leefwijze en sterfte in relatie tot opleiding.) T SOCGezondheidsz 1988;66:345-348.
13. Appels A, Otten F, Mendes de Leon C, Sturmans F, Mulder P,
Schuurman J. The KRIS follow-up study VII. Socio-economic
status and health. (De KRIS follow-up studie VII. SociaalGezondheidsz 1990;
economische status en gezondheid.) T SOC
68~298-305.
14. Folstein MF, Folstein SE, McHugh PR. Mini-mental state: a
practical method for grading the cognitive state of patients for
the clinician. J Psychiatr Res 1975;12:189-198.
15. Roth M, Huppert FA, Tym E, Mountjoy CQ. CAMDEX. The
Cambridge examination for mental disorders of the elderly.
Cambridge: Cambridge University Press, 1988.
16. Katz S, Ford AB, Moskowitz RW, Jackson BA, Jaffe MW.
Studies of illness in the aged. The index of ADL: a standardized measure of biological and psychosocial function. JAMA
1963;185:914-919.
17. Lawton PM, Brody EM. Assessment of older people: self-

maintaining and instrumental activities of daily living. Gerontologist 1969;9:179-186.
18. McKhann G, Drachman D, Folstein M, Katzman R, Price D,
Stadlan EM. Clinical diagnosis of Alzheimer’s disease: report
of the NINCDS-ADRDA Work Group under the auspices of
Department of Health and Human Services Task Force on
Alzheimer’s disease. Neurology 1984;34:939-944.
19. Kaplan EL, Meier P. Nonparametric estimation from incomplete observations. J Am Stat Assoc 1958;53:457-481.
20. Cox DR. Regression models and life tables. J R Stat SOC1972;
34~187-220.
21. Manton KG, Poss SS, Wing S. The blacwwhite mortality
crossover: investigation from the perspective of the components of aging. Gerontologist 1979;19:291-300.
22. Guralnik JM, Land KC, Blazer D, Fillenbaum GG, Branch
LG. Educational status and active life expectancy among older
blacks and whites. N Engl J Med 1993;329:110-116.

Anterior translocation of language in
patients with left cerebral
arteriovenous malformation
R.M. Lazar, PhD; R.S. Marshall, MD; J. Pile-Spellman, MD; L. Hacein-Bey, MD; W.L. Young, MD;
J.P. Mohr, MD; and B.M. Stein, MD

Article abstract-We studied seven patients with left cerebral atriovenous malformation (AVM) with superselective
arterial injection of anesthetics during angiography to determine whether there was translocation of some language
functions to other regions in the ispilateral hemisphere. All patients were right handed. With a catheter inserted into each
target vessel, patients underwent aphasia examination in an A-B-A design: (A) baseline, no anesthetic; (B) 1minute after
anesthetic injection; and (A) 12 minutes after injection (when its effects had dissipated). The results showed that six of
seven patients had no significant aphasia at baseline or 12 minutes after anesthetic injection. One patient had a mild
conduction aphasia at baseline and after anesthetic effects had dissipated. In the six patients with temporoparietal AVM,
anesthetic injections into vessels in the lower division of the middle cerebral artery (MCA) not feeding the AVM (e.g., the
left angular artery) produced a wide range of language function-from conduction aphasia to dense Wernicke’s syndromes.
When upper division MCA vessels were injected (e.g., the prefrontal branch), all developed a major aphasic disorder with
significant comprehension defects. A seventh patient with a frontal opercular AVM had a mild anomia, semantic paraphasias, and decreased word-list generation when the prefrontal branch was injected. Her comprehension, however, was
intact. These data show that patients with posterior cerebral AVM can show language abnormalities where such deficits
are not typically seen after acute brain injury. These findings support a posterior-to-anterior extension of some language
skills under conditions of brain disease.
NEUROLOGY 1997;49:802-808

