内啡肽和单胺类介质在脑缺血时的动态变化

建立大白鼠全脑缺血动物模型，用ＲＩＡ法及荧光分光光度计检测了缺血脑组织匀浆的ＬＥＫ、β－ＥＰ．ＤｙｎＡ１－１３及 ５－ＨＴ和 ５－ＨＩＡＡ的含量，ＬＥＫ在脑组织缺血 ６０ ｍｉｎ时含量略下降，但无统计学意义；β－ＥＰ在脑组织缺血 ３０ ｍｉｎ时显著下降（Ｐ＜０． ０５），缺血 ６０ ｍｉｎ时下降非常显著（Ｐ＜０． ０１）；ＤｙｎＡ１－１３和 ５－ＨＩＡＡ含量在缺血 ６０ ｍｉｎ时明显上升，而 ５－ＨＴ含量则显著下降。上述结果提示内啡肽和单胺类介质均参与了缺血性脑损伤的病理过程。     

急性闭合性颅脑损伤患者血清髓鞘碱性蛋白及其抗体含量的研究

用酶联免疫吸附法（ＥＬＩＳＡ）测定３６例急性闭合性颅脑损伤（ＡＣＨＴ）患者、４０例其它神经系统疾病（ＯＮＤ）患者及３２名正常人的血清髓鞘碱性蛋白（ＭＢＰ）及其抗体（Ａｎｔｉ－ＭＢＰ）含量。结果表明：ＡＣＨＴ组患者血清ＭＢＰ含量显著高于ＯＮＤ组与正常人组（均Ｐ＜０．０１），ＡＣＨＴ患者中脑挫裂伤组和脑内血肿组血清ＭＢＰ含量较脑震荡组明显增高（均Ｐ＜０．０１）；而ＯＮＤ组与正常人组比较则无明显差异（Ｐ＞０．０５）。ＡＣＨＴ组患者血清Ａｎｔｉ－ＭＢＰ含量与ＯＮＤ组比较差别无显著性（Ｐ＞０．０５）。提示血清ＭＢＰ含量对判断颅脑损伤的病情有重要价值。     

精神分裂症患者氯丙嗪治疗前后血小板聚集功能观察

目的 探讨精神分裂症患者血小板聚集功能及氯丙嗪治疗对血小板聚集功能的影响。方法 对３３例首次住院的男性精神分裂症患者氯丙嗪治疗前后进行ＢＰＲＳ评定及肾上腺素致聚下的血小板聚集功能检测，并与５５名正常对照相比较。结果 精神分裂症患者血小板１分钟聚集率（ＰＡＲ１）、５分钟聚集率（ＰＡＲ５）显著高于对照组（Ｐ〈０．０５，Ｐ〈０．０１）；用氯丙嗪治疗１个月后，患者临床症状缓解，ＢＰＲＳ评定分值下降（Ｐ〈０．０１），血小板聚集功能ＰＡＲ１无显著性改变（Ｐ〉０．０５），ＰＡＲ５明显升高（Ｐ〈０．０１）。结论 精神分裂症患者血小板聚集功能增强；氯丙嗪治疗可导致血小板的激活状态。     

高血压伴无症状脑梗死患者动态血压监测分析

目的观察无症状脑梗死（ＡＣＩ）与动态血压的关系。方法对３８例高血压伴ＡＣＩ（ＨＴ－Ａ）组患者及７０例高血压病不伴脑卒中（ＨＴ－Ｂ）组患者分别进行了２４ｈ动态血压监测（ＡＢＰＭ）。结果ＨＴ－Ａ组夜间收缩压和舒张压负荷值明显高于ＨＴ－Ｂ组（Ｐ＜０．０１），日间收缩压和舒张压负荷值及２４ｈ平均收缩压和舒张压两组比较差异亦有显著性（Ｐ均＜０．０５），ＨＴ－Ａ组的血压昼夜节律紊乱检出率（６５．８％）显著高于ＨＴ－Ｂ组（３４．２％）（Ｐ＜０．０１），表明ＡＣＩ与动态血压均值、血压负荷值及血压昼夜节律紊乱密切相关，以夜间血压负荷的持续时间及昼夜节律消失的关系为明显。结论高血压患者预测高血压性脑血管损害方面，动态血压监测有重要意义。     

