42242ournal ofNeurology, Neurosurgery, and Psychiatry 1995;58:422-427

Vascular ataxic : a re-evaluation J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.58.4.422 on 1 April 1995. Downloaded from

Thierry Moulin, Julien Bogousslavsky, Jean-Luc Chopard, Joseph Ghika, Thierry Crepin-Leblond, Valerie Martin, Philippe Maeder

Abstract reports emphasised several sites, Ataxic hemiparesis is commonly consid- including the and frontal lobe.6-9 ered as one of the "typical" lacunar syn- Fisher introduced the term ataxic hemi- dromes. Using the prospective in 1978 to designate a clinical picture registries from Lausanne and Besancon, associating hemiparesis with ipsilateral 100 patients were selected consecutively .10 He emphasised that the lesion might (73% men, 27% women; age 64-7 (SD be the result of an infarct in the , corona 13-6) years) with a first stroke and ataxic radiata, or , and that it is sug- hemiparesis (hemiparesis or pyramidal gestive of "lacunar infarction" (a small infarct signs and ipsilateral incoordination with- in the territory of a deep perforator due to out sensory loss). CT or MRI was small disease)."* 12 Initially described as performed on all patients. A primary a homolateral ataxia and crural paresis,'3 haemorrhage was present in 5%, an ataxic hemiparesis is currently defined by the infarct in 72%, isolated leukoaraiosis in association of hemiparesis or corticospinal 9%, and no apparent abnormality in 14%. signs (weakness or , Babinski's The locations of were the internal sign) with ipsilateral cerebellar incoordina- capsule (39%), pons (19%), thalamus tion. This picture has usually been explained (13%), corona radiata (13%), lentiform by a lesion in the white matter, involving both nucleus (8%), (superior the corticospinal and the cerebello-thalamo- cerebellar artery territory) (4%), and cortico-ponto-cerebellar tracts'0 12; however, it frontal cortex (anterior cerebral artery has also been found to involve the thalamus territory) (4%). The clinical features of or cortical areas.'4 16 Ataxic hemiparesis is ataxic hemiparesis with different loca- not the commonest "lacunar syndrome" tions were almost identical. Only minor (<10%).17 19 associated signs allowed the localisation Our purpose was to study the features of of the lesions (paraesthesiae with a lesion ataxic hemiparesis and its association with in the thalamus; nystagmus or lacunar infarction in a general population with with a cerebellar or pontine location). first stroke. Crural paresis with homolateral ataxia was seen only with cortical paramedian frontal lesions. Presumed hypertensive Methods http://jnnp.bmj.com/ small artery disease was not always We studied 100 patients with ataxic hemi- found, but was still the leading cause of paresis and first stroke. The patients were stroke, being present in 59% of the selected consecutively between 1986 and patients and in 62% of those with small 1990 from all patients admitted to two deep infarcts. A potential source of primary care centres; all patients were part of (arterial or cardiac) was found prospective stroke registries (Lausanne and

