Pemicu 4

BLOK SARAF
Jessica Gracia
405140041
LI
• 1. MM anatomi
• 2. MM histologi
• 3. MM fisiologi SSP
• 4. MM definisi penyakit UMN
Anatomi
SSP
• Telencephalon (Endbrain)
• Diencephalon (Interbrain)
• Mesencephalon (Midbrain)
• Metencephalon (Afterbrain)
• Myelencephalon (Narrow Brain)
SCALP (Dinding SSP)
• The scalp consists of  skin (normally hair bearing) & subcutaneous tissue
(cover the neurocranium from the superior nuchal lines on the occipital
bone to the supra- orbital margins of the frontal bone. Laterally, the scalp
extends over the temporal fascia to the zygomatic arches.
• composed of 5 layers  1st 3 of which are connected intimately & move as
a unit
• Skin.
• Connective tissue
• Aponeurosis (epicranial aponeurosis)
• Loose areolar tissue
• Pericranium
SCALP (Dinding SSP)
Cranial Meninges
• The cranial meninges  membranous coverings of the brain that lie
immediately internal to the cranium
• The cranial meninges:
• Protect the brain.
• Form the supporting framework for arteries, veins, and venous sinuses.
• Enclose a fluid-filled cavity, the subarachnoid space, which is vital to the
normal function of the brain.
• The meninges  composed of 3 membranous connective tissue
• Dura mater (dura): tough, thick external fibrous layer.
• Arachnoid mater (arachnoid): thin intermediate layer.
• Pia mater (pia): delicate internal vasculated layer.
Cranial Meninges
• The cranial meninges  membranous coverings of the brain that lie immediately
internal to the cranium
• The cranial meninges:
• Protect the brain.
• Form the supporting framework for arteries, veins, and venous sinuses.
• Enclose a fluid-filled cavity, the subarachnoid space, which is vital to the normal function of
the brain.
• The meninges  composed of 3 membranous connective tissue
• Dura mater (dura): tough, thick external fibrous layer.
• Arachnoid mater (arachnoid): thin intermediate layer.
• Pia mater (pia): delicate internal vasculated layer.

