NEUROVASCULAR

Carotis-cavernosis Fistula (CCF)

Sign
- proptosis
- chemosis
- parese cranial nerve
- bruit, dsb.
Type CCF:
 Direct internal carotid artery and Sinus Cavernosus
 Indirect from Dural Artery
o Tye B : Meningeal branch –ICA
o Type C : Meningeal branch –ECA
o Type D : Meningeal branch –ECA + ICA
Carotid cavernous fistula
- Pasti ada riwayat SBF anterior (bila ada trauma)
- Trias klasik CCF : proptosis, kemosis, bruit
Kemosis
Diebabkan oleh karena V. oftalmika superior dan inferior terbendung  vena-
vena membesar  arteri tertekan  arteri membuat kolateral (arteriolization)
 kemosis.

Proptosis
Karena vena-vena yang akan memasuki sinus cavernosus terbendung jadi
membesar.

Bruit
Disebabkan oleh high flow (KA) melalui fistula arteriovenosus .
Apabila GCS tidak 15, jangan tulis kekuatan motorik dan sensorik.
Tulis : eyeball movement : dolls eye (+)
Motorik = no hemiparesis
Sensorik = response to pain
Temuan CT Scan = edema serebri : kompresi sulkus x girus, sylvian fissure,
ventrikel dan cisterna.
Indikasi cito pada Fracture depress :
- Open depress
- < 8 jam.

Jika ada penekanan pada brainstem karena faktor mekanik, maka harus
ditemukan sejumlah gejala brainstem :
- Gangguan pola nafas
- Gangguan cranial nerves
 Gangguan reflex jika pasien tidak sadar
 CN lainnya sulit karena GCS pasien jelek.
Apabila ditemukan lesi intraparenkim, maka disarankan untuk dilakukan open
craniotomy karena kita tidak dapat kontrol perdarahan, apalagi bila vena
kortikal terkena puncture saat burrhole aspirasi.
Abses boleh dipungsi apabila letaknya dekat dengan korteks, dan karena
abses bersifat slow flow. Setelah itu dilanjutkan dengan craniotomy = ada CT
control.
EDH  bila ada faktor yang melewati sutura, EDH bisa melewati sutura.
Subgaleal  lewat sutura.
Subperiosteal  tidak lewat sutura
EDH dengan fraktur memanjang depan  belakang dapat membentuk aesent
shape.
Hernia uncal : anisokor, yang disusul dengan kesadaran 
Hernia hipokampus : kesadaran , lalu anisokor.
Anak-anak jarang mengalami perdarahan, karena :
- Durameter menempel
- Otak masih ada space
- LCS lebih banyak.
Misalnya : ada EDH minimal  sudah 4 hari; paling baik : CT kontrol.
Kriteria x-ray cervical pada pasien trauma (ada 10, cari!)
- Pasien tidak sadar dengan kemungkinan riwayat trauma
- Mekanisme trauma yang menandakan adanya resiko spine injury
- Multiple trauma
- Trauma berat di atas klavikula
- Trauma yang disertai dengan gejala hipotensi
- Riwayat trauma leher
- Neck tenderness
- Pasien sadar dengan neck pain.
- Pasien dengan defisit neurologis
- Adanya trauma besar lainnya (contohnya : trauma abdominal, dsb).

Durret’s haemorrhage: Perdarahan mikro yang disebabkan karena

tertariknya brainstem ke atas (upward).

DlC
dynamic condition of clotting activation and trombin generation resulting in
trombosis and bleeding due to consumption of coagulation factors, fibrin deposition
and fibrinolysis.
Causes:
Over 100 identified. Most frequent causes:
- sepsis - shock & blood loss - crush injuries - head injury
- hypoxia - obstetric complications - burns
- transfusion reaction - Fat embolism - malignancy

Pathophysiology
Sudden release of tromboplastic material into the vascular system results in
widespread deposition of fibrin in the microcirculation (with resultant consumption of
fibrinogen) Fibrin degradation products (FDP) are produced, further impairing
coagulation. The resultant effecti is major bleeding and tissue ischaemia from the
microvascular trombi.

