NC453G-2思婷

NC453G-2王思婷 9580047

撰寫人：9580047 王思婷NC453- Glossary

Archicerebellum

Oldest part of the cerebellum. Includes the flocculus and nodulus and is related to equilibrium.

【譯】古/原小腦：小腦最老的一部份。其包含小腦的絨球和小結以及它和平衡有關。

【補充】

The Cerebellum (小腦) →http://basic.shsmu.edu.cn/passw/anatomy_new/wskt/Cerebellum.swf →202.194.14.235/xtjpx/ppt2/20.The%20Cerebellum.ppt

小腦外形(相關介紹、圖片及影片) http://202.116.0.143/jnujpx/ziyuan/zhongshu/gelun/50xiaonaowaixing.htm

小腦位於大腦半球後方，覆蓋在腦橋及延髓之上，橫跨在中腦和延髓之間。它由胚胎早期的菱腦分化而來，是腦六個組成部分中僅次於大腦的第二大結構。

外部形態

中部狹窄稱小腦蚓vermis，兩側膨大部稱小腦半球，小腦下面靠小腦蚓兩側小腦半球突起稱小腦扁桃體tonsil of cerebellum。

內部結構

皮質

髓質(髓體)：頂核、中間核(拴狀核、球狀核)、齒狀核。

小腦的分葉

按形態結構和進化可分為：絨球小結葉flocculonodular lobe(原小腦或古小腦)，小腦前葉anterior lobe(舊小腦)，小腦後葉posterior lobe(新小腦)。

按機能可分為：前庭小腦(原小腦或古小腦archicerebellum)，脊髓小腦(舊小腦paleocerebellum)，大腦小腦(新小腦neocerebellum)

小腦的纖維聯繫和功能

前庭小腦：調整肌緊張，維持身體平衡。

脊髓小腦：控制肌肉的張力和協調。

大腦小腦：影響運動的起始、計畫和協調，包括確定運動的力量、方向和範圍。

小腦的進化

原始的小腦出現在圓口類的七鰓鰻。在大多數魚類，小腦還不發達，體積小，表面光滑，它只是橫跨在第四腦室上方的一小塊凸起的頂壁。軟骨魚綱中的鯊魚小腦較大，表面甚至出現溝裂，這是比較特殊的例外。兩栖類和爬行類的小腦不發達，表面也缺乏溝回。少數在海中洄游的龜類小腦的體積在整個腦中佔有較大的比重。爬行類的小腦內部開始出現神經核團，這標誌小腦接受傳入資訊和發出傳出聯繫增多。鳥類的小腦非常發達，在種系發生上顯得突出。它的小腦體積大，表面溝回緊湊，位於內側的新小腦部分特別發達，接受來自脊髓的傳入纖維和來自上位腦結構的投射纖維數量增多，與之相應的傳出聯繫也更為廣泛，因而腦橋及橄欖核亦隨之發達。到了哺乳類，小腦進一步發展，新小腦、舊小腦及古小腦分部清楚，表面的溝回變得更為複雜，神經核團更加分化、發達，其生理功能也更為完善和重要。

解剖

從外觀上看，小腦中間有一條縱貫上下的狹窄部分，捲曲如蟲，稱為蚓部。蚓部兩側有兩個膨隆團塊稱為小腦半球。在小腦蚓部和半球表面有一些橫行的溝和裂，將小腦分成許多回、葉和小葉。在這些橫貫小腦表面的溝和裂中，後外側裂和原裂是小腦分葉的依據。後外側裂將小腦分成絨球小結葉和小腦體兩大部分，而原裂又將小腦體分成前葉和後葉。這樣，前葉、後葉和絨球小結葉便構成了小腦3個橫向組成的分部。在小腦的分葉中，為了簡化命名，拉塞爾提出羅馬字的命名系統，他將小腦蚓部從前到後按Ⅰ～Ⅹ次序分成10個小葉；對小葉的半球部分，則在代表各小葉的羅馬字前冠以H，例如HⅥ即表示小腦第Ⅵ小葉的半球部分。從發生學的觀點來看，絨球小結葉出現最早，是小腦最古老的部分，被稱為古小腦，它主要接受來自前庭核和前庭神經的傳入纖維，調節軀幹肌肉的活動，在維持肌緊張、身體平衡和姿勢等方面起重要作用；前、後葉的蚓部及後葉蚓部的後外側部出現得稍晚，稱為舊小腦，其主要功能與頭部和身體的本體感受和外感受的傳入資訊有關，有調節肌緊張的作用；小腦半球的大部分和部分蚓部發展得最晚，稱為新小腦，它在人類最為發達，主要接受經腦橋接轉的來自大腦皮質的纖維，參與由大腦皮層發起的隨意運動的調節。在位相性的活動和肌肉的協調運動過程中起重要作用。

小腦的表面被覆著一層灰質，叫做小腦皮層；皮層的下方是小腦髓質，由出入小腦的神經纖維和4對小腦深部核團組成。小腦皮層分為3層，從表及裏分別為分子層、浦肯野氏細胞層和顆粒細胞層，皮層裏含有星狀細胞、籃狀細胞、浦肯野氏細胞、高爾基氏細胞和顆粒細胞等5種神經元。在這些細胞中只有浦肯野氏細胞發出軸突離開小腦皮層，成為小腦皮層中唯一的傳出神經元；其他4種均為中間神經元，它們的神經末梢都分佈在小腦皮層之內。所有小腦葉片都有同樣的神經組織結構（圖2）。在分子層內，星狀細胞和籃狀細胞（亦稱內星狀細胞）的軸突走向均與小腦葉片的長軸相垂直。每個星狀細胞都有抑制性的軸樹突觸與數個浦肯野氏細胞的樹突相接觸，每個籃狀細胞都有抑制性的軸體突觸通過它的筐籃狀神經末梢與數個浦肯野氏細胞的胞體相接觸；在顆粒層內，每個顆粒細胞有一個胞體和4～6支短的樹突。顆粒細胞的軸突向上伸至分子層，在那裏呈T字形分成兩支，以相反的方向沿著葉片的長軸走行，被稱為平行纖維，其長度可達5～7毫米。平行纖維與浦肯野氏細胞、星狀細胞、籃狀細胞和高爾基氏細胞的樹突形成興奮性的軸樹突觸。高爾基氏細胞位於顆粒層的上部，它的樹突分支伸向分子屋，軸突卻終止於顆粒層，與顆粒細胞的樹突和苔狀纖維的末梢共同組成小腦小球，成為一種突觸複合體，即苔狀纖維的末梢與顆粒細胞的樹突之間為興奮性突觸，高爾基氏細胞的軸突與顆粒細胞的樹突之間為抑制性突觸；在浦肯野氏細胞層內，浦肯野氏細胞的胞體排列整齊有序，其樹突分支伸向分子層，沿與葉片相垂直的平面分佈，而它的軸突則向下穿出小腦皮層，與小腦深部核團的神經元接觸而形成抑制性突觸。每個浦肯野氏細胞的軸突都有返行的側支與其他的浦肯野氏細胞、高爾基氏細胞及籃狀細胞構成抑制性突觸。在小腦左、右半球深部的髓質中，每側各埋藏著4個由神經細胞群構成的神經核團，由內側向外側分別為頂核、栓狀核、球狀核和齒狀核，其中栓狀核和球狀核常合稱為間位核。 小腦與外部的聯繫通過3對由小腦傳入和傳出纖維組成的巨大神經纖維束進行，分別稱為上、中、下小腦腳或小腦臂。小腦借這3對腳與腦幹相連，而且通過它們與其他的神經結構相聯繫，是小腦與外部聯繫的必經之路。在小腦腳中，傳出纖維占四分之一，而傳入纖維約占四分之三。

