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1.
目的 探讨直立倾斜试验对血管迷走性晕厥的诊断价值及其局限性。方法 对 12 9例不明原因晕厥患者及 5 4名无晕厥病史健康对照者进行直立倾斜试验 ,先进行基础倾斜试验 (倾斜 70°、持续 30 min) ,阴性者再进行两阶段的异丙肾上腺素的激发试验。结果  112 9例晕厥患者中 ,倾斜试验阳性者 88例 (阳性率 6 8.2 % ) ,5 4名对照组中阳性者 6名 (阳性率 11.1% ) ,晕厥组阳性率明显高于对照组 ,差异有显著性 (P<0 .0 0 5 )。本次试验的灵敏度 6 8.2 % ,特异度 88.9%。 2患者年龄越大阳性反应率越低 (P<0 .0 5 ) ,性别对试验的阳性反应率影响不显著 (P=0 .31)。结论 倾斜试验设备简单、易于操作、是血管迷走性晕厥的一项比较安全有效的诊断方法。  相似文献   

2.
我们对8名不明原因晕厥病人及14名对照者经基础直立倾斜试验后,进行舌下含服消心中加直立倾斜试验。S.ISD-HUT在诱发血管迷走性晕厥病人的敏感性为71%,特异性为92%。  相似文献   

3.
目的 探讨小儿晕厥的病因及美托洛尔治疗小儿血管迷走性晕厥(VVS)的疗效,为临床诊治提供依据.方法 采用卧位立位血压、血常规、血糖浓度、血气分析、心电图、超声心动图、头颅CT、脑电图、24h动态心电图以及直立倾斜试验(HUT)等检测指标,以鉴别得病的原因;将VVS患儿随机平均分为治疗组(口服美托洛尔片)及对照组(口服复合维生素B片),观察两组患者临床晕厥发作次数及HUT结果.结果 小儿自主神经介导晕厥发病率最高(64.3%),其中VVS晕厥发病最多(66.7%).治疗组经美托洛尔治疗后有效率为85.7%,HUT阴转率为66.7%;对照组有效率为42.8%,HUT阴转率为44.4%;两组有效率差异有统计学意义(P<0.05).结论 小儿自主神经介导晕厥发病率最高,尤其以VVS晕厥最多见;口服美托洛尔片可有效治疗小儿VVS晕厥.  相似文献   

4.
The disorders of autonomic control associated with orthostatic intolerance are a diverse group of syndromes that can result in syncope and near-syncope. A basic understanding of the pathophysiology of these disorders is essential to diagnosis and proper treatment. It is especially important to recognise the difference between the effect of prolonged upright posture on a failing autonomic nervous system (a hyposensitive or dysautonomic response) and the vasovagal response (which may be a hypersensitive response). Vasovagal syncope is the most common abnormal response to upright posture and occurs in all age groups. The advent of tilt table testing has helped define a population with an objective finding during provocative testing that has enabled researchers to study the mechanism of vasovagal syncope and to evaluate the efficacy of treatments. In most patients, vasovagal syncope occurs infrequently and only under exceptional circumstances and treatment is not needed. Treatment may be indicated in patients with recurrent syncope or with syncope that has been associated with physical injury or potential occupational hazard. Based on study data, patients with vasovagal syncope can now be risk stratified into a high-risk group likely to have recurrent syncope and a low-risk group. Many patients with vasovagal syncope can be effectively treated with education, reassurance and a simple increase in dietary salt and fluid intake. In others, treatment involves removal or avoidance of agents that predispose to hypotension or dehydration. However, when these measures fail to prevent the recurrence of symptoms, pharmacological therapy is usually recommended. Although many pharmacological agents have been proposed and/or demonstrated to be effective based on nonrandomised clinical trials, there is a remarkable absence of data from large prospective clinical trials. Data from randomised placebo-controlled studies support the efficacy of beta-blockers, midodrine, serotonin reuptake inhibitors and ACE inhibitors. There is also considerable clinical experience and a consensus suggesting that fludrocortisone is effective. Encouraging new data suggest that a programme involving tilt training can effectively prevent vasovagal syncope. For patients with recurrent vasovagal syncope that is refractory to these treatments, implantation of a permanent pacemaker with specialised sensing/pacing algorithms appears to be effective. A number of larger clinical trials are underway which should help further define the efficacy of a number of different treatments for vasovagal syncope.  相似文献   

