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目的 探讨阻塞性睡眠呼吸暂停综合征患者 (OSAS)认知障碍的生化机制。方法 对OSAS组 36例 ,对照组 18例进行睡眠多导仪和神经心理测验量表检查 ,用放射免疫方法检测血清胰岛素样生长因子 1(IGF I)水平 ,观察患者血清IGF I变化 ,并比较它与认知功能、夜间低氧和睡眠结构紊乱间的关系。结果 OSAS患者视觉再生 (用于检测短时记忆能力 )和数字符号 (用于检测一般学习能力 )两项神经心理测验分数明显低于对照组 (视觉再生 :患者为 8 4± 2 7;对照为 11 6± 1 4 ;P <0 0 1;数字符号 :患者为 36 9± 8 3;对照为 4 7 8± 6 8,P <0 0 1) ,血清IGF I水平显著降低 (患者为12 7 2± 87 0 ;对照为 194 0± 77 3;P <0 0 5 ) ,且与视觉再生 (r=0 381,P <0 0 5 )和数字符号 (r =0 330 ,P <0 0 5 )两项受损神经心理测验分数呈正相关 ,与最低血氧饱和度 (r=0 371,P <0 0 5 )、平均血氧饱和度 (r=0 333,P <0 0 5 )和REM睡眠长短 (r=0 5 98,P <0 0 1)呈正相关。结论 OSAS患者短时记忆能力和一般学习能力受损 ,血清IGF I水平降低 ,且可能是其认知功能障碍的生化机制之一。夜间低氧和REM期睡眠剥夺可能是导致血清IGF I降低的原因。
Objective To investigate the biochemical mechanism of cognitive impairment in obstructive sleep apnea syndrome (OSAS). Methods 36 cases of OSAS group and 18 cases of control group were inspected by polysomnography and neuropsychological test. The level of serum insulin-like growth factor 1 (IGF-I) was detected by radioimmunoassay and the changes of serum IGF-I in patients were observed. It is associated with cognitive function, nocturnal hypoxia and disturbances of sleep structure. Results Two neuropsychological test scores were significantly lower in OSAS patients with visual regeneration (for short-term memory tests) and numeric symbols (for general learning tests) than those in the control group (visual regeneration: 8 4 ± 2 7; control 11 6 ± 1 4; P <0 0 1; number sign: 36 9 ± 8 3 in patients; control was 478 ± 6 8, P 0 01), and the level of serum IGF I was significantly decreased 2 ± 87 0; control was 194 0 ± 77 3; P <0 05), and was significantly correlated with visual reproduction (r = 0 381, P 0 05) ) Were positively correlated with the scores of the two neuropsychological tests, and were positively correlated with the lowest oxygen saturation (r = 0 371, P 0 05), mean oxygen saturation (r 0 333, P 0 05) and REM The length of sleep (r = 0 5 98, P <0.01) was positively correlated. Conclusion Short-term memory and general learning ability are impaired in patients with OSAS, and serum IGF-I level is decreased, which may be one of the biochemical mechanisms of cognitive impairment. Nighttime hypoxia and REM sleep deprivation may be responsible for the reduction of serum IGF I.