FOCUSED ISSUE OF THIS MONTH J Korean Med Assoc 2014 April; 57(4): pissn / eissn

FOCUSED ISSUE OF THIS MONTH J Korean Med Assoc 2014 April; 57(4): 300-307 pissn 1975-8456 / eissn 2093-5951 http://dx.doi.org/10.5124/jkma.2014.57.4.300 요추및경추통증을유발하는퇴행성척추질환의병태생리 이인식 1 정선근 2 1 건국대학교의학전문대학원건국대학교병원, 2 서울대학교의과대학재활의학과 Pathophysiology of degenerative spinal disease causing lumbar and cervical spinal pain In-Sik Lee, MD 1 Sun G. Chung, MD 2 Department of Rehabilitation Medicine, 1 Konkuk University Medical Center, Konkuk University School of Medicine, 2 Seoul National University College of Medicine, Seoul, Korea As degenerative spinal disease among spinal diseases causing lumbar and cervical spinal pain is the endless repetition of the biological healing of mechanical damage occurring over a lifetime, spinal pain by degenerative spinal disease occurs as a series of successive changes through the repetitive damage-healing process of various spinal structures including the intervertebral disc rather than a temporary phenomenon of any given pathophysiologic change in one moment. Degenerative spinal disease generally begins with degeneration of the intervertebral disc. Then herniation of the intervertebral disc resulting in subsequent radicular pain occurs when the nucleus pulposus with degeneration located in the intervertebral disc tears and penetrates the annulus fibrosus. Subsequently, disc space narrowing occurs and alters the spinal biomechanics, followed by degenerative changes to the vertebral endplate, vertebra itself, and facet joint. Finally, these changes lead to spinal stenosis, which is the final destination of degenerative spine disease. Although the exact pathogenesis of spinal pain could be still unclear because of some inconsistencies between the degenerative changes in the spine and the clinical manifestations of spinal pain, an accurate understanding of the pathophysiology and future predictions for further mechanical injury as well as thorough history taking and careful attention to the long-term clinical courses and other associated risk factors including daily life posture and work posture are needed for successful treatment of spinal pain. Key Words: Intervetebral disc degeneration; Physiopathology; Low back pain; Neck pain; Spinal stenosis 서론 요추혹은경추통증을유발하는척추질환의평생유병률 (life-time prevalence) 은 65-80% 에이르는것으로알려져 Received: January 2, 2014 Corresponding author: Sun G. Chung E-mail: suncg@snu.ac.kr Accepted: January 16, 2014 ㅈ Korean Medical Association This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons. org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. 