Acquired disorders of language can arise from many
etiologies, such as stroke,l trauma,2 tumor,3 and
most other causes of cerebral dysf~nction.~
Although
there is extensive literature on the relationship between lesion location and aphasia s y n d r ~ m e ,much
~,~
less is known regarding the neural networks responsible for language function in patients with brain

lesions. The purpose of this study was to delineate
some of the features of the neural compensatory
mechanism that may be associated with language
reorganization.
We chose cerebral atriovenous malformation
(AVM) as our disease model because its evaluation
and treatment represented a unique opportunity to

From the Departments of Neurology (Drs. Lazar, Marshall, and Mohr), Radiology (Drs. Pile-Spellman, Hacein-Bey, and Young), Anesthesiology (Dr. Young),
and Neurological Surgery (Drs. Lazar, Mohr, Young, and Stein), Columbia-Presbyterian Medical Center, New York, NY.
Supported in part by PHS grant NS27713.
Presented in part at the 48th annual meeting of the American Academy of Neurology, San Francisco, CA, February 1996.
Received October 3, 1996. Accepted in final form April 2, 1997.
Address correspondence and reprint requests to Dr. Ronald M. Lazar, Neurological Institute, Columbia-Presbyterian Medical Center, 710 West 168th Street,
New York, N Y 10032.
802

Copyright 0 1997 by the American Academy of Neurology

study the localization of higher cerebral functions.
Arteriovenous malformations in the brain are
thought to be the result of dysvasculogenesis during
fetal development7 but patients usually do not become symptomatic until the middle decades of life.8
As part of the work-up for treatment consideration
at our center, the territories of feeding, and adjacent,
and remote arteries are studied in conscious patients
with superselective neuroangiographic techniques,
not only to assess hemodynamic contributions of
blood vessels but also to ensure that therapeutic embolization or subsequent surgical resection will not
affect eloquent f ~ n c t i o n s .Prior
~
to the delivery of
embolic material (N-butyl cyanoacrylate), amobarbital sodium (USP) and a contrast medium are injected
into a target vessel distal t o the circle of Willis to
produce temporary anesthesia in the focal brain region supplied by the artery. This superselective anesthetic technique is an adaptation of Wada’s test
used to determine cerebral dominance for memory
and language in presurgical epileptic patients.1° The
objective of this paper is t o describe how the superselective anesthetic technique demonstrated an unexpected pattern of language organization in the brains
of patients with left-hemisphere AVM.
Methods. Patients. Seven patients (two men and five
women) were studied after informed consent was obtained
for neuroangiography and possible embolization for a cerebral AVM. All patients were right handed and were studied between November 1994 and June 1996. Because of the
idiosyncrasies often seen in the history and presentation of
AVM, a brief clinical summary for each patient follows.
Patient 1was a 27-year-old man who had a history of
headache and was discovered to have a left parietooccipital AVM in 1990. He underwent nine previous embolizations in 1990 and 1991. He never had a hemorrhage. His last embolization was associated with an
ischemic stroke that produced speech difficulties. He returned to our center in 1994 with worsening headaches.
On presentation he was found t o have mild sensory
aphasia but normal physical examination. Noncontrast
CT of the brain (figure lA, left) showed multiple coil and
silastic bead embolic material, and acrylite in the left
occipitoparietal region and left thalamus. There was a
persistent lucency, compared with previous films, in the
left posterior temporal and parietal region thought t o
represent the old infarct. Repeat angiogram (figure lA,
right) revealed a large, left occipitoparietal AVM with
both superficial and deep drainage. Multiple arterial
feeders were seen from the left middle cerebral artery
(MCA), including a left angular artery feeder and a left
posterior temporal artery feeder. There were also multiple left external carotid artery feeders as well as feeders
from the left occipital artery and the left meningeal
artery. There was occlusion of the left P2 segment of the
posterior cerebral artery (PCA) and there were multiple
posterior choroidal feeders off the proximal PCA.
Patient 2 was a 37-year-old woman who presented in
August 1995 with a 6-month history of headache. Her neurologic examination was entirely normal. CT of the brain
(figure lB, left) suggested an AVM in the left temporal