in one fourth of the patients. Therefore B¢sancon). All were examined by at least one on October 1, 2021 by guest. Protected copyright. no definite association can be made of us. Selection criteria included: (a) hemi- Service de Neurologie, between ataxic hemiparesis and lacunar paresis with a motor deficit of mild or moder- Hopital J Minjoz, infarction. In particular, so called ate severity with or without increased tendon CHU Besganon, uncommon lesion locations may not be reflexes and Babinski's sign. Involvement of France rare. a T Moulin After extensive investigations the face, upper limb, and lower limb was J-L Chopard diagnosis of lacunar infarct can be assessed; (b) cerebellar type of incoordination, T Crepin-Leblond retained in only slightly more than half of with , defined as poorly controlled V Martin the cases. direction movement on finger to nose or fin- Service de Neurologie, ger to finger and heel to knee tests nor- CHU Vaudois, (with Lausanne, (J Neurol Neurosurg Psychiatry 1995;58:422-427) mal initiation and velocity but irregular Switzerland acceleration or deceleration producing oscilla- J Bogousslavsky tions near the target with a series of secondary J Ghika P Maeder Keywords: ataxic hemiparesis; lacunar infarction movements, eyes open or closed), rebound Correspondence to: phenomenon (Steward-Holmes test), and Dr Julien Bogousslavsky, Several decades ago, French neurologists ; (c) no sensory deficit, but Service de Neurologie, CHU Vaudois, CH-1O1 1 wrote on the clinical aspect of ataxic hemi- subjective dyaesthesia or paraesthesia was Lausanne, Switzerland. paresis, though they did not use this term.'-4 allowed, as was dysarthria or gaze evoked nys- Received 22 September The first vascular case was reported by tagmus; (d) no evidence for , apraxia, 1994 and in revised form 21 December 1994 Nicolesco et a15 in a patient with an anterior other neuropsychological dysfunction or Accepted 22 December 1994 cerebral artery territory infarct. Further visual field defect. Vascular ataxic hemiparesis: a re-evaluation 423

Table 1 Distribution ofrisk factors and type ofstroke J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.58.4.422 on 1 April 1995. Downloaded from No lesion Deep Superficial Primary leukoairosis infarct infarct infarct haemorrhage Total Risk factor (n = 23) (n = 53) (n = 14) (n = 6*) (n = 4*) (n = 100) Age (y) 69-9 63-6 62-2 616 59-5 64-7 (SD) (9 9) (13-6) (14.1) (21 6) (15-8) (13-5) Male/female 16/7 40/12 10/5 5/1 2/2 (% male) (69 5) (76-9) (66 6) (83 3) (50) (73) 19t 28 lit 3 1 (62) (%) (83) (53) (79) (50) (25) 3 9 3 1 0 (16) (%) (13) (17) (21) (16) 00 Smoking 6 21 5 4 3 (39) (%) (26) (40) (36) (67) (75) Hypercholest 6 13 3 1 1 (24) (%) (26) (25) (21) (16) (25) PCV >45% 11 28 5 2 2 (48) (%) (47) (53) (36) (33) (50) Previous TIAs 1 9 3 1 1 (15) % (4) (16) (21) (16) (25) *One primary haemorrhage was considered as an intrainfarct haematoma. tPercentage among patients with brainstem infarct or without lesion differed significantly (p > 0 05) from other patients. Hypercholest = Hypercholesterolaemia; PCV = packed cell volume.

The protocol of investigations and analysis tory of thalamogeniculate ); (e) frontal of associated factors followed the guidelines of cortex (superficial territory of anterior cere- the Lausanne stroke registry, as reported in bral artery); (t) pons (territory of paramedian detail previously.'9 Risk factors included arteries); (g) corona radiata/centrum ovale hypertension; blood pressure higher than (involving the territory of medullary branches 160/90 mm Hg at least twice before the of the superficial branches of middle cerebral stroke; diabetes mellitus; known fasting blood artery); (h) lentiform nucleus and adjacent glucose >6 mmol/l before the stroke; hyper- part of internal capsule (territory of lenticulo- cholesterolaemia; fasting blood cholesterol striate arteries). The location and volume of higher than 6-5 mmol/l, and current cigarette lesions were determined independently by at smoking. All patients had Doppler ultra- least two of us (including a neurologist and a sounds and B mode echotomography, ECG, radiologist).22 and standard blood and urine tests. Presumed infarct aetiologies were separated Angiography, trans-thoracic/trans-oesopha- into the following groups as previously geal echocardiography, and transcranial defined'9: large artery disease (>50% Doppler were performed in selected patients. in the appropriate large artery); potential car- In selected instances CT and MRI were diac source of embolism; small artery disease performed at least once within one month of (hypertension or diabetes mellitus, in the the stroke; all emergency CTs were followed absence of a potential arterial or cardiac by another CT or MRI four to 10 days later. source of embolism, and with a <15 mm The topographic diagnosis of infarct or infarct limited to the territory of a deep