由小腦皮層的傳出神經元浦肯野氏細胞軸突構成的傳出纖維，首先到達小腦的深部核團，在這些核團轉換神經元後，再離開小腦。從小腦皮層浦肯野氏細胞到小腦深部核團的纖維聯繫，稱為皮層—核團投射。這種投射具有一定的方位特徵，蚓部皮層的浦肯野氏細胞主要投射到頂核，部分投射到前庭外側核；半球部皮層的浦肯野氏細胞投射到齒狀核；介於蚓部和半球之間的旁蚓皮層的浦肯野氏細胞則投射到頂核和齒狀核之間的間位核。根據皮層—核團投射的這種解剖學特徵，可將小腦分成三個縱向區：①內側區，由蚓部皮層和它所投射到的頂核共同組成，該縱區管理整個軀體的姿勢、肌緊張和平衡；②外側區，由半球皮層和齒狀核組成，管理同側肢體的靈巧運動；③間位區，由旁蚓皮層和間位核組成，管理同側肢體的姿勢和靈巧運動。近年的研究，又進一步將上述3個縱區劃分為7個縱區。

在小腦的傳入方面，一般可分為苔狀纖維和攀緣纖維兩個傳入系統。苔狀纖維傳入系統包括：來自身體的本體感受器和外感受器的衝動，通過脊髓小腦束、楔小腦束傳至小腦前葉，來自腦幹及小腦深部核團的衝動，通過網狀核群經網狀小腦束投射到小腦前葉和蚓部，這些纖維大部分為不交叉的投射；來自頭部本體感受器和外感受器的衝動，經三叉神經核和三叉小腦束投射到小腦的第Ⅴ和第Ⅵ小葉;來自前庭神經的第1級纖維和前庭神經核的第2級纖維，組成前庭小腦束投射到絨球小結葉皮層和鄰近小腦皮層，以及終止於頂核；來自大腦皮層的衝動，經皮層腦橋束下行到達腦橋核，再經腦橋小腦束投射到新、舊小腦的皮層。這些傳入小腦的纖維共同組成了苔狀纖維傳入系統。攀緣纖維傳入系統包括來自大腦皮層、腦幹網狀核群、紅核以及小腦深部核團的衝動，投射到延髓的下橄欖核，然後投射到對側的全部小腦皮層。從下橄欖核到小腦皮層的投射有著相當精細的對應關係。下橄欖核為一板層結構，由背側副橄欖核、主橄欖核和內側副橄欖核等3個部分組成。副橄欖核的不同部分投射到小腦蚓部皮層的不同縱區，主橄欖核的背板和腹板投射到一側小腦半球，而主橄核的外側枝和背帽則投射到絨球小結葉。此外，由於研究的不斷深入，還提出了小腦第3傳入系統，即單胺能神經元傳入投射。它與苔狀纖維和攀緣纖維有著不同的形態學和生理學特徵。這種單胺能神經纖維的數量較苔狀纖維和攀緣纖維要少得多。根據單胺能神經元傳入末梢產生和釋放的遞質不同，又可將它進一步分為去甲腎上腺素能投射和5-羥色胺能投射。前者起源于延髓的藍斑，投射到整個小腦皮層，以蚓部、絨球和腹側旁絨球最為密集；後者起源於中縫核群，投射到除小腦皮層第Ⅵ小葉以外的幾乎所有區域，其中第ⅥAⅩ小葉的蚓部和HⅧA部位的皮層投射密度最大。第3傳入系統在小腦可能起一種調節作用，而不是象苔狀纖維或攀緣纖維傳入系統那樣起著特異資訊的傳遞作用。 形態學和電生理學研究證明在小腦有一種皮層核團的微複合體的結構與機能單位。這一單位是由小腦皮層核團投射的微縱區，以及與它相對應的下橄欖核—小腦皮層區投射共同組成。有人測算人類小腦的結構與機能單位多達5 000個。由於皮層核團微複合體的活動，使小腦在調控運動中對於信號的處理更為精確。

功能

小腦通過它與大腦、腦幹和脊髓之間豐富的傳入和傳出聯繫，參與軀體平衡和肌肉張力（肌緊張）的調節，以及隨意運動的協調。小腦就象一個大的調節器。人喝醉酒時走路會晃晃悠悠，就是因為酒精麻痹了小腦。有一個實驗：將一隻狗摘除小腦，狗走路就會失去協調。

調節軀體平衡

小腦對於軀體平衡的調節，是由絨球小結葉，即古小腦進行的。軀體的平衡調節是一個反射性過程，絨球小結葉是這一反射活動的中樞裝置。軀體平衡變化的資訊由前庭器官所感知，經前庭神經和前庭核傳入小腦的絨球小結葉，小腦據此發出對軀體平衡的調節衝動，經前庭脊髓束到達脊髓前角運動神經元，再經脊神經到達肌肉，協調了有關頡頏肌群的運動和張力，從而使軀體保持平衡。例如，當人站立而頭向後部仰時，膝和踝關節將自動地作屈曲運動，以對抗由於頭後仰所造成的身體重心的轉移，使身體保持平衡而不跌倒。在這一過程中，膝與踝關節為配合頭向後仰而作的輔助性屈曲運動，就是由於小腦發出的調節性衝動，協調了有關肌肉的運動和張力的結果。如果絨球小結葉受到損傷，將破壞軀體的平衡機能。切除了絨球小結葉的猴不能站立，總是坐在籠子的角落裏，以籠子的兩邊支撐身體來保持平衡。在人類，絨小結葉如受損傷或壓迫，患者的身體平衡將嚴重失調，身體傾斜，走路時步態蹣跚。研究還表明，蚓部皮層也接受與軀體平衡有關的本體感覺和視覺衝動的傳入，頂核與前庭核之間有許多纖維來往。因此，由蚓部皮層和頂核組成的縱向內側區也參與了軀體平衡，主要是站立的調節。內側區的損傷也將造成平衡和站立的困難。

