小儿轻度闭合性颅脑损伤的脑电图检查

①目的　观察小儿轻度闭合性颅脑损伤病人的脑波改变。②方法　应用脑电图对１３３ 例轻度闭合性颅脑损伤病儿进行检查,并与１５５ 例成人轻度闭合性颅脑损伤脑电图结果进行比较。③结果　小儿脑电图异常率为６４．７％ ,明显高于成人１９．４％ ,差异有极显著意义（χ２＝ ６１．０８,Ｐ＜ ０．００５）;小儿组有意识障碍者脑电图异常率为９４．３％ ,高于无意识障碍者（５４．１％ ）,差异有显著意义（χ２ ＝ １８．２４,Ｐ＜ ０．０１）; 脑电图异常率随病程的延长而下降（χ２ ＝ １５．１４,Ｐ＜ ０．０１）。④结论　脑电图检查可以反映小儿轻度闭合性颅脑损伤的程度及病情变化。     

A New Approach to an Old Problem

A patient with progressive visual loss was found to have an optic nerve sheath meningioma. The patient was treated with stereotactic radiotherapy, a computer-guided stereotactic technique that minimizes the risk of radiation-induced optic neuropathy. Six months after treatment, the patient was doing well and showed no signs of radiation-induced optic neuropathy.     

Changes in optic nerve head blood flow and retrobular hemodynamics following calcium-channel blocker treatment of normal-tension glaucoma

Background: Because calcium channel blockers reduce vascularresistance, they may have a clinical application in the treatment ofnormal-tension glaucoma (NTG). This study investigates changes inboth the optic disc blood flow and the hemodynamics of retrobulbarvessels in NTG patients after the systemic administration of a calcium channel blocker. Methods: Twelve eyes of 12 NTG patients (meanage 57 6 ± 15.3 years) were examined before and after a 4-weektreatment with 2 mg b.i.d. oral nilvadipine, an L-typc calcium channel blocker. By scanning laser-Doppler flowmetry (SLDF), we obtained the velocity, flow, and volume from within a 10 × 10 pixel windowplaced on the temporal rim region of the optic disc perfusion map. Byultrasound color Doppler imaging (CDI), we measured the peak systolicvelocity (PSV) and the end diastolic velocity (EDV) of the ophthalmicartery (OA), central retinal artery (CRA), nasal posterior ciliary artery (NPCA), and temporal posterior ciliary artery (TPCA). We then calculated a resistance index (RI) for each vessel. Results: After treatment, the flow and velocity of the optic disc blood flow significantly increased (P < 0.05).Nilvadipine also significantly reduced RIs of the CRA, NPCA, and TPCA(P <0 .05), and increased both the PSV of the NPCA and the EDVs of the CRA, NPCA, and TPCA. The percent change in velocity correlated significantly with the percent changes of the CRA RI and NPCA RI. Conclusions: Oral nilvadipine appears to reduce orbital vascular resistance, which consequentlyincreases the optic disc blood flow. Abbreviations.BP – blood pressure;CRA – central retinal artery;CDI – ultrasound color Doppler imaging;EDV – end diastolic velocity;NPCA – short posterior ciliary arteries located nasal to optic nerve;NTG – normal-tension glaucoma;OA – ophthalmic artery;PP – perfusion pressure;PSV – peak systolic velocity;RI – resistance index;SLDF scanning laser-Doppler flowmetry;TPCA – short posterior ciliary arteries locatedtemporal to optic nerve.     

