85454ournal of Neurology, Neurosurgery, and Psychiatry 1992;55:854-856 SHORT REPORT Lacunar thalamic stroke with pure cerebellar and proprioceptive deficits Jose A Gutrecht, Amir A Zamani, Deepak N Pandya Abstract Case reports of two patients with cerebellar ataxia and proprioceptive sensory loss are presented. MRI of the brain revealed lesions of the ventroposterior part of the thalamus. These patients illustrate clinically the anatomical independence of cerebelkar and sensory pathways in the thalamus. We suggest that the ataxic deficit is caused by interruption of cerebellar outflow pathways in the thalamus and not secondary to sensory deafferentation. (3 Neurol Neurosurg Psychiatry 1992;55:854-856) Department of Neurology, Lahey Clinic Medical Center, Burlington, Massachusetts J A Gutrecht Department of Radiology, Brigham and Women's Hospital, Boston, Massachusetts A A Zamani Department of Anatomy and Neurology, Boston University Medical School, Boston, Massachusetts, and the Bedford Veterans Administration Hospital, Bedford, Massachusetts, USA D N Pandya Correspondence to: Dr Gutrecht, Department of Neurology, Lahey Clinic Medical Center, 41 Mall Road, Burlington, MA 01805. Received 12 September 1991 and in revised form 6 December 1991. Accepted 18 December 1991 Ischaemic lacunar strokes occur frequently in the thalamus.' 2 Small haemorrhages in the thalamus may also produce lacunar strokes3 4 with similar clinical deficits.5 The lateral syndrome is the most common and has one of the best known cluster of findings of the thalamic syndromes.6This syndrome and its anatomical location of the responsible lesion were first described by Dejerine and Roussy7 in 1906. Reported cases of "pure" thalamic syndromes with deficits in only one or two tracts or systems deficits are rare.8-" We report two cases of lacunar thalamic stroke that produced a contralateral combination of a cerebellar deficit and proprioceptive sensory loss. Case reports A 63 year old right handed man was seen at the Lahey Clinic Medical Center because of the sudden onset of dysaesthesia of the right side of the face and distal right limbs and an inability to walk that lasted for one hour. Three days earlier, he had had an episode of nausea, decreased concentration, and an inability to read that lasted for a few hours. The patient has diabetes mellitus and hypertension, and he was taking tolbutamide and metoprolol. Neurological examination demonstrated dysdiadochokinesis and dysmetria with terminal tremor in the right limbs that did not worsen with closed eyes. A mild subjective decreased pain sensation was observed in the right side of the face and right hand, but touch, position, and temperature sensation were normal. Two-point discrimination and stereognosis were greatly decreased in the right hand. No weakness was noted. Stretch reflexes were hypoactive but symmetrical. Plantar reflexes were normal. MRI of the brain showed a small lesion in the lateral posterior aspect of the left thalamus (fig 1). No source of an embolus was found. Cerebral angiography was not performed. The deficits abated in several days. A 74 year old right handed man complained of sudden onset of inability to control the right arm and leg despite normal strength, unsteadiness, and a "frozen feeling" in the right side of the face and right hand. History included hypertension treated with methyldopa and triamterene/hydrochlorothiazide. Mild dysarthria, inconsistently decreased pain sensation, dysdiadochokinesis, and decomposition of movements in the right limbs were noted. CT of the head showed a small left lateral thalamic haemorrhage. The findings improved in a few weeks. Neurological examination at the Lahey Clinic seven months later revealed slightly decreased touch and pain sensations but normal temperature sensation and position sense with moderately diminished two-point discrimination and graphaesthesia in the right hand. Mild dysmetria, terminal tremor, and decreased finger and foot tapping ability were present on the right side. No weakness was present, and the stretch reflexes were normoactive and symmetrical. Plantar reflexes were normal. MRI of the brain performed .5 . ....S. *A4~~~~~~~~~~~.. ... ...S..;...: Figure 1 (Case 1). Coronal T,-weighted (Magneton 1 *0 T, TR 065 s, TE 17 ms, 3 mm slice) image through posterior thalamic regions demonstrates a well-defined irregular area of low intensity in the lateral portion of the left thalamus. Lacunar thalamic stroke with pure cerebeUlar and proprioceptive deficits Figure 2 (Case 2). Coronal T,-weighted (Magneton 1 -07T TR 0-65 s, TE 20 ms, 4 mm slice) image through posterior thalamic regions demonstrates a linear area of low signal intensity in the lateral portion of the left thalamus. 855 Lack of causal correlation of sensory and cerebellar deficits was further suggested by the case reported by Garcin and Lapresle" in 1969. Their patient had no sensory deficits, and the lacuna found at necropsy was on the medial aspect of the contralateral thalamus. In the series of Bogousslavsky et al"4 five of 18 patients with the lateral thalamic syndrome had severe ataxia "unrelated" to sensory deficits. Other cases of sensory deficits without ataxia have been reported,5 thus strongly suggesting 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 incoordination 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 cerebellum and terminate in the cell-sparse ventral Discussion posterolateral nucleus, oral division and venThalamic 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 adjasubthalamic 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 thaladuce 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 conceivdromes 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 accordsensory loss,8 pure sensory deficit,9 ataxic ing to its location. The size and location of the hemiparesis,1' and cerebellar syndromes" lacunar lesion would be defined by the terrihave been reported. tory of the blood supply and size of the Our two patients had deficits in the proprio- terminal perforating branches of the thalamoceptive 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 a lesion in the ventral posterior nucleus. The of the cerebellar and proprioceptive sensation origin of hemiataxia 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. Neurolenter the thalamus, although no pathological ogy 1965;15:774-84. JM, Bogousslavsky J. Lacunar syndromes. In: confirmation was available. Dejerine and 2 Orgogozo Toole JF, ed. Handbook of dinical neurology. Vascular diseases Part II. NewYork: Elsevier, 1989:235-69. Roussy,7 however, believed that the ataxic 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. 4 Millikan C, Futrell N. The fallacy of the lacune hypothesis. sensory deficits. In 1955, Garcin'3 presented 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 proprioUemura K. CT classification of small thalamic hemorrhages and their clinical implications. Neurology ceptive sensation in the same limbs subsided. 1986;36: 165-72. Anatomical examination of the brain revealed a 6 Martin JJ. Thalamic syndromes. In: Vinken PJ, Bruyn GW, Handbook of clinical neurology. Amsterdam: Northeds, lacuna in the posterolateral region of the Holland, 1968:469-96. contralateral thalamus. He'3 stated that the cerebellar deficits were explained by the thalamic lesion without subthalamic involvement. 7 Dejerine J, Roussy G. Le syndrome thalamique (1). Rev Neurol 1906;12:521-32. 8 Fisher CM. Pure sensory stroke involving face, arm, and leg. Neurology 1965;15:76-80. 856 Gutrecht, Zamani, Pandya 9 Sacco RL, Bello JA, Traub R, Brust JCM. Selective proprioceptive loss from a thalamic lacunar stroke. Stroke 1987;18:1160-3. 10 Boiten J, Lodder J. Ataxic hemiparesis following thalamic infarction. Stroke 1990;21:339-40. 11 Garcin R, Lapresle J. 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