【摘要】：【研究背景】創(chuàng)傷性腦損傷（traumatic brain injury，TBI）后認(rèn)知功能障礙是法醫(yī)臨床學(xué)鑒定的難點(diǎn)之一，其發(fā)生機(jī)制迄今尚未闡明，而精神量表測(cè)評(píng)方法的客觀性欠佳，不能有效鑒別避免夸大病情甚至偽裝。因此，選擇適宜的實(shí)驗(yàn)動(dòng)物模型，尋求認(rèn)知功能障礙的客觀檢測(cè)指標(biāo)和方法，可能是揭示TBI后認(rèn)知功能障礙本質(zhì)的關(guān)鍵環(huán)節(jié)，具有重要的理論和實(shí)踐價(jià)值。 【目的】嘗試建立創(chuàng)傷性腦損傷（TBI）后認(rèn)知功能障礙大鼠模型，探索SD大鼠創(chuàng)傷性腦損傷基礎(chǔ)上空間學(xué)習(xí)記憶能力與神經(jīng)電生理指標(biāo)之間的關(guān)聯(lián)，，尋求TBI后認(rèn)知功能障礙的客觀檢測(cè)指標(biāo)和方法，為后續(xù)研究提供初步研究支持。 【方法】選擇雄性SD大鼠為研究對(duì)象，隨機(jī)分組為對(duì)照組、假損傷組、損傷組（傷后3d組、傷后7d組、傷后14d組）。對(duì)照組不做任何處理，假損傷組僅顱骨開窗而不予打擊，損傷組開露骨窗后，采用自制自由落體打擊裝置，制作SD大鼠創(chuàng)傷性腦損傷。采用Morris水迷宮系統(tǒng)進(jìn)行行為學(xué)測(cè)試：定位航行實(shí)驗(yàn)連續(xù)4d，記錄MWM逃避潛伏期；空間探索實(shí)驗(yàn)1d，記錄穿臺(tái)次數(shù)。神經(jīng)電生理檢測(cè)：大鼠麻醉后，給予oddball paradigm刺激，顱外電極記錄事件相關(guān)電位P300波幅和潛伏期。采用SPSS11.5軟件，進(jìn)行數(shù)據(jù)統(tǒng)計(jì)處理。 【結(jié)果】各組大鼠均可引出典型P300波。對(duì)照組、假損傷組、傷后3d組、傷后7d組、傷后14d組大鼠的P300潛伏期分別為305.29±34.03ms、324.33±31.30ms、446.67±49.09ms、474.00±42.05ms、388.33±22.37ms；正常對(duì)照組與假損傷組之間無顯著性差異（P=0.38），而二者均明顯小于損傷組各亞組（P＜0.01）；傷后3d組與傷后7d組無統(tǒng)計(jì)學(xué)差異（P=0.28）；但二者均明顯大于傷后14d組（P≤0.04）。正常對(duì)照組、假損傷組、傷后3d組、傷后7d組、傷后14d組大鼠的P300波幅分別為26.97±5.83μV、25.18±6.79μV、17.03±5.54μV、15.35±6.89μV和14.77±3.51μV；正常對(duì)照組與假損傷組之間無顯著性差異（P=0.60），而二組均明顯大于損傷組各亞組（P＜0.05）；損傷組各亞組之間無統(tǒng)計(jì)學(xué)差異。各組大鼠Morris水迷宮逃避潛伏期均大體呈下降趨勢(shì)；對(duì)照組與假損傷組之間不具有統(tǒng)計(jì)學(xué)差異（P=0.19），而二者均顯著小于損傷組各亞組（P＜0.01）；傷后3d組、7d組之間不具有統(tǒng)計(jì)學(xué)顯著性差異（P=0.826），而二者均明顯大于傷后14d組（P㩳0.05）。對(duì)照組與假損傷組穿臺(tái)次數(shù)無顯著性差異，二者與損傷各亞組均存在顯著性差異；而傷后3d組、7d組和14d組穿臺(tái)次數(shù)均無顯著性差異。Morris水迷宮逃避潛伏期與P300潛伏期之間存在正相關(guān)關(guān)系，r=0.606，P=0.002。Morris水迷宮逃避潛伏期與P300波幅大體呈負(fù)相關(guān)趨勢(shì)，但不具有統(tǒng)計(jì)學(xué)顯著性。 【結(jié)論】Morris水迷宮逃避潛伏期能反映SD大鼠腦損傷后認(rèn)知功能障礙，且與腦損傷動(dòng)態(tài)過程相一致。事件相關(guān)電位P300潛伏期能相對(duì)客觀、靈敏地反映SD大鼠腦損傷后認(rèn)知功能障礙。SD雄性大鼠創(chuàng)傷性腦損傷模型適于TBI后認(rèn)知功能障礙研究。
[Abstract]:[background] Cognitive dysfunction after traumatic brain injury (traumatic brain injury-TBI) is one of the difficulties in forensic clinic identification, the mechanism of which has not been elucidated so far, but the objectivity of mental scale evaluation method is not good. Can not be effectively identified to avoid exaggerating the disease or even camouflage. Therefore, the selection of appropriate animal models and the objective detection of cognitive dysfunction may be the key link to reveal the nature of cognitive dysfunction after TBI. It has important theoretical and practical value. [objective] to establish a rat model of cognitive dysfunction after traumatic brain injury (TBI). To explore the relationship between spatial learning and memory ability and electrophysiologic indexes on the basis of traumatic brain injury in SD rats, and to explore the objective detection indexes and methods of cognitive dysfunction after TBI. [methods] male SD rats were randomly divided into control group, sham injury group and injury group (3 days after injury, 7 days after injury and 14 days after injury). The control group did not do any treatment, the sham injury group only opened the skull window but did not strike. After the open window, the injury group made the traumatic brain injury of SD rats by using the self-made free-fall hitting device. The behavior test of Morris water maze system was carried out: the navigation experiment was carried out for 4 consecutive days, and the escape latency of MWM was recorded, and the number of platform penetration was recorded in the space exploration experiment for 1 day. After anesthesia, rats were stimulated with oddball paradigm, and the amplitudes and latencies of event-related potentials (P300) were recorded at extracranial electrode. SPSS11.5 software was used to process the data. [results] typical P300 waves were obtained from each group of rats. The latency of P300 in the control group, the sham injury group, the 3rd day group, the 7 day group and the 14 day group were 305.29 鹵34.03 Ms ~ 324.33 鹵31.30 Ms ~ (446.67 鹵49.09 Ms) 474.00 鹵42.05 Ms ~ (388.33 鹵22.37 Ms) respectively, while there was no significant difference between the normal control group and the sham injury group (P < 0. 38), but the latency of P300 was significantly lower than that of each subgroup (P < 0. 01). There was no significant difference between the 3 d group and the 7 d group (P < 0. 28), but both of them were significantly higher than those of the 14 d group (P 鈮

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