primary haemorrhage was made from lesion perforator on CT); other aetiologies (dissec- http://jnnp.bmj.com/ mapping templates developed in the tion, haematological disorders, etc); and Lausanne stroke registry and elsewhere.2021 undetermined. The results of neuroimaging were classified Follow up data was obtained from the out- into different groups according to anatomical patient clinic. locations and vascular territories: (a) no lesion Statistical studies were carried out with visible; (b) leukoaraiosis, (c) posterior part of a descriptive univariate analysis X2 test posterior limb of internal capsule (territory of corrected by Fisher's test, and analysis of anterior choroidal artery); (d) thalamus (terri- variance (ANOVA) for volume measurement. on October 1, 2021 by guest. Protected copyright.

Results Table 2 Type ofstroke GENERAL CHARACTERISTICS Type ofstroke Number There were 51 patients from Lausanne and 49 from representing 4% of in No visible lesion 14 Besanqon, Leukoaraiosis 9 each centre. These two groups were identical Total 23 in sex, age distribution, risk factors, aetiolo- Infarcts 72 Superficial infarct 5 gies, and location of lesions. There was a pre- ACA pial territory 2(*) ponderance of men (73%). Mean age was SCA pial territory 3 Deep infarct 53 64-7 (SD 13-6) (table 1). Brainstem infarct 14 Pons (upper and medial part) 14 Primary haemorrhage 5 STROKE TYPE AND TOPOGRAPHY Lentiform nucleus 2 No lesion was found in 14 but 10 Corona radiata 1 patients, of Pons 1 these patients had only one CT and none had Lobar (intrainfarct haematoma; ACA) 1 * MRI. In nine patients, the only abnormality Total 100 was leukoaraiosis, which was found in nearly a *One primary haemorrhage was considered as an intrainfarct quarter of the patients. At least one lesion was haematoma. ACA = Anterior cerebral artery; SCA = superior cerebellar found in 77 patients (table 2). An infarct was artery. found in 94% of these cases (72/77) and a 424 Moulin, Bogousslavsky, Chopard, Ghika, Crepin-Leblond, Martin, Maeder

Table 3 Location ofstroke locations showed an expected difference, in J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.58.4.422 on 1 April 1995. Downloaded from Location Number (%0) Volume (ml) that smaller volumes were found in the pons and thalamus and volumes in the Frontal cortex (ACA territory) 3 (4) - larger Corona radiata: anterior part 10 (13) 0 71 + lentiform nucleus (table 3). Corona radiata: posterior part 9 (12) 0 45 Brain MRI was Internal capsule 21 (39) 0 39 performed in 23 patients; in Lentiform nucleus 6 (8) 1-24* half of them it confirmed the location of the Thalamus 10 (13) 0-12** lesion seen on Pons 15 (19) 018** CT, whereas in 39% of the Cerebellum (SCA territory) 3 (4) - cases it identified a new lesion. Brain MRI Total 77 (100) 0-43 showed a double lesion in 10-5% (8/77) of the ACA = Anterior cerebral artery; SCA = superior cerebellar artery. patients (pons and internal capsule in five < *p 0 05; **p < 0-01, ANOVA test. patients and corona radiata and internal cap- sule in three).

