12ournalof Neurology, Neurosurgery, and Psychiatry 1992;55:1162-1167

Movement disorders in astrocytomas of the basalganglia and the thalamus

Joachim K Krauss, Fritz Nobbe, Ajay K Wakhloo, Mohsen Mohadjer, Werner Vach,Fritz Mundinger

AbstractIn a series of 225 patients with astro-cytomas (grades I-IV) of the basal gangliaand the thalamus, 20 had a movementdisorder. In all patients the histologicaldiagnosis was verified by stereotacticbiopsy. Tremor was observed in twelvepatients, dystonia in eight, chorea inthree, and chorealballismus and myoclo-nus in one. The tumour involved thethalamus in 16 patients. Corticospinaltract dysfunction was evident in 70% ofthepatients with movement disorders and in73% ofthose without. Demographic, clini-cal, histological and neuroradiologicaldata of the patients with a movementdisorder were compared with the data ofpatients without. CT data yielded no dif-ferences with respect to the involvement ofanatomical structures. Movement disor-ders were significantly associated withlow-grade astrocytomas.

(7 Neurol Neurosurg Psychiatry 1992;55: 1162-1167)

Albert-Ludwigs-UniversitAit, Freiburg,GermanyDepartment ofNeurosurgeryJ K KraussF NobbeDepartment ofStereotaxy andNeuronuclearMedicineM MohadjerSection ofNeuroradiologyA KWakhlooInstitute of MedicalBiometry and MedicalInformaticsWVachSt Josefs-Krankenhaus,Freiburg, GermanyF MundingerCorrespondence to:Dr Krauss,NeurochirurgischeUniversitatsklinik,Hugstetter Str 55, D-7800Freiburg, Germany.Received 20 January 1992and in revised form9 March 1992.Accepted 16 March 1992

Tumours of the thalamus and the basal gangliaare relatively rare. They are estimated to makeup 1-2 5% of intracranial tumours. 1-4 Most ofthese neoplasms are benign or malignant astro-cytomas.'-7 Since craniotomy and partialresection was associated with high mortalityand morbidity, stereotactic diagnostic andtherapeutic techniques have been favoured in

7 8

recent years.As movement disorders (MDs) are often

related to dysfunction or structural lesions ofthe basal ganglia, a high incidence in intrinsictumours might be expected, but they seem tobe infrequent. While in some series they are noteven mentioned,9 they range from 1-7% in

3 4

recent57 and from 4-33% in earlier series.Since 1965,'° no large series has focused on

the subject. To characterise better this rela-tively uncommon cause of MDs, we reviewedthe literature and retrospectively analysed a

series of 225 patients with histologically veri-fied astrocytomas of the basal ganglia and thethalamus. Among those we identified 20 withMDs (classified according to criteria publishedelsewhere)' 1-16 at the time of biopsy.

MethodsThis study is based on a retrospective evalu-ation of 225 patients with low- or high-gradeastrocytomas of the basal ganglia and thethalamus histologically confirmed by stereo-

tactic biopsy. Fifteen patients were operated onbefore 1975 and 210 between 1975-86. Thepatients were referred from other neurosurg-ical or neurological clinics to the department ofstereotaxy. CT scans, (available in our institu-tion since 1975) and also MRI were laterobtained before biopsy. In patients operatedupon before 1975, CT was performed as soonas it became available. The patients werefollowed up at various times, with latest followups in 1989, 90 or 91. Patients' clinicalreports, the register of a tumour data bank,and film recordings were reviewed to identify20 patients with MDs.

Stereotactic biopsy and interstitial radiother-apy were performed using the Riechert-Mundinger system as described elsewhere. 17 19

The histological diagnosis was made usingintraoperative smear preparations by methyl-ene blue staining and was confirmed withparaffin sections. The tumours were gradedaccording to the classification of the WorldHealth Organisation (WHO).Demographic, clinical and histopathological

data of patients with an MD were comparedwith those of patients without. For statisticalanalysis Fisher's exact test, the Wilcoxon, andthe Chi-square test were applied.

