Klinische Neurophysiologie 2004; 35 - 282
DOI: 10.1055/s-2004-832194

Maintained Activity of Contralateral SII in Patients with Thalamic Infarction Affecting the VPL

B Taskin 1, GJ Jungehülsing 2, F Blankenburg 3, J Ruben 4, A Villringer 5
  • 1Berlin
  • 2Berlin
  • 3Berlin
  • 4Berlin
  • 5Berlin

Cortical representations may change when somatosensory input is altered. Here, we investigated the functional consequences of partial central deafferentation of the somatosensory cortex due to a lesion of the ventroposteriolateral nucleus (VPL). We applied event-related functional magnetic resonance imaging (fMRI) during electrical index finger stimulation of the affected and non-affected side in patients exhibiting contralesional sensory deficits. Six right-handed subjects (age 60–68 years) with non-acute (>60 days) solitary unilateral thalamic infarctions participated in the study. For localization of lesions, images at high spatial resolution using a T1-weighted inversion recovery sequence were acquired. In all patients the lesions were found to involve the VPL. Imaging was performed on a 1.5 T scanner using a T2*-weighted BOLD-sensitive echoplanar sequence (TR=2s, TE=60 ms, voxel size 4×4×5mm, 16 slices). For somatosensory stimulation, electrical current pulse trains (4 pulses at 7Hz, duration 200µs) were delivered scan-triggered to the left and right index finger at a low and a high amplitude (60 presentations each) in a randomized order with a mean interstimulus interval of ˜6s. The low and high intensities were equal for both sides and were set closely above sensory and below pain threshold of the non-hypaesthetic side. Analysis of imaging data was performed with SPM99. For the group, statistical parametric maps showed a reduced activation of the contralateral primary somatosensory cortex (SI) in response to stimulation of the affected side. However, no significant difference in activation of the contralateral secondary somatosensory cortex (SII) compared to stimulation of the non-affected side was detected. For the preserved responsiveness of SII in thalamic stroke comparable to that of the contralesional hemisphere, possible explanations are a direct thalamocortical input to SII mediating parallel information processing, a non-linear response behavior of SII in serial processing, or reorganizational processes that evolved over time.