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a major division of the vertebrate brain; situated above the medulla oblongata and beneath the cerebrum in humans

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小脳

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/06/03 13:48:31」(JST)

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小脳（しょうのう、英: cerebellum、ラテン語で「小さな脳」を意味する）は、脳の部位の名称。脳を背側から見たときに大脳の尾側に位置し、外観がカリフラワー状をし、脳幹の後ろの方からコブのように張り出した小さな器官である。脳幹と小脳の間には第四脳室が存在する。重さは成人で120～140グラムで、脳全体の重さの10％強をしめる。大脳の10分の1しかないのに、大脳の神経細胞よりもはるかに多くの神経細胞がある。脳の神経細胞の大部分は、小脳にあり、その数は1000億個以上である。小脳の主要な機能は知覚と運動機能の統合であり、平衡・筋緊張・随意筋運動の調節などを司る。このため、小脳が損傷を受けると、運動や平衡感覚に異常をきたし、精密な運動ができなくなったり酒に酔っているようなふらふらとした歩行となることがある。小脳が損傷されると、そうした症状が起きるが、意識に異常をきたしたり知覚に異常を引き起こすことはない。このため、かつては高次の脳機能には関係がなく、もっぱら運動を巧緻に行うための調節器官だとみなされ、脳死問題に関する議論が起きた際も人の生死には関係がないので、小脳は脳死判定の検査対象から外すべきと主張する学者もいた。ところがその後、小脳がもっと高次な機能を有していると考えられる現象が相次いで報告された。また、アルツハイマー病の患者の脳をPETで調べたところ、頭頂連合野や側頭連合野が全く機能していないにもかかわらず、小脳が活発に活動していることが判明した。アルツハイマー病の患者では例外なく小脳が活動しており、通常より強化されている。これは大脳から失われたメンタルな機能を小脳が代替していると考えられている。伊藤正男は、小脳は大脳のシミュレーターであって、体で覚える記憶の座と表現した^[1]。

小脳の傷害が運動障害を引き起こすことを最初に示したのは、18世紀の生理学者たちであった。その後19世紀初頭～中盤にかけて、実験動物を用いた小脳切除・病変形成実験が行われ、小脳傷害が異常運動・異常歩様・筋力低下の原因となることが明らかにされた。これらの研究成果に基づき、小脳が運動制御に重要な役割を果たすという結論が導かれたのである^[2]。

協調運動制御のため、小脳と大脳運動野（情報を筋肉に伝達し運動を起こさせる）および脊髄小脳路（身体位置保持のための固有受容フィードバックを起こす）を結ぶ多くの神経回路が存在する。小脳は運動を微調整するため体位に対し絶えずフィードバックをかけることで、これらの経路を統合している^[2]。

1 発生と進化
2 構造と機能
- 2.1 区分
- 2.2 深部小脳核
- 2.3 小脳皮質
- 2.4 小脳脚
- 2.5 小脳髄質
3 血液供給
4 機能障害
- 4.1 小脳症候
- 4.2 上肢の小脳症候診察
- 4.3 下肢、体幹の小脳症候診察
5 出典・脚注
6 関連文献
7 関連項目
8 外部リンク

発生と進化

小脳の位置を様々な角度から見た動画。赤いところが小脳。

S. カハールによるニワトリ小脳のスケッチ。その構造や構成細胞は、ヒトを含む哺乳類とほとんど変化が無い。左上に見える、樹状の突起を伸ばした細胞がプルキンエ細胞である。

脳の発生は、胚発生の早期における前脳・中脳・菱脳の形成から始まる。菱脳は胚脳の最も尾側に位置し、ここから小脳の発生が起こる。菱脳から菱形部（rhombomeres）と呼ばれる8つの隆起が形成され、このうち神経管（最終的に脳と脊髄になる）の翼板に位置する2つから小脳が発生する。

小脳を構成する神経細胞は2つの領域から発生すると考えられている。1つ目の領域は第四脳室上方に位置する脳室帯である。この領域からは、小脳皮質の主要な出力ニューロンであるプルキンエ細胞と深部小脳核神経細胞が作られる。2つ目の領域は外顆粒層として知られる領域である。この細胞層は小脳の外側を覆い、顆粒細胞を産生する。ヒトの場合、外顆粒層の顆粒細胞は出生後に内側に移動し、内顆粒層に到達する。この移動により、外顆粒層は成熟した小脳では消失している。これら2つの領域に加え、小脳白質からも神経細胞の発生があるかについては統一見解が得られていない。

小脳の系統発生学的起源は、古皮質（archipallium）と呼ばれる最も原始的な脳の構成領域の1つにまでさかのぼる。小脳皮質の神経回路は、魚類から哺乳類に至る脊椎動物全般にほぼ共通した構造を持つ。これは小脳が全脊椎動物において重要な機能を果たしていることの証拠であると考えられている。

構造と機能

小脳縦断面の模式図。白質（図の白色部分）の分岐による小脳活樹の構造が明瞭である。

小脳は頭尾方向正中に存在する小脳虫部と左右一対の小脳半球から成っている。小脳表面には横走する溝（小脳溝）が存在し、小脳溝により小脳回が分けられている。小脳は上小脳脚、中小脳脚、下小脳脚によってそれぞれ中脳、橋、延髄と結ばれていて、多くの入出力線維が通っている。

小脳は大脳と同じく、灰白質と白質を持つ。白質はその樹木に類似した分岐構造から小脳活樹（arbor vitae、生命の木）と呼ばれ、4つの深部小脳核を含んでいる。小脳は大まかな機能に基づいて、3つの発生学的（肉眼的でもある）部位に分けられている。3層から成る小脳皮質には特徴的な細胞群が見られ、様々な入出力回路を形成している。酸素を含んだ血液が、脳底動脈・椎骨動脈より分岐する3本の動脈枝から供給される。

区分

小脳は3つの異なる観点（解剖学、系統発生学および機能）から区分される。

解剖学的区分

小脳は肉眼的に、片葉小節葉、前葉（小脳第一裂の吻側）、後葉（小脳第一裂の背側）の3部位に区分される。後二者は正中線に位置する小脳虫部と、外側の小脳半球にさらに分けられる。

系統発生学的・機能的区分

小脳は系統発生学的、あるいは機能的区分に基づいて3つに分類することができる（下表参照）。小脳機能の多くは、小脳傷害・病変に罹患した患者からのデータ分析、あるいは動物実験によって理解されてきた。

機能的名称（系統発生学的名称）	解剖学的部位	役割
前庭小脳 (古小脳)	片葉小節葉（小脳虫部に隣接する）	身体平衡と眼球運動を調節する。半規管と前庭神経核からの入力信号を受け取り、前庭神経外側核・内側核に出力する。また、上丘と視覚野からの視覚信号の入力（後者は橋核を経由する）を受け取る。前庭小脳の傷害は、平衡と歩様の異常を引き起こす。
脊髄小脳（旧小脳）	小脳虫部および小脳半球の中間部分（"paravermis"）	体幹と四肢の運動を制御する。三叉神経、視覚系、聴覚系および脊髄後索（脊髄小脳路を含む）からの固有受容信号を受信する。深部小脳核へと出力された信号は大脳皮質と脳幹に達し、下位の運動系を調節する。脊髄小脳には感覚地図が存在し、身体部位の空間的位置データを受け取っている（小脳虫部は体幹と四肢の近位、paravermisは四肢の遠位）。運動の最中に、身体のある部位がどこへ動くかを予測するため、固有受容入力信号の詳細な調節を行うことができる。
大脳小脳（新小脳）	小脳半球の側面部分	運動の計画と感覚情報の評価を行う^[3]。大脳皮質（特に頭頂葉からの全入力を、橋核を経由して受け取り、主に視床腹外側に出力する。信号は前運動野、一次運動野および赤核に達し、下オリーブ核を通って再び小脳半球へとリンクする。

深部小脳核

橋における横断面。第4脳室の背側に深部小脳核を認める。

小脳の中心、白質の内部に4対の神経核、深部小脳核が存在する。これらの神経核は小脳皮質のプルキンエ細胞から抑制性の入力信号（GABA介在性）を、苔状線維からは興奮性の信号（グルタミン酸介在性）を受け取る。小脳の出力線維の大半は小脳核から起始する。例外的に、片葉小節葉からの線維は小脳核を経由することなく、直接前庭神経核にシナプスを形成する。脳幹にあるこの前庭神経核は、苔状線維とプルキンエ細胞からの入力信号を両方受け取るという点で、深部小脳核と類似した構造である。

外側から中央部にかけ、歯状核・栓状核・球状核・室頂核の4つの深部小脳核が位置する。一部の動物種では栓状核と球状核の区別が不明瞭で、代わりに挿入核と呼ばれる単一の神経核を持つ。栓状核と球状核が明瞭に分かれている動物種においても、挿入核という用語は二核をまとめた意味でしばしば使用される。

一般的に、どの神経核も小脳の解剖学的区分と関連している。歯状核は小脳半球外側の深部にあり、挿入核は中間帯に、室頂核は小脳虫部に位置する。これらの構造的関連性は、神経核と小脳皮質の神経回路において維持されている。すなわち、歯状核は小脳半球外側からの神経刺激の大半を受け取り、挿入核・室頂核はそれぞれ中間帯・虫部からの信号のほとんどを担当している。

小脳皮質

小脳の表面は、小脳皮質と呼ばれる灰白質が覆っており、3層の層構造を示す。表層から順に分子層、プルキンエ細胞層、顆粒層の3層である。皮質の機能は、深部小脳核へと送られる情報を制御することである。苔状線維と登上線維（下オリーブ核から起始）によって深部小脳核に伝達された感覚運動情報は、そこから様々な運動野へと転送され、運動の出力とタイミングを制御する。苔状線維・登上線維はさらに、この情報を小脳皮質にも送り込み、プルキンエ細胞の「発火」を調節する。プルキンエ細胞は強力な抑制性シナプスを通じて、小脳核へのフィードバックを行う。この抑制刺激は苔状線維・登上線維が活性化できる小脳核の範囲を調節し、小脳が運動機能に果たす最終的な効果をコントロールしている。小脳皮質のシナプスの強さは、その可塑性にあることが示されている。これにより小脳皮質の回路は常時適切に保たれ、出力を微調整し、運動の学習・協調の基礎を形成することが可能となっている。小脳皮質のどの層にも、この回路を構成する様々な細胞が含まれている。

顆粒層

マウス小脳皮質の共焦点顕微鏡画像。プルキンエ細胞層には、洋梨状のプルキンエ細胞（GFPにより緑色蛍光を発している）が一列に並んでいる。これより上方の、樹状突起が伸びている部分が分子層、下方の暗い領域が顆粒層である。顆粒層のさらに下、横方向に線維が走行している部位（画像のほぼ中央）が白質にあたる。

皮質の最深部にある顆粒層には、2種類の神経細胞－小型で数の多い顆粒細胞と、大型のゴルジ細胞－が分布する。主に橋核から起始する苔状線維は、顆粒細胞と興奮性シナプスを形成する。顆粒細胞は、平行線維と呼ばれる特徴的なT字型の軸索を分子層に伸ばしており、プルキンエ細胞の樹状突起と非常に多くの（数百から数千）シナプスを作る。ヒトの小脳には600～800億個もの顆粒細胞が存在し、これは脳と脊髄にある全神経細胞の、実に7割を占めている。

ゴルジ細胞は顆粒細胞とシナプスを形成し、抑制性刺激を伝達する。

プルキンエ細胞層

皮質の中間層に存在する神経細胞は、大型のプルキンエ細胞のみである。プルキンエ細胞は小脳皮質を代表する統合的ニューロンであり、小脳からの出力信号を発する唯一の神経細胞である。その細胞体からは樹状突起と呼ばれる突起が分子層に伸び、数百におよぶ分岐を持つ。樹状突起の伸び方は平面的であり、隣同士の樹状突起が平行に重なり合うような構造をとっている。顆粒細胞から伸びる平行線維とは直角に交わる。プルキンエ細胞はGABA作動性であり、深部小脳核および脳幹の前庭神経核と抑制性シナプスを形成する。1つのプルキンエ細胞が、およそ10万～20万本の平行線維からの興奮性刺激を受け取る。

分子層

小脳皮質の最外層である分子層には、2種類の抑制性ニューロン（星状細胞と籠細胞）が存在する。また、プルキンエ細胞の樹状突起や顆粒細胞から伸長する平行線維も、分子層の重要な構成要素である。星状細胞・籠細胞はともに、プルキンエ細胞の樹状突起とGABA作動性シナプスを形成する。

小脳脚

小脳脚の走行を示した模式図。小脳は3種類の小脳脚によって中脳・橋・延髄と結ばれている。

小脳は3種類の脳脚（束状の神経線維）によって、出入力信号を外部の臓器と伝達し合う。それぞれの小脳脚は上小脳脚（結合腕）・中小脳脚（橋腕）・下小脳脚（索状体）と呼ばれる。

小脳脚の名称	機能
上小脳脚（superior peduncle）	小脳の主要な出力経路で、赤核・視床外側腹側核/前腹側核・延髄などと連絡する。大半は歯状核から起始する遠心性線維から成るが、前脊髄小脳路から小脳前葉へと繋がる求心性線維の一部が、上小脳脚を経由している。「歯状核 → 赤核 → 視床 → 前運動皮質」と「小脳 → 視床 → 前運動皮質」の2経路が、上小脳脚を通る主なルートであり、運動の立案に重要な役割を果たす。
中小脳脚（middle peduncle）	最大の小脳脚であり、「大脳皮質 → 橋 → 小脳」を結ぶ壮大な経路の一部を成す。全て橋核に起始する遠心性線維で構成される。この経路は大脳新皮質の感覚・運動野から下行する。
下小脳脚（inferior peduncle）	様々な種類の出入力線維を含む。平衡や姿勢の保持など、運動前庭機能を伴う固有感覚入力の統合に、主に関与する。全身からの固有情報は後脊髄小脳路を通じて下小脳脚に伝達され、旧小脳にシナプスを形成する。前庭の情報は古小脳に至る。また、下オリーブ核から起始する登上線維も下小脳脚を通るほか、プルキンエ細胞から直接受け取った情報を、脳幹背側に位置する前庭神経核に送る役割を持つ。