ABC－ELISA法检测重症肌无力患者三种自身抗体的研究

本文利用ＡＢＣ－ＥＬＩＳＡ法检测了９７例ＭＧ病人血清内三种抗体：ＡｃｈＲａｂ、Ｐｒ－Ｍａｂ、ＣＡＥａｂ。结果发现：（１）全身型ＡｃｈＲａｂ、ｐｒ－Ｍａｂ阳性率明显高于眼肌型（Ｐ＜０．０１）；ＡｃｈＲａｂ与Ｐｒ－ＭａｂＰ／Ｎ值呈线性正相关（ｒ＝０．７９７Ｐ＜０．０１）。（２）合并胸腺异常者ＣＡＥａｂ阳性率为８４．２％，明显高于对照组（Ｐ＜０．０１）；此组病人ＡｃｈＲａｂ与ＣＡＥａｂＰ／Ｎ值呈显著正相关，Ｐｒ－Ｍａｂ与ＣＡＥａｂＰ／Ｎ值呈非常显著正相关。（ｒ＝０．５１２和ｒ＝０．５９８Ｐ＜０．０１）。（３）８例病人作了治疗前后抗体检测。激素治疗后或切除异常胸腺后，抗体滴度多数下降或有转阴趋势。     

脑血管病患者血小板α颗粒膜蛋白－140的临床研究

采用放射免疫方法对４５例脑血管病患者血浆及血小板膜表面的ＧＭＰ－１４０进行测定。发现病人组血浆中ＧＭＰ－１４０均高于正常对照组（Ｐ＜０．０１）。脑梗塞及脑出血急性期组血浆及血小板膜表面的ＧＭＰ－１４０均高于脑动脉硬化症组（Ｐ＜０．０１）。恢复期上述数据逐渐下降，接近脑动脉硬化症组水平。结果提示ＧＭＰ－１４０的检测可作为脑血管病发病、病情监测及疗效观察的一项新指标     

精神发育迟滞患者的单胺类物质代谢研究

用高效液相色谱法测定３３例精神发育迟滞（ＭＲ）患者及１２例对照者脑脊液（ＣＳＦ）和血清中单胺类物质，结果显示：精神发育迟滞患者ＣＳＦ中高香草酸（Ｃ－ＨＶＡ）和５－羟吲哚乙酸（Ｃ－５－ＨＩＡＡ）高于对照组（Ｐ＜０．０５）；先天愚型组Ｃ－ＨＶＡ明显高于其它三组（Ｐ＜０．０１），Ｃ－５－ＨＩＡＡ高于对照组和脆性Ｘ综合征组（Ｐ＜０．０１），而先天愚型组血清中５－羟色胺低于其它三组（Ｐ＜０．０１）；脆性Ｘ综合征组的游离色氨酸高于其它三组（Ｐ＜０．０５）。     

电针对慢性应激抑郁模型大鼠脑单胺类神经递质的影响

目的　探讨电针刺激百会、印堂穴对慢性应激抑郁模型大鼠脑内单胺类神经递质的影响及治疗抑郁症的机理。方法　将２４ 只ＳｐｒａｇｕｅＤａｗｌｅｙ 雄性大鼠随机分为对照组、抑郁模型组、抑郁模型加电针组和抑郁模型加阿米替林组,每组６ 只。用高效液相电化学法测定大鼠脑内单胺类神经递质及其代谢产物的含量,比较含量的比值。结果　抑郁模型组大鼠脑皮层５羟色胺（５ＨＴ）／５羟吲哚乙酸（５ＨＩＡＡ） 、纹状体多巴胺（ＤＡ）／３,４二羟基苯乙酸（ＤＯＰＡＣ） 分别为０－５０ ±０－１７,１０－３７ ±１－４０,低于对照组（ 分别为０－８８±０－２５ ,１２－３６ ±１－５０）,Ｐ＜ ０－０５ ;皮层去甲肾上腺素（ＮＥ）／５ＨＴ（２－８８ ±１－００） 高于对照组（１－７３±０－４０） ,Ｐ＜ ０－０５。电针刺激百会、印堂穴可使模型大鼠脑皮层５ＨＴ／５ＨＩＡＡ 与ＮＥ／５ＨＴ恢复正常（Ｐ＜０－０５） ,对纹状体ＤＡ／ＤＯＰＡＣ 的降低无影响（ Ｐ＞ ０－０５）。结论　提示电针刺激百会、印堂穴通过降低皮层５ＨＴ的代谢,提高５ＨＴ能神经的活性,并协调ＮＥ 与５ＨＴ之间的平衡来发挥抗抑郁作用。     

