肺脏保存的影响.方法 健康日本大耳白兔24对,随机分为4组,每组6对.D组用改良型低钾右旋糖酐液(对照组,改良LPD液)行肺灌洗保存,Y组用改良LPD液+异博定(2 mg/kg体重),H组用改良LPD液+还原型谷胱甘肽(3 mmol/L),L组用改良LPD液+异博定(2 mg/kg体重)+还原型谷胱甘肽(3 mmol/L).实验结束时取肺组织测定湿/干比,细胞内钙离子浓度,丙二醛(blDA)含量与超氧化物歧化酶(SOD)活性,并行细胞凋亡测定.结果 L组的肺组织湿/干比、细胞内钙离子浓度、丙二醛(NDA)含量与超氧化物歧化酶(SOD)活性均优于D组(P值均＜0.01),细胞凋亡L组平均灰度值和阳性单位明显好于D组(P＜0.01、P＜0.05).结论 联合应用异博定和还原型谷胱甘肽对于肺缺血再灌注损伤的作用均优于两药单独应用.     

Effects of alfentanil on cerebral haemodynamics in an experimental model of traumatic brain injury

Alfentanil is reported to increase intracranial pressure (ICP) after neurotrauma. A direct cerebral vasodilator effect has been postulated. We studied 17 Sprague-Dawley rats allocated to one of three groups. Animals were anaesthetized and their lungs ventilated, and arterial pressure, ICP and/or regional cerebral blood flow (CBF) measurements were undertaken. Group 1 (n = 6) received a severe closed head injury while group 2 (n = 5) received no injury. ICP and mean arterial pressure (MAP) were measured before, during and after rapid infusion of alfentanil 250, 500 and 750 micrograms kg-1. CBF was measured by hydrogen clearance before rapid infusions and at 30-min intervals after starting a subsequent slow infusion of alfentanil 500 micrograms kg-1 h- 1. Group 3 (n = 6) underwent CBF measurement only, for comparison with those of groups 1 and 2. They received an injury but no alfentanil. ICP or MAP values did not differ significantly between groups 1 and 2. Rapid i.v. doses of alfentanil produced increases in ICP and reductions in MAP. ICP changes were consistent with a drug effect (P < 0.001) but were small. Reductions in MAP were significant (P < 0.05) and preceded changes in ICP. CBF values were similar and unaffected by slow alfentanil infusion in groups 1 and 2, and did not differ significantly between groups 1 and 3. We conclude that alfentanil did not appear to exert a direct effect on the cerebral circulation. Changes in ICP after rapid infusion were secondary to reductions in SAP. Slow infusion did not cause such changes.      

胆碱酯酶抑制剂他克林对兔内毒素性脑损伤的影响

目的 评价胆碱酯酶抑制剂他克林对兔内毒素性脑损伤的影响.方法 健康成年雄性新西兰大白兔21只,体重1.7～2.3 ks,采用随机数字表法,将其随机分为3组(n＝7):假手术组(S组)脑池内注射生理盐水；内毒素组(LPS组)脑池内注射内毒素200 μg/kg;胆碱酯酶抑制剂组(THA组)脑池内注射内毒素200 μg/kg和盐酸他克林150 μg/kg.注射后4h时处死动物,取脑组织,提取细胞核蛋白,采用Western blot法测定NF-κBp65表达,ELISA法测定血浆、脑脊液和脑组织TNF-α水平,采用分光光度法测定脑组织髓过氧化物酶(MPO)活性,称重后计算湿干重比.结果 与S组比较,LPS组和THA组NF-κB p65表达上调,血浆、脑脊液和脑组织TNF-α水平、MPO活性和湿干重比升高(P<0.05)；与LPS组比较,THA组NF-κB p65表达下调,血浆、脑脊液和脑组织TNF-α水平、MPO活性和湿干重比降低(P<0.05).结论 胆碱酯酶抑制剂他克林可通过抑制局部炎性反应减轻兔内毒素性脑损伤.     

Clinical study of intracranial pressure and auditory brain stem response in the cases of diffuse axonal injury]

The course of intracranial pressure (ICP) and the finding of auditory brain stem response (ABR) was discussed in the cases diagnosed as diffuse axonal injury (DAI) established by Gennarelli. ICP was measured in twenty-six cases which were divided into three groups according to the course of ICP: Group (1), in which ICP remained below 20 mmHg (group I, 9 cases). Group (2), in which ICP rose above 20 mmHg but was controlled by therapy (group II, 8 cases). Group (3), in which ICP rose above 20 mmHg and could not be controlled by any therapies (group III, 9 cases). Glasgow outcome scale 3 months after the injury in the cases of group I and II was severe disability (SD) and/or persistent vegetative state (PVS), but all of the cases in group III died. The findings of serial ABR were divided into 3 groups. These were group A (2 cases) which showed normal record, group B (5 cases) which showed elongation of latencies between the first and fifth waves, and group C (5 cases) in which there was no response in ABR. GOS in group A or B was SD and/or PVS, but all of the cases in group C were shown to be dead in GOS. Our studies suggest that the level of ICP in DAI is rather higher than that published in previous reports, and the continuous measurements of ICP and serial records of ABR are useful for evaluating the outcome of DAI.