ResultsTwenty (9%) patients with astrocytomas of thebasal ganglia and the thalamus displayed anMD at the time of biopsy. The MD was theinitial symptom of the tumour in threepatients. The mean latency between onset ofany symptoms and biopsy was 3 years. Variousother clinical symptoms were found (table 1).Signs of raised intracranial pressure at biopsywere evident in patients 2, 5, 6, 8, and 15.Obstructive hydrocephalus at biopsy wasfound in patients 5, 6, and 8. Five patients hadreceived ventriculoatrial or ventriculoperito-neal shunts before stereotactic biopsy. Two hadno MD before the shunt operation, in twoothers shunting did not alter the MD, and inpatient 14 hemiparesis improved while tremordid not.CT or additional MRI findings were

obtained in 18 of the 20 patients (two had diedbefore 1975). The tumour involved the thala-mus in 16. Downward extension to the sub-thalamus or the upper midbrain varied. Thiscould not always be determined exactly due tothe compressive effect of the tumour onadjacent structures or due to peritumouraloedema, or because some patients had hadonly axial CT scans. In 15 patients the tumour

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Table 1 Clinical features, histological grading and neuroradiological findings of 20 patients with movement disorders in basal ganglia and thalamicastrocytomas

Sex/Age at TumourBiopsylAge Preop. Other Clinical Symptoms Grade of Volume

Case at Onset KPS Movement Disorder at Biopsy Hemiparesis Astrocytoma Brain Imaging Study Results cm3

1 M/25/13 60 Tremor, 3-4 Hz1 arm: rest, post, int

2 M13/3 80 Tremor, 3-5 HzI arm > leg: post, intAthetosis, 1 hand: restHead tilt

3 M/50/44 60 Tremor, 3-4 HzI arm > leg: rest, post, int

4 F/49/43 60 Choreaface, bilateral I > rI arm > leg

5 F/70/70 40 Parkinsonism hypokinesia,bilateral rigidity + tremor:rest, post, int

6 M/37/31 60 Tremor, 4-5 HzI arm: rest, post, int

7 F/I 1/10 60 DystoniaI arm: rest, on action

8 M/12/9 70 DystoniaI hand: on actionTremor, 4-5 HzI arm: post, int

9 M/42/41 70 Tremor, 4 Hzr arm: rest, post, int

10 M125/25 60 Dystoniar arm: rest, on action

11 M/15/13 70 Tremor, 4-5 Hzr arm: rest, post, int

12 F/11/9 70 Chorear arm > legmarked on action

13 F/ 10/9 60 DystoniaI arm > legChorea-BallismusI arm > leg

14 F/1 2/3 60 Tremor, 3-5 HzI arm: rest, post, int

15 M/16/15 40 Dystonia + ChoreaI arm > leg > face: rest, onaction

16 Ff62/59 60 Tremor, high-frequencybilateral, 1 > rfingers + eyelids

17 F/13/11 70 Dystonia, r arm: rest,on actionMyoclonus, r shoulder

18 F/3/2 70 Tremor, 3-4 Hzr arm: int

19 F/55 60 Dystonia, r arm: rest, onaction

20 F/12/10 60 Tremor, 3-4 Hzr arm: int

R hypacusis, nystagmus - I R thalamus, cyst extending to midbrain -25

Papilloedema

R optic atrophy, r 3rdnerve palsy, dysarthria,gait ataxiaImpaired memory,seizures

Impaired memory,obstructivehydrocephalus,Parinaud's syndrome,lethargyImpaired memory,seizures, aphasia

Lethargy,Neurofibromatosistype I

Impaired memory,obstructivehydrocephalus,I hemihypaesthesia, 1 6thnerve palsy, Parinaud'ssyndromeSeizures, headaches

Impaired memory,aphasia, behaviouraldisorder, seizures,r hemihypaesthesiaImpaired memory

Behavioural disorder,r hemihypesthesia

Precocious puberty

Seizures, gait ataxia

Obtundation, 3rd nervepalsy, cachexia

Psychosis, lethargy,dysarthria

Dysarthria

Behavioural disorder,anorexia, diminishedvision I eyeBehavioural disorder,diminished vision I eye

Impaired memory,behavioural disorder,diminished vision I eye

(circumscribed)R thialamus, internal capsule, pallidum -22(circumscribed)

L I R postero-basal thalamus, nucleus ruber -1.5(circumscribed)

