Extrapyramidal dysfunction with cerebral arteriovenous ... · JournalofNeurology, Neurosurgery,...

Journal of Neurology, Neurosurgery, and Psychiatry, 1974, 37, 259-268

Extrapyramidal dysfunction with cerebralarteriovenous malformations'

JOAO LOBO-ANTUNES, MELVIN D. YAHR2, AND SADEK K. HILAL

From the Clinical Center for Research in Parkinsonism and Allied Diseases, The Mount SinaiSchool of Medicine, Columbia University College ofPhysicians and Surgeons, and the Departments of

Neurosurgery and Neuroradiology, New York Neurological Institute, New York, N. Y., U.S.A.

SYNOPSIS Arteriovenous malformations have only rarely been implicated as a cause of basalganglia dysfunction. In four instances where such a lesion was uncovered, abnormal involuntarymovements were present. In two, tremor involving the contralateral limbs occurred, while in othersthe head and neck were involved in dystonic movements and posture. The clinical and angiographiccharacteristics of these four patients have been assessed and are presented in detail in this report. Thepossible mechanism by which arteriovenous malformations may disturb the internal circuitry of thebasal ganglia and induce symptoms are discussed.

The clinical manifestations and natural historyof arteriovenous malformations of the brain(AVM) have been previously well documented(Olivecrona and Riives, 1948; Mackenzie, 1953;Paterson and McKissock, 1956; Anderson andKorbin, 1958; Tonnis et al., 1958; Svien andMcRae, 1965; Perret and Nishioka, 1966; Kellyet al., 1969; Moody and Poppen, 1970). In theirclassical form they are distinguished by theoccurrence of hemicrania, convulsive seizures,and subarachnoid bleeding. In most instances,and usually over a period of time, a variety ofneurological deficits accrue to this triad, thoughextrapyramidal signs appear to be a rarity. In ourreview of several reported series of arteriovenousmalformations encompassing more than athousand cases, abnormal involuntary move-ments were described on only one occasion(Paterson and McKissock, 1956). An additionalcase was briefly reported by Shaw et al. (1972).

It is the exception rather than the rule to en-counter discrete structural lesions of the brain asan underlying cause of classical extrapyramidaldisorders. It is, therefore, of more than passinginterest to find four cases in which specific in-voluntary movement disorders were a major

1 Supported in part by the Parkinson Disease Foundation, New Yorkand NINDS Grant No. 05184.2 Address for reprints: Dr. Yahr, Mount Sinai School of Medicine.

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manifestation of a cerebral arteriovenous mal-formation. In three of these cases the vesselsinvolved were those that normally supply thebasal ganglia structures. The clinical and angio-graphic features of these exceptional cases, aswell as some physiopathological implications arethe basis of this report.

CASE 1

This 21 year old right-handed man was admitted tothe Neurological Institute for the first time in 1964.He was the product of a full-term uncomplicatedpregnancy and, although he was always consideredto be a clumsy child, his milestones were normal.When he was 1 year old the mother noted peculiarwaving movements of the right arm. Over the yearsthis progressed and at the age of 13 years he wasnoted to have tremor of the right hand, and troublein performing fine movements; his handwritingdeteriorated and he began to prefer the left hand. Atthe age of 14, he had been admitted to another hos-pital for evaluation. He was thought to be mentallyslow; nystagmus on lateral and upward gaze andbilateral hypertrophy of the sternocleidomastoidmuscles were noted. There was an involuntarypronation-supination tremor of the right arm, andthe performance of rapid succession movements withthe right foot was defective. Radiographs of the skullrevealed a 10 mm left to right shift of the pinealgland. A pneumoencephalogram failed to visualize

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Joao Lobo-Antunes, Melvin D. Yahr, and Sadek K. Hilal

FIG. 1. Case 1. (a) AP view of the left carotid angiogram(initial study). Deep A VM supplied predominantly by theanterior choroidal artery (arrows), and posterior cerebralartery. A smaller supply may be coming from the lenticulo-striate vessels. (b) Lateral view of the same case. (c) APview of the left carotid angiogram obtained at the time ofthe second admission. Note the shift of the anterior cerebralartery and lateral displacement of the middle cerebralartery. Also note the increased size of the avascular zone inthe medial aspect of the malformation (arrows).

adequately the ventricular system, though the basalcisterns and sulci were normal.