RISK FACTORS AND STROKE AETIOLOGY haemorrhage in 6% (one intrainfarct Tables 1 and 4 summarise the risk factors and haematoma located in anterior cerebral artery aetiology. The prevalence of risk factors in the territory, four primary haematomas located in small deep infarct group were: hypertension the corona radiata (one patient), pons (one (62%), smoking (39%), and hypercholestero- patient) or lentiform nucleus (two patients)). laemia (24%). Diabetes was less frequent There were 67 small deep infarcts (53 in the (16%). A potential arterial (10%) or cardiac anterior circulation and 14 in the posterior (12%) source of embolism was present in circulation) and five superficial infarcts. 22% of the patients. The commonest pre- The main location of lesion was the pos- sumed cause of stroke was hypertensive small terior part of the internal capsule (30/77; artery disease (59% overall). In deep and 39%) (table 3). As CT section variability brainstem infarcts, this frequency increased sometimes rendered the lesion more difficult (62%); several locations were associated with to localise, we considered that the lower part an even higher prevalence of small artery dis- of the internal capsule (21/30) and the supe- ease (thalamus (70%) and pons (80%)). rior part of the internal capsule located in the Presumed aetiologies were similarly distrib- posterior part of corona radiata near the ven- uted among the different subtypes and loca- tricular body (9/30) corresponded to the same tions of stroke, except for embolic events, territory. The volume of infarcts in these two which were more common with superficial areas was very close (0-39-0 45 ml) and the infarcts (50%) and with infarcts in the ante- clinical aspects were also similar. The second rior part of the corona radiata (40%). most common location was the pons, in 19% (15/77), followed by the anterior part of the CLINICAL PATTERNS (TABLE 5) corona radiata (remote from the ventricular Ataxia was present in both the upper and wall) in 13% (10/77), and thalamus in 13% lower limb in 98% of the patients. Dysmetria (10/77) (involving the territory of the thalamo- and hypermetria were present in all patients, geniculate artery (9/10) except in one patient but hypotonia or dysdiadochokinesis were with a thalamotuberal infarct). Two locations found in only one quarter of the patients. were rare: in 8% the was (6/77), lesion in the Face-upper limb-lower limb (FUL) hemi- http://jnnp.bmj.com/ lentiform nucleus (medial lenticulostriate paresis was almost as frequent with pontine arteries territory), being a primary haemor- (53%) and capsular lesions (57%). A partial rhage in two of the six patients; superficial motor deficit (FU, UL, or F/U/L) was more infarcts were found in 8% (6/77) of the common with lentiform nucleus (67%) patients, three infarcts involving the anterior involvement, followed by the anterior part of cerebral artery territory (one patient with the corona radiata (30%), the thalamus intrainfarct haematoma), and three the (20%), and the pons (17%). The frequency of superior cerebellar artery territory. was similar with lesion of the on October 1, 2021 by guest. Protected copyright. The volume of lesions was calculated only pons (60%), anterior part of the corona radi- for deep lesions (mean 0 43 ml). The statistical ata (50%), lentiform nucleus (50%), and thal- analysis of the volume according to different amus (40%). In infarcts involving the anterior

Table 4 Relationship between aetiology and stroke type (n (%)) No lesion Deep Brainstem Superficial Primary leucoairosis infarct infarct infarct haemorrhage Total Aetiology (n = 23) (n = 53) (n = 14) (n = 6*) (n= 4*) (n = 100) Undetermined 4 9 3 2 1 19 (17) (17) (22) (33) (25) Large artery 2 6 1 0 1 10 diseaset (9) (11) (7) (25) Embolic heart 1 8 0 3 0 12 disease (4) (15) (50) AF - 7 - 2 - 9 Akinesia 1 1 - - - 2 MVP - - - 1 - 1 Hypertensive 16 30 10 1 2 arteriolopathy (70) (57) (71) (17) (50) 59 *One primary haemorrhage was considered as an intra-infarct haematoma; t>50% stenosis in the appropriate artery or dissection. AF = Atrial ; MVP = mitral valve prolapse. Vascular ataxic hemiparesis: a re-evaluation 425

