Athens University Medical School, Department of Psychiatry, Eginition Hospital, Athens, Greece.
World J Biol Psychiatry. 2009;10(4 Pt 3):953-5. doi: 10.1080/15622970701739526.
Despite the recent progress in the pharmacological treatment of obsessive-compulsive disorder (OCD)--especially with high doses of serotonin reuptake inhibitors, alone or in combination with low doses of antipsychotics--a non-negligible proportion of patients remains refractory to it. For these patients augmentation tactics with drugs from other chemical classes, including antiepileptic drugs, seems advisable. We report on the case of a female inpatient with OCD, whereby the adjunction of tiagabine, a selective GABA reuptake inhibitor at 15 mg/day, to a fluvoxamine (400 mg/day)-risperidone (1 mg/day) combination led to the patient's marked improvement as reflected in the reduction by almost 47% of her score on the Yale-Brown Obsessive Compulsive Scale. With respect to tiagabine's specifically anti-OCD mechanism of action, we note that enhanced inhibitory GABAergic neurotransmission slows down excitatory glutamatergic transmission in the cortico-striato-thalamic system, which presumably constitutes the core pathophysiological mechanism of OCD symptoms.
尽管在强迫症(OCD)的药物治疗方面最近取得了进展——尤其是高剂量的选择性 5-羟色胺再摄取抑制剂(SSRIs)单独或与低剂量的抗精神病药物联合使用——但仍有相当一部分患者对此无反应。对于这些患者,使用其他化学类别的药物进行增效治疗,包括抗癫痫药物,似乎是明智的。我们报告了一例强迫症住院女患者的病例,加用每日 15 毫克的选择性 GABA 再摄取抑制剂噻加宾(tiagabine),联合氟伏沙明(400 毫克/天)和利培酮(1 毫克/天)治疗,使患者的病情明显改善,耶鲁-布朗强迫症量表评分降低近 47%。关于噻加宾治疗强迫症的具体作用机制,我们注意到增强抑制性 GABA 能神经传递会减缓皮质-纹状体-丘脑系统中的兴奋性谷氨酸能传递,这可能构成强迫症症状的核心病理生理机制。