L II

11-III (8m)IV

R frontomedial, basal, septum >50pellucidum, corpus callosum, caudate(diffuse)R + L posteromedial thalamus, 3rd -20ventricle, corpus pineale, spleniumcorporis callosi (circumscribed)-upperbrainstem compression

- II R thalamus, internal capsule, pallidum,putamen, corpus callosum, septumpellucidum, r frontal + temporal,I frontal (diffuse)

L I R pallidum, subthalamus, internalcapsule (circumscribed) +quadrigeminal plate + bilateral pons +cerebellum (diffuse)

L I R thalamus (circumscribed)

- II L basal ganglia + hemisphere, corpuscallosum (diffuse, multifocal)

R I L thalamus, subthalamus, caudate,putamen, pallidum, internal capsule,corona radiata (circumscribed)

>100

-12

-15

>100

-40

R I L pailidum, putamen, corona radiata -18(circumscribed)-compression ofthalamus

R II L subthalamus, internal capsule, medial -18caudate, posterobasal pallidum(circumscribed)

L I R subthalamus, thalamus, internal -25III (4y) capsule, corona radiata, crus cerebri

(circumscribed)

L II R thalamus, quadrigeminal plate(circumscribed)

L IV R thalamus, upper brainstem (0 CT)

R II L anterior-ventrolateral thalamussubthalamus, internal capsule, cruscerebri (circumscribed)

R I L hypothalamus, thalamus extendingover midline and to midbrain (0 CT)

- I L hypothalamus, thalamus(circumscribed)

R I L subthalamus, thalamus, caudate,internal capsule, pallidum, putamen,insula, uncus (circumscribed)

R I L thalamus, subthalamus, crus cerebri(circumscribed)

-25

>30

-7

-25

-20

-20

-16

M = male, F = female, KPS = Karnofsky Performance Scale, R = right, L = left. Tremor is qualified as: rest-tremor at rest, post-postural tremor and int-intentiontremor.

appeared to be more or less circumscribed. Inpatients 6 and 9 (fig 1) the neoplasm involvedthe basal ganglia and large parts of the hemi-sphere diffusely. The tumour volume rangedfrom 1 5 to more than 100 cm3. It was locatedin the contralateral basal ganglia in patientswith unilateral MDs.

Twelve patients had tremor. Only patient 5had Parkinsonism with bilateral rigidity, rest-ing and postural tremor, akinesia, masked face,and loss of postural reflexes, though tremorwas also present on action. In this case thetumour was located in the midline andinvolved both thalami, but exerted markedcompression on the midbrain. Patient 16 had ahigh-frequency tremor of fingers and eyelids,

presumably essential tremor, which was lesssevere on the right, slightly hemiparetic sidecontralateral to the tumour. The tumour pre-dominantly involved the anterior and ven-trolateral thalamus (fig 2). Ten patients hadunilateral tremor, which in two was onlypresent on action, in two others on action andon maintaining antigravity posture, and in six acombined resting-postural-intention tremorwas found. These tremors had a frequency of 3to 5 Hz. The slight increase in tone in somepatients with an ipsilateral hemiparesis hadfeatures of spasticity rather than of rigidity.Tremor in these patients was not associatedwith akinesia or impaired postural reflexes. Innine of these patients the tumour involved the

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Figure 1 Axial enhancedCT scans ofpatient 9 withright resting, postural andintention 4 Hz tremorshow a diffusely spreadingWHO grade IIastrocytoma of the leftbasal ganglia andhemisphere extendingcontralaterally via thecorpus callosum.

thalamus. In the tenth (case 11) the tumourwas predominantly located in the pallidum andputamen, sparing the thalamus, but never-theless exerted considerable compression onthe thalamus. In patient 3 the tumour waslocated mainly in the red nucleus and to alesser degree in the postero-basal thalamus(fig 3). In patient 14 the astrocytoma extendedfrom the thalamus to the quadrigeminal plate(fig 4).Hemidystonia or hemiathetosis was seen in

eight patients, in five of whom it was partic-ularly marked on action. The arm was affectedin all these patients, with additional involve-ment of the leg in two. Patients 2 and 8 withinvolvement only of hand and fingers had anastrocytoma confined to the thalamus. Inpatients 10 and 19 the tumour mainly involvedthe caudate and putamen, to a lesser degree

Figure 2 Enhanced CT scans ofpatient 16 with essential tremor showing a WHO gradeII astrocytoma (focal anaplastic transformation could not be excluded) locatedpredominantly in the left anteriorlventrolateral thalamus and the genu of the internalcapsule.

