敖然 于生元

光學(xué)相干斷層掃描術(shù)在中樞神經(jīng)系統(tǒng)疾病中的應(yīng)用

敖然 于生元

中樞神經(jīng)系統(tǒng)疾病較為復(fù)雜，常規(guī)檢查方法易受患者主觀因素的影響而缺乏準(zhǔn)確性，通過(guò)光學(xué)相干斷層掃描術(shù)（OCT）可以客觀檢測(cè)眼球后結(jié)構(gòu)改變，進(jìn)而反映神經(jīng)元變性情況。本文旨在探討OCT技術(shù)在中樞神經(jīng)系統(tǒng)疾病中的應(yīng)用，并尋找新型生物學(xué)標(biāo)志物。

體層攝影術(shù)，光學(xué)相干； 中樞神經(jīng)系統(tǒng)疾??； 綜述?

視神經(jīng)在胚胎發(fā)育過(guò)程中起源于外胚層，屬于中樞神經(jīng)的一部分［1］。視神經(jīng)和眼底結(jié)構(gòu)可以在一定程度上反映中樞神經(jīng)系統(tǒng)疾病。中樞或周?chē)窠?jīng)系統(tǒng)病理性損害可以導(dǎo)致神經(jīng)元變性［2］，神經(jīng)元變性可發(fā)生于視覺(jué)通路［3］。視覺(jué)通路由三級(jí)神經(jīng)元組成，一級(jí)神經(jīng)元為視網(wǎng)膜雙極細(xì)胞，其周?chē)c視覺(jué)感受器視錐細(xì)胞和視桿細(xì)胞形成突觸，其中樞支與二級(jí)神經(jīng)元節(jié)細(xì)胞形成突觸，節(jié)細(xì)胞軸突形成視神經(jīng)，向后延伸形成視束，止于外側(cè)膝狀體三級(jí)神經(jīng)元，其軸突形成視輻射，止于枕葉皮質(zhì)［4］。順行神經(jīng)元變性自視網(wǎng)膜至視輻射或視皮質(zhì)，逆行神經(jīng)元變性則自視皮質(zhì)或視輻射至視網(wǎng)膜［5］。上述病理改變?cè)诩膊〕跗谕ǔ３蕘喤R床變化，常規(guī)檢測(cè)難以發(fā)現(xiàn)，光學(xué)相干斷層掃描術(shù)（OCT）可以早期發(fā)現(xiàn)組織結(jié)構(gòu)改變，為及時(shí)治療提供時(shí)機(jī)。

OCT技術(shù)是一種非侵襲性、可重復(fù)性、無(wú)創(chuàng)性眼科檢查方法，其技術(shù)原理與超聲類(lèi)似，根據(jù)眼部各組織結(jié)構(gòu)不同折光率獲得眼底結(jié)構(gòu)的橫斷面成像，從而檢測(cè)視網(wǎng)膜、脈絡(luò)膜等結(jié)構(gòu)，分辨率達(dá)5～10 μm，接近病理結(jié)構(gòu)水平［6］。OCT 技術(shù)還可以檢測(cè)視乳頭旁和黃斑區(qū)視網(wǎng)膜神經(jīng)纖維層（RNFL）厚度。光學(xué)相干斷層掃描增強(qiáng)深部成像（EDI?OCT）是新型OCT技術(shù)，與傳統(tǒng)OCT技術(shù)相比，具有較高的信噪比（SNR），分辨率高達(dá)2 μm，同時(shí)增加視覺(jué)追蹤系統(tǒng)，可于數(shù)微秒內(nèi)捕捉到眼球后結(jié)構(gòu)變化，呈現(xiàn)視網(wǎng)膜各層結(jié)構(gòu)和脈絡(luò)膜結(jié)構(gòu)，并形成三維圖像，從而更直觀地觀察中樞神經(jīng)系統(tǒng)疾?。??8］。脈絡(luò)膜是血供最豐富的結(jié)構(gòu)，為視網(wǎng)膜外層和部分視神經(jīng)供血，其結(jié)構(gòu)改變可以在一定程度上反映血供異常［9］。既往主要采用超聲或熒光素眼底血管造影（FFA）對(duì)脈絡(luò)膜進(jìn)行檢測(cè)，不能直觀反應(yīng)脈絡(luò)膜結(jié)構(gòu)，EDI?OCT技術(shù)由于更靠近眼球，可以清晰獲得脈絡(luò)膜圖像，實(shí)現(xiàn)快捷、無(wú)創(chuàng)性檢測(cè)脈絡(luò)膜。