있으며 [1,2], 최근 6개월간한차례이상의요통을호소하는비율이 40% 에이르며 [3], 경추부통증의경우에는이전에통증이없는사람의 15-20% 에서새로운통증이발현된다 [4]. 요통의경우 20대부터발생하기시작하여전체유병률은 65세까지지속적으로증가하는양상을보이다가그이후부터는서서히감소한다 [5,6]. 급성요통의경우, 특별한치료없이시간이경과함에따라호전되는경우가대부분인것으로알려져있는데, 여러가이드라인에서급성요통환자의 90% 가 6주내로호전되며, 요통이발생한지 1년이지난시점에서통증이호전된비율은 54-90% 에달하는것으로보고되었다 [7,8]. 이와같이 300 대한의사협회지

Lee IS Chung SG Pathophysiology of degenerative spinal disease 요통의자연경과에대해낙관적인통계수치는요통을포함한척추통증을아주가벼운증상으로오해하게만든다. 하지만, 요통은재발이매우흔한데, 첫증상발생후 1년내로재발할확률이 50%, 2년내로재발할확률이 60%, 5년내로재발할확률은 70% 에달하며, 급성요통환자의상당수는만성요통또는지속적인통증으로증상의양상이변화하게된다 [9]. 따라서, 요추혹은경추통증을유발하는척추질환은일생을걸쳐일어나는 기계적손상에대한생물학적치유 의끝없는반복의과정이기에척추통증은어떤한순간에갑자기발생한증상이아니라반복적인손상, 치유과정을거쳐서발현되는증상임을이해하고, 한번의시술또는수술로요통을완전히해결할수있다는잘못된믿음을버려야한다. 요추및경추통증을유발하는척추질환들의분류혹은감별진단들로는통증의발병원인및방사통여부, 그리고병태생리등에따라서염좌와긴장, 퇴행성척추질환, 퇴행성변형 ( 전방전위증, 측만및후만등 ), 골절을포함한외상성병변, 척추종양, 감염그리고강직성척추염과같은염증성질환등으로분류할수있다 [10,11]. 이장에서는일생을걸쳐일어나는일련의연속적인변화과정인퇴행성척추질환 ( 추간판변성, 신경근병증, 척추관협착증등 ) 을중심으로병태생리를살펴보고, 이에따른경막외스테로이드주사치료와같은비수술중재적치료의적응기전에관해정리해보고자한다. 퇴행성척추질환의병태생리 척추는 20대부터퇴행성변화가일어나기시작하는데추간판변성부터시작되어변성된수핵이후방섬유륜을뚫고추간판탈출을일으키며결국에는척추종판 (endplate) 과척추뼈, 그리고척추의후방에위치한척추후관절까지퇴행성변화가일어나게된다. 이러한퇴행성변화가중심척추관이나추간공 (intervertebral foramen) 을침범하게되면중심성혹은외측성척추관협착증이초래되는데, 척추관협착증은궁극적으로척추의퇴행성변화의종착역이라고할수있다 (Figure 1) [11,12]. 이러한일련의과정으로척추의퇴행성변화가어떻게일어나는지잘설명되지만, 척추의퇴행성변화와실제발현하는척추통증간에는괴리가있는경우를자주보게되며, 실제발현된통증의정확한발생기전에대해서여전히잘설명되지않는경우도흔하다 [13,14]. 1. 추간판변성및퇴행추간판은무혈관조직이고수분을다량함유한수핵에는신경이분포하지않으나, 섬유륜의바깥부위는혈관과신경이분포되어있어침해수용성및기계적감각을전달하는신경섬유가분포되어있다. 이러한감각수용체들은추간판이정상적인기능을하는경우에는일상적인하중에반응하지않지만, 추간판에변성, 염증, 손상등이있으면일상적인하중에도통증을전달하게된다. 수핵의내부는아교질 (gelatinous substance) 로차있으며, 아교질은수분, 프로테오글라이칸, 콜라겐으로구성된다. 출생당시에는수핵의성분중 90% 가수분이지만, 시간이지날수록수분이줄고추간판의퇴행이진행하면서수핵의높이도낮아지게된다. 수핵에대사산물이축척되고조직내의산소이용이감소되면서여러염증성효소작용에의해황산케라탄과같은프로테오글라이칸성분이증가하고 aggrecan이소실및분절화되고이로인해수핵의구조적변형이발생되어사방으로퍼지는압력이척추종판및섬유륜에압력을미치게되어섬유륜에틈새가생기기시작하여이들이점차연결되고방사성으로갈라져수핵이빠져나오게된다. 척추종판도두터워지거나균열을일으키고척추뼈몸통에연결되는추간판가장자리에는골증식체가생기는등의퇴행성변화를보인다 (Figure 2) [15]. 이러한추간판내부의손상과퇴행으로인하여발생하는통증을추간판성 (discogenic) 통증이라지칭하며, 요통의경우 39% 가이에해당하는것으로알려져있다 [16]. 추간판의탈출 ( 팽윤과돌출을포함 ) 로인하여신경근에자극이가해짐으로써발생하는소위좌골신경통을신경근통증 (radicular pain) 으로부르는데, 요통의약 30% 정도를차지한다 [17]. 그러나후방관절증이나척추관협착증과같은척추통증의다른원인들도결국추간판의손상과퇴행에의 요추및경추통증을유발하는퇴행성척추질환의병태생리 301

