夏賀南,韓成甫
(北京市健宮醫(yī)院神經(jīng)內(nèi)科,北京 100054)
帕羅西汀緩解腦卒中后焦慮抑郁的臨床觀察
夏賀南,韓成甫
(北京市健宮醫(yī)院神經(jīng)內(nèi)科,北京 100054)
目的 觀察帕羅西汀治療腦卒中后焦慮抑郁的臨床療效。方法 選取確診為腦卒中后抑郁焦慮患者70例,隨機(jī)平均分成對(duì)照組和研究組。對(duì)照組給予腦血管病常規(guī)治療和心理治療,研究組在對(duì)照組治療的基礎(chǔ)上加服帕羅西汀治療,療程為30 d。兩組患者均在治療前后進(jìn)行漢密爾頓抑郁量表(HAMD)和焦慮量表(HAMA)評(píng)分,并根據(jù)得分減少率判定臨床療效。結(jié)果 (1)對(duì)照組治療后HAMD評(píng)分(8.85±2.16)與治療前(11.98±2.61)相比,差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05),HAMD評(píng)分差值為(3.24±1.78);研究組HAMD評(píng)分(6.29±2.35)與治療前(11.39±2.27)相比,差異有統(tǒng)計(jì)學(xué)意義(P<0.05),HAMD評(píng)分差值為(5.23±1.96)。兩組HAMD差值相比,差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。(2)對(duì)照組治療后HAMA評(píng)分(7.55±1.36)與治療前(9.52±1.64)相比,差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05),HAMA評(píng)分差值為(2.05±1.78);而研究組HAMA評(píng)分(4.29±1.05)與治療前(9.63±1.28)相比,差異有統(tǒng)計(jì)學(xué)意義(P<0.05),HAMA評(píng)分差值為(5.44±1.13)。兩組HAMA差值相比,差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。(3)與對(duì)照組治療總有效率28.6%相比,研究組的總有效率提高到91.4%,差異有顯著統(tǒng)計(jì)學(xué)意義(P<0.01)。結(jié)論 帕羅西汀治療腦卒中后焦慮抑郁臨床療效明顯,值得推廣。
卒中;焦慮;抑郁;帕羅西汀
卒中后抑郁和焦慮是腦卒中后常見(jiàn)的并發(fā)癥之一,也是常見(jiàn)的心理障礙病之一,發(fā)病率為20~60%,其中輕、中度的抑郁占91.8%[1]。主要表現(xiàn)為情緒低落、郁悶或是焦慮,是對(duì)喪失、失望或者失敗所產(chǎn)生的一種正?;虍惓5呢?fù)性情緒反應(yīng),是目前阻礙卒中病人神經(jīng)功能及日常生活能力恢復(fù)的重要因素[2]。卒中后抑郁焦慮不僅可以使神經(jīng)功能缺損恢復(fù)時(shí)間延長(zhǎng)、生活質(zhì)量下降,甚至可以使死亡率增加[3-4]。因此對(duì)卒中后焦慮抑郁早期診斷,干預(yù)非常重要。本研究旨在通過(guò)觀察比較腦血管病常規(guī)藥物對(duì)癥治療并合心理治療和在此基礎(chǔ)上加用帕羅西汀治療對(duì)腦卒中后焦慮抑郁的緩解情況,以探討帕羅西汀治療卒中后焦慮抑郁的臨床療效,現(xiàn)報(bào)道如下。
1.1 一般資料
將2011年10月-2012年9月來(lái)我院就診,按第四屆全國(guó)腦血管病會(huì)議確定的診斷標(biāo)準(zhǔn),經(jīng)過(guò)CT和MRI證實(shí)發(fā)生腦卒中,且采用漢密爾頓抑郁量表(HAMD)對(duì)患者評(píng)分,≥7分的患者70例。在本研究排除急性出血性腦卒中(卒中發(fā)生兩周內(nèi)),有抑郁焦慮病史、老年癡呆、腫瘤、自身免疫性、感染性等其他疾病者。70例患者隨機(jī)平均分為2組,研究組和對(duì)照組。其中研究組35例,其中男22例, 女13例,年齡52~71歲,平均年齡(60.8±7.9)歲;對(duì)照組35例,其中男20例,女15例,年齡49~70歲,平均年齡(58.7±8.5)歲。兩組患者年齡、性別和病程等資料差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05),具有可比性。
1.2 治療方法
對(duì)照組患者給予腦血管病常規(guī)藥物對(duì)癥治療及康復(fù)并合心理治療,研究組除對(duì)照組相同治療外另加用帕羅西汀,口服20 mg/d,持續(xù)治療30 d。
1.3 評(píng)價(jià)方法
采用漢密爾頓抑郁量表(HAMD)和焦慮量表(HAMA)在治療前后對(duì)所有患者評(píng)分。
1.4 療效評(píng)定標(biāo)準(zhǔn)
根據(jù)抑郁量表(HAMD)的得分減少率作為療效評(píng)定標(biāo)準(zhǔn),得分減少率=(治療前得分-治療后得分)/治療前得分×100%。治愈:得分減少率大于75%;顯效:得分減少率51~75%;改善:得分減少率25~50%;無(wú)效:得分減少率小于25%。
