42242ournal ofNeurology, Neurosurgery, and Psychiatry 1995;58:422-427 Vascular ataxic hemiparesis: 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 lesion sites, Ataxic hemiparesis is commonly consid- including the thalamus and frontal lobe.6-9 ered as one of the "typical" lacunar syn- Fisher introduced the term ataxic hemi- dromes. Using the prospective stroke paresis in 1978 to designate a clinical picture registries from Lausanne and Besancon, associating hemiparesis with ipsilateral 100 patients were selected consecutively ataxia.10 He emphasised that the lesion might (73% men, 27% women; age 64-7 (SD be the result of an infarct in the pons, corona 13-6) years) with a first stroke and ataxic radiata, or internal capsule, 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). Brain CT or MRI was small artery 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 hyperreflexia, Babinski's The locations of lesions 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%), cerebellum (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 dysarthria 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 embolism (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 dysmetria, 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 dysdiadochokinesia; (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 aphasia, 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 Brainstem 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) Hypertension 19t 28 lit 3 1 (62) (%) (83) (53) (79) (50) (25) Diabetes 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 arteries); (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% stenosis 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 strokes 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).