Abstract

We performed stereotactic VIM (ventralis intermedius), VIM-CL (centralis lateralis) or VIM-Vcpc (ventralis caudalis parvo-cellularis) thalamotomy in 19 patients with thalamic pain. The electrophysiological characteristics of the thalamus in patients with thalamic pain were analyzed. Patients were classified into non-thalamic and thalamic lesion groups on CT scan. Of 19 patients 13 were men (46-76 years) and 6 women (43-69 years); 11 showed cerebral infarct and 8 hemorrhage. Abnormal sensations including pain developed 1 month to 6 years (mean 11 months) after stroke. The clinical features of thalamic pain were referred to as “superficial pain” and “deep pain”. In the non-thalamic lesion group, we could usually recognize more deep than superficial pain, while, in the thalamic lesion group, superficial pain was predominant. We analyzed thalamic electrical activities [unitary spike discharges and background neural activity (BNA)], and compared them with those of parkinsonian patients. Furthermore, sensory neurons identified mainly in the thalamic sensory nucleus were studied with regard to the modality of peripheral natural stimulation, the distribution of peripheral receptive fields and the location of response sites in the thalamus.Thalamic electrical activity was correlated with the state of thalamic lesions on CT scan and non-thalamic lesions, respectively. In the non-thalamic lesion group, thalamic BNA was relatively preserved in the ventral thalamus, but was not uniform in the VIM nucleus (compared with that of parkinsonian patients). Furthermore, the peripheral receptive field of sensory (kinesthetic) neurons was predominantly the face or mouth area, deviating from standard thalamic topography in the VIM nucleus. These findings suggest that functional change or reorganization in the thalamic sensory nucleus occurred in this group. In the thalamic lesion group, BNA decreased markedly in the ventral thalamus, particularly in the VC nucleus, and sensory (kinesthesic) neurons were rarely identified. Additionally, in about half the operated cases irregular burst discharges in and around the VIM nucleus were frequently observed. It was suggested that the different character of thalamic pain, both deep and superficial, is associated with that of local pathophysiology in the thalamic sensory nucleus.

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