延髄の横断面。下オリーブ核と下小脳脚、オリーブ小脳路を含む。

小脳に入力信号を送るルートに苔状線維と登上線維がある。苔状線維は主に橋核に始まり、対側大脳皮質からの情報を伝達するが、脊髄小脳路から起始し同側脊髄からの情報を伝えるものもある。登上線維は下オリーブ核に由来する。1個のプルキンエ細胞の樹状突起につき、1本の登上線維が興奮性シナプスを形成する。

小脳からの出力信号のほとんどは、小脳脚に送られる前に小脳核を経由する。重要な例外ルートとして、プルキンエ細胞による前庭神経核の直接抑制がある。

小脳髄質

小脳皮質の下は、小脳髄質と呼ばれる白質である。

血液供給

上小脳動脈・前下小脳動脈・後下小脳動脈の3種類の動脈が、小脳に血液を供給している。

上小脳動脈（SCA）

脳底動脈の側面、後大脳動脈に繋がる部分の下流から分岐する。橋を経由して小脳に到達する。SCAは小脳皮質・小脳核・上小脳脚・中小脳脚で使われる血液の大半を供給する。

前下小脳動脈（AICA）

脳底動脈の側面、椎骨動脈との接続部の上流から分岐する。橋の下部、小脳橋角を通過して小脳に至る。小脳前下部のほか、顔面神経と内耳神経にも血液を供給する。AICAの損傷は不全麻痺・麻痺・顔面感覚の喪失、さらには聴覚障害の原因となる。小脳橋角に梗塞が起きると、鐙骨筋（顔面神経の支配を受ける）の機能障害による聴覚過敏や、内リンパ流の加速（内耳神経の影響を受ける）によるめまいが発症する。

後下小脳動脈（PICA）

脳底動脈の側面、椎骨動脈との接続部の下流から分岐する。小脳後部表層に達する前に延髄でも分岐し、いくつかの脳神経核にも血液を送り込む。PICAは小脳後下部のほか、下小脳脚・疑核・迷走神経運動核・三叉脊髄核・孤束核・内耳神経核への血液供給を担う。

機能障害

運動失調は小脳に損傷を受けた場合にしばしば見られる症状で、一般的には協調運動の欠如による複雑な病態である。小脳の異常を見つけるために、歩様と姿勢の検査を含む神経学的検査が行われる。出血・梗塞・腫瘍・変性などの構造的異常は、断層撮影で明らかになることもある。小脳の検査には、MRI検査の方がCTスキャンよりも感受性が強いとされる^[4]。

小脳症候

小脳失調を考える上で理解する必要がある小脳の運動機能は2つである。1つは意図する運動全体の企画やプランの具体的実行司令を作成するという事である。目的の運動を達成するためにはどの筋肉をどの順番で動かせばよいかというような意識に上らない実行司令の作成である。2つ目は運動の実行司令と実際の運動との差の補正である。これは起こってしまった運動だけではなく起こりつつあると予想される運動の補正も含まれる。運動の補正に関しては小脳のfunctional unitの関与がわかっている。このユニットへの情報入力は中小脳脚と下小脳脚を介しており出力系はプルキンエ細胞である。プルキンエ細胞では入力された様々な情報が処理されて実行司令を小脳核から上小脳脚を介して大脳に送っている。小脳徴候は実行司令の不良と補正の不良を見る場合がほとんどである。古典的な神経診断学では小脳症候を小脳遠心系の障害、小脳歯状核の障害、中小脳脚の障害と分類することはほとんどできない。多くの小脳症候は深部感覚障害、麻痺、錐体外路障害でもみられる。しかし異常のパターンが病態によって異なる。

測定障害(dysmetria)

目的物めがけて運動している時に、目的物の空間的位置に対する実行司令が障害されており目的物に到着しないことである。空間的な位置に関する実行プランの不良である。目的物を通り過ぎる測定過大（hypermetria）と手前で止まる測定過小（hypometria）がある。測定過大が小脳症候として特徴的である。麻痺、深部感覚障害、錐体外路障害でも測定障害は認められる。深部感覚障害では測定過大と測定過小ともに認められミスの仕方に一貫性がない。錐体外路障害では測定過小、麻痺では測定過大が多い。被験者が測定過大することを見越して運動することもあるが、素早く行わせるとこの補正も効かなくなるので検査時はすばやく運動させることも重要である。

運動の分解（decomposition）と共同運動障害（dyssynergia）

運動がスムーズに行えず、一つ一つに分解されてしまうことをいう。

変換運動障害（dysdiadochokinesis）

ある運動を繰り返し行うことが難しく、リズムが乱れたり（時間的に乱れる）、運動そのものが空間的に乱れたりする現象である。この障害の原因は時間測定障害（dyschronometria）と考えられている。麻痺や深部感覚障害、錐体外路障害でも認められるが、小脳症候では運動を早くすると悪化し、ゆっくりすると改善する傾向がある。

時間測定障害（dyschronometria）

運動を始めようとした時に開始が遅くなるという所見としてあらわれる。

筋肉のトーヌスの低下（hypotonus）

小脳の筋紡錘への制御に異常が生じて筋トーヌスが下がるとされている。

眼球運動障害

測定過大が眼球運動にも認められocular dysmetriaといわれる。眼振は小脳特有のものは少なく、rebound nystagmusが比較的特有である。これは注視した後、正中位に戻した時に逆向きに認められる眼振である。また小脳片葉病変ではdown beat nystagmusが認められる。

不随意運動

不随意運動としては口蓋帆振戦（口蓋帆ミオクローヌス）とaction myoclonusとaction tremorが知られている。口蓋帆振戦は規則的に軟口蓋が動く病態であり歯状核オリーブ路が傷害されると認められる。action myoclonusとaction tremorは安静時には何も症状がないが運動を始めようとすると大きな不随意運動が出現することである。

上肢の小脳症候診察

指鼻指試験（finger-nose-finger test）

自分の鼻と検者の指を交互にさわる検査である。測定過大と運動分解を評価できる。深部感覚障害では閉眼で行うと悪化する視覚補正がある。また深部感覚障害ではずれ方に傾向がない。小脳失調では測定過大となり、パーキンソン病など固縮がある場合は測定過小をおこす。軽度の麻痺でも異常をしめす。

手回内試験（hand pronation test）

閉眼した状態で両手を回外位で挙上させ、合図とともに両上肢を回内させる。小脳失調があると回内しすぎてしまう。測定過大、時間的測定障害を評価している。

手回内回外試験（hand pronation-spination test）

手の回内、回外を繰り返す検査である。変換障害を評価するものである。小脳に障害があるとリズムが乱れ、遅くなり、運動の大きさも不規則になる。片手ずつべつべつに検査する。一般に利き手のほうが早く上手にできる。指のタッピングも同様の返還運動障害の試験である。

holmes-stewart試験
筋トーヌスの評価

筋トーヌス評価として肩揺すり試験をおこなうこともある。

下肢、体幹の小脳症候診察

踵膝試験（heel knee test)

小脳失調では運動分解と測定過大が認められる。深部感覚障害ではズレかたに一貫性がない。

膝たたき試験（knee-tapping test）

指のtapping試験に相当する。

足の到達動作試験

母趾で検者の指を触るように指示する。

膝立試験

仰向けに寝て片足の膝をたてる。両足をつけずに対側の足を同じ角度に立てるように指示する。深部感覚障害では測定過大、測定過小どちらも示すが小脳失調では測定過大が目立つ。

出典・脚注

^ 立花隆『脳を究める』朝日文庫 2001年3月1日
^ ^a ^b Fine EJ, Ionita CC, Lohr L (2002). “The history of the development of the cerebellar examination”. Semin Neurol 22 (4): 375-84. PMID 12539058.
^ Kingsley, R. E. (2000). Consise Text of Neuroscience (2nd edition ed.). Lippincott Williams and Wilkins. ISBN 0-683-30460-7.
^ Gilman S (1998). “Imaging the brain. Second of two parts”. NEJM. 338 (13): 889-96. PMID 9516225.

外部リンク

小脳 - 看護士による簡潔な概説
小脳、外景、内景、機能 - 慶應義塾大学医学部に勤務する医師による解説
小脳 - 脳科学辞典

wiki en

[Wiki en表示]

The cerebellum (Latin for "little brain") is a region of the brain that plays an important role in motor control. It may also be involved in some cognitive functions such as attention and language, and in regulating fear and pleasure responses,^[1] but its movement-related functions are the most solidly established. The cerebellum does not initiate movement, but it contributes to coordination, precision, and accurate timing. It receives input from sensory systems of the spinal cord and from other parts of the brain, and integrates these inputs to fine-tune motor activity.^[2] Cerebellar damage produces disorders in fine movement, equilibrium, posture, and motor learning.^[2]

Anatomically, the cerebellum has the appearance of a separate structure attached to the bottom of the brain, tucked underneath the cerebral hemispheres. Its cortical surface is covered with finely spaced parallel grooves, in striking contrast to the broad irregular convolutions of the cerebral cortex. These parallel grooves conceal the fact that the cerebellar cortex is actually a continuous thin layer of tissue tightly folded in the style of an accordion. Within this thin layer are several types of neurons with a highly regular arrangement, the most important being Purkinje cells and granule cells. This complex neural organization gives rise to a massive signal-processing capability, but almost all of its output passes through a set of small deep cerebellar nuclei lying in the interior of the cerebellum.

In addition to its direct role in motor control, the cerebellum is necessary for several types of motor learning, most notably learning to adjust to changes in sensorimotor relationships. Several theoretical models have been developed to explain sensorimotor calibration in terms of synaptic plasticity within the cerebellum. Most of them derive from models formulated by David Marr and James Albus, which were based on the observation that each cerebellar Purkinje cell receives two dramatically different types of input: one type of input is made up of thousands of weak inputs from the parallel fibers; the other type is that of an extremely strong input from a single climbing fiber. The basic concept of the Marr–Albus theory is that the climbing fiber serves as a "teaching signal", which induces a long-lasting change in the strength of parallel fiber inputs. Observations of long-term depression in parallel fiber inputs have provided support for theories of this type, but their validity remains controversial.

1 Structure
- 1.1 Gross anatomy
  - 1.1.1 Subdivisions
- 1.2 Microanatomy
  - 1.2.1 Purkinje cells
  - 1.2.2 Granule cells
  - 1.2.3 Mossy fibers
  - 1.2.4 Climbing fibers
  - 1.2.5 Deep nuclei
  - 1.2.6 Compartments
2 Function
- 2.1 Principles
- 2.2 Learning
- 2.3 Theories and computational models
3 Clinical significance
- 3.1 Aging
- 3.2 Developmental and degenerative disorders
4 Comparative anatomy and evolution
- 4.1 Cerebellum-like structures
5 History
- 5.1 Descriptions
- 5.2 Etymology
6 References
7 External links

Structure

At the level of gross anatomy, the cerebellum consists of a tightly folded layer of cortex, with white matter underneath and a fluid-filled ventricle at the base. At the microscopic level, there are four deep nuclei embedded in the white matter. Each part of the cortex consists of the same small set of neuronal elements, laid out in a highly stereotyped geometry. At an intermediate level, the cerebellum and its auxiliary structures can be separated into several hundred or thousand independently functioning modules called "microzones" or "microcompartments".

Gross anatomy

View of the cerebellum from above and behind

The cerebellum is located in the posterior cranial fossa. The fourth ventricle, pons and medulla are in front of the cerebellum.^[3] It is separated from the overlying cerebrum by a layer of leathery dura mater, the tentorium cerebelli; all of its connections with other parts of the brain travel through the pons. Anatomists classify the cerebellum as part of the metencephalon, which also includes the pons; the metencephalon is the upper part of the rhombencephalon or "hindbrain". Like the cerebral cortex, the cerebellum is divided into two hemispheres; it also contains a narrow midline zone (the vermis). A set of large folds is, by convention, used to divide the overall structure into 10 smaller "lobules". Because of its large number of tiny granule cells, the cerebellum contains more neurons than the total from the rest of the brain, but takes up only 10% of the total brain volume.^[4] The number of neurons in the cerebellum is related to the number of neurons in the neocortex. There are about 3.6 times as many neurons in the cerebellum as in the neocortex, a ratio that is conserved across many different mammalian species.^[5]

The unusual surface appearance of the cerebellum conceals the fact that most of its volume is made up of a very tightly folded layer of gray matter: the cerebellar cortex. Each ridge or gyrus in this layer is called a folium. It is estimated that, if the human cerebellar cortex were completely unfolded, it would give rise to a layer of neural tissue about 1 meter long and averaging 5 centimeters wide—a total surface area of about 500 square cm, packed within a volume of dimensions 6 cm × 5 cm × 10 cm.^[4] Underneath the gray matter of the cortex lies white matter, made up largely of myelinated nerve fibers running to and from the cortex. Embedded within the white matter—which is sometimes called the arbor vitae (Tree of Life) because of its branched, tree-like appearance in cross-section—are four deep cerebellar nuclei, composed of gray matter.^[6]

Subdivisions

Schematic representation of the major anatomical subdivisions of the cerebellum. Superior view of an "unrolled" cerebellum, placing the vermis in one plane.