• Pachymeninx  Duramater
• Leptomeninx  Arachnoid and pia.
Cranial Meninges
Cranial Meninges [Dura mater]
• Suatu jaringan ikat kolagen  merekat erat dgn stratum meningeale
• Terdapat spatium epidurale  celah antara lamina interna tulang
dengan dura.
Cranial Meninges
ANATOMI SISTEM SARAF
Sistem saraf dibagi menjadi 2  sistem saraf pusat(CNS) & sistem
saraf perifer (PNS)
Susunan saraf pusat
1. Telencephalon
2. Diencephalon
3. Mesencephalon
4. Metencephalon
5. Myelencephalon
6. Medula spinalis
TELENCEPHALON/CEREBRUM HEMISPHERE
• Cerebrum  (+) 2 hemisfer
• Memiliki 3 kutub  frontal, occipital dan temporal
(aspek lateral)
• Memiliki 4 lobus
CEREBRAL HEMISPHERE
• Hemisfer  (+) 3 batas superomedial,
inferolateral dan inferomedial (potongan
koronal)
• Batas2 membagi otak mjd bbrp bagian
• Superolateral
• Medial
• Inferior  terbagi menjadi bg anterior
(orbital) & posterior (tentorial)
CEREBRAL HEMISPHERES
Permukaan superolateral
Terdapat 2 sulkus prominen
• Ramus posterior sulcus lateralis
• Sulcus centralis  midpoint dari lobus frontalis dan occipitalis
Permukaan medial
• Sulcus parietooccipitalis
Terdapat batas inferomedial anterior dari lobus occipitalis 
preoccipital notch (incisura preoccipitalis)
CEREBRAL HEMISPHERE
Pembagian permukaan superolateral
• Lobus frontalis
• (+) sulcus precentralis  membagi pracentral gy & postcentral gy
• (+) sulcus frontalis inf & sup  mmbg gyrus sup & mid , mid dan inf
• Ramus ant ascendens sulcus lateralis
• Ke anterior  pars orbitalis
• b/w ant & ascending  pars triangularis
• Posterior  pars opercularis
CEREBRAL HEMISPHERE
• Lobus temporalis
• (+) sulcus temporalis superior  mmbagi gyrus temporalis sup & medialis
• (+) sulcus temporalis inferior  mmbagi gyrus temporalis medialis & inf
• Lobus parietalis
• (+) sulcus postcentralis & sulcus centralis  ruang diantara dsbt gyrus postcentralis
• Intraparietal sulcus  membagi lobus parietalis sup & inf
• Ujung dari ramus posterior sulcus lateralis ekstensi sampai ke lobus parietalis inf 
mmbagi lobus mjd 3 bagian
• Supramarginal gyrus  lanjutan dr ramus post sulcus lateralis melengkung keatas
• Angular gyrus  lanjutan yg melengkung sampai ke sulcus temporalis sup
• Arcus temporooccipitalis  bagian yg melengkung pada ujung post dan ing dari sulcus
temporalis
CEREBRAL HEMISPHERE
• Lobus occipitalis
• Sulcus occipitalis lateralis  membagi gyrus occipital inf dan sup
• Sulcus lunatus
• Gyrus descenden  vertical strip yg berada didepan kutub occipital
• Sulcus occipitalis transversalis  bagian plg atas dari kutub occipitalis
• Arcus parieto osccipitalis
• Insula
• Bagian dalam dari batang & ramus posterior sulcus lateralis
• Dikelilingi o/ sulcus circularis
• Operculum
• Frontal operculum
• Frontoparietal operculum
• Temporal operculum
CEREBRAL HEMISPHERE
(permukaan medial)
Corpus callosum
• Membagi ke2 hesmifer
• tdd  splenium (posterior), trunk (central) dan genu (anterior)
• Bagian dr inf corpus callosum  3rd ventricle
• Foramen intraventrikuler  menghubungkan 3rd ventricle dgn lateral
ventricle
• Thalamus  dinding lateral ventricle yg dibentuk o/ masa besar dari
substansia grisea
• Thalamus kanan dan kiri dibatasi o/ connexus interthalamic
• Hypothalamus  bagian anteroinferior dari dinding lateral 3rd ventricle
• Fornix  t’ltk diatas thalamus, berbentuk gumpalan serat
• Posterior  corpus callosum
• Septum pellucidum
• lamina tipis diantara fornix dan corpus callosum
• Memisalahkan ventrikel lateral kanan dan kiri
• Commissura anterior & lamina terminalis (lamina tipis dari jaringan saraf) dinding ant dari 3rd ventricle
• Rostrum  penghub antara commissura ant dgn corpus callosum
• Paraterminal gyrus & Para olfactorius gyrus  terletak di ant dari lamina terminalis
• Pineal body/glands  T’ltk di posterior dr 3rd ventrikel
• Serebri hipofisis  T’ltk di inferior dr 3rd ventrikel
• Sulcus cingulate
• Batas ant  rostrum
• Batas post  sulcus centralis
• Gyrus cinguli  dibatasi o/ sulcus callosus dgn corpus callosum
• Terdapat lobus paracentral yg dipisah kan o/ sulcus centralis dgn gyrus
frontalis media
• Cuneus  permukaan medial dibelakang lobus paracentral dan gyrus
cinguli, tdpt 2 sulcus mayor yg memotong suatu area segitiga
• Batas ant & sup  sulcus parieto-occipitalis
• Inf  sulcus calcarine
• Post  hemisfer superomedial
• Isthmus  area kecil yg memisahkan splenium dari sulcus calcarine
• Precuneus  area quadrilateral yg tltk diantara sulcus parieto-occipitalis
dan lobus paracentralis
• Ant & post dari precuneus dipisahkan o/ sulcus suprasplenial/subparietal
CEREBRAL HEMISPHERE
(Bagian inf)
• Fossa interpeduncularis
• Batas ant  Optic chiasma
• Batas lat dan med  traktus opticus
• Medial & Lateral geniculate
• traktus opticus yang memotong aspek posterolateral dari midbrain
• Mamillary bodies
• Pembengkakan bulat yg tdpt pd bagian ant dan media dari crura midbrain
• Di bagian ant  tdpt elevasi median  tuber cinereum  T4 melekatnya infundibulum dr
hypophysis
• Posterior perforated substance  triangular interval antara mamillary bodies dan midbrain
yg di perforasi o/ bnyk P.D
• Anterior perforated substance  dpt pd sisi optic chiasma
• Batas anterolateral  stria olfaktorius lateralis
• Batas posterolateral  uncus
• Berhub dgn insula o/ substansia grisea yg disebut limen insulae
Sulcus dan gyrus pada permukaan orbitas
• Sulcus olfactorius  sulcus anteroposterior pada permukaan orbitalis
• (+) area medial dari sulcus olfactorius  gyrus rectus
• sisa dr permukaan orbital dibagi o/ sulcus orbitalis dlm pola ‘H’ mnjd
 gyrus orbitalis ant, post, med dan lar
Sulcus dan gyrus pada permukaan tentorial
• Sulcus collateralis  medial
• Bg post berjalan parallel dgn sulcus calcarine yg mmbtk area diantaranya yg
dsbt  gyrus lingualis
• ant dr gyrus lingualis lanjut mjd gyrus parahippocampal  berhub pd medial
midbrain dan fossa interpeduncularis
• Sulcus rhinalis  bagian yg memotong gyrus hippocampus dgn lekukan kutub
temporal
• Sulcus occipito-temporalis  lateral
• Gyrus occipitotemporalis area diantara sulcus occipitotemporalis, sulcus
collateralis dan sulcus rhinalis
STRUKTUR DIDALAM HEMISFER SEREBRALIS
• Cerebral cortex  permukaan hemisfer serebral yg berwarna abu2
• Dilateral dari 3rd ventricle  (+) thalamus dan hypothalamus  derivat dr
diencephalon
• Corpus striatum  derivat telencephalon yg tdd
• Nucleus caudatus
• Nucleus lentiformis  diantara nuclues lentiformis dan insula tdpt lapisan kecil abu2
 claustrum
• Nucleus caudatus + nucleus lentiformis + claustrum + massa pada substansia grisea
yg mrupakan derivat dari telencephalon  basal nuclei
• Internal capsule  substansia alba yg mengokupasi thalamus dan nucleus
caudatus dan nucleus lentiformis
• corona radiata  substansia alba yg berasal dari internal capsule menuju
cortex
Fungsi Area dari Korteks
Serebral
• Area Motorik
• Lokasi  gyrus pracentral pada permukaan
superolateral + bagian anterior dari lobus
paracentral pd permukaan medial
• Broadman  4
• Lobus paracentralis  u/ pergerakan
tungkai bwh
• Gyrus precentralis (bg atas) badan dan
tungkai atas
• Gyrus precentralis (bg bwh  wajah &
kepala
Fungsi Area dari Korteks
Serebral
Area Premotorik
• Terletak didepan area motorik
• Gyrus frontalis sup dan mid (Broadman) 
6 dan 8
• Gyrus frontalis inf (Motor speech area
/broca ) 44 dan 45
• Frontal eye field (bg anterior dari gyrus
pracentral)  Broadman 6,8, dan 9
• u/ gerakan conjugat ( menggerakan
kepala dan dilatasi pupil)
Fungsi Area dari Korteks
Serebral
• Area Sensorik
• Broadman 1,2,3
• Respon dpt di rekam dari area
sensorik ketika tubuh distimulasi
• Bagian tubuh yg plg sensitif 
digital, lidah dan bibir
Fungsi Area dari Korteks
Serebral
• Area Visual
• Terletak di lobus occipitalis t.u di
permukaan medial diwbh & diatas
sulcus calcarina ( area 17)
• Area 17 berkelanjutan mjd area 18 dan
19
• Area 18 & 19  u/ interpretasi hasil
mnju are 17 (area phychovisual)
Fungsi Area dari Korteks
Serebral
• Area Acoustic (auditory)
• Tdpt pd lobus temporalis
• Terdapat 2 gyrus oblik yg disebut gyrus
temporalis transversalis ant dan post (area
41,41 dan 52
• Gyrus temporalis transversalis ant (area41)
memanjang mmbtk ke gyrus temporalis
sup
ARTERI YG MENSUPPLY OTAK
• Otak di supply o/ cabang dr A. carotid interna & A.
vertebralis
• A. carotid interna  bercabang mnjd
• A. cerebralis Anterior
• A. cerebralis media
• 2 A. vertebralis berjalan naik secara anterolateral  pada
batas bawah dr pons bergabung dan membentuk A. basilaris
• Pada batas atas pons  A. basilaris mengalami bifurkasi
mnjd 2 A. cerebralis posterior
• Sistem internal carotid dan vertebro-basilaris dihub dgn A.
communis post
• 2 A. cerebralis ant di hub kan o/ A. communis ant
• Hasil dr anastomosis Arteri diatas membentuk cincin
arteri/circulus of willis/ arteriosus
ARTERI YG MENSUPPLY OTAK
• A. carotid interna mempunyai cabang kecil
• A. choroidal ant (cbg lgsng)  berjalan mundur kearah traktus optikus dan
masuk ke tanduk ind ventrikel lateral lewat fissura choroidalis
• Cabang rekuren dari A. cerebralis ant/ Artery of heubner  (+) trombosis
 paralysis kontralateral pd wajah dan ekstremitas atas
• A. cerebralis ant, mid dan post bercabang menjadi
• A. corticalis  memperdarahi korteks