調節肌緊張

肌緊張是肌肉中不同肌纖維群輪換地收縮，使整個肌肉處於經常的輕度收縮狀態，從而維持了軀體站立姿勢的一種基本的反射活動。小腦可以調節肌緊張活動，其調節作用表現為抑制肌緊張和易化肌緊張兩個方面。小腦抑制肌緊張的作用主要是前葉（舊小腦）蚓部的機能，這一抑制作用在去大腦動物上表現得最為明顯。刺激去大腦貓小腦前葉的蚓部，可以減弱動物因去大腦而造成的伸肌過度緊張現象；反之，切除該部位則使去大腦僵直加強，這些現象都說明小腦有抑制肌緊張的作用。小腦對肌緊張的易化作用是由前葉的兩側部位來實現的。刺激猴的小腦前葉兩側部位，可加強伸肌的緊張狀態，並減弱層肌的緊張；在人類，這個部位的損傷則引起肌無力或低緊張現象。小腦前葉對於肌緊張的抑制或易化作用是通過腦幹網狀結構中的肌緊張抑制區和易化區實現的。這兩個區是控制骨骼肌緊張的中樞部位，它們通過下行的網狀脊髓束控制脊髓前角的γ運動神經元的活動。易化區的下行衝動可以加強γ運動神經元的活動，使肌緊張加強；抑制區則可減弱γ運動神經元的活動，使肌緊張減弱。在正常情況下，腦幹網狀結構的肌緊張抑制區和易化區的活動，在高級中樞大腦、紋狀體和小腦等的影響下保持著動態的平衡，從而使肌緊張維持在正常的狀態，如果由於某種原因加強或減弱了小腦（前葉的蚓部或外側部）對腦幹網狀結構肌緊張抑制區或易化區的影響，將會破壞這兩個低級中樞之間原有的平衡，使肌緊張活動加強或減弱。此外，小腦還可以通過前庭外側核調節肌緊張活動。從前庭外側核有前庭脊髓束到達脊髓，緊張性衝動通過這條下行的傳導束，提高脊髓前角α運動神經元的活動，使肌緊張加強。從小腦的蚓部皮質到前庭外側核有直接的和經頂核接轉的間接纖維投射，其中的直接纖維投射對於前庭外側核來說是一條抑制性的通路，它減弱前庭外側核的緊張性活動，進而使脊髓前角α運動神經元的活動水平下降，導致肌緊張的減弱；從蚓部皮層經頂核到前庭外側核的間接投射則是一條興奮性的通路，頂核可以通過這條通路加強前庭外側核的活動，其最終結果是使肌緊張活動加強。所以，局限於蚓部皮層的損傷，使去大腦動物的僵直現象加強；頂核的損傷則使去大腦動物的肌張力減弱。

協調隨意運動

意運動是大腦皮層發動的意向性運動，而對隨意運動的協調則是由小腦的半球部分，即新小腦完成的。新小腦的損傷，將使受害者的肌緊張減退和隨意運動的協調性紊亂，稱為小腦性共濟失調。主要的表現有：①運動的準確性發生障礙。產生意向性震顫現象，當病人留意做某動作，如用手指鼻時，手指發生顫抖，愈接近目標，手指顫抖得愈厲害，因而不能把握運動的準確方向。②動作的協調性發生障礙。患者喪失使一個動作停止而立即轉換為相反方向的動作的能力，運動時動作分解不連續。例如，病人不能完成快速翻轉手掌這類簡單、快速的輪替運動，稱為輪替運動失常；當完成一個方向的運動並需要轉換運動的方向時，患者必須先停下來思考下一步的動作，才能再重新開始新的運動。所有這些列舉的症狀只在運動中表現出來，說明新小腦對隨意運動起著重要的協調作用，這種協調作用，是小腦對大腦皮層和脊髓活動進行調節的結果。在大腦皮層與小腦之間存在著雙向的神經連接，大腦皮層發出傳導運動資訊的錐體束在下行過程中，有側枝在橋腦的腦橋核換神經元，再由腦橋核發出纖維進入小腦，形成皮層—腦橋小腦束；而小腦向大腦皮層的投射，由新小腦皮層的浦肯野氏細胞的軸突投射到深部的齒狀核，再由齒狀核發出纖維出小腦，經丘腦腹外側核到達大腦皮層的運動區，這就是齒狀核—丘腦皮層束，這兩條傳導束構成了小腦調節大腦皮層運動區活動的基本環路。當大腦皮層運動區將引起肌肉收縮的運動衝動經錐體束傳向脊髓的時候，也同時有側枝衝動經皮層—腦橋小腦束到達小腦。有關的肌肉在接受到這些運動衝動而發生收縮時，肌肉中的肌梭等本體感受器又將它們所感受的有關肌肉運動的本體衝動，經脊髓小腦束傳入小腦。這樣，在隨意運動進行的每一瞬間，小腦即接受到大腦皮層給出的引起運動的指令，又獲取了肌肉執行運動指令的資訊。在對兩者進行比較之後，小腦皮層的浦肯野氏細胞發出的衝動對小腦深部核團，主要是齒狀核的活動進行調整，再由齒狀核發出衝動經齒狀核—丘腦皮層束反饋到大腦皮層運動區，通過易化或抑制作用相應地調整了大腦皮層運動區的活動。在另一方面，小腦在接受脊髓小腦束傳來的肌肉運動的本體資訊後，還經紅核和紅核脊髓束將調節性衝動傳向脊髓，調整運動神經元的活動。小腦就是這樣在隨意運動進行的過程中，即時、不斷地調整著大腦皮層運動區、紅核和脊髓的活動，使運動能夠準確、平穩和順利地進行。 新小腦皮層的外側部（外側區）和內側部（間位區）及其相應的投射核團齒狀核和間位核，在隨意運動的起始和完成中起著不同的作用。小腦皮層的外側區和齒狀核，通過其與大腦皮層之間的交互聯繫，在隨意運動發生的早期與大腦皮層聯絡區、基底神經節、丘腦腹外側核等神經結構一起，參加了隨意運動的設計和運動程式的編制；而小腦皮層的間位區和間位核則參加了隨意運動的執行。例如，在猴開始做腕關節的屈或伸運動之前，小腦深部的齒狀核和間位核就有細胞放電的變化，但是，齒狀核細胞的放電變化卻發生在間位元核細胞之前，而且放電的型式也較間位核細胞複雜，這種反應時間的先後及反應型式的差別，表明小腦半球的這兩個縱區及其相應的投射核團，在隨意運動中起著不同的作用。 此外小腦與運動性的學習記憶和心血管活動也有一定的關係。在家兔瞬膜條件反射的形成和保持中，海馬CA1、CA3區、小腦皮層第Ⅵ小葉的半球部分（H Ⅵ）以及間位核的有關神經元均能產生學習關聯性發放。損毀小腦皮層H Ⅵ和間位核，可使上述條件反射以及海馬CA1、CA3區的學習關聯性發放消失。電刺激小腦頂核的嘴側部能引起明顯的心血管反應，包括動脈血壓明顯升高；心率加快、心律異常，壓力感受性和化學感受性調製作用的改變等，這種心血管反應稱為頂核升壓反應。