Table S Clinicalfeatures and stroke location J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.58.4.422 on 1 April 1995. Downloaded from Isolated No motor ataxic Static Location deficit FUL FUIUL FIUIL No F hemiparesis Paraesthesia Dysarthria ataxia Nystagmus Frontal cortex (ACA 0 0 0 0/0/3 3 3 1 territory) (100) (100) (100) 0 0 (33) 0 Corona radiata 0 4 0/3 0/2/1 5 6 1 3 3 anterior part (40) (30) (30) (50) (60) (10) (30) (30) 0 Corona radiata 0 4 3/0 0/1/1 2 4 0 4 1 posterior part (44) (30) (26) (22) (44) (44) (11) 0 Internal 12 5/1 0/2/1 3 11 3 2 6 capsule 0 (57) (29) (14) (14) (52) (14) (9 5) (29) 0 Lentiform 2 1/0/3 3 3 1 1 1 nucleus 0 (33) 0 (67) (50) (50) (17) (17) (17) 0 Thalamus 2 4 0/2 0/2/0 6 1 8 2 3 (20) (40) (20) (20) (60) (10) (80) (20) (30) 0 Pons 8 0/5 1/1/0 6 3 10 10 1 0 (53) (30) (17) (40) (20) 0 (67) (67) (7) Cerebellum (SCA 2 1/0 0/0/0 1 1 1 2 territory) 0 (67) (33) 0 (33) 0 (33) (33) (67) Total 2 36 9/15 2/7/3 28 32 14 23 26 3 (2-5) (47) (31) (16) (36) (42) (18) (30) (34) (4) F = Face; U = upper limb; L = lower limb; ACA = anterior cerebral artery; SCA = cerebellar artery.

cerebral artery territory, the clinical picture (53%). Nine patients had sequelae which lim- was characteristic, with crural and ited activities. A severe persisted in homolateral brachial ataxia. In half of the all patients with infarcts in the anterior cere- patients with thalamic infarct, pyramidal signs bral artery territory. were hardly apparent (only increased tendon reflexes or Babinski's sign). Minor associated signs such as ataxia when Discussion standing or dysarthria (67% of patients) sug- The existence of ataxic hemiparesis is contro- gested a pontine lesion. In thalamic infarct, versial, dysmetria sometimes being attributed paraesthesia or pain was frequent (80%). to corticospinal dysfunction itself.23 When the internal capsule was involved, Furthermore, its definition has been variable paraesthesia was less common (14%), while and at times confused with other clinical syn- ataxia and dysarthria was found in one dromes such as dysarthria-clumsy hand."024 quarter of the patients (23%). On the other This probably explains our difficulty in com- hand, no associated disturbance was found in paring the previously reported series with each 42% (32/77) of our patients (mainly with other. Overall, 4% of our patients with first involvement of the corona radiata (60%; stroke had ataxic hemiparesis, which corre- 6/10), internal capsule (50%; 15/30), or sponds with published findings.'7 18 25-28 lentiform nucleus (50%; 3/6). Although ataxia has usually been consid- ered to be severe in over two thirds of cases,29 it SHORT TERM EVOLUTION was often moderate in our patients, nearly The initial evolution of stroke followed the always involving the arm and leg with equal http://jnnp.bmj.com/ classical pattern of lacunar infarction with intensity. Some authors proposed that partial progressive or initially fluctuating onset in one hemiparesis, nystagmus, and dysarthria are third of the patients, with no differences suggestive of an infratentorial lesion,30 between stroke type (table 6). At one month, whereas facial sparing and lack of dysarthria no patient had died. Some weakness remained and paraesthesia would be associated with a in 20% of patients, and ataxia persisted in hemispherical lesion.29-31 Actually, minor