Except for a slight increase in tremor his con-dition remained essentially unchanged. In 1964, hewas admitted to the New York Neurological Insti-tute for evaluation. Apart from a mild right-sided

reflex preponderance, and a questionable left centralfacial paresis his neurological examination was un-changed. An intravenous RISA scan (1131) revealedan area of increased uptake over the left mid-tem-poral region thought to be of vascular origin. Apneumoencephalogram revealed a slight displace-

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ment to the right of the posterior portion of the thirdventricle. A lumbar puncture disclosed cerebrospinalfluid under normal pressure with a protein content of59 mg/100 ml. An electroencephalogram was nor-mal. An angiographic study was refused by thefamily and the patient was discharged.He was readmitted in July 1965. On the day of

admission he awoke with a severe, generalized head-ache, followed by nausea and vomiting. Neurologicalexamination on admission revealed a lethargicpatient with marked nuchal rigidity and positivemeningeal signs. Speech was dysarthric and mildweakness and increase in tone of the right upperextremity were noted. There were flailing dystonicmovements of the right arm and motor coordinationwas poor. Pain, touch, position, and vibratory sensa-tions as well as stereognostic sensibilities were de-creased over the right hand. There was paralysis ofupward gaze. A right central facial paresis waspresent and on protrusion the tongue deviated to theright. No bruits were heard. Again, bilateral hyper-trophy of the sternocleidomastoid muscles was ob-served. Lumbar puncture revealed grossly bloodyfluid under increased pressure. An angiographicstudy revealed a large arteriovenous malformationoccupying the left basal ganglia, thalamus, and uppermesencephalon which was fed predominantly by theanterior choroidal artery in its lateral aspect, and bybranches of the posterior cerebral artery in its medialaspect (Fig. la, b). The major drainage was throughthe basilar vein which was markedly enlarged in itsposterior portion. Approximately a week after thehaemorrhage, it was noted that the abnormal move-ments had disappeared, but the patient maintaineda dystonic posture of the right hand. He received acourse of radiotherapy and was discharged onemonth later.He was readmitted two months later with a second

episode of subarachnoid bleeding. His neurologicalstatus remained essentially unchanged. Two furtherhaemorrhages occurred during his hospitalization.He did well until May 1972 when he was readmittedafter another episode of bleeding. His neurologicalcondition was essentially unchanged. A secondangiographic study was performed. A 7 mm shift ofthe left anterior cerebral artery to the right, and alateral displacement of the middle cerebral arterywere present indicating a centrosylvian mass effectwhich was much greater than on the initial studies(Fig. Ic). There was also an increase in the size of thelucent area in the medial aspect of the malformationsuggesting the presence of a haematoma.

CASE 2

This 39 year old woman was admitted to the New

York Neurological Institute in February 1959. Fivedays before admission she experienced sudden,severe, generalized headaches, followed by vomiting.She was admitted to another hospital and a mild lefthemiparesis was noted; she remained severelylethargic over the next few days and was subse-quently transferred to the Neurological Institute.Past medical history was significant in that thepatient had suffered from a left torticollis since earlychildhood, which had been successfully treated bytenotomy of the sternal head of the left sternocleido-mastoid muscle six years before this event. Whenseen on admission, the patient was quite drowsy withsevere neck stiffness and positive meningeal signs.No bruits were heard. Mild left hemiparesis waspresent. Lumbar puncture revealed grossly bloodyspinal fluid under a pressure of 200 mm H20. Bi-lateral carotid angiograms revealed an arteriovenousmalformation in the right posterior thalamic regionfed mostly by the posterior choroidal branches of theposterior cerebral artery. A pneumoencephalogramdemonstrated mild ventricular dilatation and anincisural block. The patient improved progressivelyand returned to work four months later.

In October 1966 a sclerosing haemiangioma of thesternum was removed. When last seen in April 1968she was free of symptoms.

