Abstract
Acute facial palsy was produced by compressing the extratemporal facial nerve of guinea pigs using a microsurgical needle holder. The compressive force was 1.6kgW. The compression lasting for 5 seconds resulted in facial palsy which consistently healed within 4 weeks after the compression.
In the 10 guinea pigs, methylcobalamin was injected intramuscularly immediately after the compression and at intervals of every 48 hours. In the 10 control guinea pigs, the same amount of physiological saline was injected in the same manner. The grade of functional recovery of the facial nerve was assessed by the blink reflex evoked by air puff and an electromyogram of the orbicularis oculi muscle evoked by electrical stimuli central to the compressive site, which was recorded 1 and 2 weeks after the compression. In 4 guinea pigs of each group, light-microscopic histological findings of myelin was obtained at the compressive site of the nerve. The nerve specimen was taken 2 weeks after the compression and stained with toluidine blue.
In the methylcobalamin group, the blink reflex was restored significantly earlier (Fig. 4). The evoked electromyographic response in the methylcobalamin group appeared about 1 week earlier than in the control group (Fig. 6). Histologically, as shown in Fig. 8, a more active remyelinative process was apparent in the methylcobalamin group.
The results of the animal experiment indicated that injection of methylcobalamin accelerated repair of mechanical injury of the facial nerve. The present animal model and experimental design are found to be practical in testing the therapeutic effects of neurotropic drugs used in facial paralysis.