J Korean Med Assoc 2014 April; 57(4): 300-307 Normal disc Disc degeneration and bulging Herniated intervertebral disc Disc space narrowing Discovertebral degeneration and spondylosis 해유발되므로 [18], 추간판손상과퇴행이척추통증의가장 근본적인문제로볼수있다. Facet joint Intervertebral foramen Annular tears and fissures Extrusion of disc Facet joint degeneration Foraminal stenosis 추간판성요통은추간판탈출증 (her-niated intervertebral disc) 으로인한신경근통증의소견없이추간판 의손상과퇴행으로인하여발생하는요통을뜻하며추간판 내부의퇴행과척추종판 (endplate) 의손상으로발생된염 증이추간판내부의감각신경을자극하여발생하는것으로 알려져있다. 특히, 수핵이외측섬유륜에있는신경과접 Hypertrophy of ligament flavum Central canal stenosis Figure 1. The degenerative cascade of L4-5 spinal segment. (A) Normal disc, (B) degeneration of the intervertebral disc, (C) herniated intervertebral disc, (D) disc space narrowing and facet joint degeneration, and (E) spinal stenosis with discovertebral degeneration and spondylosis. A B C D E 촉하게되면, 신경이손상되고손상된 신경말단이추간판내부인내측섬유 륜, 수핵까지침투하는것으로알려져 있다 [19]. 이때혈관과골지힘줄기관 (golgi tendon organ) 과같은감각수용 체와교감신경도새롭게생성된다 [20]. 즉, 추간판성척추통증의가장중요한 요소는다양한손상과퇴행에의해발 생된염증과통각신경의만남이다. 염 증을유발하는퇴행과손상의원인으로 는나이, 비만, 흡연, 진동, 강한기계적 인압박, 그리고유전적인소인을들수 있다. 기계적인압박은부하가가해진 상태로굴곡운동을하거나 [21,22], 굴 곡운동과비틀림운동이동시에일어날 때발생하는것으로알려져있다 [23]. 이러한추간판성척추통증에대한치 료로경피적추간판내감압술및경피적 수핵성형술 (nucleoplasty) 등과같은추 간판내부시술이비수술중재적치료 로임상에서사용되고있다. 이러한추 간판내부시술은추간판의후방섬유 륜부위에고열을가하여추간판내감 압및섬유륜파열부위의신경통증완 화, 그리고탈출된수핵을감입시키는 목적으로사용되지만, 아직효과에임 상적근거가높은상태가아니며 [24], 추간판퇴행에미치는악영향때문에 아직논란의여지가많다 [25]. 그외최근에는인공추간판 치환술, 성장인자를이용한생물학적치료, 추간판내세포 치료및줄기세포치료등을추간판성척추통증의치료에이 용하고있으나, 아직많은부분이실험적단계에있다 [26]. 2. 신경근통증 신경근통증 (radicular pain) 은신경근에기계적압박이가 해지거나염증반응과같은화학적반응에의해발생하며, 가 302 대한의사협회지

Lee IS Chung SG Pathophysiology of degenerative spinal disease Loss and fragmentation of aggrecan Greater amount of keratan sulfate with age Change in the distribution and type of collagen; type 1 collagen in nucleus Impairment of nutrition with diffusion Enzymatic activation Enzymatic activity and inhibition (MMPs, ADAMTS, TIMPs) 장흔히발생하는요천추신경병증의위치는요추 5 번과천추 1 번이며, 경추신경병증의위치는경추 6 번과 7 번이다. 신경 근중배측신경근혹은배측신경절에서발산되는이소성방출 (ectopic discharge) 에의한통증이며 2-3 인치두께로찌르는 듯한통증이하지로방사되는양상을보인다 [27]. 이러한통증 양상은말초신경에서는보이지않고배측신경근이나배측신 경절을자극했을때만보이는것으로알려져있다. 