Movement related slow cortical potentials in severely paralyzed chronic stroke patients

Yilmaz Ö., Birbaumer N., Ramos-Murguialday A.

Frontiers in Human Neuroscience, cilt.8, sa.JAN, 2015 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 8 Sayı: JAN
  • Basım Tarihi: 2015
  • Doi Numarası: 10.3389/fnhum.2014.01033
  • Dergi Adı: Frontiers in Human Neuroscience
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Anahtar Kelimeler: EEG, Intention to move, Movement preparation, Movement related slow cortical potentials, Stroke
  • Marmara Üniversitesi Adresli: Hayır

Özet

Movement-related slow cortical potentials (SCPs) are proposed as reliable and immediate indicators of cortical reorganization in motor learning. SCP amplitude and latency have been reported as markers for the brain's computational effort, attention and movement planning. SCPs have been used as an EEG signature of motor control and as a main feature in Brain-Machine-Interfaces (BMIs). Some reports suggest SCPs are modified following stroke. In this study, we investigated movement-related SCPs in severe chronic stroke patients with no residual paretic hand movements preceding and during paretic (when they try to move) and healthy hand movements. The aim was to identify SCP signatures related to cortex integrity and complete paralysis due to stroke in the chronic stage. Twenty severely impaired (no residual finger extension) chronic stoke patients, of whom ten presented subcortical and ten cortical and subcortical lesions, underwent EEG and EMG recordings during a cue triggered hand movement (open/close) paradigm. SCP onset appeared and peaked significantly earlier during paretic hand movements than during healthy hand movements. Amplitudes were significantly larger over the midline (Cz, Fz) for paretic hand movements while contralateral (C4, F4) and midline (Cz, Fz) amplitudes were significantly larger than ipsilateral activity for healthy hand movements. Dividing the participants into subcortical only and mixed lesioned patient groups, no significant differences observed in SCP amplitude and latency between groups. This suggests lesions in the thalamocortical loop as the main factor in SCP changes after stroke. Furthermore, we demonstrated how, after long-term complete paralysis, post-stroke intention to move a paralyzed hand resulted in longer and larger SCPs originating in the frontal areas. These results suggest SCP are a valuable feature that should be incorporated in the design of new neurofeedback strategies for motor neurorehabilitation.