Subarachnoid Bleeding and aneurysm

 Traumatic : most common SAH
 Spontaeous:
o ruptured intracranial aneurysms: 75-80% of spontaneous SAH
o cerebral arteriovenous malformation (A VM): 4-5% of cases (A VMs
more commonly cause ICH & IVH than SAH)
Fact about SAH
• peak age for aneurysmal SAH is 55-60 years, .. 20% of cases occur between ages
15-45 yrs25
• 30% of aneurysmal SAH occurs during sleep
• 50% of patients with aneurysms have warning symptoms, usually 6-20 days before
SAH
• headache is lateralized in 30%, most to the side of the aneurysm
• SAH is complicated by intracerebral hemorrhage in 20-40%, by intraventricular
hemorrhage in 13-28% and by subdural blood in 2-5% (usually due to p-comm
aneurysm when over convexity, or distal anterior intracerebral artecy (DACA)
aneurysm with interhemispheric subdural

Risk factors for SAH

• hypertension
• oral contraceptives
• substance abuse
i. cigarette smoking
ii. following cocaine abuse
iii. alcohol consumption
• diurnal variations in blood pressure
• pregnancy and parturition
• slight increased risk during lumbar puncture and/or cerebral angiography in
patient with cerebral aneucysm
• slight increased risk with advancing age
• conditions with an increased incidence of cerebral aneurysms

Symptoms of SAH
 Sudden onset of severe HIA usually with vomiting
 syncope (apoplexy)
 neck pain (meningismus)
 photophobia.
 Focal cranial nerve deficits may occur (e.g. third nerve palsy from aneurysmal
compression, causing diplopia and/or ptosis).
Radiologic in SAH
  CT non contrast : distribution SAH
 MRA : no radiation, does not use contrast. Poor sensitivity for aneurysm
detection early after SAH
sensitivity is 87% and specificity is 92% for detecting intracranial
aneurysms, significantly poorer sensitivity for aneurysms< 3
mm diameter,
 CTA : Contrast Iodine ( Depend on renal function)
detecting 97% of aneurysms and demonstrating CTA as safe and effective
when used as the initial and sole imaging study for ruptured and
unruptured cerebral
aneurysms61• CTA shows a 3-dimensional image
 DSA : may be necessary after a positive CTA to better delineate the anatomy,
or to determine dominant filling and cross flow, The gold standard for
evaluation of cerebral aneurysms,

Risk from SAH

1. rebleeding: the major concern during the initial stabilization
2. hydrocephalus: precipitous development acute hydrocephalus may be
obstructive (due to blockage of CSF flow by blood clot), but presence
ofventriculomegaly early after SAH as well as at later stages is often due to
communicating hydrocephalus (due toxic effect ofblood breakdown products
on arachnoid granulations)
3. delayed ischemic neurologic deficit (DIND), usually attributed to
vasospasm. Begins to be of concern several days following the SAH
4. hyponatremia with hypovolemia
5. DVT and pulmonary embolism
6. seizures

Treated for vasospasme

Nimotop can be used for traumatic and nontraumatic SAB
 POSTRAUMATIC SUBARACHNOID HEMORRHAGE AKA traumatic
SAH (tSAH). Trauma is the most common cause of SAH. There is some
evidence that nimodipine (Nimotop®) may improve outcome in head-injured
patients with subarachnoid blood detected on CT58• &: 60 mg PO or per NG
q 4 hrs, hold for hypotension. (Greenberg 7th edition pg:862)
Cerebral aneurysms
Type:
 Saccular aneurysms : AKA berry aneurysms are usually located on major
named cerebral arteries at the apex of branch points which is the site of
maximum hemodynamic stress in a vessel. More peripheral aneurysms do
occur, but tend to be associated with infection (mycotic aneurysms) or trauma.
 Fusiform aneurysms are more common in the vertebrobasilar system.
Dissecting aneurysms should be categorized with arterial dissection

Saccular aneurysms location:

• 85-95% in carotid system, with the following 3 most common locations:
• ACoA (single most common): 30% (ACoA & ACA more common in males)
• p-comm: 25%
• middle cerebral artery (MCA): 20%
• 5-15% in posterior circulation (vertebra-basilar)
 • -10% on basilar artery: basilar bifurcation, AKA basilar tip, is the most
common
• 5% on vertebral artery: VA-PICAjunction is the most common
• 20-30% of aneurysm patients have multiple aneurysms
Timing of aneurysm surgery

