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  • Title: Pure sensory syndromes in thalamic stroke.
    Author: Paciaroni M, Bogousslavsky J.
    Journal: Eur Neurol; 1998; 39(4):211-7. PubMed ID: 9635471.
    Abstract:
    We studied 25 patients with an acute thalamic stroke (infarct or hemorrhage) on CT or MRI scan and sensory dysfunction, among the 3,628 patients with first-time stroke included in the Lausanne Stroke Registry. Twelve patients had a right-sided infarct, 11 a left-sided infarct, and 2 a left-sided thalamic hemorrhage. Sensory symptoms or signs were the only clinical abnormality. The presumed causes of stroke were small artery disease in 21 patients including both cases of hemorrhage, emboligenic heart disease in 2, while the etiology of ischemic stroke was undetermined in 2 patients. Nine patients had a loss of all modalities of sensation with faciobrachiocrural distribution, 5 patients suffered dissociated sensory loss with faciobrachiocrural distribution and 11 patients showed a dissociated involvement of sensation with a partial distribution pattern. The inferolateral region (thalamogeniculate arteries) was involved in all patients. Six patients complained of pain and/or dysesthesias during the stroke; 5 of them had involvement of the nucleus ventrocaudalis (in 3 with damage to the nucleus ventro-oralis intermedius, and in one to the pulvinar) and 1 patient had involvement of the nucleus ventro-oralis intermedius. Eighteen patients complained 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 ventro-oralis intermedius, and nucleus ventro-oralis externus, and in one with damage to the nucleus parvocellularis and pulvinar). Four patients developed delayed pain and/or dysesthesias; all of them had involvement of the nucleus ventrocaudalis (in 1 with damage to the nucleus parvocellularis and pulvinar). Time lag from stroke onset to developing pain ranged from 2 to 15 days (mean 10.5 days). One patient with dissociated involvement of sensation with a partial distribution pattern had paresthesias and dissociated hemisensory loss involving position sense without pain and temperature sensations. This patient had involvement of the posterolateral part of the nucleus ventrocaudalis. In conclusion, sensory dysfunction and delayed pain are more often found in thalamic lesions that involve the nucleus ventrocaudalis, and nucleus ventro-oralis intermedius. Restricted sensory abnormalities correlate with very small lesions located in critical areas within these nuclei.
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