Based on the surface appearance, three lobes can be distinguished within the cerebellum: the anterior lobe (above the primary fissure), the posterior lobe (below the primary fissure), and the flocculonodular lobe (below the posterior fissure). These lobes divide the cerebellum from rostral to caudal (in humans, top to bottom). In terms of function, however, there is a more important distinction along the medial-to-lateral dimension. Leaving out the flocculonodular lobe, which has distinct connections and functions, the cerebellum can be parsed functionally into a medial sector called the spinocerebellum and a larger lateral sector called the cerebrocerebellum.^[6] A narrow strip of protruding tissue along the midline is called the cerebellar vermis. (Vermis is Latin for "worm".)^[6]

The smallest region, the flocculonodular lobe, is often called the vestibulocerebellum. It is the oldest part in evolutionary terms (archicerebellum) and participates mainly in balance and spatial orientation; its primary connections are with the vestibular nuclei, although it also receives visual and other sensory input. Damage to this region causes disturbances of balance and gait.^[6]

The medial zone of the anterior and posterior lobes constitutes the spinocerebellum, also known as paleocerebellum. This sector of the cerebellum functions mainly to fine-tune body and limb movements. It receives proprioceptive input from the dorsal columns of the spinal cord (including the spinocerebellar tract) and from the cranial trigeminal nerve, as well as from visual and auditory systems. It sends fibers to deep cerebellar nuclei that, in turn, project to both the cerebral cortex and the brain stem, thus providing modulation of descending motor systems.^[6]

The lateral zone, which in humans is by far the largest part, constitutes the cerebrocerebellum, also known as neocerebellum. It receives input exclusively from the cerebral cortex (especially the parietal lobe) via the pontine nuclei (forming cortico-ponto-cerebellar pathways), and sends output mainly to the ventrolateral thalamus (in turn connected to motor areas of the premotor cortex and primary motor area of the cerebral cortex) and to the red nucleus.^[6] There is disagreement about the best way to describe the functions of the lateral cerebellum: It is thought to be involved in planning movement that is about to occur,^[7] in evaluating sensory information for action,^[6] and in a number of purely cognitive functions, such as determining the verb which best fits with a certain noun (as in "sit" for "chair").^[8]^[9]^[10]^[11]

Microanatomy

Microcircuitry of the cerebellum. (+): excitatory; (-): inhibitory; MF: Mossy fiber; DCN: Deep cerebellar nuclei; IO: Inferior olive; CF: Climbing fiber; GC: Granule cell; PF: Parallel fiber; PC: Purkinje cell; GgC: Golgi cell; SC: Stellate cell; BC: Basket cell

Transverse section of a cerebellar folium, showing principal cell types and connections

Two types of neuron play dominant roles in the cerebellar circuit: Purkinje cells and granule cells. Three types of axons also play dominant roles: mossy fibers and climbing fibers (which enter the cerebellum from outside), and parallel fibers (which are the axons of granule cells). There are two main pathways through the cerebellar circuit, originating from mossy fibers and climbing fibers, both eventually terminating in the deep cerebellar nuclei.^[4]

Mossy fibers project directly to the deep nuclei, but also give rise to the following pathway: mossy fibers → granule cells → parallel fibers → Purkinje cells → deep nuclei. Climbing fibers project to Purkinje cells and also send collaterals directly to the deep nuclei.^[4] The mossy fiber and climbing fiber inputs each carry fiber-specific information; the cerebellum also receives dopaminergic, serotonergic, noradrenergic, and cholinergic inputs that presumably perform global modulation.^[12]

The cerebellar cortex is divided into three layers. At the bottom lies the thick granular layer, densely packed with granule cells, along with interneurons, mainly Golgi cells but also including Lugaro cells and unipolar brush cells. In the middle lies the Purkinje layer, a narrow zone that contains the cell bodies of Purkinje cells and Bergmann glial cells. At the top lies the molecular layer, which contains the flattened dendritic trees of Purkinje cells, along with the huge array of parallel fibers penetrating the Purkinje cell dendritic trees at right angles. This outermost layer of the cerebellar cortex also contains two types of inhibitory interneuron: stellate cells and basket cells. Both stellate and basket cells form GABAergic synapses onto Purkinje cell dendrites.^[4]

Purkinje cells

A mouse Purkinje cell injected with fluorescent dye

Purkinje cells in the human cerebellum (in orange, from top to bottom 40X, 100X and 200X magnification) stained according to published methods^[13]

Purkinje cells are among the most distinctive neurons in the brain, and one of the earliest types to be recognized—they were first described by the Czech anatomist Jan Evangelista Purkyně in 1837. They are distinguished by the shape of their dendritic tree: The dendrites branch very profusely, but are severely flattened in a plane perpendicular to the cerebellar folds. Thus, the dendrites of a Purkinje cell form a dense planar net, through which parallel fibers pass at right angles.^[4] The dendrites are covered with dendritic spines, each of which receives synaptic input from a parallel fiber. Purkinje cells receive more synaptic inputs than any other type of cell in the brain—estimates of the number of spines on a single human Purkinje cell run as high as 200,000.^[4] The large, spherical cell bodies of Purkinje cells are packed into a narrow layer (one cell thick) of the cerebellar cortex, called the Purkinje layer. After emitting collaterals that innervate nearby parts of the cortex, their axons travel into the deep cerebellar nuclei, where they make on the order of 1,000 contacts each with several types of nuclear cells, all within a small domain. Purkinje cells use GABA as their neurotransmitter, and therefore exert inhibitory effects on their targets.^[4]

Purkinje cells form the heart of the cerebellar circuit, and their large size and distinctive activity patterns have made it relatively easy to study their response patterns in behaving animals using extracellular recording techniques. Purkinje cells normally emit action potentials at a high rate even in the absence of the synaptic input. In awake, behaving animals, mean rates averaging around 40 Hz are typical. The spike trains show a mixture of what are called simple and complex spikes. A simple spike is a single action potential followed by a refractory period of about 10 ms; a complex spike is a stereotyped sequence of action potentials with very short inter-spike intervals and declining amplitudes.^[14] Physiological studies have shown that complex spikes (which occur at baseline rates around 1 Hz and never at rates much higher than 10 Hz) are reliably associated with climbing fiber activation, while simple spikes are produced by a combination of baseline activity and parallel fiber input. Complex spikes are often followed by a pause of several hundred milliseconds during which simple spike activity is suppressed.^[15]

Granule cells

Granule cells (GR, bottom), parallel fibers (horizontal lines, top), and Purkinje cells (P, middle) with flattened dendritic trees

Cerebellar granule cells, in contrast to Purkinje cells, are among the smallest neurons in the brain. They are also easily the most numerous neurons in the brain: In humans, estimates of their total number average around 50 billion, which means that about 3/4 of the brain's neurons are cerebellar granule cells.^[4] Their cell bodies are packed into a thick layer at the bottom of the cerebellar cortex. A granule cell emits only four to five dendrites, each of which ends in an enlargement called a dendritic claw.^[4] These enlargements are sites of excitatory input from mossy fibers and inhibitory input from Golgi cells.^[4]

The thin, unmyelinated axons of granule cells rise vertically to the upper (molecular) layer of the cortex, where they split in two, with each branch traveling horizontally to form a parallel fiber; the splitting of the vertical branch into two horizontal branches gives rise to a distinctive "T" shape. A human parallel fiber runs for an average of 3 mm in each direction from the split, for a total length of about 6 mm (about 1/10 of the total width of the cortical layer).^[4] As they run along, the parallel fibers pass through the dendritic trees of Purkinje cells, contacting one of every 3–5 that they pass, making a total of 80–100 synaptic connections with Purkinje cell dendritic spines.^[4] Granule cells use glutamate as their neurotransmitter, and therefore exert excitatory effects on their targets.^[4]

Granule cells receive all of their input from mossy fibers, but outnumber them by 200 to 1 (in humans). Thus, the information in the granule cell population activity state is the same as the information in the mossy fibers, but recoded in a much more expansive way. Because granule cells are so small and so densely packed, it is difficult to record their spike activity in behaving animals, so there is little data to use as a basis for theorizing. The most popular concept of their function was proposed in 1969 by David Marr, who suggested that they could encode combinations of mossy fiber inputs. The idea is that with each granule cell receiving input from only 4–5 mossy fibers, a granule cell would not respond if only a single one of its inputs were active, but would respond if more than one were active. This combinatorial coding scheme would potentially allow the cerebellum to make much finer distinctions between input patterns than the mossy fibers alone would permit.^[16]

Mossy fibers

Mossy fibers enter the granular layer from their points of origin, many arising from the pontine nuclei, others from the spinal cord, vestibular nuclei etc. In the human cerebellum, the total number of mossy fibers has been estimated at about 200 million.^[4] These fibers form excitatory synapses with the granule cells and the cells of the deep cerebellar nuclei. Within the granular layer, a mossy fiber generates a series of enlargements called rosettes. The contacts between mossy fibers and granule cell dendrites take place within structures called glomeruli. Each glomerulus has a mossy fiber rosette at its center, and up to 20 granule cell dendritic claws contacting it. Terminals from Golgi cells infiltrate the structure and make inhibitory synapses onto the granule cell dendrites. The entire assemblage is surrounded by a sheath of glial cells.^[4] Each mossy fiber sends collateral branches to several cerebellar folia, generating a total of 20–30 rosettes; thus a single mossy fiber makes contact with an estimated 400–600 granule cells.^[4]

Climbing fibers

Purkinje cells also receive input from the inferior olivary nucleus on the contralateral side of the brainstem via climbing fibers. Although the inferior olive lies in the medulla oblongata and receives input from the spinal cord, brainstem and cerebral cortex, its output goes entirely to the cerebellum. A climbing fiber gives off collaterals to the deep cerebellar nuclei before entering the cerebellar cortex, where it splits into about 10 terminal branches, each of which innervates a single Purkinje cell.^[4] In striking contrast to the 100,000-plus inputs from parallel fibers, each Purkinje cell receives input from exactly one climbing fiber; but this single fiber "climbs" the dendrites of the Purkinje cell, winding around them and making a total of up to 300 synapses as it goes.^[4] The net input is so strong that a single action potential from a climbing fiber is capable of producing an extended complex spike in the Purkinje cell: a burst of several spikes in a row, with diminishing amplitude, followed by a pause during which activity is suppressed. The climbing fiber synapses cover the cell body and proximal dendrites; this zone is devoid of parallel fiber inputs.^[4]

Climbing fibers fire at low rates, but a single climbing fiber action potential induces a burst of several action potentials in a target Purkinje cell (a complex spike). The contrast between parallel fiber and climbing fiber inputs to Purkinje cells (over 100,000 of one type versus exactly one of the other type) is perhaps the most provocative feature of cerebellar anatomy, and has motivated much of the theorizing. In fact, the function of climbing fibers is the most controversial topic concerning the cerebellum. There are two schools of thought, one following Marr and Albus in holding that climbing fiber input serves primarily as a teaching signal, the other holding that its function is to shape cerebellar output directly. Both views have been defended in great length in numerous publications. In the words of one review, "In trying to synthesize the various hypotheses on the function of the climbing fibers, one has the sense of looking at a drawing by Escher. Each point of view seems to account for a certain collection of findings, but when one attempts to put the different views together, a coherent picture of what the climbing fibers are doing does not appear. For the majority of researchers, the climbing fibers signal errors in motor performance, either in the usual manner of discharge frequency modulation or as a single announcement of an 'unexpected event'. For other investigators, the message lies in the degree of ensemble synchrony and rhythmicity among a population of climbing fibers."^[15]

Deep nuclei

Sagittal cross-section of human cerebellum, showing the dentate nucleus, as well as the pons and inferior olivary nucleus

The deep nuclei of the cerebellum are clusters of gray matter lying within the white matter at the core of the cerebellum. They are, with the minor exception of the nearby vestibular nuclei, the sole sources of output from the cerebellum. These nuclei receive collateral projections from mossy fibers and climbing fibers as well as inhibitory input from the Purkinje cells of the cerebellar cortex. The four nuclei (dentate, globose, emboliform, and fastigial) each communicate with different parts of the brain and cerebellar cortex. (The globose and the emboliform nuclei are also referred to as combined in the interposed nucleus). The fastigial and interposed nuclei belong to the spinocerebellum. The dentate nucleus, which in mammals is much larger than the others, is formed as a thin, convoluted layer of gray matter, and communicates exclusively with the lateral parts of the cerebellar cortex. The flocculonodular lobe is the only part of the cerebellar cortex that does not project to the deep nuclei—its output goes to the vestibular nuclei instead.^[4]

The majority of neurons in the deep nuclei have large cell bodies and spherical dendritic trees with a radius of about 400 μm, and use glutamate as their neurotransmitter. These cells project to a variety of targets outside the cerebellum. Intermixed with them are a lesser number of small cells, which use GABA as a neurotransmitter and project exclusively to the inferior olivary nucleus, the source of climbing fibers. Thus, the nucleo-olivary projection provides an inhibitory feedback to match the excitatory projection of climbing fibers to the nuclei. There is evidence that each small cluster of nuclear cells projects to the same cluster of olivary cells that send climbing fibers to it; there is strong and matching topography in both directions.^[4]

When a Purkinje cell axon enters one of the deep nuclei, it branches to make contact with both large and small nuclear cells, but the total number of cells contacted is only about 35 (in cats). Conversely, a single deep nuclear cell receives input from approximately 860 Purkinje cells (again in cats).^[4]

Compartments

Schematic illustration of the structure of zones and microzones in the cerebellar cortex

From the viewpoint of gross anatomy, the cerebellar cortex appears to be a homogeneous sheet of tissue, and, from the viewpoint of microanatomy, all parts of this sheet appear to have the same internal structure. There are, however, a number of respects in which the structure of the cerebellum is compartmentalized. There are large compartments that are generally known as zones; these can be decomposed into smaller compartments known as microzones.^[17]

The first indications of compartmental structure came from studies of the receptive fields of cells in various parts of the cerebellar cortex.^[17] Each body part maps to specific points in the cerebellum, but there are numerous repetitions of the basic map, forming an arrangement that has been called "fractured somatotopy".^[18] A clearer indication of compartmentalization is obtained by immunostaining the cerebellum for certain types of protein. The best-known of these markers are called "zebrins", because staining for them gives rise to a complex pattern reminiscent of the stripes on a zebra. The stripes generated by zebrins and other compartmentalization markers are oriented perpendicular to the cerebellar folds—that is, they are narrow in the mediolateral direction, but much more extended in the longitudinal direction. Different markers generate different sets of stripes, the widths and lengths vary as a function of location, but they all have the same general shape.^[17]

Oscarsson in the late 1970s proposed that these cortical zones can be partitioned into smaller units called microzones.^[19] A microzone is defined as a group of Purkinje cells all having the same somatotopic receptive field. Microzones were found to contain on the order of 1000 Purkinje cells each, arranged in a long, narrow strip, oriented perpendicular to the cortical folds.^[17] Thus, as the adjoining diagram illustrates, Purkinje cell dendrites are flattened in the same direction as the microzones extend, while parallel fibers cross them at right angles.^[4]

It is not only receptive fields that define the microzone structure: The climbing fiber input from the inferior olivary nucleus is equally important. The branches of a climbing fiber (usually numbering about 10) usually innervate Purkinje cells belonging to the same microzone. Moreover, olivary neurons that send climbing fibers to the same microzone tend to be coupled by gap junctions, which synchronize their activity, causing Purkinje cells within a microzone to show correlated complex spike activity on a millisecond time scale.^[17] Also, the Purkinje cells belonging to a microzone all send their axons to the same small cluster of output cells within the deep cerebellar nuclei.^[17] Finally, the axons of basket cells are much longer in the longitudinal direction than in the mediolateral direction, causing them to be confined largely to a single microzone.^[17] The consequence of all this structure is that cellular interactions within a microzone are much stronger than interactions between different microzones.^[17]