more than 60%. Most patients had no func- associated signs were common in our on October 1, 2021 by guest. Protected copyright. tional disability (38%) or had minor sequelae patients-for example, paraesthesia with thala- without limitation of previous activities mic infarct and dysarthria or ataxia with a pontine infarct. Hemiparesis involved the face, arm, and leg in half our patients with capsular, corona radiata or pontine stroke, but Table 6 Clinical course, outcome, and stroke type (n (%)) facial sparing was not uncommon, mainly No lesion Deep Brainstem Superficial Primary with lentiform nucleus lesions. Sudden onset leukoaraiosis infarct infarct infarct haemorrhage Total without progression occurred more often in Aetiology (n = 23) (n = 53) (n = 14) (n = 6*) (n = 4*) (n 100) our patients than in previous reports.'7 192632 Onset: Overall, short term recovery was good, espe- Sudden 16 32 12 6 4 (69) (60) (86) (100) (100) 70 cially in patients with small deep infarct or Progressive 5 13 1 haemorrhage.1458 26 The poorest functional (22) (25) (7) - - 19 Fluctuating 2 8 1 outcome may correspond to anterior cerebral (9) (15) (7) - _11 artery territory infarct with large cortical Evolution: No sequellae 9 18 7 3 1 involvement.33 (39) (34) (50) (50) (25) 38 The prevalence of risk factors in our group Moderate 12 30 7 1 3 (52) (57) (50) (17) (75) 53 with small deep infarcts was similar to previ- Severe 2 5 0 2 0 ous reports, except for diabetes, which was (9) (9) (33) 9 higher in our series.28 Presumed hypertensive One primary haemorrhage was considered as an intrainfarct haematoma. small artery disease is the main cause of small 426 Moulin, Bogousslavsky, Chopard, Ghika, Cripin-Leblond, Martin, Maeder

deep infarcts (lacunar infarct).171826-2934 Sixty most frequent location of lesion. Dysarthria two per cent of our cases fulfilled the criteria and gait ataxia were suggestive of this loca- J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.58.4.422 on 1 April 1995. Downloaded from for lacunar infarct, which was particularly tion. Clinical variants have also been common in the thalamus and the pons. On reported, with bilateral motor dysfunction,53 the other hand, potential cardiac or arterial trigeminal nerve impairment,54 or slight ataxia sources of embolism were not uncommon, in the contralateral lower extremity.55 We had mainly with superficial infarcts and infarcts in no patient with a infarct.56 the anterior part of the corona radiata.2' In Although ataxic hemiparesis was usually infarcts of the corona radiata, a haemody- due to a small deep infarct, superficial infarcts namic mechanism in the end zone territory were not uncommon and involved the ante- has been suggested.2' Low flow could be a rior cerebral artery or superior cerebellar consequence of several conditions, such as artery territories. Infarcts of the anterior cere- vascular , cardiac failure, hypo- bral artery territory with ataxic hemiparesis volaemic state, and hyperviscosity. No have commonly been reported.5'3 In these haemodynamic factor or trigger could be cases, the corticopontocerebellar pathway identified in our patients. (Tiirck's tract) may be affected within the In previous CT studies, lesions have been frontal lobe, explaining "cerebellar" ataxia." detected in 30-70% of the cases.'83536 Size The clinical features in our patients with ante- and location are probably determinant, so rior cerebral artery infarcts were characteris- that infarcts could remain undetected when tic, with crural weakness and homolateral small or located in the brainstem.'418 Only brachial ataxia. Interestingly, these features 14% of our patients had no visible lesion, were first reported as typical of a lacunar syn- however. In these cases, associated distur- drome, with a lesion in the pons." Our find- bances (nystagmus, gait ataxia, or dysarthria), ings do not support this. Infarcts in the partial hemiparesis, and presumed hyperten- superior cerebellar artery territory have rarely sive arteriolopathy were common. Only a few been reported with ataxic hemiparesis,5 more cases with a double lesion have been often with dysarthria clumsy hand syn- reported.3738 In a larger series using MRI, one drome.56 58 59 sixth of the cases examined for possible lacu- Thalamic lesions with ataxic hemiparesis nar infarct showed double lesions,35 as in our have rarely been reported,46 556>63 but we study. We found that ataxic hemiparesis can found this location to occur quite often. The develop after different types of stroke, includ- lateral part of the thalamus was the most com- ing haemorrhage, superficial infarct, or deep monly involved area. The dentatorubrothala- infarct. Haemorrhage as a cause of lacunar mic tracts may be affected within the syndrome has been reported in 5% of the ventrolateral part of the thalamus, so that in cases,5 35 in agreement with our own findings. thalamic infarct with ataxic hemiparesis, cere- Most haemorrhages involve the lenticulo- bellar ataxia may be explained by the inter- striate region,29 and other locations (internal ruption of this afferent pathway. The lack of capsule,39 capsulothalamic region,40 and reports of ataxic hemiparesis from thalamic pons4' 42) are rare. In our study, lenticulo- infarct may be because corticospinal signs are striate haemorrhages were larger than the usually slight; they are probably due to other haemorrhages associated with ataxic ischaemia or oedema compressing the adja- hemiparesis. On clinical grounds, it was not cent corticospinal tract.460 Another possible http://jnnp.bmj.com/ possible to distinguish ataxic hemiparesis due explanation of mild hemiparesis in thalamic to haemorrhage from ataxic hemiparesis due infarct is associated infarction of the adjacent to infarct. internal capsule, as the thalamogeniculate The most common lesion associated with branches may sometimes contribute to the ataxic hemiparesis was a small deep infarct.2829 supply to the innermost part of the posterior As in recent studies, 26 28-30 43-48 we found that limb of the internal capsule.64 Because of