:S,.S. ............-

Figure 3 Axial enhanced CT scans (lower row) withsagittal (upper row) and coronal (middle row)reconstructions ofpatient 3 with left resting, postural andintention 3-4 Hz tremor showing a relatively smallcircumscribedWHO grade I astrocytoma, predominantlylocated in the right red nucleus and posterobasal thalamus.

the thalamus. In cases 13, 15, and 17 the maintumour mass was found in the thalamus,whereas in case 7 the thalamus only wascompressed.

Choreatic MDs were seen in four patients.Two had hemichorea, one left hemichoreainvolving the face markedly on the left side,and one hemichorea/hemiballismus. Patients13 and 15 presented with hemichorea anddystonia appearing as "choreoathetosis".Hemichorea was associated in two patientswith involvement of the head of the caudate. Inthe patient with hemichorea/hemiballismus,the thalamic tumour involved the subthalamicnucleus. Choreatic hyperkinesias disappearedin all patients in the long term.The following data were analysed compar-

atively for patients with and without MDs. Thefemale/male ratio was 1 2: 1 (11 females/9males) for MD patients and 1:1 for thosewithout (102/103). The 20 astrocytomas of theMD patients and the 205 astrocytomas ofthose without were distributed according tohistological grading as follows: WHO I-12(60%)/41 (20%); WHO II-6 (30%)/71(35%); WHO III-0/56 (27%); and WHOIV-2 (10%)/37 (18%). In patient 16 thetumour was graded histologically as an astro-cytoma WHO II, however, focal anaplastictransformation could not be excluded. Thefrequency of MDs in patients with low-grade(I + II) astrocytomas was 15%, in patientswith high-grade (III + IV) astrocytomas2- 1%. This difference was statistically sig-nificant (p = 0-0017). The mean age ofpatients with MDs at the time of biopsy waslower (24 years) than that of the patientswithout (36 years), however, the proportion oflow-grade astrocytomas was higher in MDpatients and the mean age correlated withhistological grading as follows: WHO I (meanage in years, MD patients/patients without)-15/20;WHO II-36/35;WHO III- -/42; andWHO IV-43/47. There was also a trend forthe mean age in patients with astrocytomas

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Figure 4 Sagittal SE 1040/40 and axial SE 1200/80 MR images ofpatient 14 withleft resting, postural and intention 3-5 Hz tremor reveal a WHO grade II astrocytoma,predominantly located in the right thalamus and the quadrigeminal plate.

WHO I to be lower in MD patients (15 years)compared with those without (20 years).

Analysis of the CT data of patients with andwithout MD yielded no difference concerningthe involvement of different anatomical struc-tures. Comparing tumour volumes there was adifferent distribution, which reached statisticalsignificance: MD patients more often hadtumour volumes ranging from 16 to 25 ccm(55%) than those without (17%). However,large tumours were found more often inastrocytomasWHO III and IV.

Seventy per cent of patients with MDs and73% of patients without had a hemiparesis ofvariable degree contralateral to the tumour. Inthe astrocytoma WHO I group there was atendency for MD patients to present moreoften with hemiparesis (75%) than those with-out (61%). The median Karnofsky Perform-ance Score20 (KPS) in MD patients was 60.Considering the interrater variability the dis-tribution of the KPS of patients with andwithout MD was similar.

