卡马西平联合喹硫平对痴呆患者精神行为症状的疗效

目的观察卡马西平联合喹硫平治疗痴呆患者精神行为症状的临床疗效。方法痴呆患者96例,分为治疗组46例,对照组50例。治疗组给予喹硫平25～300 mg.d-1,平均(160.4±135.2)mg.d-1;卡马西平0.3～0.6 g.d-1,平均(0.49±0.25)g.d-1,在1周内联合用药;对照组给予喹硫平25～400 mg.d-1,平均(260.5±235.4)mg.d-1,均口服,共观察8周。治疗期间禁用其他抗精神病药,锥体外系反应明显时可使用苯海索1～2 mg.d-1;严重失眠者晚间可短期使用苯二氮类药物辅助睡眠。用简易智能状态检查量表(MMSE)、痴呆病理行为评定量表(BEHAVE-AD)和不良反应量表(TESS)于治疗前,治疗第1,2,4,6,8周末评价临床疗效及不良反应。结果治疗组和对照组总有效率分别为84.8%,87.5%。两组疗效在第4周差异有统计学意义,在第8周差异无统计学意义(P>0.05),且两组间治疗4,6周末BEHAVE-AD总分和攻击行为因子分差异有统计学意义(P<0.05),两组间不良反应发生率差异有统计学意义(P<0.01)。结论卡马西平联合喹硫平对痴呆患者精神行为症状疗效确切,可减少喹硫平用量及不良反应,对精神行为控制较快,疗效相对明显。     

喹硫平和利培酮治疗老年期痴呆精神行为障碍对照研究

目的比较喹硫平和利培酮治疗老年期痴呆精神行为症状的疗效和安全性。方法将55例老年期痴呆患者随机分为喹硫平组28例,利培酮组27例,共观察8周。治疗前及治疗后第2,4,8周分别采用阿尔茨海默病病理行为评定量表(BEHAVE-AD)评定疗效,采用不良反应量表(TESS)评定不良反应,采用简易智力状态检查(MMSE)评定认知功能。结果两组临床总有效率分别为82.14%和88.89%,无显著性差异(P>0.05);2组在治疗后2周末起BEHAVE-AD评分有显著下降(P<0.01或P<0.05),治疗结束后组间BEHAVE-AD评分和MMSE评分均无显著性差异(P>0.05);两组锥体外系反应发生率比较有显著性差异,喹硫平组更低(P<0.01)。结论喹硫平治疗老年期痴呆精神行为障碍疗效与利培酮相当,但锥体外系反应较利培酮少,更适用于老年患者。     

喹硫平与利培酮治疗血管性痴呆精神行为症状比较

目的比较喹硫平与利培酮对血管性疾呆(VD)精神行为症状(BPSD)的疗效和安全性。方法将66例VD患者随机分为喹硫平组与利培酮组,治疗8周,治疗前、治疗2、4和8周以简易智力状态检查表(MMSE)评定患者痴呆状况;以痴呆病理行为评定量表(BEHAVE-AD)评定疗效,治疗中出现的症状量表(TESS)评定不良反应。结果喹硫平组有效率88.6%,利培酮组有效率86.7%,喹硫平组不良反应低于利培酮组。结论喹硫平与利培酮均能显著改善VD患者BPSD,喹硫平安全性更高。     

喹硫平与奥氮平治疗老年期痴呆伴行为和精神障碍(BPSD)的疗效及不良反应

目的分析喹硫平与奥氮平治疗老年期痴呆伴行为和精神障碍(BPSD)的疗效及不良反应。方法选取本院2013年9月至2016年4月收治的老年期痴呆伴行为和精神障碍患者75例,随机分组,38例行喹硫平用药治疗,37例采用奥氮平用药,对比两组临床疗效。结果两组治疗后,在BEHAVE-AD、MMSE、ADL评分均明显改善;奥氮平组的口干、体质量增加、锥体外系反应要明显多于喹硫平组,差异明显有统计学意义(P<0.05)。结论喹硫平与奥氮平治疗老年期痴呆伴行为和精神障碍均有确切疗效,结合药物不良反应,喹硫平更具有优势。     

