PURE SENSORY SYNDROMES IN THALAMIC STROKE

We studied 25 patients with an acute thalamic stroke (infarct or hemor rhage) on CT or MRI scan and sensory dysfunction, among the 3,628 pati ents with first-time stroke included in the Lausanne Stroke Registry. Twelve patients had a right-sided infarct, 11 a left-sided infarct, an d 2 a left-sided thalamic hemorrhage. Sensory symptoms or signs were t he only clinical abnormality. The presumed causes of stroke were small artery disease in 21 patients including both cases of hemorrhage, emb oligenic heart disease in 2, while the etiology of ischemic stroke was undetermined in 2 patients. Nine patients had a loss of all modalitie s of sensation with faciobrachiocrural distribution, 5 patients suffer ed dissociated sensory loss with faciobrachiocrural distribution and 1 1 patients showed a dissociated involvement of sensation with a partia l distribution pattern. The inferolateral region (thalamogeniculate ar teries) was involved in all patients. Six patients complained of pain and/or dysesthesias during the stroke; 5 of them had involvement of th e nucleus ventrocaudalis (in 3 with damage to the nucleus ventro-orali s intermedius, and in one to the pulvinar) and 1 patient had involveme nt of the nucleus ventro-oralis intermedius. Eighteen patients complai ned of paresthesias in the contralateral part of the body; 16 of them had involvement of the nucleus ventrocaudalis (in 4 with damage to the nucleus ventro-oralis intermedius, in 1 with damage to the nucleus ve ntro-oralis intermedius, and nucleus ventro-oralis externus, and in on e with damage to the nucleus parvocellularis and pulvinar). Four patie nts developed delayed pain and/or dysesthesias; all of them had involv ement of the nucleus ventrocaudalis (in 1 with damage to the nucleus p arvocellularis and pulvinar). Time lag from stroke onset to developing pain ranged from 2 to 15 days (mean 10.5 days). One patient with diss ociated involvement of sensation with a partial distribution pattern h ad paresthesias and dissociated hemisensory loss involving position se nse without pain and temperature sensations. This patient had involvem ent of the posterolateral part of the nucleus ventrocaudalis. In concl usion, sensory dysfunction and delayed pain are more often found in th alamic lesions that involve the nucleus ventrocaudalis, and nucleus ve ntro-oralis intermedius. Restricted sensory abnormalities correlate wi th very small lesions located in critical areas within these nuclei.