DiscussionThe frequency reported for MDs in patientswith tumours of the basal ganglia and thethalamus varies considerably. It ranged from 1to 33%1-7 9 10 21-24 (table 2) in previous studies

Table 2 Large series ofpatients with tumours of thethalamus and the basal ganglia

Literature Review Number of patients with movement(by first author) disorders/Total number ofpatients

Ody, 1932 4/25 16%Globus, 1942 3/21 * 14%Arseni, 1958 5/50 * 10%Roth, 1958 7/34 * 21%McKissock, 1958 8/24 ** 33%Tovi, 1961 2/49 */** 4%Tolosa, 1965 15/61 25%Cheek, 1966 ?/51 */** "rare"Paillas, 1970 13/55 * 23%Hirose, 1975 4/18 ** 22%Bernstein, 1984 4/60 */** 7%Beks, 1987 ?/27 */**Kelly, 1989 1/72 1%Krauss, 1992 20/225 9%

*: Series with different types of histological diagnoses, butmainly astrocytomas I-IV.**: Histological diagnosis was not obtained in all patients.

and our study was 9%. However, in somestudies a histological diagnosis was not estab-lished in all patients and different histologicaldiagnoses were grouped together withoutspecifying separately those with astrocytomas,so that an exact comparison cannot be made.Only three series on tumours of the basalganglia and the thalamus which mentionedpatients with movement disorders dealt withhistologically verified astrocytomas for thetotal study population or a defined sub-group.' 1 2 Since the involvement of the basalganglia and thalamus in astrocytomas is differ-ent from that in other neoplasms, it may bebetter to consider the former tumours sepa-rately. The incidence of MDs seems to begenerally lower in recent than in earlier studies.This might be explained by the availability ofCT and MRI which also reveal smaller andoligosymptomatic tumours, and by the use ofstereotactic techniques to establish an earlierhistological diagnosis. We chose biopsy as thetimepoint for calculating the incidence ofMDs, since later MDs may be altered by, oreven result from, therapeutic measures.

Previous series on basal ganglia and thalamictumours differ considerably with respect to theproportion of low- or high-grade astrocytomasin MD patients. While some series report thatthe majority of patients had "malignant glio-mas"23 or glioblastomas,10 others stress thatmost of the tumours producing "extrapyr-amidal" symptoms grow "very or rather"slowly.25 In our study MDs were found sig-nificantly more often in low-grade astrocyto-mas.Although well documented cases of basal

ganglia and thalamic tumours presenting withMDs and ipsilateral hemiparesis had beenpublished earlier21 26 sparing of the corticospi-nal tract was regarded as essential for MDs tooccur.23 25 In contrast, our data show thattremors as well as dystonia and chorea may beassociated with a mild or moderate degree ofhemiparesis. Comparing the patients with andwithout MDs we did not find a significantdifference in the frequency of corticospinaltract dysfunction.

Unlike previous series and case reports onhistologically verified astrocytomas of the basalganglia and the thalamus the distribution ofMDs differs in our study2 7 8 10 12 21-23 251(table 3). We observed comparatively morecases with dystonia and chorea. In patientswith dystonia the thalamus was involved morefrequently than the caudate or putamen. How-ever, there may be secondary putaminalinvolvement due to the mass effect of thetumour. Clinicopathological correlationsreported previously demonstrate primarylesions in caudate or putamen in the majorityof cases with secondary dystonia. 12 42 43 Chor-eatic hyperkinesias, which were transient in ourpatients, seem to be rare in basal gangliatumours. We found only one case in theliterature and six of "choreoathetosis". Hemi-ballismus was described in a cystic midbrainglioma, 4 but as far as we know, not in thalamicor basal ganglia astrocytomas.Tremor was the most frequent MD in our

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Table 3 Movement disorders in patients with histologically verified astrocytomas of thethalamus and the basal ganglia: literature review and present series

Present Study Literature Review By first AuthorMovement Disorder Number of Patients Number of Patients (Number of Patients)

Tremor/Parkinsonism 12 47 Alexander (1), Arseni (5),Bailey (1), Brzezicki (1),Cheek (3), Coers (1),Garcin (1), Globus (2),Kelly (1), Kulali (1),McGirr (1), Mettler (1),Ody (3), Polyzoidis (1),Roth (5), Sciarra 3),' Smyth (1),Tolosa (15)27 S1II

