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盧令一 巴金森氏症等引起之膀胱功能異常之處置指引 2016/7/28 下午 05:58:36 0
原 文 題  目 A guideline for the management of bladder dysfunction in Parkinsons disease and other gait disorders
作  者 Ryuji SakakibaraJalesh Panicker,Enrico Finazzi-Agro,Valerio Iacovelli,Homero Bruschini
出  處 Neurourology and Urodynamics 35(5):551-563
出版日期 Jun.18 2016
評 論 這篇是國際尿控協會(International Continence Society,ICS)的Neurourology Promotion Committee中的Parkinsons Disease Subcomittee針對巴金森氏症(Parkinsons disease,以下簡稱PD)的膀胱功能障礙所做的治療建議,並不針對個別的文章或研究做討論。PD患者由於dopamine D1-GABAergic direct pathway受到破壞,容易有下泌尿道症候群(LUTS)的產生,而膀胱過動症(OAB)則是LUTS中最常見的症狀,尿路動力學檢查也確實發現PD患者容易有detrusor overactivity(DO),且PVR通常也不多,這與multiple system atrophy (MSA)常見有尿滯留的情況相反。臨床上PD患者有detrusor hypocontractility的情形也不少見,但是關於這部分的研究則缺少具有實證的數據及資料可參考。至於夜尿在PD患者也有超過70%的盛行率,但是夜尿的成因非常複雜,很難歸因於就是PD所引起。治療PD的三大類藥物中(levodopa, dopaminergic agonists, monoamine oxidase type B inhibitors),LUTS並不會因為使用levodopa控制PD而得到改善,而dopaminergic 藥物可能使PD患者的LUTS改善,但也可能變得更嚴重,目前只有MAO-B inhibitors中的rasagiline證實對於初期的PD患者可以同時改善其LUTS。因此對於PD同時有LUTS的患者經常需要加上抗膽鹼藥物治療,雖然效果普遍不錯,但是目前卻乏以抗膽鹼藥物治療PD的LUTS的大規模研究。新近上市的Beta-3 adrenergic agonists因為對中樞認知功能的影響非常小,對於PD患者的LUTS治療效果相當值得期待。目前的數據顯示介入性治療deep brain stimulation (DBS)對PD患者的LUTS的治療效果很好,但是接受治療的病患數目都不多。膀胱內肉毒桿菌素注射對於有頑固性尿失禁的PD患者有很好的治療效果。以前有些證據認為PD患者若有BPH,經尿道攝護腺切除手術(TURP)未必能改善患者的排尿障礙,但是現在認為只要排除MSA,則TURP對於同時患有PD和BPH的患者並不是禁忌症。
abstract Parkinsons disease (PD) is a common neurodegenerative disorder, and lower urinary tract (LUT) dysfunction is one of the most common autonomic disorders with an estimated incidence rate of 27–80%. Studies have shown that bladder dysfunction significantly influences quality-of-life (QOL) measures, early institutionalisation, and health economics. We review the pathophysiology of bladder dysfunction in PD, lower urinary tract symptoms (LUTS), objective assessment, and treatment options. In patients with PD, disruption of the dopamine D1-GABAergic direct pathway may lead to LUTS. Overactive bladder (OAB) is the most common LUT symptom in PD patients, and an objective assessment using urodynamics commonly shows detrusor overactivity (DO) in these patients. The post-void residual (PVR) volume is minimal in PD, which differs significantly from multiple system atrophy (MSA) patients who have a more progressive disease that leads to urinary retention. However, subclinical detrusor weakness during voiding may also occur in PD. Regarding bladder management, there are no large, double-blind, prospective studies in this area. It is well recognised that dopaminergic drugs can improve or worsen LUTS in PD patients. Therefore, an add-on therapy with anticholinergics is required. Beta-3 adrenergic agonists are a potential treatment option because there are little to no central cognitive events. Newer interventions, such as deep brain stimulation (DBS), are expected to improve bladder dysfunction in PD. Botulinum toxin injections can be used to treat intractable urinary incontinence in PD. Transurethral resection of the prostate gland (TURP) for comorbid BPH in PD is now recognised to be not contraindicated if MSA is excluded. Collaboration of urologists with neurologists is highly recommended to maximise a patients bladder-associated QOL.
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