Archicerebellum：The small, phylogenetically oldest portion of the cerebellum, also called vestibulocerebellum because its afferents arise from the vestibular ganglion and nuclei; in mammals, it is represented by four subdivisions of the cerebellum: nodulus, uvula vermis, flocculus, and lingula of cerebellum. That portion of the cerebral cortex that, with the paleocortex, develops in association with the olfactory system, and which is phylogenetically older than the neocortex and lacks its layered structure. The embryonic archicortex corresponds to the cortex of the dentate gyrus and hippocampus in mature mammals. Called also archaeocortex or archeocortex, archipallium, and olfactory cortex.

Origin：[archi- + cerebellum] archi- 表示〝主要的〞；〝為首的〞；〝大的〞；〝第一的〞。

維基百科http://en.wikipedia.org/wiki/Archicerebellum

arcuate fasciculus

Fibers of the superior longitudinal fasciculus known to connect the association cortices of Broca area with Wernicke area.

【譯】弓狀束：縱向的上神經纖維束。連接大腦皮層的布洛卡氏區和韋尼克氏區。

Picture?

http://www.lib.mcg.edu/edu/eshuphysio/program/section8/8ch15/s8c15_14.htm

http://williamcalvin.com/LOS96.html

【補充】

弓狀束（Arcuate fasciculus）：額葉和顳葉間主要的傳導徑路，將字的音、形傳入Broca區。 傳導型失語症 (Conduction aphasia)：其主要的特徵是明顯的複誦障礙，患者也有命名上的困難，但卻有不錯的聽覺和閱讀理解能力。這類患者在語音上的錯誤是常見的，但病患常傾向於自我更正這方面的錯誤，但最後並不見得會成功，這種現象就是所謂的「conduitee d’approche」。此型和威氏型的比較是患者的理解能力比複述能力好；和布氏型的比較是其口語表達是流暢的。此類型的病患，腦病變常涉及緣上回或其下白質部分，也就是弓狀束（arcuate fasciculus）。

大部份成人的左大腦半球是處於語言最重要的部位。用右手的人當中，約99%的人的語言中樞是在左大腦半球，其他慣用左手的人，約65%的人的語言中樞也是在左大腦半球。 一個人了解別人所講，所寫或將這些訊息表達出來的能力，需要大腦皮質許多區域協調。聽到一種訊息後，神經衝動便由耳朵傳到大腦第一聽覺區。而了解這訊息代表之意義前，則必須經過大腦皮質中Wernicke區的處理（位於temporal lobe中，緊接第一聽覺區旁邊）。 若訊息是由寫的，這時候在第一視覺區所接收的訊息就必須傳道角回（Angular gyrus位於頂葉，為視覺性語言中樞，在Wernicke區的上面，才能了解所看到的影像的意義）。 輸出口語訊息時必須先將要傳遞的思考形式化，再選擇適當的用字連接起來成為輸出的訊息，思考的形式化及用字的選擇就是Wernicke區與角回的功能。在Frontal lobe的後側方有一個Broca區，可控制用字的各種形式。至於Wernicke區與Broca區的聯繫，則由一很大的神經纖維束稱為弓形束（Arcuate fasciculus），將這些神經訊息由Temporal lobe的Wernicke區傳遞到位於Frontal lobe的Broca區，進而使其相鄰的運動皮質興奮，然後作用於講話的肌肉，使其完成作用。

傳達性失語症（Conduction Aphasia）： 病人在接受語言及表達語言上沒有困難，但無法覆誦或朗讀。這種情形發生在弓形束（Arcutate Fasciculus）的傷害，也就是顳葉與額葉之間的聯絡被阻隔。此類的病人能自由自在的講話而沒有人任何困難，可了解自己及別人所講的話，其主要的缺陷是在選字方面，所以病人常因說話錯誤而感到挫折。 臨床表徵： 1.說話平順流暢，但措詞不當。 2.病人可了解對方談話內容和書報雜誌的內容，但無法與對方交談，也無法照書出聲朗讀。 3.無法重複對方談話。 4.無法說出物件名稱。 5.書寫字體端正清晰，但內容雜亂。

Speech Functions: The Arcuate Fasciculus

Good picture! Web source?

Lesions affecting the arcuate fasciculus, a white matter tract connecting Wernicke's and Broca's speech regions, results in conduction aphasia. Like persons with Wernicke's aphasia, conduction aphasiacs have many paraphasic errors, in which incorrect words or sounds are substituted. Speech fluency may be less than typical Wernicke's patients, but comprehension is usually good. Lack of normal input from Wernicke's cortex to Broca's cortex deprives affected persons of the ability to repeat and name. Although reading aloud is abnormal, conduction aphasiacs are able to read silently with good comprehension.

Good picture! Web source?

The arcuate fasciculus (Latin, curved bundle) is the neural pathway connecting the posterior part of the temporoparietal junction with the frontal cortex in the brain. 《Function》 In the cerebral hemisphere specialised for language, this pathway is thought to connect Broca's area to Wernicke's area. It is thought to connect areas of the brain involved in the generation and understanding of language. 《Pathology》 Damage to this pathway can cause a form of aphasia known as conduction aphasia, where auditory comprehension and speech articulation are preserved, but people find it difficult to repeat heard speech.

arcuate fasciculus -->superior longitudinal fasciculus Long association fibre bundle lateral to the centrum ovale of the cerebral hemisphere, connecting the frontal, occipital, and temporal lobes; the fibres pass from the frontal lobe through the operculum to the posterior end of the lateral sulcus where many fibres radiate into the occipital lobe and others turn downward and forward around the putamen and pass to anterior portions of the temporal lobe.

相關網站http://thebrain.mcgill.ca/flash/d/d_10/d_10_cr/d_10_cr_lan/d_10_cr_lan.html http://www.dls.ym.edu.tw/neuroscience/lang_c.htm

Argyll Robertson pupil

Impaired papillary reaction to light while the near vision reflex is preserved. Commonly seen with degenerative brain diseases such as Alzheimer disease and with encephalopathy and diabetes.