Early surgery defined as < 48-96 hrs post SAH):

Advantage
 if successful, virtually eliminates the risk of rebleeding which occurs most
frequently in the period immediately following SAH
 facilitates treatment of vasospasm which peaks in incidence between days 6-8
post SAH (never seen before day 3) by allowing induction of arterial
hypertension and volume expansion without danger of aneurysmal rupture
 allows lavage to remove potentially vasospasmogenic agents from contact
with vessels
 although operative mortality is higher, overall patient mortality is loweriJM
Disadvantage
 inflammation and brain edema are most severe immediately following SAH
 the presence of solid clot that has not had time to lyse impedes surgery
 the risk of intra-operative rupture is higher with early surgery
 possible increased incidence of vasospasm following early surgery from
mechanotrauma to vessels
Late surgery defined as < 10-14 days post SAH):
Advantage
 poor medical condition and/or advanced age of patient (age may not be a
separate factor related to outcome, when patients are stratified by H&H grade)
 poor neurologic condition of patient (H&H grade~ 4): controversial.
 aneurysms difficult to clip because of large size, or difficult location
necessitating a lax brain during surgery (e.g. difficult basilar bifurcation or
mid-basilar artery aneurysms, giant aneurysms)
 significant cerebral edema seen on CT
 the presence of active vasospasm
Hunt & Hess classification of SAH
Coma following SAH
 increased ICP
 damage to brain tissue from intraparenchymal hemorrhage (may also
contribute to increased ICP)
 hydrocephalus
 diffuse ischemia (may be secondary to increased ICP)
 seizure
 low blood flow (reduced CBF) due to reduced cardiac output

Fisher grade for vasospasme

Intracerebral Haemorhage
Common arterial feeders of ICHs:
 lenticulostriates: the source of putaminal hemorrhages (possibly secondary to
microaneurysms of Charcot-Bouchard)
 thalamoperforators
 paramedian branches of BA

Common site Spontaneous ICH

ICH score : associated 30 day mortality

Management ICH
NON-SURGICAL: factors that favor medical management
 minimally symptomatic lesions: e.g. alert patient with subtle hemiparesis
(especially patients with GCS > 10)
 situations with little chance of good outcome
1. high ICH score (see page 1126), which overlaps with the following
2. massive hemorrhage with significant neuronal destruction (see
below)
3. large hemorrhage in dominant hemisphere
4. poor neurologic condition: e.g. comatose with posturing (i.e. GCS ~
5), loss of brain stem function
5. age > 75 yrs: do not do well with surgery for this
 severe coagulopathy or other significant underlying medical disorder
  basal ganglion (putaminal) or thalamic hemorrhage: surgery is no better than
medical management

SURGICAL: factors that favor rapid surgical removal of the blood clot
 lesions with marked mass effect, edema, or midline shift on imaging (removal
is considered due to the potential for herniation)
 lesions where the symptoms (e.g. hemiparesis/plegia, aphasia, or sometimes
just confusion or agitation ) appear to be due to increased ICP
 volume: surgery for moderate volume hematomas (30 cc)
 persistent elevated ICP in spite of therapy (failure of medical management).

Management of cerebellar hemorrhage

 patients with a Glasgow Coma Scale (GCS) score 0! 14 and hematoma < 4 em
diameter:
treat conservatively
 patients with GCS ~ 13 or with a hematoma :I! 4 em: surgical evacuation
 patients with absent brain stem reflexes and flaccid quadriplegia: intensive
therapy is not indicated
 patients with hydrocephalus: ventricular catheter (if no coagulopathy).
Caution: do not overdrain to avoid upward cerebellar herniation. Most
caseswith hydrocephalus also require evacuation of the clot

ICH in young adults

Posterior cerebral artery occlusions:

 A. Hemianopsia
B. Memory loss
C. Cognitive abnormalities
D. Occcsionally (25%) PCA & ICA branch (fetal pattern persists)

Syndromes of the cerebral arteries:

Internal carotid artery occlusion
- contralateral hemiplegia, facial palsy, hemianopia, hemianestesia and urinary
incontinentia.
- if infarction of the dominant left hemisphere will result in disphasia (mixed type)
- confusion (in some patients) t.u pd psn usia lanjut & sering disalahartikan sbg
dementia.