齐拉西酮和喹硫平治疗痴呆患者精神行为症状的疗效观察

目的评估喹硫平和齐拉西酮治疗痴呆患者精神行为症状的临床疗效及安全性。方法在双盲对照试验中,127名伴有精神与行为症状的痴呆的门诊患者被随机地给予接受喹硫平,齐拉西酮治疗;剂量根据需要调整患者跟踪至36周;采用阿尔茨海默病行为病理评定量表(BehaveAD)、Co-hen-Mansfield激惹性问卷(CMAI)评定的临床疗效及治疗前及治疗第6及12周末对血糖、血脂、心电图进行检测及分析而得到。采用TESS量表评定不良反应。结果①两组治疗后BehaveAD和CMAI评分均显著下降(P<0.01),治疗后两组间疗效差异无统计学意义(P>0.05)。②齐拉西酮组治疗前后空腹血糖、总胆固醇及三酰甘油差异均无统计学意义(P>0.05),而喹硫平组治疗后血糖及TG水平明显升高,与治疗前比较差异有统计学意义(P<0.05)。③治疗后两组间心电图异常发生率无显著性差异(P>0.05)。④两组患者治疗后出现不良反应率的比较无显著性差异,使用齐拉西酮的患者不良反应少。结论齐拉西酮和喹硫平治疗痴呆患者的精神行为症状均有效,但是使用齐拉西酮的患者不良反应少,其耐受性好,对患者的血糖、血脂影响较喹硫平小。故新型抗精神病药齐拉西酮是治疗BPSD较为理想的药物。     

喹硫平增效治疗老年抑郁症的疗效及安全性

目的:探讨米氮平合并喹硫平治疗老年抑郁症的疗效及安全性。方法:将40例老年抑郁症患者根据随机分为研究组(米氮平并喹硫平)20例和对照组(单用米氮平)20例,疗程8周。于治疗前及治疗后第2、4、6、8wk末应用汉密尔顿抑郁量表(HAMD),副反应量表(TESS)分别评定疗效和治疗中出现的副反应。结果:治疗后第4、6、8周末,研究组HAMD评分较治疗前均显著降低(P<0.05);治疗后第6、8周末,对照组HAMD评分较治疗前均显著降低(P<0.05);治疗后第4、6、8周末,研究组的HAMD评分均低于对照组(P<0.05)。研究组、对照组的有效率分别为80%、45%,两组之间疗效有显著性差异(P<0.05);两组不良反应比较差异无显著性(P>0.05)。结论:米氮平合并喹硫平治疗老年抑郁症安全有效。     

哌罗匹隆与喹硫平治疗老年痴呆患者精神行为症状的对照研究

目的：探讨哌罗匹隆治疗老年痴呆患者精神行为症状（BPSD）的临床疗效及安全性。方法：将106例老年痴呆患者随机分成哌罗匹隆组和喹硫平组,于治疗前及治疗后12周采用阿尔茨海默病病理行为评分表（BEHAVE-AD）、Cohen-Mansfied激越问卷（CMAI）、简易智力状态检查（MMSE）、日常生活能力评分（ADL）、不良反应量表（TESS）评价疗效及不良反应。结果：治疗12周后哌罗匹隆组有效率为82.0％,喹硫平组有效率为85.7％,两组差异无统计学意义（P〉 0.05）。哌罗匹隆治疗12周后BEHAVE-AD总分及各因子分均下降,其中在幻觉、行为紊乱、攻击行为3个因子的得分明显下降（P〈 0.01）。两组患者治疗12周后的MMSE及ADL评分均较治疗前有所增加,但治疗前后差异无统计学意义。哌罗匹隆的不良反应较喹硫平轻,但差异无显著性。结论：与喹硫平相比,哌罗匹隆治疗老年期痴呆精神行为障碍的疗效与安全性相当,不良反应较少。     

帕利哌酮缓释片与喹硫平治疗精神分裂症的对照研究

目的探讨帕利哌酮缓释片治疗精神分裂症的疗效及安全性。方法将67例精神分裂症患者随机分为帕利哌酮组(34例)和喹硫平组(33例),疗程8周,在治疗前及治疗后2,4,6,8周时采用阳性及阴性症状量表(PANSS)、治疗中出现的症状量表(TESS)评定疗效和不良反应。并于治疗前、中、后检测泌乳素水平。结果治疗结束时,帕利哌酮组显效率62%,有效率88%;喹硫平组显效率64%,有效率85%,两组间的疗效差异无显著性(P>0.05)。两组PANSS总分和各因子分均较治疗前明显下降(P<0.01),帕利哌酮组在第二周末的评分明显低于喹硫平组(P<0.05),余时点组间比较差异无显著性(P>0.05)。不良反应总体发生率两组间差异无显著性(P>0.05)。帕利哌酮组催乳素水平明显升高,喹硫平组则无影响,二组间比较有显著性差异(P<0.01)。结论帕利哌酮缓释片对精神分裂症患者的总体疗效与喹硫平相当,但起效更早,且耐受性更高。     

