Facial nerve surgery inevitably leads to partial pareses, abnormally associated movements and pathologically altered reflexes. The reason for this "post-paralytic syndrome" is the misdirected reinnervation of targets, which consists of two major components. First, due to malfunctioning axonal guidance, a muscle gets reinnervated by a "foreign" axon, that has been misrouted along a "wrong" fascicle. Second, the supernumerary collateral branches emerging from all transected axons simultaneously innervate antagonistic muscles and cause severe impairment of their coordinated activity. Since it is hardly possible to influence the first major component and improve the guidance of several thousands axons, the authors concentrated on the second major component and tried to reduce the collateral axonal branching.
Recovery of mimic function after facial nerve transection is poor: the successful regrowth of axotomized motoneurons to their targets is compromised by (i) poor axonal navigation and excessive collateral branching, (ii) abnormal exchange of nerve impulses between adjacent regrowing axons and (iii) insufficient synaptic input to facial motoneurons. As a result, axotomized motoneurons get hyperexcitable and unable to discharge. Since improvement of growth cone navigation and reduction of the ephaptic cross-talk between axons turn out be very difficult, the authorsa concentrated on the third detrimental component and proposed that an intensification of the trigeminal input to axotomized electrophysiologically silent facial motoneurons might improve specificity of reinnervation. To test the hypothesis they compared behavioral, electrophysiological and morphological parameters after single reconstructive surgery on the facial nerve with those obtained after identical facial nerve surgery, but combined with direct or indirect stimulation of the ipsilateral infraorbital (ION) nerve. The authors found that in all cases trigeminal stimulation was beneficial for the outcome by improving the quality of target reinnervation and recovery of vibrissal motor performance.
Following an exhaustive literature review on the global issue of intracerebral presentation of antigen, this monograph summarizes results from voluminous work to establish which indigenous cerebral cells might present (auto)antigen to the immune system and thus initiate an (auto)immune reaction. Employing the combination of (a) a lesion model in which neuronal degeneration and neuronophagia are caused without disruption of the blood--brain barrier, (b) stable labeling of the neuronophages via phagocytosis of the permanent nontoxic fluorescent marker Fluoro-Gold from preloaded neurons, and (c) immunocytochemical identification of all FG-labeled brain neuronophages, the authors provide evidence that the only cells in the rat CNS which can be regarded as the resident antigen presenting cells of the brain are perivascular cells.
Using a combined morpho-functional approach the author recently found that polyinnervation of the neuro-muscular juction (NMJ) is the critical factor for recovery of function after transection and suture of the facial nerve. Since polyinnervation is activity-dependent and can be manipulated, he tried to design a clinically feasible therapy by electrical stimulation or by soft tissue massage. First, electrical stimulation was applied to the transected facial nerve or to paralysed facial muscles. Both procedures did not improve vibrissal motor performance (video-based motion analysis of whisking), failed to diminish polyinnervation and even reduced the number of innervated NMJ to one fifth of normal values. In contrast, gentle stroking of the paralysed vibrissal muscles by hand resulted in full recovery of whisking. Manual stimulation was also effective after hypoglossal-facial anastomosis and after interpositional nerve grafting. The author concludes that manual stimulation is a non-invasive procedure with immediate potential for clinical rehabilitation following facial nerve reconstruction.
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