Efficacy evaluation of gadoteridol for MR angiography of intracranial vascular lesions

A phase III multicenter study was conducted in 89 patients with known intracranial vascular lesions to evaluate an extracellular gadolinium contrast agent, gadoteridol, for intracranial magnetic resonance (MR) angiography. The pre- and postcontrast MR angiograms of 82 patients were evaluated by the unblinded investigators and by two blinded readers (A and B) for visualization of lesions; arterial and venous anatomy; extent, size, and number of lesions; and disease classification. The unblinded readers indicated that lesions were visualized better on postcontrast images in the following categories: venous anatomy, 87 (81%) of 107 lesions; arterial anatomy, 43 lesions (40%); and extent or size of lesions, 38 lesions (36%). In 29 (35%) of 82 patients, the unblinded readers determined that enhanced MR angiography provided more diagnostic information than unenhanced MR angiography. The blinded readers determined that enhanced MR angiography provided more information for visualization of vascular anatomy in more than 60% of cases. The additional information provided with gadoteridol would have changed the diagnosis in nine (8%) of 107 lesions seen by the unblinded readers, 11 (12%) of 90 lesions seen by reader A, and three (3%) of 93 lesions seen by reader B. The results confirm that the use of gadoteridol improves the visualization of intracranial vascular lesions with MR angiography. The authors conclude that development of new postprocessing algorithms will improve the utility of contrast-enhanced MR angiography.     

32例出血性梗塞研究分析

对32例出血性梗塞研究分析，发现常出现于脑栓塞及大面积脑血栓病人。以治疗中病情突然加重或持久症状不改善为特征，动态CT检查对本病的诊断及治疗有重要意义。     

Protective effects of serotonin reuptake inhibitors, citalopram and clomipramine, against hippocampal CA1 neuronal damage following transient ischemia in the gerbil

To clarify the role of serotonin in cerebral ischemia, we examined the effects of selective serotonin reuptake inhibitors, citalopram and clomipramine, on ischemic neuronal damage in the gerbil. Pretreatment with citalopram (40 mg/kg i.p.) and clomipramine (20 mg/kg i.p.) protected against neuronal destruction of hippocampal CA1 pyramidal cells following 5 min of forebrain ischemia. Furthermore, microdialysis assays showed that a striking increase in extracellular excitatory amino acid levels during ischemia was significantly inhibited by pretreatment with citalopram and clomipramine. However, citalopram (40 mg/kg i.p.) did not alter the extracellular amino acid concentrations in normal gerbils. Thus, serotonin reuptake inhibitors have a protective effect against ischemic neuronal damage. Furthermore, the present result suggests that the protective effect is mediated through prevention of the accumulation of extracellular excitatory amino acids during and after ischemia.     

在大鼠大脑皮质发育过程中5—HT受体亚型的改变

５－ＨＴ灌流幼年组及成年组大鼠脑片。幼年组６６．７％额叶后部Ⅳ层神经元的兴奋性突触后电位（ＥＰＳＰ）幅度降低７３．９％，膜电位和膜电阻无变化；此作用为５－ＨＴ１β激动剂ＴＦＭＰＰ模拟，为５－ＨＴ１Ａ／１β拮抗剂ｐｉｎｄｏｌｏｌ阻抑；５－ＨＴ不降低低钙高镁液中谷氨酸钠的去极化反应。提示幼年期５－ＨＴ经突触前膜５－ＨＴ１β受体抑制突触传递。５－ＨＴ灌流使成年组６０．９％神经ＥＰＳＰ降低３６．２％，伴随     

Velocity and flow quantitation in the superior sagittal sinus with ungated and cine (gated) phase-contrast MR imaging

Normal blood flow and velocity in the superior sagittal sinus were measured in 30 patients. A fast two-dimensional ungated phase-contrast (PC) pulse sequence was compared with a peripherally gated cine PC technique for velocity and flow quantitation. The same imaging parameters were used for both methods. Measured values for mean velocity and flow obtained with the two methods were compared by using regression analysis and t testing. For blood flow, the correlation coefficient was 0.976. For velocity measurements, r was 0.950. Mean flow was 285 mL/min ± 19 with the ungated PC method and 281 mL/min ± 19 with the cine PC method. The mean velocities measured with the two methods were 12.94 cm/sec ± 1.1 and 13.59 cm/sec ± 1.1, respectively. There was no significant difference (paired t test) between the methods for mean flow or velocity data. This was true even though flow in the superior sagittal sinus is moderately pulsatile, as shown with the cine PC technique. The ungated PC method provided these data in 13 seconds versus 3.5 minutes for the cine PC method.     

大鼠马桑内酯急性局灶型癫痫大脑运动皮质的形态计量研究

用微量马桑内酯注入Ｗｉｓｔａｒ大鼠左侧前肢运动皮质，造成急性局灶型癫痫。用光镜、电镜和体视学方法研究其运动皮质第Ｖ层结构的改变。结果显示：癫痫大鼠运动皮质灶区、灶旁区的神经细胞数和胶质细胞数均分别比对照大鼠灶区和灶旁区显著减少；灶区神经毡中突触性终末数，显著减少；突触性终末的面积分数明显减少，而树突的面积分数无变化；神经胶质突起的面积分数增加。     

Interocular mismatch in spatial frequency and directionality characteristics of striate cortical neurones

Summary Spatial-frequency dependence of directional tuning and directional bias was compared, for both eyes, in four previously established discrete classes of binocular feline striate cortical neurones. Two classes (respectively direction-selective or bidirectional at optimal spatial frequency) were directionality invariant at all spatial frequencies. In the remaining two classes, both directionbiased at optimal spatial frequency, directional bias either altered or reversed with change in spatial frequency. In all four classes, the directional tuning of a majority of neurones sharpened at high spatial frequency through either eye, although the bandpass characteristics were sometimes dissimilar for the two eyes. All neurones were of the same type through either eye. Amongst the two classes of direction-biased neurones, the strength of bias was commonly different through the two eyes. Where reversal of bias occurred, that reversal took place at different spatial frequencies for each eye. Thus, the direction and orientation preferences of cortical neurones are fixed at optimal spatial frequency, but their envelope of tuning to a gamut of spatial frequencies is not. These differences are potentially related to binocular coding of visual perspective, including dynamic object rotation in visual space.     

脑梗塞患者血清脂蛋白（a）测定及其临床意义

应用酶标法测定58例脑梗塞患者和56例健康对照者血清脂蛋白(a)[LP(a)]含量,并同时测定了其他脂代谢指标,对其中26例脑梗塞患者还测定了血浆纤维蛋白溶解(简称纤溶)指标。结果表明脑梗塞组存在显著的脂代谢和纤溶功能紊乱。LP(a)含量增高,与所测脂代谢、纤溶指标无显著相关,是脑梗塞发病独立的危险因素。     

Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II

Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na⁺)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na⁺] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema. It is possible that excessive administration of electrolyte-free solutions and high doses of insulin may increase the risk of this complication. While there are some data to suggest that brain cell size is disturbed during acute uremia, additional work is necessary to clarify the role of cerebral cell volume regulation during acute and chronic uremia.