lobe. An angiogram (see figure lB, right) showed a small
left anterior temporal AVM supplied by the anterior temporal branch of the left MCA draining into superficial cortical veins as well as into the basal vein of Rosenthal.
Patient 3 was a 25-year-old woman who reported a
1-year history of paresthesias in the right arm, blurring of
visual fields, and recent episodes of speech difficulty and
inability to understand language. She also developed nausea and dizziness. An EEG was negative. Neuropsychological evaluation showed some minor changes in verbal function but no aphasia. MRI (figure lC, left), taken after her
superselective Wada’s test and first embolization, showed
a 2 X 2.5 x 3-cm left parietal opercular AVM. There was
no evidence of midline shift or significant mass effect. Cerebral angiography (see figure lC, right) showed the AVM
on the posterior aspect of the sylvian fissure, fed mainly by
distal left MCA sylvian branches, and draining through a
large vein of Trolard and a large vein of LabbB. Her data
(later) were collected prior to embolization.
Patient 4 was a 42-year-old woman with increasing
headaches for the year prior to April 1996 when she found
that she was experiencing confused speech at work. A first
seizure brought her to a local hospital. CT of the brain
showed a left parietal lobe hemorrhage. She was placed on
Dilantin and discharged. Seven days later she had a second seizure with aphasic features. CT and MRI (figure lD,
left) revealed a subacute hemorrhage. An angiogram
showed a 1.5-cm AVM in the region of the hemorrhage and
she was referred to our center for further treatment. The
neurologic examination showed a mild conduction aphasia
with some dysprosodic features in her speech. A left internal carotid injection during neuroangiography (see figure
lD, right) revealed a 2 x 3-cm AVM in the left temporosylvian region a t the junction between the temporal and parietal lobes, supplied mainly by the left angular artery and
draining into the sigmoid sinus.
Patient 5 was a 29-year-old man who was well until
April 1991 when he had a mild, focal seizure. MRI and
angiographic evaluation a t that time revealed a left parietal AVM, and he was treated with anticonvulsants alone.
In July 1995 he developed a severe headache, diplopia, and
impaired speech, and he was found t o have a left temporal
hemorrhage (figure l E , left). He recovered significantly,
with neuropsychologic testing disclosing some learning
problems and a subtle language disorder at the time he
presented a t our center. His physical examination was normal. An angiogram (see figure lE, right) demonstrated a
small AVM in the left temporoparietal region supplied by
the left angular artery with numerous branches in passage. The venous drainage was primarily superficial.
Patient 6 was a 15-year-old girl who experienced seven
episodes of difficulty in using her right hand in April 1996.
She was brought to a local hospital where she had the
same problem in paroxysmal fashion in addition to nausea
and vomiting. MRI of the brain showed a large left parietal
AVM. After referral to our center, neuropsychological examination revealed a very mild sensory aphasia with otherwise normal reading comprehension. Her physical examination was normal. Neuroangiographic evaluation on
6/7/96 (figure l F , right) revealed a moderate-size left central AVM supplied by the left MCA and anterior cerebral
artery (ACA) branches with superficial venous drainage.
Patient 7 was a 29-year-old woman with migraine headSeptember 1997 NEUROLOGY 49 803

Figure 1. Left column shows representative CT or MRI for six of the seven study patients. CT for Patient 7 (lG, left) was
postsurgical. The right column displays corresponding angiograms for all seven patients at the time of superselective
Wada’s testing.
ache who had sudden onset of severe headache, neck pain,
and nausea and vomiting in June 1994. She improved to
normal within 2 weeks, but 1 month later her symptoms
recurred. CT of the brain revealed no new hemorrhage but
a left frontal AVM. Following referral to our center, an
angiogram (figure lG, right) demonstrated a left frontal
AVM with its main supply via left ACA branches (orbital
frontal, frontal polar, anterior internal frontal arteries) as
well as left MCA opercular and frontal branches. Following
two embolizations she began to complain of memory problems, and neuropsychological examination showed her to
804 NEUROLOGY 49

