IN VIVO 31-P NMR STUDIES IN SCHIZOPHRENICS

由动物研究支持的临床研究表明， 前额叶皮层在精神分裂症认知缺陷中的作用 迄今为止的生理学研究表明， 脑血流量（氙133）和2-脱氧葡萄糖摄取（正电子 发射断层扫描，PET）在一些精神分裂症患者。 相比之下 自闭症的PET研究报告了自闭症患者2-脱氧葡萄糖的摄取增加， 成年自闭症患者的额叶 31 P NMR光谱学提供了 高能磷酸盐和膜代谢的体内评估 直接和非侵入性地促进纵向研究。 初步 该实验室的31 P NMR研究揭示了膜的变化 8例首发未服药精神分裂症患者的磷脂代谢 与正常衰老时观察到的惊人相似。 在 此外，PCr水平与严重程度呈正相关， 阳性症状 相似的磷脂但不同的高能 在5例智商正常的成人孤独症患者中观察到磷酸盐的发现。 基于这些初步研究结果，本研究建议先研究30个 发作，入组时以及第4周、第6周和第12周时从未接受过药物治疗的精神分裂症患者 入组研究后3个月和2年。 结果在30 精神分裂症患者将与对照组（30名正常人）的结果进行比较 对照组和30名自闭症患者）在入组时和术后1年和2年获得 入境 正常智商的成年自闭症患者被选为对照组， 这些自闭症患者与精神分裂症患者有许多共同的阴性症状， 有时被误诊为精神分裂症，但发病年龄不同 和不同的临床过程。

Clinical studies supported by animal research have implicated the dorsal prefrontal cortex in the cognitive deficits observed in schizophrenia. Physiological studies to date have demonstrated decreased frontal lobe cerebral blood flow (xenon 133) and 2-deoxyglucose uptake (positron emission tomography, PET) in some patients with schizophrenia. In contrast PET studies in autism have reported increased uptake of 2-deoxyglucose in the frontal lobes of adult autistic men. 31P NMR spectroscopy provides in vivo assessment of both high-energy phosphate and membrane metabolism directly and non-invasively facilitating longitudinal studies. Preliminary 31P NMR studies from this laboratory reveal alterations in membrane phospholipid metabolism in 8 first episode, never medicated schizophrenics that are strikingly similar to those observed with normal aging. In addition the levels of PCr have a positive correlation with the severity of positive symptoms. Similar phospholipid but different high energy phosphate findings have been observed in 5 normal IQ adult autistics. Based on these preliminary findings, this study proposes to study 30 first episode, never medicated schizophrenics at entry and at 4 weeks, 6 and 12 months and 2 years after entry into the study. Results in the 30 schizophrenics will be compared with results in controls (30 normal controls and 30 autistics) obtained at entry and at 1 and 2 years after entry. The normal IQ adult autistics are chosen as a comparison group as these autistics share many of the negative symptoms with schizophrenia, are sometimes misdiagnosed as schizophrenia but have a different age of onset and a different clinical course.