一、中樞神經(jīng)系統(tǒng)脫髓鞘疾病

多發(fā)性硬化（MS）、視神經(jīng)脊髓炎譜系疾?。∟MOSD）是中樞神經(jīng)系統(tǒng)脫髓鞘疾病，病變常累及視神經(jīng)，導(dǎo)致視神經(jīng)炎。視神經(jīng)炎包括炎癥反應(yīng)、脫髓鞘改變、軸索損傷等，這一過(guò)程可能導(dǎo)致視網(wǎng)膜節(jié)細(xì)胞死亡、黃斑體積縮小、視覺(jué)功能障礙或永久性失明［10］。疾病早期影像學(xué)檢查可能無(wú)異常，眼科檢查僅發(fā)現(xiàn)亞臨床改變，如果能夠獲得早期診斷和及時(shí)治療，患者預(yù)后良好。

1.多發(fā)性硬化 有25%～50%以急性視神經(jīng)炎首發(fā)的患者最終證實(shí)為多發(fā)性硬化［11］。尸檢顯示，49例多發(fā)性硬化患者中35例發(fā)生視網(wǎng)膜神經(jīng)纖維層萎縮［12］。1999 年，Parisi等［13］首次將 OCT 技術(shù)用于多發(fā)性硬化，他們對(duì)有視神經(jīng)炎表現(xiàn)且視力恢復(fù)較好的患者進(jìn)行OCT檢測(cè)，發(fā)現(xiàn)仍有6/14例患側(cè)視網(wǎng)膜神經(jīng)纖維層和4/14例健側(cè)視網(wǎng)膜神經(jīng)纖維層較正常對(duì)照者變薄。視神經(jīng)炎致視網(wǎng)膜神經(jīng)纖維層厚度改變與視覺(jué)誘發(fā)電位（VEP）P100波幅降低相一致，提示軸索變性［14］。視神經(jīng)損害早期視網(wǎng)膜節(jié)細(xì)胞內(nèi)叢狀層即變薄，故可準(zhǔn)確篩查出早期視神經(jīng)損害［15］。

2.視神經(jīng)脊髓炎譜系疾病 研究顯示，視神經(jīng)脊髓炎譜系疾病患者視乳頭周?chē)飨笙抟暰W(wǎng)膜神經(jīng)纖維層均變薄，特別是上象限和下象限，提示軸索直徑較薄的區(qū)域不易受累。與多發(fā)性硬化患者相比，視神經(jīng)脊髓炎譜系疾病患者黃斑區(qū)視網(wǎng)膜神經(jīng)纖維層顯著變?。?6］，提示后者的視神經(jīng)炎較前者更易導(dǎo)致視網(wǎng)膜神經(jīng)纖維層變薄，且出現(xiàn)時(shí)間更早，這可能是由于抗水通道蛋白4（AQP4）抗體聚集使血?腦屏障（BBB）通透性增加［17］。

