Keywords
cerebellar arteriovenous malformation - precipitating hydrophobic injectable liquid
embolization
Introduction
Posterior fossa arteriovenous malformations (AVM) represent 10 to 15% of all AVMs,
whereas cerebellar AVMs represent around the 75% of all posterior fossa AVMs.[1]
[2] The most frequent clinical presentation is hemorrhage in around 60 to 80% of the
cases, which may present as parenchymal, intraventricular, or subarachnoid.
The gold standard treatment of this lesions is microsurgery, with high rates of total
obliteration, but moderate morbidity and mortality.[3] Nevertheless, other options are available such as endovascular embolization and
radiosurgery.
Little is known about the curative results of endovascular embolization of posterior
fossa AVMs because it is mainly used as an adjuvant therapy prior to microsurgery
or radiosurgery.[4] A lack of clinical studies and case reports exist regarding the endovascular management
of posterior fossa AVMs. Moreover, new embolic agents and endovascular devices are
increasingly used to treat this pathology more frequently.
To the best of our knowledge, this is the first report of an immediate and midterm
follow-up of complete obliteration of a posterior fossa AVM following embolization
with precipitating hydrophobic injectable liquid (PHIL; Microvention, Tustin, CA,
United States).
Case Report
In a previously healthy 39-year-old woman, with a 5-year history of headache that
improves with analgesics, MRI is performed, revealing a left petrous unruptured cerebellar
AVM.
The patient visits the emergency department of our hospital because of headache and
vomiting, a brain CT scan is performed ruling out bleeding. She is hospitalized in
the emergency department. Digital subtraction angiography (DSA) is performed, revealing
a cerebellar AVM with feeders arising from the left posterior cerebral artery (PCA),
left anterior superior cerebellar artery (ASCA), and left anterior inferior cerebellar
artery (AICA), with venous drainage to the straight and transverse sinus and an associated
large venous aneurysm. The AVM dimensions were 20mm × 18mm. We decided to perform
embolization through the AICA ([Fig. 1]).
Fig. 1 Brain CT scan revealing vasogenic edema with an aneurysm (A). CTA confirms the presence of a nidus with an associated aneurysm (B). CTA with three-dimensional reconstruction shows the presence of a cerebellar AVM
with a venous aneurysm (C); feeders from the posterior cerebral artery (PCA) and ASCA can be seen (D). DSA of the left vertebral artery with three-dimensional reconstruction shows feeders
from the left ASCA and the AICA (double arrow) (E). DSA shows the three feeders (PCA, ASCA, and AICA) with an associated large venous
aneurysm and drainage to the straight sinus (F, G, H). PCA = arrow, ASCA = dotted arrow, AICA = double arrow. AICA, anterior inferior
cerebellar artery; ASCA, anterior superior cerebellar artery; AVM, arteriovenous malformation;
PCA, posterior cerebral artery.
Endovascular procedure: The right femoral artery was approached by Seldinger’s technique.
A guide catheter Boston 6F was navigated to the right vertebral artery; then, a Headway
Duo microcatheter (Microvention), Hybrid 007 microwire (Balt Extrusion, Montmorency,
France), and liquid embolic agent PHIL (Microvention) were used. The microcatheter
was navigated over the microwire into the left AICA, and then a superselective angiogram
was performed showing the AVM nidus and the venous drainage. Once in the appropriate
position, embolization was performed with 4 mL of liquid embolic agent PHIL, achieving
good penetration to the nidus. A control DSA showed absence of the nidus with little
reflux to the left AICA, and there was also absence of the venous aneurysm and the
venous drainage ([Fig. 2]).
Fig. 2 Brain CT postembolization showing embolic agent artifact and no bleeding (A, B). DSA of the left vertebral artery revealing complete obliteration of the nidus without
venous drainage and venous aneurysm. The procedure was performed through the left
AICA (C, D,
E). DSA of the left ICA showing absence of the nidus (F). Abbreviations: AICA, anterior inferior cerebellar artery; ICA, internal carotid
artery; DSA, digital subtraction angiography.