September 1997

have some verbal memory dysfunction, dysnomia, and dyscalculia. Her physical examination was normal.
Superselective Wada’s test. All testing was performed
in the Embolization Suite. Patients were lightly sedated
with midazolam, fentanyl, and propofol. The right common
femoral artery was then punctured using a Pott’s needle. A
7.5 French vascular sheath was inserted over a guide wire.
A coaxial system, consisting of a 5 French inner hockey
stick catheter and a 7 French outer guiding catheter, was
then used to catheterize selectively the left internal carotid
artery. After angiographic verification of catheter place-

Table The results of the language examination following
injection of anesthetic i n each target vessel for each patient. *

Patient
1

2
3

Injected vessel

Elicited syndrome

Angular artery
Prefrontal artery
Angular artery
Prefrontal artery
Angular artery
Insular artery

Wernicke’s aphasia
Global aphasia
Wernicke’s aphasia
Global aphasia
Wernicke’s aphasia
Semantic conduction
aphasia

4

5

Figure 2. An angiograin demonstrating placement of a
microcatheter into the left angular artery just prior to injection of amobarbital sodiumllidocaine and metrizamide.

Prefrontal artery
Supramarginal
artery
Angular artery
Frontal opercular
branch of MCA
Superior
temporal
branch
Angular artery
Posterior rolandic
artery
Upper division of

Global aphasia
Conduction aphasia
Conduction aphasia
Mixed nonfluent
aphasia
Conduction aphasia

No aphasia
No aphasia

Global aphasia

MCA

ment, the 5 French hockey stick catheter was replaced by a
1.8 French Magic Balt microcatheter. The latter was navigated to the target vessel, such as to the left angular
artery for Patient 1 as shown in figure 2. Mean arterial
feeding pressures were measured a t the catheter tip both
in the arteries feeding AVMs and in the vessels undergoing superselective Wada’s testing.
With the microcatheter in place in the target vessel,
sedation was discontinued and patients underwent aphasia examination in an A-B-A design: (A) A 4-to 5-minute
baseline language examination evaluating fluency, comprehension, naming, repetition, and oral reading. Materials were generally adapted from the Boston Diagnostic
Aphasia Examination,ll Boston Naming Test,12 and the
Wide Range Achievement Test.13 Then, 50 to 75 mg of
amobarbital sodium and 20 mg of lidocaine opacified with
metrizamide were injected, followed 1 minute later by (B)
a repeat language examination. Twelve to 15 minutes after
anesthetic injection, when the anesthetic effects were presumed to have dissipated, the language evaluation was
performed again (A). The microcatheter was then removed
from the initial artery and placed into the next target
vessel, and the evaluative process was repeated until all
vessels of interest had been studied. Determination of a
change in language function was based on guidelines from
the Boston Diagnostic Aphasia Examinationll with an audio recording used for later verification. Because of variation in neurovascular architecture and the patients’ tolerance of procedures, the same arterial territories could not
be evaluated in all patients.

Results. All patients performed at their baseline clinical
state in the Embolization Suite before and 12 to 15 minutes after amobarbital sodium injection. The table shows
the nature and extent of language abnormality for the
seven study patients during superselective Wada’s testing.

Lower division of
MCA

Upper division of
MCA

7

Prerolandic
artery
Prefrontal artery

Mild decrease in fluency
but no aphasia
Impaired
comprehension,
dysfluency, anomia,
normal reading aloud
Anomia
Semantic paraphasias,
decreased word-list
generation
.-

“ ~ 1 1arteries were in the left hemisphere,
MCA = middle cerebral artery.