Middle Cerebral Artery

- commonly involved in cerebral thromboembolism
- occlusion will result in contralateral hemiplegia, sensory loss, motor aphasia and
hemianopia.

Anterior cerebral artery

- contralateral hemiplegia with greater weaknas of leg than arm, cortical sensory loss,
aphasia & apraxia.
- The arm may show lnvoluntary movements. Incontinentia of urine and self neglect
maybe additional problems.

Posterior cerebral artery

- contralateral homonymous hemianopia
- contralateral thalamic syndrome
- visual association area in the dominant hemisphere is affected, there will be visual
agnosia
- bilateral lesion of occipital lobes will cause total blindness of cortical type.
- pupillary reflexes are normal
- frequently there is loss of memory and confusion
- mortality rate is high
Vertebrobasilar territory syndromes.
- Total occlusion of the basilar artery is immediately fatal.
- Smaller infarcts will impair respiration, heart beat and level of consciousness.
- involvement of the lower brain stem causes paralysis and sensory impairment in all
limbs, and dysphagia.
- lesion higher in the brainstem present with vertigo, vomiting, disarthria, dysphagia
and cerebellar signs. Occlusion of individual branches of the basilar artery can
produce crossed hemiplegias. These are:
- Weber's syndrome: - unilateral 3rd cranial nerve palsy witn contralateral hemiplegia.
- Benedict's syndrome : - 3rd nerve palsy with ipsilateral cerebellar ataxia.
- Millard-Gubler syndrome - paralysis of 6th and 7th cranial nerves on one side with
contralateral hemiplegia.
- Foville's syndrome : - 6th nerve palsy, paralysis of conjugate ocular deviation and
contralateral hemiplegia.

Vertebrobasiler ischaemia:
- common in the elderly
- can cause symptoms of loss of balance, poor posture control, dizzihess, recurrent
falls and drop attacks.

Posterior Inferior cerebellar artery

- vertigo
- vomiting
- unilateral facial paiy
- disphagia
- paralysis of the palate on the side of the lesion, cerebellar signs in the limbs on the
affected side
- ipsilateral Horner's syndrome, dissociated anaesthesia to pain and temperature on the
same side of the face and over the opposite half of the body below the neck.

Arterio venous malformation (AVM)

Abnormal collection of blood vessel arteri blood flow directly into draining veins
without the and interposed capillary no interveiting neural pareucyme
AVM – medium- high pressure and high flow

1) Parencymal AVM
2) Pure deural AVM
3) Mixed ( rare)

Presentation :

1) Hemorrhage
2) Seizuras
3) Mass effect (tigeneival neuralgia )
4) Ischenic
5) Migranes (headace rare)
6) Brit in dural AVM
7) ICP
8) HCP, coufestive heart fail w/ cardiomogali provenance of torehead veins. See
GB 1098

Moya-moya disease

progressive spoutanous occulation of one or both ICAS (@level sipkon) and their
brances w/ secondary formation a aquastomatic coll ateral capillary network at the
base of the brain Associated w/ aneurism, rarely w/AVMs.

Presentation

 Juvenile form : ischemic include TIAs hemiplegic and infarat. Headace most
common, also way seizures, focal neurologic deficit, hemorrape.
 adult form : hemmorage – rupture of MM bleeding into ganglia basal (GB),
Tudamus, ventricles.

SAB spontan vs non spontan

- Etiologi
- Kriteria diagnostik
- Patofisiologi dan anatomis
IV H
- Anatomi, patofisiologi
- Cabang arteri

Pertanyaan :
- Kenapa pasien didiagnosa tersebut ?
- Rencana terapi.
Mis : rencana coiling, definisi ? syarat, waktu, prosedur, komplikasi
Lokasi aneurisma tersering ?
Basilar tetap pecah  Isi darah di sistema interpedunkular & prepontin
A communicans pecah  Bisa ke ventrikel III, indikasi evakuasi ICH
infratentoriial
- Volume > 10 cc
- Diameter > 2,5 cm
- Obliterasi ventrikel 4.
Kalau Relatif dan absolut pada pasien dengan kelainan darah, ITP, leukemia
cari cabang-cabang MCA, M1-M7.

