Introduction arteries that supply blood to the normal brain,

pass through the nidus and also contribute to

Spontaneous Intracerebral hemorrhage (ICH)
is one of the disease with high mortality rate
in the world. Many factors that cause the
occurence of spontaneous ICH. One of them,
expecially that attack young age, is
arteriovenous malformation (AVM).
Hemorrhage from cerebral venous
malformation represents 2% of all
hemorrhagic stroke, which one of the causes
of non-hypertensive spontaneous ICH.1
the shunt before supply blood to normal
brain. In a similar manner to the arteries, for
the draining vein, one should note the
number, size, and locations of the major
veins. Like the transit arteries, it is important
to recognize the possible existence of normal
veins draining functional cerebral tissue that
may be adjacent to the lesion.

AVM is congenital lession of the complex

tanggle of the blood vessel (arteries and
veins)connected by one or more fistulae. It
can occured in all over the body including
brain and spinal cord. Normally, the blood wil
flow to whole area of the body from the heart
by large artery. Then become samller until a
small cell capillary that supply nutritions and
oxygen to the cell. The place of exchanging
nutrition or oxygenitation is capillary bed. CO2
and other residual of cell metabolisme will be
transfered to vein by capilary bed, and the
back to the heart. But in AVM, arteries direcly
connect to the vein without capilary bed
betwen them. Because theres a different Feature 1. Arteriovenous malformation. Showed a nidus,
pressure between arteries (high flow) and the some feeders arteries and draining vein
veins (low flow, then will develop a problem
When AVM ruptures, it will has nine fold risk
was called high pressure shunt. The veins will
for rerupture in the first year.2 A clear
not be able to withstand a high pressure flow.
understanding of the diagntic and treatment
So it wil scretch and became larger and thin,
of the AVMis imperative.
and will be vulnerable to rupture.
Epidemiology
AVM consist of three component. Feeding
vessels, nidus and darining veins. The vascular Insidence of AVM is vary in each country. In
conglomarate is called the nidus. Size of nidus New York island insidence of AVM is about
is resemble the size of the avm. There are 1,34 per 100.000 person-years. Theres a
three types of feeding vessel in AVM: direct report that insidence rate from australia and
feeders, transit feeders and indirect feeder sweden is 0,89-1,24 per 100.000 person-
(artery en passage). Direct feeders are arteries years, and in scotland about 18 per 100.000
that end directly and exlusively in the nidus. persons-years.3 Al-shahi et al (2001), from his
Transit feeders are the arteries that supply systematic review, found that insidence of
blood to the normal brain but they pass AVM is 1 per 100.000 persons per year in
through the nidus. Indirect feeders are the unselected population, and in adult is 18 per
100.000 person-years. AVMs account for
between 1 and 2% of all strokes, 3% of strokes
in young adults, 9% of subarachnoid
haemorrhages and, of all primary
intracerebral haemorrhages, they are
responsible for 4% overall, but for as much as
one-third in young adults.
Many factors make the AVMs vurnarable to
rupture. Small nidus and single draining vein is
common factor. Also thre’s connection
between size of the AVM and rupture rate.
Smaller the AVM higher chance to rupture.
May be it’s because the small has the higher
feeding pressure compared to larger AVM, the
high pressure can make the AVM easy to
rupture.4 The other factors that assosiated
with the risk of rupture are previous rupture,
infratentorIal, and deep location.5,6
AVMs are the most common cause of
spontaneous ICH in young adult. Maybe
because the lessions are congenital lession.
Aproximately it occured on the age of 20-
40.7,8,9 Risk of bleeding can be simply
approximated with the linier formula10:
% lifetime risk = 105 – patient’s age
For example 25 years old man has % lime time
risk of bleeding by 80%, at least once in a life
time. There’s no distinc between sex for the
AVM. It affects male and female in the same
rate.
Pathological squelae
AVMs make neurological defficites through 3
main mechanisms.11 First, hemorrhage may
occur in the subarachnoid space, the
intraventricular space or, most commonly, the
brain parenchyma. Second, in the absence of
hemorrhage, seizures may occur as a
consequence of AVM: approximately 15-40%
of patients present with seizure disorder.
