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5.6.3.2 Multiple Arteriovenous Malformations
Therapeutic decision-making is usually complex in children with multiple AV shunts and should be approached on an individual basis (Iizuka et
al. 1992; Willinsky et al. 1990a). At neonatal age, the most prominent
shunt should be attacked first, as well as the shunt that gives rise to the
most prominent pial congestion, in order to obtain systemic relief and
brain drainage improvement.
5.6.4 Children
The clinical history in combination with the MRI and angiographic findings help determine which lesion or lesions cause symptoms and therefore need prompt treatment (Tables 5.4–5.8).
For CAVMs other than the AVF and multiple AV shunts, the rules of
management are similar to those in adults (see Berenstein 1992a).
When reading the literature, it seems that the expected bleeding rate
reduction is the only indicator for successful treatment. It is our experience that CAVMs do not bleed more frequently in children than in adults,
while on the other hand cerebral damage and the ongoing risk of seizures
constitute a major restriction for schoolchildren and adolescents.
5Cerebral Arteriovenous Malformations342
Ta ble 5.4. Pial AVMs in children (<16 years): clinical presentation in children
Hemorrhage 50%
Epilepsy 16.6%
Deficit 15%
Headaches 7.7%
Incidental 3.3%
Cardiac overload 2.2%
Mental retardation 1.6%
Macrocrania 1.1%
Other 2.2%
Ta ble 5.5. Cerebral arteriovenous malformations in children (<15years) in Japan,
1986–1988 (Tamaki 1992)
Patients
(n) (%)
Neonatal hemorrhages 432 56.2
CAVM (all pial) 125 16.3
Idiopathic 101 13.2
Coagulation disorders 61 7.9
Ruptured aneurysms 27 3.5
Tu mo r 13 1.6
Occlusive disease 10 1.3
To tal 769 100
343Children
Ta ble 5.6. Classification of seizures
IGeneralized seizures
Bilaterally symmetric and without focal clinical onset
To nicoclonic seizures (grand mal)
Isolated tonic or clonic seizures
Bilateral myoclonus
Infantile spasms
Aton ic or astatic seizures (infants and children)
Absences
Simple (petit mal)
Complex (with various symptoms)
Myoclonic
To n i c , a t o n i c
With automatisms
With autonomic (visceral) symptoms
II Partial seizures (seizures beginning locally)
Simple seizures,generally without loss of consciousness
Complex seizures with loss of consciousness
III Partial seizures with secondary generalizations
IV Unilateral seizures (infancy) concerning only one cerebral hemisphere
Ta ble 5.7. Va rious types of partial seizures
Ty pe of seizure Site
Simple seizures
Motor seizures
Dysarthria, jacksonian seizures Prerolandic gyrus
Non-jacksonian seizures
Adversive seizures Frontal cortex
Masticatory seizures Amygdaloid nucleus
Sensory seizures
Somatosensory seizures Postrolandic gyrus
Visual seizures Occipital or temporal cortex
Auditory seizures Temporal cortex
Olfactory seizures Mesial temporal cortex
Gustatory seizures Insular cortex
Ve r t i g i n o us seizures
Abdominal pain
Vo c a l
Phonatory seizures Inferior rolandic cortex or supplementary
motor cortex
Aphasic seizures Posterior temporal or inferior frontal cortex
Complex seizures
Psychomotor automatisms Temporal cortex
Psychosensory automatisms
Intellectual seizures
(dreamy states,depersonalization)
Affective seizures (joy,sadness,
fear,hunger,déjà vu impression)
These symptoms will interfere with the future quality of life to a great
extent and are not as such fully appreciated by the Glasgow Outcome
Score. Failure to thrive, mental retardation, physical atrophy, and facial
collateral circulation all reflect irreversible changes that have been the
result of active treatment.
It has not been our experience that symptoms worsen at the time of
puberty. Headaches may sometimes start at that time, but either they reveal an already large lesion or this is a retrospective finding in an incidentally discovered AVM at adult age.
5.6.5 Rebleeding
Rebleeding occurrence is an important point, since the delay between
embolization sessions can be variable. During a 12-year period, the rebleed rate in embolized pediatric CAVMs seems to be low,except in large
deeply located lesions that were poorly controlled. This empirical statement also illustrates the fact that hemorrhagic episodes are often difficult
to identify in the past history of children. The information from the literature is also difficult to interpret. For example, Hladky (1994) reported
that a hemorrhage occurred at the former AVM site in 5.7% of CAVM
patients believed to have been successfully treated surgically.