1.5 統(tǒng)計(jì)學(xué)分析
采用SPSS 13.3軟件分析。所有數(shù)據(jù)采用“±s”表示,計(jì)量資料比較采用t檢驗(yàn),計(jì)數(shù)資料比較采用卡方檢驗(yàn),以P<0.05為差異有統(tǒng)計(jì)學(xué)意義。
2.1 兩組患者治療前后HAMD評(píng)分比較
對(duì)照組治療后HAMD評(píng)分與治療前相比,差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05);而研究組HAMD評(píng)分與治療前相比,差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。兩組HAMD差值相比,差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。見(jiàn)表1。
表1 兩組患者治療前后HAMD評(píng)分情況比較(±s,n=35)
表1 兩組患者治療前后HAMD評(píng)分情況比較(±s,n=35)
注:與治療前相比,*P<0.05;與對(duì)照組相比,#P<0.05
組別 治療前 治療后 治療前后差值研究組 11.39±2.27 6.29±2.35* 5.23±1.96#對(duì)照組 11.98±2.61 8.85±2.16 3.24±1.78
2.2 兩組患者治療前后HAMA評(píng)分情況比較
對(duì)照組治療后H A M A評(píng)分與治療前相比,差異無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05);而研究組HAMA評(píng)分與治療前相比,差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。兩組HAMA差值相比,差異有統(tǒng)計(jì)學(xué)意義(P<0.05)。見(jiàn)表2。
表2 兩組患者治療前后HAMA評(píng)分情況比較(±s,n=35)
表2 兩組患者治療前后HAMA評(píng)分情況比較(±s,n=35)
注:與治療前相比,*P<0.05;與對(duì)照組相比,#P<0.05
組別 治療前 治療后 治療前后差值研究組 9.63±1.28 4.29±1.05* 5.44±1.13#對(duì)照組 9.52±1.64 7.55±1.36 2.05±1.78
2.3 兩組患者治療后臨床療效情況比較
對(duì)照組總有效率為28.6%,研究組為91.4%,兩組治療的總有效率對(duì)比差異有顯著統(tǒng)計(jì)學(xué)意義(P<0.01)。見(jiàn)表3。
表3 兩組臨床療效情況比較 [例,(%)]
目前卒中后焦慮抑郁的發(fā)病機(jī)制尚不完全清楚。大量的研究表明,卒中后焦慮抑郁的發(fā)生發(fā)展與大腦受損后的神經(jīng)生物學(xué)特性改變有關(guān)[5]。去甲腎上腺素能和5-羥色胺能神經(jīng)元胞體位于腦干,其軸突通過(guò)丘腦及基底節(jié)到達(dá)額葉皮質(zhì),病灶累及以上部位時(shí),可影響區(qū)域內(nèi)的5-羥色胺能和去甲腎上腺素能神經(jīng)通路,導(dǎo)致去甲腎上腺素和 5-羥色胺含量下降而導(dǎo)致抑郁。腦卒中后抑郁患者腦內(nèi)的去甲腎上腺素和5-羥色胺也發(fā)現(xiàn)明顯下降[6-7]。
帕羅西汀是一種選擇性5-羥色胺再攝取抑制劑,對(duì)其他遞質(zhì)無(wú)明顯影響[8]。通過(guò)阻止5-羥色胺的再吸收而提高神經(jīng)突觸間隙內(nèi)5-羥色胺的濃度,從而產(chǎn)生抗抑郁作用[9-10]。腦卒中后焦慮抑郁患者的5-羥色胺含量明顯下降,所以阻止患者5-羥色胺再攝取可以相對(duì)提高突觸間隙內(nèi)的5-羥色胺[11]。
在本臨床研究中我們觀察到,在常規(guī)腦血管藥物治療和心理治療的基礎(chǔ)上,加用帕羅西汀,H A M D評(píng)分差值由對(duì)照組的(3.24±1.78)升高到(5.23±1.96),HAMA評(píng)分差值由對(duì)照組的(2.05±1.78)升高到(5.44±1.13),說(shuō)明加用帕羅西汀后,研究組患者的焦慮和抑郁癥狀比對(duì)照組得到了更明顯的緩解。與對(duì)照組總有效率為28.6%相比,研究組的總有效率提高明顯提高,達(dá)到91.4%(P<0.01)。這些結(jié)果顯示帕羅西汀在緩解腦卒中后焦慮抑郁癥有很好的臨床療效,值得推廣。
[1] Sagen, U,Finset A,Moum T,et al.Early detection of patients at risk for anxiety,depression and apathy after stroke[J].General hospital psychiat ry,2010,32(1):80-85.