喹硫平和奥氮平治疗阿尔茨海默病精神行为症状比较

目的 探讨喹硫平和奥氮平治疗阿尔茨海默病(Alzheimer’s disease,AD)患者精神行为症状(behavioral and psychological symptom of dementia,BPSD)的临床疗效和不良反应. 方法 将70例AD患者随机分为喹硫平组和奥氮平组各35例,喹硫平组口服喹硫平,起始剂量25 mg.d^-1,根据临床疗效和不良反应调整剂量,4周内渐增至200～400 mg.d^-1,平均(235.3±98.7) mg.d^-1;奥氮平组口服奥氮平,起始剂量2.5 mg.d^-1,根据临床疗效和不良反应调整剂量,4周内渐增至5～15 mg.d^-1,平均剂量(10.3±4.6) mg.d^-1;两组禁止使用其他抗精神病药物,疗程均为12周. 采用阿尔茨海默病病理行为评定量(behavioral pathology in Alzheimer’ s disase,BEHAVE-AD)和简易智力状态检查(mini-mental state examination,MMSE)评价疗效,采用不良反应症状量表(treatment emergent symptom scale,TESS)评价不良反应. 结果 两组治疗后第12周MMSE评分较治疗前均显著提高(P<0.05),两组之间评分差异无统计学意义,两组BEHAVE-AD总分均明显下降(P<0.01). 喹硫平组总有效率为85.7%,奥氮平组总有效率82.9%,差异无统计学意义. 两组各项不良反应发生率差异无统计学意义(P＞0.05),主要不良反应为嗜睡、头晕和便秘. 结论 喹硫平和奥氮平治疗AD的精神行为症状疗效肯定,不良反应轻,安全性良好.     

艾司西酞普兰联合喹硫平治疗广泛性焦虑障碍的疗效观察

目的 评价艾司西酞普兰联合喹硫平治疗广泛性焦虑障碍(GAD)的疗效、安全性和可行性。方法 采用随机、双盲、平行对照研究。60例患者随机分为艾司西酞普兰喹硫平组(研究组)和艾司西酞普兰(对照组),每组30例,疗程为8周。在治疗前和第1,2,4,6,8周末进行汉密尔顿焦虑量表(HAMA)及临床疗效总评量表的病情严重度(CGI-SI)等评定疗效。用副反应量表(TESS)、心电图(ECG)检查、实验室检查评定安全性。结果 与治疗前比较,2组在第8周末HAMA、CGI-SI评分均显著下降(P<0.05);第1周末,研究组显著下降(P<0.05),对照组下降无统计学差异。组间HAMA比较有统计学意义(P<0.05)。CGI-SI在第1,2,4周末比较有统计学意义(P<0.05)。研究组和对照组治疗有效率分别为86.7％和70％,差异有统计学意义(P<0.05);不良反应发生率分别为20.0％和23.3％,差异无统计学意义。结论 喹硫平联用艾司西酞普兰治疗广泛性焦虑障碍疗效确切、起效快、不良反应轻。     

喹硫平和氟哌啶醇治疗老年痴呆精神行为症状的对照研究

目的：观察喹硫平和氟哌啶醇治疗老年痴呆精神行为症状的疗效和安全性。方法：采用随机对照研究,喹硫平组28例,剂量(130±s 60)mg·d~(-1),25～400mg·d~(-1),氟哌啶醇组23例,剂量(4．8±1．4)mg·d~(-1),2～20mg·d~(-1),疗程12wk,治疗前后采用痴呆病理分析评定量表(BEHAVE-AD)和治疗时出现的症状量表(TESS)评定疗效和不良反应。结果：2组病人治疗后BEHAVE-AD评分显著下降(P＜0．01),2组病人之间治疗前后BEHANE-AD的减分值无显著差异(P＞0．05),氟哌啶醇组44%有锥体外系反应,明显高于喹硫平组的7%,有显著差异(P＜0．05)。结论：喹硫平和氟哌啶醇治疗老年痴呆精神行为症状疗效确切,喹硫平不良反应少。     