【譯】Argyll Robertson氏瞳孔：(對光無調節反應，見於中樞神經性梅毒及近視)。對於光，瞳孔的反應受損。常見於一些退化的腦性疾病，例如：阿茲海默症、腦病及糖尿病。

【補充】

亞羅伯頓氏瞳孔(Argyll Robertson pupil--兩眼會協同動作，但不會對光反應。) 代表可能有梅毒、糖尿病或是中樞神經的疾病。

Definition：pupil unconstricted in bright light: a pupil that does not constrict when exposed to bright light but that contracts normally when the eye focuses on a near object.

Pupils of the eye which react to accommodation but not to light. Seen in cases of tertiary syphilis.

Argyll Robertson pupil：a form of reflex iridoplegia characterized by miosis, irregular shape, and a loss of the direct and consensual pupillary reflex to light, with normal pupillary constriction to a near vision effort (light-near dissociation); often present in tabetic neurosyphilis.

Argyll Robertson pupil(From Wikipedia, the free encyclopedia) Argyll Robertson pupils (“AR pupils”) are bilateral small pupils that constrict when the patient focuses on a near object (they “accommodate” with near vision), but do not constrict when exposed to bright light (they do not “react” to light). They were formerly known as "prostitute's pupils" because of their association with syphilis and because, like a prostitute, they “accommodate but do not react.”). They are a highly specific sign of neurosyphilis. Pupils that “accommodate but do not react” are said to show light-near dissociation. A video of AR pupils and light-near dissociation is available at http://content.lib.utah.edu/u?/EHSL-Moran-Neuro-opth,60 AR pupils are extremely uncommon in the developed world. There is continued interest in the underlying pathophysiology, but the scarcity of cases makes ongoing research difficult. 《History》 The AR pupil was named after Douglas Moray Cooper Lamb Argyll Robertson, a Scottish ophthalmologist who noted the association with syphilis in 1869. When serological tests for syphilis became available, patients with AR pupils usually tested positive for syphilis. The AR pupil became known as a reliable clinical sign of syphilis. In the early 20th century, Adie described a second type of pupil that could “accommodate but not react.” Adie’s tonic pupil is usually associated with a benign peripheral neuropathy (Adie syndrome), not with syphilis. When penicillin became widely available in the 1940s, the prevalence of AR pupils (which develop only after decades of untreated infection) decreased dramatically. AR pupils are now quite rare. A patient whose pupil “accommodates but does not react” almost always has a tonic pupil, not an AR pupil. In the 1950s, Loewenfeld distinguished between the two types of pupils by carefully observing the exact way in which the pupils constrict with near vision. The near response in AR pupils is brisk and immediate. The near response in tonic pupils is slow and prolonged.《Pathophysiology》 The two different types of near response are caused by different underlying disease processes. Adie's pupil is caused by damage to peripheral pathways to the pupil (parasympathetic neurons in the ciliary ganglion that cause pupillary constriction to bright light and with near vision). The AR pupil is thought to be caused by damage to central pathways for pupillary constriction. Specifically, the AR pupil is thought to be caused by selective damage to pathways from the retina to the Edinger-Westphal nucleus. These light-sensitive pathways allow the pupil to constrict to bright light. The accommodation pathways – pathways to the Edinger-Westphal nucleus that cause the pupils to constrict with near vision – are thought to be spared because of their more ventral course in the brainstem. The exact relationship between syphilis and the two types of pupils (AR pupils and tonic pupils) is not known at the present time. The older literature on AR pupils did not report the details of pupillary constriction (brisk vs. tonic) that are necessary to distinguish AR pupils from tonic pupils. Tonic pupils can occur in neurosyphilis. It is not known whether neurosyphilis itself (infection by Treponema pallidum) can cause tonic pupils, or whether tonic pupils in syphilis simply reflect a coexisting peripheral neuropathy. Thompson and Kardon (2006) summarize the present view: The evidence supports a midbrain cause of the AR pupil, provided one follows Loewenfeld’s definition of the AR pupil as small pupils that react very poorly to light and yet seem to retain a normal pupillary near response that is definitely not tonic. To settle the question of whether the AR pupil is of central or peripheral origin, it will be necessary to perform iris transillumination (or a magnified slit-lamp examination) in a substantial number of patients who have a pupillary light-near dissociation (with and without tonicity of the near reaction), perhaps in many parts of the world. 《Parinaud syndrome》 A third cause of light-near dissociation is Parinaud syndrome, also called dorsal midbrain syndrome. This uncommon syndrome involves vertical gaze palsy associated with pupils that “accommodate but do not react.” The causes of Parinaud syndrome include brain tumors (pinealomas), multiple sclerosis and brainstem infarction. Due to the lack of detail in the older literature and the scarcity of AR pupils at the present time, it is not known whether syphilis can cause Parinaud syndrome. It is not known whether AR pupils are any different from the pupils seen in other dorsal midbrain lesions.

Good picture! Web source?

Arnold-Chiari malformation

Developmental malformation marked by a downward herniation of the medulla and cerebellum in the vertebral canal of the cervical region. Often associated with spinal bifida and hydrocephaly.

【譯】先天性小腦延髓下疝畸形：是後顱窩中線結構在胚胎時期的異常發育，使小腦扁桃體疝入枕骨大孔內，從而引起延髓、上頸髓受壓、腦脊液迴圈不暢導致顱內壓升高等所表現的一組綜合症。

http://www.thefetus.net/page.php?id=88

http://faculty.washington.edu/alexbert/MEDEX/Fall/csf.jpg

【補充】

Chiari畸形 小腦扁桃體下疝畸形（Arnold-Chiari malformation），又稱Chiari畸形，是因後顱凹中線腦結構在胚胎期中的發育異常，小腦扁桃體向下延伸，或和延髓下部甚至Ⅳ腦室，經枕大孔突入頸椎管的一種先天性發育異常。 　　【病理與發病】 　　目前，對本病的發病機制意見不一，多認為下疝是在胚胎期後顱凹中線結構腦組織過度生長延伸，加之後顱凹的容積縮小，更促使其向下穿經枕大孔疝入頸椎管內。有的甚至降至樞椎或更低，以至嚴重損害小腦、腦幹和高位頸髓、頸神經等，並可引起腦積水。本病常合併其他枕大畸形，如顱底凹陷、寰枕融合、扁平顱底、頸椎分節不全等。 【臨床表現】 輕度小腦扁桃體下疝可無症狀，外傷、感染、咳嗽及腰椎穿刺可誘發症狀或使症狀加重。由小腦扁桃體下疝引起的症狀大體有以下幾方面： 　顱神經和頸神經症狀　 表現為聲音嘶啞、吞咽困難、頸項部疼痛及活動受限等。 　　腦幹延髓症狀　　 可出現肢體運動障礙，偏癱和四肢癱，四肢感覺障礙，及大小便障礙等。 　　 小腦症狀　　　 可出現共濟失調，走路不穩及眼球震顫。 顱內壓增高症狀　 可出現頭疼、嘔吐、眼底水腫及視力下降等腦積水表現的。 脊髓空洞症表現　 伴有脊髓空洞時可出現感覺分離或雙上肢肌萎縮等。 　　【診斷】 　　根據以上的臨床表現，結合MRI檢查，診斷不難成立。 MRI檢查可以清楚地顯示小腦扁桃體下疝的具體部位，有無延髓及第四腦室下疝，腦幹的移位，有無脊髓空洞及腦積水等。X線平片檢查及CT可瞭解顱頸部骨性畸形情況。 　　【治療】 　　以手術治療為主要手段，其目的是解除枕大孔及頸椎對小腦、腦幹、脊髓、第四腦室及其他神經組織的壓迫，疏通腦脊液迴圈，緩解神經受壓症狀和腦積水。 　　對少數小腦扁桃體下疝嚴重的病人，可考慮切除小腦扁桃體；有證據提示Ⅳ腦室正中孔粘連者，可予顯微分離；有腦積水者酌情行分流術。