Finally, but rarely, a progressive neurological
deficit may occur in 6-12% of patients over a
few months to several years. These slowly
progressive neurological deficits are thought
to relate to siphoning of blood flow away
from adjacent brain tissue that is called the
"steal phenomenon", a concept that has been
recently challenged. Neurological deficits may
be explained alternatively by the mass effect
of an enlarging AVM or venous hypertension
in the draining veins.
Seizure is the second most commont
presenting symptom, assosiated with
supratentorial AVM. Aproximately 15%-30%
AVM patient With focal or generelized
seizure.12,13,14 Angiographic characteristics of
epileptogenic AVMs include cortical location
of the nidus or feeding artery, feeding by the
middle cerebral artery, absence of aneurysms,
presence of varices in the venous drainage,
and association of varix and absence of
intranidal aneurysms. Other factors
significantly associated with the onset of
seizures include AVMs fed by the external
carotid artery and a temporal or parietal
cortical location.15
Another pathological squelae is headache.
Headaches are the presenting symptom in
approximately 15% of patients without
evidence of rupture.12 Headache and seizure
also can be assosiated to the hemorrhage.
Classification and Grading System
AVM included into category of dysplastic
vascular malformation, where there have
been four pathological entities:
developmental venous anomalu (venous
angioma), cappilary telangiectasias, cavernous
malformation, and AVM.16,17,18 One of them can
follow another, altough it’s rare.
Avm may be classified as :
1. Parenchymal AVM
a. Pial
b. Subcortical
c. Paraventricular
 d. Combined
2. Pure dural AVM
3. Mix parenchimal and dural AVM
The AVM is classified to know the outcomes after
surgery. So the surgeon can predict the risk of
permanent neurological deficits after surgery. It’s
“Spetzler-Martin Scale” that be used. Grade 1 and
2 has very low risk of morbidity after surgery, but
the grade 4 and 5 has higher risk of neurological
deficits after surgery. It very usefull for surgical
decision making.
Diagnostic Radiology
Many imaging technic can visualize a AVM,
including: MRI, MR angiography (MRA), CT, CT
Angiography (CTA) and angiography. MRI is usefull
in diagnostic and management of AVM. MRI not
only can visualize the AVM but also can show
better visualization of location of the AVMs and
surrounding structure that relate to AVM. On T2-
weighted images, hypointense signal of the lession
are indicated to flow void. Peripheral to the nidus,
Table Structure visualized during DSA
hypointense on T2 and gradient echo can also
show hemosiderin depocites that sign a previous
hematoma.
Non contrast CT scan cannot visualize AVM clearly.
But, it’s necessary to recognize the key feature
around hematoma that was suspected AVM. 25%
to 30% AVMs have calcium depocition
(calsification) that may be seen even in the mass of
the hematoma.19 CTA and MRA can deliniate the
nidus and assosiated vessels without exposed any
complication of angiography.
But in CTA and MRA, is very hard to determine
dinamic aspec of malformation. because in MRA
CTA the vessels enhance contrast simultanly. So,
its dufficult to see where is the nidus, feeding
arteries and draining veins. For that angigraphy is
required. Angiography, expecially digital
substraction angiography (DSA), can substract out
static components of the image, so we can clearly
visualize nidus, feeder artries and darining veins.
Structure visualized in every phase during DSA are
seen on the table below. But the angiography is
lack of geometrical of the nidus.
Treatment
Unlike the anuerisme, risk of rebleeding imediately
for AVM rupture is very rare. Although surgical
evacuation of the hematoma caused by AVM
rupture for life treatening is must be done
imediately, resection of the AVM can be delayed
until hematoma is resolved and the AVM stabilize
its form. And then wait until swelling decreased for
easier surgical intervention. But if if neurological
deficits happen progressively, surgical intervention
must be done urgently.