应用视神经纤维分析仪检测正常人视网膜神经纤维层厚度

目的 探讨正常人的视网膜神经纤维层厚度及其象限比值与年龄的关系。方法 应用视神经每人义检测１９８例（１９８只眼）正常志愿者,并按年龄分组进行统计分析。结果 ＲＮＦＬＴ与年龄成负相关,上、下方象限厚度较鼻、颞侧大,与年龄相关、鼻、颞侧无此特点。上、下方象限厚度比值平均为１．０４１。结论 ＮＦＡ是测量ＲＮＦＬＴ的可靠方法,正常人的ＲＮＦＬＴ随年龄的增长而减少。     

应用彩色多普勒血流显像检测眼前部缺血性视神经病变

应用彩色多普勒血流显像检测眼前部缺血性视神经病变,以探讨其血流动力学变化特征。     

正常眼共焦扫描激光多普勒视网膜血流图

目的　探讨共焦扫描激光多普勒视网膜血流图的临床应用价值。方法　应用Ｈｅｉｄｅｌｂｅｒｇ共焦扫描激光多普勒视网膜血流图仪对４８ 例（８２ 只正常眼）视乳头及视网膜血流灌注进行检测。结果　视乳头大血管血流量为２０３１４ ±７４７７,血流速为６ ２７２４３ ±２ ２６００７ ,红细胞移动速率为１３１４ ±２５８ ;视乳头筛板处的血流量为２６３６ ±１４７４ ,血流速为４６７９９ ±２７０１５ ,红细胞移动速率为１９３ ±１０７ 。颞侧视乳头盘沿的血流量为２２９０ ±１１３２,血流速为５１４５３ ±３７０２１,红细胞移动速率为１６９±１１２ ;鼻侧视乳头盘沿的血流量为２１７７ ±９８３,血流速为４９３２１ ±２９０２９,红细胞移动速率为１６５±０９０;颞侧与鼻侧比较差异无显著性（ｔ 值分别为０６８２ ５ ,０４１０ ４,０２５０ １,Ｐ＞ ００５） 。颞侧视乳头旁视网膜的血流量为３２５５ ±１３００,血流速为５５８６３ ±２９３４５ ,红细胞移动速率为１７８ ±０８３;鼻侧视乳头旁视网膜的血流量为２０６１ ±８９２ ,血流速为３５８６４ ±２１２６６ ,红细胞移动速率为１２     

大鼠实验性视网膜光损伤中的视细胞凋亡

目的 进一步探讨视网膜光损伤的发病机制。 方法 20只Wistar大鼠分为实验组、对照组,分别在光照后12,24,36小时摘除眼球,视网膜组织行HE染色和核苷酸末端转移酶介导的DUTP缺口翻译法(TdT-mediated dUTP nick end labelling method,TUNEL)标记凋亡细胞。 结果 光照后12小时,视杆细胞外节出现少量空泡变性;24小时后,外核层出现明显的细胞核破碎、浓染和DNA裂解;36小时后,视杆细胞内、外节溶解,外核层大量细胞核丢失。 结论 视细胞凋亡是大鼠实验性视网膜光损伤的重要机制之一。 (中华眼底病杂志, 1999, 15: 167-169)     

Statins and peripheral neuropathy

Within the past 3 years seven cases of reversible peripheral neuropathy apparently caused by statins have been reported. Here we report seven additional cases associated with long-term statin therapy, in which other causes of neuropathy were thoroughly excluded. The neuropathy was in all cases axonal and with affection of both thick and thin nerve fibers. The symptoms of neuropathy persisted during an observation period lasting from 10 weeks to 1 year in four cases after statin treatment had been withdrawn. We suggest that long-term statin treatment may be associated with chronic peripheral neuropathy. Received: 6 July 1998 / Accepted in revised form: 1 October 1998     

Interactions between essential fatty acid,prostanoid, polyol pathway and nitric oxide mechanisms in the neurovascular deficit of diabetic rats