• A. centralis /perforating  masuk kdlm substansia cerebral 
memperdarahi bagian dlm
A. CENTRALIS
• A. central tdd 6 group utama
• Anteromedial  berasal dr A. communis Ant dan A. cerebralis ant
• Posteromedial  berasal dr A. communis posterior & A. serebralis posterior
 masuk ke regio interpeduncularis
• Anterolateral dextra dan sinistra/striae arteries
• Berasal t.u dr A. cerebralis media , dan bbrpa A. A. cerebralis ant
• Perforasi kdlm area substansia dan dibagi mjd :
• Bagian lateral  A . Striae lateralis  (+) cabang Arteri yg > bsr dr yg lainnya  A.charcot’s /
A.cerebralis hemoragikus
• Bagian medial  A, Striae medialis  memperdarahi nucleus lentiformis, caudatus dan
capsula interna
• Posterolateral dextra & sinistra  brasal dari A. cerebralis post dan berjalan
disekitar pedunculus cerebralis
• A. vertebralis bercabang mnjd
• A. spinalis Ant dan Post  memperdarahi medulla
• A. cerebeRALIS post inf  memperdarahi medulla dan cerebellum
• A. basilaris bercabang mjd
• A. cerebeRALIS ant inf
• A. cerebeRALIS sup
• A. cereberalis post (bercabang mjd A. choroidal post) cabang terminal dr A.
basillaris
Arteri Korteks Serebral
Permukaan superolateral
• A. cerebralis ant  ½ - 1 inch lebar
disepanjang batas superomedial dari bagian
frontalis – sulcus parieto-occipitalis
• A. cerebralis post  lobus occipitalis & gyrus
temporalis inf (x) tmsk kutub temporal
Permukaan medial
• Main artery  A. cerebralis Ant
• Bagian medial dr lobus occipitalis  A.
cerebralis post
Permukaan inferior
• Permukaan orbitalis  A. cerebralis media dan
pada bagian medial o/ A, cerebralis ant
• Permukaan tentorial  A. cerebralis post & pada
kutub temporalis di perdarahi o/ A. cerebralis
media
Bagian somatik motorik dan sensorik  diperdarahi
o/ A. cerebralis media, KECUALI bg plg atas (legs
area) yg di supp o/ A. cerebralis ant
Area akustik  A. cerebralis media
Area visual  A. cerebralis post
INTERNAL CAPSULE
• Arteri utama yg memperdarahi adalah
• A. cerebralis media cabang dari A. striate lateral dan media
• A. cerebralis ant cabang rekuren,
• A. choroidal Ant
• Bagian atas dari ekstremitas ant, genu dan post di perdarahi o/ A.
cerebralis media cabang striate
• Bagian bawah ekstremitas diperdarahi o/
• Bg bawah dari anterior limb  cabang rekuren dari A. cerebralis ant
• Bg bwh dari genu  cabang lgsg dr A. carotid interna dan A. communis posterior
• Bg bwh posterior limb  A. choroidal ant
• Bg retrolentiform & sublentiform  A. choroidal ant
Thalamus Hypothalamus
• Disupply t.u o/ A. cerebralis • Anterior  cabang centralis
post cabang perforata dari group anteromedial (
• Bg medial & anterior  A. cabang dr A. cerebralis ant)
thalamo-perforata (cabang • Posterior  cabang centralis
group posteromedial)
dari group posteromedial
• Posterior & lateral  cabang (cabang dari A. cerebralis
thalamo-geniculate (group post dan communis post)
posterolateral)
• Thalamus jg mndptkan
perdarahan dr  A,
communis posterior,
choroidal ant, dan cerebral
arteri
Corpus Striatum
• Nucleus caudatus dan putemen  t.u o/ A.
cerebralis media cabang striate medial dan
lateral
• Bagian paling dpn(tmsk caput nucleus
caudatus)  A. cerebralis ant cabang rekuren
• Bagian posterior ( caudal nucleus caudatus )
 A. choroidal ant
• Globus pallidus  A. choroidal ant, lateral
segment ( (+) A. striate) dan bg plg medial
(cabang dari A. communis posterior )
CEREBELLUM
• Permukaan superior  cabang superior cerebellar dari A. basilaris
• Bg anterior dari permukaan inferior  Cabang anteroinferior dari A.
basilaris
• Bg posterior dari permukaan inferior  cabang inferoposterior
cerebellar dari A. vertebralis
PERDARAHAN BALIK OTAK/ DRAINASE VENA
• Drainase vena otak terbuka lewat sinus venosus duralis (sup sagittal, inf sagittal,
straight, transverse, sigmoid, cavernous, sphenoparietal, petrosal dan occipital
sinuses)
• Darah sinus2  sinus sigmoideus  vena jugularis interna
• Sinus venosus intracranialis berhub dgn vena diluar tengkorak lewat vena
emissary
Sinus Otak
VENA DARI HEMISFER CEREBRAL
Tdd vena superficial dan profunda
• V. superficialis  drainase kdlm sinus venosus yg berdekatan
• V. cerebralis sup  drainase ke bagian atas dari permukaan superolateral dan
medial dan berakhir di sinus sagitalis sup
• V. cerebralis inf  drainase ke bagian bawah dari hemisfer
• V. cerebralis media superficialis  pad permukaan superolateral , tdpt
sepanjang sulcus lateralis dan ramus posterior
• Ujung posterior yg berhub dgn SSS  V. anastomotic sup
• Berhub dgn sinus transversus  V. anastomotic inf
VENA SEREBRALIS
Vena profunda
• Tdpt 2 V. cerebralis interna  bergabung mmbtk V. cerebralis mayor
• dimulai di foramen interventricularis  choroidea tela pada atap dari 3rd
ventricle  mmbtk V. thalamostriae pd bg bwg dr ventricle lateral
• Tdpt 2 V. basilaris  sepanjang midbrain dan berakhir ke V. cerebralis
mayor, dan dibtk dr gabungan :
• V. cerebralis ant  bersama A. cerebralis Ant
• V. cerebralis media profunda  tdpt pada bagian dlm batang dan ramus post
sulcus lateralis
• V. striate inf  gabungan dr Substansia perforata anterior
VENA SEREBRALIS
• V. serebralis mayor  dibtk dari gabungan 2 V. cerebralis interna 
menerima darah dr v. basalis & bbrp V. dari occipital dan corpus
callosum
• V. cerebralis profunda  drainase dari thalamus, hypothalamus ,
corpus striatum, capsula interna, corpus callosum, septum
pellucidum dan plexus choroidalis
• Berperan sbg channel alternatif mnj korteks serebral
• Berhub dgn v. superficialis cerebri
VENA CEREBERALIS
• Vena dari permukaan atas  masuk ke sinus venosus rectus,
transversalis dan petrosal superior
• Vena dari permukaan inf  drainase kedalam sinus sigmoidalis dan
petrosal inf, Sinus occipitalis dan sinus rectus
Medula spinalis
Medula spinalis
• Suatu struktur yang terletak di dalam canalis vertebralis, yang
bentuknya memanjang seperti tabung silindris dengan sedikit
mendatar di daerah sisi dorso ventral
• Panjang : 40-45 cm
• 31 pasang saraf spinal  segmen2 (8 segmen cervikal, 12 segmen
thoracal, 5 segmen lumbal, 5 segmen sacral, 1 segmen coccygeal)
Medula spinalis
• Vaskularisasi:
• a. vertebralis
• a. cervicalis
• a. intercostales, lumbales, dan sacralis  3 anyaman: a. spinal anterior dan
sepasang a. spinal posterior
• Saddle block anestesi: injeksi obat ke dalam ruang epidural dibawah
S2operasi daera pelvis, pasien dalam keadaan sadar
Medula spinalis
• Radix ventralis: cabang saraf yang keluar dari medulla spinalis bagian
depan
• Radix dorsalis: cabang saraf yang keluar dari medulla spinalis
bagianbelakang
• Ganglion radix posterior: bagian dari radix posterior yang membesar
(tempat badan sel)
• Cornu anterior: bagian dalam dari medulla spinalis yang berwarna
abu-abu dan berbentuk seperti tanduk di bagian depan
• Cornu posterior: bagian dalam dari medulla spinalis yang berwarna
abu-abu dan berbentuk seperti tanduk di bagianbelakang
Medula spinalis
• Filum terminale: ujung daripada medulla spinalis yang berbentuk
lancip seperti jarum
• Cauda equine: kumpulan nervi spinalis yang berbentuk seperti ekor
kuda, pada bagian akhir medulla spinalis
Vaskularisasi Medulla Spinalis
• A. Spinalis posterior
• A. Spinalis anterior
• A. Spinalis segmentalis
• Vena-vena medulla spinalis mengalir ke dalam plexus venosus
vertebralis interna
Traktus Piramidal dan
Ekstrapiramidal
Batang Otak
BATANG OTAK
BATANG OTAK
Batang Otak (truncus encephali)
• Bagian otak yang tertinggal setelah hemispherium cerebri dan
cerebellum diangkat
• Medulla oblongata + pons + mesencephalon
• Letak: fossa cranii posterior
• Penghubung medulla spinalis – prosencephalon
• Di batang otak sampai talamus  jar. Neuron (formasio retikularis)
 mengintegrasikan semua masukan / info asenden  menyebarkan
ke serebrum dalam bentuk sinyal (Reticular Activating System / RAS)
Batang Otak
3 fungsi utama :
• Penyalur tractus asendens dan desendens  penghubung medulla
dan pusat atas prosencephalon
• Mengandung pusat-pusat refleks  kontrol respirasi + KV, dan terkait
kendali tingkat kesadaran
• Mengandung nuclei penting saraf kranial III-XII
 PERBEDAAN ANTARA MESENCEFALON, PONS, & MEDULLA OBLONGATA
MESENCEFALON PONS MEDULLA OBLONGATA
• Traktus ascendens (Sensorik) & •Traktus sensorik •Traktus sensorik &
descendens (motorik) & motorik motorik
• Pusat kardiovaskuler  atur •Nuklei pontin  •Colliculi superior 
detak jantung & diameter kirimkan impuls2 koordinasi pgerakan
pembuluh darah area motorik kepala, mata, tubuh thp
• Medullary rhythmicity area  korteks cerebri ke stimuli visual
atur bernapas (dgn pons) serebelum •Colliculi inferior 
• Nucleus gracilis, cuneate, •Nuklei vestibuler koordinasi pgerakan
gustatori, koklear, vestibuli   bag jalur kepala, mata, tubuh thp
komponen jalur sensori ke otak keseimbangan ke stimuli audio
• Nukleus olivari inferior  otak •Substansia nigra & red
dukung instruksi ke cerebellum •Area nucleus  kontrol
utk mngkondisikan otot ketika pneumotoksik & pergerakan
mplajari keterampilan motorik yg apneustik  •Nuklei saraf otak III & IV
baru regulasi napas
• Nuklei saraf otak VII, IX, X, XI, (bsama medulla)
XII •Nuklei saraf otak
• Nuklei lainnya  muntah, V, VI VII, VIII
menelan, bersin, batuk, bsendawa
• Formatio reticularis (pons,
diensefalon)  kesadaran &
nafsu seks (arousal)
 Formasio
Retikular