The first six patients (Patients 1 to 6) had cerebral AVMs
in temporoparietal regions, whereas Patient 7 had a frontal lobe AVM. All AVMs had low feeding pressures.
Five of the six patients with retrorolandic AVM had
injections of the angular artery with a wide range of outcomes. Patients 2 and 3 developed dense Wernicke’s aphasias (fluent speech with literal and verbal paraphasias,
inability to follow any commands, poor repetition, and inability to name pictures), but Patient 1 only had a mild
Wernicke’s syndrome, demonstrated by mild comprehension defect, mildly impaired repetition (“They heard him
speak on the rag. . .radio last night” for They heard him
speak on the radio last night), and mild dysnomia with
literal paraphasic errors (“bool” for broom; “pretza” for
pretzel). Patient 4 had a conduction aphasia (“Fry the tin
lid off’ for Pry the tin lid ofk “The phantom ducella across
the foggy firth” for The phantom soared across the foggy
heath) that was no different from her clinical level of function. Patient 5 showed no language changes in this condition, but he had a conduction aphasia following injection of
September 1997 NEUROLOGY 49 806

a medial temporal sylvian branch off the lower division of
the MCA (“The vak leaks” for The vat leaks; “The fleece
fled to Greece” for The spy fled to Greece). Patient 6 had a
more global injection into the main branch of the lower
division of the MCA, but there was no change in language
except for dysfluency. Patient 3 also had injection of the
insular artery, which produced an unusual form of “conduction” aphasia characterized by a disorder of repetition
in which many of her errors were semantic rather than
phonemic in nature. Whereas she made some literal paraphasias during animal naming such as “turkio” for turkey
and “monkley”for monkey, she repeated the dictated sentence The phantom soared across the foggy heath as “The
phantom flew over the. . .field.” Semantic substitutions
during repetition have recently been described following
infarction limited t o the posterior insula and immediately
adjacent intrasylvian parietal operculum.14
There was greater uniformity in language abnormality
during the peak anesthetic effect when the six patients
with posterior AVM had injections in vessels in frontal
regions anterior to their lesions. All developed a major
aphasic syndrome with significant receptive language dysfunction. Following injection of the prefrontal artery, Patients l, 2, and 3 became globally aphasic so that in addition to impaired vocalizations, they were unable to perform
consistently even simple tasks on command. Patient 1
opened his mouth and stuck out his tongue to the plane of
his lips when asked to “Stick out your tongue.” When next
asked to “Say the days of the week,” he opened his mouth.
When asked t o show one finger, he responded by drawing a
circle in the air and tapping each finger successively. He
was unable to read any single words aloud or repeat single
words. Patient 2 said numbers aloud when asked to say
the days of the week. She appropriately opened her eyes
when asked to do so, but when asked to repeat single
words, she responded by saying numbers. Patient 3 developed a dense receptive aphasia and was unable to execute
correctly any dictated commands. Her speech contained
literal, semantic, and neologistic paraphasic errors.
Patient 4 received an injection into the frontal opercular
branch in the upper division of the MCA. When asked t o
say the names of animals, she responded, “Six, six, six.”
She answered “No,” to each of the initial eight questions
from the Complex Ideational Material section (e.g., Does a
stone sink in water?) from the Boston Diagnostic Aphasia
Examination.
Patients 5 and 6 had an injection of the entire upper
division of the MCA. The former developed a severe global
aphasia with virtually no measurable language. Patient 6
was dysfluent and dysarthric with significant receptive
dysfunction. She answered 5 of 8 questions correctly on the
initial eight questions from the Complex Ideational Material. She could not provide the names of any animals in 1
minute. The dictated sentence The spy fled to Greece
yielded “The sply full to Greece.” Her oral reading of single
words, however, was normal with no alexic errors.
Patient 7 was the only example in this cohort of patients with an AVM in the left frontal lobe. No vessel in
the lower MCA division was explored. In the frontal region, an injection in the prerolandic artery produced a mild
anomia. When the prefrontal artery was investigated she
produced semantic paraphasic errors and her word-list
806 NEUROLOGY 49 September 1997

generation decreased from her preinjection baseline. Her
comprehension, however, remained intact.

