Lahti A C, Koffel B, LaPorte D, Tamminga C A
Department of Psychiatry, Maryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore 21228, USA.
Neuropsychopharmacology. 1995 Aug;13(1):9-19. doi: 10.1016/0893-133X(94)00131-I.
We administered ketamine to schizophrenic individuals in a double-blind, placebo-controlled design using a range of subanesthetic doses (0.1, 0.3, and 0.5 mg/kg) to evaluate the nature, dose characteristics, time course, and neuroleptic modulation of N-methyl-D-aspartate (NMDA) antagonist action on mental status in schizophrenia. Ketamine induced a dose-related, short (< 30 minutes) worsening in mental status in the haloperidol-treated condition, reflected by a significant increase in BPRS total score for the 0.3 mg/kg (p = .005) and 0.5 mg/kg (p = .01) challenges. Positive symptoms (hallucinations, delusions, thought disorder), not negative symptoms accounted for these changes. These ketamine-induced psychotic symptoms were strikingly reminiscent of the subject's symptoms during active episodes of their illness. Results from six patients who were retested in the same design after being neuroleptic-free for 4 weeks failed to indicate that haloperidol blocks ketamine-induced psychosis. Several subjects evidenced delayed or prolonged (8-24 hours) psychotomimetic effects such as worsening of psychosis with visual hallucinations. These data suggest that antagonism of NMDA-sensitive glutamatergic transmission in brain exacerbates symptoms of schizophrenia.
我们采用双盲、安慰剂对照设计,对精神分裂症患者给予一系列亚麻醉剂量(0.1、0.3和0.5毫克/千克)的氯胺酮,以评估N-甲基-D-天冬氨酸(NMDA)拮抗剂对精神分裂症患者精神状态作用的性质、剂量特征、时间过程及抗精神病药调节作用。在氟哌啶醇治疗的情况下,氯胺酮导致精神状态出现剂量相关的短期(<30分钟)恶化,0.3毫克/千克(p = 0.005)和0.5毫克/千克(p = 0.01)剂量激发时,简明精神病评定量表(BPRS)总分显著增加,反映了这一情况。导致这些变化的是阳性症状(幻觉、妄想、思维紊乱),而非阴性症状。这些氯胺酮诱发的精神病性症状与患者疾病活动期的症状惊人地相似。6名患者在停用抗精神病药4周后,按照相同设计重新接受测试,结果未能表明氟哌啶醇能阻断氯胺酮诱发的精神病。几名受试者出现了延迟或延长(8 - 24小时)的拟精神病效应,如伴有视幻觉的精神病恶化。这些数据表明,脑内NMDA敏感的谷氨酸能传递拮抗作用会加重精神分裂症症状。