急性脑卒中患者血小板超微结构的观察

为了探讨急性脑卒中患者血小板超微结构的变化，采用ＤＸＡ４～１０型电子显微镜对５０例急性脑卒中患者血小板中α颗粒数及每平方微米中血小板α颗粒数进行观察。结果：脑卒中组上述指标显著低于对照组（Ｐ＜０．０１）。其中缺血性脑卒中者降低更显著（Ｐ＜０．００１）。梗塞面积大于５ｃｍ的患者α颗粒较小面积损伤者显著减少（Ｐ＜０．０５），而与梗塞部位无关。血液稀释和阿司匹林（ＡＳＡ）治疗后α颗粒数减少显著改善（Ｐ＜０．０５）。另外还发现，血小板α颗粒减少与血钙减少呈正相关（ｒ≥０．３４，Ｐ＜０．０５）。结果提示，血小板超微结构的改变可作为判断脑卒中诊断、治疗及预后的客观指标。     

血可溶性白细胞介素2受体与不同精神疾病的相关性研究

为了解精神疾病与可溶性白细胞介素２受体（ＳＩＬ－２Ｒ）的关系，采用双抗体夹心步骤的酶联免疫吸附测定（ＥＬＩＳＡ）来检测精神分裂症４０例、躁狂症１８例、抑郁症２０例及４９名健康者的血清ＳＩＬ－２Ｒ含量。结果显示，精神分裂症和抑郁症患者血清ＳＩＬ－２Ｒ基础值较健康对照组显著升高（Ｐ＜０．０１），躁狂症组较对照组显著降低（Ｐ＜０．０１），而精神分裂症和抑郁症患者经治疗后血清ＳＩＬ－２Ｒ显著降低（Ｐ＜０．０１），躁狂症则明显增高（Ｐ＜０．０１）。提示精神疾病患者存在有免疫缺陷，血清ＳＩＬ－２Ｒ是可供判断免疫缺陷和精神症状演变的一个参考指标。     

Whole blood serotonin in juvenile obsessive-compulsive disorder

Whole blood serotonin (5-HT) concentration was assessed in 16 children and adolescents with severe obsessive-compulsive disorder (OCD) and in 14 normal adolescent controls. There was no difference in blood 5-HT content between the OCD patients and the normal controls. However, the OCD patients with a family history of OCD had significantly higher blood 5-HT levels than did either the OCD patients without a family history of OCD or the normal controls. Blood 5-HT content was not associated with a history of major depressive disorder or chronic tic disorder. These preliminary results suggest that studies of serotonergic functioning in OCD may need to control for family history of OCD and that blood 5-HT may be a useful biochemical measure in family-genetic studies of OCD.     

No correlation between aggression and platelet (3)H-paroxetine binding in obsessive-compulsive disorder patients

Different findings suggest that the serotonin (5-HT) system may be involved in both the regulation of aggression and the pathophysiology of obsessive-compulsive disorder (OCD). Our study aimed to evaluate the aggressive features of a group of OCD patients and to explore possible correlations with a serotonergic marker, namely platelet 5-HT transporter. Psychopathological and biological patterns were compared with those of a group of healthy controls and those of patients with major depression. Twenty-one patients affected by OCD, 21 by depression and 21 healthy controls were included in the study. Aggressive features were measured by means of the Buss and Durkee Hostility Inventory (BDHI). The platelet 5-HT transporter was evaluated by means of the (3)H-paroxetine binding parameters (maximum binding capacity, B(max) and dissociation constant, K(d)). The OCD patients showed a total score on the BDHI not significantly different from that of healthy controls and lower than that of depressed patients. The factor profile was similar in the 3 groups, but higher in the depressed patients. The irritability, resentment, guilt, negativism and suspiciousness factors were significantly more pronounced in depressed patients. Some sex-related difference in single factors were also observed. The B(max) of (3)H-paroxetine binding was lower in OCD patients than in depressives or healthy controls. OCD patients were more similar to healthy controls than to depressed patients with regard to aggressive features measured by means of the BDHI. This suggests that aggression in OCD is a complex phenomenon that probably requires specific instruments of evaluation.     