5.
OBJECTIVE: Pharmacological treatment with selective serotonin reuptake inhibitors (SSRIs) is thought to decrease coronary risk in patients with depressive disorder. Selective serotonin reuptake inhibitor intake may (1) attenuate the hypothalamus-pituitary-adrenal (HPA) system, (2) improve disturbances of the autonomous nervous system, and (3) dampen the aggregability of platelets. There is only limited information about the influence of acute treatment with SSRIs on these systems, which is especially important for the initiation of therapy in high-risk cardiac patients. We compared the reaction of these systems to physical stress with single-dose SSRI treatment (100 mg) with that of placebo treatment. METHODS: Using a double-blind, crossover, placebo-controlled design, we assessed HPA system activity via serum cortisol and corticotropin as well as sympathetic nervous system by determining serum norepinephrine and epinephrine levels at baseline and as a response to stress. Analysis of heart rate variability (HRV) provided information on sympathetic/parasympathetic balance. Platelet activity was measured via flow-cytometric determination of platelet surface activation markers along with the serotonin (5-HT) uptake of platelets. RESULTS: We studied 12 healthy young men under placebo and verum conditions. We found higher HPA system activity at baseline and after physical activity under sertraline when compared with placebo, no difference in sympathetic nervous system activity after physical exertion and only slightly heightened baseline epinephrine values after sertraline intake. No difference was seen between sertraline and placebo intake regarding platelet activity and 5-HT uptake, HRV, blood pressure, and HR. CONCLUSIONS: Initiating sertraline treatment increases HPA system activity and epinephrine concentrations. We found no clinically relevant effect of single-dose sertraline treatment on autonomous nervous function, platelet activity, or platelet 5-HT uptake. These findings may not be extrapolated to patients with affective or cardiac disorders or to other SSRIs.  相似文献   

6.
The responses of electrophysiologically identified sympathetic preganglionic neurones (SPGN) and interneurones activated by sympathetic visceral afferents (VA), to iontophoretic application of 5-hydroxytryptamine (serotonin) and serotonin receptor antagonists: methysergide and cinanserin, were tested in the T3 segment of the spinal cord of the cat. Serotonin had a definite and dose-dependent excitatory action on sympathetic preganglionic neurones and neurones activated by visceral afferents. This excitatory response to serotonin was characterized by the rapid development of tachyphylaxis. Methysergide antagonized the effects of serotonin in preganglionic neurones and neurones activated by visceral afferents. Cinanserin was less effective than methysergide. Preliminary data on the effect of inhibitors of serotonin uptake: chloroimipramine and fluoxetine are also reported. These findings support the idea that sympathetic output and the activity of neurones activated by sympathetic visceroafferents is modulated by an excitatory serotoninergic supraspinal input.  相似文献   

7.
Drug-free symptomatic panic patients, drug-treated nonsymptomatic patients and healthy controls were submitted to simulated public speaking. Subjective anxiety, cognitive impairment and discomfort measured by the visual analog mood scale as well as skin conductance level were higher in symptomatic patients than in controls at the beginning of the experimental session, nonsymptomatic patients lying in between. Subjective sedation, spontaneous fluctuations of skin conductance, heart rate and blood pressure were similar in the three groups. Preparation and performance of speech decreased sedation while increasing anxiety, cognitive impairment, level and fluctuations of skin conductance, heart rate and blood pressure. Anxiety, cognitive impairment and conductance level were less increased in symptomatic patients than in controls. Electrodermal activity, but not cardiovascular measures of sympathetic arousal correlated with anticipatory anxiety. Chronic treatment with serotonin uptake inhibitors attenuated the differences between panic patients and controls, supporting the participation of serotonin in panic disorder.  相似文献   

