Facial nerve injury-induced disinhibition in the primary motor cortices ofboth hemispheres

Unilateral facial nerve transection induces plastic reorganization of the s omatotopic order in the primary motor cortex area (MI). This process is bip hasic and starts with a transient disinhibition of connections between cort ical areas in both hemispheres. Little is known about the underlying mechan isms. Here, cortical excitability has been studied by paired pulse electric al stimulation, applied either within the MI or peripherally to the trigemi nal nerve, while the responses were recorded bilaterally in the MI. The rat ios between the amplitudes of the second and first evoked potentials (EPs o r fEPSPs) were taken as measures of the inhibitory capacity in the MI ipsil ateral or contralateral to the nerve injury. A skin wound or unilateral fac ial nerve exposure immediately caused a transient facilitation, which was f ollowed by a reset to some level of inhibition in the MI on both sides. Aft er facial nerve transection, the first relatively mild reduction of inhibit ion started shortly (within 10 min) after denervation. This was followed by a second step, involving a stronger decrease in inhibition, 40-45 min late r. Previous publications have proved that sensory nerve injury (deafferenta tion) induces disinhibition in corresponding areas of the sensory cortex. I t is now demonstrated that sham operation and, to an even greater extent, u nilateral transection of the purely motoric facial nerve (deefferentation), each induce extended disinhibition in the MIs on both sides.