抄録
It was reported that after the lesion of the corticospinal tract (CST) at C5, recovery of the finger dexterity was completed in 1-3 months (Sasaki et al. 2004, Nishimura et al. 2005). In this study, to clarify the neuronal mechanism of the functional recovery, we performed following two experiments; 1) In 3 monkeys, we performed functional imaging by positron emission tomography (PET) during precision grip. At postoperative 1 month (during early recovery), increased activity was observed in bilateral primary motor cortex (M1). At postoperative 3 months (after complete recovery), in addition to bilateral M1, activities in bilateral ventral premotor cortex (PMv) were increased. 2) In 2 monkeys we investigated the effect of reversible inactivation of areas where we found increased activity in the PET study. Inactivation of M1 contralateral (c) to the lesion caused deficit in control of independent finger movements both at postoperative 1 and 3 months. Inactivation of M1 ipsilateral (i) to the lesion caused deficit in precision grip at postoperative 1 month. Inactivation of iPMv also caused deficit in precision grip at postoperative 3 months. These results indicate that bilateral M1 and iPMv play an important role in the functional recovery. [J Physiol Sci. 2006;56 Suppl:S92]
