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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3644_Библиотеки_им_академика_М_И_Перельмана
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5Cerebral Arteriovenous Malformations322
Fig. 5.22A–D. A, B Right internal carotid artery (RICA) demonstrated slow-flow AVM
(arrow, A) draining into a cortical vein (arrows,B) and no filling of the giant distal ar-
terial aneurysm or venous pouch. C, D Three weeks later, the child presented a 2-h
episode of transient weakness and numbness involving the left side of his body as well
as slurred speech and incapacitating headaches (enhancing portion of the venous
ectasia; arrow, D). E–I see pp.323, 324
323Ve nous Enlargement
Fig. 5.22E–H. (continued) E,F MRI T2 W showed evidence of flow artifact (arrow) as
well as slight edema posterior to the giant distal arterial aneurysm or venous pouch.
G, H Angiogram at that time demonstrated partial re-opacification of the previously
thrombosed giant distal arterial aneurysm or venous pouch (arrow, G), apparently
causing worsening clinical symptoms.There is also residual AVM nidus draining into
a separate cortical vein (arrows, H). I see p.324
5.5.6 Arterial Angiopathy
Arterial changes are sometimes observed in older children and rarely in
neonates or infants. Localized stenotic or diffuse stenotic changes in our
series occurred only after many years (Scheme 5.2A–C). They require a
certain degree of angiogenesis, as indicated by the occurrence of a dramatic transdural supply. They have minimal symptoms in comparison to
the vascularization status, again indicating the unique level of tolerance
of the cerebral tissue in childhood. This contrasts with the obvious vulnerability in the first few years of life.The subclinical course of CAVMs in
children comes at the expense of compliance, and as soon as the system
fails, the overall equilibrium is difficult to restore. In our experience,
headaches in children are often associated with arterial stenosis and
rarely with an increase in intracranial pressure. There is no relationship
between the transdural supply and headaches. These headaches often
indicate a pseudo-migrainous course (Fig. 5.1).
As a result of this proximal arterial angiopathy, the brain tissue surrounding the CAVM may produce seizures or deficits. These are usually
progressive and while they can be stabilized they are rarely fully reversible, as the subischemic state of arterial origin will not be improved
by partial or total exclusion of the lesion. Diffuse arterial involvement is
rare and in older children may produce moyamoya phenomena associated with true CAVM (Garcia Monaco et al. 1991c).
Arterial enlargement (Scheme 5.2D) can theoretically cause compression, but we have never observed this phenomenon in this age group.We
do not believe that it constitutes a morphological goal for partial treatment.
Mural (wall) abnormalities are the most important angioarchitectural
artery-related characteristic; however,they are extremely rare in children
(Scheme 5.2E). Flow-related aneurysms are thought to be caused by the
5Cerebral Arteriovenous Malformations324
Fig. 5.22. (continued)
I Obliteration of the entry
(arrow) into the giant distal
arterial aneurysm or venous
pouch resulted in dramatic
reversal of clinical symptoms
325Arterial Angiopathy
Scheme 5.2a. Arterial high-flow angiopathy in cerebral arteriovenous malformations
(AV M ) in children
Scheme 5.2b. Arterial high-flow angiopathy in cerebral arteriovenous malformations
(AV M ) in children
5Cerebral Arteriovenous Malformations326
Scheme 5.2c. Arterial high-flow angiopathy in cerebral arteriovenous malformations
(AV M ) in children
Scheme 5.2d. Arterial high-flow angiopathy in cerebral arteriovenous malformations
(AV M ) in children
increased shear forces established on the endothelial cells proximal to an
AV s h u nt, b ut the time required to overcome the remodeling capabilities
of the vessel wall is long, and the individual host response capabilities
make this development highly unpredictable (Fig. 5.23). Flow-related
aneurysms should be distinguished from extradural and distal internal
carotid aneurysms. The latter are exceptional in this age group and even
more so in association with a CAVM. Distally or intranidally located arterial pouches are less rare in older children. In our strategy,they will lead
to the same therapeutic decisions as in adults. The clinical symptoms that
express this type of arterial wall abnormality relate to hemorrhagic
events. False arterial aneurysms are very rare in children (Fig. 5.24) and
indicate again that most bleeding episodes are due to abnormalities
involving the venous system.
We know the extent to which high-flow angiopathy can modify the angioarchitecture of a given AVM. Angiogenesis following hemorrhage or
ischemia and angiectasia following local arterial steal phenomena as well
as stenosis and enlargement of the venous sector following outlet restriction can all be causes of enlargement of an AVM (Fig. 5.21).
