85454ournal of , Neurosurgery, and Psychiatry 1992;55:854-856 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.9.854 on 1 September 1992. Downloaded from SHORT REPORT

Lacunar thalamic stroke with pure cerebellar and proprioceptive deficits

Jose A Gutrecht, Amir A Zamani, Deepak N Pandya

Abstract MRI of the showed a small lesion in the Case reports of two patients with cere- lateral posterior aspect of the left (fig bellar and proprioceptive sensory 1). No source of an embolus was found. loss are presented. MRI of the brain Cerebral angiography was not performed. The revealed lesions of the ventroposterior deficits abated in several days. part of the thalamus. These patients illus- A 74 year old right handed man complained trate clinically the anatomical independ- of sudden onset of inability to control the right ence ofcerebelkar and sensory pathways in arm and leg despite normal strength, unsteadi- the thalamus. We suggest that the ataxic ness, and a "frozen feeling" in the right side of deficit is caused by interruption of cere- the face and right hand. History included bellar outflow pathways in the thalamus hypertension treated with methyldopa and and not secondary to sensory deaffer- triamterene/hydrochlorothiazide. Mild dysar- entation. thria, inconsistently decreased pain sensation, dysdiadochokinesis, and decomposition of (3 Neurol Neurosurg Psychiatry 1992;55:854-856) movements in the right limbs were noted. CT of the head showed a small left lateral thalamic haemorrhage. The findings improved in a few Ischaemic lacunar strokes occur frequently in weeks. Neurological examination at the Lahey the thalamus.' 2 Small haemorrhages in the Clinic seven months later revealed slightly thalamus may also produce lacunar strokes3 4 decreased touch and pain sensations but nor- with similar clinical deficits.5 The lateral syn- mal temperature sensation and position sense drome is the most common and has one of the with moderately diminished two-point dis- best known cluster of findings of the thalamic crimination and graphaesthesia in the right syndromes.6This syndrome and its anatomical hand. Mild , terminal , and location of the responsible lesion were first decreased finger and foot tapping ability were described by Dejerine and Roussy7 in 1906. present on the right side. No weakness was Reported cases of "pure" thalamic syn- present, and the stretch reflexes were dromes with deficits in only one or two tracts normoactive and symmetrical. Plantar reflexes

or systems deficits are rare.8-" We report two were normal. MRI of the brain performed http://jnnp.bmj.com/ cases of lacunar thalamic stroke that produced Department of a contralateral combination of a cerebellar Neurology, Lahey Clinic Medical Center, deficit and proprioceptive sensory loss. Burlington, Massachusetts J A Gutrecht Case reports Department of A 63 year old right handed man was seen at the