二、神經(jīng)變性病

1.帕金森病 帕金森病（PD）是臨床常見(jiàn)的神經(jīng)變性病，其病理改變是黑質(zhì)多巴胺能神經(jīng)元變性缺失和路易小體（LB）形成，臨床以運(yùn)動(dòng)癥狀為主，表現(xiàn)為運(yùn)動(dòng)遲緩、靜止性震顫、肌張力增高、姿勢(shì)平衡障礙［18］。視覺(jué)障礙在帕金森病患者中較為常見(jiàn)，主要表現(xiàn)為視物模糊、視物成雙、幻視等［19］。視覺(jué)相關(guān)檢查常受帕金森病患者認(rèn)知功能障礙的影響而缺乏準(zhǔn)確性，影像學(xué)檢查可以較客觀地反映眼部各組織結(jié)構(gòu)異常。有學(xué)者提出，多巴胺在視網(wǎng)膜視覺(jué)成像過(guò)程中發(fā)揮一定作用［20］，而帕金森病患者視網(wǎng)膜多巴胺水平減少可能導(dǎo)致視覺(jué)障礙，補(bǔ)充左旋多巴制劑可以改善癥狀［21］。OCT技術(shù)是客觀檢測(cè)視網(wǎng)膜形態(tài)學(xué)的方法，可以反映出神經(jīng)元功能和突觸傳遞。Bodis?Wollner等［22］對(duì) 24 例帕金森病患者和17例性別、年齡相匹配的正常對(duì)照者進(jìn)行OCT檢查，結(jié)果顯示，帕金森病患者視網(wǎng)膜、視網(wǎng)膜神經(jīng)纖維層內(nèi)上和內(nèi)下象限均較正常對(duì)照者變薄。Jiménez等［23］認(rèn)為，帕金森病嚴(yán)重程度與視乳頭旁視網(wǎng)膜神經(jīng)纖維層厚度有關(guān)，帕金森病患者視乳頭旁各象限視網(wǎng)膜神經(jīng)纖維層均較正常對(duì)照者變薄。Garcia?Martin等［24］探討帕金森病患者生活質(zhì)量與中央凹視網(wǎng)膜神經(jīng)纖維層厚度的相關(guān)性，發(fā)現(xiàn)中央凹視網(wǎng)膜神經(jīng)纖維層厚度減少與帕金森病嚴(yán)重程度相關(guān)。α?突觸核蛋白（α?Syn）在帕金森病的發(fā)生與發(fā)展中發(fā)揮重要作用，其聚集與路易小體（LB）形成和多巴胺能神經(jīng)元變性缺失密切相關(guān)。α?Syn參與脂質(zhì)連接、線粒體功能和突觸傳遞［25］。有研究顯示，α?突觸核蛋白基因（SNCA）表達(dá)于脊椎動(dòng)物視網(wǎng)膜外叢狀層［26］。病理學(xué)研究顯示，視網(wǎng)膜內(nèi)層細(xì)胞間質(zhì)α?Syn 表達(dá)上調(diào)［19］。Satue等［27］采用 OCT 技術(shù)檢測(cè)帕金森病患者視網(wǎng)膜神經(jīng)纖維層厚度，發(fā)現(xiàn)視網(wǎng)膜外叢狀層視網(wǎng)膜神經(jīng)纖維層較正常對(duì)照者變??；亦有研究顯示，視網(wǎng)膜其他層視網(wǎng)膜神經(jīng)纖維層也變?。?8?29］。因此，α?Syn 對(duì)視網(wǎng)膜結(jié)構(gòu)的影響尚待進(jìn)一步驗(yàn)證。

2.阿爾茨海默病 近年關(guān)于阿爾茨海默?。ˋD）患者視覺(jué)障礙的研究逐漸增多，眼部癥狀常出現(xiàn)在癡呆前［30］。OCT技術(shù)可以在阿爾茨海默病早期即發(fā)現(xiàn)亞臨床證據(jù)，從而早期診斷阿爾茨海默病。研究顯示，隨著阿爾茨海默病的進(jìn)展，視網(wǎng)膜神經(jīng)纖維層逐漸變薄，黃斑體積與簡(jiǎn)易智能狀態(tài)檢查量表（MMSE）評(píng)分顯著相關(guān)［31］。因此，OCT 技術(shù)是評(píng)價(jià)阿爾茨海默病嚴(yán)重程度的便捷方法。

三、原發(fā)性頭痛

1.偏頭痛 偏頭痛是發(fā)作性神經(jīng)系統(tǒng)疾病，我國(guó)患病率約為9%［32］。皮質(zhì)擴(kuò)散性抑制（CSD）是公認(rèn)的有先兆偏頭痛的病理生理學(xué)機(jī)制［33］，是神經(jīng)元去極化后出現(xiàn)的興奮性抑制，通過(guò)釋放大量炎性因子和神經(jīng)遞質(zhì)以激活三叉神經(jīng)血管系統(tǒng)，最終導(dǎo)致偏頭痛［34］。三叉神經(jīng)血管系統(tǒng)包括三叉神經(jīng)、顱內(nèi)外腦膜血管，以及腦干、顱外軟組織、眼部等［35］。亦有學(xué)者開(kāi)始關(guān)注偏頭痛患者眼球后結(jié)構(gòu)變化。研究顯示，偏頭痛發(fā)作期脈絡(luò)膜厚度顯著增加［36］，偏頭痛非發(fā)作期脈絡(luò)膜厚度較正常對(duì)照者減少，可能是由于偏頭痛反復(fù)發(fā)作致腦血流量減少，使脈絡(luò)膜變薄；其中，有先兆偏頭痛組脈絡(luò)膜厚度減少得更明顯［37］，此與有先兆偏頭痛易引起顱內(nèi)血管事件相一致［38］。Martinez等［39］發(fā)現(xiàn)，偏頭痛組患者視網(wǎng)膜神經(jīng)纖維層厚度較對(duì)照組減少，視網(wǎng)膜神經(jīng)纖維層厚度與偏頭痛殘疾程度評(píng)價(jià)問(wèn)卷（MIDAS）、偏頭痛發(fā)作頻率和病程相關(guān)。視網(wǎng)膜神經(jīng)纖維層變薄可能是逆行性神經(jīng)元變性所致，皮質(zhì)擴(kuò)散性抑制源于枕葉皮質(zhì)，視覺(jué)先兆發(fā)生時(shí)枕葉血流量減少［40］，偏頭痛反復(fù)發(fā)作可以引起視覺(jué)皮質(zhì)神經(jīng)元逆行性變性，從而導(dǎo)致視網(wǎng)膜神經(jīng)纖維層變薄。