배측신경 과신경절을자극하는가장흔한원인은추간판탈출증이다. 추간판탈출증을수핵탈출증 (herniated nucleus pulposus) 로부르는경우도있으나, 추간판탈출증수술에서얻은조직 을분석해보면수핵만탈출되는경우보다수핵, 섬유륜, 종판 성분이혼합되어탈출되는경우가더많으므로 [28], 수핵탈 출증으로만부르는것은옳지않다. 앞서추간판성척추통증 에서설명된것과마찬가지로추간판탈출증의원인도나이, 비만, 흡연, 진동, 강한기계적인압박, 그리고유전적인소인 을들수있다 [29]. Adams 등 [21] 은사체실험에서요추가중 립위에서압박을받으면척추종판의손상이오고굴곡상태에 서반복적인압박을받으면처음에는수핵이섬유륜을손상 시키며후방으로열상을만들다가반복이지속되면섬유륜을 뚫고탈출이되는소견을기술하였다. 즉, 반복적인굴곡부하 가추간판탈출증의기계적인원인임을밝힌것이다. 오랜기 간동안추간판탈출에의한기계적인압박이신경근통증의 원인으로간주되었으나 1990 년대말과 2000 년대초반이되 Extracellular matrix structure Loss of hydration Failure of the structural framework No longer behave hydrostatically under load Disc bulging under a load Stress conc. along the endplate or in the annulus Strong influence on other spinal structures Affect disc function Predispose disc to injury Figure 2. The spectrum of pathogenesis of the degenerative changes in the intervertebral disc. MMPS, matrix metalloproteinases; ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs, TIMPs, tissue inhibitors of metalloproteinases (From Choi YS. Asian Spine J 2009;3:39-44, according to the Creative Commons license) [15]. 면서동물실험에서수핵의내용물을배 측신경절에접촉시키는것만으로도신 경근통증이생기고축삭의손상을동반 한신경전도속도의감소를일으키는것 이보고된후 [30,31], 탈출된추간판의 구조물중, 신경근에염증을일으키는요 소는섬유륜보다는수핵이라는것도실 험적으로증명되었으며 [32], 수핵이배 측신경근에강력한염증반응을일으키 는것은수핵속에존재하는수핵세포에 의한것으로실험적연구에서밝혀졌다 [33,34]. 이후의연구에서수핵세포에 존재하는종양괴사인자 (tumor necrosis factor-α) [35-39] 와아산화질소 (nitrous oxide) 등에의해염 증반응이발생한다고밝혀졌다 [40,41]. 실험적으로수핵에의 해발생된신경근의염증반응을국소적인스테로이드나 [42], 항종양괴사인자물질로 [38,39,43,44] 감소시킬수있음이밝 혀져실제임상적으로경막외스테로이드주사가신경근통증 의치료에널리사용되고있는데급성기통증혹은일정기간 보존적치료를하였음에도증상의호전이없는경우에사용되 어 3 개월이내에자연경과보다유의하게높은증상완화효과 를볼수있다 [45-47]. 하지만, 수핵에의한비기계적인염증 반응과탈출된추간판물질에의한기계적인압박이동시에 작용하면더심한신경근병변을일으키며, 해당척추분절의 불안정성등으로인한동적인압박까지가중될경우에는경막 외스테로이드주사치료만으로는충분한치료가되지않는경 우도드물지않다. 3. 척추증및척추후관절증 Kirkaldy-Willis 등 [12] 은최종적으로는척추관협착증까 지이르게되는퇴행성요추질환에서일어나는연쇄반응에 대한이론을제시하면서비록추간판과후관절 (facet joint) 이해부학적으로는분리되어있으나, 어느한구조물에작 용하는외력과병소는다른구조물에도영향을준다고주장 하였다. 만약척추에과도한압축력이가해지면퇴행성추간 판질환이발생하고이로인해후관절에부하가가해지면후 요추및경추통증을유발하는퇴행성척추질환의병태생리 303