Effects of chronic fluoxetine treatment on behavioral and neuroendocrine responses to meta-chlorophenylpiperazine in obsessive-compulsive disorder

To investigate the effect of fluoxetine on serotonergic sensitivity in obsessive-compulsive disorder (OCD), the partial serotonin agonist metachlorophenylpiperazine (mCPP) was compared to placebo under double-blind conditions in six patients with OCD before and during treatment with fluoxetine. Readministration of oral mCPP (0.5 mg/kg) after at least 12 weeks of fluoxetine treatment did not increase obsessive-compulsive (OC) symptoms, in contrast to exacerbation of OC symptoms produced by mCPP before treatment. Chronic fluoxetine treatment resulted in a significant increase in prolactin and cortisol response to mCPP. This may be accounted for, however, by substantially increased plasma mCPP levels during fluoxetine treatment. Chronic fluoxetine treatment diminished the behavioral sensitivity to mCPP and did not diminish, but may have partially normalized, the neuroendocrine response to mCPP in patients with OCD. These adaptive homeostatic effects may reflect fluoxetine's antiobsessional mechanism.     

强迫症患者的防御方式及其家庭因素研究

目的 探讨强迫症患者的防御方式、家庭环境及其父母教养方式的特点。方法 采用防御方式问卷（DSQ）、家庭环境量表（FES—CV）及父母教养方式评价量表（EMBU）对36例强迫症患者（强迫症组）进行了问卷调查，并与36例正常受试者（对照组）加以比较。结果 ①强迫症组不成熟和中间防御机制因子评分均明显高于对照组，而成熟防御机制因子评分则明显低于对照组（P〈0．05或P〈0．01）；②强迫症组家庭亲密度、情感表达及娱乐性评分均明显低于对照组，而矛盾性及控制性评分则明显高于对照组（P〈0．05或P〈0．01）；③强迫症组父母惩罚及过分拒绝因子评分均明显高于对照组（P〈0．05或P〈0．01）；另外患者父亲的情感温暖因子评分极明显低于对照组（P〈0．01），而过度保护因子评分则明显高于对照组（P〈0．05）。结论 强迫症患者的防御方式、家庭环境及父母教养方式与正常人相比有其特点，可以针对其特点进行相应的心理干预。     

强迫症与抑郁症的脑单光子发射计算机断层扫描对照研究

目的探讨强迫症、抑郁症局部脑血流量(rCBF)特点。方法应用单光子发射计算机断层扫描(SPECT)技术,对首发且未经治疗的39例强迫症患者、36例抑郁症患者和39名正常人于静息状态下行脑血流显像。以小脑皮质的放射性计数值为参考,对局部脑血流进行半定量分析。结果强迫症组两侧前额叶、前颞叶rCBF高于正常组(P<0.01);抑郁症组两侧前额叶、枕叶、扣带回及右前颞叶、右顶叶rCBF低于正常组(P<0.05);在两侧前额叶、前颞叶、顶叶、枕叶及右后额叶、扣带回,强迫症组rCBF高于抑郁症组(P<0.05)。结论强迫症组的前额叶及前颞叶呈高灌注改变,抑郁症组脑血流普遍低灌注,SPECT技术可望作为二者鉴别诊断的客观依据之一。     

Lack of effects on core obsessive-compulsive symptoms of tryptophan depletion during symptom provocation in remitted obsessive-compulsive disorder patients.

BACKGROUND: Pharmacological evidence support that enhancement of serotonin (5-HT) neurotransmission is critical for treatment efficacy in obsessive-compulsive disorder (OCD). Surprisingly, acute tryptophan depletion (ATD), a procedure known to reduce 5-HT neurotransmission, carried out in remitted OCD patients on selective serotonin reuptake inhibitors (SSRIs) failed to worsen obsessive-compulsive (OC) symptoms. We hypothesized that the putative symptom exacerbation resulting from ATD would only be observed during symptom provocation but not at rest. METHODS: Double-blind placebo-controlled ATD study conducted in 16 OCD patients with stable improvement under either SSRI (n = 8) or specialized cognitive behavior therapy alone (n = 8), coupled with gradual symptom provocation, performed 5 hours after drink ingestion. RESULTS: Acute tryptophan depletion markedly reduced total and free plasma tryptophan levels but did not significantly increase obsessions or compulsions at rest or following symptom provocation. However, subjective distress in response to triggering situations was significantly higher during ATD; significant mood lowering was also present during ATD. CONCLUSIONS: These results are consistent with the view that relapses in OC core symptoms in remitted OCD patients may not depend solely on short-term changes in presynaptic 5-HT availability. In contrast to its apparent lack of effect on core OC symptoms, ATD affected the patient's mood and distress level resulting from provocation.     