In 2005, Richard Apps and Martin Garwicz summarized evidence that microzones themselves form part of a larger entity they call a multizonal microcomplex. Such a microcomplex includes several spatially separated cortical microzones, all of which project to the same group of deep cerebellar neurons, plus a group of coupled olivary neurons that project to all of the included microzones as well as to the deep nuclear area.^[17]

Function

The strongest clues to the function of the cerebellum have come from examining the consequences of damage to it. Animals and humans with cerebellar dysfunction show, above all, problems with motor control, on the same side of the body as the damaged part of the cerebellum. They continue to be able to generate motor activity, but it loses precision, producing erratic, uncoordinated, or incorrectly timed movements. A standard test of cerebellar function is to reach with the tip of the finger for a target at arm's length: A healthy person will move the fingertip in a rapid straight trajectory, whereas a person with cerebellar damage will reach slowly and erratically, with many mid-course corrections. Deficits in non-motor functions are more difficult to detect. Thus, the general conclusion reached decades ago is that the basic function of the cerebellum is to calibrate the detailed form of a movement, not to initiate movements or to decide which movements to execute.^[6]

Prior to the 1990s the function of the cerebellum was almost universally believed to be purely motor-related, but newer findings have brought that view into question. Functional imaging studies have shown cerebellar activation in relation to language, attention, and mental imagery; correlation studies have shown interactions between the cerebellum and non-motor areas of the cerebral cortex; and a variety of non-motor symptoms have been recognized in people with damage that appears to be confined to the cerebellum.^[20]^[21] In particular, the cerebellar cognitive affective syndrome has been described in adults^[22] and children.^[23] Estimates based on functional mapping of the cerebellum using functional MRI suggest that more than half of the cerebellar cortex is interconnected with association zones of the cerebral cortex.^[24]

Kenji Doya has argued that the function of the cerebellum is best understood not in terms of what behaviors it is involved in, but rather in terms of what neural computations it performs; the cerebellum consists of a large number of more or less independent modules, all with the same geometrically regular internal structure, and therefore all, it is presumed, performing the same computation. If the input and output connections of a module are with motor areas (as many are), then the module will be involved in motor behavior; but, if the connections are with areas involved in non-motor cognition, the module will show other types of behavioral correlates. Thus the cerebellum has been implicated in the regulation of many differing functional traits such as affection, emotion and behavior.^[25]^[26] The cerebellum, Doya proposes, is best understood as predictive action selection based on "internal models" of the environment or a device for supervised learning, in contrast to the basal ganglia, which perform reinforcement learning, and the cerebral cortex, which performs unsupervised learning.^[21]^[27]

Principles

The comparative simplicity and regularity of the cerebellar anatomy led to an early hope that it might imply a similar simplicity of computational function, as expressed in one of the first books on cerebellar electrophysiology, The Cerebellum as a Neuronal Machine by John C. Eccles, Masao Ito, and János Szentágothai.^[28] Although a full understanding of cerebellar function has remained elusive, at least four principles have been identified as important: (1) feedforward processing, (2) divergence and convergence, (3) modularity, and (4) plasticity.

Feedforward processing: The cerebellum differs from most other parts of the brain (especially the cerebral cortex) in that the signal processing is almost entirely feedforward—that is, signals move unidirectionally through the system from input to output, with very little recurrent internal transmission. The small amount of recurrence that does exist consists of mutual inhibition; there are no mutually excitatory circuits. This feedforward mode of operation means that the cerebellum, in contrast to the cerebral cortex, cannot generate self-sustaining patterns of neural activity. Signals enter the circuit, are processed by each stage in sequential order, and then leave. As Eccles, Ito, and Szentágothai wrote, "This elimination in the design of all possibility of reverberatory chains of neuronal excitation is undoubtedly a great advantage in the performance of the cerebellum as a computer, because what the rest of the nervous system requires from the cerebellum is presumably not some output expressing the operation of complex reverberatory circuits in the cerebellum but rather a quick and clear response to the input of any particular set of information."^[29]
Divergence and convergence: In the human cerebellum, information from 200 million mossy fiber inputs is expanded to 40 billion granule cells, whose parallel fiber outputs then converge onto 15 million Purkinje cells.^[4] Because of the way that they are lined up longitudinally, the 1000 or so Purkinje cells belonging to a microzone may receive input from as many as 100 million parallel fibers, and focus their own output down to a group of less than 50 deep nuclear cells.^[17] Thus, the cerebellar network receives a modest number of inputs, processes them very extensively through its rigorously structured internal network, and sends out the results via a very limited number of output cells.
Modularity: The cerebellar system is functionally divided into more or less independent modules, which probably number in the hundreds to thousands. All modules have a similar internal structure, but different inputs and outputs. A module (a multizonal microcompartment in the terminology of Apps and Garwicz) consists of a small cluster of neurons in the inferior olivary nucleus, a set of long narrow strips of Purkinje cells in the cerebellar cortex (microzones), and a small cluster of neurons in one of the deep cerebellar nuclei. Different modules share input from mossy fibers and parallel fibers, but in other respects they appear to function independently—the output of one module does not appear to significantly influence the activity of other modules.^[17]
Plasticity: The synapses between parallel fibers and Purkinje cells, and the synapses between mossy fibers and deep nuclear cells, are both susceptible to modification of their strength. In a single cerebellar module, input from as many as a billion parallel fibers converges onto a group of less than 50 deep nuclear cells, and the influence of each parallel fiber on those nuclear cells is adjustable. This arrangement gives tremendous flexibility for fine-tuning the relationship between the cerebellar inputs and outputs.^[30]

Learning

There is considerable evidence that the cerebellum plays an essential role in some types of motor learning. The tasks where the cerebellum most clearly comes into play are those in which it is necessary to make fine adjustments to the way an action is performed. There has, however, been much dispute about whether learning takes place within the cerebellum itself, or whether it merely serves to provide signals that promote learning in other brain structures.^[30] Most theories that assign learning to the circuitry of the cerebellum are derived from the ideas of David Marr^[16] and James Albus,^[31] who postulated that climbing fibers provide a teaching signal that induces synaptic modification in parallel fiber–Purkinje cell synapses.^[32] Marr assumed that climbing fiber input would cause synchronously activated parallel fiber inputs to be strengthened. Most subsequent cerebellar-learning models, however, have followed Albus in assuming that climbing fiber activity would be an error signal, and would cause synchronously activated parallel fiber inputs to be weakened. Some of these later models, such as the Adaptive Filter model of Fujita^[33] made attempts to understand cerebellar function in terms of optimal control theory.

The idea that climbing fiber activity functions as an error signal has been examined in many experimental studies, with some supporting it but others casting doubt.^[15] In a pioneering study by Gilbert and Thach from 1977, Purkinje cells from monkeys learning a reaching task showed increased complex spike activity—which is known to reliably indicate activity of the cell's climbing fiber input—during periods when performance was poor.^[34] Several studies of motor learning in cats observed complex spike activity when there was a mismatch between an intended movement and the movement that was actually executed. Studies of the vestibulo–ocular reflex (which stabilizes the visual image on the retina when the head turns) found that climbing fiber activity indicated "retinal slip", although not in a very straightforward way.^[15]

One of the most extensively studied cerebellar learning tasks is the eyeblink conditioning paradigm, in which a neutral conditioned stimulus (CS) such as a tone or a light is repeatedly paired with an unconditioned stimulus (US), such as an air puff, that elicits a blink response. After such repeated presentations of the CS and US, the CS will eventually elicit a blink before the US, a conditioned response or CR. Experiments showed that lesions localized either to a specific part of the interposed nucleus (one of the deep cerebellar nuclei) or to a few specific points in the cerebellar cortex would abolish learning of a conditionally timed blink response. If cerebellar outputs are pharmacologically inactivated while leaving the inputs and intracellular circuits intact, learning takes place even while the animal fails to show any response, whereas, if intracerebellar circuits are disrupted, no learning takes place—these facts taken together make a strong case that the learning, indeed, occurs inside the cerebellum.^[35]

Theories and computational models

Model of a cerebellar perceptron, as formulated by James Albus

The large base of knowledge about the anatomical structure and behavioral functions of the cerebellum have made it a fertile ground for theorizing—there are perhaps more theories of the function of the cerebellum than of any other part of the brain. The most basic distinction among them is between "learning theories" and "performance theories"—that is, theories that make use of synaptic plasticity within the cerebellum to account for its role in learning, versus theories that account for aspects of ongoing behavior on the basis of cerebellar signal processing. Several theories of both types have been formulated as mathematical models and simulated using computers.^[32]

Perhaps the earliest "performance" theory was the "delay line" hypothesis of Valentino Braitenberg. The original theory put forth by Braitenberg and Roger Atwood in 1958 proposed that slow propagation of signals along parallel fibers imposes predictable delays that allow the cerebellum to detect time relationships within a certain window.^[36] Experimental data did not support the original form of the theory, but Braitenberg continued to argue for modified versions.^[37] The hypothesis that the cerebellum functions essentially as a timing system has also been advocated by Richard Ivry.^[38] Another influential "performance" theory is the Tensor network theory of Pellionisz and Llinás, which provided an advanced mathematical formulation of the idea that the fundamental computation performed by the cerebellum is to transform sensory into motor coordinates.^[39]

Theories in the "learning" category almost all derive from publications by Marr and Albus. Marr's 1969 paper proposed that the cerebellum is a device for learning to associate elemental movements encoded by climbing fibers with mossy fiber inputs that encode the sensory context.^[16] Albus proposed in 1971 that a cerebellar Purkinje cell functions as a perceptron, a neurally inspired abstract learning device.^[31] The most basic difference between the Marr and Albus theories is that Marr assumed that climbing fiber activity would cause parallel fiber synapses to be strengthened, whereas Albus proposed that they would be weakened. Albus also formulated his version as a software algorithm he called a CMAC (Cerebellar Model Articulation Controller), which has been tested in a number of applications.^[40]

Clinical significance

Altered walking gait of a woman with cerebellar disease

The most salient symptoms of cerebellar dysfunction are motor-related—the specific symptoms depend on which part of the cerebellum is involved and how it is disrupted. Damage to the flocculonodular lobe (the vestibular part) may show up as a loss of equilibrium and, in particular, an altered walking gait, with a wide stance that indicates difficulty in balancing.^[6] Damage to the lateral zone, or the cerebrocerebellum, results in problems with skilled voluntary and planned movements. This can cause errors in the force, direction, speed and amplitude of movements. Some manifestations include hypotonia (decreased muscle tone), dysarthria (problems with speech articulation), dysmetria (problems judging distances or ranges of movement), dysdiadochokinesia (inability to perform rapid alternating movements), impaired check reflex or rebound phenomenon, and intention tremor (involuntary movement caused by alternating contractions of opposing muscle groups).^[41] Damage to the midline portion may disrupt whole-body movements, whereas damage localized more laterally is more likely to disrupt fine movements of the hands or limbs. Damage to the upper part of the cerebellum tends to cause gait impairments and other problems with leg coordination; damage to the lower part is more likely to cause uncoordinated or poorly aimed movements of the arms and hands, as well as difficulties in speed.^[6] This complex of motor symptoms is called ataxia.

To identify cerebellar problems, neurological examination includes assessment of gait (a broad-based gait being indicative of ataxia), finger-pointing tests and assessment of posture.^[2] If cerebellar dysfunction is indicated, a magnetic resonance imaging scan can be used to obtain a detailed picture of any structural alterations that may exist.^[42]

The lower trace shows an attempt by a patient with cerebellar disease to reproduce the upper trace.

The list of medical problems that can produce cerebellar damage is long, including stroke, hemorrhage, swelling of the brain (cerebral edema), tumors, alcoholism, physical trauma such as gunshot wounds or explosives, and chronic degenerative conditions such as olivopontocerebellar atrophy.^[43]^[44] Some forms of migraine headache may also produce temporary dysfunction of the cerebellum, of variable severity.^[45] Infection can result in cerebellar damage in such conditions as the prion diseases^[46] and Miller Fisher syndrome, a variant of Guillain–Barré syndrome.

Aging

The human cerebellum changes with age. These changes may differ from those of other parts of the brain. The cerebellum is the youngest brain region (and body part) in centenarians according to an epigenetic biomarker of tissue age known as epigenetic clock: it is about 15 years younger than expected in a centenarian.^[47] Further, gene expression patterns in the human cerebellum show less age-related alteration than that in the cerebral cortex.^[48] Some studies have reported reductions in numbers of cells or volume of tissue, but the amount of data relating to this question is not very large.^[49]^[50]

Developmental and degenerative disorders

Congenital malformation, hereditary disorders, and acquired conditions can affect cerebellar structure and, consequently, cerebellar function. Unless the causative condition is reversible, the only possible treatment is to help people live with their problems.^[51]

In normal development, endogenous Sonic hedgehog signaling stimulates rapid proliferation of cerebellar granule neuron progenitors (CGNPs) in the external granule layer (EGL). Cerebellar development occurs during late embryogenesis and the early postnatal period, with CGNP proliferation in the EGL peaking during early development (postnatal day 7 in the mouse).^[52] As CGNPs terminally differentiate into cerebellum granule cells (also called cerebellar granule neurons, CGNs), they migrate to the internal granule layer (IGL), forming the mature cerebellum (by post-natal day 20 in the mouse).^[52] Mutations that abnormally activate Sonic hedgehog signaling predispose to cancer of the cerebellum (medulloblastoma) in humans with Gorlin Syndrome and in genetically engineered mouse models.^[53]^[54]

Congenital malformation or underdevelopment (hypoplasia) of the cerebellar vermis is a characteristic of both Dandy–Walker syndrome and Joubert syndrome.^[55]^[56] In very rare cases, the entire cerebellum may be absent.^[57] The inherited neurological disorders Machado–Joseph disease, ataxia telangiectasia, and Friedreich's ataxia cause progressive neurodegeneration linked to cerebellar loss.^[43]^[51] Congenital brain malformations outside the cerebellum can, in turn, cause herniation of cerebellar tissue, as seen in some forms of Arnold–Chiari malformation.^[58]

Other conditions that are closely linked to cerebellar degeneration include the idiopathic progressive neurological disorders multiple system atrophy and Ramsay Hunt syndrome type I,^[59]^[60] and the autoimmune disorder paraneoplastic cerebellar degeneration, in which tumors elsewhere in the body elicit an autoimmune response that causes neuronal loss in the cerebellum.^[61] Cerebellar atrophy can result from an acute deficiency of vitamin B1 (thiamine) as seen in beriberi and in Wernicke–Korsakoff syndrome,^[62] or from vitamin E deficiency.^[51]

Cerebellar atrophy has been observed in many other neurological disorders including Huntington's disease, multiple sclerosis,^[46] essential tremor, progressive myoclonus epilepsy, and Niemann–Pick disease. Cerebellar atrophy can also occur as a result of exposure to toxins including heavy metals or pharmaceutical or recreational drugs.^[51]

Comparative anatomy and evolution

Cross-section of the brain of a porbeagle shark, with the cerebellum highlighted in blue

The circuits in the cerebellum are similar across all classes of vertebrates, including fish, reptiles, birds, and mammals.^[63] There is also an analogous brain structure in cephalopods with well-developed brains, such as octopuses.^[64] This has been taken as evidence that the cerebellum performs functions important to all animal species with a brain.