AVM
Definisi :
- Kumpulan pembuluh darah abnormal dimana aliran arteri langsung menuju
draining vein tanpa melalui capillary beds
- Tidak ada parenkim otak dalam nodus AVM.
- Kelainan kongenital yang cenderung bertambah besar seiring
bertambahnya usia dan progress dari low flow. Lesion saat lahir menjadi
medium to high flow lesion saat dewasa.

AVM dapat diklasifikasikan :

1. Parenkimal AVM
a. Pial
b. Subcortical
c. Paraventricular
d. Combined
2. Pure dural AVM
3. Mixed parenchymal dan dural (rare)

Epidemiologi
1. Malformasi congenital
- 15-20% PS Osler-Weber-Rendu syndrome have cerebral AVM.
- ± Diagnosa usia 33 th.
- 64% AVM terdiagnosa sebelum usia 40
- Puncak usia hemorrhage 15-20 th
 - Mortalitas 10% morbiditas 30-50%
Manifestasi klinis
1. Hemorrhage (most common) : 50% (Aneurisma : 92%) (paling sering
intraparenkimal)
2. Kejang
3. Mass effect
4. Ischemia by steal
5. Headache
6. Bruit (terutama dural AVM)
7. TTIK

Lokasi perdarahan pada AVM :

1. Intra parenkim : 82% (the most common site of bleeding)
2. Intraventricular
A : Biasanya karena ICH yang ruptur masuk ventrikel
P : pure intraventricular (with no ICH)  curiga intraventricular AVM.
3. SAH : bisa karena ruptur dari aneurisma pada feeding artery
4. SPH : uncommon

AVM kecil lebih lethal dari ukuran besar karena resiko perdarahan lebih besar
karena higher pressure of feeding artery.
AVM besar lebih cenderung bikin kejang karena lebih melibatkan korteks.
Average risk of hemorrhage for AVM is 2-4% per year.
Grading AVM Spetzlier Martin
Poin
Ukuran small (< 8 cm) 1
Ukuran medium (3-6 cm) 2
Ukuran largel (> 6 cm) 3
Non eloquent 0
Eloquent 1
Drainase vena superficial 0
Deep 1
Eloquent : Korteks sensori motor, bahasa, visual hipotalamus dan thalamus,
capsula interna, brainstem, pedonkulus serebelar, deep cerebellar nucler.
Spetzler Martin  tidak bisa dipakai pada pediatrik karena AVM nya masih
immature.
AVM matur saat usia 18 th dan cenderung jadi lebi padat.

Treatment
1. Surgery = Treatment of choice untuk AVM.
(+) : mengurangi resiko bleeding segera, seizure control improve.
(-) : invasif, risiko operasi.
2. Radiasi konvensional, efektif pada < 20% kasus  efektif.
Stereotactic radio surgery :
Untuk small AVM ( 2,5 – 3 cm nidus), deep avm
(+) bisa dikerjakan di ODS, non mvasif, reduksi gradual AVM flow, no
recovery period.
(-) butuh (- 3 th) untuk bekerja (selama waktu tersebut resiko bleeding)
hanya bisa pada lesi dengan nidus  3 cm.
3. Endovascular = embolisasi
(+) memfasilitasi pembedahan
(-) kadang tidak adekuat untuk membuat obliterasi permanen,
menginduksi perubahan hemodinamik, memerlukan prosedur multipel.

Kombinasi : embolisasi untuk mengecilkan nodus diikuti stereoactic

radiosurgery.

Vascular malformation : merupakan hasil dari diferensiasi mamplete plexus

cerebral primordial menjadi arteri, vena dan kapiler, gagal memisah di dura
dan pial circulation.
ICH : Faktor resiko :
1. Usia insidens meningkat signifikan > 55 th.
2. Laki-laki > wanita
3. Konsumsi alkohol sering = ICH lebar.

Ischemic stroke
Modalitas : Stage
- CT non kontras 1. Early hyperacute : 0-6 jam
- CT perfusion 2. Late hyperacute : 6-24 jam
- CT angiogafi 3. Acute : 24 jam – 1 mg
- MRI 4. Subacute : 1-3 minggu
5. Chronic : > 3 minggu

CT Scan :
Keuntungan : cepat, murah
Kerugian : sensitivitas terbatas
1. Immediate
Hyperdense segment of vessels
- MCA : MCA dot sign (M2)
- Top of the basilar syndrome
2. Early hyperacute
Paling rentan : daerah dengan poor collateral.
Tanda :
- Loss of grey matter differentiation
- Hypo attenuation of deep nuclear lentiform nuclear hypoattention (3
jam)
- Cortical hypodensity – parenchimal swelling + gyral effacement (loss of
insular ribbon)
3. Acute
-hypoattenuation dan swelling lebih nyata  mass effect.
4. Subacute
Swelling   fogging phenomenon.
5. Chronic
Swelling  , gliosis (+) ,  hipodens tanpa mass effect.