malformed posterior fossa structures associated with caudad traction and displacement of the rhombencephalon as caused by tethering of the spinal cord; may or may not be accompanied by spina bifida and associated anomalies such as meningomyelocele; this malformation is usually multifactorial in inheritance; very weak evidence of autosomal recessive inheritance.

arnold-chiari malformation： Chiari I herniation of medulla and cerebellar tonsils, 4th ventricle in normal position, Chiari II herniation of medulla, tonsils, vermis, 4th ventricle at foramen magnum, myelomeningocele, aqueductal stenosis most likely to be hydrocephalus, Chiari III further herniation, 4th ventricle below foramen magnum, encephalocele or myelomeningocele associated with: agenesis of corpus callosum, syrinx

Arnold-Chiari malformation(From Wikipedia, the free encyclopedia) Arnold-Chiari malformation, sometimes referred to as Chiari II malformation or ACM, is a congenital malformation of the brain. Arnold-Chiari Malformation (Chiari II malformation) occurs in almost all children born with both spina bifida and hydrocephalus. German pathologist Hans Chiari in the late 1800's described seemingly related anomalies of the hindbrain, the so called Chiari malformations I, II and III. Later, other investigators added a fourth (Chiari IV) malformation. The scale of severity is rated I - IV, with IV being the most severe. Arnold Chiari Malformation specifically refers to the Chiari II malformation. 《Cause》 The cerebellar tonsils are elongated and pushed down through the opening of the base of the skull (see foramen magnum), blocking the flow of cerebrospinal fluid (CSF). The brainstem, cranial nerves, and the lower portion of the cerebellum may be stretched or compressed. Therefore, any of the functions controlled by these areas may be affected. The blockage of CSF flow may also cause a syrinx to form, eventually leading to syringomyelia. Many sufferers turn to The Chiari Institute in Long Island, NY for specialized medical attention and medication. Established in 2001, The Chiari Institute is a division of the Harvey Cushing Institutes of Neuroscience of the North Shore-Long Island Jewish Health System. 《Presentation》 In infants, the most common symptoms are stridor and swallowing difficulties. In older children, upper (and lower as age marches on) limb weakness and breathing difficulties may occur. Patients may experience no symptoms or remain asymptomatic until early adulthood, at which point they will often experience quick onset severe headaches and neck pain. Fatigue, dizziness, vertigo, neuropathic pain, pain at the point of tethering, visual disturbances, difficulty swallowing, ringing in the ears, sleep apnea, impaired fine motor skills, muscle weakness, and palpitations and excessive clearing of the throat with no obstructions are other common symptoms. Because of the complex combination of symptoms and the lack of experience with ACM1 had by many, even outstanding, neurologists and neurosurgeons, patients are frequently misdiagnosed. Some patients may go an entire lifetime without having noticeable symptoms. Or, symptoms can be minimal, then turn severe suddenly due to head trauma which alters the condition of the spine, brain, or cerebellar tonsils and begins to cause more difficulties. A Chiari malformation may be congenital or acquired. Research is still being done to determine its causes. In some cases it can be hereditary, and numerous cases exist of multiple members of one family having the condition. It is common for adults to start showing noticeable symptoms when they are in the mid to late 30's. It is more common in women than in men. 《Treatment》 Once symptomatic onset occurs, the most frequent treatment is decompression surgery, in which a neurosurgeon seeks to open the base of the skull and through various methods unrestrict CSF flow to the spine. This treatment is well recognized and accepted with many studies published (involving a total of hundreds of patients) in well respected peer reviewed medical journals showing that about 80% of patients obtain improvement. A small number of neurological surgeons believe that detethering the spinal cord as an alternate approach relieves the compression of the brain against the skull opening (foramen magnum) obviating the need for decompression surgery and associated trauma. However, this approach is significantly less documented in the medical literature with reports on only a handfull of patients. It should be noted that the alternative spinal surgery is also not without risk. 《History》 An Austrian pathologist, Hans Chiari, first described these hindbrain malformations in the 1890s. A colleague of Professor Chiari, Dr. Julius Arnold later contributed to the definition of the condition, and students of Dr. Arnold suggested the term "Arnold-Chiari malformation" to henceforth refer to the condition.