CASE 3

This 60 year old right-handed man was admitted tothe New York Neurological Institute for the firsttime in 1963, with a history of spasmodic retrocollissince the age of 19 years. Because of the increasedfrequency and severity of his movement disorder hewas admitted to a hospital in Florida where bilateralcarotid angiograms revealed a large AVM in theright parietal region fed by branches of the rightmiddle cerebral artery. He was transferred to theNew York Neurological Institute for further manage-ment. On admission he was noted to have episodesof spasmodic involuntary hyperextension of thehead, which was also slightly tilted to the right. Theexamination was otherwise normal. During hishospitalization he underwent section of the rightanterior Cl, C2, and C3 spinal nerve roots, withslight improvement of the dystonia. In May 1972 hehad a brief episode of loss of consciousness, but hiscondition has remained stable.

CASE 4

This 10 year old, right-handed white boy wasadmitted to the Babies Hospital, Columbia-Presbyterian Medical Center in January 1972 with ahistory of bifrontal, pulsating headaches and in-

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FIG. 2. Case 4. (a) AP view of the rightcarotid angiogram. The lateral segment ofthe A VM is supplied by the lenticulostriatevessels, and the medial segment by theanterior choroidal artery (arrows). Notethe triangular shape of the malformation inthis projection. (b) Lateral view of thesame study. (c) Left vertebral angiogramshowing the supply to the A VMfrom theposterior choroidal arteries and the thala-moperforate arteries (arrows). Note theavascular area between these two groups ofvessels.

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voluntary movements of the left upper extremity,consisting of a gross tremor of the proximal segmentand fine movements of the fingers. He was the pro-duct of an uncomplicated pregnancy and normaldelivery. The acquisition of developmental mile-stones was normal. Six months before the admissionthe parents noted an intermittent tremor of the leftarm, which increased with tension and action. Thisbecame progressively worse and he started to com-plain of headaches, sensation of pressure over theright retro-orbital region, blurred vision, anddiplopia on conjugate gaze to the left. Because ofthis, he was admitted to another hospital where bi-lateral carotid angiograms showed an arteriovenousmalformation. He was subsequently transferred toour institution for further management.On admission he was alert and cooperative, in no

distress. The head circumference was 56-5 cm, bloodpressure 116/80 mmHg and pulse rate 92/min andregular. A prominent bruit was heard over bothfrontoparietal areas, synchronous with the systolicimpulse. He tended to tilt the head to the left. Leftcentral facial paresis and hemiparesis were noted,with increased tendon reflexes and an extensorplantar response on that side. There was a prominenttremor of the left upper extremity, of about 3-4 Hzpresent at rest and increased with voluntary motion,the hand being postured in a pseudo-athetoid way.

Rapid alternating and succession movements on theleft side were performed with difficulty.An electroencephalogram was normal. Right

carotid and left vertebral angiograms were obtainedby a femoral approach (Fig. 2a, b, c). These showed alarge AVM occupying the right basal ganglia, thala-mus, and upper mesencephalon. This malformationwas supplied by hypertrophied lenticulostriatearteries, anterior choroidal artery, and perforatingbranches of the posterior communicating andposterior cerebral arteries. The superior and dorsalsegments were nourished by large posterior choroidalvessels. An area of avascularity was noted in theventral segment of the upper mesencephalon. Thevenous drainage depended upon enlarged thalamo-striate and internal cerebral veins.The patient was discharged but was readmitted

two months later because of increasing headaches,anorexia, and vomiting. The neurological examina-tion was unchanged except for evidence of earlypapilloedema. Lumbar puncture revealed clear fluidunder a pressure of 320 mm H20, with normal cells,sugar, and protein. Six days later bifrontal trephina-tions were done and a pneumoventriculogram per-formed which revealed dilatation of both lateralventricles, with obstruction of both foramina ofMonro. This was thought to be due to dilatation ofthe thalamostriate veins. A biventricular-atrial shunt

ACA

\gl <s FIG. 3. Perforatingarteries at the base of

2 S the brain. ICA:{PCA internal carotid

artery; ACA:anterior cerebralartery; PCA: pos-terior communicatin)gartery; ACH:anterior choroidalartery (modified fromAlexander, 1941).