Discussion. The application of Wada’s test to the
selective study of vessels prior to embolization of
AVM feeding vessels has seen considerable recent
development. Rauch et al.15 found 23 positive amobarbital sodium tests out of 109 injections, and Han
et al.16 found 11positive tests out of 66 vessels evaluated. In all patients, however, the arteries undergoing superselective testing were those feeding the
AVM. To our knowledge, our study is the first to
explore vessels remote from the lesion.
Our series of mainly posterior AVM demonstrated
varying degrees of aphasia during the peak anesthetic effect when vessels supplying posterior parietal and temporal brain regions were injected, findings consistent with the expected involvement of
these regions in speech-language processes. The major new finding in these patients was that when arteries in the superior division of the MCA in the
frontal lobe were anesthetized, all six patients developed a major aphasic syndrome that included severe
comprehension deficits. We interpret these data to
indicate that patients with posterior AVM in the left
hemisphere can show language abnormalities in
frontal regions where such deficits are not typically
seen after acute focal brain injury, such as stroke.
These findings support a posterior-to-anterior extension of some language functions under conditions of
brain abnormality. The only patient not to demonstrate such profound receptive language deficits with
a frontal injection was Patient 7, who had a frontal
lobe AVM, indicating that frontal artery anesthesia
per se was not sufficient to produce comprehension
defects in this setting. Simple learning effects could
not account for our findings since the order of arterial studies varied randomly across patients and repeated exposures to language tests did not improve
performance. Patients 1, 2, 3, and 5 , for example,
demonstrated their most severe disorders in the last
vessel studied.
Patients with acute infarction in the territory of
the upper division of the MCA can present with
global aphasia, but the lesion is very large, encompassing not only Broca’s area but also the insula and
the adjacent operculum from the frontal to the parietal lobe.4Alexander et al.17reported comprehension
deficits in nine patients with infarcts in the region of
the left frontal operculum. Their CT data, however,
showed that in every patient the lesion extended to
the insula cortex. Injury to the left insula, has been
shown to produce aphasias with sensory features.18
In the series reported here, anesthetic injections in
the prefrontal and frontal opercular branches, with
no radiographic evidence of perisylvian involvement,
produced marked comprehension defects. Lesions restricted to Broca’s area may produce an initial mutism with buccofacial dyspraxia, but comprehension
of auditory and visual language information is virtually intact.lg The simultaneous injection of contrast

material with amobarbital sodium provided a means
of determining the region of induced anesthesia in
the present study, and in four of the six patients
with posterior AVMs, the affected territory in the
single arterial branch of the frontal lobe more closely
approximated the size seen in Broca’s area infarction. The defect in receptive language seen in Patients 5 and 6 with complete upper division injections was not
merely the grammatical
comprehension difficulty seen in Broca’s aphasia,5
but gross dysfunction for even simple, auditory comprehension.
Other authors have made observations consistent
with this interpretation in individual patients. Martin et a1.20reported the case of a right-handed patient with a 3.5-cm AVM involving the posterior temporal branches of the left MCA and two temporal
branches of the left PCA. Superselective testing was
performed in the posterior temporal branch of the
left MCA with contrast medium that demonstrated
filling of a branch supplying the superior temporal
gyrus. There were no receptive or expressive language deficits identified, suggesting the absence of
language function in that regon. Our data suggest
that language skills could have extended to new regions in this patient.
Our observations do not modify the welldocumented evidence that patients with stroke, the
most common cause of aphasia, have extremely variable language recovery. Factors involved in the outcome are thought to be related to location and size of
infarcted brain tissue,21and the degree of severity of
the initial aphasic ~ y n d r o m e .Since
~ ~ - ~the
~ brain does
not regenerate its neural tissue, a functional reorganization must be assumed.26
It is not yet clear how such improvements or
changes occur, but evidence supports a role in both
the ipsilateral (left) and contralateral (right) hemi~ p h e r e , findings
~ ~ , ~ ~ supported by regional cerebral
blood flow (rCBF)
More recently there
has been increasing evidence in PET studies that the
left hemisphere may play a crucial role in recovery
from aphasia. Heiss et al.,32using resting and activation (with spontaneous speech) procedures, studied
patients 12 to 18 days following left MCA stroke and
again after 4 months. They found that in addition to
metabolic rates in the mirror region in the right
hemisphere, the intactness of the left hemisphere
was an important predictor of recovery. Kamimoto et
al.33evaluated patients with PET after acute, lefthemisphere stroke, and again after 3 to 49 months.
All patients demonstrated improvement on a clinical
stroke scale during the study period. Among these
regions both rCBF and CMRO, were significantly
increased in the middle frontal gyrus, inferior frontal
gyrus, supramarginal gyrus, and angular gyrus. In
the right hemisphere, both rCBF and CMRO, were
increased in every measured region except the thalamus, especially in the supramarginal gyrus. Collectively these data therefore suggest that intact re-