Axonnya berjalan asendens dan desendens sepanjang axis

batang otak :
– Axon asendens dibawa ke central tegmental tract
– Axon desendens dibawa ke reticulospinal tract
Formasio Retikular
• Fungsi :
• Mengontrol seluruh derajat kewaspadaan korteks
• Penting dalam kemampuan mengarahkan perhatian
• RF memfiltrasi informasi sensoris
• Mengkoordinasi aktifitas otot

• Ketika informasi sensoris mencapai R.F  R.F memiliki serat2 asendens 

membawa sinyal untuk mengaktifasi korteks cerebri  serat2 ini menyusun
ARAS (Ascending Reticular Activating System)

• Penurunan fungsi R.F  efek tidur

Cerebellum
Cerebellum
• Dalam fossa cranii posterior
• Posterior terhadap pons dan medula oblongata
• 2 hemispherium dihubungkan vermis
• Hubungan dengan:
• Mesencephalon melalui pedunculus cerebellaris superior
• Pons melalui pedunculus cerebellaris media
• Medulla oblongata melalui pedunculus cerebellaris inferior
Cerebellum
• Lapisan permukaan hemispherium = korteks  terdiri substansia
grisea
• Lipatan-lipatan korteks dibatasi fissura-fissura transversal
• Massa substansia grisea tertanam dalam substansia alba = nucleus
dentatus (terbesar)
• Medulla oblongata, pons dan cerebellum mengelilingi ventriculus IV
Cerebellum
• Hubungan ventriculus IV:
• Superior  ventriculus tertius melalui aqueductus cerebri
• Inferior  canalis centralis medulla spinalis
• Dengan ruang subarakhnoid melalui 3 lubang  aliran LCS SSP
Nervus Craniales
KORDA SPINALIS
• Korda spinalis/medulla spinalis  bagian penting dari canalis
vertebralis
• Upper border  1st cervical
• Lower border  1st lumbal
• Bagian terendah dari corda spinalis  conus medullaris 
berkelanjutan kebwh membentuk corda fibrosa/filum terminalis
CORDA SPINALIS
• ᴓ transversalis  massa berbentuk H
• Gray matter yg luas collumna
ventralis/anterior
• Gray matter yg sempit dan memanjang 
collumna posterior/dorsalis
• Lateral projection of gray matter  collumna
lateralis
CORDA SPINALIS
• Commisura grisea  pembatas antara substansia grisea korda
spinalis kanan dan kiri
• Canalis centralis  memotong commisura grisea
• Bagian terbawah dari canalis centralis meluas dan mmbtk ventrikalis
terminalis  brda disepanjang conus medullaris
• Disepanjang canalis spinalis (+) sel epyndima  (+) CSF pada corda
spinalis
CORDA SPINALIS
• Substansia alba korda spinalis tdd
• Anterior  fissura medianus anterior
• Posterior  septum medianus posterior
• Funiculus posterior/ collumna posterior alba
• Funiculus anterior
• Funiculus lateralis
SARAF SPINALIS DAN SEGMEN SPINALIS
Nervus spinalis melekat pada kedua sisi dari korda spinalis
N. Spinalis b’asal dari 2 akar  dorsal/posterior & ventral/anterior
FAAL
FUNGSI SISTEM SARAF
• Memproses informasi dari lingkungan melalui komponen sensoris
• Mengkoordinasikan dan melakukan fungsi motorik
• Fungsi kognitif yang lebih tinggi
• Sensory input  integration (interpretation of sensory input) 
motor output
Neuron
• Neuron aferen
• Neuron eferen
• Antarneuron
Neuroglia
• Astrosit
• Oligodendrosit
• Sel ependimal
• Mikroglia
Otak  oksigen dependent
• Otak tidak dapat membentuk ATP tanpa oksigen

• Otak hanya bisa menggunakan glukosa

• Kekurangan oksigen 4-5 menit, kekurangan glukosa 10-15 menit 

kerusakan otak
P.d otak (serebrum) robek/ ruptur/ tersumbat oleh bekuan

p.d jaringan otak ke(-)an pasokan O2 & glukosa

kerusakan/kematian jaringan

mengeluarkan glutamat merusak lb byk lagi

merusak neuron-neuron di sekitarnya

mengeluarkan lebih banyak glutamat

Fungsi motorik lain
• Daerah motorik suplementer
• Korteks pramotorik
• Korteks parietalis posterior
Kemampuan berbahasa
• Hanya di jumpai di 1 hemisfer  umumnya kiri

• Daerah primer spesialisasi kortikal bahasa

• Daerah broca
• Daerah wernicke
Daerah asosiasi
• Korteks asosiasi prafrontalis
• Korteks asosiasi parietalis-temporalis-oksipitalis
• Korteks asosiasi limbik
Hemisfer
• Hemisfer kiri  logis, analitis, sekuensial, dan verbal

• Hemisfer kanan  persepsi spasial, kemampuan artistik & musik

Batang otak
• Fungsi
• Sebagian besar 12 pasang saraf kranial
berasal dari otak
• Terdapat pusat yg mengontrol fungsi
vaskuler, respirasi, pencernaan, tidur
• Modulasi sensasi nyeri
• Mengatur refleks otot yg terlibat dalam
keseimbangan & postur
• Menyusun RAS
Amnesia Pasca Trauma (3A)
• A disorder of memory (amnestic syndrome)
•  may occur as one feature of an acute confusional state or dementia, or as an isolated
abnormality.
• Declarative (conscious) memory
• includes working memory,  newly presented information,
• as well as longer-term semantic (factual) and
• episodic (personal) memory.
• Nondeclarative (unconscious) memory
• includes procedural memory  automatic tasks, and
• emotional memory
 • Phases of registration, storage, and retrieval of information.
• hippocampus, parahippocampal region of the medial temporal lobe, and neocortical
 association memory processing.
• Bilateral damage to these regions
•  results in impairment of short-term memory,
• Long-term memory, relatively preserved,  stored more diffusely

• ACUTE AMNESIA
• HEAD TRAUMA
• Head injuries  in loss of consciousness associated with an amnestic syndrome.
• shortly after such an injury exhibit a confusional state  unable to incorporate new
memories (anterograde, or posttraumatic amnesia;)
• although they may behave in an apparently normal
• In addition, retrograde amnesia is present, covering a variable period prior to the trauma.
• As full consciousness returns  the ability to form new memories is restored.
• Events occurring in the confusional interval tend to be permanently lost to memory,
• Exceptions are islands of memory for a lucid interval between trauma and
unconsciousness,
INTRACRANIAL HEMORRHAGE (2)