the most common location was the posterior commonly associated sensory disturbances, on October 1, 2021 by guest. Protected copyright. limb of the internal capsule, usually also ataxic hemiparesis may be less frequent than involving the upper part of the internal cap- "hypaesthetic ataxic hemiparesis" or "painful sule near the ventricular body. By contrast ataxic hemiparesis".44 56 60 61 In "hemiataxia- with a recent study,49 we suggest that these hypaesthesia syndrome", also associated with infarcts may involve the anterior choroidal small lateral thalamic infarcts, no sign of cor- artery territory as they commonly extended ticospinal dysfunction is present.65 These four into the posterior limb of the internal capsule. syndromes, ataxic hemiparesis, hemiataxia- Identification of the supply to this area hypaesthesia syndrome, painful ataxic hemi- requires further study.4850 In ataxic hemipare- paresis, and hypaesthesic ataxic hemiparesis sis, few reports have documented involvement might be explained by variations in the blood of the anterior part of the corona radiata as in supply to the capsulothalamic region.66 When our series; such infarcts were clearly located the blood supply is predominantly through at some distance from the ventricular body, the posterior circulation (thalamogeniculate corresponding to the territory of the white arteries), infarction may be limited to the lat- matter medullary arteries,21 46 47 51 although eral thalamus, with hemiataxia-hypaesthesia part of this area could also be supplied by syndrome or painful ataxic hemiparesis. On the lateral lenticulostriate arteries.20 In the the other hand, when the blood supply is brainstem, pontine involvement in the terri- mainly through the anterior circulation (ante- tory of the basilar paramedian arteries is com- rior choroidal artery), infarction may involve mon. 0 35-384152 We found it to be the second both the thalamus and the internal capsule, Vascular ataxic hemiparesis: a re-evaluation 427

leading to hypaesthesic ataxic hemiparesis. 29 Sanguineti L, Tredici G, Beghi E, Aiello U, Bogliun G, Di

Lelio A, Tagliabue M. Ataxic hemiparesis syndrome: J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.58.4.422 on 1 April 1995. Downloaded from Our findings suggest that there is no defi- clinical and CT study of 20 new cases and review of the nite association between ataxic hemiparesis literature. ItalJ7 Neurol Sci 1986;7:51-9. 30 Huang CY, Lui FS. Ataxic hemiparesis, localization and and lacunar infarct due to small artery dis- clinical features. Stroke 1984;15:363-6. ease. Uncommon locations of lesion occur- 31 Combarros 0, Diez C, Cano J, Berciano J. Ataxic hemi- paresis with cheiro-oral syndrome in capsular infarction. for instance, in the thalamus, cerebellum, J7Neurol Neurosurg Psychiatry 1992;55:859. lentiform nucleus, and cerebral cortex. Minor 32 Norrving B, Cronqvist S. Clinical and radiologic features of lacunar versus nonlacunar minor stroke. 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