In our series of CAVM patients waiting for embolization, three children bled and one rebled.One of the former three suffered delayed hemorrhage 1 month before his scheduled first session of embolization. Two
of the three patients (one with a diencephalic AVM and one with a mesencephalic AVM) bled between the third and fourth sessions. The first of
them, who was initially not operable,was subsequently successfully operated on and had a moderate residual sensory motor deficit; the second
had a nonoperable AVM and died from the hemorrhage. The fourth patient died from a recurrent hemorrhage 5 years after the first bleeding
episode and 1 year following the embolization session, in which incomplete occlusion had been achieved.Our group had felt that the therapeutic risks involved in completing the treatment by any method were too
high.
5Cerebral Arteriovenous Malformations344
Ta ble 5.8. Hemorrhagic episode in cerebral arteriovenous malformations in children
and adults (Celli et al. 1984)
Children (%) Adults (%)
Frequency 55–77 37–41
Mortality 7–13 3–10
Coma 23–31 11–17
Immediate morbidity 78–89 50–53
Ve ntricular hemorrhage 56 40
5.7 Technical Management
5.7.1 General Remarks
When discussing partial or complete endovascular exclusion in CAVM patients, we are referring to transarterial embolization with glue. From published and unpublished experience in CAVM in children,coils,particles,balloons, cocktails, threads, collagen mixture, and other methods have shown
no reliable and predictable results,even if they were useful in some isolated
situations,nor are they safer.In our experience,they have never constituted
an improved embolic agent to reach the therapeutic goal, nor are they a satisfactory alternative as a primary embolic agent.It must be emphasized that
frequent changes in the type of embolic material used have been a significant hindrance for many teams in their attempts to increase their technical
experience and develop a reliable follow-up with a given agent.
Our technique is the same as the one described in Chap. 3 of this volume.
Complete exclusion,if it can be obtained,is the goal (Figs. 5.30,5.31),but can
not be achieved as frequently as in VGAMs. Even if endovascular management is the primary choice, complementary treatment is usually planned
(see Sect. 5.3.2). The basic technical challenge consists in occluding the arterial part of the nidus with the immediate portion of the draining vein in
AVFs. The entire nidus demonstrated may not have to be occluded,as secondary regression of other supplies can sometimes be seen in young children. Superselective injections are rarely helpful in making this decision.
The dangers related to the venous passage of glue and possible subsequent
hemorrhage depends on the converging or diverging position of the venous
outlets. Multiplicity of the nidal veins and the length of the course in the
subpial compartment indicate the distal point of possible venous occlusion.
In addition, one should never forget that children with CAVMs, in particular those who are known to have HHT disorder, also need management of their associated vascular disease, such as the pulmonary AVSs,
which can be a major cause of neurological sequelae (Fig. 5.32).
5.7.2 Other Techniques
5.7.2.1 Surgery
Interpretation of published results is very difficult, since the age limits
include children up to 20years. In our review of several series between
1941 and 1990, 80% of children were operated on and approximately 65%
had complete exclusion of their lesion. In a more recent review (Hladky
1994) of 62 cases admitted between 1975 and 1992, 75% eventually had
complete exclusion of their malformation with a very good neurological
outcome. This is superior to all previously published management data: a
mortality rate of 7.6% and a recurrence rate of 5.6% was reported.Epilepsy occurred in 14.8% of patients after surgery,although it was not present
prior to surgery; it was felt that it was an acceptable drawback.Reviewing
the latest series, the mortality rate in nonoperated patients varies from
20% to 57%. These numbers are particularly high considering that there
were few young children in these series (Table 5.9).
345Surgery
5Cerebral Arteriovenous Malformations346
Fig. 5.31A–C. A 14-year-old girl presenting with sudden headaches with a moderate
right upper limb deficit. CT (A) revealed a subcortical parietorolandic hematoma.Angiography disclosed a parietal arteriovenous malformation (B).We decided to follow
up the patient after resolution of the hematic collection in order to better visualize the
malformation and to attempt the endovascular approach during the same session.
