普罗巴诺洛尔有效抑制在扩散轴突损伤的急性阶段发生的发性交感性过活性的攻击:一个案例报告
Satoshi Shinoda1,2, Takafumi Tanei2, Hirotaka Nakanishi3
1Neurosurgery, Ogaki Municipal Hospital, Gifu, JPN.
Cureus
|February 19, 2025
概括
性交感性多动症是严重脑损伤后的一种情况,呈现出模仿或败血症的症状. 普罗普拉诺洛尔有效地治疗了十几岁的青少年患者的这些过活期,允许停用镇静剂.
科学领域:
- 神经科学是一个神经科学.
- 关键护理医学 关键护理医学
- 药理学 药理学是指药理学的学科.
背景情况:
- 松性交感性多动性 (PSH) 是严重创伤性脑损伤 (TBI) 后的一个关键神经疾病.
- PSH的特点是同情神经系统活动的激增,症状可能被误诊为或败血症.
- 准确的诊断和有效的PSH治疗对于TBI患者的治疗结果至关重要.
研究的目的:
- 报告一个青少年患有严重TBI的PSH病例.
- 突出PSH症状带来的诊断挑战.
- 评估普罗普拉诺洛尔在控制PSH方面的疗效.
主要方法:
- 一名16岁的男性患有严重的TBI,接受了标准药物治疗.
- 在停用镇静剂后出现了PSH症状,有阴性败血症和的治疗.
- 在初始疗法显示有限的成功后,治疗被升级为包括propranolol.
主要成果:
- 患者在停用镇静剂后经历了高温,心跳缓慢,出汗和高血压的反复发作.
- 最初使用巴克洛芬和丹特罗林的治疗只提供了轻微的缓解,并且需要镇静剂超过40天.
- 添加醇 (30毫克/天) 完全解决了PSH攻击,使得停用镇静剂成为可能.
结论:
- 作为口服β-阻断剂的普罗普拉诺洛尔是一种有效的治疗 Paroxysmal Sympathetic Hyperactivity 的方法.
- 这一案例强调了在TBI患者中识别PSH的重要性,这些患者呈现自主失调.
- 早期和准确的诊断和有针对性的药理干预,如用普拉诺洛尔,可以改善患者的管理.
相关概念视频
Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers
525
β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in...
525
Adrenergic Agonists: Therapeutic Uses
719
Adrenergic agonists have diverse therapeutic uses across various medical conditions and emergencies.
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and...
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
Allergies and...
719
Drugs Acting on Autonomic Ganglia: Blockers
943
Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:
943
Heart Failure Drugs: β-Blockers
308
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
308
Antihypertensive Drugs: Types of β-Blockers
566
β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and...
566
Depolarizing Blockers: Pharmocokinetics
302
Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
302