After the embolization, the patient developed sixth cranial nerve paresis, hearing
loss, left dysdiadochokinesia, nausea and vomiting, but no motor deficit. A brain
CT scan was performed and showed no bleeding. She was discharged home 7 days after
the procedure. A 9-month follow-up DSA demonstrated total obliteration of the AVM
nidus and disappearance of the previous impairments.
Discussion
Current treatment of AVMs includes microsurgery, endovascular therapy, radiosurgery,
and a combination of these modalities, depending on multiple features. It is well-established
that microsurgery is the treatment of choice for cerebellar AVMs, and embolization
is mainly indicated prior to surgery or prior to radiosurgery as an adjuvant treatment
to reduce the blood flow and size of the nidus.
Compared with supratentorial AVMs, these lesions carry a higher risk of morbidity
and mortality: the high-rate of rupture with compromise of vital structures and hydrocephalus
must be a cause of concern.[5]
The standard classification system for AVMs is the Spetzler–-Martin classification,
which predicts the complication rate when surgery is performed, but not when endovascular
approach is chosen. The Spetzler–Martin classification is the most widely used in
all types of AVMs,[6] especially supratentorial AVMs, but is not suitable for posterior fossa lesions.
This can be explained because the only eloquent structures in the cerebellum are the
deep nuclei, and the deep venous drainage is not a good indicator of AVM depth.[7]
Currently, there is no standard classification for cerebellar AVMs.
From the morphological and anatomical perspective, Rodriguez–Hernández et al classified
the cerebellar AVMs into five types: suboccipital, vermian, tonsillar, tentorial,
and petrosal.[7] This can be correlated with angiographic studies and helps in preoperative planification.
From the endovascular counterpart, the Buffalo Score is a newly developed system that
predicts complications if endovascular treatment is selected.[8] Unfortunately, this score does not include posterior fossa AVMs.
In selected cases, endovascular therapy can cure these complex lesions. New embolic
agents such as PHIL were developed for this purpose. This novel product is a nonadhesive
dimethyl sulfoxide (DMSO)-based liquid embolic agent with iodine for radiopacity.[9] This product has some advantages over Onyx (Medtronic Neurovascular, Irvine, CA,
USA).[10]
Posterior fossa AVMs should be treated promptly because of the high-rate of rupture
compared with supratentorial AVMs.[5]
The association with aneurysms occurs in 20% of all AVMs and ranges from 5 to 20%.[11]
[12]
If the aneurysms are located in the infratentorial space, the risk of rupture rises
to 60%.[11]
Possible complications during treatment are rupture, infarctions, and hydrocephalus.
Moreover, these lesions can cause hydrocephalus due to mechanical obstruction in the
ventricular system.[13]
Robert et al treated 69 patients with posterior fossa AVMs, achieving an obliteration
rate of 72.5% with subsequent microsurgery or radiosurgery in 15 patients.[14]
Feng et al treated a total of 63 patients with posterior fossa AVM, of which 20 received
endovascular treatment. Of these 20 patients, only two patients achieved complete
obliteration.[4]
At our institution, we treat all AVMs with endovascular therapy. In this case, we
chose the embolic agent PHIL because of its properties to penetrate the nidus.
The patient of this report did not fortunately develop any vascular complications.
The initial complaints were due to the mass effect of the embolic agent and its relation
with surrounding neurovascular structures.
We do not believe that endovascular therapy is an adjunct treatment for cerebellar
AVMs. As many papers describe, it is mainly used prior to microsurgery and radiosurgery
to reduce the size. We think that in well-selected cases, the embolization of the
AVM could achieve complete obliteration, as in our case. It will depend on the feeding
vessels, angioarchitecture of the nidus, and location within the posterior fossa.
Conclusions
Microsurgery is the treatment of choice for cerebellar AVMs; nevertheless, endovascular
treatment is an option in selected cases with curative results.
Currently, endovascular neurosurgeons are provided with a wide armamentarium of endovascular
devices, such as liquid embolic agents that allow penetration to the AVM nidus with
complete obliteration and achievement of definitive cure.