2.叢集性頭痛 叢集性頭痛是臨床最為常見(jiàn)的三叉神經(jīng)自主神經(jīng)性頭痛，表現(xiàn)為偏側(cè)頭痛、程度劇烈，嚴(yán)重影響生活質(zhì)量［41］。多項(xiàng)研究顯示，叢集性頭痛發(fā)作時(shí)眼部血管發(fā)生血流動(dòng)力學(xué)改變，從而導(dǎo) 致 視 覺(jué) 障 礙［42］。Ewering 等［43］采 用 OCT 技 術(shù) 對(duì)107例叢集性頭痛患者視網(wǎng)膜神經(jīng)纖維層厚度進(jìn)行檢測(cè)，發(fā)現(xiàn)雙眼顳側(cè)象限視網(wǎng)膜神經(jīng)纖維層厚度均較正常對(duì)照者減少，其中，慢性叢集性頭痛患者黃斑區(qū)視網(wǎng)膜神經(jīng)纖維層厚度較偶有頭痛發(fā)作者和正常對(duì)照者均減少，提示視網(wǎng)膜神經(jīng)纖維層厚度改變可能是長(zhǎng)期血供異常所致。

綜上所述，OCT技術(shù)是非侵襲性、可重復(fù)性、無(wú)創(chuàng)性檢測(cè)方法，不受患者主觀影響，可以客觀、精確地捕捉眼球后結(jié)構(gòu)變化，廣泛應(yīng)用于中樞神經(jīng)系統(tǒng)疾病的早期診斷，尤其對(duì)存在眼部癥狀的中樞神經(jīng)系統(tǒng)疾病、神經(jīng)變性病和發(fā)作性疾病具有重要臨床意義。視網(wǎng)膜神經(jīng)纖維層厚度有望成為新型生物學(xué)標(biāo)志物，可以早期發(fā)現(xiàn)亞臨床改變，為疾病早期診斷提供依據(jù)。

［1］Wilson SW,Houart C.Early steps in the development of the forebrain.Dev Cell,2004,6:167?181.

［2］Wang JT,Medress ZA,Barres BA.Axon degeneration:molecular mechanisms of a self?destruction pathway.J Cell Biol,2012,196:7?18.

［3］Kelle J,Sánchez?Dalmau BF,Villoslada P.Lesions in the posterior visual pathway promote trans?synaptic degeneration of retinal ganglion cells.PLoS One,2014,9:E97444.

［4］Jia JP,Chen SD.Neurology.7th ed.Beijing:People's Medical Publishing House,2013:5?6［.賈建平,陳生弟.神經(jīng)病學(xué).7版.北京:人民衛(wèi)生出版社,2013:5?6.］

［5］Graham SL,Klistorner AI,Grigg JR,Billson FA.Objective VEP perimetry in glaucoma:asymmetry analysis to identify early deficits.J Glaucoma,2000,9:10?19.

［6］Podoleanu AG.Optical coherence tomography.Br J Radiol,2005,78:976?988.

［7］Nakano T,Hayashi T,Nakagawa T,Honda T,Owada S,Endo H,Tatemichi M.Applicability of automatic spectral domain optical coherence tomography forglaucomamassscreening.Clin Ophthalmol,2016,11:97?103.

［8］Bock M,Brandt AU,D?rr J,Pfueller CF,Ohlraun S,Zipp F,Paul F.Time domain and spectral domain optical coherence tomography in multiple sclerosis:a comparative cross?sectional study.Mult Scler,2010,16:893?896.

［9］Spaide RF,Koizumi H,Pozonni MC.Enhanced depth imaging spectral?domain optical coherence tomography. Am J Ophthalmol,2008,146:496?500．

［10］Frohman EM,Frohman TC,Zee DS,McColl R,Galetta S.The neuroophthalmology of multiple sclerosis.Lancet Neurol,2005,4:111?121.