Radiology, Brigham on September 27, 2021 by guest. Protected copyright. and Women's Hospital, Lahey Clinic Medical Center because of the Boston, Massachusetts sudden onset of dysaesthesia of the right side A A Zamani of the face and distal right limbs and an Department of inability to walk that lasted for one hour. Three Anatomy and Neurology, Boston days earlier, he had had an episode of nausea, University Medical decreased concentration, and an inability to School, Boston, read that lasted for a few hours. The patient has Massachusetts, and the Bedford Veterans diabetes mellitus and hypertension, and he was Administration taking tolbutamide and metoprolol. Neuro- Hospital, Bedford, logical examination demonstrated dysdiado- Massachusetts, USA chokinesis and dysmetria with terminal tremor D N Pandya in the right limbs that did not worsen with Correspondence to: Dr Gutrecht, Department of closed eyes. A mild subjective decreased pain Neurology, Lahey Clinic sensation was observed in the right side of the Medical Center, 41 Mall face and right hand, but touch, position, and .5 . *A4~~~~~~~~~~~.. ... Road, Burlington, MA ....S. ...S..;...: 01805. temperature sensation were normal. Two-point Received 12 September discrimination and stereognosis were greatly Figure 1 (Case 1). Coronal T,-weighted (Magneton 1 *0 1991 TR 065 TE 17 3 mm slice) image through and in revised form decreased in the right hand. No weakness was T, s, ms, 6 December 1991. noted. Stretch reflexes were hypoactive but posterior thalamic regions demonstrates a well-defined Accepted 18 December irregular area of low intensity in the lateral portion of the 1991 symmetrical. Plantar reflexes were normal. left thalamus. Lacunar thalamic stroke with pure cerebeUlar and proprioceptive deficits 855 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.9.854 on 1 September 1992. Downloaded from Figure 2 (Case 2). Lack of causal correlation of sensory and Coronal T,-weighted (Magneton 1-07T TR 0-65 cerebellar deficits was further suggested by the s, TE 20 ms, 4 mm slice) case reported by Garcin and Lapresle" in image through posterior 1969. Their patient had no sensory deficits, thalamic regions demonstrates a linear area and the lacuna found at necropsy was on the of low signal intensity in medial aspect of the contralateral thalamus. In the lateral portion of the the series of Bogousslavsky et al"4 five of 18 left thalamus. patients with the lateral thalamic syndrome had severe ataxia "unrelated" to sensory defi- cits. Other cases of sensory deficits without ataxia have been reported,5 thus strongly sug- gesting independence of ataxic limb movement and sensory deficits. The patient described by Boiten and Lodder'0 had cerebellar ataxia without sensory deficits. Sacco et al9 suggested that the limb ataxia in one patient with "pure" proprioceptive sensory loss was caused by the sensory deficits although the ataxic movements were present only in the arm and not in the leg despite sensory loss in both limbs. Recently, Dobato et al" suggested that the incoordina- tion of limb movements was caused by sensory deafferentation rather than involvement of cerebellar pathways. almost one year later showed a lesion in the Anatomical studies'6 in monkeys have lateral posterior area of the left thalamus (fig shown that dense input of cerebellar fibres to 2). the contralateral thalamus exists. These fibres arise in the dentate nucleus of the and terminate in the cell-sparse ventral Discussion posterolateral nucleus, oral division and ven- Thalamic ischaemic strokes frequently pro- tral lateral nucleus, caudal division of the duce multiple symptoms and signs because of thalamus whereas the posterior columns involvement of different nuclei as well as medial lemniscal fibres terminate in the adja- subthalamic regions that share blood supply. cent ventral posterolateral caudalis nucleus. Small haemorrhages in these areas may pro- These two tracts do not overlap in the thala- duce similar symptoms.5 The best known and mus. However, some overlap of cerebellar and most common thalamic syndrome is the classic spinothalamic fibres occurs as some of the lateral or Dejerine-Roussy7 syndrome. On the latter terminate in the ventral posterolateral other hand, well-defined "pure" thalamic syn- nucleus, oral division."6 It is therefore conceiv- dromes are uncommon. These "pure" syn- able that a small lesion in the ventroposterior dromes are characterised by involvement of area of the thalamus could produce deficits in one or two tracts. Isolated proprioceptive sensory or cerebellar pathways or both accord- sensory loss,8 pure sensory deficit,9 ataxic ing to its location. The size and location of the ,1' and cerebellar syndromes" lacunar lesion would be defined by the terri- http://jnnp.bmj.com/ have been reported. tory of the blood supply and size of the Our two patients had deficits in the proprio- terminal perforating branches of the thalamo- ceptive and more impressively, cerebellar geniculate arterial stalk or haemorrhage. domains. The cerebellar deficits were typical We suggest that the hemiataxia in our two and did not worsen with closure of the eyes. patients is independent of the sensory deficits Since the original description by Dejerine and and is caused by involvement of cerebellar