• Traumatic intracranial hemorrhage can be epidural, subdural, or intracerebral

• Epidural hematoma
• most often results from a lateral skull fracture that lacerates the middle
meningeal artery or vein.
• may or may not lose consciousness initially,
• event a lucid interval (several hours to 1 to 2 days )
• of headache,
• progressive obtundation,
• hemiparesis, and
• finally ipsilateral pupillary dilatation from uncal herniation.
• Death may follow if treatment is delayed.
• Subdural hematoma
• after head injury can be acute, subacute, or chronic.
• In each case, headache and altered consciousness are the principal
manifestations.
• Delay in diagnosis and treatment  fatal outcome.
• In contrast to epidural hematoma,
• the time between trauma and the onset of symptoms is typically longer,
• the hemorrhage tends to be located over the cerebral convexities, and
• associated skull fractures are uncommon.
• diagnosis  CT scan or MRI.
 • Epidural hematoma 
• appear as a biconvex, lens-shaped, extra-
axial mass that may cross the midline or the
tentorium
• but not the cranial sutures.
• Subdural hematoma 
• is typically crescent shaped and may cross
the cranial sutures
• but not the midline or tentorium.
• treated by surgical evacuation.
• depends on the clinical course and
location.
• Evacuation, decompression, or shunting
for hydrocephalus may be indicated.
Intracerebral Hemorrhage
• Etiology
• The most common cause of nontraumatic intracerebral hemorrhage 
chronic hypertension
• Clinical Findings
• Intracerebral hemorrhage occurs while  patient is awake.
• Hemorrhage  not preceded by transient prodromal symptoms (TIAs 
associated with cerebral infarction)
• Headache  moderate to severe.
• may be localized to the site of hemorrhage or generalized.
• Nausea & vomiting  common.
• Altered consciousness  may progress steadily to stupor or coma over
minutes to hours.
Intracerebral Hemorrhage
• Clinical Findings
• On examination  nearly always hypertensive (BP 170/90 mm Hg or higher),
even in the late stages of transtentorial herniation.
• The funduscopic examination  shows vascular changes associated with
chronic hypertension.
• Nuchal rigidity is common.
• Gaze deviation  (toward the side of a putaminal or lobar hemorrhage or
downward and medially in thalamic hemorrhage)
• Hemiparesis is frequent because of the proximity of common hemorrhage
sites, such as the basal ganglia and thalamus, to the internal capsule, which
conveys descending motor fibers from the cerebral cortex.
• Seizures occur in approximately 10% of cases and are often focal. Neurologic
deficits do not fluctuate spontaneously.
Intracerebral Hemorrhage
• Investigative Studies
• CT scan without contrast
• MRI shows intra parenchymal blood and confirms the diagnosis
Intracerebral Hemorrhage
• Treatment
• Blood pressure
• Systolic BP  should be reduced to 140 mm Hg or less  limit hematoma expansion 
excessive BP reduction should be avoided (may compromise blood flow in brain tissue
adjacent to the hemorrhage)
• Cerebral edema
• The mass effect of intracerebral hemorrhage  typically compounded by progressive cerebral
edema  approximately 24 hours and maximal within 5 to 6 days.
• Cerebral edema  treated with mannitol or IV hypertonic saline, but this is usually only
useful as a temporizing measure prior to surgery
• Surgical treatment
• Evacuation of the clot  if hemorrhage is located superficially in the cerebral hemisphere
and produces a mass effect.
• most hemorrhages are deep within the brain  less accessible to surgery.
STROKE (3B)
• characterized by four key features:
• 1. Sudden onset
• 2. Focal involvement of the central nervous system
• suggested by the symptoms and signs, neurologic examination, and [CT] or [MRI).
• 3. Lack of rapid resolution
• classic definition required for at least 24 hours to distinguish stroke from transient
ischemic attack (TIA)
• transient ischemic attacks usually resolve within 1 hour.
• 4. Vascular cause
• the acute onset of symptoms and often from the patient’s age,
• referable to the territory of a particular cerebral blood vessel.
• ACUTE ONSET
• Strokes begin abruptly.
• Neurologic deficits maximal at onset or may
progress over seconds to hours (or
occasionally days).
• Focal cerebral deficits
• that develop slowly (over weeks to months)
 unlikely to be due to stroke and suggest
another process,
• such as tumor or inflammatory or degenerative
disease.
• FOCAL INVOLVEMENT
• Stroke produces focal symptoms and signs  correlate with the area of the brain
supplied by the affected blood vessel.
• Ischemic stroke,
•  interfering with neurologic functions dependent on that region and producing a more or
less stereotyped pattern of deficits.
• Hemorrhage
• less predictable pattern of focal involvement
• because complications such as:
• increased intracranial pressure,
• cerebral edema,
• compression of brain tissue and blood vessels, or
• dispersion of blood through the subarachnoid space or cerebral ventricles
•  can impair brain function at sites remote from the hemorrhage.
 • Global cerebral ischemia
• (usually from cardiac arrest) and subarachnoid hemorrhage
• affect the brain in more diffuse fashion and produce global cerebral dysfunction
• the term stroke is not usually applied in these cases.
• History and neurologic examination provide enough information to
localize the lesion to one side of the brain
• (eg, to the side opposite a hemiparesis or hemisensory deficit or
• to the left side if aphasia is present) and to the anterior or posterior cerebral
circulation.
• ANTERIOR CAROTID CIRCULATION
• supplies most of the cerebral cortex and subcortical white matter, basal
ganglia, and internal capsule.
• It consists of the internal carotid artery and its branches:
• the anterior choroidal, anterior cerebral, and middle cerebral arteries.
• commonly associated with symptoms and signs that indicate hemispheric dysfunction
•  aphasia, apraxia, or agnosia
• They also often produce hemiparesis, hemi- sensory disturbances, and visual field defects,
• but these can occur with posterior circulation strokes as well.
• POSTERIOR VERTEBROBASILAR CIRCULATION
• supplies the brainstem, cerebellum, thalamus, and portions of the occipital and
temporal lobes.
• It consists of the paired vertebral arteries, the basilar artery, and their branches:
• the posterior inferior cerebellar, anterior inferior cerebellar, superior cerebellar, and
posterior cerebral arteries).
• Posterior circulation strokes  symptoms and signs of brainstem or cerebellar dysfunction or
both
• including coma,
• drop attacks
• vertigo, nausea and vomiting,
• cranial nerve palsies, ataxia, and crossed sensorimotor deficits that affect the face on one side of
the body and the limbs on the other.
• Hemiparesis, hemisensory disturbances, and visual field deficits also occur, but are not specific to
posterior circulation strokes.
• DURATION OF DEFICITS
• Stroke  neurologic deficits that persist.
• When symptoms and signs resolve completely after briefer periods (usually within 1 hour) without
evidence of cerebral infarction,  transient ischemic attack (TIA)
• Recurrent TIAs
• caused by thrombosis or embolism arising from the same site within the cerebral circulation.
• approximately one-third of patients with TIAs  stroke within 5 years—and because this risk may be reduced
with treatment.
• VASCULAR ORIGIN
• term stroke is used only when such events are caused by vascular disease.
• The underlying pathologic  can be either ischemia or hemorrhage, usually arising from an
arterial lesion.
• Ischemia and hemorrhage account for approximately 90% and 10% of strokes
• CT scan or MRI permits definitive diagnosis.
• ischemic strokes, about 50% are attributed to cardiac embolism, 25% to large artery
occlusion, and 10% to small artery occlusion, with the remainder of unknown origin
(cryptogenic)
• ISCHEMIA
• Interruption of blood flow to the brain deprives neurons, glia, and vascular cells of substrate
glucose and oxygen.
•  leads to ischemic death of brain tissue (infarction) within the ischemic core, where flow is typically
less than 20% of normal.
• Complete, permanent ischemia, such as occurs in stroke without reperfusion,  pannecrosis, affecting
all cell types, resulting in chronic cavitary lesions.
• incomplete ischemia(20%-40% of normal blood flow)
•  cell damage is potentially reversible and cell survival may be prolonged.
• Brain edema is another determinant of stroke outcome.
• Ischemia  vasogenic edema as fluid leaks from the intravascular compartment into brain
parenchyma.
• usually 2 to 3 days after stroke
•  may be sufficiently severe that it produces a mass  herniation
• Two pathogenetic mechanisms can produce ischemic stroke
• thrombosis and embolism.
• Thrombosis