Summary Impaired -6 essential fatty acid metabolism and exaggerated polyol pathway flux contribute to the neurovascular abnormalities in streptozotocin-diabetic rats. The potential interactions between these mechanisms were examined by comparing the effects of threshold doses of aldose reductase inhibitors and evening primrose oil, alone and in combination, on neurovascular deficits. In addition, highdose aldose reductase inhibitor and evening primrose oil treatment effects were challenged by co-treatment with the cyclo-oxygenase inhibitor, flurbiprofen, or the nitric oxide synthase inhibitor, N^G-nitro-l-arginine. Eight weeks of diabetes caused an 18.9% reduction in sciatic motor conduction velocity (p<0.001). This was only modestly ameliorated by a 0.1% dietary supplement of evening primrose oil or the aldose reductase inhibitors ZD5522 (0.25 mg · kg^–1 · day^–1) and WAY121509 (0.2 mg · kg^–1· day^–1) for the final 2 weeks. However, joint treatment with primrose oil and ZD5522 or WAY121509 caused marked 71.5 and 82.4% corrections, respectively, of the conduction deficit. Sciatic nutritive blood flow was 43.1% reduced by diabetes (p<0.001) and this was corrected by 67.8% with joint ZD5522 and primrose oil treatment (p<0.001). High-dose WAY121509 (10 mg · kg^–1 · day^–1) and primrose oil (10% dietary supplement) prevented sciatic conduction velocity and nutritive blood flow deficits in 1-month diabetic rats (p<0.001). However, these effects were abolished by flurbiprofen (5 mg · kg^–1 · day^–1) and N^G-nitro-l-arginine (10 mg · kg^–1 · day^–1) co-treatment (p<0.001). Thus, the data provide evidence for synergistic interactions between polyol pathway/nitric oxide and essential fatty acid/cyclo-oxygenase systems in the control of neurovascular function in diabetic rats, from which a potential therapeutic advantage could be derived.Abbreviations ARI Aldose reductase inhibitor - EPO evening primrose oil - NCV nerve conduction velocity - NO nitric oxide - NOLA N^G-nitro-l-arginine     

The effect of trimethyltin on acetylcholine release in the guinea-pig trachea

The purpose of the present work was to characterise the effects of trimethyltin on the release of acetylcholine from parasympathetic nerves and its effect on the postjunctional cholinergic stimulation of a smooth muscle. The guinea-pig trachea has been used as a model. Prejunctionally, trimethyltin (3.0 × 10⁻³ M) significantly enhanced in a reversible manner the high K⁺ (75 mM) evoked release of endogenous acetylcholine and [³H]acetylcholine. The evoked release of endogenous acetylcholine and [³H]acetylcholine was released from a pool of acetylcholine being independent of extraneuronal Ca²⁺ in the presence, but not in the absence of trimethyltin. The effect of trimethyltin on the release was not inhibited by low Ca²⁺ (0 mM and 1.0 × 10⁻⁴ M) or by Ca²⁺ channel blockers (verapamil, 1.0 × 10⁻⁴ M, flunarizine, 1.0 × 10⁻⁴ M, ω-conotoxin GVIA, 2.0 × 10⁻⁷ M and ω-agatoxin, 2.0 × 10⁻⁷ M). The present results also demonstrate that trimethyltin induce emptying of a non-vesicular, probably a cytoplasmic storage pool of acetylcholine, since AH5183 (2.0 × 10⁻⁵ M), an inhibitor of the translocation of acetylcholine into synaptic vesicles, and -latrotoxin (1.0 × 10⁻⁸ M), a toxin from black widow spider venom inducing vesicle depletion, had no inhibitory effects on the release of [³H]acetylcholine evoked by trimethyltin (3.0 × 10⁻³ M). The release of [³H]acetylcholine was moreover enhanced by trimethyltin when the vesicular uptake of [³H]acetylcholine was inhibited by AH5183, probably as a result of a higher cytoplasmic concentration of [³H]acetylcholine. Trimethyltin also reduced the neuronal uptake of [³H]choline and this was probably due to a depolarising effect of trimethyltin on the cholinergic nerve terminals. A similar depolarisation induced by trimethyltin was observed during patch clamping of GH₄ C₁ neuronal cells. Postjunctionally, trimethyltin had no effect by itself or on the carbachol-induced smooth muscle contraction, indicating that trimethyltin did not have a general depolarising effect on smooth muscle cells or an effect on muscarinic receptors. Furthermore, the reduced electrical field-induced contraction and the subsequent increase in the basal smooth muscle tension that was observed by addition of trimethyltin was activity-dependent, and was most probably due to emptying of a nervous non-vesicular storage pool of acetylcholine, followed by rapid hydrolysis of acetylcholine by acetyl- and pseudocholinesterases.