The silent cortex revisited: Multimodal evidence for a reorganisation in the hand region of the primary somatosensory cortex in hand amputation and hand dysmelia

Amputation as well as dysmelia is known to induce a reorganisation of the primary somatosensory cortex (SI). This reorganisation is reflected in a reduced or increased amount of neurons in SI representing the affected part of the body surface. Moreover, the amount of reorganisation in SI was shown to be strongly correlated with dysfunctional effects like phantom pain. While animal studies allow for a direct measurement of the extent of the deafferented areas in SI, studies in humans with phantom pain or dysmelia used rather indirect measures like interhemispheric differences of distances in SI. Thus, little is known about the fate of the particular part of the human cortex that receives input from a smaller amount or even no somatosensory receptors at all. The present study aimed to investigate the reorganization in SI in a patient with phantom pain following hand amputation and a patient with hand dysmelia. We measured bilaterally tactile thresholds and two-point discrimination in six different regions adjacent to the affected body part. In addition, in the amputee we stimulated the median nerve bilaterally at the wrist, thus eliciting sensations in the intact hand and in the phantom. In the dysmelic patient we stimulated the intact and the dysmelic thumb. The evoked neuronal activity was estimated by means of a simultaneous EEG and fMRI measurement and a subsequent dipole analysis. In both patients we found a reduction in two-point discrimination adjacent to the affected hand compared to the intact side. The same holds true for the tactile thresholds in the dysmelic patient. The smaller the peripheral thresholds the smaller was the distance between the cortical representation of the tested region and the hand in SI. In the amputee dipole data as well as fMRI data revealed a reduction of neuronal activity contralateral in Brodmann Area 3b (BA 3b) and the secondary somatosensory cortex (SII) on the affected side. Activity in BA1 could only be shown after stimulation of the intact side. In the dysmelic patient the dipole in SI was weaker and dipoles in SII could not be shown following stimulation on the affected as compared to the intact side. While fMRI revealed concordant evidence for SII, the activation in BA3b was larger for the affected side. Both single case studies point to a continuous reorganisation in SI after amputation or in dysmelia. Particularly, parts of the former hand representation in BA3b, BA1 and SII dramatically change their extent and response to afferent stimulation. This is reflected in a concordant change of the characteristics of the somatosensory perception along the affected body surface.