相關病變─Louis-Bar氏綜合症

又稱共濟失調—毛細血管擴張症，為一種特殊類型的原發性免疫缺陷病，是一獨立疾病。 病因病理病機 病因未明。屬常染色體隱性遺傳。由於DNA修復缺陷，第14對染色體易位所引起，具有體液免疫和細胞免疫異常，突出的表現為胸腺發育障礙、淋巴系統形成不全、皮膚粘膜毛細血管擴張，各臟器可見巨核症。 臨床表現 特徵為進行性小腦變性、眼結膜和皮膚毛細血管擴張以及感染傾向等三個主要症狀。 男女發病率相等。嬰兒期即出現小腦性共濟失調，開始主要影響軀幹和頭部，10歲左右即不能獨行，在意向性震顫、構音障礙、假性球麻痹、眼球震顫、面具樣臉、震動覺減退及手足徐動症等。20 ～30歲時脊髓受累，深感覺缺失，病理反射陽性。毛細血管擴張通常在3～6歲出現，見於全部病人的眼結膜，50%病人的皮膚暴露部位，偶見於耳殼。1/3病人智力減退，有時性功能障礙。60～80%有感染傾向，多數病孩伴發惡性腫瘤，多數病孩因反復呼吸道感染和（或）淋巴系統腫瘤而於青春期死亡。血液低球蛋白血症，IgA和IgE選擇性缺乏。周圍血淋巴細胞減少。氣腦造影見小腦萎縮。 鑒別診斷 （一）顱底陷入症（basilar invagination） 為先天性畸形。絕大多數在成年後起病，臨床症狀與畸形程度可不一致，病情多進展緩慢，但呈進行性加重。主要表現聲音嘶啞、舌肌萎縮、言語不清、吞咽困難等後組顱神經症狀，以及枕頂部疼痛、上肝麻木、腿反射減低或消失等，眼球震顫、小腦共濟失調等症狀較輕。枕大孔區X線攝片上測量樞椎齒狀突的位置可診斷。 （二）先天性小腦延髓下疝畸形（Arnold- Chiari malformation） 為先天性畸形。主要表現為延髓、上頸髓受壓症狀，以及顱神經、頸神經為根症狀，小腦症狀表現為眼球震顫、步態不穩等，可合併顱內高壓征。為明確診斷和鑒別診斷，可做椎動脈造影、CT、MRI。 （三）多發性硬化（multiple Sclerosis） （四）小腦腫瘤（cerebellar tumor） 主要表現為患側肢體協調動作障礙、語音不清、眼球震顫。肌張力明顯減低，腿反射遲鈍或消失，或有步態不穩，逐漸發展為行走不能，站立時向後傾倒，可伴有顱內壓增高症狀。CT、MRI可明確診斷 。 （五）進行性核上性麻痹（progressive supranuclear plasy） 多見於中年或老年，病程呈進行性。主要表現為核上性眼肌麻痹、錐體外系性肌強直、癡呆、球麻痹及步態不協調等。常規檢驗均正常，腦脊液也無顯著異常。腦電圖示不規則慢波，但無局灶性改變。CT見橋腦及中腦萎縮。

Arteriosclerosis

Narrowing of arterial lumen owing to accumulation of lipids, fatty substance, and cholesterol along intimal walls of blood vessels. Also called atherosclerosis.

【譯】動脈硬化：由於血管內膜壁積聚脂質、脂肪的物質和膽固醇，造成逐漸狹窄的動脈內腔。也稱作〝(動脈)粥樣硬化〞。

lipids = fatty substance

【補充】

中華民國血脂及動脈硬化學會 http://202.168.199.76/tas/index.htm

動脈硬化之病理成因

隨著西風東漸，心臟及腦血管疾病已經分別躍居93 年國人死因亞軍、季軍。而動脈粥狀硬化造成的急慢性缺血性疾病則是其主 流。 愈來愈多的証據支持「動脈粥狀硬化是一種發炎性疾病」的論點。藉由不利的遺傳特質、糖尿病、高血壓、高血脂症、抽菸等危險因子的搧風點火，啟動免疫系統，在動脈管域建立灘頭堡、伺機茁壯並開花結果，危害生命的延續。 透過高血脂症對血管的肆虐模式可以管窺動脈粥狀硬化的病理機轉。或因血管內皮的通透性增強，或因與蛋白多糖結合而延長停留期間，低密度脂蛋白膽固醇得以滲透並局部聚積於動脈內膜。聚積於動脈內膜而與蛋白多糖結合的低密度脂蛋白膽固醇容易被氧化並釋出磷脂質，進而激活覆蓋在表層的內皮細胞，喚醒其炎性基因、增加附著器的佈署。內皮細胞一旦接合上血小板就會被啟動合成白血球接受器。內膜區緊接著釋出化學物質，召喚已接合、以單核球及淋巴球為主的白血球進入內膜區，蛻變為巨噬細胞。大量的巨噬細胞吞噬脂蛋白顆粒形成最初期的病灶－脂肪斑紋－粥狀動脈硬化斑塊的前身。脂肪斑紋雖然可以發展成為粥狀動脈硬化斑塊，它也可能消褪、不留痕跡。 一些生長因子可以誘使平滑肌細胞由中皮層移居內皮層並且開始分裂繁殖、生產膠原纖維。因此，相對於以滿腹脂肪之巨噬細胞為主的脂肪斑紋，粥狀動脈硬化斑塊則富含由平滑肌細胞所合成的細胞外膠原纖維性基質；除了外圍以膠原纖維為主的頂冠，核心盡是泡沫細胞和細胞外脂肪粒。肥大細胞、巨噬細胞、T細胞等炎性細胞會滲透浸潤硬化斑塊；緊臨正常內膜的斑塊區－肩部－通常炎性細胞的數量最多、活性最強、釋放的炎性物質最多，因此頂冠比較薄、脆弱。硬化斑塊的裂痕常見於肩部，吸引血小板等的粘黏、聚集，形成血栓、阻滯血流，臨床上呈現不穩定心絞痛、急性心肌梗塞、中風等急症。 免疫系統中備有抗發炎的剎車機制，藉以遏止粥狀動脈硬化的建立及推進。動脈硬化之緩和或惡化決定於炎性及抗炎性強度的平衡。良好的生活型態，包括戒菸、低脂飲食、多運動等，可以強化抗炎性因子，趨吉避凶，減緩甚或避開動脈硬化的厄運。

Atherosclerosis http://www.nlm.nih.gov/medlineplus/ency/article/000171.htm http://en.wikipedia.org/wiki/Arteriosclerosis

Atherosclerosis is a Disease affecting the Arterial Blood Vessel. It is commonly referred to as a "hardening" or "furring" of the Arteries. It is caused by the Formation of Multiple Plaques Within the Arteries.

A group of diseases in which the walls of the arteries get thick and hard. In one type of arteriosclerosis, fat builds up inside the walls and slows the blood flow. These diseases often occur in people who have had diabetes for a long time.

Arteriosclerosis: Hardening and thickening of the walls of the arteries. Arteriosclerosis can occur because of fatty deposits on the inner lining of arteries (atherosclerosis), calcification of the wall of the arteries, or thickening of the muscular wall of the arteries from chronically elevated blood pressure (hypertension).

Imprecise term for various disorders of arteries, particularly hardening due to fibrosis or calcium deposition, often used as a synonym for atherosclerosis.

Arteriosclerosis： Main Entry: ar·te·rio·scle·ro·sis Pronunciation: \är-ˌtir-ē-ō-sklə-ˈrō-səs\ Function: noun Etymology: New Latin Date: 1881 : a chronic disease characterized by abnormal thickening and hardening of the arterial walls with resulting loss of elasticity

arteriovenous malformation

Congenital condition in which tangled and twisted arteries and veins are interconnected in a localized area, where the arterial blood shunts to the veins, bypassing the cortical tissue.