J Korean Med Assoc 2014 April; 57(4): 300-307 관절의퇴행이발생한다. 이러한손상이특정레벨에서발생하게되면위쪽과아래쪽구조물도영향을받게되어결과적으로광범위한척추증 (spondylosis) 의형태로진행하게된다 (Figure 1D,1E) [48]. 후관절에미세손상이반복되면연골이파괴되고활막이두꺼워지는퇴행성변화가일어난다. 후관절의퇴행성변화는관절의불안정성과골관절비대의원인으로작용한다. 비대해진골관절로인해척추관및추간신경공이좁아지고신경근을압박한다 (Figure 1E). 이러한연쇄반응은추간판에서도마찬가지로일어나는데, 반복된미세손상으로섬유륜의파열이일어나게된다. 섬유륜파열방향이후외측으로진행하게되면추간판탈출이발생하고내부로진행하면추간판내장증이발생하며, 이두가지문제는추간판의높이를낮추고, 척추의불안정성을유발하여결과적으로외측함요와추간신경공의협착이일어난다. 경추부척추증도추간판퇴행의결과로초래되는데수핵변성및섬유륜팽윤에의해연골종판에서의기계적부하가증가되어골막하골형성이촉진되어골극들이형성되며, 척수관의앞쪽혹은추간신경공을침범하게된다 [49]. 이러한현상은추간판이소실된경추분절의과운동성을안정시키기위해추간판이소실된분절의인접경추분절에서흔히시작된다. 또한, 구상돌기 (uncinate process) 의비후로인해추간신경공의협착이발생하며, 아시아인에게더흔한후종인대골화증도척추퇴행증과함께발생하여심한경수압박을유발할수있다. 유병률에대한여러보고들에의하면남성의경우 70세에이르면거의 100% 에서, 여성의경우에도 96% 에서척추퇴행증을가진다고하며, 사후생검을통한보고에서는 60세남성의 1/2, 여성의 1/3에서유의한척추퇴행증이관찰되었다고보고되고있다 [50]. 1992년방상선학적검사를통한유병률조사에서는궁극적으로남녀모두 70% 이상에서척추퇴행증을가지며, 남성이방사학적인정도가더심하다고보고하고있다 [51]. 4. 척추관협착증 1) 요추부 : 신경인성파행상기기전들만으로도척추관협착증 (spinal stenosis) 에 의한신경인성파행을설명할수도있으나최근에는척추주위혈관의역할이중요하게대두되고있다. 요추부척추관협착증의전형적인증상인신경인성파행은좁아진척수관의기계적압박외에주위혈관의혈류문제에의해서유발되는것으로알려져있다. 이는척추협착증의증상이감압술만으로호전되지않는다는사실에서도확인할수있다. 척추관협착증과관련된혈류문제는크게두가지로구분되는데, 하나는정맥확장 (venous engorgement) 이고다른하나는동맥부전 (arrterial insufficiency) 이다. 정맥확장이론은, 척추협착증환자의정맥이확장되어울혈과혈류정체를일으키고울혈과정체된부위가경막외압력과경막내압력을증가시켜미세순환문제와신경허혈손상을유발함으로써전형적인신경인성파행증상이나타나게된다는것이다. 이와반대로동맥부전이론에서는정상적인혈관확장반응이척추협착증환자에서는나타나지않는다는것이다. 특히척추관협착증과죽상동맥경화증은모두고령에서호발하는질환이므로동맥부전이동반될가능성이높다 [52]. 2) 경추부 : 경추부퇴행성척수병증경추부퇴행성척수병증 (cervical spondylotic myelopathy) 은척추관협착을기본으로한여러병태생리학적인자들의합산물로서, 정적기계적인자, 동적기계적인자, 척수허혈, 그리고신장과연관된손상등이병발하여발생하게된다. 정적기계적인자들부터살펴보면, 척추체의후면골극이커지면서, 척추중심관이좁아지게되며, 선천적으로좁은척추중심관 (10-13 mm) 이동반되어있는경우더잘발생하게된다. 연령과관련된황색인대비후및척추뼈자체의비후, 그리고퇴행성후만증및아탈구등도경추부퇴행성척수병증의발생에일조를하게되며, 동적기계적인자로는정상적인경추부의굴곡-신전이기존의척수압박에의해기시된척수손상을악화시키게된다. 즉, 굴곡동작에서는척수가길이가늘어남으로써척추체의골극에의해척수가신장되게되며, 신전동작에서는황색인대가접히면서척수가황색인대와척추체골극사이에서끼이게된다 [53]. 경추부퇴행성척수병증의병리조직학검사상에서백질은최소한의침범을보이면서주로회백질을침범하는소견으로미루어척수허혈도병태생리에서중요한역할을하는 304 대한의사협회지

Lee IS Chung SG Pathophysiology of degenerative spinal disease 것으로밝혀졌는데, 허혈은미세혈류순환이저해된분절단위에서발생하게된다 [54]. 신장과관련된손상이경추부퇴행성척수병증의좁아진중심척추관과비정상적인움직임을보이는척추분절에서장력및전단력의상승을야기시켜척수내의국소적축삭손상을유발하게된다 [55]. 나가는자연경과와이를방해할수있는기계적손상의가능 성에대해서도정확히예측할수있어야할것이다. 찾아보기말 : 추간판퇴행 ; 병태생리 ; 요통 ; 경부통 ; 척추관협착증 5. 그외척추통증을유발하거나영향을미치는인자허리와목은여러조직이합쳐진구조물이며통증의원인인구조물도다양하며, 통증의발생기전도복합적인경우가많다. 척추분절불안정성 (segmental instability), 척추주위근육들의불균형, 우울증과같은사회정신적요소, 그리고통증의중심화 (centralization) 등을포함한여러인자들이척추통증의발현에직접혹은간접적으로영향을미치는것으로알려져있다. 결론 요추혹은경추통증을유발하는척추질환들중퇴행성척추질환은일생을걸쳐일어나는 기계적손상에대한생물학적치유 의끝없는반복의과정이기에퇴행성척추질환으로인해발생하는척추통증은어떤한순간의병태생리학적변화에의한일시적현상이라기보다는추간판을포함한여러척추구조물들의반복적인손상, 치유과정을통해일련의연속적인변화과정속에서발현하게된다. 