The definitif treatments for AVM including:
1. Medical or symptomatic therapy
2. Embolization
3. Microsurgery
4. Radiosurgery
5. Multi modal therapy
That must be considered for treatment of the AVM 1. Malformation is very extensive
are: 2. Deep location in the brain
1. Size of the AVM 3. Primary blood supply origin from deep
2. Location perforating vessels
3. Vascular anatomy 4. Advance age
4. Age 5. Poor medical condition. (such as: advance
5. Medical condition heart disease, insuficiency respiratory, or
The current American Heart Association cancer with metastatic.
multidisciplinary management guidelines for the
treatment of brain AVMs recommend the Embolization
following approach:20
Embolization is used for pre operative, pre
1. Surgical extirpation is strongly suggested
radiosurgery or paliatif embolization. Embolization
as the primary treatment for Spetzler-
involves occluding blood flow to an arteriovenous
Martin grade I and II if surgically
malformation by using endovascular catheters to
accessible with low risk.
deposit occlusive materials into the feeding
2. Radiation therapy alone is recommended
arteries and nidus. It can be used to reduce size of
for Spetzler-Martin grade I or II if the
the AVMs, and symptoms. Embolization can be
AVM is less than 3 cm in size and surgery
curative in a minority of cases, particularly for
has an increased surgical risk based on
lesions less than 1 cm in diameter that are fed by a
location and vascular anatomy.
single artery.21,22 It is usually inadequate by itself
3. Brain AVM of Spetzler-Martin grades III
to treat the AVM, because it may recanalize later.
can often be treated by a multimodal
AVMs that are embolized have a rate of
approach with embolization followed by
permanent morbidity between 4% and 14%.23
surgical extirpation. If the lesion has a
If the embolization is followed by surgical
high surgical risk based on location and
intervention, the surgery can be done 3-30 days
vascular anatomy, radiation therapy may
after embolization. If its followed by radiosurgery,
be performed after embolization.
the surgery can be done 30 days after the
4. AVMs of Spetzler-Martin grade IV and V
embolization.24
are often not amenable to surgical
The agents for embolization are classified to three
treatment alone because of the high
cathegories, they are: occlusive devices,
procedural risk. These AVMs can be
microparticles, and liquids. Occlusive devices
approached by a combined multimodal
include balloons for large vessel occlusions,braided
approach of a combination of
silk threads which are highly thrombogenic, and
embolization, radiosurgery, and/or
coils. Many earlier reports of embolizations used
surgery.
particles, specifically, polyvinyl alcohol (PVA)
5. In general, embolization should only be
(Counter PVA particles, Boston Scientific, Fremont,
performed if the goal is complete AVM
CA). Two liquid agents are currently in use in the
eradication with other treatment
United States for embolization: NBCA and EVOH
modalities. The only exception is palliative
(Onyx). Improved obliteration rates (of
embolization in patients with an AVM of
approximately 20%) have been reported for the
Spetzler-Martin grade IV or V with venous
use of a recently developed embolic agent
outflow obstruction or true steal
(Onyx).25
phenomenon in order to reduce arterial
inflow to control edema or to reduce the Radiosurgery
amount of shunt, respectively.
Radiosurgery is an option that is generally used to
Medical treatment treat AVMs that are approximately 3 cm in
diameter or less. Proton beam, linear accelerator,
Indications for medical treatment including:
or gamma knife methods are used to deliver a high
dose of radiation to the AVM, while minimizing the Susupicious for the AVM. The MRI was done, and
effects to surrounding brain tissue; a single dose showed some heterogen lession with a flow void
generally is given. AVMs with nidal volumes less feature. And from CTA showed a tanggle of some
than 10 mL (diameter <3 cm) are frequently vessels that refers to AVM with size aproximately
curable by radiosurgery, with rates of obliteration 5.6 cc. From angiography found involvement of
at 2 years estimated at between 80% and 88%. 26,27 two feeder arteries branch of MCA and one
Radiosurgery may take 1-3 years to achieve darining vein.
thrombosis of an AVM, thus the patient remains at The patient was diagnosed with arteriovenous
risk for hemorrhage from AVM during the malformation. And performed surgery for AVM
treatment period. resection. And the AVM was resected by en-block
resection. No significant neuroligical deficits was
found after surgery.
Surgical treatment
Decisions as to which lesions are most amenable
to surgery are commonly based on the Spetzler–
Martin scale. Grade I, II, or III AVMs were found to
have low treatment-associated morbidity. In case
series for grade I – III, reported rates of permanent
weakness or paralysis, aphasia, and hemianopsia
are 0 to 15%, and most report no deaths.28,29
However, grade IV lesions conferred 31.2%
treatment-associated morbidity, and grade V
lesions had 50% new treatment-associated
morbidity.30 Surgery is recomended for all grade I
and II lesions. Grade III lesions should be treated
on a case-by-case basis. Grade IV and V lesions
require a multidisciplinary approach with
individual analysis. Surgical outcome predicted by
Spetzler–Martin scale are showed on the table
below.31

Case report
A 42 years-old man was pressented with
spontaneous inrtracerebral hemorrhage 3 moths
ago. He was underwent surgery for evacuation clot
emergency. No history of hypertension before.