Myoclonus 1 -Chorea/Ballismus 1 -

Chorea 3 1 Alexander (1)27"Choreoathetosis" (2) 6 Arseni (2), Millichap (1),

Ody (1), Parker (1),Roth (1)21 23 26 63

Dystonia/Athetosis 8 7 Chorobski (1), Marsden (2),Masten (1), Narbona (I38Sciarra (1), Urechia (1)

series as well as in the literature. Interpretationof the literature is limited, since in the 47 casesof basal ganglia and thalamic astrocytomas wecollected from 1927-91 (table 3) data con-cerning frequency and characteristics of thetremor were not always reported and theinterpretations have differed considerably.While McKissock pointed out that the tremorwas not "parkinsonian" in any of the eightcases he presented,3 it was stated to be"parkinsonian" in all patients with tremor inother series.6 'O As was pointed out by Ody,"rigor" or "rigidity" in some patients withspace occupying cerebral tumours may havebeen more a sign of partial decerebration thana Parkinsonian feature.21 Although the tremorobserved in some patients of this study had afrequency corresponding to Parkinsoniantremor, it differed in other characteristics. Itwas present on, or even only on, intendedmovements and was not accompanied byrigidity. Only one patient had tumour-inducedParkinsonism. Categorisation of these tremorsraises certain difficulties.16 44 45 Tremors havebeen denominated according to proven orassumed distinct lesions generating differenttypes of tremor. In our opinion, however,denotation following clinical phenomenashould not have topological or anatomicalimplications: "midbrain tremor", "rubraltremor" or "cerebellar tremor at rest". Thus wewould not label the tremor in our patients as

"thalamic", although there is evidence thattremor-driving impulses might originate in thethalamus.46 Furthermore, as stated above,axial CT scans may be inadequate to deter-mine exactly the direct or indirect extension ofinvolvement of the upper midbrain. Involve-ment of thalamic projections from cerebellarnuclei might be the common denominator forpostural and intention tremors, with an addi-tional structural or functional lesion of the rednucleus and/or the substantia nigra and theirprojections being necessary to produce resttremor. Tumour-induced Parkinsonism seemsto be more common in extra-axial than inintrinsic tumours.33We could not find previous reports on the

effect of thalamic or basal ganglia tumours onpre-existing movement disorders. In patient16, who presumably had essential tremor, the

rightsided tremor may have been less markedbecause of slight hemiparesis. However, it isalso conceivable that it was reduced due to thetumour being located mainly in the left ven-trolateral thalamus exerting a functional sup-pression.We think that clinicopathological correla-

tions in thalamic and basal ganglia astro-cytomas should be made only with certainreservations. Interaction of different mechan-isms may or may not lead to clinical symptoms.Functional lesions of the structures involvedprimarily by the tumour might result from"internal" compression of neurons or neuralpathways or from altered metabolism byreduced vascular supply. But tumours or aperitumoural oedema may also induce symp-toms by "external" compression of adjacentstructures or their vascular supply.47 The ques-tion has been raised as to why tumours of thebasal ganglia are not associated with MDsmore often. The situation becomes more com-plex, since these tumours may also involvestructures ofthe basal ganglia which are knownto abolish or to reduce MDs when lesioned-(predominantly the ventrolateral thalamus, thezona incerta, the pulvinar thalami and theinternal pallidum and their fibre connections).Again these structures may be functionallydamaged by "external" compression.

Neither necropsy findings nor the presentcomparative analysis of in vivo CT datashowed topographical differences in thalamicand basal ganglia astrocytomas that do or donot cause MDs. However, tumours which areapparently identical on imaging studies maynevertheless differ in functional terms. Theseaspects might be at least partly explained usingmodels such as that of parallel distributedprocessing48 provided more detailed informa-tion were available. However, the functionalstate of the basal ganglia in brain tumourscausing MDs has only rarely been studied. In acase of a left frontal meningioma with righthemi-Parkinsonism PET indicated impairedoxygen metabolism and tissue perfusion in thestriatopallidal region.49 In one case of Parkin-sonism secondary to a craniopharyngiomabiochemical findings on necropsy revealedconsiderably reduced striatal catecholaminesand severely decreased dopamine receptorbinding sites in the caudate.5" Further func-tional studies are needed and should providedeeper insights into the pathophysiologicalprocesses underlying the generation of move-ment disorders.

We thank G Pfister, H Forster and V Sonntag-O'Brien fortechnical assistance and preparation of the manuscript and HKrauss for translation of the French literature.