ACH

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using a medium pressure Hakim valve was theninserted with good improvement of the headache.Two weeks later selective embolization of the mal-formation in the left vertebral artery was attempted.Thirty-one silastic balls of 1 and 1 5 mm in diameterwere instilled with slight reduction of the vascularityof the lesion.

In April, he was admitted again because of lowback pain. The neurological examination was un-changed. Lumbar puncture revealed a pressure ofO mm H20. The following month he reentered thehospital for another embolization. The procedurewas terminated after one ball entered the rightposterior inferior cerebellar artery. His condition hasremained unchanged.

DISCUSSION

Few areas of the brain receive as rich and over-lapping a blood supply as the basal ganglia

I41

>: :

V-

MCA

ACH

PCAFIG. 4. Vascular supply of the thalamus and basalganglia. CA: caudate nucleus; PU: putamen; PA:pallidum; IC: internal capsule; TH: thalamus; RN:red nucleus; SN: substantia nigra; MCA: middlecerebral artery; ACH: anterior choroidal artery;PCA: posterior communicating artery (modifiedfromMettler et al., 1954).

region (Foix and Hillemand, 1925; Abbie, 1933;Alexander, 1942; Mettler et al., 1956; Kaplan,1958; Truex and Carpenter, 1969; Salamon,1971). The central or ganglionic branchesoriginating from the proximal segments of all themajor intracranial arteries feed this region (Figs3 and 4). The striatum is nourished by the per-forating branches of the anterior and middlecerebral artery, except for the most caudal partof the putamen and the tail of the caudatenucleus which are fed by the anterior choroidalartery. This vessel also supplies the globuspallidus, except for its lateral portions which arefed by the lenticulostriate branches of the middlecerebral artery. On occasion, part of the medialsegment may receive branches from the posteriorcommunicating artery. The vascularization ofthe thalamus has been reviewed recently(Lazorthes and Salamon, 1971). It receives itsmajor supply from branches of the posteriorcommunicating and posterior cerebral arteriesthrough perforating branches (thalamoperfora-ting arteries) and the posterior choroidal vessels.Branches of the anterior choroidal artery nourishthe ventrolateral segment of the thalamus. Thevascular supply of the subthalamic nucleus, rednucleus, and substantia nigra depends onbranches of the posterior communicating andposterior cerebral arteries. The venous drainageof the basal ganglia is through the deep cerebralveins, by way of the internal cerebral vein and thegreat cerebral vein of Galen. These are thevessels primarily involved in AVMs of the basalganglia and thalamus as one would expect fromthe embryological development of the vascularsystem of the brain (Kaplan et al., 1961).

Despite this plethora of vascular channels,arteriovenous malformations are infrequentlyfound in the region of the basal ganglia andthalamus. In our survey only 7-6% of supra-tentorial AVMs were found to involve thesestructures. The same appears to be true for neo-plastic lesions (McKissock and Paine, 1958;Tovi et al., 1961; Cheek and Taveras, 1966). It istherefore not surprising that extrapyramidal syn-dromes are only rarely seen with such lesions.Equally rare in such instances is the so-called'thalamic syndrome' originally described byDejerine and Roussy (1906), in which choreo-athetoid movements involving the paretic limbsmay occur. In two cases an AVM causing this

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TABLECLINICAL AND ANGIOGRAPHIC CHARACTERISTICS

Cases Sex Age of First Sub- Type and site of Site ofAVM Feeding vessels Follow-uponset symptoms arachnoid involuntary movements(yr) haemorrhage (AIM)t

(SAH)

Paterson NR NR* NR NR Athetoid movements 'Central' NR NRet al. (1956) of the hemiparetic

limbs (site?)Shaw et al. M 19 Subarachnoid + L. torticollis NR R. middle AIM subsided

(1927) bleeding cerebral artery completelytwo years later

Our casesCase 1 M 1 'Waving' + AIM unclassifiable L. thalamus, L. anterior AIM subsided

movements (5 episodes) ; basal ganglia choroidal and after firstof R. arm Tremor and upper perforating SAH

mesencephalon branches ofDystonia (R. upper post. comm.

extremity) and post.cereb.