This was done 2 months later.The lesion was embolized with glue (C), resulting in the
total elimination of the nidus
347Surgery
Fig. 5.32A–D. This 23-month-old girl presented with congestive heart failure (IVC,
pulmonary stenosis), mental retardation on the Denver score (<20%), and progressive left hemiparesis, leading to the diagnosis of PF AVFs. MRI (A, B) and angiography (C, D) demonstrated three AVFs in the right parietal temporal cortex and brain
stem. The brain stem lesion was of the AVF type, fed from the basilar tip.She had no
significant family history, but was highly suspected of having HHT1 on the basis of
multifocality and fistulous architecture. The fistulas were embolized in three sessions,
four feeders were occluded with N-Butyl CyanoAcrylate (NBCA),and the fistulas were
reduced to 50% over a 1-year period (E–I).Another session was proposed 1year later,
but her family refused further treatment. The child unfortunately had an ischemic
stroke related to a pulmonary AVF and died 14 months after the last embolization,
confirming the diagnostic suspicion of HHT1. E–I see p. 348
5Cerebral Arteriovenous Malformations348
Fig. 5.32E–I. Legend see p. 347
349Surgery
Ta b l e5.9. Review of the literature on surgical treatment of pial arteriovenous malformations (Lasjaunias et al.1995)
Authors Upper Study Patients Operations for Patients with total exclusion Operative Remarks
age period CAVM/VGAM mortality
limit Neurologically Neurologically
(years) normal abnormal
(n)(n)(n) (%) (n) (%) (n) (%)
Gerosa et al. 1981 16 1954–1979 56 38 17 45 6 16 3 8 Partial treatments included
Eiras et al. 1987 17 1975–1985 17 14 9 64 2 14 0 0 Partial treatments not
included
Fong and Chan 1988 16 1971–1987 39 27 23 85 3 11 1 4 No distinction made
between TE and PE; all cases
taken to be TE
Amacher et al. 1979 18 ? 20 20 15 75 1 5 0 0
Celli et al. 1984 15 1951–1980 19 11 6 55 5 45 0 0
Yasargil 1988 15 ? 60 60 54 90 6 10 0 0
Martin 1989 ? ? 35 35 30 86 1 3 1 3 Ages not stated
Mori et al. 1980 15 ? 28 18 – – – – 3 17 Some discrepancy between
tables and text
Mazza et al. 1983 16 1971–1982 24 18 15 83 1 6 2 11
Lapras et al. 1990 15 ? 65 62 26 42 25 40 6 10 Total actually 65,but two
had VP shunts only and one
had embolization (excluded)
Humphreys 1989 17 1954–1986 100 72 43 60 23 32 6 8 Figures vary in text; 74 patients
but only 72 accounted for;
54 removals of AVM; no
distinction made between TE
and PE; all cases taken to be TE
Partington et al. 1989 16 1985–1988 12 12 11 92 1 8 0 0 Stereotactic surgery; includes
cavernoma and venous
angioma
Garza-Mercado 18 1968–1985 19 12 3 25 4 33 4 33
et al. 1987
Malik et al. 1991 18 1941–1989 46 27 23 85 2 7 2 7 Over 19 patients below 16 years;
only four were cured and
neurologically normal out of
seven surgically treated
Laine et al. 1981 20 1950–1980 20 20 12 60 4 20 4 20
5Cerebral Arteriovenous Malformations350
Ta ble 5.9. (continued)
Authors Upper Study Patients Operations for Patients with total exclusion Operative Remarks
age period CAVM/VGAM mortality
limit Neurologically Neurologically
(years) normal abnormal
(n)(n)(n) (%) (n) (%) (n) (%)
Tamaki et al.1991 19 1970–1990 25 25 23 92 2 8 0 0 No distinction made between
TE and PE; all cases taken
to be TE
Suarez and Viano 1989 15 ? 15 10 7 70 0 – 3 30 Computation of percentage not
accurate
Nelson et al. 1992 19 1978–1990 13 11 7 64 – – 1 9 Surgery alone, embolization
alone or combined
Ve ntureyra 18 1975–1985 23 18 9 50 3 16 3 16 22% Of lesions were occult; full
and Herder 1987 activity is counted as normal;
in this group some children had
had lobectomy or chronic
epilepsy
To tal 15–20 1941–1990 636 510 388 66 89 17 39 8 112 counted as TE and neuro
logically normal
AVM, arteriovenous malformation; CAVM, cerebral AVM; VGAM, vein of Galen aneurysmal malformation; TE, total exclusion; PE partial, exclusion;
VP, ventriculoperitoneal shunt.
Fig. 5.33A–F. A 10-year-old
female presented with intracerebral hemorrhage and neurological
deficit. The left internal carotid
angiogram frontal view (A) and
lateral view (B) showed that she
had a moderate-sized medial left
frontal parietal AVM, which was
embolized to reduce the size,as
shown on the follow-up angiogram, frontal (C) and lateral (D)
views,which was then radiated.
One year after radiosurgery,
she had a second hemorrhage
resulting again in neurological
deficit. She underwent surgical
removal of the AVM, as shown on
follow-up angiogram, frontal (E)
and lateral (F) views. She has
made near complete recovery
▲
351Surgery
Fig. 5.33A–F. Legend see p. 350
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