Patient has hystory of the seazure 2 years ago,
twice, generelize seizure, but controled by the
drug. He complaint mild headache sometimes, but
it didn’t really disturbe his daily activities. Phsisical
diagnostic was normal and neurological state in
the normal range.
From the CT finding shows calsification feeture on
the left temporal near the remains of hematoma.
 hemorrhage is imperative. It’s including age,
simptom, history of hypertension and feature of
Discussion radio imaging,
Spontaneous ICH from rupture of the AVM are still
a rare case. Neverthless, to know the things
relating to the AVM as etiology of cerebral
This patient is 42 years-old, no history of the
hypertension and has hystory of generalized
seizure. With this datas, it’s supposedly the priority
6.
of it’s etiology is AVM. And phsysician before
prepare for the resection of the AVM. Because the
ruptered AVM has the high risk of reccurent
bleeding as 18% in the first year. This may be
resulting poorer prognosis. 7.
In caso, presenting lobar AVM with 2,5 cm
diameter, located in non-eloquen area, with
superficial venous drainage. With this so the
spetzel-martin grade is 1, and its recomended for
surgical resection of the AVM, suitable to the 8.
surgical intervention that already done. Because
from the some trials, surgical is generally
considered appropriate for AVM that are grade I
9.
and II.
Summary
10.
Comperhension of natural history, signs and
symptoms, and imaging for the AVM case is
necessary for receiving an optimal treatment.
Decision making for treatment of the AVM is
according to spetzel-martin grade, age of the 11.
patient, presenting of assosiated aneurisme, and
pattern of the vessels.
Referrences
12.
1. Rustam al shahi, charles warlow, a systematic
review of the frequency and prognosis of
arteriovenous malformation of the brain in
adults, brain (2001), 124, 1900-1926
2. Mast H, Young WL, Koennecke H-C, Sciacca RR,
Osipov A, Pile-Spellman J, et al. Risk of 13.
spontaneous haemorrhage after diagnosis of
cerebral arteriovenous
malformation. Lancet 1997; 350: 1065–8 14.
3. Stapf C, Mast H, Sciacca RR, Berenstein A,
Nelson PK, Gobin YP, et al. The New York
Islands AVM Study: design, study progress,
and initial results. Stroke. May 2003;34(5):e29-
15.
33.
4. Spletzer R.F., Hargraves R.W., McCormick
P.W., et al: relationship of perfussion pressure
and size to risk of hemorrhage from
arteriovenous malformation. J neurosurg 16.
1992;76(6): 918-923.
5. Hernesniemi J.A., Dashti R., Juvela S., et
17.
al: Natural history of brain arteriovenous
malformations: a long-term follow-up study of
risk of hemorrhage in 238
patients. Neurosurgery 2008; 63(5):823-
829.discussion 829-831
Laakso A., Dashti R., Seppänen J., et al: Long-
term excess mortality in 623 patients with
brain arteriovenous
malformations. Neurosurgery 2008; 63(2):244
-253.discussion 253-255
Brown RD Jr, Wiebers DO, Torner JC, O’Fallon
WM. Frequency of intracranial hemorrhage as
a presenting symptom and subtype analysis: a
population-based study of intracranial vascular
malformations in Olmsted Country,
Minnesota. J Neurosurg 1996;85:29-32.
ApSimon HT, Reef H, Phadke RV, Popovic EA. A
population-based study of brain arteriovenous
malformation: longterm treatment outcomes.
Stroke 2002;33: 2794-800.
Crawford PM, West CR, Chadwick DW, Shaw
MD. Arteriovenous malformations of the
brain: natural history in unoperated patients. J
Neurol Neurosurg Psychiatry 1986;49:1-10.
Fleming K., Brown R.D.: Natural history of
intracranial vascular
malformations. In: Winn H.R., ed. Youmans
Neurological Surgery, 5th ed.. St.
Louis: Elsevier; 2004:2160.