Pilot trial of ondansetron in the treatment of 8 patients with obsessive-compulsive disorder

BACKGROUND: Serotonin (5-HT) neuronal systems have been implicated in the modulation of obsessive-compulsive disorder (OCD) symptoms. 5-HT3 receptor antagonists have been found to act as anxiolytics in selected animal models of anxiety; in particular, those involving an element of risk assessment. Since the compulsions of OCD are frequently triggered by an abnormal perception of risk, a pilot study was initiated to determine whether the 5-HT3 receptor antagonist ondansetron might have efficacy in the treatment of OCD. METHOD: Eight medication-free subjects with a DSM-IV diagnosis of OCD and a Yale-Brown Obsessive Compulsive Scale (YBOCS) score > or = 16 entered an 8-week open-label trial of ondansetron at a fixed dose of 1 mg 3 times daily in a study conducted between February and October 1998. RESULTS: Six subjects completed the trial. Three subjects (37%) achieved a clinically significant response (> or = 35% reduction in YBOCS score). For these subjects, the average reduction in YBOCS-rated symptoms was 55%. In aggregate, the 8 patients exhibited a 28% reduction in YBOCS-rated symptoms over the course of the trial. The medication was well tolerated. CONCLUSION: These results suggest that low-dose ondansetron may have promise as a monotherapy for some patients suffering from OCD.     

强迫症与精神分裂症错误相关负电位的比较研究

目的 比较强迫症和精神分裂症患者的错误相关负电位(error-related negativity,ERN).方法 检测21例强迫症患者和19例首发精神分裂症患者的ERN和正确相关负电位(correct-related negativity,CRN),并与23名正常对照进行比较.结果与正常对照组相比,强迫症组ERN波幅增高(Z=-2.60,P＜0.01),精神分裂症组ERN波幅降低(Z=-2.16,P＜0.05)而潜伏期延长(t=3.60,P＜0.01).与强迫症组相比,精神分裂症组的ERN波幅降低(Z=-3.75,P＜0.01)而ERN潜伏期延长(t=2.70,P＜0.05).CRN波幅和潜伏期在三组间差异无统计学意义(P>0.05).无论是强迫症组,还是精神分裂症组,其ERN/CRN指标与临床精神症状之间均未见相关(P>0.05).结论 强迫症和精神分裂症的ERN均存在异常但方向相反,提示ERN可能作为二者鉴别诊断的参考.     

Platelet imipramine binding and serotonin uptake in obsessive-compulsive patients

Platelet imipramine binding was measured in 16 drug-free nondepressed patients (aged 20-61 years, mean ± SD 35 ± 8) suffering from obsessive-compulsive disorder (OCD) and in 16 sex-, race- and age-matched healthy controls. Imipramine binding capacity and affinity were not different in the 2 groups. Platelet serotonin (5-HT) uptake capacity, V_max, was also measured in 15 of these patients and their matched controls. V_max was significantly higher in the patients (309 ± 149 pmol/10⁹ cells/min) than in the controls (181 ± 110). An increase in platelet 5-HT uptake supports the involvement of 5-HT in OCD and may suggest that a hyperactive serotonergic system is present in this disorder.     

Controlled comparisons of clomipramine and fluoxetine in the treatment of obsessive-compulsive disorder. Behavioral and biological results

Treatment with fluoxetine hydrochloride was compared with treatment with clomipramine hydrochloride in two groups of patients with obsessive-compulsive disorder using two different experimental designs. In the first group of 11 patients with obsessive-compulsive disorder studied using a randomized, double-blind, crossover design, treatment with fluoxetine for 10 weeks was found to produce therapeutic effects similar to treatment with clomipramine for 10 weeks. There were significantly fewer total side effects reported during fluoxetine than clomipramine treatment. Drug tapering and placebo substitution in the 4-week crossover interval phase led to substantial relapses in obsessive-compulsive disorder symptoms and depression. Furthermore, responses to the second drug took as long to occur as responses to the first drug, although both drugs are thought to act by a common mechanism, serotonin uptake inhibition. A second group of 21 patients with obsessive-compulsive disorder that had been previously stabilized on clomipramine treatment with at least partial benefit were crossed over to fluoxetine treatment in a double-blind fashion. After 10 weeks of fluoxetine administration, most patients manifested behavioral rating scores of obsessive-compulsive disorder and depressive symptoms that were comparable with precrossover ratings completed during clomipramine treatment. A significant exacerbation in obsessive-compulsive disorder and depression ratings as well as a similar lag in therapeutic efficacy were also noted in this second cohort of patients with obsessive-compulsive disorder. Platelet 5-HT concentrations were reduced 95% during both clomipramine and fluoxetine treatment periods. These results suggest that fluoxetine may represent a viable alternative to clomipramine in the treatment of obsessive-compulsive disorder, although further studies with larger sample sizes are needed.