gions ipsilateral to the damaged brain are important
for language recovery.
There are little data showing that such brain
structures are necessary for language recovery to
take place. Indeed, the PET studies described have
shown bilateral activation with language tasks but a
single, ischemic stroke in the homologous region in
the right hemisphere rarely produces aphasia. A recent study4 with normal subjects using functional
MRI demonstrated extensive left prefrontal activation, but the investigators noted that functional imaging techniques do not distinguish between critical
areas from those that participate in a task. To confirm the importance of a region t o recovery, an experimental model is needed to establish a causal relationship between a brain site and a target function.
The application of superselective testing with amobarbital sodium in target arteries using an A-B-A
experimental design may represent such a model.
The reorganizational process for language recovery following stroke may not represent the same
mechanism of language relocation in patients with
cerebral vascular malformations. Neuropsychological
investigations of patients before surgical resection of
AVMs have yielded variable results with respect to
localization of function, and most neurocognitive
studies have not been able to demonstrate the kind
of impairment typically seen with acute focal lesions
in comparable brain region^.^^,^^ Brown et al.37 and
Mahalick et al.38suggest that one possible reason for
the variability of neuropsychological impairment
seen among AVM patients could be atypical organization of language function. Moreover, intracranial
AVMs are congenital lesions composed of a coiled
mass of arteries and veins lying in a bed formed by
displacement rather than invasion of normal brain
tissue. AVMs appear to undergo an unclear development process for many years until some critical mass
is reached and symptoms (often seizures or hemorrhage) occur. “Steal” is unlikely to account for the
redistribution of function since recent data have suggested that focal neurologic deficits are rare at the
time of presentation, except in cases of hemorrhage.39Moreover, many of the vessels serving language areas injected in this series had very low feeding pressures. At this point it is not known when this
reorganization begins, or whether it needs to begin
in childhood or can occur later in life.
There were several matters that this study did not
address. First, we examined only selected vessels in
each patient, and not all patients underwent the
same superselective studies. All patients had cerebral AVMs as a common feature but one had infarction 3 years earlier, one a cerebral hemorrhage 1
year earlier, and one a cerebral hemorrhage 1month
earlier than the superselective study. We were able
to demonstrate that certain regions were necessary
for language function but other regions that were not
evaluated could have also been important. In addition, we did not determine the contribution of the
right hemisphere to language function in these paSeptember 1997 NEUROLOGY 49 807

tients. Nevertheless, this research demonstrates a
new method of study in the cerebral localization of
behavior and some of the redistribution of function
from posterior to anterior regions that can occur.
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Anterior translocation of language in patients with left cerebral arteriovenous
malformation
R. M. Lazar, R. S. Marshall, J. Pile-Spellman, et al.
Neurology 1997;49;802-808
DOI 10.1212/WNL.49.3.802
This information is current as of September 1, 1997
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