Laakso A, Dashti R, Juvela S, Niemelä M,
Hernesniemi J. Natural history of
arteriovenous malformations: presentation,
risk of hemorrhage and mortality. Acta
Neurochir Suppl. 2010;107:65-9.
Brown R.D., Wiebers D.O., Torner J.C., O’Fallo
n W.M.: Frequency of intracranial hemorrhage
as a presenting symptom and subtype
analysis: a population-based study of
intracranial vascular malformations in Olmsted
Country, Minnesota. J
Neurosurg 1996; 85(1):29-32.
Crawford P.M., West C.R., Chadwick D.W., Sha
w M.D.: Arteriovenous malformations of the
brain: natural history in unoperated patients. J
Neurol Neurosurg Psychiatr 1986; 49(1):1-10.
Mast H., Young W.L., Koennecke H.C., et
al: Risk of spontaneous haemorrhage after
diagnosis of cerebral arteriovenous
malformation. Lancet 1997; 350(9084):1065-
1068.
Turjman F., Massoud T., Sayre J., et al: Epilepsy
associated with cerebral arteriovenous
malformations: a multivariate analysis of
angioarchitectural characteristics. AJNR Am J
Neuroradiol 1995; 16(2):345-350.
McCormick W.F.: The pathology of vascular
(“arteriovenous”) malformations. J
Neurosurg 1966; 24(4):807-816.
McCormick W.F., Nofzinger J.D.: “Cryptic”
vascular malformations of the central nervous
system. J Neurosurg 1966; 24(5):865-875.
18. McCormick W.F., Hardman J.M., Boulter T.R.:
Vascular malformations (“angiomas”) of the
brain, with special reference to those
occurring in the posterior fossa. J
Neurosurg 1968; 28(3):241-251.
19. Osborn A.: Diagnostic Imaging. Salt Lake
City, Amirsys, 2004.
20. Ogilvy CS, Stieg PE, Awad I, Brown RD Jr,
Kondziolka D, Rosenwasser R. AHA Scientific
Statement: Recommendations for the
management of intracranial arteriovenous
malformations: a statement for healthcare
professionals from a special writing group of
the Stroke Council, American Stroke
Association. Stroke. Jun 2001;32(6):1458-71.
21. Soderman M, Andersson T, Karlsson B, Wallace
MC, Edner G. Management of patients with
brain arteriovenous malformations. Eur J
Radiol 2003;46:195-205.
22. Weber W, Kis B, Siekmann R, Kuehne D.
Endovascular treatment of intracranial
arteriovenous malformations with onyx:
technical aspects. AJNR Am J Neuroradiol
2007;28:371-7.
23. Haw C.S., ter
Brugge K., Willinsky R., Tomlinson G.: Complica
tions of embolization of arteriovenous
malformations of the brain. J
Neurosurg 2006; 104(2):226-232.
24. Greeberg.
25. Weber W, Kis B, Siekmann R, Kuehne D.
Endovascular treatment of intracranial
arteriovenous malformations with onyx:
technical aspects. AJNR Am J Neuroradiol
2007;28:371-7.
26. Yu SCH, Chan MSY, Lam JMK, Tam PHT, Poon
WS. Complete obliteration of intracranial
arteriovenous malformation with
endovascular cyanoacrylate embolization:
initial success and rate of permanent cure.
AJNR Am J Neuroradiol 2004;25(7):1139–1143
27. Lunsford LD, Kondziolka D, Flickinger JC, et al.
Stereotactic radiosurgery for arteriovenous
malformations of the brain. J Neurosurg
1991;75(4):512–524.
28. Hamilton MG, Spetzler RF. The prospective
application of a grading system for
arteriovenous malformations. Neurosurgery
1994;34:2-6.
29. Pikus HJ, Beach ML, Harbaugh RE.
Microsurgical treatment of arteriovenous
malformations: analysis and comparison with
stereotactic radiosurgery. J Neurosurg
1998;88:641-6.
30. Hamilton MG, Spetzler RF. The prospective
application of a grading system for
arteriovenous malformations. Neurosurgery
1994;34(1):2–6, discussion 6–7
31. Spetzler RF, Martin NA. A proposed grading
system for arteriovenous malformations. J
Neurosurg 1986;65(4):476–483