8.
Evidence is reviewed linking clinical effects of ethanol with actions on the sympathetic and parasympathetic nervous systems. The studies reported include a series of investigations by the authors. Acutely, ethanol causes peripheral vasodilation and may also result in changes in heart rate and blood pressure. Ethanol may contribute to acute problems which may present clinically, including micturition syncope, accidental hypothermia and facial flushing. However, increased sympathetic nervous activity plays a role in causing hypertension and other symptoms during ethanol withdrawal in chronic alcoholics. Some chronic alcoholics may have neuropathy involving sympathetic nerves, and this can result in distal sweating loss and occasionally in orthostatic hypotension. Also, hypothalamic lesions associated with Wernicke's encephalopathy may result in hypothermia. Neuropathy involving parasympathetic nerves in not uncommon in alcoholics with other evidence of nervous system damage, but it is generally asymptomatic. Occasionally, vagal neuropathy may cause disorder of gastrointestinal motility, and neuropathy affecting the sacral innervation may be a factor in alcoholic impotence.  相似文献   

9.
Systolic time intervals (STI) are sensitive indices of myocardial function. Passive tilting is a rapidly reversible and non-invasive method for inducing cardiovascular stress. The present work was conducted to study the effect of graded head-up tilt (HUT) on STI. 20 male medical students were subjected to 30 degrees, 60 degrees and 80 degrees HUT on a tilting table. ECG, phonocardiogram and carotid pulse were recorded simultaneously on Grass polygraph. Electromechanical systole (QS2), left ventricular ejection time (LVET), pre-ejection period (PEP), PEP/LEVT ratio, heart rate (HR) and corrected STI were determined immediately after and at 1, 2, 3, 4 and 5 min after each angle tilt. HUT produced a decrease in QS2 which was more pronounced at higher angle tilt. LVET decreased after 60 degrees and 80 degrees HUT. PEP and PEP/LVET ratio decreased after each angle tilt. These changes in STI can be explained on the basis of sympathetic stimulation-induced increase in the inotropic state of the heart.  相似文献   

10.
Massin M 《Paediatric drugs》2003,5(5):327-334
A wide variety of pharmacologic agents are currently used for the prevention of recurrent neurocardiogenic syncope in children and adolescents. Significant advances in the understanding of this syncopal disorder have occurred in the past decade, and the list of medications recommended has changed, reflecting the evolving understanding of the pathophysiology and development of agents with enhanced efficacy and fewer adverse effects. Clinicians have few randomized controlled trials available to guide their decisions about treating neurocardiogenic syncope, and even fewer when it comes to medications targeting the pediatric population. At the present time, beta-adrenergic receptor blockers, fludrocortisone, and also specific serotonin reuptake inhibitors and midodrine, appear to be favored treatment options. Ideally, specific therapy would be tailored to specific pathophysiologic mechanisms. Unfortunately, at present, specific treatments based on those abnormalities have not been identified.  相似文献   

11.
To study mechanisms underlying the cardiovascular effects of centrally administered serotonin, we recorded responses to intracerebroventricular (i.c.v.) injections of serotonin in urethane-anesthetized rats. Dose-related increases in blood pressure accompanied by reductions in heart rate and sympathetic nerve firing were elicited consistently. The diminution in sympathetic nerve activity implies that while sympathetic inhibition could contribute to the bradycardia, sympathetic activation alone cannot account for the pressor response. Pressor and bradycardic responses must have been caused by activation of specific serotonergic receptors in the brain because both responses were inhibited following serotonin blockade produced by i.c.v. injection of methysergide. By contrast, intravenous injection of a vasopressin antagonist inhibited the pressor response selectively, thereby suggesting that peripheral mediation of the pressor (but not the bradycardic) response involves release of endogenous vasopressin. Collectively, our results are compatible with the interpretation that i.c.v.-injected serotonin acts on serotonergic brain receptors to elevate blood pressure by releasing endogenous vasopressin, and slow the heart through sympathetic inhibition.  相似文献   

12.
Chronic constipation is a highly prevalent disorder that is associated with significant direct and indirect costs and has substantial impact on patient quality of life. It is more common among women and non-white populations and is evenly distributed across adult age groups. Constipation is a heterogeneous disorder associated with multiple symptoms and aetiologies. Recent research has increased our understanding of the pathogenesis of this disorder and the central role of the neurotransmitter serotonin in mediating gastrointestinal motility, secretion and sensation. Abnormal serotonin signalling and reuptake appear to play central roles in the symptoms of a subset of patients with chronic constipation. This observation provides a rationale for the use of targeted serotonergic agents for the treatment of chronic constipation. As the role of serotonin in gastrointestinal function is further elucidated and additional candidate drugs are developed, it is likely that serotonergic agents will afford additional treatment options for patients with chronic constipation. This article provides a concise review of the evidence supporting a role for serotonin in the pathogenesis of chronic constipation and a summary of the currently available evidence supporting the use of serotonergic agents for this disorder.  相似文献   

