UNRUPTURED

INTRACRANIAL
AVM
Presented by
dr. Yunni Diansari
Supervisor
Dr. Alwi Shahab,SpS(K)

PREFACE
AVM : uncommon case
Unruptured AVM 1:1000
Symptoms : vary
headache, seizure, progressif neurological
deficit, intracranial bleeding>>>, or
asymptomatic
Multidisciplinary Management ~case by
case

CASE REPORT
Identification
Male, 32 yo
Palembang
Admitted to hospital : sept, 4th 2008

Anamnesis

1 year before hospitalized Throbbing

Headache, unilateral
3 month before hospitalized
headache>>, vomitus (-), visual disturbance(-),
hearing disturbance (-), seizure (-)
2 month before hospitalized
weakness in the right arm& right leg, legs are
more weaker than arm, headache (+)
1 month before hospitalized
weakness became worse, Assymetry face,
disarthry

 History
Hypertension (-)
Head Injury 3 years ago
Seizures (-)

First time

Physical Examination
General Status
Sens : compos mentis , GCS : 15
BP: 120/80 mmHg
Pulse : 72x/m
RR : 22x/m
T: 36,80C

Neurological Status
Nn. Craniales
N II : Visus OD 6/6, OS 6/6,
edema papil(-)
N VII : right paresis; assimetry face,
lagophthalmus (-),
N XII : tongue deviate to the right,
disartry (+), athropy papil (-),
fasiculation (-)

Motoric Function
Right
arm

Left arm Right

leg

Left
leg

Movement

enough

enough

enough

enough

Strength

Tonus

Klonus
Phy ref

Pat ref

+(B,C)

+(B,C)

Head CT Scan without contrast(20-6-08)

Intracerebral SOL in left temporoparietal lobes ~susp
oligodendroglioma +bleeding intraventricle

Head CT Scan with contrast (25-6-08)

Radiologist suspected hemangioma appearance in left
temporoparietal lobes
DD: A-V malformation

CD : Right hemiparesis spastic type

Right paresis N VII&XII central type

TD : Temporoparietal lobes, left

hemisferium cerebri

ED :- SOL
- Intracranial AVM

Therapy
IVFD RL gtt xx/m
Inj Dexametason 3x2 amp iv
Inj Ranitidin 2x1 amp iv
Mefenamic Acid 3x500mg
Chest X-Ray
ECG
Lab

Prognosis

Quo ad Vitam : Dubia ad malam

Quo ad functionam : Dubia ad malam

Follow up
Sept 5th 2008
Comp : headache
General Status
sens : cm
BP:120/80, P:72x/m, RR:20x/m, T:afebris
Neurological status: stqa
Neurological diagnosis : idem
Therapy : continued
planning for Head MRI & Head
MRA

Supporting Examination
Laboratorium
Routin blood count : within normal value
Chemistry clinic blood count : within
normal value
Chest X-Ray : normal

Sept 6th 2008 Sept 9th 2008

Comp : headache <<

General status
Vital sign: within normal range
Neurological status : stqa
Head MRI
On T1: there is tubuler structure in left temporoparietal
lobes
On T2: there is hiperintens with hipointens appereance.
Post contrast there is enhancement in the wall. Narrowed of
Left hemisphere cortical sulci. There is a mass enlarge to
the complex of N VII &hipofisis

Narrowed of Left ventricle. Both of left fissura

sylvii & cysterna obliterated. There is midline shift
to the right. Differentiation of alba
substantia&gricea are good. Pons ,Cerebellum, &
paranasalis sinus are normal
AVM in left temporoparietal lobes
CD: right hemiparesis spastic type
right paresis N VII&XII sentra type
TD: temporoparietal lobes, left cerebral
hemisferium
ED:Intracranial AVM

Head MRI (8-9-08)

Head MRI with contras

Therapy
Continued
Consult to neurosurgery

Sept 10th

2008

Comp : headache (-)