Case 2 F 'Child- L. torticollis + L. torticollis R. posterior R. lateral post. Improvementhood' thalamus choroidal after tenotomy

L. sterno-cleidomastoid

Case 3 M 19 Retrocollis 0 Retrocollis R. parietal lobe R. middle Minimal im-cerebral provement

after section ofR. C1, C2, C39ant. roots

Case 4 M 9 Tremor of L. 0 Tremor and dystonic R. thalamus, R. lenticulo- No improvementarm posture of L. upper basal ganglia striate, ant. after partial

extremity and upper choroidal, and selectivemesencephalon perforating embolization

branches of of AVMpost. comm.and post.cereb.

* NR: not recorded.t AIM: abnormal involuntary movements.

type of picture, but without abnormal move-ments, have been documented (Silver, 1957;Waltz and Ehni, 1966).The clinical and angiographic characteristics

of two previously reported patients and the fourcases in this series are summarized in the Table.An intimate correlation exists between thelaterality of the symptoms and the site of theAVM. However the symptomatology is variableand may result from differing mechanisms.

Arteriovenous malformations may becomesymptomatic in several different ways (Pool,1972). The large volume of blood which isshunted through the AVM may result in a 'stealeffect' from normal tissues with temporary orpermanent ischaemia of neuronal structures. Inour case 3, and in the case reported by Shaw etal. (1972) this type of phenomenon can be impli-cated. The size of the AVM may be such as toproduce a mass effect with impingement on basal

ganglia structures. This may well have beenoperative in case 1 where a shift of the midlinestructures to the opposite side was consistentlyfound long before a known or significant bleed-ing episode occurred. Major or minor haemor-rhages may occur within and contiguous to theabnormal vessels and lead to the formation ofhaematomas with pressure upon and necrosis ofadjacent neural tissue. It is also conceivable that,in association with maldeveloped blood vessels,abnormalities in brain development may occur.Because of these various factors, the clinical pic-ture may be variable and labile. Initial symptomsmay subside, increase in severity, or be replacedby new ones as any one of the above mechanismsbecome operative.Case 1 in our series is particularly illustrative

of many of these aspects. In this patient 'waving'movements of one hand, undoubtedly dyskineticin nature, were noted at 1 year of age. At the age

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of 12 years they were replaced by tremor at rest,and, after an episode of bleeding at the age of 25,he began to have flailing dystonic movements;the latter subsided completely within one week.Hence, an interesting spectrum of abnormalmovements occurred whose pathological sub-strate is difficult to establish. However, from thesite at which the AVM was located, which in-cluded the mesencephalon, one might suspect thepathways involved. Experimentally, tremor atrest simulating tremor of Parkinsonism has beenproduced in the monkey by lesions placed in theventromedial tegmental area of the mesen-cephalon at the level of the substantia nigra andred nuclei (Poirier et al., 1966). Such lesionsdestroy the pars compacta of the substantia nigraand interrupt pathways to the striatum, palli-dum, and thalamus as well as rubrospinal andtegmentospinal tracts. It is postulated thattremor results from interruption of the dopamin-ergic nigrostriatal pathway which is thought toexert an inhibitory effect on the pallidum(Poirier et al., 1965). Other types of dyskineticmovements may similarly represent disturbancesof internal circuitry in the basal ganglia resultingin loss of inhibitory phenomena. Experimentally,choreoid and ballistic movements may bq pro-duced in monkeys by lesions localized to thecontralateral subthalamic nucleus, which prob-ably has an inhibitory influence upon the globuspallidus (Carpenter et al., 1950). The disappear-ance of the abnormal movements in this casewas probably due to involvement of the cortico-spinal tract at the posterior limb of the internalcapsule with development of mild hemiparesis.However, destruction of the pallidum, ventro-lateral nuclei of the thalamus, or the pallido-thalamic connection fibres could well haveoccurred and abolished the dyskinetic move-ments. As is well known, lesions placed in thesestructures in man have effectively alleviated ab-normal movements. Angiographically, the mal-formation was fed in its lateral portion by theanterior choroidal artery, and in its posterior andmost medial aspect by large thalamoperforatingvessels. These involved primarily the pallidum,thalamus, upper mesencephalon, and probablypart of the internal capsule. It should be empha-sized that both anterior and posterior segmentsof the internal capsule are supplied by perfora-ting branches of the middle cerebral artery,