多奈哌齐与利司哌酮治疗阿尔采末病痴呆的精神行为症状疗效

目的：比较多奈哌齐与利司哌酮治疗阿尔采末病(AD)的痴呆的精神行为症状(BPSD)的疗效及不良反应。方法：52例AD病人随机分为2组(多奈哌齐组和利司哌酮组各26例),分别予多奈哌齐片5mg·d~(-1)和利司哌酮片1～2mg·d~(-1)治疗,疗程3mo,以AD病理行为评分表(BEHAVE-AD),简易智力状态检查(MMSE)评定疗效,以治疗时出现的症状量表(TESS)评定不良反应。结果：对BPSD的疗效及不良反应2组比较差异无显著意义(P＞0．05)；多奈哌齐组治疗1mo后MMSE评分与治疗前比较,差异即有非常显著意义(P＜0．01)；多奈哌齐对中、重度AD病人的BPSD有效。结论：对有行为紊乱、攻击行为以及情感障碍的中、重度AD病人,可首选多奈哌齐治疗。     

奥氮平与利司哌酮治疗痴呆病人的精神行为症状的比较

目的：比较奥氮平与利司哌酮(又名利培酮)治疗痴呆病人的精神行为症状(BPSD)的疗效和不良反应。方法：67例痴呆病人分为2组。奥氮平组32例[剂量(4．1±s 1．8)mg·d~(-1)；2．5～7．5mg·d~(-1)],利司哌酮组35例[剂量(0．8±0．5)mg·d~(-1),0．25～2mg·d~(-1)],疗程8wk。分别采用痴呆行为量表(BE- HAVE-AD)和副反应量表(TESS)评定疗效和不良反应。结果：奥氮平组和利司哌酮组显效率分别为50%和40%(P＞0．05)；2组BEHAVE-AD评分治疗前后配对比较均有非常显著差异(P＜0．01)。2组不良反应发生率分别为28%和49%(P＞0．05)；奥氮平组的不良反应主要为嗜睡(12%)和体重增加(16%)。结论：低剂量的奥氮平或利司哌酮治疗可以显著改善BPSD,但奥氮平不良反应少。     

Oxcarbazepine: an update of its efficacy in the management of epilepsy

Oxcarbazepine (10,11-dihydro-10-oxo-5H-dibenz[b,f]azepine-5-carboxamide) is a 10-keto analogue of carbamazepine with anticonvulsant activity. In newly diagnosed adult patients, oxcarbazepine monotherapy is as effective as phenytoin and vaiproic acid at reducing generalised tonic-clonic and partial seizure frequency. Furthermore, oxcarbazepine 2400 mg/day as monotherapy has also proved effective in the treatment of refractory partial seizures in adult patients. Oxcarbazepine 600, 1200 and 2400 mg/day as adjunctive therapy significantly reduced seizure frequency compared with placebo in 692 patients with refractory partial seizures. The efficacy of oxcarbazepine monotherapy is similar to that of phenytoin in the treatment of children and adolescents with newly diagnosed partial or generalised tonic-clonic seizures. Additionally, adjunctive therapy with oxcarbazepine was significantly more effective than placebo at reducing seizure frequency in children and adolescents with refractory partial seizures. The most commonly reported adverse events associated with oxcarbazepine monotherapy and/or adjunctive therapy in adults and/or children are somnolence, dizziness, headache, nausea and vomiting. Oxcarbazepine monotherapy is better tolerated than phenytoin (in both adults and children) and valproic acid (in adults), and although 75 to 90% of adult patients in 5 recent monotherapy studies reported adverse events while receiving oxcarbazepine, <8% withdrew from treatment because of them. Acute hyponatraemia, although usually asymptomatic, develops in 2.7% of patients treated with oxcarbazepine. Adverse events most likely to resolve upon switching to oxcarbazepine therapy from treatment with carbamazepine are undetermined skin reactions (rashes, pruritus, eczema), allergic reactions and a combination of malaise, dizziness and headache. Although oxcarbazepine does have a clinically significant interaction with some drugs (e.g. phenytoin and oral contraceptives), it has a lower propensity for interactions than older antiepileptic drugs (AEDs) because its major metabolic pathway is mediated by noninducible enzymes. CONCLUSION: Oxcarbazepine as monotherapy is a viable alternative to established AEDs in the treatment of partial and generalised tonic-clonic seizures in adults and children. Furthermore, it is also effective as adjunctive therapy in the treatment of refractory partial seizures in both age groups. In addition, the drug is tolerated better than the older, established AEDs, and has a lower potential for drug interactions. These attributes make oxcarbazepine an effective component in the initial treatment of newly diagnosed partial and generalised tonic-clonic seizures, and also as an adjunct for medically intractable partial seizures in both adults and children.     