［11］Kale N.Management of optic neuritis as a clinically first event of multiple sclerosis.Curr Opin Ophthalmol,2012,23:472?476.

［12］Serbecic N,Beutelspacher SC,Kircher K,Reitner A,Schmidt?Erfurth U.Interpretation of RNFLT values in multiple sclerosis?associated acute optic neuritis using high?resolution SD?OCT device.Acta Ophthalmol,2012,90:540?545.

［13］Parisi V,Manni G,SpadaroM,Colacino G,Restuccia R,Marchi S, Bucci MG, Pierelli F. Correlation between morphological and functional retinal impairment in multiple sclerosis patients.Invest Ophthalmol Vis Sci,1999,40:2520?2527.

［14］Trip SA,Schlottmann PG,Jones SJ,Altmann DR,Garway?Heath DF,Thompson AJ,Plant GT,Miller DH.Retinal nerve fiber layer axonal loss and visual dysfunction in optic neuritis.Ann Neurol,2005,58:383?391.

［15］Al?Louzi OA,Bhargava P,Newsome SD,Balcer LJ,Frohman EM,Crainiceanu C,Calabresi PA,Saidha S.Outer retinal changes following acute optic neuritis.Mult Scler,2016,22:362?372.

［16］Bennett JL,de Seze J,Lana?Peixoto M,Palace J,Waldman A,Schippling S,Tenembaum S,Banwell B,Greenberg B,Levy M,Fujihara K,Chan KH,Kim HJ,Asgari N,Sato DK,Saiz A,Wuerfel J,Zimmermann H,Green A,Villoslada P,Paul F;GJCF?ICC&BR.Neuromyelitis optica and multiple sclerosis:seeing differences through optical coherence tomography.Mult Scler,2015,21:678?688.

［17］Hofman P,Hoyng P,vanderWerf F,Vrensen GF,Schlingemann RO.Lack of blood?brain barrier properties in microvessels of the prelaminar optic nerve head.Invest Ophthalmol Vis Sci,2001,42:895?901.

［18］Armstrong RA. Visual symptoms in Parkinson's disease.Parkinsons Dis,2011:ID908306.

［19］Schulz?Schaeffer WJ.The synaptic pathology of alpha?synuclein aggregation in dementia with Lewy bodies,Parkinson's disease and Parkinson's disease dementia.Acta Neuropathol,2010,120:131?143.

［20］Rodnitzky R.Visual dysfunction in Parkinson's disease.Clin Neurosci,1998,5:102?106.

［21］Rohani M,Langroodi AS,Ghourchian S,Falavarjani KG,Soudi R,Shahidi G.Retinal nerve changes in patients with tremor dominant and akinetic rigid Parkinson's disease.Neurol Sci,2013,34:689?693.

［22］Bodis?Wollner I,Kozlowski P,Glazman S,Miri S. α?Synuclein in the inner retina in Parkinson disease.Ann Neurol,2014,75:964?966.

［23］Jiménez B,Ascaso FJ,CristóbalJA,López delValJ.Developmentofa prediction formula ofParkinson disease severity by optical coherence tomography.Mov Disord,2014,29:68?74.

［24］Garcia?Martin E,Rodriguez?Mena D,Satue M,Almarcegui C,Dolz I,Alarcia R,Seral M,Polo V,Larrosa JM,Pablo LE.Electrophysiology and optical coherence tomography to evaluate Parkinson disease severity.Invest Opthalmol Vis Sci,2014,55:696?705.

［25］Uversky VN.Alpha?synuclein misfolding and neurodegenerative diseases.Curr Protein Pept Sci,2008,9:507?540.

［26］Martinez?Navarrete G,Martin?Nieto J,Esteve?Rudd J,Angulo A,Cuenca N.Alpha synuclein gene expression profile in the retina of vertebrates.Mol Vis,2007,18:949?961.

［27］Satue M,Garcia?Martin E,Fuertes I,Otin S,Alarcia R,Herrero R,Bambo MP,Pablo LE,Fernandez FJ.Use of fourier domain OCT to detectretinalnerve fiber layer degeneration in Parkinson's disease patients.Eye,2013,27:507?514.

［28］Albrecht P,Müller AK,Südmeyer M,Ferrea S,Ringelstein M,Cohn E,Aktas O,Dietlein T,Lappas A,Foerster A,Hartung HP,Schnitzler A,Methner A.Optical coherence tomography in parkinsonian syndromes.PLoS One,2012,7:E34891.