1 Arseni C. Tumors of the basal ganglia. Arch Neurol Psychiat1958;80: 18-24.

2 Cheek WR, Taveras JM. Thalamic tumors. J Neurosurg1966;24:505-1 3.

3 McKissock W, Paine KWE. Primary tumours of thethalamus. Brain 1958;81:41-63.

4 Tovi D, Schisano G, Liliequist B. Primary tumors of theregion of the thalamus. J Neurosurg 1961;18:730-40.

5 Bemstein M, Hoffman HJ, Halliday WC, Hendrick EB,Humphreys RB. Thalamic tumors in children. J Neurosurg1984;61:649-56.

6 Paillas JE, Legre J, Alliez B, Dufour M. Approche dudiagnostic et du traitement des tumeurs des noyaux gris

1166 on 17 F

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/J N

eurol Neurosurg P

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ber 1992. Dow

nloaded from

Movement disorders in astrocytomas of the basal ganglia and the thalamus

centraux. Neurochirurgie 1970;216:89-115.7 Kelly PJ. Stereotactic biopsy and resection of thalamic

astrocytomas. Neurosurgery 1989;25:185-95.8 McGirr SJ, Kelly PJ, Scheithauer BW. Stereotactic resection

of juvenile pilocytic astrocytomas of the thalamus andbasal ganglia. Neurosurgery 1987;20:447-52.

9 Beks JWF, Bouma GJ, Journee HL. Tumours of thethalamic region. Acta Neurochir 1987;85: 125-7.

10 Tolosa E, Vilato J, Fuenmayor P. Parkinsonisme tumoral.Neurochirurgie 1966;12:555-60.

11 Lakke JPWF, Barbeau A, Duvoisin RC, Gerstenbrand F,Marsden CD, Stern G. Classification of extrapyramidaldisorders. J Neurol Sci 1981;51:311-27.

12 Marsden CD, Obeso JA, Zarranz nJ, Lang AE. Theanatomical basis of symptomatic hemidystonia. Brain1985;108:463-83.

13 Krauss JK, Mohadjer M, Wakhloo AK, Mundinger F.Dystonia and akinesia due to pallidoputaminal lesionsafter disulfiram intoxication. Mov Disord 1991 ;6:166-70.

14 Dewey RB Jr, Jankovic J. Hemiballism-Hemichorea. Clin-ical and Pharmacological Findings in 21 Patients. ArchNeurol 1989;46:862-7.

15 Krauss JK, Mohadjer M, Nobbe F, Mundinger F. Bilateralballismus in children. Child's Nerv Syst 199 1;7:342-6.

16 Sabra AF, Hallett M. Action tremor with alternating activityin antagonist muscles. Neurology 1984;34: 151-6.

17 Riechert T, Mundinger F. Beschreibung und Anwendungeines Zielgerates fur stereotaktische Hirnoperationen(2. Modell). Acta Neurochir 1956;3:308-37.

18 Mundinger F. CT-stereotactic biopsy for optimizing thetherapy of intracranial processes. Acta Neurochir Suppl1985;35:70-4.

19 Mundinger F, Braus DF, Krauss JK, Birg W Long-termoutcome of 89 low-grade brain-stem gliomas after inter-stitial radiation therapy. J Neurosurg 1991 ;75:740-6.

20 Karnofsky DA, Burchenal JH. The clinical evaluation ofchemotherapeutic agents in cancer. In: MacLeod CM,ed. Evaluation of Chemotherapeutic Agents. New York:Columbia University Press, 1949:191-205.

21 Ody F. Tumors of the basal ganglia. Arch Neurol Psychiatr1932;27:249-69.

22 Globus JH, Kuhlenbeck H. Tumors of the striatothalamicand related regions. Arch Pathol 1942;34:674-734.

23 Roth RL, Bebin J. Cerebral hemispheric tumors andextrapyramidal signs and symptoms. Neurology 1958;8:277-84.

24 Hirose G, Lombroso CT, Eisenberg H. Thalamic tumors inchildhood. Arch Neurol 1975;32:740-4.

25 Arseni C, Nash F, Samitka DC. Extra-pyramidal syndromeswith intracranial tumour. Psychiat Neurol 1959;137:230-44.

26 Mettler FA, Davidoff LM, Grimes R. Static tremor withhemiplegia. Arch Neurol Psychiat 1947;57:423-9.

27 Alexander L. The fundamental types of histopathologicchanges encountered in cases of athetosis and paralysisagitans. In: Basal ganglia, ARNMD: XXI. Baltimore:Williams and Wilkins, 1942:464-8. (cited by Roth etBebin).