阿立哌唑与奥氮平治疗老年期痴呆精神行为症状的对照研究

目的：观察阿立哌唑和奥氮平治疗老年痴呆精神行为症状的疗效和安全性。方法：68例老年痴呆精神行为症状的患者随机分为两组,分别采用阿立哌唑和奥氮平治疗,疗程12周。治疗前及治疗4、8、12周末,应用痴呆病理行为评定量表（BEHAVE-AD）评定两组疗效,用副反应量表（TESS）评定两组不良反应。结果：两组患者治疗后BEHAVE-AD评分均较治疗前显著下降（P〈0.01）,两组治疗前后BEHAVE-AD减分值差异无统计学意义（P〉0.05）,两组不良反应差异也无统计学意义（P〉0.05）,有效率分别为82.4%和80.6%。结论：阿立哌唑和奥氮平两种新型抗精神病药治疗老年痴呆精神行为症状疗效均确切,起效快、不良反应少。     

利培酮和氟哌啶醇随机双盲治疗痴呆的行为和精神症状

目的 :评价利培酮和氟哌啶醇治疗痴呆的行为和精神症状的疗效和安全性。方法 :采用随机双盲对照研究 ,利培酮组 2 8例 ,剂量 (1.3±s 0 .5 )mg·d- 1,0 .5～ 2mg·d- 1。氟哌啶醇组 2 5例 ,剂量(2 .8± 0 .9)mg·d- 1,1～ 4mg·d- 1,疗程均 8wk。治疗前后进行阿尔采末病病理行为评分表 (BE HAVE AD)、Cohen Mansfield激越问卷 (CMAI)等量表评定及实验室检查。结果 :2组病人治疗后BEHAVE AD和CMAI评分显著下降 (P <0 .0 1) ,2组病人之间治疗后的BEHAVE AD和CMAI减分值无显著差异 (P >0 .0 5 )。 2组病人的不良反应均以锥体外系反应为主 ,利培酮组 2 3% ,氟哌啶醇组4 0 %。结论 :低剂量的利培酮和氟哌啶醇治疗BPSD疗效确切 ,病人耐受性好。     

阿立哌唑治疗阿尔茨海默病行为和精神症状的临床对照研究

目的探讨阿立哌唑治疗阿尔茨海默病(AD)行为和精神症状(BPSD)的疗效和安全性。方法 72例AD伴BPSD患者随机分为阿立哌唑组37例,利培酮组35例,疗程8周,采用Cohen-Mansfield(CMAI)激越问卷和痴呆病理行为量表(BEHAVE-AD)评定疗效,采用副反应量表(TESS)评定副反应。结果阿立哌唑组总有效率86.5%,利培酮组总有效率85.7%,组间比较差异无统计学意义(P>0.05),组内比较差异有显著统计学意义(P<0.01)。两组不良反应比较,阿立哌唑组EPS发生率明显低于利培酮组,差异有统计学意义(P<0.05)。结论阿立哌唑和利培酮治疗AD伴发BPSD均有较好疗效,两者总体疗效、起效时间相当,而阿立哌唑的安全性及不良反应优于利培酮。     