• by occluding large cerebral arteries
•  (especially the internal carotid, middle cerebral, or basilar), small penetrating arteries (as in lacunar
stroke), cerebral veins, or venous sinuses.
• minutes to hours.
• often preceded by TIAs, which tend to produce similar symptoms because they affect the same territory
recurrently.
• Embolism
• when cerebral arteries are occluded by the distal passage of thrombus from the heart, aortic
arch, or large cerebral arteries.
• Emboli in the anterior cerebral circulation  occlude the middle cerebral artery or its branches
• Emboli in the posterior cerebral circulation  lodge at the apex of the basilar artery or in the posterior
cerebral arteries.
• produce neurologic deficits that are maximal at onset.
• When TIAs precede embolic strokes, especially from a cardiac source,
• symptoms typically vary between attacks because different vascular territories are affected.
• HEMORRHAGE
• destruction or compression of brain tissue,
• compression of vascular structures, and edema.
• Intracranial hemorrhage
• is classified by its location as intracerebral, subarachnoid, subdural, or epidural, all of
which—except subdural hemorrhage—are usually caused by arterial bleeding.
• Intracerebral Hemorrhage
• causes symptoms by destroying or compressing brain tissue.
• Unlike ischemic stroke, intra-cerebral hemorrhage
•  cause more severe headache and depression of consciousness as well as neurologic
deficits
• Subarachnoid Hemorrhage
• leads to cerebral dysfunction due to increased intracranial pressure
•  resulting hypoperfusion,
• direct destruction of tissue, and
• toxic constituents of subarachnoid blood.
• may be complicated by vasospasm (leading to ischemia), rebleeding, extension of
blood into brain tissue (producing an intracerebral hematoma), or hydrocephalus.
• typically presents with headache rather than focal neurologic deficits
• Subdural or Epidural Hemorrhage
• produces a mass lesion that can compress the underlying brain.
• often traumatic in origin
• usually present with headache or altered consciousness.
• Clinical finding
• Predisposing Factors
• such as TIAs, hypertension, diabetes, dyslipidemia,
ischemic or valvular heart disease, cardiac
arrhythmia, cigarette smoking, and oral
contraceptive use should be sought.
• Hematologic and other systemic disorders can also
increase the risk of stroke.
• Antihypertensive drugs can precipitate
cerebrovascular symptoms
• if the blood pressure is lowered excessively in patients
with nearly total cerebrovascular occlusion and poor
collateral circulation.
• The history may also suggest a thrombotic or embolic etiology.
• Features suggesting thrombotic stroke
• often presents with stepwise progression of neurologic deficits and may be preceded by
one or more TIAs with identical symptoms.
• Lacunar infarcts are also characteristically thrombotic.
• Features suggesting embolic stroke
• Cardioembolic stroke is suggested by maximal deficit within 5 minutes of onset,
• impaired consciousness at onset, sudden regression of deficit, multifocal infarction,
• Wernicke or global aphasia without associated hemiparesis, top-of- the-basilar
syndrome,
• hemorrhagic transformation of infarct, or associated valvular disease, cardiomegaly,
arrhythmia, or endocarditis.
• Associated Symptoms action.
• Headache
• 25% of patients with ischemic stroke and is especially common in intra- cranial arterial dissection and venous or
sinus thrombosis.
• Seizures
• can accompany the onset of stroke or follow stroke by weeks to years, but do not definitively distinguish
embolic from thrombotic stroke.
• General Physical Examination
• The blood pressure  a major risk factor for stroke.
• Comparison of blood pressure and pulse on the two sides
• Ophthalmoscopic examination  evidence of embolization in the anterior circulation
• Neck examination absence of carotid pulses or the presence of carotid bruits.
• Cardiac examination  detect arrhythmias, or murmurs related to valvular diseas
• which may predispose to cardioembolic stroke.
• Temporal artery palpation
• Skin examination may show signs of a coagulation disorder, such as ecchymoses or petechiae.
• Neurological examination
• 1. Cognitive deficits
• aphasia, unilateral neglect or constructional apraxia  cortical lesion in the anterior circulation.
• Coma implies brainstem or bihemispheric involvement.
• 2. Visual field abnormalities
• hemianopia can occur  occlusion of either the middle or posterior cerebral artery,
• Isolated hemianopia  posterior cerebral artery stroke,
• because middle cerebral artery stroke should produce additional (motor and somatosensory) deficits.
• 3. Ocular palsy, nystagmus, or internuclear ophthalmoplegia
•  underlying lesion to the brainstem and thus the posterior cerebral circulation.
• 4. Hemiparesis.
• face, hand, and arm more than the leg  middle cerebral artery lesions.
• Crossed hemiparesis, face on one side and the rest of the body on the other,
• assigns the lesion to the brainstem between the facial (VII) nerve nucleus in the pons and the decussation of the pyramids in the
medulla.
• 5. Cortical sensory deficits
• astereognosis or agraphesthesia  middle cerebral artery territory.
• Hemisensory deficits without motor involvement are usually lacunar
• 6. Hemiataxia
•  lesion in the ipsilateral brainstem or cerebellum but can also be produced by lacunar stroke in the internal capsule.
• Treatment of cerebrovascular disease
• related to specific underlying vascular, cardiac,
and hematologic causes of stroke
•  (eg, anti-inflammatory, antibiotic or
antiarrhythmic drugs)
• PRIMARY PREVENTION
• Lifestyle
• aerobic activity for 30 to 40 min per day, 3 to
4 times per week, is recommended.
• A diet low in sodium and saturated fats and
rich in fruits, vegetables, low-fat dairy
products, and nuts  reduce stroke risk,
• as may weight reduction in overweight or
obese patients, cessation of smoking, and
moderation of heavy alcohol use.
• Statins
• recommended for patients, with or without dyslipidemia, who are at increased (>10%)
10-year risk for cardiovascular events, including stroke.
• statins have vasoprotective (eg, anti-inflammatory) actions besides their lipid-lowering
effects.
• Blood Pressure Control
• lifestyle modification, antihypertensive drugs, or both for patients
• Glycemic Control
• Diabetes increases the risk of stroke
• Antiplatelet Drugs
• Low-dose aspirin (81-100 mg/d)  reduce the risk of stroke
• TRANSIENT ISCHEMIC ATTACK & ACUTE ISCHEMIC STROKE
• Transient ischemic attack, or TIA,
• focal cerebral ischemia that resolves fully and rapidly, usually within 1 hour, without
evidence of cerebral infarction.
• The goal of treatment is to prevent subsequent stroke
• 10% of patients in 2 days and up to 20% of patients in 90 days.
• Acute ischemic stroke
• persistent focal neurologic deficit, which may be improving, stable, or worsening.
• Evaluation and treatment are largely the same in both cases
• the major difference is that thrombolytic therapy is not usually considered for TIA
• Investigation
• evaluated urgently with blood tests (complete blood count, prothrombin and
partial thrombo- plastin time, erythrocyte sedimentation rate, treponemal
test for syphilis, glucose) and ECG to identify underlying causes or mimics of
cerebrovascular disease, and CT scan or MRI with diffusion-weighted
imaging to document stroke and exclude other disorders.
• anterior circulation ischemia
• who are good surgical candidates should undergo MR angiography, CT angiog- raphy, or
Doppler ultrasonography to detect operable lesions in the extracranial carotid artery.
• Echocardiography  if there is a predisposing cardiac disorder or if
symptoms suggest cardiogenic embolus (
• Medical Treatment
• 1. Blood pressure
• When acute antihypertensive therapy is indicated, recommended drugs include intravenous labetalol or
nicardipine.
• Hyperthermia  corrected, and any infectious cause identified.
• Hypoxia (oxygen saturation ≤94%) should be treated with supplemental oxygen.
• Hypoglycemia (blood glucose <60 mg/dL) should be corrected.
• Anticoagulation
• with heparin, given by continuous intravenous infusion to achieve an activated partial thromboplastin
time (aPTT) 1.5 to 2.5 times control,
• followed by warfarin, given orally daily to achieve an INR of 2.5±0.5,
• or another oral anticoagulant is indicated if a cardiac embolic source.
• Antiplatelet therapy
• with aspirin (325 mg orally once, followed by 81-325 mg orally daily) is recommended for presumed
noncardiogenic TIA or acute ischemic stroke
• Statins should be continued for patients receiving long- term statin treatment.
 Strategies for Preventing Stroke and
Reducing Stroke Disability
stroke
blood pressure mortality
glucose
smoking mass popl.
lipids strategy acute treatment