CT perfusion
- CBV CBV = MTT  : infark
- CBF CBV = MTT  : penumbra
- Mean transit time
- Time to peak
MRI
Keuntungan : sensitivitas dan spesifitas dalam beberapa jam setelah onset.
Kerugian : waktu lebih lama, kurang available
1. Early hyperacute
Dalam beberapa menit : signal BWI , ADC  = Infarction non
slow/stagnant vessel = loss of normal flow word high signal on T2 / flair.
Jika infarction complete : cortical contrast enhancement dalam 2-4 jam.
2. Late hyperacute
Setelah 6 jam : high T2 signal (flair)
T1 hipointens baru nampak dalam 16 jam.
3. Acute
-dalam minggu 1 :  DWI signal,  ACS signal,
 ADC mulai minggu I
Infarct tetap hyperintense on T2/flair  meningkat dalam 4 hari pertama.
4. Subacute
- ADC : pseudonormalisation antara 10-15 hari
- Infarcted tissue
- Persistent high T2 flair
- Minggu ke2 : T2 fogging
- T1 hipointense
5. Chronic
T1 : tetap hypointense
T2 :
Cortical contrast enhancement (+) 2-4 bln , DWI mulai 

Gambaran Klinis SAH

1. Nyeri kepala (97%) mendadak, severe, hilang dalam 1 hari.
2. Muntah
3. Syncope
4. Nyeri leher (meningismus)
5. Fotofobia
Tanda : - Meningismus (6-24 jam onset awal)
- hipertensi
- defisit neurologis fokal (N III palsy)
 - koma
- perdarahan okular

Faktor predisposisi perkembangan aneurisma (Nica et. Al 2010)

1. TBI (< 1% kasus)
2. Infeksi (2%)
3. Herediter (20% dari seluruh aneurisma)
4. Merokok dan hipertensi
5. Obat : kokain & amfetamin
6. Gangguan darah :
- Fibromuscular dysplasia
- Arteritis cerebral
- Arterial dissection

Komplikasi SAH
1. Vasopasme : 4-7 post SAB, defisit sesuai lokasi arteri, deteriorasi,
rebleeding, HCP, edema, kejang, hipoksia, sepsis.
2. HCP

Perdarahan di brainstem yang sudah memenuhi brainstem tidak ada gunanya

di EVD, tidak ada goal, walaupun GCS E1MUV+
Aneurisma  jadi IVH – bisa asal dari distal basiler tapi 2. A.Communicans 
lamina terminalis, 3 distal AICA , 4. Distal Plexus coroid terminalis.

DSA paling maksimal masuk di segmen A2, M2, V2 kalau lebih dari itu,
pembuluh darahnya sudah terlalu kecil, sehingga ujung probe tidak bisa
masuk.
EVD rusak sistem sirkulasi ICS, ventrikel jadi menciut beda dengan VP shunt,
karena VP shunt masuk ke rongga peritoneum. Idealnya pada ICH spontan :
CT serial per 6 jam karena turn over ICS tiap 6-8 jam.
ICH tensi  , kalau pas buka dura otak menciut  outcome jelek pada pasien
geriatri, hati-hati terhadap hidrosefalus akut.
Otak atrofi, kaku, sedikit gambaran edema periventrikel sudah menunjukkan
TTIK .
Pada aneurisma , IVH terjadi pada 13-28% dengan prognosis lebih buruk .
- Distal PICA  ke ventrikel dan ML + luschka
- A comm aneurysm  In lamina terminalis  ventrikel 3 dan lateral
- Distal basilar artery  floor 3rd ventricle  ventrikel 3

Cavernoma / cavernous angioma

- Vascular malformation, congenital. Gejala : headache, seizure, smal
parenchimal hemorrhage.
1% dari intracranial vascular lesion
15% dari cerebrovascular malformation
Cavernoma tidak memiliki vaskularisasi
Pada T2 : popcorn pattern (mixed signal core with low signal)
Gejala : seizure 60%, neurologic deficit 50%, hemorrhage 20%.

