Is aberrant neuronal plasticity related to previously identified abnormalities of neuronal inhibition?
Exactly what caused neuronal plasticity to transgress normal boundaries in writer’s cramp remains unknown. Because our protocol comprised activation of an afferent somatosensory pathway as well as external activation of the motor cortex, the spatial abnormalities of PAS-induced plasticity could be due to a disturbance in any neuronal processing stage before or within the motor cortex. Indeed, previous findings have provided evidence both for spatial de-differentiation of somatosensory representation (Bara-Jimenez et al., 1998; Elbert et al., 1998; Tinazzi et al., 2000) and for a disturbance of sensorimotor integration (Abbruzzese et al., 2001; Tamburin et al., 2002; Bertolasi et al., 2003) in dystonia. However, while somatosensory de-differentiation may contribute to spatial de-differentiation in motor cortex, it would not easily explain the increased gain of motor cortical plasticity. Deficiencies in homeostatic dynamic plasticity mechanisms [such as synaptic scaling (Turrigiano and N