[2] 鄧建中,齊進(jìn)興,趙彥玲,等.腦梗死后抑郁焦慮狀態(tài)相關(guān)因素分析[J].中國(guó)實(shí)用神經(jīng)疾病雜志,2010,13(2):26-27.
[3] 洪 莉.早期綜合心理護(hù)理對(duì)腦梗死后抑郁狀態(tài)的改善作用[J].安徽醫(yī)學(xué),2009,30(6):681-683.
[4] 郝吉莉,周蘭蘭.腦卒中后抑郁的研究現(xiàn)狀及治療進(jìn)展[J].安徽醫(yī)藥,2006,10(7):481-483.
[5] Fang J,Cheng Q.Etiological mechanisms of post-stroke depression: a rev iew[J].Neurological Research,2009,31(9):904-909.
[6] 張 勇,孫建中.米氮平聯(lián)合認(rèn)知療法治療腦卒中后抑郁的療效觀察[J].安徽醫(yī)學(xué),2009,30(5):532-534.
[7] 孫建田.氟西汀治療急性首發(fā)腦卒中后抑郁的臨床對(duì)照研究[J].安徽醫(yī)學(xué),2009,30(4):440-442.
[8] Huang Y,Chen W,Li Y,et al.Effects of antidepressant treatment on N-ace tyl aspartate and choline levels in the hippocampus and thalami of poststroke depression patients: a study using (1) H magnetic resonance spec troscopy[J].Psychiatry research,2010,182(1):48.
[9] Paslakis G,Kopf D,Westphal S,et al.Treatment with paroxetine, but not amitriptyline, lowers levels of lipoprotein (a) in patients with major dep ression[J].Journal of Psychopharmacology,2011,25(10):1 344-1 346.
[10] 費(fèi)慧芝,王 涵,胡小婭,等.帕羅西汀抗抑郁作用涉及改善氧化應(yīng)激狀態(tài),HPA軸功能和海馬腦源性神經(jīng)營(yíng)養(yǎng)因子表達(dá)[J].中國(guó)臨床藥理學(xué)與治療學(xué),2012,17(10):1 137-1 142.
[11] Loubinoux I,Kronenberg G,Endres M,et al.Post-stroke depression: me chanisms, translation and therapy[J].Journal of Cellular and Molecular Medicine,2012,16(9):1 961-1 969.
(本文編輯 李新剛)
The study on the clinical ef fi cacy of Paroxetine on treatment in patients with anxiety and depression after stroke
XIA He-nan,HAN Cheng-fu
(Beijing Jiangong Hospital,Beijing 100054,China)
Objective To observe the clinical ef fi cacy of paroxetine on treatment in patients with anxiety and depression after stroke. Methods 70 patients who were diagnosed as anxiety and depression after stroke were taken. They were randomly, equally divided into control group and treatment group. The control group was given conventional therapy for cerebral vascular disease and psychological treatment. The treatment group was given the same treatment. Besides that, paroxetine was taken. The treatment was for 30 days. The patients of two groups were scored according to Hamilton Depression Scale (HAMD) and self-rating anxiety scale (HAMA) at the time of pre-treatment and post-treatment. The clinical ef fi cacy was judged by the score reduction rate. Results (1) The per-treatment HAMD score v.s. post-treatment is (8.85 ± 2.16) v.s. (11.98 ± 2.61) in the control group. There is no signi fi cant difference (P>0.05), HAMD score difference was (3.24 ± 1.78); and the per-treatment HAMD score v.s. post-treatment is (6.29 ± 2.35) v.s. (11.39 ± 2.27) in treatment group, there were signi fi cant differences (P<0.05), HAMD score difference was (5.23 ± 1.96). Compared two groups of HAMD difference, there is a statistically significant difference (P<0.05). (2) The per-treatment HAMA score v.s. post-treatment is (7.55 ± 1.36) v.s. (9.52 ± 1.64) in the control group. There is no signi fi cant difference (P>0.05), HAMA score difference was (2.05 ± 1.78); and the per-treatment HAMA score v.s. post-treatment is (4.29 ± 1.05) V.S. (9.63 ± 1.28) in treatment group, there were signi fi cant differences (P<0.05), HAMA score difference was (5.44 ± 1.13). Compared two groups of HAMA difference, there is a statistically significant difference (P<0.05). (3) The total effective rate of control group was 28.6%, and the total effective rate of treatment group was increased to 91.4%, there were signi fi cant differences (P<0.01). Conclusion Paroxetine had clinical curative effect in the treatment of anxiety and depression after stroke, and it was worthy of promotion.
Stroke; Anxiety; Depression; Paroxetine
R749.1
B
10.3969/j.issn.1674-070X.2014.02.002.002.02
2013-05-08
夏賀南,女,本科,主治醫(yī)師,主要從事內(nèi)科、神經(jīng)內(nèi)科臨床工作。