13.
Because of reports of reduced serotonin uptake in depression and the frequent association between panic disorder and depression, this study was designed to assess the neurobiologic relationship between panic disorder and depression. Platelet serotonin uptake studies were done on 47 patients with panic disorder, 17 patients with primary major depression, and 15 healthy volunteers. The authors found that the rate of uptake of serotonin to platelets (Bmax) was significantly lower in both the depressed and panic disorder groups than the healthy control group. The panic disorder patients with a present or past history of major depression had slightly higher values than the panic disorder patients without such a history.  相似文献   

14.
《Substance use & misuse》2013,48(5):413-419
A follow-up review of 45 patients with cough syncope was performed to ascertain the effect of therapy in relieving symptoms. These patients constituted 2.5% of all Mayo Clinic patients evaluated over a 3-year period for syncope. Cough syncope patients were predominantly male (43:2), the average weight was 96.1 kg, and the average age was 53.2 years. Eighty-two percent were current or ex-smokers at the time of the the initial evaluation and 86% of those having pulmonary function tests demonstrated findings consistent with obstructive lung disease. Treatment was determined by their primary physician and, in general, was aimed at decreasing the cough. Cough-related symptoms were abolished or improved in 97% of patients. Smoking cessation was closely asso ciated with decreased symptoms. Although felt by both patient and physician to be a benign disorder, cough syncope can result in severe bodily injury. Patients with a vigorous cough, especially smokers, should be questioned thoroughly about cough syncope. Treatment of cough is effective in relieving symptoms.  相似文献   

15.
Patients with bipolar disorder are often prescribed lithium in combination with a selective serotonin reuptake inhibitor. Doubts still remain, however, about the safety of the combination, particularly with regard to the risk of developing a serotonin syndrome. The authors retrospectively evaluated the safety of the combination of lithium and paroxetine when the two medications were sequentially prescribed in patients with bipolar disorder. The authors examined a sample of 17 patients with bipolar disorder who were treated with lithium during a depressive episode and who required paroxetine as an adjunctive antidepressant to ongoing lithium treatment. Averaging across all subjects, no statistically significant increase was found for any of the somatic symptoms that were assessed before and after paroxetine was added to ongoing lithium therapy. Examining the clinical records of each patient in detail; however, four patients who developed significant adverse events, possibly related to an emerging serotonin syndrome were identified. Clinicians should be aware of the possible development of a serotonin syndrome among patients in whom paroxetine is added to ongoing lithium treatment.  相似文献   

16.
Maternal smoking during pregnancy greatly enhances perinatal morbidity/mortality and is the major risk factor for Sudden Infant Death Syndrome (SIDS). Studies in developing rodents indicate that nicotine is a neuroteratogen that targets monoamine pathways involved in the responses to hypoxia that are in turn, hypothesized to contribute to these adverse events. We administered nicotine to pregnant Rhesus monkeys from gestational day 30 through 160 by continuous infusion, achieving maternal plasma levels comparable to those in smokers; we examined neurochemical parameters immediately after Cesarean delivery at the end of the exposure period. Nicotine evoked elevations in brainstem serotonin levels and serotonin turnover, indicating hyperactivity of these pathways. The same treatment evoked a deficit in cardiac norepinephrine levels. Both effects were offset by coadministration of the antioxidant, Vitamin C. Brainstem serotonin hyperinnervation is a hallmark of SIDS, and the hyperactivity seen here can also account for the downregulation of serotonin receptors noted in this disorder. Deficient cardiac sympathetic innervation is also consistent with increased vulnerability to hypoxia during delivery or in the agonal event in SIDS. Our results thus indicate that nicotine exposure in a primate model produces brainstem and autonomic abnormalities of the key monoamine systems that govern the response to hypoxia, indicate an important role of oxidative stress in the adverse effects, and point to potential amelioration strategies that could offset these particular effects of nicotine.  相似文献   