First stroke Secondary recurrent

prevention stroke
high risk strategy
Rehabilitation
hypertension
TIA
Atrial fibrillation
other vascular disease Stroke related
disability
Thrombolysis therapy
Therapies to Prevent Ischemic Stroke

• Oral anticoagulants
• Low dose enoxaparin (LMWH) 40 mg daily
• Subcutaneous heparin 5000 U twice daily
• Warfarin 5-10 mg daily
• Antiplatelet agents
• Aspirin 50-325 mg/day

• Ticlopidine 250 mg twice daily

• Clopidogrel 75 mg/day

• Aspirin (25 mg) plus extended-release dipyridamole

(200 mg) twice a day
• Antihypertensive agent
• ACE-inhibitor, diuretic, beta blocker for maintenance
• For acute stroke,. BP >220/120 mmHg, IV labetalol or
nicardipine IV
 DSA (Digital Subtraction
angiogram)
• It is done under local anaesthesia, via the transfemoral
route, on a cathlab containing special DSA & ‘roadmap’
software’ & takes just 20 to 30 minutes.
• the machine subtracts the skull, brain, CSF, meninges etc
from the image, making the contrast flowing through the
blood vessels stand out. Thus it is highly accurate &
detects abnormalities in blood vessels. It is a real-time
study which does not involve any reconstruction as in MR
angio or CT angio. Also views are taken in different
projections after cannulating all vessels selectively so that
maximum dynamic information is gathered about the
pathology. Maneuvers like cross- compression are done to
ascertain cross-flow across the circle of Willis.
Indication for DSA
• The common indications of DSA are:
• ALL patients of Subarachnoid hemorrhage (SAH)
• Patients of TIA or ischemic stroke in whom either Doppler or
MRA have detected extracranial or intracranial atheromatous
disease.
• Patients with recurrent / crescendo TIAs in the same territory
• Suspected carotid or vertebral artery dissection when MRI is
inconclusive
• Patients with intracerebral bleed when an underlying AVM is
suspected (young patients, peripheral location of the bleed, no
evidence or history of hypertension, recurrent bleeds in the same
territory etc.)
• Suspected venous sinus thrombosis when MRI is inconclusive.
• Highly vascular CNS or ENT tumors when pre-op embolisation is
required.
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
• Spontaneous subarachnoid hemorrhage  result of a ruptured cerebral arterial
aneurysm or an AVM.
• Rupture  5th & 6th decades (most often)
• Approximately equal sex distribution.
• Hypertension  not been conclusively predispose to the formation of aneurysms
• Acute elevation of BP (eg, at orgasm)  may be responsible for rupture.
• Fusiform aneurysms  result from circumferential dilation of a cerebral arterial trunk.
• Saccular aneurysms  caused by atherosclerosis or dissection, affect the vertebrobasilar
system preferentially, and can present with symptoms from ischemia or mass effect, in
addition to rupture.
• Intracranial AVMs  less frequent cause of subarachnoid hemorrhage (10%)  usually
bleed in the 2nd – 4th decades
• Blood in the subarachnoid space can also result from intracerebral hemorrhage, embolic
stroke, and trauma.
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
[Pathophysiology]
• Rupture of an intracranial artery  ⬆ intracranial pressure  distorts
pain-sensitive structures  headache.
• Intracranial pressure may reach systemic perfusion pressure 
acutely ⬇ cerebral blood flow  loss of consciousness (occurs at the
onset in ±50% of patients)
• Rapid ⬆ of ICP  produce subhyaloid retinal hemorrhages
Subarachnoid Hemorrhage
[Symptoms & Signs]
• The classic presentation  sudden onset of severe generalized headache
(“WORST HEADACHE OF MY LIFE”)
• (-) of headache essentially  precludes the diagnosis.
• 1/3 of patients present with headache alone.
• duration of the hemorrhage is brief BUT the intensity of the headache  remain
unchanged for several days & may subside slowly over ⬇ 2 weeks.
• Recurrence of the headache  rebleeding.
• Loss of consciousness  frequent at onset
• Vomiting & neck stiffness.
• Milder similar headache (sentinel headache)  in the weeks prior to the
acute event
•  represent small prodromal hemorrhages or aneurysmal stretch.
• Hemorrhage from a ruptured AVM  headache not always severe.
Subarachnoid Hemorrhage
[Symptoms & Signs]
• BP ⬆  result of the hemorrhage.
• Meningeal irritation  temperature ⬆ up to 39°C (102.2°F) during the first 2 weeks.
• Frequently associated confusion, stupor, or coma.
• Nuchal rigidity & other evidence of meningeal irritation  are common, but may
not occur for several hours after the onset of headache.
• Preretinal globular subhyaloid hemorrhages  most suggestive of the diagnosis.
• Aneurysmal rupture  bleeding mainly in the subarachnoid space Vs brain
parenchyma.
• Therefore, prominent focal neurologic signs  uncommon
• If present  no relationship to the site of the aneurysm.
• Oculomotor (III) nerve palsy  due to compression of the nerve ipsilateral to a
posterior communicating artery aneurysm.
• Abducens (VI) nerve palsy  nonlocalizing signs  result from ⬆ ICP
• Ruptured AVMs  focal neurologic signs, such as hemiparesis, aphasia, or visual
field defects
Subarachnoid Hemorrhage
[Laboratory Findings]
• Investigated 1st  CT scan (confirms the hemorrhage >90% with
aneurysmal rupture & help identify a focal source).
• most sensitive  on the day bleeding & in patients with altered
consciousness.
• Aneurysms  may not be evident on CT
• most AVMs  can be seen after administration of contrast material.
• MRI  useful for detecting small AVMs in the brainstem
• Complications
• Intracerebral or intraventricular extension of blood
• Hydrocephalus
• Infarction.
Subarachnoid Hemorrhage
• Imaging Findings
Subarachnoid Hemorrhage
[Laboratory Findings]
• If normal neurologic examination  a normal CT scan within 6 hours of symptom
onset is held some authorities to exclude subarachnoid hemorrhage.
• CT scans are inadequate or delayed, or fail to confirm the diagnosis  lumbar puncture
• The CSF in subarachnoid hemorrhage
• markedly ⬆ opening pressure
• grossly bloody, containing 100,000 to >1 million/μL RBC.
• Bloody initially, xanthochromic supernatant with centrifugation (“yellow”) by ~12 h, lasts 2
wk
• As heme is degraded  green pigment
• Biliverdin  yellow pigment
• WBC  initially (+) in the CSF in the same proportion to RBC as in the peripheral blood.
• Chemical meningitis caused by blood in the subarachnoid space 
• produce a pleocytosis of several thousand WBC (first 48 hours)
• ⬇ in CSF glucose 4 to 8 days after hemorrhage.
• In the absence of pleocytosis, CSF glucose after subarachnoid hemorrhage is normal.
• The peripheral WBC count  modestly ⬆ but rarely exceeds 15,000/μL.
Subarachnoid Hemorrhage
[Laboratory Findings]
• ECG  abnormalities (peaked or deeply inverted T waves, short PR
interval, or tall U waves)
• Once the diagnosis confirmed by CT or lumbar puncture  four-vessel
cerebral arteriography is undertaken.
• Carotid & vertebral arteries  studied to visualize the entire cerebral vascular
anatomy
• Angiography should be performed at the earliest time convenient for radiology
department personnel; emergency studies in the middle of the night are rarely
indicated.
• Angiography is a prerequisite to the rational planning of surgical treatment and is
therefore not necessary for patients who are not surgical candidates, such as those
who are deeply comatose. CT and magnetic resonance angiography are approaching
the sensitivity of conventional catheter angiography.
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
[DDx/]
• The sudden onset of severe headache
• confusion or obtundation
highly specific for
• nuchal rigidity subarachnoid hemorrhage
• absence of focal neurologic deficits
• bloody spinal fluid.