There is considerable variation in the size and shape of the cerebellum in different vertebrate species. In amphibians, it is little developed, and in lampreys, and hagfish, the cerebellum is barely distinguishable from the brain-stem. Although the spinocerebellum is present in these groups, the primary structures are small, paired-nuclei corresponding to the vestibulocerebellum.^[65] The cerebellum is a bit larger in reptiles, considerably larger in birds, and larger yet in mammals. The large paired and convoluted lobes found in humans are typical of mammals, but the cerebellum is, in general, a single median lobe in other groups, and is either smooth or only slightly grooved. In mammals, the neocerebellum is the major part of the cerebellum by mass, but, in other vertebrates, it is typically the spinocerebellum.^[65]

The cerebellum of cartilaginous and bony fishes is extraordinarily large and complex. In at least one important respect, it differs in internal structure from the mammalian cerebellum: The fish cerebellum does not contain discrete deep cerebellar nuclei. Instead, the primary targets of Purkinje cells are a distinct type of cell distributed across the cerebellar cortex, a type not seen in mammals. In mormyrid fish (a family of weakly electrosensitive freshwater fish), the cerebellum is considerably larger than the rest of the brain put together. The largest part of it is a special structure called the valvula, which has an unusually regular architecture and receives much of its input from the electrosensory system.^[66]

The hallmark of the mammalian cerebellum is an expansion of the lateral lobes, whose main interactions are with the neocortex. As monkeys evolved into great apes, the expansion of the lateral lobes continued, in tandem with the expansion of the frontal lobes of the neocortex. In ancestral hominids, and in Homo sapiens until the middle Pleistocene period, the cerebellum continued to expand, but the frontal lobes expanded more rapidly. The most recent period of human evolution, however, may actually have been associated with an increase in the relative size of the cerebellum, as the neocortex reduced its size somewhat while the cerebellum expanded.^[67] The size of the human cerebellum, compared to the rest of the brain, has been increasing in size while the cerebrum decreased in size ^[68] With both the development and implementation of motor tasks, visual-spatial skills and learning taking place in the cerebellum, the growth of the cerebellum is thought to have some form of correlation to greater human cognitive abilities.^[69] The lateral hemispheres of the cerebellum are now 2.7 times greater in both humans and apes than they are in monkeys.^[68] These changes in the cerebellum size cannot be explained by greater muscle mass. They show that either the development of the cerebellum is tightly linked to that of the rest of the brain or that neural activities taking place in the cerebellum were important during Hominidae evolution. Due to the cerebellum's role in cognitive functions, the increase in its size may have played a role in cognitive expansion.^[68]

Cerebellum-like structures

Many vertebrate species have brain areas that resemble the cerebellum in terms of cytoarchitecture and neurochemistry.^[63] The only one found in mammals is the dorsal cochlear nucleus (DCN), one of the two primary sensory nuclei that receive input directly from the auditory nerve. The DCN is a layered structure, with the bottom layer containing granule cells similar to those of the cerebellum, giving rise to parallel fibers that rise to the superficial layer and travel across it horizontally. The superficial layer contains a set of GABAergic neurons called cartwheel cells that resemble Purkinje cells anatomically and chemically—they receive parallel fiber input, but do not have any inputs that resemble climbing fibers. The output neurons of the DCN are pyramidal cells. They are glutamatergic, but also resemble Purkinje cells in some respects—they have spiny, flattened superficial dendritic trees that receive parallel fiber input, but they also have basal dendrites that receive input from auditory nerve fibers, which travel across the DCN in a direction at right angles to the parallel fibers. The DCN is most highly developed in rodents and other small animals, and is considerably reduced in primates. Its function is not well understood; the most popular speculations relate it to spatial hearing in one way or another.^[70]

Most species of fish and amphibians possess a lateral line system that senses pressure waves in water. One of the brain areas that receives primary input from the lateral line organ, the medial octavolateral nucleus, has a cerebellum-like structure, with granule cells and parallel fibers. In electrosensitive fish, the input from the electrosensory system goes to the dorsal octavolateral nucleus, which also has a cerebellum-like structure. In ray-finned fishes (by far the largest group), the optic tectum has a layer—the marginal layer—that is cerebellum-like.^[63]

All of these cerebellum-like structures appear to be primarily sensory-related rather than motor-related. All of them have granule cells that give rise to parallel fibers that connect to Purkinje-like neurons with modifiable synapses, but none have climbing fibers comparable to those of the cerebellum—instead they receive direct input from peripheral sensory organs. None has a demonstrated function, but the most influential speculation is that they serve to transform sensory inputs in some sophisticated way, perhaps to compensate for changes in body posture.^[63] In fact, James M. Bower and others have argued, partly on the basis of these structures and partly on the basis of cerebellar studies, that the cerebellum itself is fundamentally a sensory structure, and that it contributes to motor control by moving the body in a way that controls the resulting sensory signals.^[71] Despite Bower's viewpoint, there is also strong evidence that the cerebellum directly influences motor output in mammals.^[72]^[73]

History

Base of the human brain, as drawn by Andreas Vesalius in 1543

Descriptions

Even the earliest anatomists were able to recognize the cerebellum by its distinctive appearance. Aristotle and Herophilus (quoted in Galen) called it the parencephalis, as opposed to the encephalon or brain proper. Galen's extensive description is the earliest that survives. He speculated that the cerebellum was the source of motor nerves.^[74]

Further significant developments did not come until the Renaissance. Vesalius discussed the cerebellum briefly, and the anatomy was described more thoroughly by Thomas Willis in 1664. More anatomical work was done during the 18th century, but it was not until early in the 19th century that the first insights into the function of the cerebellum were obtained. Luigi Rolando in 1809 established the key finding that damage to the cerebellum results in motor disturbances. Jean Pierre Flourens in the first half of the 19th century carried out detailed experimental work, which revealed that animals with cerebellar damage can still move, but with a loss of coordination (strange movements, awkward gait, and muscular weakness), and that recovery after the lesion can be nearly complete unless the lesion is very extensive.^[75] By the beginning of the 20th century, it was widely accepted that the primary function of the cerebellum relates to motor control; the first half of the 20th century produced several detailed descriptions of the clinical symptoms associated with cerebellar disease in humans.^[2]

Etymology

The name cerebellum is a diminutive of cerebrum (brain);^[76] it can be translated literally as little brain. The Latin name is a direct translation of the Ancient Greek Παρεγκεφαλίς (parencephalis), which was used in the works of Aristotle, the first known writer to describe the structure.^[77] No other name is used in the English-language literature, but historically a variety of Greek or Latin-derived names have been used, including cerebrum parvum,^[78] encephalion,^[79] encranion,^[78] cerebrum posterius,^[80] and parencephalis.^[78]