Collection of dilated blood vessel, tapi bisa terjadi linkage penyebab seizure
karena penekanan, bisa juga karena daerah sekitar yang scaring.
Indikasi surgery :
1. Accesible lesion
- Focal deficit
- Smptomativ hemorrhage
- Seizure
2. Less accessible : repeatedly bleeding, progressive

Etiologi lobar hemorrhage (10-32% of spontaneous ICH)

1. Ekstensi dari deep hemorrhage
2. Cerebral amyloid angiopathy : the most common cause of lobar ICH pada
elderly dengan normotensi.
3. Trauma
4. Hemorrhagic transformation of ischemic infarct
5. Tumor
6. AVM
7. Ruptur aneurisma
8. Idiopatik
Cerebral amiloid angiopathy/congophilic angiopathy should be suspended in
patient with recurent hemorrhage dengan lokasi lobar. Insidens ± 50% usia >
70 thn.

Kriteria diagnosis of CAA :

Definitif CAA ; Full postmortem exam show 3 of the :
a. Lobar cortical or corticosubcortical hemorrhage
b. Severe CAA
c. Absence of another diagnostic lesion

Possible CAA with supporting pathological evidence. Clinical data ,

pathological tissue showing 3 of the following :
a. Lobar, cortical or corticosubcortical hemorrhage
b. Some degree of vascular amylodi deposition in spearmen
c. Absence of another diagnostic lesson

Probable CAA
Clinical data dan MRI findings showing 3 of all the following :
a. Age ≥ 60 y.o.
b. Multiple hemorrhages restricted to the lobar, cortical or corecosuncortical
region
c. Absence of another cause of hemorrhage.

Possible CAA. Clinical data-data MRI findings :

a. Age ≥ 60 th
b. Single, lobar, cortical or corecosuncortical hemorrhage without another
cause, or multiple hemorrhages with a possible but not definitie cause or
with some hemorrhage in a atypical location. Mis : brain stem.

Intratumoral bleeding (apoplexy)

Malignant tumors most commonly cause ICH :
1. Glioblastoma
2. Limfoma
3. Metastatic tumors
 A. Melanoma  40% hemorrhage
B. Chronocarcinoma 40% hemorrhage
C. Renal cell carcinoma
D. Bronchogenic carcinoma
Although only 9% tapi tumor ini paling sering metastase ke otak,
jadi khususnya cukup sering.
Surgical untuk ICH
a. Lesion with marked mass effect, edema dan MLS
b. Lesion with ICP  symptoms, mass effect and edema
c. Volume : favourable : 10-30 cc
< 10 cc : konservatif
> 30 cc : poor outcome
> 60 cc dengan GCS  8 mortalitas 91%
> 85 cc no patients survived
d. Favourable location : lobar, cerebellar, external capsule non dominant
hemisphere.
e. Usia < 50 th
f. Durasi < 24 jam.
Cabang A. Carotis externa :
S uperior thyroid
A scending pharyngeal
L ingual
Facial anastomosis dengan A. ophtalmic
O cciptal
P osterior avricular
S uperficial temporal : cb frontal
cb parietal
Internal maxillary – middle meningeal
House Brackman VII grade
1. None normal
2. Mild slight weakness on close inspection
3. Moderate obvious, not disfiguring
4. Moderate severe obvious + disfiguring asimetri
5. Severe barely perceptible motion
 6. Total paralysis
Penunjang :
CT / MRI : proptosis
Pembuluh darah intraokular membesar (termasuk sup. Ophtal nueveub
(best seen on T2 coronal) dan convexity of lateral wall covernous sinus.
Angiography : shunting of blood from ICA into covernous sinus.
Rapid opafication of petrosal sinus dan /ophtalmic vein
Terapi :
20-50% of low flow CCF spontaneously thrombose, hanya observasi selama
visual acvity stabil dan tekanan bola mata < 25
High flow CCF jarang resolve spontan, progressive visual deterioration urgent
treatment is usually indicated.
Tx : embolisasi / dippring
Indikasi treatment :
1. Proptosis
2. Visual loss
3. Cranial nerve VI palsy
4. Intractable burit
5. Severely elevated intraocular pressive.
6. Increased filling of cortical veins in angiography
Koma pada SAH, karena :
1. ICP 
2. Damage brain tissue
3. Hidrosefalus
4. Diffuse ischemia
5. Seizure
6. CBF  karena CO 
 tekanan CSF  kompresi vena retina sentral dan retinochoroidal
anastomosis
 hipertensi vena dan disrupsi vena retina  accular hemorrhage
1. Sub hyaloid (preretinal) hemorrhage
2. Intra retinal hemorrhage
3. Hemorhage within vitreous tumor
CT Scan : untuk subtle SAH; lih occipital horn dan silvian fissure
Lihat : - ventrikel
- hematoma
-infark
-darah di sisema dan fisura
- deteksi lokasi aneurisma
MRI/MRA :
1. Poor sensitivity for aneurism detection earl ofter SAB (the 1 st 24-48 jam)
karena met Hb terlalu sedikit.
2. Significantly poorer sensitivit for aneurysm < 3 mm untuk screening test
pada pasien resiko tinggi (two first degree relatives with aneurism,
merokok dan HT.
3. Waktu terbaik setelah 4-7 hari.