• Hypertensive intracerebral hemorrhage

•  Obtundation & bloody spinal fluid + prominent focal neurologic deficits
• Ruptured mycotic aneurysm
•  Obtundation & bloody spinal fluid + sign of endocarditis.
Subarachnoid Hemorrhage
[DDx/]
• Traumatic lumbar puncture can be excluded as the cause of bloody
CSF by
•  comparing RBC counts in the 1st & last tubes of CSF obtained and
examination of the centrifuged CSF specimen.
• Blood clears as fluid is removed after a traumatic tap, but not after
subarachnoid hemorrhage.
• As blood introduced by traumatic lumbar puncture  not have time to
undergo enzymatic break- down to bilirubin, centrifugation of the specimen
reveals a colorless supernatant.
• Bacterial meningitis  excluded by the (+) of blood in the CSF or on
CT scan.
Subarachnoid Hemorrhage
[Complications]
• Recurrence of Hemorrhage
• occurs in ±20% over 10 to 14 days.
• major acute complication & roughly doubles the mortality rate.
• Acute recurrence of hemorrhage from AVM is less common.
• Intraparenchymal Extension of Hemorrhage
• Hemorrhages from an AVM  commonly involve the brain parenchyma
• Aneurysmal hemorrhage less commonly involve the brain parenchyma .
• rupture of an aneurysm of the anterior cerebral or middle cerebral artery  direct a jet of blood into the brain w/ resultant
intracerebral hematoma  hemiparesis, aphasia, and transtentorial herniation.
• Arterial Vasospasm
• Vasospasm  occurs in area surrounded by subarachnoid blood  associated w/ ischemic neurologic
deficits.
• Clinical ischemia  day 4 after the hemorrhage, peaks at day 7 to 8, then resolves spontaneously.
• The diagnosis  by transcranial Doppler or cerebral angiography.
• The severity of vasospasm is related to  amount of subarachnoid blood
• Vasospasm  less common when less blood is present (after traumatic subarachnoid hemorrhage or rupture
of an AVM).
Subarachnoid Hemorrhage
[Complications]
• Acute or Subacute Hydrocephalus
• Acute or subacute hydrocephalus  during the first three days or after several
weeks  as a result of impaired CSF absorption in the subarachnoid space.
• Progressive somnolence, nonfocal findings, & impaired upgaze due to downward
pressure on the midbrain  suggest the diagnosis.
• Seizures
• Seizures occur in fewer than 10% of cases and only after damage to the cerebral
cortex.
• Decorticate or decerebrate posturing  common acutely  may mistaken for
seizures.
• Other Complications
• Although inappropriate secretion of antidiuretic hormone and resultant diabetes
insipidus can occur, they are uncommon.
Subarachnoid Hemorrhage
[Medical Treatment]
• Preventing ⬆ of arterial or ICP that might re-rupture the aneurysm or AVM.
• Absolute bed rest w/ the head of the bed elevated 15 to 20o
• Mild sedation
• Analgesics for headache (antiplatelet  avoided).
• Patients w/ hypertensive on admission  ⬆ mortality
• ⬇ BP (to ±160/100 mm Hg)  bed rest & mild sedation  often adequate.
• Hypotension  should prevented to ensure adequate cerebral perfusion
• IV fluids should be isosmotic (normal saline)
• overhydration  exacerbate cerebral swelling.
• Hyponatremia  managed by NaCl PO/ IV 3% normal saline, rather than by
fluid restriction.
Subarachnoid Hemorrhage
[Medical Treatment]
• Following definitive surgical treatment (in the (-) of other aneurysms)
 vasospasm can be treated
•  induced HTN w/ phenylephrine or dopamine.
• The calcium channel antagonist
• Nimodipine, 60 mg PO (or by NGT) every 4 hours for 21 days  ⬇ delayed ischemic
neurologic deficits (through neuroprotective mechanisms).
• Seizures  uncommon after aneurysmal rupture
• HTN accompanying an acute seizure  ⬆the risk of re-rupture.
• prophylactic administration of an anticonvulsant (phenytoin, 300 mg/d) 
recommended in the perioperative period and then is discontinued.
Subarachnoid Hemorrhage
[Surgical Treatment]
• Aneurysm
• Definitive surgical th/ of a ruptured aneurysm  cut the neck of the
aneurysm or endovascular placement of a coil to induce clotting.
• Neurologic examination  grade the patient’s surgical candidacy.
• Patients fully alert (Hunt and Hess grades I & II) or only mildly confused (grade III) 
surgery has been shown to improve the clinical outcome.
• Stuporous (grade IV) or comatose (grade V) patients  not appear to benefit.
• Maximal rebleeding (first 24 hours) following aneurysmal rupture  early
surgical intervention, is indicated.
Subarachnoid Hemorrhage
[Surgical Treatment]
Subarachnoid Hemorrhage
[Surgical Treatment]
• AVM
• Surgically accessible AVMs  removed by en-bloc resection or obliterated by
ligation of feeding vessels or by embolization with a local intra-arterial
catheter.
• Risk of an early 2nd hemorrhage  much less with AVMs Vs aneurysms 
surgical treatment can be undertaken electively at a convenient time after the
bleeding episode.
Parkinsonism
Parkinsonism
[Etiology]
• Idiopathic
• Occurs w.o obvious cause  called Parkinson disease or paralysis agitans
• No atypical features & sustained response to dopaminergic medication.
• During a preclinical phase (back for several years before the motor deficit) hyposmia,
constipation, anxiety, depression, and REM sleep behavior disorder (+).
• Encephalitis
• Drug-or Toxic-induced parkinsonism
• Vascular parkinsonism
• Post-traumatic parkinsonism
• Familial & genetic parkinsonism
• Associated with other neurologic disease
Parkinsonism
[Clinical Findings]
• Tremor
• The 4- to 6-Hz tremor of parkinsonism is characteristically most conspicuous
at rest
• ⬆ at times of emotional stress & often ⬆during voluntary activity.
• begins with 
• rhythmic, opposing circular movements of the thumb & index finger (“pill-rolling”)
• rhythmic flexion–extension of the fingers or of the hand or foot
• rhythmic pronation–supination of the forearm.
• frequently involves  lower jaw & chin as well.
• May be (+) in all limbs
• not uncommon  confined to one limb—or both limbs on one side—for months or
years before it becomes more generalized.
Parkinsonism
[Clinical Findings]
• Rigidity
• Rigidity or ⬆ tone (ie, ⬆ resistance to passive movement)  characteristic of
parkinsonism.
• The disturbance in tone  flexed posture.
• The resistance  uniform  affects agonist and antagonist muscles alike
• In contrast to spasticity  clasp-knife phenomenon.
• described as cogwheel rigidity  ratchet-like interruptions of passive
movement
Parkinsonism
[Clinical Findings]
• Akinesia/Bradikinesia
• The most disabling feature  hypokinesia (bradykinesia /akinesia)
• ⬇ of voluntary movement & ⬇ in automatic movement (swinging the arms while walking)
• face 
• immobile (hypomimia or mask- like facies)
• widened palpebral fissures
• infrequent blinking
• certain fixity of facial expression
• smile that develops & fades slowly.
• The voice is soft (hypophonia) & poorly modulated.
• Fine or rapidly alternating movements  impaired
• The handwriting  small (micrographia), tremulous, and hard to read.
Parkinsonism
[Clinical Findings]
• Abnormal Gait & Posture
• difficult to get up from bed or an easy chair
• flexed posture on standing.
• difficult to start walking  lean farther & farther forward while
walking
• In advanced  tends to walk with ⬆ speed to prevent a fall (festinating
gait)  altered center of gravity that results from the abnormal
posture.
• The gait is characterized 
• small, shuffling steps
• (-) of the arm swing that normally accompanies
• unsteadiness on turning
• there may be difficulty in stopping.
• Retained arm swing, wide-based gait, or marked imbalance at an
early stage  non-parkinsonian disorder.
Parkinsonism
[Clinical Findings]
• Other Motor Abnormalities
• mild blepharoclonus (fluttering of the closed eyelids)
• blepharospasm (involuntary closure of the eyelids).
• Drool  due to impairment of swallowing.
• No alteration in the tendon reflexes (although a mild hyperreflexia may occur
on the affected side in asymmetric parkinsonism)
• Repetitive tapping (approximately twice per second) over the bridge of the
nose produces a sustained blink response (Myerson sign)
Parkinsonism
[Clinical Findings]
• Nonmotor Manifestations
• Anosmia  early symptom (not a specific indicator of Parkinson disease).
• Cognitive decline
• executive dysfunction
• personality changes
• depression
• anxiety.
• Apathy may be conspicuous.
• fatigue  prominent, and some patients complain of pain or sensory disturbances.
• Dysautonomic symptoms (urinary urgency & urge incontinence, and constipation)
• postural hypotension (relates to dopaminergic th/ or inactivity but may also reflect
baroreflex failure or denervation of cardiac muscle)
• Sleep disorders (REM behavior disorder).
• Seborrheic dermatitis may occur.
Parkinsonism
[Treatment]
• Early parkinsonism  no drug treatment
• Discuss about the nature of the disorder & the availability of
medical treatment if symptoms become more severe
• Treatment of the motor symptoms  directed toward restoring
the dopaminergic–cholinergic balance in the striatum by
blocking the effect of acetylcholine (anticholinergic drugs) or by
enhancing dopaminergic transmission
• Anticholinergic Drugs
• Amantadine
• Levodopa
• Dopamine Antagonist
• Catechol-O-Methyltransferase Inhibitors
• Monoamine Oxidase Inhibitors
Parkinsonism
[Treatment]