References

^ Wolf U, Rapoport MJ, Schweizer TA (2009). "Evaluating the affective component of the cerebellar cognitive affective syndrome". J. Neuropsychiatry Clin. Neurosci. 21 (3): 245–53. doi:10.1176/jnp.2009.21.3.245. PMID 19776302.
^ ^a ^b ^c ^d Fine EJ, Ionita CC, Lohr L (2002). "The history of the development of the cerebellar examination". Semin. Neurol. 22 (4): 375–84. doi:10.1055/s-2002-36759. PMID 12539058.
^ "Chapter 20". Gray's Anatomy (40th ed.). 2008. p. 297. ISBN 978-0-8089-2371-8.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x ^y Llinas RR, Walton KD, Lang EJ (2004). "Ch. 7 Cerebellum". In Shepherd GM. The Synaptic Organization of the Brain. New York: Oxford University Press. ISBN 0-19-515955-1.
^ Herculano-Houzel S (2010). "Coordinated scaling of cortical and cerebellar numbers of neurons". Front. Neuroanat. 4:12. doi:10.3389/fnana.2010.00012.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j Ghez C, Fahn S (1985). "The cerebellum". In Kandel ER, Schwartz JH. Principles of Neural Science, 2nd edition. New York: Elsevier. pp. 502–522.
^ Kingsley RE (2000). Concise Text of Neuroscience (2nd ed.). Lippincott Williams and Wilkins. ISBN 0-683-30460-7.
^ Petersen SE, Fox PT, Posner MI, Mintun M, Raichle ME (1989). "Positron emission tomographic studies of the processing of single words". Journal of Cognitive Neuroscience 1: 153–170. doi:10.1080/14734220701496448. PMID 17786810.
^ Timmann D, Daum I (2007). "Cerebellar contributions to cognitive functions: a progress report after two decades of research". Cerebellum 6 (3): 159–62. doi:10.1162/jocn.1989.1.2.153. PMID 23968463.
^ Strick PL, Dum RP, Fiez JA (2009). "Cerebellum and nonmotor function". Annual Review of Neuroscience 32: 413–434. doi:10.1146/annurev.neuro.31.060407.125606. PMID 19555291.
^ Buckner RL (2013). "The cerebellum and cognitive function: 25 years of insight from anatomy and neuroimaging". Neuron 80 (3): 807–815. doi:10.1016/j.neuron.2013.10.044. PMID 24183029.
^ Schweighofer N, Doya K, Kuroda S (2004). "Cerebellar aminergic neuromodulation: towards a functional understanding". Brain Res. Brain Res. Rev. 44 (2–3): 103–116. doi:10.1016/j.brainresrev.2003.10.004. PMID 15003388.
^ Felizola SJ, Nakamura Y, Ono Y, Kitamura K, Kikuchi K, Onodera Y, Ise K, Takase K, Sugawara A, Hattangady N, Rainey WE, Satoh F, Sasano H (2014). "PCP4: a regulator of aldosterone synthesis in human adrenocortical tissues.". J. Mol. Endocrinol. 52 (2): 159–167. doi:10.1530/JME-13-0248. PMC 4103644. PMID 24403568.
^ Eccles JC, Llinás R, Sasaki K (1966). "The excitatory synaptic action of climbing fibers on the purkinje cells of the cerebellum". J. Physiol. 182 (2): 268–96. doi:10.1113/jphysiol.1966.sp007824. PMC 1357472. PMID 5944665.
^ ^a ^b ^c ^d Simpson JI, Wylie DR, De Zeeuw CI (1996). "On climbing fiber signals and their consequence(s)". Behav. Brain Sci. 19 (3): 384–398. doi:10.1017/S0140525X00081486.
^ ^a ^b ^c Marr D (1969). "A theory of cerebellar cortex". J. Physiol. 202 (2): 437–70. doi:10.1113/jphysiol.1969.sp008820. PMC 1351491. PMID 5784296.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k Apps R, Garwicz M (2005). "Anatomical and physiological foundations of cerebellar information processing". Nature Rev. Neurosci. 6 (4): 297–311. doi:10.1038/nrn1646. PMID 15803161.
^ Manni E, Petrosini L (2004). "A century of cerebellar somatotopy: a debated representation". Nature Rev. Neurosci. 5 (3): 241–9. doi:10.1038/nrn1347. PMID 14976523.
^ Oscarsson O (1979). "Functional units of the cerebellum-sagittal zones and microzones". Trends Neurosci. 2: 143–145. doi:10.1016/0166-2236(79)90057-2.
^ Rapp B (2001). The Handbook of Cognitive Neuropsychology: What Deficits Reveal about the Human Mind. Psychology Press. p. 481. ISBN 1-84169-044-9.
^ ^a ^b Doya K (2000). "Complementary roles of basal ganglia and cerebellum in learning and motor control". Curr. Opin. Neurobiol. 10 (6): 732–739. doi:10.1016/S0959-4388(00)00153-7. PMID 11240282.
^ Schmahmann JD, Sherman JC (April 1998). "The cerebellar cognitive affective syndrome". Brain 121 (4): 561–79. doi:10.1093/brain/121.4.561. PMID 9577385.
^ Levisohn L, Cronin-Golomb A, Schmahmann JD (May 2000). "Neuropsychological consequences of cerebellar tumour resection in children: cerebellar cognitive affective syndrome in a paediatric population". Brain 123 (5): 1041–50. doi:10.1093/brain/123.5.1041. PMID 10775548.
^ Buckner RL, Krienen FM, Castellanos A, Diaz JC, Yeo BT (2011). "The organization of the human cerebellum estimated by intrinsic functional connectivity". J. Neurophysiol. 106 (5): 2322–2345. doi:10.1152/jn.00339.2011. PMC 3214121. PMID 21795627.
^ Hernáez-Goñi P, Tirapu-Ustárroz J, Iglesias-Fernández L, Luna-Lario P (November 2010). "Participación del cerebelo en la regulación del afecto, la emoción y la conducta" [The role of the cerebellum in the regulation of affection, emotion and behavior]. Revista de Neurologia (in Spanish) 51 (10): 597–609. PMID 21069639.
^ Turner BM, Paradiso S, Marvel CL, Pierson R, Boles Ponto LL, Hichwa RD, Robinson RG (March 2007). "The cerebellum and emotional experience". Neuropsychologia 45 (6): 1331–41. doi:10.1016/j.neuropsychologia.2006.09.023. PMC 1868674. PMID 17123557.
^ Doya K (1999). "What are the computations of the cerebellum, the basal ganglia and the cerebral cortex?". Neural Networks 12 (7–8): 961–974. doi:10.1016/S0893-6080(99)00046-5. PMID 12662639.
^ Eccles JC, Ito M, Szentágothai J (1967). The Cerebellum as a Neuronal Machine. Springer-Verlag.
^ The Cerebellum as a Neuronal Machine, p. 311
^ ^a ^b Boyden ES, Katoh A, Raymond JL (2004). "Cerebellum-dependent learning: the role of multiple plasticity mechanisms". Annu. Rev. Neurosci. 27: 581–609. doi:10.1146/annurev.neuro.27.070203.144238. PMID 15217344.
^ ^a ^b Albus JS (1971). "A theory of cerebellar function". Math. Biosciences 10 (1–2): 25–61. doi:10.1016/0025-5564(71)90051-4.
^ ^a ^b Houk JC, Buckingham JT, Barto AG (1996). "Models of the cerebellum and motor learning". Behav. Brain Sci. 19 (3): 368–383. doi:10.1017/S0140525X00081474.
^ Fujita M (1982). "Adaptive filter model of the cerebellum". Biol. Cybern. 45 (3): 195–206. doi:10.1007/BF00336192. PMID 7171642.
^ Gilbert PF, Thach WT (1977). "Purkinje cell activity during motor learning". Brain Res. 128 (2): 309–28. doi:10.1016/0006-8993(77)90997-0. PMID 194656.
^ Christian KM, Thompson RF (2003). "Neural substrates of eyeblink conditioning: acquisition and retention". Learn. Mem. 10 (6): 427–55. doi:10.1101/lm.59603. PMID 14657256.
^ Braitenberg V, Atwood RP (1958). "Morphological observations on the cerebellar cortex". J. Comp. Neurol. 109 (1): 1–33. doi:10.1002/cne.901090102. PMID 13563670.
^ Braitenberg V, Heck D, Sultan F (1997). "The detection and generation of sequences as a key to cerebellar function: Experiments and theory". Behav. Brain Sciences 20 (2): 229–277. doi:10.1017/s0140525x9700143x. PMID 10096998.
^ Ivry RB, Spencer RM, Zelaznik HN, Diedrichsen J (2002). "The cerebellum and event timing". Ann. N. Y. Acad. Sci. 978: 302–307. Bibcode:2002NYASA.978..302I. doi:10.1111/j.1749-6632.2002.tb07576.x. PMID 12582062.
^ Pellionisz A, Llinás R (1982). "Space-time representation in the brain. The cerebellum as a predictive space-time metric tensor". Neuroscience 7 (12): 2949–70. doi:10.1016/0306-4522(82)90224-X. PMID 7162624.
^ Horváth G (2003). "CMAC: Reconsidering an old neural network" (PDF). Intelligent Control Systems and Signal Processing. Retrieved 2009-12-24.
^ Schmitz TJ (2007). "Examination of Coordination". In O'Sullivan SB, Schmitz TJ. Physical Rehabilitation. Philadelphia: F. A. Davis. pp. 193–225.
^ Gilman S (1998). "Imaging the brain. Second of two parts". N. Engl. J. Med. 338 (13): 889–96. doi:10.1056/NEJM199803263381307. PMID 9516225.
^ ^a ^b "NINDS Ataxias and Cerebellar or Spinocerebellar Degeneration Information Page". National Institutes of Health. 16 April 2014. Retrieved 2 February 2015.
^ Yuhas, D (January 15, 2016). "Veterans of Iraq, Afghanistan Show Brain Changes Related to Explosion Exposure". Scientific American. Retrieved January 21, 2016.
^ Vincent M, Hadjikhani N (2007). "The cerebellum and migraine". Headache 47 (6): 820–33. doi:10.1111/j.1526-4610.2006.00715.x. PMC 3761082. PMID 17578530.
^ ^a ^b "NINDS Cerebellar Degeneration Information Page". National Institutes of Health. 28 February 2014. Retrieved 2 February 2015.
^ Horvath S, Mah V, Lu AT, Woo JS, Choi OW, Jasinska AJ, Riancho JA, Tung S, Coles NS, Braun J, Vinters HV, Coles LS (2015). "The cerebellum ages slowly according to the epigenetic clock." (PDF). Age 7 (5): 294–306. doi:10.18632/aging.100742. PMID 26000617.
^ Fraser HB; Khaitovich P; Plotkin JB; Pääbo S; Eisen MB (2005). "Aging and gene expression in the primate brain". PLoS Biology 3 (9): e274. doi:10.1371/journal.pbio.0030274. PMC 1181540. PMID 16048372.
^ Andersen BB, Gunderson HJ, Pakkenberg B (2003). "Aging of the human cerebellum: A stereological study". J. Comp. Neurol. 466 (3): 356–365. doi:10.1002/cne.10884. PMID 14556293.
^ Raz N, Gunning-Dixon F, Head D, Williamson A, Acker JD (2001). "Age and sex differences in the cerebellum and the ventral pons: A prospective MR study of healthy adults" (PDF). Am. J. Neuroradiol. 22 (6): 1161–1167. PMID 11415913.
^ ^a ^b ^c ^d Albert, Richard K.; Porter, Robert S., eds. (2006). The Merck Manual of Diagnosis and Therapy (18th ed.). Whitehouse Station, New Jersey: Merck Research Libraries. pp. 1886–1887.
^ ^a ^b Hatten, M (1995). "Mechanisms of neural patterning and specification in the developing cerebellum". Annu Rev Neurosci 18: 385–408. doi:10.1146/annurev.ne.18.030195.002125. PMID 7605067.
^ Polkinghorn, W (2007). "Medulloblastoma: tumorigenesis, current clinical paradigm, and efforts to improve risk stratification". Nat Clin Pract Oncol 4: 295–304. doi:10.1038/ncponc0794. PMID 17464337.
^ Roussel, M (2011). "Cerebellum development and medulloblastoma". Curr Top Dev Biol 94: 235–82. doi:10.1016/B978-0-12-380916-2.00008-5. PMC 3213765. PMID 21295689.
^ "NINDS Joubert Syndrome Information Page". National Institutes of Health. 23 December 2013. Retrieved 9 January 2015.
^ "NINDS Dandy-Walker Information Page". National Institutes of Health. 14 February 2014. Retrieved 9 January 2015.
^ "NINDS Cerebellar Hypoplasia Information Page". National Institutes of Health. 29 September 2011. Retrieved 9 January 2015.
^ "Chiari Malformation Fact Sheet". National Institutes of Health. 10 December 2014. Retrieved 9 January 2015.
^ "NINDS Dyssynergia Cerebellaris Myoclonica Information Page". National Institutes of Health. 14 February 2011. Retrieved 1 February 2015.
^ "NINDS Olivopontocerebellar Atrophy Information Page". National Institutes of Health. 16 April 2014. Retrieved 9 January 2015.
^ "NINDS Paraneoplastic Syndromes Information Page". National Institutes of Health. 12 March 2009. Retrieved 9 January 2015.
^ "NINDS Wernicke-Korsakoff Syndrome Information Page". National Institutes of Health. 14 February 2007. Retrieved 9 January 2015.
^ ^a ^b ^c ^d Bell CC, Han V, Sawtell NB (2008). "Cerebellum-like structures and their implications for cerebellar function". Annu. Rev. Neurosci. 31: 1–24. doi:10.1146/annurev.neuro.30.051606.094225. PMID 18275284.
^ Woodhams PL (1977). "The ultrastructure of a cerebellar analogue in octopus". J. Comp. Neurol. 174 (2): 329–45. doi:10.1002/cne.901740209. PMID 864041.
^ ^a ^b Romer AS, Parsons TS (1977). The Vertebrate Body. Philadelphia: Holt-Saunders International. p. 531. ISBN 0-03-910284-X.
^ Shi Z, Zhang Y, Meek J, Qiao J, Han VZ (2008). "The neuronal organization of a unique cerebellar specialization: the valvula cerebelli of a mormyrid fish". J. Comp. Neurol. 509 (5): 449–73. doi:10.1002/cne.21735. PMID 18537139.
^ Weaver AH (2005). "Reciprocal evolution of the cerebellum and neocortex in fossil humans". Proc. Natl. Acad. Sci. U.S.A. 102 (10): 3576–3580. Bibcode:2005PNAS..102.3576W. doi:10.1073/pnas.0500692102. PMC 553338. PMID 15731345.
^ ^a ^b ^c Schoenemann PT (December 1, 2009). "Evolution of Brain and Language". Language Learning 59: 162–186. doi:10.1111/j.1467-9922.2009.00539.x.
^ MacLeod CE, Zilles K, Schleicher A, Rilling JK, Gibson KR (2003). "Expansion of the neocerebellum in Hominoidea". J. Hum. Evol. 44 (4): 401–429. doi:10.1016/S0047-2484(03)00028-9. PMID 12727461.
^ Roberts PD, Portfors CV (2008). "Design principles of sensory processing in cerebellum-like structures. Early stage processing of electrosensory and auditory objects". Biol. Cybern. 98 (6): 491–507. doi:10.1007/s00422-008-0217-1. PMID 18491162.
^ Bower JM (1997). "Is the cerebellum sensory for motor's sake, or motor for sensory's sake: the view from the whiskers of a rat?". Prog. Brain Res. 114: 463–96. doi:10.1016/S0079-6123(08)63381-6. ISBN 978-0-444-82313-7. PMID 9193161.
^ Heiney SA, Kim J, Augustine GJ, Medina JF (February 2014). "Precise control of movement kinematics by optogenetic inhibition of Purkinje cell activity". J. Neurosci. 34 (6): 2321–30. doi:10.1523/JNEUROSCI.4547-13.2014. PMC 3913874. PMID 24501371.
^ Witter L, Canto CB, Hoogland TM, de Gruijl JR, De Zeeuw CI (2013). "Strength and timing of motor responses mediated by rebound firing in the cerebellar nuclei after Purkinje cell activation". Front. Neural Circuits 7: 133. doi:10.3389/fncir.2013.00133. PMC 3748751. PMID 23970855.
^ Clarke E, O'Malley CD (1996). "Ch. 11: Cerebellum". The Human Brain and Spinal Cord (2nd ed.). Norman Publishing. p. 629. ISBN 0-930405-25-0.
^ Ito M (2002). "Historical review of the significance of the cerebellum and the role of Purkinje cells in motor learning". Ann. N. Y. Acad. Sci. 978: 273–288. Bibcode:2002NYASA.978..273I. doi:10.1111/j.1749-6632.2002.tb07574.x. PMID 12582060.
^ Lewis CT, Short C (1879). A Latin dictionary founded on Andrews' edition of Freund's Latin dictionary. Oxford: Clarendon Press.
^ Marshall LH, Magoun HW (1998). Discoveries in the human brain. Neuroscience prehistory, brain structure, and function. Totowa: Humana Press.
^ ^a ^b ^c Foster FD (1891). An illustrated medical dictionary. New York: D. Appleton and Company.
^ Kraus LA (1844). Kritisch-etymologisches medicinisches Lexikon (Dritte Auflage). Göttingen: Verlag der Deuerlich- und Dieterichschen Buchhandlung.
^ Schreger CHT (1805). Synonymia anatomica. Synonymik der anatomischen Nomenclatur. Fürth.

External links

Cerebellum Rodolfo Llinas and Mario N. Negrello, Scholarpedia, 10(1):4606. doi:10.4249/scholarpedia.4606
Cerebellum–Cell Centered Database
Stained brain slice images which include the "cerebellum" at the BrainMaps project
A Man's Incomplete Brain Reveals Cerebellum's Role In Thought And Emotion
Cerebellum histology images

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 成人における小脳性運動失調の概要 overview of cerebellar ataxia in adults
2. まれな脳腫瘍 uncommon brain tumors
3. 後方循環系の脳血管症候群 posterior circulation cerebrovascular syndromes
4. 小児における急性小脳性運動失調 acute cerebellar ataxia in children
5. 成人における詳細な神経学的検査 the detailed neurologic examination in adults

English Journal

Epidemiology of primary brain tumors in childhood and adolescence in Kuwait.

Katchy KC, Alexander S, Al-Nashmi NM, Al-Ramadan A.SourceDepartment of Pathology, Al-Sabah Hospital, Safat, Kuwait ; FRCPath, FRCPC, Department of Pathology, Al-Sabah Hospital, P.O.Box 4078, 13041 Safat, Kuwait.
SpringerPlus.Springerplus.2013 Dec;2(1):58. Epub 2013 Feb 18.
The relatively high frequency of primary brain tumors (PBT) observed in childhood and adolescence in Kuwait has necessitated this epidemiological study. It is based on the records of the Department of Pathology, Al-Sabah Hospital, which examined all brain tumor biopsies done in this age group in Kuw
PMID 23519270

Running-induced epigenetic and gene expression changes in the adolescent brain.

Abel JL, Rissman EF.SourceDepartment of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA 22908, United States.
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience.Int J Dev Neurosci.2013 Oct;31(6):382-90. doi: 10.1016/j.ijdevneu.2012.11.002. Epub 2012 Nov 23.
Physical exercise is associated with positive neural functioning. Here we examined the gene expression consequences of 1 week of voluntary wheel running in adolescent male mice. We assayed expression levels of genes associated with synaptic plasticity, signaling pathways, and epigenetic modifying en
PMID 23178748

Altered synapses and gliotransmission in Alzheimer's disease and AD model mice.