CTA :
1. Dapat melihat hubungan dengan struktur tulang.
2. Bisa 3D, dapat membedakan pembuluh darah yang ada, aneurisma
dengan sekitarnya
3. Untuk evaluasi vasospasme.
4. Deteksi rupture dan unrupture

DSA
- Gold standard untuk evaluasi aneurisma.
- Maybe necessary after CTA, untuk menggambarkan anatomi untuk
menentukan pembuluh darah yang dominan mengisi aneurisma. Dan
collateral/perforasi  jangan di-clip.
- Untuk highly suspicious case with CTA (-)
Prediksi lokasi aneurisma dari pattern darah pada CT 78% (mostly for
MCA & A. comm)
A. Darah predominan di fisura interhemisfer anterior (± di ventrikel lateral) /
girus rektus  A. comm aneuris
B. Darah predominan di satu sylvian fissure  PCOM/MCA
C. Darah predominan di prepontin / sistema pedunkular  basilar/SC
D. Darah predominan di ventrikel
 - Ventrikel 3 & 4 : suggest lower posterior fossa source PICA/VA
dissection
- Ventrikel 3 : basillar
Vasospasme/delayed ischemic neurologic deficit :
- Hampir tidak pernah muncul < 3 hari post SAH
- Main time of Risk : 3 – 14 hari post SAH
- Peak incidence : 6-8 hari post SAH
- Faktor resiko : higher SAH grade, more blood on CT

Hunt dan hess grade : 1. 22%

2. 33%
3. 52% Kemungkinan vasopasme
4. 53%
5. 74%

Manifestasi klinis
Biasanya bersifat gradual, bisa juga progresif/fluktuasi
1. Non incalizing finding : new/ increasing headache, alteration in level of
conscious ness, disorientasi, meningismus
2. Focal neurological sign : vasospasme lebih sering pada distribusi ACA
dibanding MCA.
ACA syndrome : FRONTAL LOBE FINDINGS
(labura, grasps/such reflex, inkontinensia urin, mengantuk, slowness,
respon lambat, konfusi, infark pada distribusi ACA bilateral biasanya
karena ruptur Aco A.
MCA syndrome : hemiparesis, monoparesis, afasia.
ICH pada ITP
Faktor resiko :
- Trombosit < 10 – 20.000
- Penggunaan NSAID
- Trauma kepala (33%)
- Vasculitis terkait SLE
- AVM
Insidensi < 1 : 100 ps ITP
 ♀>♂
Usia 3 bulan – 17 th
Kontra indikasi mutlak / = mutlak ?

Normo pressure hydrocephalus

- Sering pada dekade ke 6 dan 7
60% NPH idiopatik
40% NPH sekunder : 1. SAB
2. Meningitis
3. Peradangan
Trias : demensia, gangguan berjalan / gait, inkontinensia urine

Gangguan berjalan/gait : Magnetic gait/kakinya seperti lengket ke lantai,

langkah-langkah kecil, lambat, sulit berbalik.