28 Bailey P, Buchanan DN, Bucy PC. Intracranial tumors ofinfancy and childhood. Chicago: University of ChicagoPress, 1939.

29 Brzezicki E. Der Parkinsonismus symptomaticus. SchweizArch Neurol Psychiat 1929;25:56-88.

30 Coers C, Kleyntjens F, Brihaye J. Syndrome parkinsoniend'origine tumorale. Acta Neurol Belg 1952;52:737-65.

31 Garcin R, Klein MR, Kipfer M, Bozec L. Hemisyndromeparkinsonien gauche par tumeur fronto-calleuse droitedisparaissant completement apres ablation de celle-ci.Rev Neurol 1943;3:80-3.

32 Kulali A, Tugtekin M, Utkiir Y, Erkurt S. Ipsilateralhemiparkinsonism secondary to an astrocytoma. J NeurolNeurosurg Psychiatry 199 1;54:653.

33 Polyzoidis KS, McQueen JD, Rajput AH, MacFadyen DJ.Parkinsonism as a manifestation of brain tumor. SurgNeurol 1985;23:59-63.

34 Sciarra D, Sproflin BE. Symptoms and signs referable tothe basal ganglia in brain tumor. Arch Neurol Psychiat1953;69:450-61.

35 Smyth GE, Stern K. Tumours of the thalamus-a clin-icopathological study. Brain 1938;61:339-74.

36 Millichap JG, Miller RH, Backus RE. Intracranial tumors inchildhood. JAMA 1962;179:589-93.

37 Parker HL. Tumors of the brain simulating epidemicencephalitis and involving the third ventricle, the fourthventricle, and the basal ganglia: report of three cases.Jf Nerv Ment Dis 1923;58:1-15.

38 Chorobski J. Involuntary movements in patients withintracranial tumors. Arch Neurol 1962;6:27-42.

39 Masten MG. Spongioblastoma of diencephalon. 7 NervMent Dis 1938;87:322-4.

40 Narbona J, Obeso JA, Tunon T, Martinez-Lage JM,Marsden CD. Hemi-dystonia secondary to localised basalganglia tumour. J Neurol Neurosurg Psychiatry 1984;47:704-9.

41 Urechia CI, Dragomir L, Usinievici G. Spasme de torsionunilateral cause par une tumeur cerebrale. Confin Neurol1942/43;5:271-80.

42 Pettigrew LC, Jankovic J. Hemidystonia: a report of 22patients and a review of the literature. Jf Neurol NeurosurgPsychiatry 1985;48:650-7.

43 Krauss JK, Mohadjer M, Braus DF, Wakhloo AK, Nobbe F,Mundinger F. Dystonia following head trauma-a reportof 9 patients and review of the literature. Mov Disord1992;7:263-72.

44 Goldberger ME, Growden JH. Tremor at rest followingcerebellar lesions in monkeys: effect of L-Dopa admin-istration. Brain Research 1971;27:183-7.

45 Koppel BS, Daras M. "Rubral" tremor due to midbraintoxoplasma abscess. Mov Disord 1990;5:254-6.

46 Narabayashi H. Tremor mechanisms. In: Schaltenbrand G,Walker AE, eds. Stereotaxy of the human brain. Stuttgart,NewYork: Thieme, 1982:510-4.

47 Krauss JK, Mohadjer M, Nobbe F, Scheremet R. Hemidys-tonia due to a contralateral parieto-occipital metastasis:disappearance after removal of the mass lesion. Neurology1991;41:1519-20.

48 Mitchell U, Brotchie JM, Brown GDA, Crossman AR.Modeling the functional organization of the basal ganglia.A parallel distributed approach. Mov Disord 1991;6:189-204.

49 Leenders KL, Findley U, Cleeves L. PET before and aftersurgery for tumor-induced parkinsonism. Neurology1986;36: 1074-8.

50 Garcia de Yebenes J, Gervas nJ, Iglesias J, Mena MA, DelRio RM, Somoza E. Biochemical findings in a case ofparkinsonism secondary to brain tumor. Ann Neurol1982;11:313-6.

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