General status
Vital sign: within normal range
Neurological status
Motoric : strength of arm 5/5
strength of leg 4/5

Neurological Diagnosis : idem

Therapy
IVFD RL gtt xx/m
Inj dexametason 3x1amp iv
Omeprazol 1x1 tab
Patient discharged from the hospital
by family request

Oct 6th 2008

Comp : (-)
Vital sign : within normal range
Neurological Status
Nn Craniales : right paresis N VII sentral
type
Motoric fc : paresis (-),phys ref n/n, Pat ref -/MRA : AVM in left hemispherium, location
could be in M1 segmen
Patient was suggested to reffer to Jakarta

Head MRA (20-9-08)

Dec 10th 2008

Comp : headache, right visual field cut

Vital sign : within normal range
Neurological status
N II : right homonymous hemianopia
Therapy
conservative symptomatic
consult to eye departement
for camfimetry (havent been done)

LITERATURE REVIEW
Epidemiology
The Incidence & Prevalence not exactly
known
USA : 0,14% symptoms 12 %
Most common : 20-40 years
Male ~ female
AVM 2% of all stroke
38% of intracerebral hemorrhage

Definition

abnormalities

of
intracranial
vessels
that
constitute
a
fistulous
connection
between the arterial
and venous system
and that lack
of a
normal intervenning
capillary bed.

Patological features
AVM consist of :
1. Nidus
2. Feeding artery
3. Draining vein

Types of AVM
1.
2.
3.
4.
5.

True arteriovenous malformation

Cryptic AVM or Cavernous malformation
Venous malformation
Capillary telangiectasia/ hemangioma
Dural fistule

Clinical symptoms
depend on type & location of AVM
40-60% intracranial hemorrhage
Seizures
Headache
Progressif neurological deficit
most common intracranial AVM assimptomatic until
the bleeding occur

Supporting examination
CT Scan
MRI/MRA
Angiography

Grading system

Management
Goals

Limited bleeding
Control of seizure
Remove the AVM ( if possible)

Methods

Conservative
Surgery
Radiosurgery
Endovascular Embolization

CASE ANALYSIS
Anamnesis
Chronic throbbing headache, unilateral,
Progresiff neurological deficit weakness
of arm&leg, assymetry face, disartry
CD: right hemiparesis spastic type
right paresis N VII&XII sentral type
ED : SOL
AVM

 Supporting examination

Head CT scan: Suspected SOL

Head CT Scan with contrast
AVM, DD: hemangioma
Head MRI : AVM
MRA : AVM, M1 segment
Lab : within normal range evaluation for
surgery

It should be done Angiography grading

Management & prognosis

Management case by case

Surgical Intervention

angiography
grading

Conservative

This patient angiography havent been

done
Supporting examination giant AVM

 Giant AVM

surgery high risk, complication >>

Radiosurgery not recommended
embolization - combined therapy (presurgical & pre
radiosurgery
- palliative therapy
Goals
- presurgical limited bleeding during surgery
- Preradiosurgery reduce the nidus size
- Paliative decreasing blood flow to AVM decreasing
neurologic deficit
Conservative risk & benefit

 This patient conservative

Progressif neurological deficit
Vasogenic edema improvement after
giving dexametason
Vascular steal ischemic around brain
This patient was suggested to reffer to
Jakarta endovascular embolization

 Prognosis
dubia ad malam
Size : giant
Progressif neurological deficit
counselling important

CONCLUSION
AVM: vascular malformation >>>
Grading system: therapy & prognosis
Management : case by case risk &
benefit
The succesfull treatment Multidiscipline
team : neurologist, neurosurgery,
neuroradiologist, radiotherapist

 This case reported the patient with

progressif neurological deficit caused by
intracranial AVM
Supporting examination gave a picture of
unruptured intracranial AVM
Management conservative (limitation of
equipment)

THANK YOU