All types of AVM have a different significance. The differences in the
physiology of the various endothelial cells with regard to their resistance
or weakness to the AVM triggers makes the natural history of the disease
depend on the weakest part and therefore may differ from one AVM to
the next.
What causes regression is also obscure,and even while thrombosis can
be an ongoing process in a CAVM,most AVMs do not thrombose.Associ-
327Arterial Angiopathy
Scheme 5.2e. Arterial high-flow angiopathy in cerebral arteriovenous malformations
(AV M ) in children
5Cerebral Arteriovenous Malformations328
Fig. 5.23A–C. Young g i r l , seen for the first time in consultation at 9 years of age, who
had suffered a first intracerebral hemorrhage at 2 months of age. This had been reported to be a brain AVM but no treatment was given at that time.At 9years, she presented a new hemorrhage with a transitory left hemianopsia. Note the intranidal
aneurysm (arrow, A) embolized as the priority target (arrow,B, C)
329Arterial Angiopathy
Fig. 5.24A–D. A 1-year-old child first presented intracerebral hemorrhage opening
into the right ventricle requiring subsequent surgical ventricular shunting. There
were two recurrent hemorrhagic episodes 5 and 8 days later (A–C). Angiography
demonstrates partial thrombosis of the draining vein in a small lenticulostriate AVM
with venous false aneurysm. Complete cure by endovascular approach was obtained
in one session (D)
ated hemorrhage or stimulation of healing processes can also induce the
thrombosis of a previously demonstrated AVM (Fig. 5.8). Even a stable
situation is only a rough appreciation of a slowly evolving process that is
beyond our abilities to discriminate. Finally, if certain good reasons can
be identified to explain a given outcome (growth, stability, regression),
then explaining why this does not occur in other similar cases remains a
challenge. Growth through neighboring angiopathic changes and scarring phenomena following acute extravascular events are distinct ways
that will modify the CAVM architecture over time.
5.5.7 Spontaneous Thrombosis of Arteriovenous Malformations
Spontaneous thrombosis is a rare progression in CAVM in children,
although it has been reported. We have seen several cases of multifocal
AVMs in which one shunt was no longer demonstrated as the result of
spontaneous thrombosis, while the other remained patent. We have never observed complete and stable occlusion of an isolated non-Galenic
AVM. Thrombosis is often seen in large lesions and large venous pouches. Thrombosis of AVMs in children has been proposed to explain the
lower proportion of multiple AVMs in adults. As mentioned above,
thrombosis is either the expression of the capacity of the endothelial cells
to repair or, in contrast,of the endothelium not being able to preserve the
normal platelet–vessel wall relationships. When looking at the perilesional extravascular changes associated with spontaneous thrombosis, it
is likely that abluminal phenomena interfere as well in the exclusion of
some CAVMs. In addition, the concentric nature of some vascular proliferations points to the possible occlusive arterial role played in such rare
favorable progression of CAVMs. It is likely, however, that single-hole
AVFs are more likely to thrombose than nidus-arranged lesions.
5.6 Objectives of Treatment
5.6.1 Complete Exclusion
Ever since AV shunts were first recognized, the aim to eradicate the lesion
has been the only satisfactory goal. This strategy was based on pathological
information that tends to demonstrate fixed changes.While complete elimination of a pediatric CAVM is an acceptable goal, it should be considered in
the context of the anticipated natural history of the CAVM in a particular
child vs the risk of treatment. If the risk of total obliteration is below the estimated natural risk, total elimination of the lesion should be pursued
(Figs. 5.25–5.27). Our capacity to exclude AVMs completely has increased,in
particular for small lesions that present with intracerebral hematomas
(Figs. 5.25, 5.27).However, for more than 25 years,our interventional neuroradiological experience has demonstrated the presence of vascular compliance and adaptability. Progress in biology has also shown that remodeling
represents the reconstructive capacity of the vascular system. The recognition of high-flow angiopathy has revealed the participation of the remain-
5Cerebral Arteriovenous Malformations330
331Complete Exclusion
Fig. 5.25A–D. A 12-year-old child presented with sudden headaches due to intracerebral hemorrhage. A,B Angiography demonstrates a micro-AVM. C–E Distal catheter-
ization with a 1.2 microcatheter was achieved, which made it possible to exclude the
lesion completely.E see p.332
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