Spotlight on oxcarbazepine in epilepsy

Oxcarbazepine (Trileptal, Timox) is structurally related to carbamazepine and has anticonvulsant activity. Studies suggest that the anticonvulsant activity of oxcarbazepine is mediated via the blocking of neuronal ion channels. In patients aged <18 years, the efficacy of oxcarbazepine monotherapy was similar to that of phenytoin in children with partial onset or generalised tonic-clonic seizures in a 48-week trial. Additional supporting findings demonstrated that 43-71% of patients with partial onset, generalised or undetermined epilepsy were seizure free after oxcarbazepine monotherapy (mean dosage 27.7-50 mg/kg/day; duration 1-5 years). In contrast, one small nonblind trial showed more patients treated with oxcarbazepine monotherapy than with carbamazepine monotherapy had recurrent seizures during 16 months of therapy (although the conclusions that can be drawn from this trial are limited). As adjunctive therapy, oxcarbazepine was significantly better than placebo at reducing seizure frequency in children and adolescents with refractory partial onset seizures with or without secondary generalisation: the median percentage change in partial onset seizure frequency was 35% versus 9%, respectively, during 16 weeks of therapy. In noncomparative trials of adjunctive oxcarbazepine (mean dosage of 34.5-56.7 mg/kg/day), 7-11% of patients with partial onset or generalised seizures were seizure free during treatment, and 20-54% had seizure reductions of > or =50%. Oxcarbazepine was generally well tolerated during monotherapy and adjunctive therapy; 2.5% and 10% of patients withdrew from well controlled trials of oxcarbazepine monotherapy and adjunctive therapy. Oxcarbazepine monotherapy was better tolerated than phenytoin and events observed in oxcarbazepine-treated patients were transient. Oxcarbazepine metabolism is largely unaffected by induction of the cytochrome (CYP) P450 system. However, oxcarbazepine can inhibit CYP2C19 and induce CYP3A4 and CYP3A5, thereby interfering with the metabolism of other drugs (e.g. phenytoin). In addition, oxcarbazepine decreases plasma levels of oral contraceptives and alternative contraceptive methods should be used. In conclusion, oxcarbazepine (as both monotherapy and adjunctive therapy) has shown efficacy in the treatment of partial onset seizures in children with epilepsy. Nevertheless, the generally favorable tolerability profile and relatively low potential for drug interactions of oxcarbazepine make it a valuable option in the treatment of childhood epilepsy.     

Oxcarbazepine: a review of its use in children with epilepsy

Oxcarbazepine (Trileptal, Timox) is structurally related to carbamazepine and has anticonvulsant activity. Studies suggest that the anticonvulsant activity of oxcarbazepine is mediated via the blocking of neuronal ion channels. In patients aged <18 years, the efficacy of oxcarbazepine monotherapy was similar to that of phenytoin in children with partial onset or generalized tonic-clonic seizures in a 48-week trial. Additional supporting findings demonstrated that 43-71% of patients with partial onset, generalized or undetermined epilepsy were seizure free after oxcarbazepine monotherapy (mean dosage 27.7-50 mg/kg/day; duration 1-5 years). In contrast, one small nonblind trial showed more patients treated with oxcarbazepine monotherapy than with carbamazepine monotherapy had recurrent seizures during 16 months of therapy (although the conclusions that can be drawn from this trial are limited). As adjunctive therapy, oxcarbazepine was significantly better than placebo at reducing seizure frequency in children and adolescents with refractory partial onset seizures with or without secondary generalization: the median percentage change in partial onset seizure frequency was 35% vs 9%, respectively, during 16 weeks of therapy. In noncomparative trials of adjunctive oxcarbazepine (mean dosage of 34.5-56.7 mg/kg/day), 7-11% of patients with partial onset or generalized seizures were seizure free during treatment, and 20-54% had seizure reductions of > or=50%. Oxcarbazepine was generally well tolerated during monotherapy and adjunctive therapy; 2.5% and 10% of patients withdrew from well controlled trials of oxcarbazepine monotherapy and adjunctive therapy. Oxcarbazepine monotherapy was better tolerated than phenytoin and events observed in oxcarbazepine-treated patients were transient. Oxcarbazepine metabolism is largely unaffected by induction of the cytochrome (CYP) P450 system. However, oxcarbazepine can inhibit CYP2C19 and induce CYP3A4 and CYP3A5, thereby interfering with the metabolism of other drugs (e.g. phenytoin). In addition, oxcarbazepine decreases plasma levels of oral contraceptives and alternative contraceptive methods should be used. In conclusion, oxcarbazepine (as both monotherapy and adjunctive therapy) has shown efficacy in the treatment of partial onset seizures in children with epilepsy. Nevertheless, the generally favorable tolerability profile and relatively low potential for drug interactions of oxcarbazepine make it a valuable option in the treatment of childhood epilepsy.