【譯】動靜脈畸形瘤：一種先天性的狀況。混亂纏繞的動脈和靜脈相互連接於局部的區域，而此處是動脈內的血液經由皮質組織轉換流通到靜脈去。

http://images.google.com/images?sourceid=gmail&q=arteriovenous+malformation&um=1&ie=UTF-8&sa=N&tab=wi

http://www.neurosurgery.ufl.edu/Patients/avm.html

http://www.neurosurgery.ufl.edu/Images/AVM1.jpg

【補充】

腦內「定時炸彈」-動靜脈畸形瘤 （Arteriovenous malformation AVM） 一般在急診處如發生年輕人突然發生劇烈頭痛噁吐，接著馬上出現神經能障礙：或手腳無力或語言障礙或癲癇發作。他們都是醫院急診處之常客‧ 一、定義與病因： 一種先天性的血管畸形(二十歲以下居多)動脈靜脈間無微血管存在, 動脈血直接流到靜脈(靜脈壓大使血管易破裂出血)畸形會隨時間直而變大(癲癇症狀變多) ；導致腦動脈瘤的病因有先天性血管異常、動脈硬化、 高血壓。
二、疾病之症狀： 1. 出血：年輕人出血性腦中風最主要的原因，因為靜脈端承受不了壓力而破裂，導致嚴重的腦出血嚴重時可以致命。 2. 頭痛：有如頭部被棒子重擊一般、頸部僵硬、噁心、嘔吐，因血流異常、血管畸形導致出現血流漩渦而發生頭痛。多半是發生在較大的AVM。 3. 神經機能障礙 ：盜血症候群慢性進行性半身無力，因為血流改道，導致 AVM周圍之神經組織缺氧而發生機能失常。通常是進行性的，也就是會逐漸惡化與加重。動脈瘤增大時，神經被壓迫的現象，例如眼瞼下垂、複視、瞳孔擴大等。 4. 癲癇發作：通常局部性及感覺性因為AVM附近之腦細胞得不到正常的血液供應而使電波異常，再誘發癲癇發作。 三、處理原則： 1. 觀察- 因每年出血機率約2%，目前主張應該手術治療。 2. 開顱手術- 對簡單的病例畸形全切除是理想的手術對某些病人是高危險群甚至是致命的，手術的成功端視AVM 之大小、位置與複雜度，手術最主要目的是完全切除AVM‧ 3. 加馬刀手術-侵襲性最小的手術；放射線照射使畸形血管內皮細胞增生血管壁逐漸變厚最後整個管壁完全堵塞血流不再通過自然沒有再出血的危險呈現的症狀也會改善(此過程約一至二年) 4. 術後的定期追蹤：治療後每隔六個月影像檢查一 次 ，第二或三年血管攝影檢查證實痊癒否。 四、預防之方法： 預防的方法除了控制高血壓和禁菸外，同時必須注意到腦動脈瘤破裂大出血前之警告信號。 五、結語： 動靜脈畸形是一種血管異常，往往在出現症狀後才會被診斷出來，有時來勢洶洶甚至導致病人之死亡‧「突發性頭部劇痛」時，別忘了找神經外科專科醫師診治，如未能及早處理其後遺症是半身不遂、失語症、意識障礙甚或死亡。

arteriovenous malformation：A congenital disorder of the veins and arteries where arteries are connected directly to veins rather than through capillaries that distribute oxygen and nutrients. These connections, often called a nidus, can be extremely fragile and prone to bleeding.

Arteriovenous malformation (AVM): An arteriovenous malformation (AVM) is a congenital disorder (one present at birth) of blood vessels in the brain, brainstem, or spinal cord that is characterized by a complex, tangled web of abnormal arteries and veins connected by one or more fistulas (abnormal communications). The AVM has no capillary bed of its own and the fistulas in the AVM permit high-speed, high-flow shunting of blood from the arterial to the venous side of the circulation. This shunting causes low blood pressure (hypotension) in the arterial vessels feeding the AVM and neighboring areas of the brain that they normally supply with blood. AVMs typically cause problems before the age of 40. The most common symptoms of AVM include hemorrhaging (bleeding), seizures, headaches, and neurological problems such as paralysis or loss of speech, memory, or vision. The frequency of hemorrhage in various series ranges from 30-82%. AVM rupture accounts for 2% of all strokes. There are three general forms of treatment for AVM: Surgery, which is the best-known and longest-standing treatment for AVM. Surgery for an AVM involves identifying the margins of the malformation, ligating (tying off) or clipping the feeder arterial vessels, obliterating the draining veins, and removing or obliterating the nidus (the nest) of the AVM. Endovascular occlusion, which involves closing off the vessels of the AVM by one of various nonsurgical means. Catheters can deliver agents to block the blood vessels that include permanent balloons, thrombosing (clogging) coils, sclerosing (hardening) drugs, and fast-acting embolization glue (embolization is often used before surgery). Radiosurgery, which involves focusing multiple radiation beams on the AVM so as to injure and thrombose (clog) the AVM. The effect of radiosurgery takes weeks to months to become fully manifest. A real danger of radiosurgery is damage to neighboring nervous system tissue, normal brain (or spinal cord) tissue around the AVM. Therefore, radiosurgery is usually reserved for AVMs that are relatively small (less than 3 cm in diameter), situated so deep within important brain tissue that surgery is hazardous, or have so many feeder arteries that embolization is not feasible. Most people (perhaps 80% or more) with AVMs never experience problems due to them. However, AVMs that hemorrhage can lead to serious neurological problems, and sometimes death.

Arteriovenous Malformation of the Brain Arteriovenous malformation (AVM) of the brain is also a "short circuit" between the arteries (which carry blood from the heart to the tissues) and veins (which carry blood from the tissues back to the heart). Normally the connection between arteries and veins is through a network of smaller vessels called capillaries, which slow the blood down and permit the exchange of food, oxygen and nutrients into the tissues. In arteriovenous malformations, the arteries and veins have a direct connection, bypassing the capillary network.

Web source of this picture?

This network of abnormal connections represents the "nidus". Arteriovenous malformation of the brain presents later in childhood or, more frequently, in adults in the second to third decade of life. AVMs present with seizures, hemorrhage, progressive neurological dysfunction or headaches. On occasion, these lesions are found incidentally during an MRI or CT scan of the brain obtained for other reasons (see below).

Web source of this picture?

An AVM nidus AVMs can be difficult to treat and often require a multidisciplinary approach to therapy. At the Center for Endovascular Surgery, embolization is the first line of attack in the management of this condition. Embolization for arteriovenous malformation may be done as the sole form of treatment or in preparation for microsurgical resection or radiation therapy. For patients with AVMs that cannot be cured due to the size or location of their lesion, palliative embolization can improve the patient's quality of life and diminish symptoms such as headaches, seizures or other problems.

arteriovenous malformation：http://en.wikipedia.org/wiki/Arteriovenous_malformation