Mitew S, Kirkcaldie MT, Dickson TC, Vickers JC.SourceWicking Dementia Research and Education Centre, University of Tasmania, Hobart, Tasmania, Australia; School of Medicine, Faculty of Health Science, University of Tasmania, Hobart, Tasmania, Australia.
Neurobiology of aging.Neurobiol Aging.2013 Oct;34(10):2341-51. doi: 10.1016/j.neurobiolaging.2013.04.010. Epub 2013 Apr 30.
Amyloid-β (Aβ) plaque accumulation in Alzheimer's disease (AD) is associated with glutamatergic synapse loss, but less is known about its effect on inhibitory synapses. Here, we demonstrate that vesicular γ-aminobutyric acid (GABA) transporter (VGAT) presynaptic bouton density is unaffected in hu
PMID 23643146

Japanese Journal

Toxicogenomics/proteomics Report : Effect of dental amalgam on gene expression profiles in rat cerebrum, cerebellum, liver and kidney

Takahashi Yoshifumi,Tsuruta Shozo,Honda Akiko [他]
The Journal of toxicological sciences 37(3), 663-666, 2012-06
NAID 40019353107

小脳・マシンインタフェースによる単一Purkinje細胞活動と運動学習の因果関係直接評価法(バイオサイバネティックス,ニューロコンピューティング)

片桐和真,田中良幸,平田豊
電子情報通信学会論文誌. D, 情報・システム J95-D(5), 1304-1311, 2012-05-01
身体運動の制御と学習の中核は小脳が担っている.小脳皮質神経回路を構成する細胞タイプのうち,Purkinje細胞は唯一小脳外へ軸索を伸ばす出力細胞である.これまでの研究により,Purkinje細胞の発火頻度は,筋系を駆動するための運動指令をコードしているものと考えられている.したがって,運動の学習はPurkinje細胞発火頻度パターンが変化することにより実現されるものと考えられている.こうした知見は …
NAID 110009444746

Related Pictures

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★リンクテーブル★

リンク元	「小脳」「脳」「大脳」「前脳」「菱脳」

「小脳」

Cerebellum
	Drawing of the human brain, showing cerebellum and pons
	Location of the human cerebellum (in red)
Details
Part of	Hindbrain
Artery	SCA, AICA, PICA
Vein	superior, inferior
Identifiers
Latin	Cerebellum
NeuroLex ID	Cerebellum
TA	A14.1.07.00166
FMA	67944
	Anatomical terms of neuroanatomy [edit on Wikidata]

脳: 小脳
	大脳間脳中脳橋延髄脊髄小脳脳の矢状断。緑色が小脳。ヒトの脳の外側面。小脳は図の右下、紫色で示す部分。脳内での小脳の位置（赤色で示す部分）。; 左図は側面から、右図は正面から見たとき。
名称
日本語	小脳
英語	cerebellum
ラテン語	cerebellum
略号	Cb
関連構造
上位構造	菱脳、後脳
構成要素	小脳虫部、小脳半球、小脳片葉、小脳核など
動脈	上小脳動脈、前下小脳動脈、後下小脳動脈
画像
アナトモグラフィー	三次元CG
Digital Anatomist	左側面; 右側面; 内側面; 前方; 下方; 後方; 脳幹; 冠状断（海馬采/脳弓）; 水平断; 傍矢状断
関連情報
IBVD	体積（面積）
Brede Database	階層関係、座標情報
NeuroNames	関連情報一覧
NIF	総合検索
MeSH	Cerebellum
グレイの解剖学	書籍中の説明（英語）
	テンプレートを表示

　　[★]

英: cerebellum

SP. 392,393
PT.105

発生

菱脳→後脳→小脳

解剖

小脳は上・中・下小脳脚によって脳幹と結合している

上小脳脚

主として小脳核から視床および脳幹へ向かう遠心性線維

中小脳脚

大脳皮質から橋核を介して主として半球外側に向かう求心性線維

下小脳脚

脳幹および延髄から主として虫部と半球中間部に向かう求心性線維

血管

機能概要

運動のタイミング決定と一つの運動から次の運動への急速な切り替え

機能

①運動開始に関与
②運動学習に関与
③多関節にわたる運動に関与
④フィードバックモード、フィードフォワードモードに関与

フィードバックモード~

熟練した運動で、早く動かさないとき

フィードフォワードモード~

素早い運動を行うとき。学習を行うとき

入力経路

1)体性感覚

①楔状核小脳路
②背側脊髄小脳路
③腹側脊髄小脳路
体の固有感覚は上小脳脚や下小脳脚から入り、脊髄小脳に投射

2)前庭感覚入力

前庭小脳路
前庭神経核→下小脳脚→前庭小脳、虫部

3)視覚、聴覚入力

中脳蓋小脳路
上丘(視覚)、下丘(聴覚)→上小脳脚→脊髄小脳路

4)大脳からの入力

橋小脳路
運動野(4,6野)、前頭前野(9,10野)、頭頂葉(5野)→橋核→中小脳脚→脊髄小脳、大脳小脳

5)運動の誤差情報の入力

障害 (KAPLAN USMLE STEP 1 QBOOK p.54)

障害

小脳性運動失調

平衡障害、筋緊張異常、運動障害に分けられる

1)片葉小節葉の障害 ... 入力は前庭器官

平衡障害

体幹失調=姿勢の制御不良
失調性歩行
注視方向への眼振(注意方向性眼振=注視眼振)

Tomberg兆候(-)(両側をそろえて開眼して立つ、その後閉眼しても倒れない)

2)虫部の障害 ...

体幹筋失調による歩行障害(体幹歩行失調, 失調性歩行)

酩酊様歩行
開脚歩行
継ぎ足歩行

3)小脳半球の障害

四肢の運動失調(協調運動障害)
①推尺障害
②変換運動障害
③運動解離
④共同運動不能
⑤失調性構音障害

筋緊張低下

中位核の障害により、皮質脊髄路、赤核脊髄路ニューロンの活動が低下する。

臨床関連

「脳」

　　[★]

英: brain
ラ: encephalon
関: 大脳、ブロードマン野

発生学

前脳	prosencephalon forebrain	終脳	telencephalon	大脳半球	cerebral hemisphere
前脳	prosencephalon forebrain	間脳	diencephalon	間脳	diencephalon
中脳	mesencephalon midbrain	中脳	mesencephalon	中脳	midbrain
菱脳	rhombencephalon hindbrain	後脳	metencephalon	橋	pons
		後脳	metencephalon	小脳	cerebellum
		髄脳	myelencephalon	延髄	medulla oblongata

解剖

重量：成人の場合体重の2.2%。2-3%ともいわれる。

新生児：約400g、成人：男性約1,350g、女性：約1,250g

脳幹に着目した分類

大脳、小脳、脳幹(中脳・橋・延髄)

発生学

外胚葉

生理学

脳血流量：心拍出量の15%　(心拍出量が5Lとしたら、毎分750ml灌流している事になる)
脳の酸素消費量：全身の消費量の20%
脳のグルコース消費量：全身の消費量の25%。1日100-150g(SCN.3)
血流限界：3分　⇔心臓は10分(see:窒息)

神経内科プリント

	脳での需要量	割合
血液	700～900 ml/分	心拍出量の	約15%
酸素	40～46 ml/分	全身需要量の	約20%
グルコース	310 μmol/分	全身需要量の	約25%

「大脳」

　　[★]

英: cerebrum
関: 脳、ブロードマン野

ブロードマン野

感覚野、運動野

身体各部局在　→

発生学

前脳	prosencephalon forebrain	終脳	telencephalon	大脳半球	cerebral hemisphere
前脳	prosencephalon forebrain	間脳	diencephalon	間脳	diencephalon
中脳	mesencephalon midbrain	中脳	mesencephalon	中脳	midbrain
菱脳	rhombencephalon hindbrain	後脳	metencephalon	橋	pons
		後脳	metencephalon	小脳	cerebellum
		髄脳	myelencephalon	延髄	medulla oblongata

機能障害

	優位半球	劣位半球
	左	右
側頭葉	感覚性失語、Wernicke失語、同名性上1/4半盲
頭頂葉	対側の感覚
	ゲルストマン症候群(手指失認、左右識別障害、失算、失書)	半側空間無視、病態失認、自己身体失認など
前頭葉	対側の運動麻痺、眼球運動(対側への追視)障害、運動性失語、知的及び精神的高次機能障害など
後頭葉	対側の同名半盲、両側後頭葉の障害ではアントン症候群
小脳	筋共同運動障害、運動・平衡障害に関係し、運動失調を呈する。測定異常、反復拮抗運動障害、筋緊張低下、運動過多、歩行異常、異常姿勢、発語障害、眼振など

「前脳」

　　[★]

pros 前方に
英: forebrain, prosencephalon
同: 前脳胞
関: 一次脳胞

図：B.3
前脳胞に由来する
終脳と間脳に分かれる

発生学

前脳	prosencephalon forebrain	終脳	telencephalon	大脳半球	cerebral hemisphere
前脳	prosencephalon forebrain	間脳	diencephalon	間脳	diencephalon
中脳	mesencephalon midbrain	中脳	mesencephalon	中脳	midbrain
菱脳	rhombencephalon hindbrain	後脳	metencephalon	橋	pons
		後脳	metencephalon	小脳	cerebellum
		髄脳	myelencephalon	延髄	medulla oblongata

「菱脳」

　　[★]

英: rhombencephalon (KL), hindbrain
関: 一次脳胞, 脳、脳胞

発生過程における脳胞の呼称
分化して、後脳と髄脳となる。

発生学

前脳	prosencephalon forebrain	終脳	telencephalon	大脳半球	cerebral hemisphere
前脳	prosencephalon forebrain	間脳	diencephalon	間脳	diencephalon
中脳	mesencephalon midbrain	中脳	mesencephalon	中脳	midbrain
菱脳	rhombencephalon hindbrain	後脳	metencephalon	橋	pons
		後脳	metencephalon	小脳	cerebellum
		髄脳	myelencephalon	延髄	medulla oblongata

[NOUWOKIWAMERU-1] 立花隆『脳を究める』朝日文庫 2001年3月1日

[Fine-2] Fine EJ, Ionita CC, Lohr L (2002). “The history of the development of the cerebellar examination”. Semin Neurol 22 (4): 375-84. PMID 12539058.

[3] Kingsley, R. E. (2000). Consise Text of Neuroscience (2nd edition ed.). Lippincott Williams and Wilkins. ISBN 0-683-30460-7.

[4] Gilman S (1998). “Imaging the brain. Second of two parts”. NEJM. 338 (13): 889-96. PMID 9516225.

[1] Wolf U, Rapoport MJ, Schweizer TA (2009). "Evaluating the affective component of the cerebellar cognitive affective syndrome". J. Neuropsychiatry Clin. Neurosci. 21 (3): 245–53. doi:10.1176/jnp.2009.21.3.245. PMID 19776302.

[Fine-2] Fine EJ, Ionita CC, Lohr L (2002). "The history of the development of the cerebellar examination". Semin. Neurol. 22 (4): 375–84. doi:10.1055/s-2002-36759. PMID 12539058.

[Gray-3] "Chapter 20". Gray's Anatomy (40th ed.). 2008. p. 297. ISBN 978-0-8089-2371-8.

[SOB-4] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x ^y Llinas RR, Walton KD, Lang EJ (2004). "Ch. 7 Cerebellum". In Shepherd GM. The Synaptic Organization of the Brain. New York: Oxford University Press. ISBN 0-19-515955-1.

[5] Herculano-Houzel S (2010). "Coordinated scaling of cortical and cerebellar numbers of neurons". Front. Neuroanat. 4:12. doi:10.3389/fnana.2010.00012.

[Ghez-6] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j Ghez C, Fahn S (1985). "The cerebellum". In Kandel ER, Schwartz JH. Principles of Neural Science, 2nd edition. New York: Elsevier. pp. 502–522.

[7] Kingsley RE (2000). Concise Text of Neuroscience (2nd ed.). Lippincott Williams and Wilkins. ISBN 0-683-30460-7.

[8] Petersen SE, Fox PT, Posner MI, Mintun M, Raichle ME (1989). "Positron emission tomographic studies of the processing of single words". Journal of Cognitive Neuroscience 1: 153–170. doi:10.1080/14734220701496448. PMID 17786810.

[9] Timmann D, Daum I (2007). "Cerebellar contributions to cognitive functions: a progress report after two decades of research". Cerebellum 6 (3): 159–62. doi:10.1162/jocn.1989.1.2.153. PMID 23968463.

[10] Strick PL, Dum RP, Fiez JA (2009). "Cerebellum and nonmotor function". Annual Review of Neuroscience 32: 413–434. doi:10.1146/annurev.neuro.31.060407.125606. PMID 19555291.

[11] Buckner RL (2013). "The cerebellum and cognitive function: 25 years of insight from anatomy and neuroimaging". Neuron 80 (3): 807–815. doi:10.1016/j.neuron.2013.10.044. PMID 24183029.

[12] Schweighofer N, Doya K, Kuroda S (2004). "Cerebellar aminergic neuromodulation: towards a functional understanding". Brain Res. Brain Res. Rev. 44 (2–3): 103–116. doi:10.1016/j.brainresrev.2003.10.004. PMID 15003388.

[Felizola_et_al-13] Felizola SJ, Nakamura Y, Ono Y, Kitamura K, Kikuchi K, Onodera Y, Ise K, Takase K, Sugawara A, Hattangady N, Rainey WE, Satoh F, Sasano H (2014). "PCP4: a regulator of aldosterone synthesis in human adrenocortical tissues.". J. Mol. Endocrinol. 52 (2): 159–167. doi:10.1530/JME-13-0248. PMC 4103644. PMID 24403568.

[14] Eccles JC, Llinás R, Sasaki K (1966). "The excitatory synaptic action of climbing fibers on the purkinje cells of the cerebellum". J. Physiol. 182 (2): 268–96. doi:10.1113/jphysiol.1966.sp007824. PMC 1357472. PMID 5944665.

[Simpson-15] Simpson JI, Wylie DR, De Zeeuw CI (1996). "On climbing fiber signals and their consequence(s)". Behav. Brain Sci. 19 (3): 384–398. doi:10.1017/S0140525X00081486.

[Marr-16] Marr D (1969). "A theory of cerebellar cortex". J. Physiol. 202 (2): 437–70. doi:10.1113/jphysiol.1969.sp008820. PMC 1351491. PMID 5784296.

[AppsGarwicz-17] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k Apps R, Garwicz M (2005). "Anatomical and physiological foundations of cerebellar information processing". Nature Rev. Neurosci. 6 (4): 297–311. doi:10.1038/nrn1646. PMID 15803161.

[18] Manni E, Petrosini L (2004). "A century of cerebellar somatotopy: a debated representation". Nature Rev. Neurosci. 5 (3): 241–9. doi:10.1038/nrn1347. PMID 14976523.

[19] Oscarsson O (1979). "Functional units of the cerebellum-sagittal zones and microzones". Trends Neurosci. 2: 143–145. doi:10.1016/0166-2236(79)90057-2.

[20] Rapp B (2001). The Handbook of Cognitive Neuropsychology: What Deficits Reveal about the Human Mind. Psychology Press. p. 481. ISBN 1-84169-044-9.

[Doya-21] Doya K (2000). "Complementary roles of basal ganglia and cerebellum in learning and motor control". Curr. Opin. Neurobiol. 10 (6): 732–739. doi:10.1016/S0959-4388(00)00153-7. PMID 11240282.

[22] Schmahmann JD, Sherman JC (April 1998). "The cerebellar cognitive affective syndrome". Brain 121 (4): 561–79. doi:10.1093/brain/121.4.561. PMID 9577385.

[23] Levisohn L, Cronin-Golomb A, Schmahmann JD (May 2000). "Neuropsychological consequences of cerebellar tumour resection in children: cerebellar cognitive affective syndrome in a paediatric population". Brain 123 (5): 1041–50. doi:10.1093/brain/123.5.1041. PMID 10775548.