17.
Several immune system modifications have been reported in pathological anxiety, such as generalized anxiety, panic and obsessive-compulsive disorders. Since serotonin transporter is a marker of peripheral blood lymphocytes and it is modified in major depression, the aim of the present work was to evaluate this transporter by the binding of [3H]paroxetine to membrane preparations of blood peripheral lymphocytes from control subjects and patients with generalized anxiety disorder. The number of transporters and the affinity for the ligand did not differ among the two groups. Serotonin and 5-hydroxyindoleacetic acid (5HIAA) were determined in platelet-rich and -poor plasma, and in lymphocytes. Nonsignificant changes were found in the patients as compared to controls. However, there was a significant positive correlation between serotonin concentration in platelet-poor plasma and in lymphocytes in the patients, but not in the controls. This finding might be an indication of a poor regulation of the transporter function by which serotonin plasma concentration might influence lymphocyte serotonin concentration. Previous results indicate that serotonin transporter is reduced in these cells in major depression disorder; however, in generalized anxiety disorder, the number of transporters was not modified, although the functional efficiency of serotonin transporter might be altered.  相似文献   

18.
Serotonin is implicated in both the biology of depression and anxiety. The aim of this study was to examine the platelet intracellular calcium response to serotonin and thrombin using spectrofluorometry in 14 patients with DSM-4 panic disorder compared to 14 matched controls. Patients did not show significantly higher baseline platelet intracellular calcium levels and serotonin stimulated levels of intracellular calcium than control subjects. There was a much smaller standard deviation in the control subjects than in the panic patients. The intracellular calcium response to thrombin activation was however greater in panic patients than in control subjects (P<0.001). The failure of this study to find enhanced sensitivity of 5-HT2 receptors in panic disorder is compatible with the findings of previous challenge studies that found no consistent dysregulation of serotonin in panic disorder. The enhanced thrombin sensitivity, nevertheless suggests some receptor mediated second messenger changes independent of serotonin in the disorder.  相似文献   

19.
The neurobiological basis of panic disorder has not been clearly established, although a role for serotonin (5-HT) has been postulated. It is clear that drugs which increase 5-HT neurotransmission are effective in treating the condition but how they do so remains a point of debate. The aim of this study was to determine if lowering brain serotonin activity using the technique of tryptophan depletion provoked a short-term relapse of panic symptoms in patients with panic disorder who had responded to drug treatment. Fourteen patients with panic disorder who had responded to treatment with the selective serotonin reuptake inhibitor (SSRI) paroxetine received a tryptophan-free amino acid drink on one occasion and a control drink on the other in a double-blind crossover design. In addition, they received an infusion of flumazenil (used as a pharmacological challenge) and placebo on each day. The tryptophan depleted drink produced an 87% reduction in plasma tryptophan concentration. Flumazenil produced a panic attack (defined by changes in the panic inventory) in seven out of 14 patients when tryptophan depleted and one out of 14 on the control day (p < 0.02). Three patients also experienced temporary depressive symptoms when tryptophan depleted, with no mood changes being seen on the control days. We conclude that rapid lowering of brain serotonin function can allow the precipitation of panic symptoms in response to flumazenil in panic disorder patients who have responded to treatment with an SSRI. This implies that in panic disorder increased 5-HT availability is important in maintaining the response to SSRIs.  相似文献   

20.
余永强  谷欣  刘毅君 《中国医药科学》2014,(13):199-202,207
目的:探讨GCS评分和止血药物使用时间(HUT)对颅脑外伤术后患者下肢深静脉血栓形成的影响。方法选取120例需手术的颅脑外伤患者,按GCS分值分为A组(n=34)、B组(n=38)、C组(n=30)和D组(n=18),按HUT分为E组、F组和G组,每组患者40例。分析GCS评分、HUT与DVT发生率的关系并进行DVT的危险因素分析。结果 C组和D组患者DVT发病率高于A组和B组且F组和G组DVT发病率高于E组(P<0.05),GCS分值与DVT发病率呈负相关(r=-0.832,P<0.01),HUT与DVT发病率呈正相关(r=0.758,P<0.01)。危险因素分析结果显示术前GCS评分、术后HUT和卧床时间是DVT的危险因素。结论术前低GCS评分和长时间卧床及使用止血药物等因素是颅脑外伤患者术后下肢深静脉血栓形成的危险因素。  相似文献   

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