이러한퇴행성척추질환은일반적으로추간판변성및퇴행으로시작되며, 변성된추간판내의수핵이섬유륜을뚫고나오는추간판탈출증과이로인한신경근병증이발생하게되며, 이어서추간판간격이좁아짐으로써척추종판, 척추뼈및척추후관절등에퇴행변화가발생하게되어궁극적으로는퇴행성척추질환의종착역에해당하는척추관협착증에이르게된다. 척추의퇴행성변화와실제발현하는척추통증간에는괴리가있어실제발현된척추통증의정확한발생기전에대해서여전히잘설명되지않는경우도있지만, 성공적인치료를위해서는환자의기나긴병력에귀를기울이고일상생활자세, 작업자세등에대해서도관심을가져야하며, 향후치유되어 ORCID In-Sik Lee, http://orcid.org/0000-0001-8167-7168 Sun G. Chung, http://orcid.org/0000-0001-5785-8110 REFERENCES 1. Bovim G, Schrader H, Sand T. Neck pain in the general population. Spine (Phila Pa 1976) 1994;19:1307-1379. 2. Walker BF. The prevalence of low back pain: a systematic review of the literature from 1966 to 1998. J Spinal Disord 2000; 13:205-217. 3. Von Korff M, Dworkin SF, Le Resche L, Kruger A. An epidemiologic comparison of pain complaints. Pain 1988;32:173-183. 4. Carroll LJ, Hogg-Johnson S, van der Velde G, Haldeman S, Holm LW, Carragee EJ, Hurwitz EL, Cote P, Nordin M, Peloso PM, Guzman J, Cassidy JD; Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Course and prognostic factors for neck pain in the general population: results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine (Phila Pa 1976) 2008;33(4 Suppl):S75-S82. 5. Lawrence RC, Helmick CG, Arnett FC, Deyo RA, Felson DT, Giannini EH, Heyse SP, Hirsch R, Hochberg MC, Hunder GG, Liang MH, Pillemer SR, Steen VD, Wolfe F. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum 1998;41:778-799. 6. Loney PL, Stratford PW. The prevalence of low back pain in adults: a methodological review of the literature. Phys Ther 1999;79:384-396. 7. Schiottz-Christensen B, Nielsen GL, Hansen VK, Schodt T, Sorensen HT, Olesen F. Long-term prognosis of acute low back pain in patients seen in general practice: a 1-year prospective follow-up study. Fam Pract 1999;16:223-232. 8. Van den Hoogen HJ, Koes BW, Deville W, van Eijk JT, Bouter LM. The prognosis of low back pain in general practice. Spine (Phila Pa 1976) 1997;22:1515-1521. 9. Stanton TR, Henschke N, Maher CG, Refshauge KM, Latimer J, McAuley JH. After an episode of acute low back pain, recurrence is unpredictable and not as common as previously thought. Spine (Phila Pa 1976) 2008;33:2923-2928. 10. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002;137:586-597. 11. Jeong GK, Bendo JA. Spinal disorders in the elderly. Clin Orthop Relat Res 2004;(425):110-125. 요추및경추통증을유발하는퇴행성척추질환의병태생리 305

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