[24] Buckner RL, Krienen FM, Castellanos A, Diaz JC, Yeo BT (2011). "The organization of the human cerebellum estimated by intrinsic functional connectivity". J. Neurophysiol. 106 (5): 2322–2345. doi:10.1152/jn.00339.2011. PMC 3214121. PMID 21795627.

[25] Hernáez-Goñi P, Tirapu-Ustárroz J, Iglesias-Fernández L, Luna-Lario P (November 2010). "Participación del cerebelo en la regulación del afecto, la emoción y la conducta" [The role of the cerebellum in the regulation of affection, emotion and behavior]. Revista de Neurologia (in Spanish) 51 (10): 597–609. PMID 21069639.

[26] Turner BM, Paradiso S, Marvel CL, Pierson R, Boles Ponto LL, Hichwa RD, Robinson RG (March 2007). "The cerebellum and emotional experience". Neuropsychologia 45 (6): 1331–41. doi:10.1016/j.neuropsychologia.2006.09.023. PMC 1868674. PMID 17123557.

[27] Doya K (1999). "What are the computations of the cerebellum, the basal ganglia and the cerebral cortex?". Neural Networks 12 (7–8): 961–974. doi:10.1016/S0893-6080(99)00046-5. PMID 12662639.

[28] Eccles JC, Ito M, Szentágothai J (1967). The Cerebellum as a Neuronal Machine. Springer-Verlag.

[29] The Cerebellum as a Neuronal Machine, p. 311

[Boyden-30] Boyden ES, Katoh A, Raymond JL (2004). "Cerebellum-dependent learning: the role of multiple plasticity mechanisms". Annu. Rev. Neurosci. 27: 581–609. doi:10.1146/annurev.neuro.27.070203.144238. PMID 15217344.

[Albus-31] Albus JS (1971). "A theory of cerebellar function". Math. Biosciences 10 (1–2): 25–61. doi:10.1016/0025-5564(71)90051-4.

[Houk1996-32] Houk JC, Buckingham JT, Barto AG (1996). "Models of the cerebellum and motor learning". Behav. Brain Sci. 19 (3): 368–383. doi:10.1017/S0140525X00081474.

[33] Fujita M (1982). "Adaptive filter model of the cerebellum". Biol. Cybern. 45 (3): 195–206. doi:10.1007/BF00336192. PMID 7171642.

[34] Gilbert PF, Thach WT (1977). "Purkinje cell activity during motor learning". Brain Res. 128 (2): 309–28. doi:10.1016/0006-8993(77)90997-0. PMID 194656.

[35] Christian KM, Thompson RF (2003). "Neural substrates of eyeblink conditioning: acquisition and retention". Learn. Mem. 10 (6): 427–55. doi:10.1101/lm.59603. PMID 14657256.

[36] Braitenberg V, Atwood RP (1958). "Morphological observations on the cerebellar cortex". J. Comp. Neurol. 109 (1): 1–33. doi:10.1002/cne.901090102. PMID 13563670.

[37] Braitenberg V, Heck D, Sultan F (1997). "The detection and generation of sequences as a key to cerebellar function: Experiments and theory". Behav. Brain Sciences 20 (2): 229–277. doi:10.1017/s0140525x9700143x. PMID 10096998.

[38] Ivry RB, Spencer RM, Zelaznik HN, Diedrichsen J (2002). "The cerebellum and event timing". Ann. N. Y. Acad. Sci. 978: 302–307. Bibcode:2002NYASA.978..302I. doi:10.1111/j.1749-6632.2002.tb07576.x. PMID 12582062.

[39] Pellionisz A, Llinás R (1982). "Space-time representation in the brain. The cerebellum as a predictive space-time metric tensor". Neuroscience 7 (12): 2949–70. doi:10.1016/0306-4522(82)90224-X. PMID 7162624.

[40] Horváth G (2003). "CMAC: Reconsidering an old neural network" (PDF). Intelligent Control Systems and Signal Processing. Retrieved 2009-12-24.

[41] Schmitz TJ (2007). "Examination of Coordination". In O'Sullivan SB, Schmitz TJ. Physical Rehabilitation. Philadelphia: F. A. Davis. pp. 193–225.

[42] Gilman S (1998). "Imaging the brain. Second of two parts". N. Engl. J. Med. 338 (13): 889–96. doi:10.1056/NEJM199803263381307. PMID 9516225.

[NINDS-ataxias-43] "NINDS Ataxias and Cerebellar or Spinocerebellar Degeneration Information Page". National Institutes of Health. 16 April 2014. Retrieved 2 February 2015.

[44] Yuhas, D (January 15, 2016). "Veterans of Iraq, Afghanistan Show Brain Changes Related to Explosion Exposure". Scientific American. Retrieved January 21, 2016.

[45] Vincent M, Hadjikhani N (2007). "The cerebellum and migraine". Headache 47 (6): 820–33. doi:10.1111/j.1526-4610.2006.00715.x. PMC 3761082. PMID 17578530.

[NINDS-degen-46] "NINDS Cerebellar Degeneration Information Page". National Institutes of Health. 28 February 2014. Retrieved 2 February 2015.

[47] Horvath S, Mah V, Lu AT, Woo JS, Choi OW, Jasinska AJ, Riancho JA, Tung S, Coles NS, Braun J, Vinters HV, Coles LS (2015). "The cerebellum ages slowly according to the epigenetic clock." (PDF). Age 7 (5): 294–306. doi:10.18632/aging.100742. PMID 26000617.

[48] Fraser HB; Khaitovich P; Plotkin JB; Pääbo S; Eisen MB (2005). "Aging and gene expression in the primate brain". PLoS Biology 3 (9): e274. doi:10.1371/journal.pbio.0030274. PMC 1181540. PMID 16048372.

[49] Andersen BB, Gunderson HJ, Pakkenberg B (2003). "Aging of the human cerebellum: A stereological study". J. Comp. Neurol. 466 (3): 356–365. doi:10.1002/cne.10884. PMID 14556293.

[50] Raz N, Gunning-Dixon F, Head D, Williamson A, Acker JD (2001). "Age and sex differences in the cerebellum and the ventral pons: A prospective MR study of healthy adults" (PDF). Am. J. Neuroradiol. 22 (6): 1161–1167. PMID 11415913.

[Merck_1886-1887-51] Albert, Richard K.; Porter, Robert S., eds. (2006). The Merck Manual of Diagnosis and Therapy (18th ed.). Whitehouse Station, New Jersey: Merck Research Libraries. pp. 1886–1887.

[:0-52] Hatten, M (1995). "Mechanisms of neural patterning and specification in the developing cerebellum". Annu Rev Neurosci 18: 385–408. doi:10.1146/annurev.ne.18.030195.002125. PMID 7605067.

[53] Polkinghorn, W (2007). "Medulloblastoma: tumorigenesis, current clinical paradigm, and efforts to improve risk stratification". Nat Clin Pract Oncol 4: 295–304. doi:10.1038/ncponc0794. PMID 17464337.

[54] Roussel, M (2011). "Cerebellum development and medulloblastoma". Curr Top Dev Biol 94: 235–82. doi:10.1016/B978-0-12-380916-2.00008-5. PMC 3213765. PMID 21295689.

[55] "NINDS Joubert Syndrome Information Page". National Institutes of Health. 23 December 2013. Retrieved 9 January 2015.

[56] "NINDS Dandy-Walker Information Page". National Institutes of Health. 14 February 2014. Retrieved 9 January 2015.

[57] "NINDS Cerebellar Hypoplasia Information Page". National Institutes of Health. 29 September 2011. Retrieved 9 January 2015.

[58] "Chiari Malformation Fact Sheet". National Institutes of Health. 10 December 2014. Retrieved 9 January 2015.

[59] "NINDS Dyssynergia Cerebellaris Myoclonica Information Page". National Institutes of Health. 14 February 2011. Retrieved 1 February 2015.

[60] "NINDS Olivopontocerebellar Atrophy Information Page". National Institutes of Health. 16 April 2014. Retrieved 9 January 2015.

[61] "NINDS Paraneoplastic Syndromes Information Page". National Institutes of Health. 12 March 2009. Retrieved 9 January 2015.

[62] "NINDS Wernicke-Korsakoff Syndrome Information Page". National Institutes of Health. 14 February 2007. Retrieved 9 January 2015.

[Bell-63] Bell CC, Han V, Sawtell NB (2008). "Cerebellum-like structures and their implications for cerebellar function". Annu. Rev. Neurosci. 31: 1–24. doi:10.1146/annurev.neuro.30.051606.094225. PMID 18275284.

[64] Woodhams PL (1977). "The ultrastructure of a cerebellar analogue in octopus". J. Comp. Neurol. 174 (2): 329–45. doi:10.1002/cne.901740209. PMID 864041.

[VB-65] Romer AS, Parsons TS (1977). The Vertebrate Body. Philadelphia: Holt-Saunders International. p. 531. ISBN 0-03-910284-X.

[66] Shi Z, Zhang Y, Meek J, Qiao J, Han VZ (2008). "The neuronal organization of a unique cerebellar specialization: the valvula cerebelli of a mormyrid fish". J. Comp. Neurol. 509 (5): 449–73. doi:10.1002/cne.21735. PMID 18537139.

[67] Weaver AH (2005). "Reciprocal evolution of the cerebellum and neocortex in fossil humans". Proc. Natl. Acad. Sci. U.S.A. 102 (10): 3576–3580. Bibcode:2005PNAS..102.3576W. doi:10.1073/pnas.0500692102. PMC 553338. PMID 15731345.

[Schoenemann.2C_2009-68] Schoenemann PT (December 1, 2009). "Evolution of Brain and Language". Language Learning 59: 162–186. doi:10.1111/j.1467-9922.2009.00539.x.

[69] MacLeod CE, Zilles K, Schleicher A, Rilling JK, Gibson KR (2003). "Expansion of the neocerebellum in Hominoidea". J. Hum. Evol. 44 (4): 401–429. doi:10.1016/S0047-2484(03)00028-9. PMID 12727461.

[70] Roberts PD, Portfors CV (2008). "Design principles of sensory processing in cerebellum-like structures. Early stage processing of electrosensory and auditory objects". Biol. Cybern. 98 (6): 491–507. doi:10.1007/s00422-008-0217-1. PMID 18491162.

[71] Bower JM (1997). "Is the cerebellum sensory for motor's sake, or motor for sensory's sake: the view from the whiskers of a rat?". Prog. Brain Res. 114: 463–96. doi:10.1016/S0079-6123(08)63381-6. ISBN 978-0-444-82313-7. PMID 9193161.

[72] Heiney SA, Kim J, Augustine GJ, Medina JF (February 2014). "Precise control of movement kinematics by optogenetic inhibition of Purkinje cell activity". J. Neurosci. 34 (6): 2321–30. doi:10.1523/JNEUROSCI.4547-13.2014. PMC 3913874. PMID 24501371.

[73] Witter L, Canto CB, Hoogland TM, de Gruijl JR, De Zeeuw CI (2013). "Strength and timing of motor responses mediated by rebound firing in the cerebellar nuclei after Purkinje cell activation". Front. Neural Circuits 7: 133. doi:10.3389/fncir.2013.00133. PMC 3748751. PMID 23970855.

[74] Clarke E, O'Malley CD (1996). "Ch. 11: Cerebellum". The Human Brain and Spinal Cord (2nd ed.). Norman Publishing. p. 629. ISBN 0-930405-25-0.

[75] Ito M (2002). "Historical review of the significance of the cerebellum and the role of Purkinje cells in motor learning". Ann. N. Y. Acad. Sci. 978: 273–288. Bibcode:2002NYASA.978..273I. doi:10.1111/j.1749-6632.2002.tb07574.x. PMID 12582060.

[76] Lewis CT, Short C (1879). A Latin dictionary founded on Andrews' edition of Freund's Latin dictionary. Oxford: Clarendon Press.

[77] Marshall LH, Magoun HW (1998). Discoveries in the human brain. Neuroscience prehistory, brain structure, and function. Totowa: Humana Press.

[Foster1891-78] Foster FD (1891). An illustrated medical dictionary. New York: D. Appleton and Company.

[79] Kraus LA (1844). Kritisch-etymologisches medicinisches Lexikon (Dritte Auflage). Göttingen: Verlag der Deuerlich- und Dieterichschen Buchhandlung.

[80] Schreger CHT (1805). Synonymia anatomica. Synonymik der anatomischen Nomenclatur. Fürth.

脳: 小脳
大脳間脳中脳橋延髄脊髄小脳脳の矢状断。緑色が小脳。ヒトの脳の外側面。小脳は図の右下、紫色で示す部分。脳内での小脳の位置（赤色で示す部分）。左図は側面から、右図は正面から見たとき。
名称
日本語	小脳
英語	cerebellum
ラテン語	cerebellum
略号	Cb
関連構造
上位構造	菱脳、後脳
構成要素	小脳虫部、小脳半球、小脳片葉、小脳核など
動脈	上小脳動脈、前下小脳動脈、後下小脳動脈
画像
アナトモグラフィー	三次元CG
Digital Anatomist	左側面右側面内側面前方下方後方脳幹冠状断（海馬采/脳弓）水平断傍矢状断
関連情報
IBVD	体積（面積）
Brede Database	階層関係、座標情報
NeuroNames	関連情報一覧
NIF	総合検索
MeSH	Cerebellum
グレイの解剖学	書籍中の説明（英語）
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cerebellum

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目次

発生と進化

構造と機能

区分

深部小脳核

小脳皮質

小脳脚

小脳髄質

血液供給

機能障害

小脳症候

上肢の小脳症候診察

下肢、体幹の小脳症候診察

出典・脚注

関連文献

関連項目

外部リンク

wiki en

Contents

Structure

Gross anatomy

Subdivisions

Microanatomy

Purkinje cells

Granule cells

Mossy fibers

Climbing fibers

Deep nuclei

Compartments

Function

Principles

Learning

Theories and computational models

Clinical significance

Aging

Developmental and degenerative disorders

Comparative anatomy and evolution

Cerebellum-like structures

History

Descriptions

Etymology

References

External links

UpToDate Contents

English Journal

Japanese Journal

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★リンクテーブル★

「小脳」

発生

解剖

血管

機能概要

機能

入力経路

障害 (KAPLAN USMLE STEP 1 QBOOK p.54)

障害

臨床関連

「脳」

発生学

解剖

脳幹に着目した分類

発生学

生理学

神経内科プリント

「大脳」

ブロードマン野

感覚野、運動野

発生学

機能障害

「前脳」