Roussy,7 sensory deficits have been ascribed to pathways in the thalamus. The independence on September 27, 2021 by guest. Protected copyright. a lesion in the ventral posterior nucleus. The of the cerebellar and proprioceptive sensation origin ofhemiataxia in these patients, however, systems agrees with the known neuroanatomy has caused some argument. In 1908, Vincent'2 and functional connections of the thalamus.'7 was the first to suggest that the cerebellar deficit was caused by involvement of cerebellar pathways in the subthalamic region as they 1 Fisher CM. Lacunes: Small, deep cerebral infarcts. Neurol- enter the thalamus, although no pathological ogy 1965;15:774-84. 2 Orgogozo JM, Bogousslavsky J. Lacunar syndromes. In: confirmation was available. Dejerine and Toole JF, ed. Handbook of dinical neurology. Vascular Roussy,7 however, believed that the ataxic diseases Part II. NewYork: Elsevier, 1989:235-69. 3 Mori E, Tabuchi M, Yamadori A. Lacunar syndrome due to component in the syndrome was from the intracerebral hemorrhage. Stroke 1 985;16:454-9. sensory deficits. In 1955, Garcin'3 presented 4 Millikan C, Futrell N. The fallacy of the lacune hypothesis. Stroke 1990;21:1251-7. the case of a patient who had increasing 5 Kawahara N, Sato K, Muraki M, Tanaka K, Kaneko M, hemiataxia while severe deficits of proprio- Uemura K. CT classification of small thalamic hemor- rhages and their clinical implications. Neurology ceptive sensation in the same limbs subsided. 1986;36: 165-72. Anatomical examination ofthe brain revealed a 6 Martin JJ. Thalamic syndromes. In: Vinken PJ, Bruyn GW, eds, Handbook of clinical neurology. Amsterdam: North- lacuna in the posterolateral region of the Holland, 1968:469-96. contralateral thalamus. He'3 stated that the 7 Dejerine J, Roussy G. Le syndrome thalamique (1). Rev Neurol 1906;12:521-32. cerebellar deficits were explained by the tha- 8 Fisher CM. Pure sensory stroke involving face, arm, and lamic lesion without subthalamic involvement. leg. Neurology 1965;15:76-80. 856 Gutrecht, Zamani, Pandya J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.9.854 on 1 September 1992. Downloaded from 9 Sacco RL, Bello JA, Traub R, Brust JCM. Selective 14 Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: proprioceptive loss from a thalamic lacunar stroke. Stroke Clinical syndromes, etiology, and prognosis. Neurology 1987;18:1160-3. 1988;38:837-48. 10 Boiten J, Lodder J. Ataxic hemiparesis following thalamic 15 Dobato JL, Villanueva JA, Gimenez-Roldan S. Sensory infarction. Stroke 1990;21:339-40. ataxic hemiparesis in thalamic hemorrhage. Stroke 11 Garcin R, Lapresle J. Incoordination cerebelleuse du 1990;21: 1749-53. membre inferieur par lesion localisee dans la region 16 Asanuma C, Thach WT, Jones EG. Distribution of cere- interne du thalamus contro-lateral. Rev Neurol 1969; bellar terminations and their relation to other afferent 120:5-13. terminations in the ventral lateral thalamic region of the 12 Vincent C. Syndrome thalamique avec troubles cerebelleux monkey. Brain Res Rev 1983;5:237-65. et vaso-asymetrie. Rev Neurol 1908;16:553-6. 17 Ilinsky IA, Kultas-Ilinsky K. Sagittal cytoarchitectonic maps 13 Garcin R Syndrome cerebello-thalamique par lesion local- of the Macaca mulatta thalamus with a revised nomen- isee du thalamus-Avec une digression sur le "signes de clature of the motor-related nuclei validated by observa- la main creuse" et son inter&t semeiologique. Rev Neurol tions on their connectivity. Comp Neurol 1987; 1955;93: 143-9. 262:331-64. http://jnnp.bmj.com/ on September 27, 2021 by guest. Protected copyright.