except for the ventral segment of the posteriorlimb and the retrolenticular portion which de-pend upon the anterior choroidal artery. Thiswas one of the major feeding vessels. The pro-gressive nature of this lesion is evident in the twoangiograms performed seven years apart, whichreveal an increase in the bulk of the lucent areain the medial segment of the malformation. Thepresence of bilateral sternocleidomastoid hyper-trophy is certainly intriguing. This usually occursin cases of dystonia, due to the rhythmic, power-ful contractions of the muscles involved, but nodystonic or torsion movements were apparent inour case.The association of spasmodic torticollis and

AVM in our cases 2 and 3, and in the casereported by Shaw et al. (1972), deserves com-ment. In case 2, the malformation was localizedto the dorsal thalamus and was fed by theposterior choroidal arteries. In case 3, as well asin the case of Shaw et al., the AVM was nour-ished by branches of the middle cerebral artery,and one wonders whether or not the associationis merely coincidental. The contralaterality ofthe signs and the succession of events in the latterpatient suggest some intimate relationship. Thedystonia followed an episode of subarachnoidbleeding persisting for two years and then sub-siding. Possibly this resulted from relative vascu-lar insufficiency-so-called steal phenomenon-but unfortunately a study of the posterior fossacirculation was not carried out. It is of interest tonote that the anatomical substrate of this dis-order remains to be established (Tarlov, 1970).Spasmodic torticollis has been seen in patientswho have suffered an attack of encephalitislethargica. It has been reported in a patient withcolloid cyst of the third ventricle and improvedafter it was removed (Avman and Arasil, 1969).Experimentally, spasmodic torticollis has beenproduced in the monkey by lesions involving themedial mesencephalic reticular formation, caudaland dorsal to the red nucleus at the level of thedescussation of the brachium conjunctivum(Foltz et al., 1959); tonic neck torsion followslesions in the red nucleus (Carpenter, 1956) orbetween the red nucleus and the interstitialnucleus of Cajal (Denny-Brown, 1962). Itsanatomical substrate is, however, far from estab-lished.The angiographic features of the AVM in our

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case 4, are worthy of comment. In this case therostral portion of the malformation shows twodistinct segments the lateral one fed by hyper-trophied lenticulostriate arteries and the medialone supplied by a large anterior choroidal vessel.In the anteroposterior view, the AVM is tri-angular in shape conforming to the outline ofthe basal ganglia in this projection, and theangiographic film is quite similar to an injectedspecimen. The caudal part of the AVM receiveslarge perforating branches of the posterior com-municating and posterior cerebral arteries. Anarea of avascularity corresponding to the ventralpart of the upper mesencephalon is well visual-ized within the AVM. Ischaemia of that areawhich includes the substantia nigra and itsefferent fibres, either because of occlusion of thevessels or by a steal effect, may have been thecause of the extrapyramidal phenomena in thispatient. Although not entirely pertinent to oursubject we would like to call attention to thepresence of hydrocephalus in this case. This wasfelt to be due to obstruction of both foramina ofMonro by enlarged thalamostriate veins. As faras we could determine this mechanism has notbeen reported.The treatment of these malformations presents

a formidable problem for which no fully satisfac-tory therapeutic measures are available. Adirect surgical attack on the AVM is rarelyfeasible except in the exceptional case in whichthe dimensions of the lesion are small and theirproximity to the lateral ventricle allows a trans-ventricular approach (Carton and Hickey, 1955;Ralston and Papatheodorou, 1960). Attempts toreduce the size of the abnormal collection ofvessels by promoting thrombosis have been lessthan satisfactory. Initially, this was attempted byirradiation, more recently by embolization(Luessenhop et al., 1965). The latter may be moresuccessful using selective catheterization of thefeeding vessels (Hilal and Michelsen, 1972).However, at present it may be more judicious toavoid any intervention and restrict treatment tosymptoms as they occur.

We are grateful to Dr. James W. Correll and Dr.Jost Michelsen for permission to report their cases.

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