［29］Garcia?Martin E,Larrosa JM,Polo V,Satue M,Marques ML,Alarcia R,Seral M,Fuertes I,Otin S,Pablo LE.Distribution of retinal layer atrophy in patients with Parkinson disease and association with disease severity and duration. Am J Ophthalmol,2014,157:470?478.

［30］Kesler A,Vakhapova V,Korczyn AD,Naftaliev E,Neudorfer M.Retinal thickness in patients with mild cognitive impairment and Alzheimer's disease.Clin Neurol Neurosurg,2011,113:523?526.

［31］Cheung CY,Ong YT,Hilal S,Ikram MK,Low S,Ong YL,Venketasubramanian N,Yap P,Seow D,Chen CL,Wong TY.Retinal ganglion cell analysis using high?definition optical coherence tomography in patients with mild cognitive impairment and Alzheimer's disease.J Alzheimers Dis,2015,45:45?56.

［32］Yu S,Liu R,Zhao G,Yang X,Qiao X,Feng J,Fang Y,Cao X,He M,SteinerT.The prevalence and burden ofprimary headaches in China:a population?based door?to?door survey.Headache,2012,52:582?591.

［33］Woods RP,Iacoboni M,Mazziotta JC.Brief report:bilateral spreading cerebral hypoperfusion during spontaneous migraine headache.N Engl J Med,1994,331:1689?1692.

［34］Moskowitz MA,Nozaki K,Kraig RP.Neocortical spreading depression provokesthe expression ofc?fosprotein?like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms.J Neurosci,1993,13:1167?1177.

［35］Abdul?Rahman AM,Gilhotra J,Selva D.Dynamic focal retinal arteriolar vasospasm in migraine.Indian J Ophthalmol,2011,59:51?53.

［36］Dadaci Z,Doganay F,Oncel Acir N,Aydin HD,Borazan M.Enhanced depth imaging optical coherence tomography of the choroid in migraine patients:implications for the association of migraine and glaucoma.Br J Ophthalmol,2014,98:972?975.

［37］Gipponi S,Scaroni N,Venturelli E,Forbice E,Rao R,Liberini P,Padovani A,Semeraro F.Reduction in retinal nerve fiber layer thickness in migraine patients.Neurol Sci,2013,34:841?845.

［38］Murinova N, Krashin DL, Lucas S. Vascular risk in migraineurs:interaction of endothelial and cortical excitability factors.Headache,2014,54:583?590.

［39］Martinez A,Proupim N,Sanchez M.Retinal nerve fiber layer thickness measurements using optical coherence tomography in migraine patients.Br J Ophthalmol,2008,92:1069?1075.

［40］Tedeschi G,Russo A,Conte F,Corbo D,Caiazzo G,Giordano A,Conforti R,Esposito F,Tessitore A.Increased interictal visual network connectivity in patients with migraine with aura.Cephalalgia,2016,36:139?147.

［41］May A. Cluster headache: pathogenesis, diagnosis, and management.Lancet,2005,366:843?855.

［42］Buture A, Gooriah R, Nimeri R, Ahmed F. Current understanding on pain mechanism in migraineand cluster headache.Anesth Pain Med,2016,6:E35190.

［43］Ewering C,Ha?alN,Alten F,Clemens CR,Eter N,Oberwahrenbrock T,Kadas EM,Zimmermann H,Brandt AU,Osada N,Paul F,Marziniak M.Temporal retinal nerve fibre layer thinning in cluster headache patients detected by optical coherence tomography.Cephalalgia,2015,35:946?958.

The application of optical coherence tomography in central nervous system diseases

AO Ran,YU Sheng?yuan

Department of Neurology,Chinese PLA General Hospital,Beijing 100853,China

YU Sheng?yuan(Email:yusy1963@126.com)

Central nervous system diseases are complicated,and general examinations are lack of accuracy because they are easily influenced by subjective factors of patients.Objective results from optical coherence tomography(OCT)can detect the changes of ocular posterior structures,and then further reflect the neuronal degeneration.The aim of this review is to discuss the application of OCT in central nervous system diseases and look for new biomarkers.

Tomography,optical coherence; Central nervous system diseases; Review

This study was supported by the National Natural Science Foundation of China(No.81471147).

10.3969/j.issn.1672?6731.2017.05.013

國(guó)家自然科學(xué)基金資助項(xiàng)目（項(xiàng)目編號(hào)：81471147）

100853 北京，解放軍總醫(yī)院神經(jīng)內(nèi)科

于生元（Email：yusy1963@126.com）

2017?04?06）